Vasopressin Flashcards

1
Q

also known as vasopressin, argipressin or antidiuretic hormone (ADH)

A

Arginine vasopressin (AVP)

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2
Q

Vasopressin is a peptide hormone. It is derived from a ________________ precursor that is synthesized in the hypothalamus and stored in vesicles at the posterior pituitary. Most of it is stored in the posterior pituitary to be released into the blood stream; however, some of it is also released directly into the brain.

A

preprohormone

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3
Q

 It is a nonapeptide that acts on the DCT and collecting tubule of the nephron
 It decreases the production of urine by promoting the reabsorption of water by the renal tubules (maintains water homeostasis)
 Osmolality of blood is the principal regulator of ADH secretion
 A decreased in blood volume or blood pressure will stimulate ADH release

A

Vasopressin

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4
Q

It is a potent pressor agent and affects blood clotting by promoting Factor ___ release from the
hepatocytes and _____release from the endothelium

A

VII; vWF

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5
Q

 One of the most important roles of AVP is to regulate the body’s retention of _____; it is released
when the body is dehydrated and causes the kidneys to conserve water, thus concentrating the urine, and reducing urine volume.
 In high concentrations, it also raises blood pressure by inducing moderate __________________.

A

water; vasoconstriction

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6
Q

 It increases the permeability to water of the distal convoluted tubules and collecting tubules in the
nephrons of kidneys and thus allows water reabsorption and excretion of a smaller volume of concentrated urine - __________.

A

antidiuresis

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7
Q

ADH’s second effect on the kidney is to increase the permeability of the __________portion of the collecting duct to urea, allowing increased reabsorption of urea into the medullary interstitium, down the concentration gradient created from the removal of water in the cortical collecting duct.

A

papillary

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8
Q

The third effect that AVP has on the kidney is that it stimulates sodium reabsorption in the thick ascending loop of _______by increasing the activity of the Na+-K+-2Cl–cotransporter.

A

Henle

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9
Q

Vasopressin increases peripheral vascular resistance and thus increases _________ blood pressure. This effect appears small in healthy individuals; however it becomes an important compensatory mechanism for restoring blood pressure in ____________shock such as occurs during hemorrhage.

A

arterial; hypovolemic

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10
Q

 It has been implicated in memory formation, including delayed _______________________________ though the mechanism remains unknown, and these findings are controversial.

A

reflexes, image, short- and long-term memory,

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11
Q

Vasopressin released from centrally-projecting hypothalamic neurons is involved in

A

aggression, blood pressure regulation and temperature regulation

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12
Q

Vasopressin is secreted from the posterior pituitary gland in response to reductions in plasma volume, in response to increases in the plasma osmolality, and in response to _____________ by the small intestine

A

cholecystokinin

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13
Q

activated by pressure receptors in the veins, atria, and carotids.

A

Secretion in response to reduced plasma volume

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14
Q

mediated by osmoreceptors in the hypothalamus

A

Secretion in response to increases in plasma osmotic pressure

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15
Q

mediated by an unknown pathway

A

Secretion in response to increases in plasma Cholecystokinin

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16
Q

acts as an antagonist for AVP in the collecting ducts of the kidneys, which prevents aquaporins from binding to the collecting ducts, and prevents water reabsorption

A

Ethanol (alcohol)

17
Q

may stimulate the secretion of AVP

A

Angiotensin II

18
Q

The main stimulus for secretion of vasopressin is ______________osmolality of plasma. __________ volume of extracellular fluid also has this effect, but is a less sensitive mechanism.

A

increased; Reduced

19
Q

Decreased vasopressin release or decreased renal sensitivity to AVP leads to diabetes insipidus, a condition featuring

A

hypernatremia (increased blood sodium concentration),
polyuria (excess urine production), and
polydypsia (thirst)

20
Q

 Deficiency of ADH with normal ADH receptor
 Failure of the pituitary gland to secrete ADH
 There is large volume of urine excreted (3-20 L/day)

A

True Diabetes insipidus (Hypothalamic/Neurogenic/Cranial/Central Diabetes Insipidus)

21
Q

 Normal ADH but abnormal ADH receptor
 Failure of the kidney to respond to normal or elevated ADH levels

A

Nephrogenic Diabetes insipidus

22
Q

o Syndrome of inappropriate antidiuretic hormone (SIADH) and resultant hyponatremia (low blood sodium levels) occurs in brain diseases and conditions of the lungs (Small cell lung carcinoma).
o Medications such as carbamazipine, clofibrate, vinca alkaloids
o Physiologic stimuli such as nausea, pregnancy, hypoglycemia and hypoxia

A

High levels of AVP secretion

23
Q

o Urine immunoassay
o Serum immunoassay (RIA) + extraction prodecure
o Serum/urine osmolality

A

Direct measurement of ADH

24
Q

o Serum electrolyte determination
o Water load test to evaluate patient’s ability to suppress ADH secretion

A

Test for SIADH secretion