Persius/hicric huggingface dataset:
Exercise hypertension
Exercise hypertension is an excessive rise in blood pressure during exercise. Many of those with exercise hypertension have spikes in systolic pressure to 250 mmHg or greater.
A rise in systolic blood pressure to over 200 mmHg when exercising at 100 W is "pathological", and a rise in pressure over 220 mmHg needs to be controlled by the appropriate drugs.
Similarly, in healthy individuals the response of the diastolic pressure to 'dynamic' exercise (walking, running) of moderate intensity is to remain constant or to fall slightly (due to the improved blood flow), but in some individuals a rise of 10 mmHg or greater is found.
Recent work at Johns Hopkins involving a group of athletes aged 55 to 75 with mild hypertension has found a correlation of those with exercise hypertension to a reduced ability of the major blood vessels to change in size in response to increased blood flow (probably due to impaired function of the endothelial cells in the vessel walls). This is to be differentiated from stiffness of the blood-vessel walls, which was not found to be correlated with the effect.
Exophthalmos overview

# Overview
Exophthalmos is a bulging of the eye anteriorly out of the orbit. Some sources define exophthalmos as a protrusion of the globe greater than 18 mm and proptosis as a protusion equal to or less than 18 mm. (Epstein et al, 2003). Others define "exophthalmos" as protusion secondary to endocrine dysfunction and "proptosis" as any non-endocrine-mediated protusion .
Exophthalmos can be either bilateral (as is often seen in Grave's Disease) or unilateral (as is often seen in an orbital tumor).  Measurement of the degree of exophthalmos is performed using an exophthalmometer. Complete or partial dislocation from the orbit is also possible from trauma or swelling of surrounding tissue resulting from trauma.
In the case of Graves Disease, the displacement of the eye is due to abnormal connective tissue deposition in the orbit and extraocular muscles which can be visualized by CT or MRI.

# Reference
-  Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016
-  Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X
-  Owen Epstein, David Perkin, John Cookson, David P de Bono (2003). Clinical examination (3rd edition ed.). St. Louis: Mosby. ISBN 0-7234-3229-5. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link) CS1 maint: Extra text (link) .mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
External iliac artery
The external iliac artery is a large artery in the pelvic region that carries blood to the lower limb.
The external iliac artery is a paired artery, meaning there is one on each side of the body: a right external iliac artery and left external iliac artery.
The external iliac artery arises from the bifurcation of the common iliac artery.  It travels inferiorly, anteriorly, and laterally, making its ways to the lower limb:
The external iliac artery is accompanied by the external iliac vein, which is located posterior to the artery.

# Additional images
- The internal mammary artery and its branches.
- Dissection of side wall of pelvis showing sacral and pudendal plexuses.
- Sacral plexus of the right side.
- Posterior view of the anterior abdominal wall in its lower half. The peritoneum is in place, and the various cords are shining through.
- The spermatic cord in the inguinal canal.
- Front of abdomen, showing surface markings for arteries and inguinal canal.
External jugular vein
The external jugular vein receives the greater part of the blood from the exterior of the cranium and the deep parts of the face, being formed by the junction of the posterior division of the posterior facial with the posterior auricular vein.
It commences in the substance of the parotid gland, on a level with the angle of the mandible, and runs perpendicularly down the neck, in the direction of a line drawn from the angle of the mandible to the middle of the clavicle at the posterior border of the Sternocleidomastoideus.
In its course it crosses the Sternocleidomastoideus obliquely (does it cross it anteriorly?), and in the subclavian triangle perforates the deep fascia, and ends in the subclavian vein(does it ever end in the brachiocephalic trunk on the right?), lateral to or in front of the Scalenus anterior.
It is separated from the Sternocleidomastoideus by the investing layer of the deep cervical fascia, and is covered by the Platysma, the superficial fascia, and the integument; it crosses the cutaneous cervical nerve, and its upper half runs parallel with the great auricular nerve.
The external jugular vein varies in size, bearing an inverse proportion to the other veins of the neck, it is occasionally double.
It is provided with two pairs of valves, the lower pair being placed at its entrance into the subclavian vein, the upper in most cases about 4 cm. above the clavicle. The portion of vein between the two sets of valves is often dilated, and is termed the sinus.
These valves do not prevent the regurgitation of the blood, or the passage of injection from below upward.

## Tributaries
This vein receives the occipital occasionally, the posterior external jugular, and, near its termination, the transverse cervical, transverse scapular, and anterior jugular veins; in the substance of the parotid, a large branch of communication from the internal jugular joins it.

