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You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Krabbe's disease is caused by a defect of - and explain in detail? | Ans. is 'd' i.e., Galactosyl ceramidaseLipid storage disordersDisorderEnzyme defectGaucher's diseaseb glucosidaseNiemann Pick diseaseSphingomyelinaseFabry's diseasea galactosidaseGM1 gangliosidosisb galactosidaseGM2 gangliosidosisHexosaminidase ASandhoff s diseaseHexosaminidase A and BKrabbe's diseaseGalactosyl ceramidaseMetachromatic leukodystrophyAryl Sulfatase AFarber's diseaseCeramidaseWolman's diseaseAcid lipase |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 70-year-old patient presents with dizziness and headache followed by left sided hemiparesis with right eye dilatation and ptosis. Most probable blood vessel damaged is: and explain in detail? | Ans: (c) Posterior cerebral arteryRef: Adams and Victor's Principles of Neurology, 10th edition, Page 804; Localisation in Clinical Neurology, 6th edition, Chapter 105EponymSiteCranial nerves involvedTracts involvedSignsArteries involvedWeber SyndromeBase of midbrainIIICorticospinal tractOculomotor palsy with crossed hemiplegiaProximal posterior cerebral arteryClaude syndromeTegmentum of midbrainIIIRed nucleus, superior cerebellar peduncles after decussationOculomotor palsy with contralateral cerebellar ataxia and tremorProximal posterior cerebral arteryBenedict syndromeTegmentum of midbrainIIIRed nucleus, corticospinal tract superior cerebellar peduncles after decussationOculomotor palsy with contralateral cerebellar ataxia, tremor, and corticospinal signs, choreoathetosisProximal posterior cerebral arteryNothnagel syndromeTectum of midbrainUnilateral or bilateral III nerveSuperior cerebellar pedunclesOcular palsies (IV), paralysis of gaze, nystagmus and ataxia Parinaud syndromeDorsal midbrain Supranuclear mechanism for upward gaze and dorsal midbrain, periaqueductal gray matterParalysis of upward gaze and accommodation; fixed pupils Millard Gubler syndromeUnilateral lesion of the ventrocaudal ponsFascicles of cranial nerves VI and VIIPyramidal tract, cranial nerve VI, cranial nerve VIIContralateral hemiplegia, Ipsilateral lateral rectus paresis, Ipsilateral peripheral facial paresis Raymond SyndromeUnilateral lesion of the ventral medial ponsAbducens nerve fascicles and the corticospinal tract but spares cranial nerve VIIPyramidal tract, cranial nerve VIIpsilateral lateral rectus paresis, contralateral hemiplegia Locked-in syndromeBilateral ventral pontine lesions Bilateral corticospinal tract involvement in the basal pontis, involvement of the corticobulbar fibers innervating the lower cranial nerve nucleiQuadriplegia, Aphonia Foville syndromeDorsal pontine tegmentumInvolvement of the nucleus and fascicle (or both) of cranial nerve VIICorticospinal tract, involvement of the PPRF or abducens nucleus, or bothContralateral hemiplegia (with facial sparing), Ipsilateral peripheral type facial palsy, Inability to move the eyes conjugately to the ipsilateral side involvement of the PPRF or abducens nucleus, or both Raymond- Cestan syndromeRostral lesions of the dorsal pons Involvement of the cerebellum, medial lemniscus and the spinothalamic tract, PPRFCerebellar signs (ataxia), Contralateral hypoesthesia with reduction of all sensory modalities (face and extremities), contralateral hemiparesis, paralysis of conjugate gaze toward the side of the lesion Marie-Foix syndromeLateral pontine lesions brachium pontis Involvement of cerebellar connections, corticospinal tract, spinothalamic tractIpsilateral cerebellar ataxia, Contralateral hemiparesis,Variable contralateral hemihypesthesia for pain and temperature Wallenburg syndromeLateral tegmentum of medullaSpinal V, IX, X, XILateral spinothalamic tract,spinocerebellar and ollivocerebellar tractsIpsilateral V, IX, X,XI palsy, Horner syndrome,-cerebellar ataxia; contralateral loss of painand temperature senseIntracranial vertebral artery or posterior inferior cerebellar arteryMedial Medullary syndrome (Dejerine's Anterior Bulbar Syndrome)Medial medullaXIICranial nerveXII,Corticospinal tract,medial lemniscusIpsilateral paresis, atrophy, and fibrillation of the tongue, Contralateral hemiplegia, Contralateral loss of position and vibratory sensationVertebral artery, anterior spinal artery, or the lower segment of the basilar arteryAvellis syndromeTegmentum of medullaXSpinothalamic tractParalysis of soft palate and vocal cord and contralateral hemianaesthesia Thalamic syndrome of Dejerine and Roussy Occlusion of thalamogeniculate branches of PCA |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Mineral with antioxidant property: and explain in detail? | Ans. b (Selenium). (Ref. Harper, Biochemistry, 25th ed., 659,766)SeleniumFeaturesConstituent of glutathione peroxidaseSynergistic anti-oxidant with vitamin EEssential trace elementSelenocysteine is an L--amino acid found in a handful of proteins. As its name implies, a selenium atom replaces the sulfur of its structural analog, cysteine. The pK3 of selenocysteine, 5.2, is 3 units lower than that of cysteine. Since selenocysteine is inserted into polypeptides during translation, it is commonly referred to as the "21st amino acid."However, unlike the other 20 genetically encoded amino acids, selenocysteine is not specified by a simple three-letter codon.Trace elements TRACE ELEMENTDEFICIENCY STATESEXCESS STATES1ArsenicAcute Fatty (Yellow)liverHCCNeurologic dysfunctionGIT diseasesSkin cancerMee's linesAngiosarcoma of liverNCPF2Cadmium-Madness, paralysis agitans,3CopperGrowth failureWilson's diseaseNeutropenia CVS disordersGenu valgumMenke's kinky hair disease04ChromiumPEM, CVS diseaseArthritisDermatitisDiarroeaSeptal perforation5IodineGoiter, growth failureJod basedow phenomenonWolf chekoff phenomenon6Lead-Abdominal ColicAnaemiaBlue gum linesBasophilic stipplingConstipationConvulsionsDeliriumPeripheral neuropathy & ParalysisFailure of kidneysMetaphyseal lines7ManganeseImpaired growthAtaxiaManganese madnessParalysis agitansCVS disorders8MolybdenumGrowth failureGout bony defects Oral & esophageal carcinomaGenu valgum9Mercury-Minimota's disease Mercural erythesim (Hatter's shake)10SeleniumPEM, muscle dystrophy, CVS diseases(DCM), diarrhea, Keshan diseaseArthritis, dermatitis11AluminiumAlzheimer's diseaseOsteodystrophy12ZincNight blindnessHypogonadismImpaired wound healingAcrodermatitis enteropathicaGI irritationGrowth retardationFlaky paint dermatitis, loss of taste |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Man is intermediate host for - and explain in detail? | option-1- Life Cycle of Plasmodium: Malaria is caused by Plasmodium species. Definitive host: Female Anopheles mosquitoes Intermediate host: Man. option- 2-Tuberculosis is caused by Mycobacterium tuberculosis and doesn't have secondary host. option-3- In Filariasis (W. bancrofti): man is definitive host. option-4- Borrelia causes Relapsing fever and there is no secondary host. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is 30 yrs female presented with unilateral breast cancer associated with axilary lymph node enlargement. Modified radical mastectomy was done, further treatment plan will be and explain in detail? | Ans. is 'b' i.e. Adriamycin based chemotherapy followed by tamoxifen depending on.... Stage I & II breast cancers (Early invasive breast cancers) are managed byPrimary therapy for local management &Adjuvant therapyPrimary therapy consists of:Mastectomy with assessment of axillary lymph node status (or modified radical mastectomy) orBreast conservation (lumpectomy, wide local excision or quadrantectomy) with assessment of axillary lymph node status + radiotherapy.Various trials have found both these methods to be equally effective. Breast conservation is the preferred form of treatment because of cosmetic advantages However there are certain contraindications for conservative surgery (described in subsequent question)Management of axillary lymph nodesEarlier dissection of axillary lymph nodes (level I and II) was performed to assess the lymph node status (i.e. presence or absence of occult metastasis)Now Sentinel lymph node biopsy is considered the standard for evaluation of the axillary lymph nodes for metastasis in women who have clinically negative lymph nodes, (the sentinel lymph node is the first regional lymph node to receive tumor cells that metastasize along the lymphatic pathway from the primary breast cancer)Axillary Lymph node dissection is performed for clinically palpable axillary lymph nodes or metastatic disease detected in sentinel lymph node biopsy.Adjuvant chemotherapy is given to all node-positive cancersnode negative cancers if > 1 cm in size * node negative cancer > .5 cm in size with adverse prognostic factors such as blood vessel or lymph vessel invasion high nuclear grade high histological grade HER 2/neu overexpression negative hormone receptor statusAdjuvant hormone therapy (tamoxifen) is added to all those with estrogen receptor positive tumors.HER-2/neu expression is determined for all patients with newly diagnosed breast cancer and may be used to provide prognostic information in patients with node-negative breast cancer and predict the relative efficacy of various chemotherapy regimens. Trastuzumab is the HER-2/neu-targeted agent that is added to the adjuvant therapy is the tumor shows overexpression of HER-2/neu receptors.Advanced Local-Regional Breast Cancer (Stage III)(Neoadjuvant chemotherapy + MRM + adjuvant radiation therapy + chemotherapy + antiestrogen therapy)Here the disease is advanced on the chest wall or in regional lymph nodes (or both), with no evidence of metastasis to distant sites. Such patients are recognized to be at significant risk for the development of subsequent metastases, and treatment addresses the risk for both local and systemic relapse.In an effort to provide optimal local-regional disease-free survival as well as distant disease-free survival for these women, surgery is integrated with radiation therapy and chemotherapy.Neoadjuvant chemotherapy (administration of therapeutic agents prior to the main treatment) should be considered in the initial management of all patients with locally advanced stage III breast cancer.Surgical therapy for women with stage III disease is usually a modified radical mastectomy, followed by adjuvant radiation therapy and chemotherapy. Antiestrogen therapy (tamoxifen) is added for hormone receptor positive tumors.Chemotherapy is used to maximize distant disease-free survival, whereas radiation therapy is used to maximize local-regional disease-free survival.In selected patients with stage IIIA cancer, neoadjuvant (preoperative) chemotherapy can reduce the size of the primary cancer and permit breast-conserving surgery.Distant Metastases (Stage IV)(mainly palliative treatment)Treatment for stage IV breast cancer is not curative but may prolong survival and enhance a woman's quality of life.Hormonal therapies that are associated with minimal toxicity are preferred to cytotoxic chemotherapy. Appropriate candidates for initial hormonal therapy include women with hormone receptor-positive cancers; women with bone or soft tissue metastases only; and women with limited and asymptomatic visceral metastases.Systemic chemotherapy is indicated for women with hormone receptor-negative cancers, symptomatic visceral metastases, and hormone-refractory metastases.Bisphosphonates, which may be given in addition to chemotherapy or hormone therapy, should be considered in women with bone metastases.About Adjuvant TherapyAdjuvant therapy is the use of systemic therapy (chemotherapy or/and hormone therapy) in patients who have received local therapy but are at risk of relapse.The objective is to eliminate the occult metastasis responsible for late recurrences while they are microscopic and theoretically most vulnerable to anticancer agents.Adjuvant chemotherapy is given to all node-positive cancersnode negative cancers if > 1 cm in size node negative cancer > .5 cm in size with adverse prognostic factors such as blood vessel or lymph vessel invasion high nuclear grade high histological grade HER 2/neu overexpression negative hormone receptor statusAdjuvant hormone therapy (tamoxifen) is added to all those with estrogen receptor positive.* The use of chemotherapy in post-menopausal women is controversial.In post menopausal women, chemotherapy is frequently used upto age 70 yrs, if she can tolerate it.In older women, chemotherapy is performed less frequently.In estrogen positive tumors, in postmenopausal women, antiestrogen (tamoxifen/ aromatase inhibitors) therapy is the preferred form of adjuvant systemic treatment.Neoadjuvant chemotherapy it involves the administration of adjuvant therapy before primary therapy (surgery & radiation therapy) it has shown to down-stage the tumor.Previously CMF (cyclophosphamide, methotrexate & 5-fluorouracil) was the chemotherapeutic regimen of choice. "CMF is no longer considered adequate adjuvant chemotherapy and modem regimens include an anthracycline (doxorubicin or epirubicin) and the newer agents such as the taxanes (paclitaxel and docetaxel)"- Bailey and Love 25/e p844Anti-HER-2/neu antibody therapy (Trastuzumab)HER-2/neu expression for all newly diagnosed patients with breast cancer is now recommended.Trastuzumab is added to the chemotherapy for tumors overexpressing HER-2/neu receptors. (Trastuzumab is added along with taxanes) |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of following is derived from otic placode? and explain in detail? | Ans. is'd'i.e., CochleaRef: Langmann' 70th/e p. 92,403Otic placode form otic vesicle which in turn divides into :-Ventral component that gives rise to the saccule and cochlear duct.Dorsal component that forms the utricle, semicircular canals, and endolymphatic duct. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 9-month-old girl was admitted to the children's hospital with tachypnea (fast breathing) and shoness of breath. Physical examination fuher exhibits tachycardia (fast hea rate), a bounding peripheral pulse, and her angiographs reveal a patent ductus aeriosus. Which of the following embryonic aerial structures is most likely responsible for the origin of the patent ductus aeriosus? and explain in detail? | The left sixth aoic arch is responsible for the development of both the ductus aeriosus and the pulmonary aeries. The ductus aeriosus closes functionally in an infant soon after bih, with anatomic closure requiring several weeks, but persistent 6th arch aery lead to PDA. