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Flashcards in HIGHEST YIELD 4 Deck (26)
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Cushing's disease (also known as Cushing disease, tertiary or secondary hypercortisolism, tertiary or secondary hypercorticism, Itsenko-Cushing disease)

- is a cause of Cushing's syndrome characterised by increased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary (secondary hypercortisolism).

- This is most often as a result of a pituitary adenoma (specifically pituitary basophilism) or due to excess production of hypothalamus CRH (Corticotropin releasing hormone) (tertiary hypercortisolism/hypercorticism) that stimulates the synthesis of cortisol by the adrenal glands.

- Pituitary adenomas are responsible for 80% of endogenous Cushing's syndrome, when excluding Cushing's syndrome from exogenously administered corticosteroids.

- This should not be confused with ectopic Cushing syndrome or exogenous steroid use.


Cushing's disease

- usually present with one or more signs and symptoms secondary to the presence of excess cortisol or ACTH.

- Although uncommon, some patients with Cushing's disease have large pituitary tumors (macroadenomas).

- In addition to the severe hormonal effects related to increase blood cortisol levels, the large tumor can compress adjacent structures. These tumors can compress the nerves that carry information from the eyes, causing a decrease in peripheral vision.

- Glaucoma and cataracts also may occur in Cushing's syndrome. In children, the two main symptoms are obesity and decreased linear growth.

- The most common symptoms seen in male patients are purple striae, muscle atrophy, osteoporosis, and kidney stones.


Sheehan syndrome,

- also known as Simmond syndrome, postpartum hypopituitarism or postpartum pituitary gland necrosis, is hypopituitarism (decreased functioning of the pituitary gland), caused by ischemic necrosis due to blood loss and hypovolemic shock during and after childbirth.

Most common initial symptoms of Sheehan's syndrome are agalactorrhea (absence of lactation) and/or difficulties with lactation.

Many women also report amenorrhea or oligomenorrhea after delivery.

In some cases, a woman with Sheehan syndrome might be relatively asymptomatic, and the diagnosis is not made until years later, with features of hypopituitarism. Such features include secondary hypothyroidism with tiredness, intolerance to cold, constipation, weight gain, hair loss and slowed thinking, as well as a slowed heart rate and low blood pressure.

Another such feature is secondary adrenal insufficiency, which, in the rather chronic case is similar to Addison's disease with symptoms including fatigue, weight loss, hypoglycemia (low blood sugar levels), anemia and hyponatremia (low sodium levels). Such a woman may, however, become acutely exacerbated when her body is stressed by, for example, a severe infection or surgery years after her delivery, a condition equivalent with an Addisonian crisis. The symptoms of adrenal crisis should be treated immediately and can be life-threatening -

- Gonadotropin deficiency will often cause amenorrhea, oligomenorrhea, hot flushes, or decreased libido.

- Growth hormone deficiency causes many vague symptoms including fatigue and decreased muscle mass


Sheehan syndrome,

Hypertrophy and hyperplasia of lactotrophs during pregnancy results in the enlargement of the anterior pituitary, without a corresponding increase in blood supply.

Secondly, the anterior pituitary is supplied by a low pressure portal venous system.[7]

These vulnerabilities, when affected by major hemorrhage or hypotension during the peripartum period, can result in ischaemia of the affected pituitary regions leading to necrosis.

The posterior pituitary is usually not affected due to its direct arterial supply.


Addison’s disease (also Addison disease, chronic adrenal insufficiency, hypocortisolism, and hypoadrenalism)

- is a rare, chronic endocrine system disorder in which the adrenal glands do not produce sufficient steroid hormones (glucocorticoids and mineralocorticoids).

- It is characterised by a number of relatively nonspecific symptoms, such as abdominal pain and weakness, but under certain circumstances, these may progress to Addisonian crisis, a severe illness which may include very low blood pressure and coma.

- The condition arises from problems with the adrenal gland, primary adrenal insufficiency, and can be caused by damage by the body's own immune system, certain infections, or various rarer causes.

