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Endocrine Physiology > Quiz 1 Winter Term > Flashcards

Quiz 1 Winter Term Flashcards

1
Q

What is the type of receptor for ADH (AVP, Vasopressin) at a) low levels and b) high concentrations

A

a) V2 receptors on cell membrane of distal nephron/collecting duct
b) V1a receptors in vascular beds

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2
Q

How does AVP (ADH, Vasopressin) induce pressor effects?

A

V1a receptor activation increases phosphatidylinositol metabolism&raquo_space; free Ca++

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3
Q

What are the stimuli for release of ADH? Stimuli for inhibition?

A

Release: osmoreceptors in anterior hypothalamus sense increase in blood osmolality&raquo_space; increase in SON/PVN electroactivity (*Most important for acute regulation of ADH)

inhibition: atrial stretch receptors stimulated by increased venous pressure

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4
Q

AVP stimulates secretion of ____ via the ____ subtype of receptor.

A

Adrenocorticotropic hormone (ACTH) via V1b receptors.

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5
Q

What is the difference between Central (hypothalamic) diabetes insipidus and nephrogenic diabetes insipidus?

A

central: deficient in AVP
nephrogenic: kidneys are insensitive to AVP

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6
Q

What is Shwartz Bartter Syndrome?

A

syndrome of inappropriate secretion of ADH (SIADH). can result in severe hyponatremia.

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7
Q

What is the sequence of events for the release of milk from mammary ducts?

A

Nerve endings stimulated in the nipple relay a reflex to oxytocin neurons in the SON and PVN > Posterior pituitary secretes oxytocin > myoepithelial cells in mammary gland contract to eject milk

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8
Q

Hypothalamic hypophysiotropic hormones include:

A

Thyrotropin releasing hormone (TRH)
Luteinizing hormone releasing hormon (LHRH) = GnRH
Somatostatin (SS)
Growth hormone release inhibiting hormone (GHRIH)
growth hormone releasing hormone (GHRH)
Corticotropin releasing hormone (CRH)
Urocortins 1,2,3

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9
Q

If you transplanted the pituitary gland away from the hypothalamus, what would happen to hormonal secretion?

A

Increased secretion of prolactin

Decreased secretion of all other hormones affecting anterior pituitary

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10
Q

What are the 3 groups of hormones produced by the anterior pituitary?

A

Pro-opiomelanocortin polypeptides(POMC)
Glycoproteins
Somatomammotropic Proteins

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11
Q

ACTH causes increased conversion of cholesterol to pregnenolone via

A

increase in intracellular cAMP

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12
Q

Of the 39 amino acid residues of ACTH, which contain the steroidogenic activity?

A

1-24 ACTH. (4-10 = activation; 11-24= binding to receptors)

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13
Q

ACTH is regulated by:

A

negative: cortisol
positive: CRH, pain, anxiety, hypoglycemia, vasopressin

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14
Q

Endorphins are fragments of:

A

B-Lipoprotein

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15
Q

While all glycoproteins contain an alpha and beta chain, it is the ____ chain that confers specificity

A

beta chain (receptor binding probably determined by b chain)

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16
Q

What is the function of hCG

A

maintaining corpus luteum in early pregnancy to maintain progesterone & estrogen

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17
Q

What are the somatomammotropic hormones?

A

Growth hormone (hGH, somatotropin)
Prolactin (PRL)
hCS (chorionic somatomammotropin)

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18
Q

What are the two classes of hormones produced by the adrenal cortex?

A

Glucocorticoids and mineralcorticoids

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19
Q

What causes Congenital adrenal hyperplasia?

A

autosomal receissive diseases» mutations of enzymes that cause increased adrenal androgens synthesis instead of cortisol

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20
Q

Cortisol secretion is stimulated by ACTH via which receptor pathway?

A

G-protein coupled receptor stimulates adenylate cyclase&raquo_space; increased cAMP&raquo_space; activated PKA

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21
Q

How does cortisol usually circulate in the plasma?

A

bound to corticosteroid binding globulin and albumin. ONLY FREE HORMONE CAN BIND TO RECEPTORS, thus saturation must be attained before biolagical activity stimulated

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22
Q

What is the mechanism for glucocorticoid (cortisol) action?

A

binds intracellularly to receptor. Complex is translocated to nucleus, bind to nucleotide sequences (GRE Glucocorticoid-response elements) on DNA to stimulate or inhibit gene trascription

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23
Q

How do glucocorticoids affect blood glucose?

A

RAISE by:

  • stimulating hepatic gluconeogenesis via PEPCK
  • enhancing gluconeo & glycogenolysis by epi and glucagon
  • reducing uptake of glucose to peripheral cells
  • mobilizing amino acids from peripheral tissues
  • promoting synthesis of liver glycogen (long term preventative measure)
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24
Q

How is glucocorticoid related to metabolic syndrome?