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is FESS means: and explain in detail? | Indications ofFESSi) Chronic bacterial sinusitis unresponsive to adequate medical treatment.ii) Recurrentacutebacteridsinusitis.iii) Polypoid rhinosinusitis (diftrse nasal polyposis)'w) Fungal sinusitis with fungal ball or nasal polypi'v) Antrochoanal polyp and Ethmoid polypvi) Mucocele of frontoethmoid or sphenoid sinus.vii) Control of epistaxis by endoscopic cautery.viii) Removal of foreign body from the nose or sinus'ix) EndoscoPicsePtoPlastY.x) Removal of benign tumours, e.g. inveedpapillomas or an$ofibromas.xi) Orbital abscess ot cellulltls nonageme,tt.xii) DacryocYstorhinostomY.:lolii) RepaltofCSFleak,xiv) Pituitarysurgeryxv) Optic nerve decomPression.xvi) Orbitd decompression for Graves disease-xvii) Control ofposterior epistaxis(endoscopicclipping ofsphenopalatine aery).xviii) Choanal atresia. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Longest acting insulin and explain in detail? | Degludec is the longest acting insulin.it acts for 42hrs so it can be given even once every alternate day. Other long-acting which acts for 24 hrs is glargine, detemir. They are insulin analogues. Ref: KD Tripathi 8th ed. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 47-year old male, Kishore exhibited signs and symptoms of acromegaly. Radiologic studies showed the presence of a large pituitary tumor. Surgical treatment of the tumor was only paially effective in controlling the disease. At this point, which of the following drugs is most likely to be used as pharmacological therapy? and explain in detail? | Drugs useful in acromegaly are: * Bromocriptine and cabergoline * Octreotide (long acting somatostatin analogue) * Pegvisomant (growth hormone receptor antagonist) Nafarelin is a GnRH agonist. It has no role in acromegaly. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A female has episodic, recurrent headache in left hemicranium with nausea and paresthesia on right upper and lower limbs is most probably suffering from: and explain in detail? | Migraine 2nd most common cause of headache, Affects 15% of women and 6% of men over a one year period. Usually an episodic headache and associated with ceain features such as sensitivity to light, sound, or movement; nausea and vomiting often accompany the headache. May be associated with other symptoms of neurologic dysfunction in varying admixtures Migraine-prone patients do not habituate easily to sensory stimuli, which is amplified in females during the menstrual cycle. Various triggers, including glare, bright lights, sounds, or other afferent stimulation; hunger; excess stress; physical exeion; stormy weather or barometric pressure changes; hormonal fluctuations during menses; lack of or excess sleep; and alcohol or other chemical stimulation. Ref - Harrisons internal medicine 20e pg 3096 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of the following is the principal mode of heat exchange in an Infant incubator? and explain in detail? | Infants lose heat from the skin to the environment by the following methods: Convection :This is the loss of heat from the infant&;s skin to the surrounding air. Infants lose a lot of heat by convection when exposed to cold air or draughts. Reference: GHAI Essential pediatrics, 8th edition |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of the following antihypeensive drug is avoided in patients with high serum uric acid levels? and explain in detail? | Adverse effect ofHydrochlohiazideis hyperuricemia therefore contraindicated in gout. Enalapril, Prazosin and Atenolol has no affect on uric acid level. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is All of the following clinical findings are seen in Horner's syndrome, except and explain in detail? | The triad of miosis with ipsilateral ptosis and anhidrosis constitutes Horner&;s syndrome, although anhidrosis is an inconstant feature. Brainstem stroke, carotid dissection, and neoplasm impinging on the sympathetic chain occasionally are identified as the cause of Horner&;s syndrome, but most cases are idiopathic.(Ref: Harrison's 18/e p 225) |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is The mechanical system in which fresh air is blown into the room by centrifugal fans so as to create positive pressure and displace the vitiated air is termed as and explain in detail? | None |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is The efferent fiber bundle of substantia nigra transmits dopamine to which area and explain in detail? | The connections within the basal ganglia include a dopaminergic nigrostriatal projection from the substantia nigra pars compacta to the striatum and a GABAergic projection from the striatum to substantia nigra pars reticulata. There is an inhibitory projection from the striatum to both GPe and GPi. The subthalamic nucleus receives an inhibitory input from GPe, and in turn, the subthalamic nucleus has an excitatory (glutamate) projection to both GPe and GPi. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A chronic alcoholic has an elevated serum alpha fetoprotein levels. Which of the following neoplasms is most likely - and explain in detail? | Elevated levels of serum α-fetoprotein are found in 50 to 75% of patients with HCC.
False-positive results are encountered with yolk-sac tumors and many non-neoplastic conditions, including cirrhosis, massive liver necrosis, chronic hepatitis, normal pregnancy, fetal distress or death, and fetal neural tube defects such as anencephaly and spina bifida.
Concept
The staining for Glypican-3 is used to distinguish early hepatocellular carcinoma from a dysplastic nodule. Other tests cannot be used because the levels of serum α-fetoprotein are inconclusive in this condition. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A patient diagnosed with papillary carcinoma of thyroid underwent whole body iodine scan 6 weeks after surgery, which revealed residual disease. Next best step is : and explain in detail? | Post operative follow up protocol. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of the following is used to test the efficiency of sterilization in an autoclave? and explain in detail? | Autoclave: B. stearothermophillus
Hot air oven: Clostridium tetani nontoxigenic strain |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 25 year old patient presents in coma with GCS of 5 and extensor posturing after a bike accident. Which of the following will the best management of the patient? and explain in detail? | Ans. (c) Burr Hole surgeryThe image shows presence of extra-dural haemorrhage due to presence of biconvex lenticular opacity. Due to risk of brain herniation leading to death best management will be burr hole surgery. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Acute megakaryoblastic leukemia and explain in detail? | Acute megakaryoblastic leukemia (AMKL) is life-threatening leukemia in which malignant megakaryoblasts proliferate abnormally and injure various tissues. Megakaryoblasts are the most immature precursor cells in a platelet-forming lineage; they mature to promegakaryocytes and, ultimately, megakaryocytes which cells shed membrane-enclosed particles, i.e. platelets, into the circulation. Platelets are critical for the normal clotting of blood. While malignant megakaryoblasts usually are the predominant proliferating and tissue-damaging cells, their similarly malignant descendants, promegakaryocytes and megakaryocytes, are variable contributors to the malignancy.AMKL is commonly regarded as a subtype of acute myeloid leukemia (AML). More formally, it is classified under the AML-M7 category of the French-American-British classification and by the World Health Organization of 2016 in the AML-Not Otherwise Specified subcategory.Acute megakaryoblastic leukemia falls into three distinct groups which differ in underlying causes, ages of presentation, responses to therapy, and prognoses. These groups are: AMKL occurring in young children with Down syndrome, i.e. DS-AMKL; AMKL occurring in children who do not have Down syndrome, i.e. non-DS-AMKL (also termed pediatric acute megakaryoblastic leukemia or pediatric AMKL); and AMKL occurring in non-DS adults, i.e. adult-AMKL. AMKL, while rare, is the most common form of AML in DS-AMKL, occurring ~500-fold more commonly in Down syndrome children than in children without Down syndrome; non-DS-AMKL and adult-AMLK are rare, accounting for <1% of all individuals diagnosed as in the AML-M7 category of leukemia.
DS-AMKL
Pathophysiology
Individuals with Down syndrome almost always have three instead of the normal two copies of chromosome 21. The extra copies of key chromosome 21 genes underlie their increased susceptibility to AMKL by promoting the development of a certain type of inactivating mutation in the GATA1 gene. The GATA1 gene resides on the X chromosome and codes for two transcription factors, GATA1 and a shorter version, GATA1-S. GATA1 and GATA1-S contribute to regulating the expression of genes that control the maturation of megakaryoblasts to promegakaryocytes, megakaryocytes, and platelets as well as the maturation of erythroblasts to red blood cells. GATA1-S appears less active than GATA1 in controlling some of the genes that promote megakaryoblast maturation but more active than GATA1 in stimulating megakaryoblast proliferation. Various GATA1 mutations that cause this gene to make GATA1-S but unable to make GATA1 result in the excessive proliferation of platelet precursor cells, reductions in the levels of circulating blood platelets, mild reductions in the levels of circulating red blood cells, and the development of transient myeloproliferative disease (TMD). TMD is a disorder involving the excessive proliferation of non-malignant megakaryoblasts and descendent cells due to the cited truncating mutations in the GATA1 gene. TMD is a necessary predecessor to DS-AMKL.Down syndrome fetuses and neonates with one of the cited types of GATA1 truncating mutations are in rare cases asymptomatic (i.e. silent TMD) but more commonly exhibit in utero or during the first months of live accumulations of immature megakaryoblasts in, and sometimes life-threatening injury to, the fetal blood-forming organ, the liver, and other tissues. While fatal in up to 20% of cases, ~80 of infants with TMD fully recover from the diseases within 4 months. However, ~10% of individuals with a history of symptomatic or silent TMD develop DS-AMKL within 4 years. During this interval, these individuals may acquire somatic mutations in those of their megakaryoblasts that bear the original truncating GATA1 mutation. These newly acquired mutations appear to result from the interactions of GATAT1 truncating mutations with excessive copies of chromosome 21 genes. The genes with these mutations include TP53, FLT3, ERG, DYRK1A, CHAF1B, HLCS, RUNX1, MIR125B2 (which is the gene for microRNA MiR125B2CTCF, STAG2, RAD21, SMC3, SMC1A, NIPBL, SUZ12, PRC2, JAK1, JAK2, JAK3, MPL, KRAS, NRAS, and SH2B3. At least one but probably several of these mutations, whether occurring in individuals with silent or symptomatic TMD, are presumed responsible for or to contribute to the development of DS-AMKL.Rare cases of transient myeloproliferative disease and DS-AMKL occur in individuals who do not have Down syndrome. These individuals usually have a history of TMD and invariably have megakaryoblasts which bear extra copies of key chromosome 21 genes, truncating mutations in GATA1, and somatic mutations in one or more of the genes listed in the previous section. These individuals have extra copies of only a portion of the genes on chromosome 21. This duplication of only some chromosome 21 genes results from: a) Robertsonian translocations, wherein part of chromosome 21 is duplicated on another chromosome; b) partial trisomy 21, wherein only part of chromosome 21 is duplicated); c) an isochromosome, wherein chromosome 21 contains two long but no short arms); or d) duplications, wherein extra chromosome 21 genes are on this or other chromosomes. AMKL occurring in these individuals is classified as DS-AMKL.
Presentation
DS-AMKL most often presents in children 1–2 years old but almost always less than 4 years old who have a history of TMD. Given this history, these children are usually followed-up medically with complete blood count tests. and therefore often present with elevated blood levels of abnormally appearing platelets and platelet precursor cells, particularly megakaryoblasts, and reduced blood levels of red blood cells. DS-AMKL usually progresses slowly with affected children gradually developing increasingly more severe changes in their blood counts as well as slowly developing symptoms of these developments such as fatigue and shortness of breath due to anemia. In cases of advanced disease, individuals with DS-AMKL may present with signs and symptoms that are more typical of acute myeloid leukemic diseases such as liver enlargement, spleen enlargement, leukemia cutis (i.e. skin nodules caused by leukemic infiltrates), or leukostasis (i.e. an emergency situation in which excessive elevations in circulating blast (i.e. early precursor) cells plug the microcirculation to cause life-threatening heart, lung, and neurological dysfunctions).
Diagnosis
The diagnosis of DS-AMKL in young children is indicated by: a history of TMD; findings of increased presence of blast cells (e.g. ≥20% of nucleated cells) that have the megakaryoblast phenotype in blood and/or bone marrow as defined by the morphology of these cells in blood or bone marrow smears; failure to obtain a bone marrow aspirate because of marrow fibrosis; and immunophenotyping analyses of platelet precursor cells lineage as determined by flow cytometry and immunohistochemistry. Malignant megakaryoblasts are usually medium-sized to large cells with a high nuclear-cytoplasmic ratio. Nuclear chromatin is dense and homogeneous. There is scanty, variable basophilic cytoplasm which may be excessively vacuolated. An irregular cytoplasmic border is often noted in some of the megakaryoblasts and occasionally projections resembling budding atypical platelets are present. Megakaryoblasts lack myeloperoxidase (MPO) activity and stain negatively with Sudan Black B. They are alpha naphthyl butyrate esterase negative and manifest variable alpha naphthyl acetate esterase activity usually in scattered clumps or granules in the cytoplasm. PAS diastase staining varies from negative to focal or granular positivity to strongly positive. Immunochemical analyses, often conducted by flow cytometry, of the surface antigens on leukemic blast cells are positive for CD41, CD42b, CD51, and Von Willebrand factor in AMKL but not leukemia involving non-platelet malignant cells.Where indicated and available, the diagnosis of DS-AMKL is further supported by; immunophenotyping analysis using monoclonal antibody directed against megakaryocyte restricted antigen (CD41 and CD61) and DNA sequencing to detect GATA1 mutations that are projected to cause the gene to make GATA1-S but not GATA1 transcription factors.