- Addison's disease is also known as chronic primary adrenocortical insufficiency, to distinguish it from acute primary adrenocortical insufficiency, most often caused by Waterhouse–Friderichsen syndrome.

- Addison's disease should also be distinguished from secondary and tertiary adrenal insufficiency, which are caused by deficiency of ACTH (produced by the pituitary gland) and CRH (produced by the hypothalamus), respectively. Despite this distinction, Addisonian crises can happen in all forms of adrenal insufficiency.

- Addison's disease and other forms of hypoadrenalism are generally diagnosed via blood tests and medical imaging.Treatment involves replacing the absent hormones (oral hydrocortisone and fludrocortisone).


The submucous plexus, (Meissner's plexus, plexus of the submucosa, plexus submucosus)

lies in the submucosa of the intestinal wall. The nerves of this plexus are derived from the myenteric plexus which itself is derived from the plexuses of parasympathetic nerves around the superior mesenteric artery. Branches from the myenteric plexus perforate the circular muscle fibers to form the submucous plexus. Ganglia from the plexus extend into the muscularis mucosae and to the mucous membrane.

They contain Dogiel cells. The nerve bundles of the submucous plexus are finer than those of the myenteric plexus. Its function is to innervate cells in the epithelial layer and the smooth muscle of the muscularis mucosae.

14% of submucosal plexus neurons are sensory neurons - Dogiel type II, also known as enteric primary afferent neurones or intrinsic primary afferent neurons


The myenteric plexus (or Auerbach's plexus)

- provides motor innervation to both layers of the muscular layer, having both parasympathetic and sympathetic input, whereas the submucous plexus has only parasympathetic fibers and provides secretomotor innervation to the mucosa nearest the lumen of the gut.

- It arises from cells in the vagal trigone also known as the nucleus ala cinerea, the parasympathetic nucleus of origin for the tenth cranial nerve (vagus nerve), located in the medulla oblongata. The fibers are carried by both the anterior and posterior vagal nerves. The myenteric plexus is the major nerve supply to the gastrointestinal tract and controls GI tract motility.[1]


The myenteric plexus (or Auerbach's plexus)

The myenteric plexus originates in the medulla oblongata as a collection of neurons from the ventral part of the brain stem. The vagus nerve then carries the axons to their destination in the gastrointestinal tract.[4]

They contain Dogiel cells.

The enteric nervous system makes use of over 30 different neurotransmitters, most similar to those of the CNS such as acetylcholine, dopamine, and serotonin.

- More than 90% of the body's serotonin lies in the gut; as well as about 50% of the body's dopamine, which is currently being studied to further our understanding of its utility in the brain.

- The heavily studied neuropeptide known as substance P is present in significant levels and may help facilitate the production of saliva, smooth muscle contractions, and other tissue responses.


Hunger pangs

When hunger contractions start to occur in the stomach, they are informally referred to as hunger pangs.

Hunger pangs usually do not begin until 12 to 24 hours after the last ingestion of food.

A single hunger contraction lasts about 30 seconds, and pangs continue for around 30 to 45 minutes, then hunger subsides for around 30 to 150 minutes.

Individual contractions are separated at first, but are almost continuous after a certain amount of time.

Emotional states (anger, joy etc.) may inhibit hunger contractions.

Levels of hunger are increased by lower blood sugar levels, and are higher in diabetics.

They reach their greatest intensity in three to four days and may weaken in the succeeding days, although research suggests that hunger never disappears.

Hunger contractions are most intense in young, healthy people who have high degrees of gastrointestinal tonus. Periods between contractions increase with old age.


Hunger pangs

Biological mechanisms

The fluctuation of leptin and ghrelin hormone levels results in the motivation of an organism to consume food.

When an organism eats, adipocytes trigger the release of leptin into the body. Increasing levels of leptin result in a reduction of one's motivation to eat.

After hours of non-consumption, leptin levels drop significantly. These low levels of leptin cause the release of a secondary hormone, ghrelin, which in turn reinitiates the feeling of hunger.


The interstitial cell of Cajal (ICC)

is a type of interstitial cell found in the gastrointestinal tract. There are different types with different functions. Myenteric Interstitial cells of Cajal [ICC-MY] serve as a pacemaker which creates the bioelectrical slow wave potential that leads to contraction of the smooth muscle.