# Additional images
- Muscles of the head, face, and neck.
- Section of the neck at about the level of the sixth cervical vertebra.
- Diagram showing completion of development of the parietal veins.
- The veins of the neck, viewed from the front.
- The ven cav and azygos veins, with their tributaries.
- Scheme showing relative positions of primary lymph sacs.
Transcutaneous pacing
Synonyms and keywords: External pacing

# Overview
Transcutaneous pacing is a temporary means of pacing a patient's heart during a medical emergency. It is accomplished by delivering pulses of electric current through the patient's chest, which stimulates the heart to contract.

# Indications
The most common indication for transcutaneous pacing is an abnormally slow heart rate. By convention, a heart rate of less than 60 beats per minute in the adult patient is called bradycardia. Not all bradycardias require medical treatment. Many athletes have a slow resting heart rate. In addition, the heart rate is known to slow down with age. It is only when bradycardia causes signs and symptoms of shock that it requires emergency treatment with transcutaneous pacing.
Some common causes of hemodynamically significant bradycardia include acute myocardial infarction, sinus node dysfunction and complete heart block. Transcutaneous pacing is no longer indicated for the treatment of asystole (cardiac arrest associated with a "flat line" on the ECG), with the possible exception of witnessed asystole (as in the case of bifascicular block that progresses to complete heart block without an escape rhythm).

# Techniques
During transcutaneous pacing, pads are placed on the patient's chest, either in the anterior/lateral position or the anterior/posterior position. The anterior/posterior position is preferred as it minimizes transthoracic impedance by "sandwiching" the left ventricle between the two pads. The pads are then attached to a monitor/defibrillator, a heart rate is selected, and current (measured in milliamps) is increased until electrical capture (characterized by a wide QRS complex with tall, broad T wave on the ECG) is obtained, with a corresponding pulse. Pacing artifact on the ECG and severe muscle twitching may make this determination difficult. It is therefore advisable to use another instrument (e.g. SpO2 monitor or bedside doppler) to confirm mechanical capture.

# Disadvantages
Transcutaneous pacing may be uncomfortable for the patient. Sedation should therefore be considered. Prolonged transcutaneous pacing may cause burns on the skin. It is meant to stabilize the patient until a more permanent means of pacing is achieved.

# Others
Other forms of cardiac pacing are transvenous pacing, epicardial pacing, and permanent pacing with an implantable pacemaker.
Forceps in childbirth

# Overview
Forceps can be used to assist the delivery of a baby as an alternative to the ventouse method.

# Technique
The cervix must be fully dilated and the bladder emptied, perhaps with the use of a catheter.  Since mid-forceps and high forceps are rarely performed in this era, the station of the head must be at least +2. The woman is placed in the lithotomy position and a mild anaesthetic is administered (unless an epidural has been given). It is very important that adequate pain control is achieved.  After ascertaining the precise position of the fetal head (by accurately feeling the posterior fontanelle), the two sections of the forceps are individually inserted and then locked into position around the baby's head.  The fetal head is then rotated to occiput anterior position if it is not already in this position. An episiotomy is performed and then the baby is delivered.

# Possible indicating factors
- Fetal or maternal distress
- If the baby is not delivering despite maternal effort
- When (further) pushing is contra-indicated
- Arterial hypertension (high blood pressure)

# Comparisons to other forms of assisted delivery

### Positive aspects
- Can be performed even if the baby is not in the correct position, although not if the head is presenting high in the vaginal canal
- Can be used to avoid caesarean delivery
- Delivery of the infant can occur more quickly than with emergency caesarean surgery

### Negative aspects
- An episiotomy is usually required which itself involves anesthesia
- The internal tissues, particularly the pelvic floor muscles, are bruised
- Women with a previous history of sexual abuse have reported feeling as though they were raped after instrumental deliveries
- A rectovaginal fistula can result, where fecal material leaks from the bowel into the vagina
- Facial bruising or temporary marks on the baby
- Nerve damage
- Skull fractures
- Cervical cord injury to the baby that results in the baby being unable to breathe unassisted
- Brain damage which can cause mild to severe mental retardation

# History
Modern obstetrical forceps were invented by Peter Chamberlen around 1600 and kept a family secret for several generations. About 1730 the secret leaked out and a public design of the instrument became available. The first illustration of the forceps was published by Edward Hody in 1734. Forceps had a profound influence on obstetrics as it allowed for the speedy delivery of the baby in cases of difficult or obstructed labor. Kedarnath Das of Calcutta described over 550 varieties of the intrument in 1929 In the last decades, however, with the ability to perform a cesarean section relatively safely, use of forceps and training in the technique of its use has sharply declined.
Fecal bacteriotherapy
Fecal bacteriotherapy, also known as fecal transfusion, fecal transplant, or human probiotic infusion (HPI), is a medical treatment in which bacteria from feces of a healthy person are transferred into the large bowel and rectum of a patient.  It is an alternative treatment for patients with pseudomembranous colitis (caused by Clostridium difficile), ulcerative colitis and irritable bowel syndrome.