Treatment
The chemotherapy regimens used for all types of AMKL are similar to those used for AML. A final confirmation of safety and efficacy phase 3 study consisted of 4 cycles of induction therapy with cytarabine and daunorubicin followed by a single course of intensification therapy consisting of cytarabine and L-asparaginase, and concluded with a central nervous system consolidation course of 3 additional doses of intrathecal cytarabine. The dosages of cytarabine in this study were kept low because DS-AMKL patients proved highly susceptible to the toxic effects of the regimen which used a higher cytarabine dosage to treat AML. The low-dose cytarabine regimen achieved excellent results in DS-AMKL with relatively reduced overall toxicity and is currently recommended as a preferred treatment regimen for the disease.Autologous hematopoietic stem cell transplantation (i.e. transplantation of stem cells derived from the individual being transplanted) did not improve relapse-free survival in one large study of DS-AMKL. Allogenic hematopoietic stem cell transplantation (i.e. transplantation of stem cells derived another individual) has given better disease-free survival results than autologous transplantation and, based on recent uncontrolled studies, should be considered in DS-AMKL cases that have relapsed after their first chemotherapy-induced complete remission.
Prognosis
The 5-year event free survival, disease-free survival, and overall survival rate in the phase 3 clinical study in DS-AMKL were 79, 89, 84 percent, respectively. Other studies that use a treatment regimen similar to that used in the phase 3 clinical study report overall survival rates of ~80% and long-term survivals of 74-91%. However, DS-AMKL patients who relapse following chemotherapy have a far poorer outlook with 3 year overall survival rate in one study of only 26%. There also appears to be little role for stem cell transplantation in DS-AMKL given the success of initial chemotherapy and the relatively poor results in DS-AMKL patients given this transplantation.
Non-DS-AMKL
Pathophysiology
The most common genetic abnormality occurring in non-Down-AMKL is a nonreciprocal translocation between the short or p arm at position 13 on chromosome 1 (i.e. 1p13) and the p arm at position 13 on chromosome 22 (i.e. 22p13). Nonreciprocal translocations are exchanges of genes between two chromosomes that are not homologs, i.e. that are not maternal and paternal copies of the same chromosome. This particular translocation, designated t(1;22)(p13;q13), occurs mainly in infants but also is seen in children up to the age of 7 years with non-DS-AMKL. This translocation involves the RBM15 gene on chromosome 1 and the MKL1 gene (also termed MRTFA) on chromosome 22 to create a RBM15-MKL1 fusion gene. Studies in mice indicate that the Mkl1 gene (only the first letter of a mouse gene is capitalized) product, MKL1, interacts with the transcription factor SRF to stimulate the expression of various genes. MKLl is required for the maturation of mouse megakaryoblasts: in its absence, megakaryoblasts and promegakaryocytes proliferate abnormally while megakaryocytes are few in number and have an abnormal morphology. Mouse studies also indicate that the product of Rbm15, RMB15, interacts with Nuclear receptor co-repressor 1, Nuclear receptor co-repressor 2 (also termed SMRT), and RBPJ nuclear proteins to suppress the expression of various genes that are involved in the maturation of platelet, myeloid and lymphocyte precursor cells. In consequence, the RBM15-MKL1 fusion protein acts in an unregulated fashion to suppress MKL1 targeted genes while stimulating RPBJ target genes. This causes an over-active Notch signaling pathway and, among other abnormalities, expansion of fetal hematopoiesis and development of AMKL in a small percentage of adult mice. It is assumed that these events must be accompanied by other, as yet undefined, oncogenic (i.e., cancer causing) events to explain the development of human non-Down AMKL. A large number of other genetic abnormalities are associated with the development of non-DS-AMLK. These include complex chromosomal rearrangements and increases in copy number of various genes. Besides the t(1;22)(p13;q13) translocation, common genetic abnormalities in a study of 372 individuals diagnosed with non-DS-AMKL include: rearrangements of genes at position 23 on the long (i.e. q) arm of chromosome 11; inversion of chromosome 16 occurring between p13.3 and q24.3 denoted as inv(16)(p13.3q24.3) that results in the production of a CBFA2T3-GLIS2 fusion protein; and increases in chromosome numbers from a normal of 46 to anywhere from 47 to >50. The relationships of these and the many other genetic abnormalities detected in non-Down-AMKL to the diseases development require further investigations.
Presentation
Non-DS-AMKL occurs in neonates, infants, and children of all ages. Except for the lack of Down syndrome, no history of TMD, and occurrences in children that can be >4 years of age, individuals with non-DS-AMKL present with many of the symptoms, signs, and hematological findings seen in DS-AMKL. However, non-DS-AMKL is a more aggressive and rapidly progressing disorder than DS-AMKL. Nonetheless, the presentation of non-DS-AMKL is also like DS-AMKL in that it is not often accompanied by one or more extramedullary signs or symptoms of the disease such as liver enlargement, spleen enlargement, leukemia cutis, and leukostasis.
Diagnosis
The diagnosis of non-DS-AMKL is made in children who do not have Down syndrome but exhibit the same clinical symptoms, signs, hematological abnormalities, and specialized laboratory findings seen in DS-AMKL. These children should bear one or more of the genetic aberrations associated with the disease but not the inactivating GATA1 mutations, extra copies of chromosome 21 genes, or other genetic abnormalities associated with DS-AMKL. Non-DS-AMKL has many clinical and laboratory features similar to and must be distinguished from Acute panmyelosis with myelofibrosis, a disorder characterized by bone marrow fibrosis, abnormal megakaryocytes, macrocytic erythropoiesis, defects in neutrophil production, reduced blood levels of most circulating cells (i.e. pancytopenia), and low levels of circulating blast cells. Analyses of circulating and bone marrow blast cells for features of AMKL (see Diagnosis section of DS-AMKL) and genetic aberrations is helpful in distinguishing the two diseases.
Treatment
In a review of 153 patients treated for non-DS-AMKL between 1990 and 2014 with various intensive chemotherapy protocols that included cytarabine, an anthracycline (e.g. daunorubicin, doxorubicin), and in 25% of cases human stem cell transplantation, the probability of overall 4 year survival rate, probability of 4 year event-free survival, and probability of 4 year cumulative relapse rate were 56, 51, and 29%, respectively. A more recent treatment regimen that is similar to that used to treat DS-AMKL as described above (except it employs the high dose of cytarabine used to treat AML) gives better results and has been recommended for non-DS-AMKL. The response to this regimen approached that seen in non-DS-AMKL, i.e. its complete remission and estimated 10 year survival rates were both 76%. Similar to DS-AMKL treatment regimens, allogenic rather than autologous stem cell bone marrow transplantation should be considered in non-DS-AMKL cases that have relapsed following their first chemotherapy-induced complete remission. Further studies may indicate that this recent cancer chemotherapy regimen plus allogenic bone marrow transplantation in cases which relapse after the first remission are the preferred treatment for non-DS-AMKL.
Prognosis
In a review of 153 patients treated for non-DS-AMKL between 1990 and 2014 with various intensive chemotherapy protocols that included cytarabine, an anthracycline (e.g. daunorubicin, doxorubicin), and in 25% of cases human stem cell transplantation, the probability of overall 4 year survival rate, probability of 4 year event-free survival, and probability of 4 year cumulative relapse rate were 56, 51, and 29%, respectively. Patients with non-DS-AMKL given the treatment regimen described for DS-AMKL above had a much better prognosis than patients treated with earlier-devised treatment regimens: their overall survival rate using these regimen was estimated to be 76%.
Adult-AMKL
Pathophysiology
Adult-AMKL can result from the progression of other myeloproliferative neoplasms (MPN) viz., chronic myelogenous leukemia, polycythemia vera, essential thrombocytosis, and primary myelofibrosis. In one review of adult-AMKL, 25% of 49 cases were considered as secondary to one of these MPN. The mechanism behind these cases of secondary AMKL are unknown although an inversion in chromosome 3 at positions q21 and q26, i.e. inv(3)(q21q26), is often seen in these secondary cases of adult-AMKL.Rare cases of adult-AMKL also have mediastinal germ cell tumors. These tumors are malignancies of germ cells, i.e. primitive cells that give rise to sperm and ovum cells. In adult-AMKL, mediastinal germ cell tumors that are associated with adult-AMKL are not seminomas (i.e. do not originate from the sperm cell line) and occur before or concomitantly with but not after the diagnosis AMKL is made. The three most common genetic aberrations in the bone marrow cells of these individuals (representing ~65% of all cases) were inversions in the p arm of chromosome 12, trisomy 8, and an extra X chromosome. In several of these cases, the genetic aberrations in the malignant platelet precursor cells were similar to those in the malignant mediastinal germ cells. These results and those of other analyses suggest that the two malignancies derive from a common founding clone of cells (i.e. a set of genetically identical cells).Overall, the most common genetic aberrations occurring in adult-AMKL are the previously described inv((3)(q21q26) inversion, translocation between the q arm of chromosome 9 at position 34 and the q arm of chromosome 22 at position 11, i.e. (t(9:22)(q34:q11), and various aberrations in chromosome 5 or chromosome 7. Aberrations in the latter two chromosomes are also commonly seen in an AML that is associated with myelodydplastic-related changes (i.e. predominance of immature blood cells in the bone marrow). The underlying malignancy-causing mechanism, if any, behind these genetic aberrations requires further study.
Presentation
Adult-AMKL may occur in individuals who have a prior diagnosis of and/or present with chronic myelogenous leukemia, polycythemia vera, essential thrombocytosis, primary myelofibrosis, or mediastinal germ cell tumor. AMKL associated with mediastinal germ cell tumors typically occurs in younger adults, i.e. ages 13–36 (average age 24). Cases occurring in children aged ≤18 years, which represent ~20% of all cases, could be regarded in the non-DS-AMKL category |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A patient is on low calcium diet for 8 weeks. Following increases to maintain serum calcium levels and explain in detail? | Parathyroid hormone (PTH), also called parathormone or parathyrin, is a hormone secreted by the parathyroid glands that is impoant in bone remodeling, which is an ongoing process in which bone tissue is alternately resorbed and rebuilt over time.Ref: Ganong&;s review of medical physiology: 24th edition; page no: 377 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of the following is the chemical nature of hemodialysis associated with amyloid and explain in detail? | Ref Robbins 9/e p258 b2-Microglobulin, a component of MHC class I mole- cules and a normal serum protein, has been identified as the amyloid fibril subunit (Ab2m) in amyloidosis that com- plicates the course of patients on long-term hemodialysis. Ab2m fibers are structurally similar to normal b2m protein. This protein is present in high concentrations in the serum of patients with renal disease and is retained in the circulation because it is not efficiently filtered through dialysis membranes. In some series, as many as 60% to 80% of patients on long-term dialysis developed amyloid deposits in the synovium, joints, and tendon sheaths. * Amyloid deposits derived from diverse precursors such as hormones (procalcitonin) and keratin also have been repoed. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is What is the colour-coding of bag in hospitals to dispose of human anatomical wastes such as body pas and explain in detail? | Human anatomical wastes including human tissues, organs and body pas come under category no.1. - category no 1 wastes are discarded in a yellow colour plastic bag. Reference: Park&;s textbook of preventive and social medicine, 23rd edition, pg no: 793,794 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is True about cardiac O2 demand is and explain in detail? | Oxygen demand depends on the work being done. The work done is to pump the blood which is in the ventricles (preload) against the resistance in the aorta (afterload).