The interstitial cell of Cajal (ICC)

The frequency of ICC pacemaker activity differs in different regions of the GI tract:

3 per minute in the stomach
11-12 per minute in the duodenum
9-10 per minute in the ileum
3-4 per minute in the colon



also known as EPO, is a glycoprotein hormone that controls erythropoiesis, or red blood cell production. It is a cytokine (protein signaling molecule) for erythrocyte (red blood cell) precursors in the bone marrow. Human EPO has a molecular weight of 34 kDa.

Also called hematopoietin or hemopoietin,

it is produced by interstitial fibroblasts in the kidney in close association with peritubular capillary and proximal convoluted tubule.

It is also produced in perisinusoidal cells in the liver.

While liver production predominates in the fetal and perinatal period, renal production is predominant during adulthood. In addition to erythropoiesis, erythropoietin also has other known biological functions. For example, it plays an important role in the brain's response to neuronal injury.

EPO is also involved in the wound healing process.



In humans, chromosomal abnormalities arising from incorrect spermatogenesis results in congenital defects and abnormal birth defects (Down Syndrome, Klinefelter's Syndrome) and in most cases, spontaneous abortion of the developing fetus.

The process of spermatogenesis is highly sensitive to fluctuations in the environment, particularly hormones and temperature. Testosterone is required in large local concentrations to maintain the process, which is achieved via the binding of testosterone by androgen binding protein present in the seminiferous tubules. Testosterone is produced by interstitial cells, also known as Leydig cells, which reside adjacent to the seminiferous tubules.

If the pituitary gland is removed, spermatogenesis can still be initiated by follicle stimulating hormone and testosterone.

Follicle stimulating hormone stimulates both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier.

Androgen binding protein is essential to concentrating testosterone in levels high enough to initiate and maintain spermatogenesis, which can be 20–50 times higher than the concentration found in blood.

Follicle stimulating hormone may initiate the sequestering of testosterone in the testes, but once developed only testosterone is required to maintain spermatogenesis.

However, increasing the levels of follicle stimulating hormone will increase the production of spermatozoa by preventing the apoptosis of type A spermatogonia. The hormone inhibin acts to decrease the levels of follicle stimulating hormone.



- is one of many neurotransmitters in the autonomic nervous system (ANS).

- It acts on both the peripheral nervous system (PNS) and central nervous system (CNS) and is the only neurotransmitter used in the motor division of the somatic nervous system.

- Acetylcholine is also the principal neurotransmitter in all autonomic ganglia.

- In cardiac tissue acetylcholine neurotransmission has an inhibitory effect, which lowers heart rate. However, acetylcholine also behaves as an excitatory neurotransmitter at neuromuscular junctions in skeletal muscle.



stimulates the adrenal medulla release of norepinephrine.

Acetylcholine released by preganglionic sympathetic fibers of splanchnic nerves acts on nicotinic acetylcholine receptors, causing cell depolarization and an influx of calcium through voltage-gated calcium channels.

Calcium triggers the exocytosis of chromaffin granules and, thus, the release of adrenaline (and noradrenaline) into the bloodstream.

In the basal forebrain, it originates from the basal optic nucleus of Meynert and medial septal nucleus:

Damage to the cholinergic (acetylcholine-producing) system in the brain has been shown to be plausibly associated with the memory deficits associated with Alzheimer's diseases

ACh has also been shown to promote REM sleep.

Recently, it has been suggested that acetylcholine disruption may be a primary cause of depression.

Acetylcholine is synthesized in certain neurons by the enzyme choline acetyltransferase from the compounds choline and acetyl-CoA. Cholinergic neurons are capable of producing ACh. An example of a central cholinergic area is the nucleus basalis of Meynert in the basal forebrain.

The enzyme acetylcholinesterase converts acetylcholine into the inactive metabolites choline and acetate.


The alpha-2 (α2) adrenergic receptor (or adrenoceptor)

is a G protein-coupled receptor (GPCR) associated with the Gi heterotrimeric G-protein.