# Description of procedure
The procedure itself involves a 5 to 10 day treatment with enemas, made of bacterial flora from feces of a healthy donor (who needs to be tested for a wide array of bacterial and parasitic agents). The enemas are prepared and administered in a hospital environment to ensure all necessary precautions.  Regular checkups are required up to a year following the procedure.

# Theoretical basis
The hypothesis behind fecal bacteriotherapy is that ulcerative colitis may, like in the case of pseudomembranous colitis, be a previous infection by a still unidentified pathogen which somehow damages the healthy bacterial flora of the colon, causing a bacterial imbalance, which then proceeds to reinfect and damage the colon in an endless cycle which can be broken by "recolonizing" the colon with bacteria from a healthy bowel.  This may be considered an extension of probiotic research.

# Effectiveness
The procedure has been used to successfully cure C. difficile infections for a number of years, with a success rate of nearly 95% according to some sources.
While its effects on ulcerative colitis have not yet been adequately researched, small case series suggest it has positive effects.  A recent article by Dr. Borody in which he details 6 cases of severe chronic ulcerative colitis treated using Fecal bacteriotherapy suggests that the procedure may be extremely successful in these cases as well. Complete reversal of symptoms was achieved in all patients by 4 months post-HPI, by which time all other UC medications had been ceased. At 1 to 13 years post-HPI and without any UC medication, there was no clinical, colonoscopic, or histologic evidence of UC in any patient.  The Sydney group also reports a case of presumed sclerosing cholangitis, a disease frequently associated with IBD, which recovered fully after the treatment.

# History
It has been developed in recent years by Dr. Thomas J. Borody and his team in Sydney, Australia, primarily as an alternative treatment for pseudomembranous colitis.  This disease is caused by C. difficile infection, and is typically treated with antibiotics.
Fexofenadine overdose

# Overdosage topics
Signs of overdose
Treatment
Hemodialysis
Mortality

## Signs of overdose
Reports of fexofenadine hydrochloride overdose have been infrequent and contain limited
information. However, dizziness, drowsiness, and dry mouth have been reported. Single doses of fexofenadine hydrochloride up to 800 mg (six normal volunteers at this dose level), and doses up to 690 mg twice daily for 1 month (three normal volunteers at this dose level) or 240 mg once daily for 1 year (234 normal volunteers at this dose level) were administered without the development of clinically significant adverse events as compared to placebo. Return to top

## Treatment
In the event of overdose, consider standard measures to remove any unabsorbed drug.
Symptomatic and supportive treatment is recommended. Return to top

## Hemodialysis
Hemodialysis did not effectively remove fexofenadine hydrochloride from blood (1.7% removed) following terfenadine administration. Return to top

## Mortality
No deaths occurred at oral doses of fexofenadine hydrochloride up to 5000 mg/kg in mice (110 times the maximum recommended daily oral dose in adults and 200 times the maximum recommended daily oral dose in children based on mg/m2) and up to 5000 mg/kg in rats (230 times the maximum recommended daily oral dose in adults and 400 times the maximum recommended daily oral dose in children based on mg/m2). Additionally, no clinical signs of toxicity or gross pathological findings were observed. In dogs, no evidence of toxicity was observed at oral doses up to 2000 mg/kg (300 times the maximum recommended daily oral dose in adults and 530 times the maximum recommended daily oral dose in children based on mg/m2). Return to top
Adapted from the FDA Package Insert.
First pharyngeal arch

# Overview
The first branchial arch, also called the first pharyngeal arch and mandibular arch, is the first of six branchial arches that develops in fetal life.  It is located between the stomodeum and the first pharyngeal groove.

# Processes
This arch divides into a maxillary process and a mandibular process, giving rise to structures including the bones of the lower two-thirds of the face and the jaw.  The maxillary process becomes the maxilla (or upper jaw), and palate while the mandibular process becomes the lower jaw. This arch also gives rise to the muscles of mastication.
Innervation of the two processes of the first branchial arch is provided by two distinct branches of the trigeminal nerve (CN V), the mandibular and maxillary branches. The artery of the first arch is the first aortic arch, which partially persists as the maxillary artery.