So, myocardial oxygen demand depends on
- Rate- Directly proportional
- Contractility- Directly proportional
- Intramyocardial tension- Directly proportional
o After load- Directly proportional
o Preload- Directly proportional
o Wall thickness- Inversely proportional
- The oxygen demand of myocardium is not having the same change with varying external works. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of the following drug inhibits the enzyme 11-beta- hydroxylase responsible for coisol synthesis:- and explain in detail? | Etomidate Inhibits the activity of II-B- hydroxylase an enzyme necessary for the synthesis of coisol, aldosterone ,17- hydroxyl-progesterone and coicosterone. Associated with adrenocoical suppressionwhich canlast for 72 hours. Inhibits the enzyme 11b-hydroxylase, - decreased biosynthesis of coisol and mineralocoicoid and increases the formation 11-deoxycoicosterone. More potent inhibitor of steroid synthesis than as a sedative-hypnotic as the concentration which produces adrenocoical suppression(10 ng/mL)is much lower than that needed for hypnosis (>200 ng/mL). |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Von zumbusch disease is? and explain in detail? | ANSWER: (A) Pustular psoriasisREF: Bolognia 2nd ed Ch; 9Von zumbusc disease is a type of pustular psoriasisPUSTULAR VARIANTS OF PSORIASIS:Generalized pustular psoriasis: In generalized pustular psoriasis (GPP), the infiltration of neutrophils dominates the histologic picture, while erythemaand the appearance of sterile pustules dominate the clinical picture. GPP is an unusual manifestation of psoriasis, and triggering factors include pregnancy, rapid tapering of corticosteroids (or other systemic therapies), hypocalcemia, infections and, in the case of localized disease, topical irritants. GPP during pregnancy is also referred to as impetigo herpetiformis. There are four distinct patterns of GPP.von Zumbusch pattern: This is a generalized eruption starting abruptly with erythema and postulation. The skin is painful during this phase and the patient has a fever and feels ill. After several days, the pustules usually resolve and extensive scaling is observedAnnular pattern. The eruption is characterized by annular lesions, consisting of erythema and scaling with pustulation at the advancing edge. The lesions enlarge by centrifugal expansion over a period of hours to days, whilst healing occurs centrally. General malaise, localized tenderness and fever may occur.Exanthematic type. This is an acute eruption of small pustules, abruptly appearing and disappearing in a few days. It usually follows an infection or may occur as a result of administration of specific medications, e.g. lithium. Systemic symptoms usually do not occur. There is overlap between this form of pustular psoriasis and pustular drug eruptions, also referred to as acute generalized exanthematous pustulosis (AGEP).'Localized' pattern. Sometimes pustules appear within or at the edge of existing psoriatic plaques. This can be seen during the unstable phase of chronic plaque psoriasis and following the application of irritants, e.g. tars.Localized pustular psoriasis:Pustulosis of the palms and soles: It is characterized by 'sterile' pustules of the palmoplantar surfaces admixed with yellow-brown macules ,scaly erythematous plaques may also be seen. The minority of patients have chronic plaque psoriasis elsewhere. In contrast to the natural history of GPP, the pustules remain localized to the palmoplantar surfaces and the course of this disease is chronic. Focal infections and stress have been reported as triggering factors and smoking may aggravate the condition. Pustulosis of the palms and soles is one of the entities most commonly associated with sterile inflammatory bone lesions, for which there are several names: chronic recurrent multifocal osteomyelitis, pustulotic arthro-osteitis, and SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis and osteitis). Several neutrophilic dermatoses are associated with SAPHO.Acrodermatitis continua of Hallopeau: This is a rare manifestation of psoriasis. Clinically, pustules are seen on the distal portions of the fingers and sometimes the toes. Pustulation is often followed by scaling and crust formation. Pustules may also form in the nail bed (beneath the nail plate) and there may be shedding of nail plates. Transition into other forms of psoriasis can occur and acrodermatitis continua may be accompanied by annulus migrans of the tongue. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Contraindications to tranexamic acid in management of heavy menstrual bleeding are all except and explain in detail? | Intermenstrual bleeding is not a contraindication to use of tranexamic acid. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of the following are histological features of medulloblastoma as shown in the diagram? and explain in detail? | Medulloblastoma is very densely cellular, with sheets of anaplastic cells. Individual tumor cells are small, with scant cytoplasm and hyperchromatic nuclei that are frequently elongated or crescent shaped. Mitoses are abundant, and markers of cellular proliferation, such as Ki-67, are detected in a high percentage of the cells. The tumor may express neuronal (neurosecretory) granules, form Homer-Wright rosettes and express glial markers (e.g., GFAP). |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Relaxation of mesangial cells of kidney is brought about by and explain in detail? | Mesangial cells contractionMesangial cells relaxationEndothelinsAngiotensin IIVasopressinNor-epinephrinePlatelet -activation factorPlatelet-derived growth factorThromboxane A2PGF2LT-C4and D4HistamineANPDopaminePGE2cAMP(Refer: Ganong's Review of Medical Physiology 24thedition, pg no: 678-682) |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of the following is most diagnostic investigation for acute pancreatitis and explain in detail? | Diagnosis of Acute pancreatitis Corner Stone of the diagnosis of AP: Clinical findings +elevation of pancreatic enzyme level in the plasma Pancreatic enzymes A threefold or higher elevation of amylase & lipase levels confirms the diagnosis Amylase's serum half - life is shoer as compared with lipase Lipase is also a more specific marker of AP because serum amylase levels can be elevated in a number of conditions, such as peptic ulcer disease, mesentric ischaemia, salpingitis and microamylasemia Patients with AP are typically hyperglycemic; they can also have leukocytosis and abnormal elevation of liver enzyme levels Elevation of ALT levels in the serum in the context of AP has a positive predictive value of 95% in the diagnosis of acute biliary pancreatitis X-Ray abdomen Localized ileus of duodenum and proximal jejunum (sentinel loop) or that of transverse colon up to its mid point (colon cut off sign) IOC for acute pancreatitis : CECT Ref: Sabiston 20th edition Pgno :1524-1528 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Phonation in oesophageal speech in a case of laryngectomy is produced by: and explain in detail? | In a normal person phonation is produced by vocal cords which vibrate in response of force of air produced by lungs. In oesophageal speech, patient "inhales" air into the oesophagus and then ejects it by the contraction of chest muscles. Pharyngo-oesophageal segment functions for the missing vocal cords and vibrates to produce phonation. Since only limited amount of air can be ejected from the oesophagus, maximum phonatorv time is short and patient can speak only a few words. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Neck holding comes at what age - and explain in detail? | Ans. is 'b' i.e., 3 month AgeMilestone3 monthNeck holding5 monthRolls over6 monthSit with support8 monthSit without support9 monthStand with support12 monthStand without support Walk with support15 monthWalk alone, creep upstair |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is The management technique which is more promising tool for application in health field is:- and explain in detail? | Cost Effective Analysis - This is a more promising tool for application in health field than cost benefit analysis It is similar to cost benefit analysis except that benefit ,instead of being expressed in Monetary terms is expressed in terms of Results achieved eg - No. of lives saved or No. of days free from disease |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A female patient presented with depressed mood, loss of appetite and no interest in surroundings. There is associated insomnia. The onset of depression was preceeded by a history of business loss and soon after it she developed the following symptoms for the past one year. True statement regarding management of this patient is? and explain in detail? | SSRI are the drug of choice now . As TCAs have anticholinergic, cardiovascular and neurological side effects. They have low safety margin and have a lag time of 2-4 weeks before anti depressant action manifest. Hence SSRI are used based on side effect profile. ref: K D Tripati 8th ed. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Ivermectin is used for the treatment of : and explain in detail? | None |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is 28. In cadwell luc operation the nasoantral window is made through: and explain in detail? | Caldwell-Luc operation is a process of opening the maxillary antrum through canine fossa by sublabial approach and dealing with the pathology inside the antrum. Operation is also called anterior antrostomy as access to maxillary sinus is made through anterior wall of the sinus. Ref : Dhingra 7e pg 469. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is True about wilson\'s disease – and explain in detail? | Diagnosis of Wilson disease
Diagnosis includes the demonstration of a reduced ceruloplasmin level, increased urinary excretion of copper, the presence of Kayser-Fleischer rings in the cornea of the eyes, and an elevated hepatic copper level, in the appropriate clinical setting.
Ceruloplasmin
Serum glycoprotein that contains six copper atoms.
Copper incorporation into ceruloplasmin is impared in Wilson's disease.
95% of homozygotes have levels < 20mg/dL (rarely are levels > 30 mg/dL).
May also be low in other hypoproteinemic states
May be low in 20% of asymptomatic heterozygotes
Serum free copper (unbound copper)
Greater than 25 mg in symptomatic pts (normal < 10)
Slit lamp detection of Kayser Fleischer Rings
24 hour urinary copper excretion
May exceed 100 mg/24 h-use metal free container
False + with sign. Proteinuria (ceruloplasmin loss)
Liver biopsy
> 250 g/g copper dry weight in homozygotes (normal < 50).
Cholestatic diseases (PBC/PSC) may have elevated hepatic copper dry weight. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Methemoglobinemia is caused by: and explain in detail? | Ans. (A) Prilocaine(Ref: Katzung 11th/e p449)The administration of large doses (>10mg/kg) of prilocaine during regional anesthesia may lead to accumulation of the metabolite o-toluidine, an oxidizing agent capable of converting hemoglobin to methemoglobin.The treatment of methemoglobinemia involves the intravenous administration of reducing agents (eg. methylene blue or ascorbic acid), which rapidly convert methemoglobin to hemoglobin. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Best treatment of old fracture is and explain in detail? | Nonunion fracture shaft femur requires open reduction and rigid internal fixation with either intramedullary nail or DC plating and bone grafting. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 47-year-old man presents with a 6-week history of increasing fatigue and dark-colored stools. Complete blood count shows hemoglobin of 8.6 g/dL and microcytic, hypochromic RBCs. Upper gastrointestinal endoscopy reveals a peptic ulcer along the lesser curvature of the stomach. This patient's anemia is most likely caused by deficiency of which of the following? and explain in detail? | Gastrointestinal hemorrhage leads to the loss of heme iron at a rate faster than it is replaced from dietary sources. The result is microcytic hypochromic anemia. The anemias associated with deficiencies of folic acid (choice A) and vitamin B12 (choice D) are macrocytic.Diagnosis: Iron-deficiency anemia |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is All are seen in Pheochromocytoma EXCEPT and explain in detail? | Hypocalcemia REF: Harrison's Internal Medicine > Chapter 337 Pheochromocytoma Table 337-1 Repeat in December 2009 (surgery), December 2011 Pheochromocytomas and paragangliomas are catecholamine-producing tumors derived from the sympathetic or parasympathetic nervous system. These tumors may arise sporadically or be inherited as features of multiple endocrine neoplasia type 2. The "rule of tens" for pheochromocytomas states that about 10% are bilateral, 10% are extraadrenal, and 10% are malignant. However, these percentages are higher in the inherited syndromes. The clinical presentation is so variable that Pheochromocytoma has been termed "the great masquerader". The dominant sign is hypeension. Classically, patients have episodic hypeension, but sustained hypeension is also frequent. CLINICAL FEATURES ASSOCIATED WITH PHEOCHROMOCYTOMA Headaches Sweating attacks Palpitation and tachycardia Hypeension, sustained or paroxysmal Anxiety and panic attacks Pallor Nausea Abdominal pain Weakness Weight loss Paradoxical response to antihypeensive drugs Polyuria and polydipsia Constipation Ohostatic hypotension Dilated cardiomyopathy Erythrocytosis Elevated blood sugar Hypercalcemia |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Chyme is formed by- and explain in detail? | Ans. is 'b' i.e., Stomach * After food in the stomach has become throughly mixed with stomach secretions, the resulting mixture that passes down the gut is called chyme.* Chyme is usually semifluid mass. However, degree of fluidity of chyme depends on the relative amounts of food, water and stomach secretions and on the degree of digestion that has occurred. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A mutation that converts an amino acid codon to a stop codon is a: and explain in detail? | Changes one codon for an amino acid into another codon for that same amino acid - Silent mutation
Codon for one amino acid is changed into a codon of another amino acid - Missense mutation
Codon for one amino acid is changed into a translation termination codon - Non-sense mutation
Reading frame changes downstream to the mutant site - Frameshift mutation.
A purine base replaced by another pyrimidine, or pyrimidine replaced by another purine -Transversion.