The α subunit of an inhibitory G protein - Gi dissociated from the G protein, and associates with adenyl cyclase (also known as adenylate cyclase or adenylyl cyclase).

This causes the inactivation of adenyl cyclase, resulting in a decrease of cAMP produced from ATP. This leads to a decrease of intracellular cAMP.

Protein Kinase A is not able to be activated by cAMP, so proteins such as phosphorylase kinase cannot be phosphorylated by PKA. In particular, phosphorylase kinase is responsible for the phosphorylation and activation of glycogen phosphorylase, an enzyme necessary for glycogen breakdown. Thus in this pathway, the downstream effect of adenyl cyclase inactivation is decreased breakdown of glycogen.


Ménière's disease

also called endolymphatic hydrops, is a disorder of the inner ear that can affect hearing and balance to a varying degree. It is characterized by episodes of vertigo, tinnitus, and hearing loss.

The hearing loss comes and goes for some time, alternating between ears, then becomes permanent with no return to normal function.



Functional residual capacity (FRC) cannot be measured via spirometry, but it can be measured with a plethysmograph or dilution tests (for example, helium dilution test).


LGICs vs voltage-gated ion channels

LGICs can be contrasted with metabotropic receptors (which use second messenger activated ion channels), voltage-gated ion channels (which open and close depending on membrane potential), and stretch-activated ion channels (which open and close depending on mechanical deformation of the cell membrane).


high altitude aka acclimatization

One gene in particular, ADAM-17, is known to be involved in regulating response to low oxygen levels that is also found in Tibetan highlanders.


Acclimatization to altitude

The human body can adapt to high altitude through both immediate and long-term acclimatization. At high altitude, in the short term, the lack of oxygen is sensed by the carotid bodies, which causes an increase in the breathing rate (hyperventilation). However, hyperventilation also causes the adverse effect of respiratory alkalosis, inhibiting the respiratory center from enhancing the respiratory rate as much as would be required. Inability to increase the breathing rate can be caused by inadequate carotid body response or pulmonary or renal disease.

In addition, at high altitude, the heart beats faster; the stroke volume is slightly decreased; and non-essential bodily functions are suppressed, resulting in a decline in food digestion efficiency (as the body suppresses the digestive system in favor of increasing its cardiopulmonary reserves)

Full acclimatization, however, requires days or even weeks. Gradually, the body compensates for the respiratory alkalosis by renal excretion of bicarbonate, allowing adequate respiration to provide oxygen without risking alkalosis. It takes about four days at any given altitude and can be enhanced by drugs such as acetazolamide. Eventually, the body has lower lactate production (because reduced glucose breakdown decreases the amount of lactate formed), decreased plasma volume, increased hematocrit (polycythemia), increased RBC mass, a higher concentration of capillaries in skeletal muscle tissue, increased myoglobin, increased mitochondria, increased aerobic enzyme concentration, increase in 2,3-BPG, hypoxic pulmonary vasoconstriction, and right ventricular hypertrophy. Pulmonary artery pressure increases in an effort to oxygenate more blood.

Full hematological adaptation to high altitude is achieved when the increase of red blood cells reaches a plateau and stops. The length of full hematological adaptation can be approximated by multiplying the altitude in kilometers by 11.4 days. For example, to adapt to 4,000 metres (13,000 ft) of altitude would require 45.6 days. The upper altitude limit of this linear relationship has not been fully established.


enzyme that converts testosterone to estradiol.
estradiol is required for the development of female secondary sex characteristics BUT NOT MALE CHARACTERISTICS

AROMATASE DEFICIENCY (only in females)


converts 17-alpha-hydroxypregnenolone to 17-alpha-hydroxyprogesterone, pregnenolone to progesterone, dehydroepiandrosterone to androsterone, pregnenolone to progesterone, dehydroepiandrosterone to androstenedione and androstenediol to testosterone



converts 11-deoxycorticosterone to corticosterone and 11-deoxycortisol to cortisol



pregnenolone to 17-alpha-hydroxypregnenolone and progesterone to 17-alpha-hydroxyprogesterone