# Meckel's cartilage
Meckel's cartilage forms in the mesoderm of the mandibular process and eventually regresses to form the incus and malleus of the middle ear; the anterior ligament of the malleus and the sphenomandibular ligament. The mandible or lower jaw forms by intramembranous ossification using Meckel's cartilage as a 'template', but the mandible does not arise from direct ossification of Meckel's cartilage.

# Derivatives of the first arch
Derivatives of the first arch:
- Ectodermal and endodermal
mucous membrane and glands of the anterior two thirds of the tongue
- mucous membrane and glands of the anterior two thirds of the tongue
- Mesodermal
muscles of mastication (chewing)
masseter
pterygoid muscles
temporalis muscles
mylohyoid muscle
digastric muscle, anterior belly
tensor palati muscle
tensor tympani muscle
- muscles of mastication (chewing)
masseter
pterygoid muscles
temporalis muscles
- masseter
- pterygoid muscles
- temporalis muscles
- mylohyoid muscle
- digastric muscle, anterior belly
- tensor palati muscle
- tensor tympani muscle

# Additional images
- Human embryo from thirty-one to thirty-four days.
- Head end of human embryo, about the end of the fourth week.
- Floor of pharynx of embryo between 18 and 21 days.
- Head end of human embryo of about thirty to thirty-one days.
- The head and neck of a human embryo thirty-two days old, seen from the ventral surface.
Flash pulmonary edema
In medicine, flash pulmonary edema (FPE), is rapid onset pulmonary edema.  It is most often precipitated by acute myocardial infarction or mitral regurgitation, but can be caused by aortic regurgitation, heart failure, or almost any cause of elevated left ventricular filling pressures.
Treatment of FPE should be directed  at the underlying cause, but the mainstays are ensuring adequate oxygenation, diuresis, and decrease of pulmonary circulation pressures.
Reoccurrence of FPE is thought to be associated with hypertension and may signify renal artery stenosis. Prevention of reoccurrence is based on managing hypertension, coronary artery disease, renovascular hypertension, and heart failure.

# Reference
-  Kramer K, Kirkman P, Kitzman D, Little WC. Flash pulmonary edema: association with hypertension and reoccurrence despite coronary revascularization. Am Heart J. 2000 Sep;140(3):451-5. PMID 10966547.
-  Pickering TG, Herman L, Devereux RB, Sotelo JE, James GD, Sos TA, Silane MF, Laragh JH. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. Lancet 1988;2(8610):551-2. PMID 2900930.
Flushing (physiology)
For a person to flush is to become markedly red in the face and often other areas of the skin, from various physiological conditions. Flushing is generally distinguished, despite a close physiological relation between them, from blushing, which is milder, generally restricted to the face or cheeks, and generally assumed to reflect embarrassment. Flushing is also a cardinal symptom of carcinoid syndrome  the syndrome that results from hormones (often serotonin or histamine) being secreted into systemic circulation.

# Causes of flushing
- sexual arousal (see section to follow)
- emotions: anger, embarrassment
- an abrupt cessation of physical exertion (resulting in heart output in excess of current muscular need for blood flow)
- physiological response to vasodilators, for instance, a recent high dose of niacin, nitroglycerine, calcium channel blockers, or any drug that causes release of adrenal hormones that raise blood pressure such as stimulants
- post-menopausal decrease in estrogen production
- anaphylaxis
- neuroendocrine tumors: carcinoid syndrome, pheochromocytoma, VIPoma, thyroid medullary carcinoma
- mast cell tumor: mastocytosis
- Various psychedelics or other drugs, such as 3-Quiniclidinyl Benzilate(BZ) or Alcohol
- dehydration
- anxiety
- limerence
- Heat
- Topical Retinoids

# Sex flush
Commonly referred to as the sex flush, vasocongestion (increased blood flow) of the skin can occur during all four phases of the human sexual response cycle. Studies show that the sex flush occurs in approximately 50-75% of females and 25% of males, yet not consistently. The sex flush tends to occur more often under warmer conditions and may not appear at all under cooler temperatures. It has also been commonly observed that the marked degree of the sex flush can predict the intensity of orgasm to follow.
During the female sex flush, pinkish spots develop under the breasts, then spread to the breasts, torso, face, hands, soles of the feet, and possibly over the entire body. Vasocongestion is also responsible for the darkening of the clitoris and the walls of the vagina during sexual arousal. During the male sex flush, the coloration of the skin develops less consistently than in the female, but typically starts with the epigastrium (upper abdomen), spreads across the chest, then continues to the neck, face, forehead, back, and sometimes, shoulders and forearms.
The sex flush typically disappears soon after orgasm occurs, but this may take up to two hours or so, and sometimes, intense sweating will occur simultaneously. The flush usually diminishes in reverse of which it appeared.