Key Concept
Nonsense mutation
A coding codon mutated to a nonsense codon result in premature termination of polypeptide chain. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Characterstic nail finding in lichen planus - and explain in detail? | NAIL CHANGES IN LICHEN PLANUS: 1.Early change- bluish red discolouration of proximal nail fold. 2.thinning of nail plate, koilonychia, longtudinal ridging, splitting(onychoschizia) 3. pterygium formation-wing shaped growth of proximal nail fold across the nail plate due to severe nail matrix involvement. it is a characteristic nail change in lichen planus 4. pup tent sign: proximal onycholysis with elevation of nail plate and longitudinal splitting ue to involvement of nail bed. 5. anonychia 6. melanonychia IADVL textbook of dermatology, page 1075 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Treatment of dermatitis herpetiformis ? and explain in detail? | Ans. is 'a' i.e., Cong erythropoetic porphyria Tinea capitis shows greenish fluorescence. Erythrasma gives a coral pink hue. Pseudomonas infection gives a yellowish-green colour |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which of the following is not used in diagonosis of insulinoma and explain in detail? | These blood tests are needed to diagnose insulinoma: glucose insulin C-peptide If available, a proinsulin level might be useful, as well. Other blood tests may help rule out other conditions which can cause hypoglycemia Ref Davidson edition23rd pg837 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A free radical is and explain in detail? | Free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons.Reference: Khan Physics of Radiation therapy; 5th edition |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Regarding oncogenesis, all are true except: and explain in detail? | Activation of proto-oncogene results in cancer causing oncogenes by following mechanisms: |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Drug of choice for central diabetes insipidus is and explain in detail? | Desmopressin (dDAVP):- This synthetic peptide is a selective V2 agonist; but has negligible vasoconstrictor activity. It is also longer acting because enzymatic degradation is slow; t 1/2 1-2 hours; duration of action 8-12 hours. Desmopressin is the preparation of choice for all V2 receptor related indications. The intranasal route is preferred, though bioavailability is only 10-20%. Uses :- Based on V2 actions (Desmopressin is the drug of choice). 1. Diabetes insipidus DI of pituitary origin (neurogenic) is the most impoant indication for vasopressin. It is ineffective in renal (nephrogenic) DI, since kidney is unresponsive to ADH. Life- long therapy is required, except in some cases of head injury or neurosurgery, where DI occurs transiently. The dose of desmopressin is individualized by measuring 24 hour urine volume. It can be used in transient DI and to differentiate neurogenic from nephrogenic DI--urine volume is reduced and its osmolarity increased if DI is due to deficiency of ADH, but not when it is due to unresponsiveness of kidney to ADH. Ref:- kd tripathi; pg num:-596,597 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 20-year-old primigravid woman is in the third trimester and has felt minimal fetal movement. An ultrasound scan shows bilaterally enlarged echogenic kidneys and a markedly decreased amniotic fluid index. She gives birth to a stillborn male fetus at 33 weeks' gestation. At autopsy, there are deformations resulting from marked oligohydramnios, including flattening of the facies, varus deformities of the feet, and marked pulmonary hypoplasia. Microscopic examination of the liver shows multiple epithelium-lined cysts and proliferation of bile ducts. Which of the following is the most likely renal disease in this fetus? and explain in detail? | Autosomal recessive polycystic kidney disease (ARPKD) most often occurs in children, and this case with the distinctive finding of congenital hepatic fibrosis; most cases have PKHD1 gene mutations encoding for fibrocystin expressed in the kidney, liver, and pancreas. By contrast, autosomal dominant polycystic kidney disease (ADPKD) manifests with renal failure in adults and involves PKD1 and PKD2 gene mutations encoding for polycystin proteins found in renal tubules. Some less common forms of ARPKD are accompanied by survival beyond infancy, and these patients develop congenital hepatic fibrosis. Enlarged kidneys with 1- to 4-cm cysts are characteristic of ADPKD in adults. Perhaps the most common renal cystic disease seen in fetuses and infants is multicystic renal dysplasia (multicystic dysplastic kidney), with focal, unilateral, or bilateral from variably sized cysts, but congenital hepatic fibrosis is not present. Medullary sponge kidney is a benign condition usually found on radiologic imaging of adults. Urethral atresia would produce marked bladder dilation, hydroureter, and hydronephrosis. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Identity the structure in the given chest X-ray: and explain in detail? | Ans. b. Left-Cardiophrenic angle |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Most commonly lesion associated with pathological fracture in hand is - and explain in detail? | Ans. is 'a' i.e., Enchondroma Pathological fractures in hand* In hand pathological fractures are most commonly associated with benign bone tumors.* About 23 % of the bone tumors in hand present with pathological fractures.* The average age of presentation is 37 years.* The most common bone affected is the proximal phalynx, the fifth ray was involved in 44% of the patients.* Majority (approximately 88%) of the pathological fractures are caused by enchondromas. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is All of the following are anti-craving agents for alcohol withdrawal Except and explain in detail? | Nitrafezole. Disulfiram, Metronidazole and Nitrafezole are deterrents. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A patient developed wound infection post laparotomy for pyoperitoneam, was treated conservatively. Now, granulation tissue is seen in the wound. Next step in management is and explain in detail? | Answer- D. Resuturing with interrupted stitchesPresence ofgranulation tissue indicates that the wound is healthy and angiogenesis is occurring at the edges and base of the wound.This is an indication that the wound can now be safely closed with interrupted sutures without any risk of complications. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Increased pulmonary blood flow radiologically indicated by all except: and explain in detail? | (Refer – M.Satpathy’s Clinical Diagnosis of Congenital Heart Disease, 1st edition, pg no: 38)
Features of increased pulmonary blood flow
Blood vessels become visible in the outer third of lung field (At least 6 vessels can be traced to theouter third). When hilar and intrapulmonary vessels are uniformly changed, it is very suggestive of shunt lesions.
Ratio of right descending pulmonary artery to trachea > 1
Right descending pulmonary artery diameter> 14 mm suggests increased blood flow and >17 mm is very strongly suggestive
Prominent end-on vessels seen at hilum
Enface vessels below 10th posterior rib
Prominent vessels seen below crest of diaphragm
Ratio of vessels to adjacent bronchus >2:1 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Radiographic angulation recommended by the IADT: and explain in detail? | It is of importance to take radiographs in more than one angle to ascertain the extent of the injury. Radiographs of the cheek and lip lacerations are also indicated to search for embedded tooth fragments. The three radiographic angulations recommended by the International Association of Dental Traumatology (IADT) are as follows:
Ninety-degree horizontal angle, with central beam through the tooth.
Occlusal view.
Lateral view from the mesial or distal aspect of the tooth. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is The most common ophtalmic lesion in AIDS is - and explain in detail? | Ophthalmologic problems occur in ~50% of patients with advanced HIV infection. The most common abnormal findingson funduscopic examination are cotton-wool spots. These are hard white spots that appear on the surface of the retina and often have an irregular edge. They represent areas of retinal ischemia secondary to microvascular disease. At times they are associated with small areas of hemorrhage and thus can be difficult to distinguish from CMV retinitis. In contrast to CMV retinitis, however, these lesions are not associated with visual loss and tend to remain stable or improve over time. (Harrison's Principles of internal medicine, 20 th edition, page 1562) |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Fungal infections not associated with AIDS patient are - and explain in detail? | Fungal infections are Pneumocystitis jirovecii ,candidiasis, cryptoccosis, Aspergillosis, Histoplasmosis. REF:ANANTHANARAYAN AND PANIKER'S TEXTBOOK OF MICROBIOLOGY 9TH EDITION PAGE NO-576 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Unilateral clefts are more common on and explain in detail? | Distribution of cleft lip and cleft palate In unilateral cleft lip the deformity affects left side in 60% cases Typical distribution of cleft types Cleft lip alone :15% Cleft lip & palate :45% (MC) Isolated cleft palate :40% Ref: Sabiston 20th edition Pgno :1946-1947 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is All of the following disease spread through Louse except :- and explain in detail? | Louse is the vector of: Epidemic typhus Trench fever Relapsing fever Pediculosis Its control is done by insecticide -malathion . May be resistant to DDT & HCH. Personal hygiene most impoant to prevent its infestation. Q fever has no vector: Q fever is transmitted through Inhalation of infected dust Contaminated milk, meat. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Vitamin–B6 deficiency is seen with the use of all of the following drugs except : and explain in detail? | None |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Clonazepam and explain in detail? | Clonazepam, sold under the brand name Klonopin among others, is a medication used to prevent and treat seizures, panic disorder, anxiety, and the movement disorder known as akathisia. It is a tranquilizer of the benzodiazepine class. It possesses anxiolytic, anticonvulsant, sedative, hypnotic, and skeletal muscle relaxant properties. It is typically taken by mouth. Effects begin within one hour and last between six and twelve hours.Common side effects include sleepiness, poor coordination, and agitation. Long-term use may result in tolerance, dependence, and withdrawal symptoms if stopped abruptly. Dependence occurs in one-third of people who take clonazepam for longer than four weeks. There is an increased risk of suicide, particularly in people who are already depressed. If used during pregnancy it may result in harm to the fetus. Clonazepam binds to GABAA receptors, thus increasing the effect of the chief inhibitory neurotransmitter γ-aminobutyric acid (GABA).Clonazepam was patented in 1960 and went on sale in 1975 in the United States from Roche. It is available as a generic medication. In 2020, it was the 44th most commonly prescribed medication in the United States, with more than 14 million prescriptions. In many areas of the world it is commonly used as a recreational drug.
Medical uses
Clonazepam is prescribed for short term management of epilepsy, anxiety, and panic disorder with or without agoraphobia.
Seizures
Clonazepam, like other benzodiazepines, while being a first-line treatment for acute seizures, is not suitable for the long-term treatment of seizures due to the development of tolerance to the anticonvulsant effects.
Clonazepam has been found effective in treating epilepsy in children, and the inhibition of seizure activity seemed to be achieved at low plasma levels of clonazepam. As a result, clonazepam is sometimes used for certain rare childhood epilepsies; however, it has been found to be ineffective in the control of infantile spasms. Clonazepam is mainly prescribed for the acute management of epilepsies. Clonazepam has been found to be effective in the acute control of non-convulsive status epilepticus; however, the benefits tended to be transient in many people, and the addition of phenytoin for lasting control was required in these patients.It is also approved for treatment of typical and atypical absences (seizures), infantile myoclonic, myoclonic, and akinetic seizures. A subgroup of people with treatment resistant epilepsy may benefit from long-term use of clonazepam; the benzodiazepine clorazepate may be an alternative due to its slow onset of tolerance.
Anxiety disorders
Panic disorder with or without agoraphobia.
Clonazepam has also been found effective in treating other anxiety disorders, such as social phobia, but this is an off-label use.The effectiveness of clonazepam in the short-term treatment of panic disorder has been demonstrated in controlled clinical trials. Some long-term trials have suggested a benefit of clonazepam for up to three years without the development of tolerance but these trials were not placebo-controlled. Clonazepam is also effective in the management of acute mania.
Muscle disorders
Restless legs syndrome can be treated using clonazepam as a third-line treatment option as the use of clonazepam is still investigational. Bruxism also responds to clonazepam in the short-term. Rapid eye movement sleep behavior disorder responds well to low doses of clonazepam.
The treatment of acute and chronic akathisia induced by neuroleptics, also called antipsychotics.
Spasticity related to amyotrophic lateral sclerosis.
Alcohol withdrawal syndrome
Other
Benzodiazepines, such as clonazepam, are sometimes used for the treatment of mania or acute psychosis-induced aggression. In this context, benzodiazepines are given either alone, or in combination with other first-line drugs such as lithium, haloperidol or risperidone. The effectiveness of taking benzodiazepines along with antipsychotic medication is unknown, and more research is needed to determine if benzodiazepines are more effective than antipsychotics when urgent sedation is required.
Hyperekplexia
Many forms of parasomnia and other sleep disorders are treated with clonazepam.
It is not effective for preventing migraines.
Contraindications
Coma
Current alcohol use disorder
Current substance use disorder
Respiratory depression.
Adverse effects
In September 2020, the U.S. Food and Drug Administration (FDA) required the boxed warning be updated for all benzodiazepine medicines to describe the risks of abuse, misuse, addiction, physical dependence, and withdrawal reactions consistently across all the medicines in the class.
Common
Sedation
Euphoria
Motor impairment
Less common
Confusion
Irritability and aggression
Psychomotor agitation
Lack of motivation
Loss of libido
Impaired motor functionImpaired coordination
Impaired balance
Dizziness
Cognitive impairmentsHallucinations.
Short-term memory loss
Anterograde amnesia (common with higher doses)
Some users report hangover-like symptoms of drowsiness, headaches, sluggishness, and irritability upon waking up if the medication was taken before sleep. This is likely the result of the medications long half-life, which continues to affect the user after waking up. While benzodiazepines induce sleep, they tend to reduce the quality of sleep by suppressing or disrupting REM sleep. After regular use, rebound insomnia may occur when discontinuing clonazepam.
Benzodiazepines may cause or worsen depression.
Occasional
Dysphoria
Induction of seizures or increased frequency of seizures
Personality changes
Behavioural disturbances
Ataxia
Rare
Suicide through disinhibition
Psychosis
Incontinence
Liver damage
Paradoxical behavioural disinhibition (most frequently in children, the elderly, and in persons with developmental disabilities)
Rage
Excitement
ImpulsivityThe long-term effects of clonazepam can include depression, disinhibition, and sexual dysfunction.
Drowsiness
Clonazepam, like other benzodiazepines, may impair a persons ability to drive or operate machinery. The central nervous system depressing effects of the drug can be intensified by alcohol consumption, and therefore alcohol should be avoided while taking this medication. Benzodiazepines have been shown to cause dependence. Patients dependent on clonazepam should be slowly titrated off under the supervision of a qualified healthcare professional to reduce the intensity of withdrawal or rebound symptoms.
Withdrawal-related
Anxiety
Irritability
Insomnia
Tremors
Headaches
Stomach pain
Hallucinations
Suicidal thoughts or urges
Depression
Fatigue
Dizziness
Sweating
Confusion
Potential to exacerbate existing panic disorder upon discontinuation
Seizures similar to delirium tremens (with long-term use of excessive doses)Benzodiazepines such as clonazepam can be very effective in controlling status epilepticus, but, when used for longer periods of time, some potentially serious side-effects may develop, such as interference with cognitive functions and behavior. Many individuals treated on a long-term basis develop a dependence. Physiological dependence was demonstrated by flumazenil-precipitated withdrawal. Use of alcohol or other CNS depressants while taking clonazepam greatly intensifies the effects (and side effects) of the drug.
A recurrence of symptoms of the underlying disease should be separated from withdrawal symptoms.
Tolerance and withdrawal
Like all benzodiazepines, clonazepam is a GABA-positive allosteric modulator. One-third of individuals treated with benzodiazepines for longer than four weeks develop a dependence on the drug and experience a withdrawal syndrome upon dose reduction. High dosage and long-term use increase the risk and severity of dependence and withdrawal symptoms. Withdrawal seizures and psychosis can occur in severe cases of withdrawal, and anxiety and insomnia can occur in less severe cases of withdrawal. A gradual reduction in dosage reduces the severity of the benzodiazepine withdrawal syndrome. Due to the risks of tolerance and withdrawal seizures, clonazepam is generally not recommended for the long-term management of epilepsies. Increasing the dose can overcome the effects of tolerance, but tolerance to the higher dose may occur and adverse effects may intensify. The mechanism of tolerance includes receptor desensitization, down regulation, receptor decoupling, and alterations in subunit composition and in gene transcription coding.Tolerance to the anticonvulsant effects of clonazepam occurs in both animals and humans. In humans, tolerance to the anticonvulsant effects of clonazepam occurs frequently. Chronic use of benzodiazepines can lead to the development of tolerance with a decrease of benzodiazepine binding sites. The degree of tolerance is more pronounced with clonazepam than with chlordiazepoxide. In general, short-term therapy is more effective than long-term therapy with clonazepam for the treatment of epilepsy. Many studies have found that tolerance develops to the anticonvulsant properties of clonazepam with chronic use, which limits its long-term effectiveness as an anticonvulsant.Abrupt or over-rapid withdrawal from clonazepam may result in the development of the benzodiazepine withdrawal syndrome, causing psychosis characterised by dysphoric manifestations, irritability, aggressiveness, anxiety, and hallucinations. Sudden withdrawal may also induce the potentially life-threatening condition, status epilepticus. Anti-epileptic drugs, benzodiazepines such as clonazepam in particular, should be reduced in dose slowly and gradually when discontinuing the drug to mitigate withdrawal effects. Carbamazepine has been tested in the treatment of clonazepam withdrawal but was found to be ineffective in preventing clonazepam withdrawal-induced status epilepticus from occurring.
Overdose
Excess doses may result in:
Difficulty staying awake
Mental confusion
Impaired motor functions
Impaired reflexes
Impaired coordination
Impaired balance
Dizziness
Respiratory depression
Low blood pressure
ComaComa can be cyclic, with the individual alternating from a comatose state to a hyper-alert state of consciousness, which occurred in a four-year-old boy who overdosed on clonazepam. The combination of clonazepam and certain barbiturates (for example, amobarbital), at prescribed doses has resulted in a synergistic potentiation of the effects of each drug, leading to serious respiratory depression.Overdose symptoms may include extreme drowsiness, confusion, muscle weakness, and fainting.
Detection in biological fluids
Clonazepam and 7-aminoclonazepam may be quantified in plasma, serum, or whole blood in order to monitor compliance in those receiving the drug therapeutically. Results from such tests can be used to confirm the diagnosis in potential poisoning victims or to assist in the forensic investigation in a case of fatal overdosage. Both the parent drug and 7-aminoclonazepam are unstable in biofluids, and therefore specimens should be preserved with sodium fluoride, stored at the lowest possible temperature and analyzed quickly to minimize losses.
Special precautions
The elderly metabolize benzodiazepines more slowly than younger people and are also more sensitive to the effects of benzodiazepines, even at similar blood plasma levels. Doses for the elderly are recommended to be about half of that given to younger adults and are to be administered for no longer than two weeks. Long-acting benzodiazepines such as clonazepam are not generally recommended for the elderly due to the risk of drug accumulation.The elderly are especially susceptible to increased risk of harm from motor impairments and drug accumulation side effects. Benzodiazepines also require special precaution if used by individuals that may be pregnant, alcohol- or drug-dependent, or may have comorbid psychiatric disorders. Clonazepam is generally not recommended for use in elderly people for insomnia due to its high potency relative to other benzodiazepines.Clonazepam is not recommended for use in those under 18. Use in very young children may be especially hazardous. Of anticonvulsant drugs, behavioural disturbances occur most frequently with clonazepam and phenobarbital.Doses higher than 0.5–1 mg per day are associated with significant sedation.Clonazepam may aggravate hepatic porphyria.Clonazepam is not recommended for patients with chronic schizophrenia. A 1982 double-blinded, placebo-controlled study found clonazepam increases violent behavior in individuals with chronic schizophrenia.Clonazepam has similar effectiveness to other benzodiazepines at often a lower dose.
Interactions
Clonazepam decreases the levels of carbamazepine, and, likewise, clonazepams level is reduced by carbamazepine. Azole antifungals, such as ketoconazole, may inhibit the metabolism of clonazepam. Clonazepam may affect levels of phenytoin (diphenylhydantoin). In turn, Phenytoin may lower clonazepam plasma levels by increasing the speed of clonazepam clearance by approximately 50% and decreasing its half-life by 31%.
Clonazepam increases the levels of primidone and phenobarbital.Combined use of clonazepam with certain antidepressants, anticonvulsants (such as phenobarbital, phenytoin, and carbamazepine), sedative antihistamines, opiates, and antipsychotics, nonbenzodiazepines (such as zolpidem), and alcohol may result in enhanced sedative effects.
Pregnancy
There is some medical evidence of various malformations (for example, cardiac or facial deformations when used in early pregnancy); however, the data is not conclusive. The data are also inconclusive on whether benzodiazepines such as clonazepam cause developmental deficits or decreases in IQ in the developing fetus when taken by the mother during pregnancy. Clonazepam, when used late in pregnancy, may result in the development of a severe benzodiazepine withdrawal syndrome in the neonate. Withdrawal symptoms from benzodiazepines in the neonate may include hypotonia, apnoeic spells, cyanosis, and impaired metabolic responses to cold stress.The safety profile of clonazepam during pregnancy is less clear than that of other benzodiazepines, and if benzodiazepines are indicated during pregnancy, chlordiazepoxide and diazepam may be a safer choice. The use of clonazepam during pregnancy should only occur if the clinical benefits are believed to outweigh the clinical risks to the fetus. Caution is also required if clonazepam is used during breastfeeding. Possible adverse effects of use of benzodiazepines such as clonazepam during pregnancy include: miscarriage, malformation, intrauterine growth retardation, functional deficits, carcinogenesis, and mutagenesis. Neonatal withdrawal syndrome associated with benzodiazepines include hypertonia, hyperreflexia, restlessness, irritability, abnormal sleep patterns, inconsolable crying, tremors, or jerking of the extremities, bradycardia, cyanosis, suckling difficulties, apnea, risk of aspiration of feeds, diarrhea and vomiting, and growth retardation. This syndrome can develop between three days to three weeks after birth and can have a duration of up to several months. The pathway by which clonazepam is metabolized is usually impaired in newborns. If clonazepam is used during pregnancy or breastfeeding, it is recommended that serum levels of clonazepam are monitored and that signs of central nervous system depression and apnea are also checked for. In many cases, non-pharmacological treatments, such as relaxation therapy, psychotherapy, and avoidance of caffeine, can be an effective and safer alternative to the use of benzodiazepines for anxiety in pregnant women.
Pharmacology
Mechanism of action
Clonazepam enhances the activity of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the central nervous system to give its anticonvulsant, skeletal muscle relaxant, and anxiolytic effects. It acts by binding to the benzodiazepine site of the GABA receptors, which enhances the electric effect of GABA binding on neurons, resulting in an increased influx of chloride ions into the neurons. This further results in an inhibition of synaptic transmission across the central nervous system.Benzodiazepines do not have any effect on the levels of GABA in the brain. Clonazepam has no effect on GABA levels and has no effect on gamma-aminobutyric acid transaminase. Clonazepam does, however, affect glutamate decarboxylase activity. It differs from other anticonvulsant drugs it was compared to in a study.Clonazepams primary mechanism of action is the modulation of GABA function in the brain, by the benzodiazepine receptor, located on GABAA receptors, which, in turn, leads to enhanced GABAergic inhibition of neuronal firing. Benzodiazepines do not replace GABA, but instead enhance the effect of GABA at the GABAA receptor by increasing the opening frequency of chloride ion channels, which leads to an increase in GABAs inhibitory effects and resultant central nervous system depression. In addition, clonazepam decreases the utilization of 5-HT (serotonin) by neurons and has been shown to bind tightly to central-type benzodiazepine receptors. Because clonazepam is effective in low milligram doses (0.5 mg clonazepam = 10 mg diazepam), it is said to be among the class of "highly potent" benzodiazepines. The anticonvulsant properties of benzodiazepines are due to the enhancement of synaptic GABA responses, and the inhibition of sustained, high-frequency repetitive firing.Benzodiazepines, including clonazepam, bind to mouse glial cell membranes with high affinity. Clonazepam decreases release of acetylcholine in the feline brain and decreases prolactin release in rats. Benzodiazepines inhibit cold-induced thyroid-stimulating hormone (also known as TSH or thyrotropin) release. Benzodiazepines act via micromolar benzodiazepine binding sites as Ca2+ channel blockers and significantly inhibit depolarization-sensitive calcium uptake in experimentation on rat brain cell components. This has been conjectured as a mechanism for high-dose effects on seizures in the study.Clonazepam is a 2-chlorinated derivative of nitrazepam, which increases its potency due to electron-attracting effect of the halogen in the ortho-position.
Pharmacokinetics
Clonazepam is lipid-soluble, rapidly crosses the blood–brain barrier, and penetrates the placenta. It is extensively metabolised into pharmacologically inactive metabolites, with only 2% of the unchanged drug excreted in the urine. Clonazepam is metabolized extensively via nitroreduction by cytochrome P450 enzymes, including CYP3A4. Erythromycin, clarithromycin, ritonavir, itraconazole, ketoconazole, nefazodone, cimetidine, and grapefruit juice are inhibitors of CYP3A4 and can affect the metabolism of benzodiazepines. It has an elimination half-life of 19–60 hours. Peak blood concentrations of 6.5–13.5 ng/mL were usually reached within 1–2 hours following a single 2 mg oral dose of micronized clonazepam in healthy adults. In some individuals, however, peak blood concentrations were reached at 4–8 hours.Clonazepam passes rapidly into the central nervous system, with levels in the brain corresponding with levels of unbound clonazepam in the blood serum. Clonazepam plasma levels are very unreliable amongst patients. Plasma levels of clonazepam can vary as much as tenfold between different patients.Clonazepam has plasma protein binding of 85%. Clonazepam passes through the blood–brain barrier easily, with blood and brain levels corresponding equally with each other |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is The test is performed for palsy of: and explain in detail? | Ans. (a) Median nerve. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Glutaric aciduria type 1 and explain in detail? | Glutaric acidemia type 1 (GA1) is an inherited disorder in which the body is unable to completely break down the amino acids lysine, hydroxylysine and tryptophan. Excessive levels of their intermediate breakdown products (glutaric acid, glutaryl-CoA, 3-hydroxyglutaric acid, glutaconic acid) can accumulate and cause damage to the brain (and also other organs), but particularly the basal ganglia, which are regions that help regulate movement. GA1 causes secondary carnitine deficiency, as glutaric acid, like other organic acids, is detoxified by carnitine. Mental retardation may occur.
GA1 is an autosomal recessive disorder caused by deficiency of the enzyme glutaryl-CoA dehydrogenase (GCDH), encoded by the GCDH gene.
Signs and symptoms
The severity of glutaric acidemia type 1 varies widely; some individuals are only mildly affected, while others suffer severe problems. GA1 can be defined as two clinical entities: GA-1 diagnosed at birth or pre-birth and managed through dietary restrictions, and GA-1 diagnosed after an encephalopathic crisis. A crisis may occur under both headings, but the care of individuals diagnosed before a crisis can be managed to avoid most or all injury.
GA1 without encephalopathic crisis
Macrocephaly
Babies with glutaric acidemia type 1 often are born with unusually large heads (macrocephaly). Macrocephaly is amongst the earliest signs of GA1. It is thus important to investigate all cases of macrocephaly of unknown origins for GCDH deficiency, given the importance of the early diagnosis of GA1.
Macrocephaly is a pivotal clinical sign of many neurological diseases. Physicians and parents should be aware of the benefits of investigating for an underlying neurological disorder, particularly a neurometabolic one, in children with head circumferences in the highest percentiles.
GA1 after an encephalopathic crisis
Neuromotor aspects
Affected individuals may have difficulty moving and may experience spasms, jerking, rigidity or decreased muscle tone and muscle weakness (which may be the result of secondary carnitine deficiency). GA, in patients who have suffered a crisis, can be defined as a cerebral palsy of genetic origins.
Occupational therapy
A common way to manage striatal necrosis is to provide special seating. These special wheelchairs are designed to limit abnormal movements. However, spasticity can be worsened by constraint. Parents and caregivers can provide a more interactive occupational therapy by enabling the child to use his or her own excessive postural muscle tone to his or her own advantage (see picture; note the care with which minimal pressure is applied while ensuring safety).The excessive tone can also be managed with "jolly jumpers" and other aids to the upright stance that do not constrain the child but help him or her gradually tone down the rigidity.
Bleeding abnormalities
Some individuals with glutaric acidemia have developed bleeding in the brain or eyes that could be mistaken for the effects of child abuse.
Genetics
The condition is inherited in an autosomal recessive pattern: mutated copies of the gene GCDH must be provided by both parents to cause GA1. The GCDH gene encodes the enzyme glutaryl-CoA dehydrogenase. This enzyme is involved in degrading the amino acids lysine, hydroxylysine and tryptophan. Mutations in the GCDH gene prevent production of the enzyme or result in the production of a defective enzyme with very low residual activity, or an enzyme with relatively high residual activity but still phenotypic consequences. This enzyme deficiency allows glutaric acid, 3-hydroxyglutaric acid and to a lesser extent glutaconic acid to build up to abnormal levels, especially at times when the body is under stress. These intermediate breakdown products are particularly prone to affect the basal ganglia, causing many of the signs and symptoms of GA1.
GA1 occurs in approximately 1 of every 30,000 to 40,000 births. As a result of founder effect, it is much more common in the Amish community and in the Ojibway population of Canada, where up to 1 in 300 newborns may be affected.
Relatives of children with GA1 can have low GCDH activity: in an early study of GA1, GCDH activity was found to be 38%, 42%, and 42% in three of the four unaffected relatives tested, a pattern consistent with the 50% level that would be expected in heterozygous carriers. Those levels are close to those found in some heavily symptomatic GA1-affected children.
Diagnosis
Normally, magnetic resonance imaging shows the Sylvian fissure to be operculated, but in GA1-associated encephalopathy, operculation is absent. In many jurisdictions, GA1 is included in newborn screening panels. Elevated glutarylcarnitine can be detected by mass spectrometry in a dried blood spot collected shortly after birth. After a positive screening result, confirmatory testing is performed. This includes urine organic acid analysis, looking for glutaric acid and 3-hydroxyglutaric acid. Plasma and urine acylcarnitine analysis can also be informative. Molecular analysis, including gene sequencing and copy number analysis of GCDH, can be performed to confirm the diagnosis. Molecular testing can also provide information for family planning and prenatal testing, if desired.
Treatment
Correction of secondary carnitine depletion
Like many other organic acidemias, GA1 causes carnitine depletion. Whole-blood carnitine can be raised by oral supplementation. However, this does not significantly change blood concentrations of glutarylcarnitine or esterified carnitine, suggesting that oral supplementation is suboptimal in raising tissue levels of carnitine. Clinical nutrition researchers have likewise concluded that oral carnitine raises plasma levels but does not affect those in muscles, where most of it is stored and used.In contrast, regular intravenous infusions of carnitine cause distinct clinical improvements: "decreased frequency of decompensations, improved growth, improved muscle strength and decreased reliance on medical foods with liberalization of protein intake."Choline increases carnitine uptake and retention. Choline supplements are inexpensive, are safe (probably even in children requiring anticholinergics) and can increase exercise tolerance, truncal tone and general well-being, providing evidence of the suboptimal efficiency of carnitine supplementation alone.
Selective precursor restriction
Dietary control may help limit progression of the neurological damage.
Lysine
Lysine restriction, as well as carnitine supplementation, are considered the best predictors of a good prognosis for GA1. This excludes, however, patients who already suffered an encephalopathic crisis, for whom the prognosis is more related to the treatment of their acquired disorder (striatal necrosis, frontotemporal atrophy).
Protein restriction
Vegetarian diets and, for younger children, breastfeeding are common ways to limit protein intake without endangering tryptophan transport to the brain.
Tryptophan
Formulas such as XLys, XTrp Analog, XLys, XTrp Maxamaid, XLys, XTrp Maxamum or Glutarex 1 are designed to provide amino acids other than lysine and tryptophan, to help prevent protein malnutrition.
The entry of tryptophan into the brain is crucial in the proper synthesis of the neurotransmitter serotonin in the brain. One way to acutely cause depression, bulimia or anxiety in humans, in order to assess an individuals vulnerability to those disorders, is to supplement with a formula with all or most amino acids except tryptophan. Acute tryptophan depletion is a diagnostic procedure, not a treatment for GA1. The protein synthesis elicited by the amino acids leads circulating amino acids, including tryptophan, to be incorporated into proteins. Tryptophan is thus lowered in the brain as a result of the protein synthesis enhancement, causing circulating tryptophan to drop more than other amino acids. A relative excess of other large neutral amino acids may also compete with tryptophan for transport across the blood–brain barrier through the large neutral amino acid transporter 1. The consequence is acute tryptophan depletion in the brain and a consequent decrease in serotonin synthesis.
5-Hydroxytryptophan, a precursor of serotonin that is not metabolized to glutaryl-CoA, glutaric acid and secondary metabolites, could be used as an adjunct to selective tryptophan restriction, although it has risks. However, the evidence in favour of selective tryptophan restriction remains insufficient and the consensus is evolving towards the restriction of lysine only. In the Amish community, where GA1 is overrepresented, patients with GA1 typically do not receive tryptophan-free formulas, either as the sole source of amino acids or as a supplement to protein restriction.
Enhancement of precursor anabolic pathways
Lysine and hydroxylysine anabolic pathway enhancement
A possible way to prevent the build-up of metabolites is to limit lysine and hydroxylysine degradation, as lysine is one of the most abundant amino acids and tryptophan is one of the least abundant amino acids.
Interaction of GCDH deficiency with vitamin C levels
Humans lack the enzyme L-gulonolactone oxidase, which is necessary for the synthesis of ascorbic acid (vitamin C), leaving them dependent on dietary sources of this vitamin. Vitamin C is a necessary cofactor for the utilization of lysine in collagen synthesis. Collagen, the most abundant protein in the human body, requires great amounts of lysine, the most abundant amino acid in proteins. Ascorbic acid, the main hydroxyl radical quencher, works as the cofactor providing the hydroxyl radical required for collagen cross-linking; lysine thus becomes hydroxylysine.
GA1 worsens during stresses and catabolic episodes, such as fasts and infections. Endogenous catabolism of proteins could be an important route for glutaric acid production. It follows that collagen breakdown (and protein breakdown in general) should be prevented by all possible means.
Ascorbic acid is used to prevent multiple organ failure and to lessen mortality and morbidity in intensive care units. It thus appears reasonable to add sufficient doses of ascorbic acid to the treatment protocol during stresses and other challenges to growth in order to stimulate collagen synthesis and thus prevent lysine breakdown.
Tryptophan anabolic pathway enhancement
The conversion of tryptophan to serotonin and other metabolites depends on vitamin B6. If tryptophan catabolism has any impact on brain glutaric acid and other catabolite levels, vitamin B6 levels should be routinely assayed and normalized in the course of the treatment of GA1.
Management of intercurrent illnesses
Stress caused by infection, fever or other demands on the body may lead to worsening of the signs and symptoms, with only partial recovery.
Prognosis
A 2006 study of 279 patients found that of those with symptoms (185, 66%), 95% had suffered an encephalopathic crises, usually with following brain damage. Of the participants in the study, 49 children died and the median age of death was 6.6 years. A Kaplan–Meier analysis of the data estimated that about 50% of symptomatic people would die by the age of 25.
More recent studies provide an updated prognosis whereby individuals affected can, through proper dietary management and carnitine supplementation, manage the disease with a much improved prognosis. Newborn screening has allowed affected patients to avoid crises and live full lives without any injury to the brain. It is essential that patients with the disease be diagnosed at or before birth and that all variables be strictly managed in order to maintain quality of life. When suspected and in the absence of confirmed diagnosis (through genetic sequencing), it is critical that the individual maintain a diet restrictive of all proteins and that blood sugars be monitored rigorously. The WHO now considers this disease entirely manageable.
Epidemiology
GA1 can be described as a metabolic disorder, a neurometabolic disease, a cerebral palsy or a basal ganglia disorder (it may also be misdiagnosed as shaken baby syndrome).
Depending on the paradigm adopted, GA1 will mostly be managed with precursor restriction or with neurorehabilitation.
So-called "orphan diseases", such as GA1, can be adopted into wider groups of diseases (such as carnitine deficiency diseases, cerebral palsies of diverse origins, basal ganglia disorders, and others); Morton at al. (2003b) emphasize that acute striatal necrosis is a distinctive pathologic feature of at least 20 other disorders of very different etiologies, including, HIV encephalopathy–AIDS dementia complex, pneumococcal meningitis, hypoadrenal crisis, methylmalonic acidemia, propionic acidemia, middle cerebral artery occlusion, hypertensive vasculopathy, acute Mycoplasma pneumoniae infection, 3-nitropropionic acid intoxication, late-onset familial dystonia, cerebrovascular abrupt and severe neonatal asphyxia ("selective neuronal necrosis").
In a cohort of 279 patients who had been reported to have GA1, 185 were symptomatic (two-thirds); being symptomatic was seen as an indication of low treatment efficacy. Screening of those known to be at high risk, neonatal population screening and a diagnosis of macrocephaly are the ways to identify bearers of the GCDH mutation who are not frankly symptomatic. Macrocephaly remains the main sign of GA1 for those who have no relatives with GA1 and have not been included in a population screening program. GA1 is considered a treatable disease.
Two-thirds of the patients who have GA1 encephalopathy will receive little benefit from the treatment for GA1 but can benefit from treatments given to victims of middle cerebral artery occlusion, AIDS dementia and other basal ganglia disorders: brain implants, stem cell neurorestoration, growth factors, monoaminergic agents, and many other neurorehabilitation strategies.
References
Further reading
Mahfoud Hawilou, Antonieta; Domínguez Méndez, Carmen Luisa; Rizzo, Cristiano; Ribes Rubio, Antonia (2004). "Macrocefalia in utero como manifestación clínica de aciduria glutárica tipo I. Informe de una nueva mutación" [In utero macrocephaly as clinical manifestation of glutaric aciduria type I. Report of a novel mutation]. Revista de Neurología (in Spanish). 39 (10): 939–942. doi:10.33588/rn.3910.2004258. PMID 15573311.
Martínez Granero MA, Garcia Pérez A, Martínez-Pardo M, Parra E (2005). "[Macrocephaly the first manifestation of glutaric aciduria type I: the importance of early diagnosis.]". Neurologia (in Spanish) |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Neuro fibrillary tangles is seen in and explain in detail? | (Alzheimer's disease) (910-HM) (894-Basic pathology 8th)* Deposition of A b amyloid derived from amyloid precursor protein (APP) forming neuritic senile, plaques and neurofibrillary tangles - features of ALZHEIMER'S DISEASE* Lewy bodies - hall marks of Parkinsonism |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Ideal urine specimen for anerobic culture should be ? and explain in detail? | Ans. is 'd' i.e., Sample by suprapubic aspiration Suprapubic aspiration is the preferred method of urine collection when anaerobic bacteria are suspected as cause of UTI. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Copper sulphate poisoning manifests with which of the following feature? and explain in detail? | Acute copper sulphate poisoning can manifest with acute hemolysis. The pathogenesis of this effect is not known but it may be related to copper induced oxidation of intracellular glutathione, hemoglobin and NADPH as well as inhibition of Glucose 6 phosphate dehydrogenase by copper. Patients with acute copper poisoning also presents with severe nausea, vomiting, thirst, metallic taste in mouth, burning pain and salivation. Oliguria, hematuria, uremia and albuminuria is also seen. Patients usually die of shock. Ref: Toxicology of Metals, Volume 1 edited by Louis W. Chang, page 941. Concise Textbook Of Forensic Medicine & Toxicology By Sharma page 267. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Lipogenesis in liver is stimulated by and explain in detail? | Insulin |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is After overnight fasting, levels of glucose transpoers reduced in and explain in detail? | GluT4 is the major glucose transpoer in skeletal muscle and adipose tissue.GluT4 is under the control of insulin.In Type 2 diabetes mellitus, membrane GluT4 is reduced, leading to insulin resistance in muscles and fat cells.Ref: DM Vasudevan, 7th edition, page no: 107 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Cervical hostility is tested by following except: and explain in detail? | Post coital test and miller kurzrok test can detect cervical hostility as noted by rotatory/shaky movement of the sperm in post coital test, or < 3 cm of penetration of cervical mucus in 30 minutes in miller kurzrok test.
Spinbarkeit is basically a test for assessing ovulation: At the time of ovulation, the cervical mucus is thin and so profuse that the patient may notice a clear discharge, (called Normal ovulatory cascade). This ovulatory mucus has the property of great elasticity and will withstand stretching up to a distance of over 10 cm. This phenomenon is called spinbarkeit, or thread test for oestrogen activity. Under the influence of progesterone after ovulation mucus becomes thick and opaque and breaks on stretching i.e. hostile for sperms
Therefore, indirectly Spinbarkeit test can also detect cervical hostility. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Small intestinal biopsy is diagnostic in and explain in detail? | .Whipple's triad: * An attack of hypoglycaemia in fasting state * Blood sugar below 45 mg% during the attack * Symptoms relieved by glucose ref:SRB&;s manual of surgery,ed 3,pg no 638 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Cells that are identified by the presence of immunoglobulins on the surface include? and explain in detail? | The B-cell receptor or BCR is a transmembrane receptor protein located on the outer surface of B cells. The B-cell receptor is composed of two pas: i) A membrane-bound immunoglobulin molecule of one isotype (IgD, IgM, IgA, IgG, or IgE). ii) Signal transduction moiety Reff : Ananthanarayan & Panikers textbook of microbiology 9th edition pg: 136 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 36 years old female patient attends the OG department and complains of dark spots in face over the past few years. She initially noticed it after her first child birth, five years earlier. The lesions become worse in the second pregnancy, two years back. She does not have any other medical problems. She was not on any drugs except for oral contraceptive pills. She does not appear to be stressed. Blood pressure- 120/76 mmHg, Pulse rate- 84/min, temperature- 37.6 C, Respiratory rate-16/ min. On her forehead, cheeks and chin, multiple, discrete confluent well demarcated patches of brown hypopigmentation are seen. Complete blood count ant thyroid profile tests are normal. The most appropriate advice is - and explain in detail? | Answer: c) Melasma may or may not return with each subsequent pregnancyMELASMAMelasma (Greek: "a black spot") is an acquired light- or dark-brown hyperpigmentation that occurs in the exposed areas, most often on the face, and results from exposure to sunlight.It may be associated with pregnancy, with ingestion of contraceptive hormones, or possibly with certain medications such as diphenylhydantoin or it may be idiopathic.Females > males; about 10% of patients with melasma are men.Common, especially among persons with constitutive brown skin color who are taking contraceptive regimens and who live in sunny areas.Pregnancy causes melasma.Melasma has recently been appearing in menopausal women as a result of regimens for prevention of osteoporosis using a combination of estrogens and progesterone;The pigmentation usually evolves quite rapidly over weeks, particularly after exposure to sunlight.Completely macular hyperpigmentation of the face, the hue and intensity depending largely on the skin phototype of the patientMost often symmetric.Lesions have serrated, irregular and geographic borders.Two-thirds on the central part of the face: cheeks, forehead, nose, upper lip, and chin; a smaller percentage on the malar or mandibular areas of the face and occasionally the dorsa of the forearms.May disappear spontaneously over a period of months after delivery or after cessation of contraceptive hormones.Melasma may or may not return with each subsequent pregnancy.Treatment with hydroquinone can lead to a permanent loss of melanocytes with the development of a disfiguring spotty leukoderma.Prevention: opaque sunblock containing titanium dioxide and/or zinc oxide.Even the potent transparent sunscreens (with high SPF) are completely ineffective in blocking visible radiation |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Following test is used to assess the warfarin dose? and explain in detail? | Ans. is 'd' i.e. PT/INR * Monitoring of unfractionated heparin - aPTT* Monitoring of oral anticoagulants - PT/INR* Monitoring of LMW heparins - No monitoring required |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Examination of a peripheral blood smear demonstrates leukemia composed of small mature lymphocytes without blast forms. Which of the following is the most likely age of this patient? and explain in detail? | The disease described is chronic lymphocytic leukemia (CLL), which is a disease of older adults. The 1 year-old (choice A) would be most likely to have acute lymphocytic leukemia (ALL). The 45 year-old (choice C) would be likely to have either AML or chronic myelogenous leukemia (CML). |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Quinolones are not effective in the treatment of and explain in detail? | None |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Direct immunofluorescence is positive in – and explain in detail? | None |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Roots involved in Erb's palsy are and explain in detail? | Erb's point is formed by the roots of C5 and C6, anterior and posterior divisions of upper trunk, suprascapular nerve and nerve to subclavius muscle. So the nerve root involved in Erb's palsy is C5 and C6. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is The occlusal outline of the permanent mandibular first molar is usually similar to and explain in detail? | None |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Arcuate field defect akin to glaucoma is seen in- and explain in detail? | Arcuate field defect akin to glaucoma seen in conditions which cause optic nerve compressions |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Most common serotype of HPV associated with cervical carcinoma is:- and explain in detail? | More than 90% of CIN is attributed to human papillomavirus (HPV) infection. Only ceain types of HPV cause high-grade intraepithelial lesions and cancer (HPV-16, -18, -31, -33, -35, -39, -45, -51, -52, -56, -58, -59, -68). Type 16 is the most common form of HPV found in invasive cancer and in CIN 2 and CIN3; HPV-18 is more specific than HPV-16 for invasive tumors i.e. HPV 18 is the most malignant. Please note: Usually, HPV infections do not persist. Most women who are exposed have no clinical evidence of disease, and the infection is eventually suppressed or eliminated. Other women exhibit low-grade cervical lesions that mostly regress spontaneously. In the vast majority of cases, the infection will clear in 9 to 15 months. A small minority of women exposed to HPV develops persistent infection that may progress to CIN. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Organism multiplying and developing in the hosts is called as and explain in detail? | Ans. a (Cyclopropagative).(Ref. Park, PSM, 17th/pg.543)BIOLOGIC TRANSMISSIONTypeDefinitionE-g.PropagativeDisease agent undergoes no cyclical change, but multiplies in the body of the vector,Plague bacillus (rat flea)Cyclo-propagativeDisease agent undergoes cyclical change and multiplies in the body of the vector.Malarial parasite (Anopheline mosquito)Cyclo-developmentalDisease agent undergoes cyclical change, but does not multiply in the body of the vector,Filarial parasite (culex mosquito),Guineaworm (cyclops) |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is SAFE strategy does not include which of the following? and explain in detail? | SAFE strategy includes
Surgery of lids
Antibiotics
Facial cleanliness
Environmental hygiene |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is All of the following are good prognostic factors for childhood. All except – and explain in detail? | Pre B cell ALL has poor prognosis. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 35-year-Old man presents with daily headache. He describes two attacks per day over the last 3 weeks. Each attack lasts about an hour and awakens him from sleep. The patient has noticed associated tearingand reddening of the right eye as well as nasal stuffness. The pain's deep, excruciating, and limiting to the right side of the head. The neurological examination is normal. What is the most likely diagnosis? and explain in detail? | Harrison's principles of internal medicine 17th edition . *Cluster headache is associated with ipsilateral symptoms of cranial parasympathetic autonomic activation:conjunctival injection or lacrimation ,rhinorrhea or nasal congestion ,cranial sympathetic dysfunction such as ptosis *Pain is deep,retroorbital ,excruciating in intensity nonfluctuating and explosive *Atleast one of the daily attack of pain recurs at about the same hour each day for the duration of a cluster bout. *Onset is nocturnal in about 50%patients and men are effected three times more than women . Ref Harrison20th edition pg 2245 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is " Polychromatic luster" is a feature of and explain in detail? | Ans. d (Complicated cataract) (Ref. Basak's ophthalmology 2nd ed., 181)COMPLICATED CATARACTS# It is a complication of any protracted intraocular inflammation, especially heterochromia, chronic iridocyclitis, retinal vasculitis, and retinitis pigmentosa.# Complicated cataract results from a disturbance of the lens metabolism due to inflammatory or degenerative diseases.# The result is a "pumice-like posterior subcapsular cataract" that progresses axially toward the nucleus.# Vision is much impaired even in early stage, due to position of the opacity near nodal point of eye.# The opacity usually commences in posterior cortex in the axial plane (posterior cortical cataract).# The opacity appears grayish with "bread-crumb" appearance in oblique illumination.# This form of cataract produces extreme light scattering.# On slit lamp, the opacity shows a characteristic rainbow display of colors, the polychromatic luster.# Rx: Operative and visual prognosis in complicated cataract is usually poor.Note: Riders ("spoke wheel") are seen in lamellar cataract, which is the most common type of congenital cataract. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Electric nerve tester detects pain by stimulating which nerve fibres (OR) Sharp, shooting pain in reversible pulpitis indicates stimulation of (OR) In pulp hyperemia which nerve fibers are stimulated and explain in detail? | None |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 20 year old male patient came with the complaint of a decrease in the urinary output to about 400ml/day. Both RBF and GFR were decreased. Which of the following causes a decrease in both RBF and GFR? and explain in detail? | Constriction of either the afferent or efferent aeriole increases resistance, and according to Equation Q = DP/R, an increase in resistance (R) decreases flow (Q) (i.e., RBF). Dilation of either the afferent or efferent aeriole increases flow (i.e., RBF). Constriction of the afferent aeriole (A) decreases P GC because less of the aerial pressure is transmitted to the glomerulus, thereby reducing GFR. Dilation of the afferent aeriole increases P GC because more of the aerial pressure is transmitted to the glomerulus, thereby increasing GFR.Reference: Berne and Levy Medical Physiology; 6th edition; Page no: 574 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Flail chest means fracture of: PGI 12 and explain in detail? | Ans. Four ribs on two sides |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Endolymphatic duct connects which structure and explain in detail? | Endolymphatic duct formed by the union of two ducts, one each from saccule and utricle. Surgically it is exposed for the drainage or shunt operation in Meniere&;s disease. Reference Dhingra 6th edition |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Exposure keratopathy is due to involvement of which cranial nerve: March 2012 and explain in detail? | Ans: D i.e. 7th cranial nerve Exposure keratopathy is due to any cause which may produce exposure of the cornea due to incomplete closure of the eyelids (lagophthalmos), such as extreme proptosis as in exophthalmic ophthalmoplegia or orbital tumour, paralysis of the orbicularis (neuroparalytic keratopathy etc.) Keratopathy Neurotrophic keratopathy (desquamation of corneal epithelium) occurs in some cases in which trigeminal nerve is paralyzed Neuroparalytic keratopathy is seen in facial nerve palsy as occurs in Bell's palsy, leprosy or neurological disorders leading to ectropion, lagophthalmos & exposure keratopathy |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Which hormone causes increased food intake- and explain in detail? | Ans. is 'd' i.e., Ghrelin * Ghrelin is released from the stomach in fasting state. It increases hunger by inhibiting the ventromedial hypothalamus (satiety center). It also stimulate GH secretions.AnorexigenicOrexigenic* Decrease feeding* Increase feeding* Secreted after taking meala* Secreted in response to starvation1) a-melanocyte stimulating hormone (a-MSH)1) Melanin-concentrating hormone2) Leptin2) Neuropeptide Y3) Serotonin3) Agouti-related protein (AGPP)4) Norepinephrine4) Orexins A and B5) Corticotropin-releasing hormone5) Endorphins6) Insulin6) Galanin (GAL)7) Cholecystokinin (CCK)7) Cortisol8) Glucagon-like peptide (GLP)8) Ghrelin9) Cocaine and amphetamine-regulated transcript (CART)9) Amino acids (glutamate and a-aminobutyric acid)10) Peptide YY (PYY)10) Endocannabinoid |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is True statement about physis and explain in detail? | Physis / growth plate is metabolically active part and has highest turnover in the bone.
Tensile strength to bone is given by strands of collagen.
Osteoclasts help in bone resorption. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Prostate Specific Antigen is specific to and explain in detail? | (D) All of the above# PSA is secreted by the epithelial cells of the prostate gland.> PSA is not a unique indicator of prostate cancer, but may also detect prostatitis or benign prostatic hyperplasia. Only 30 percent of patients with high PSA have prostate cancer diagnosed after biopsy.> PSA is used for Prostate cancer screening and levels between 4 and 10 ng/mL (nanograms per milliliter) are considered to be suspicious and confirm the abnormal PSA with a repeat test.> PSA levels are monitored periodically every 6-36 months after treatment for prostate cancer. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Hand foot mouth disease is caused by ? and explain in detail? | |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Complex-I in electron transpo chain is and explain in detail? | ETC Complex-I i. It is also called NADH-CoQ reductase or NADH dehydrogenase complex. It is tightly bound to the inner membrane of mitochondria. ii. It contains a flavoprotein (Fp), consisting of FMN as prosthetic group and an iron-sulfur protein (Fe-S). NADH is the donor of electrons, FMN accepts them and gets reduced to FMNH2 (Fig.19.8). Two electrons and one hydrogen ion are transferred from NADH to the flavin prosthetic group of the enzyme. NADH + H+ + FMN - FMNH2 Summary of Electron Flow in ETC Complex I: NADH NADH NADH -- - FMN FMN FMN - Complex II: Succinate Succinate Succinate - -- Fe-S Fe-S Fe-S - -- CoQ -- FAD FAD FAD - -- Fe-S Complex III: CoQ CoQ CoQ - -- Fe-S Fe-S Fe-S - Fe-S Fe-S - -- cyt.b cyt.b cyt.b - CoQ CoQ - - - -- CoQ CoQ CoQ - - - -- cyt.c1 cyt.c1 cyt.c1 - - - cyt. c Complex IV: Cyt. c Cyt. c Cyt. c - -- cyt a-a3 cyt a-a3 cyt a-a3 - -- O O O222 cyt. c cyt. c iii. The electrons from FMNH2 are then transferred to Fe-S. The electrons are then transferred to coenzyme Q (ubiquinone) (CoQ). iv. The overall function of this complex is to collect the pair of electrons from NADH and pass them to CoQ. The reactions are shown in Fig. 19.8. v. There is a large negative free energy change; the energy released is 12 kcal/mol. This is utilized to drive 4 protons out of the mitochondriaRef: DM Vasudevan Textbook of Medical Biochemistry, 6th edition, page no: 228 |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is All of the following aeries are common sites of occlusion by a thrombus except: and explain in detail? | D i.e. Marginal Nodal, Acute Marginal & Posterior Descending (interventricular) aeryQ are branches of Right Coronary aery; whereas Circumflex, Diagonal, Obtuse Marginal & Anterior Descending (interventricular) aeryQ are branches of Left Coronary Aery. LAD, RCA and LCX are common whereas as marginal branches are uncommon site of thrombosis. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is Radioprotective drug is – and explain in detail? | Amifostine (WR - 2721) is one of today's most widely studied radioprotector. |
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. | What is A 50 years old male presents with massive splenomegaly. His differential diagnosis will include all, except and explain in detail? | Diseases Associated with massive splenmegaly.
Chronic myclogenous leukemia
Gaucher's disease
Lymphomas
Chronic lymphocytic leukemia
Hairy cell leukemia
Sarcoidosis
Myelofibrosis with myeloid metaplasia
Autoimmune hemolytic anemia
Polycythemia vera
Diffuse splenic human giomatosis |