A

May reduce sensitivity of several tissues to insulin, causing Type 2 diabetes

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25
Q

What are the negative consequences of excess glucocorticoids?

A

Osteoporosis, impaired skeletal growth, insulin resistance, slow wound healing; insomnia

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26
Q

What is Addison’s disease and what are its symptoms?

A 
Adrenal insufficiency (hypocortisolism, hypoadrenalism), hypo
hyper-pigmentation, weight loss, fatigue, fasting hypoglycemia, muscle pain, GI symptoms
(hypoaldosteronism causes hypotension)
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27
Q

What is Cushing’s syndrome and what are its symptoms?

A

Hypercortisolemia;

weight gain, buffalo hump, moon face, hypertension, osteoporosis, easy bruising, glucose intolerance, hirsutism

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28
Q

What are the two mineralocorticoids and what is their major effect?

A

aldosterone & 11-deoxycorticosterone (DOC): sodium retention and potassium excretion

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29
Q

Which region of the adrenal cortex produces aldosterone?

A

zona glomerulosa (glucocorticoid in zona reticularis and fasciculata)

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30
Q

How is aldosterone synthesized?

A

1st four steps same as cortisol synthesis (cholesterol to pregnenolone > progesterone.&raquo_space; DOC via 21-hydroxylase (P450c21),&raquo_space; corticosterone via P450c11 > aldosterone via 18-hydroxycorticosterone

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31
Q

Why is aldosterone inactivated more rapidly than glucocorticoids?

A

40% circulates freely in plasma and there is no binding protein comprable to corticosteroid binding globulin

32
Q

Where is aldosterone degraded? what conditions might cause increased aldosterone levels?

A

Liver; cirrhosis or severe congestive heart failure

33
Q

What are the physiological effects of aldosterone?

A

sodium reabsorption, potassium and H+ secretion

34
Q

What is the most significant difference between regulation of glucocorticoid and aldosterone secretion?

A

aldosterone is primarily regulated by renin-angiotensis system and plasma K+, while glucocorticoid secretion is controlled by the hypothalamo-hypophyseal axis.

35
Q

How does angiotensin II stimulate aldosterone biosynthesis?

A

stimulates rate-limiting steps: conversion of cholesterol to pregnenolone, conversion of corticosterone to aldosterone

36
Q

What enzyme prevents glucocorticoids from occupying mineralocorticoid receptors?

A

11B-HSD2 (hydroxysteroid dehydrogenase type 2). inactivates by oxidation. only expressed in aldosterone target tissues.

37
Q

What causes apparent mineralcorticoid excess syndrome?

A

deficiency of 11b-HSD2. active cortisol saturates mineralocorticoid receptors.

38
Q

Where is testosterone produced and how does it circulate in the plasma?

A

Leydig cells; circulates bound to testosterone-estradiol-binding globulin (TeBG) or to albumin. only 2-3% is free (active)

39
Q

Why is DHT (dihyrotestosterone) more potent than testosterone?

A
  1. cannot be converted to estrogens
  2. binds with higher affinity
  3. bound complex is transformed to DNA binding site more efficiently
40
Q

What are the 2 major endocrine functions of fetal testis?

A
  1. produce Mullerian inhibiting factor (MIF) (permits differentiation of wolfiann ducts & stimulate development of Leydig cells)
  2. produce testosterone
41
Q

What is the role of testosterone in fetal development? What is the specific action of DHT?

A

induces Wolfiann ducts to become seminiferous tubules, Vas, and epididymis. DHT responsible for external male genitalia, prostrate & male urethra

42
Q

What is SRY and what does it produce?

A

Y Sex-determining gene; TDF (testis -determining factor)

43
Q

At what point in development does the pituitary take over hormonal control of the testis?

A

8-12 weeks of gestation

44
Q

what causes Androgen insensitivity syndrome (AIS)?

A

defect is in the androgen

receptor that binds testosterone and dihydrotestosterone

45
Q

what is the clinical presentation of 5a-reductase deficiency (5-ARD)

A

born w/ Wolfiann structures & testis, (usually) primary female sex characteristics. 5-ARD converts testosterone to DHT

46
Q

What are the actions (whole body) of androgens

A
  1. Increased bone and muscle mass due to nitrogen retention (protein synthesis)
  2. Accumulation of potassium, phosphorus and calcium ions.
  3. stimulating linear bone growth
  4. Alter organ specific protein synthesis in non-sexual tissues such as the liver, kidney and salivary
    glands.
47
Q

How is spermatogenesis initiated?

A

testosterone & FSH:

FSH stimulates sertoli cells to undergo mitosis

48
Q

How do Sertoli cells regulate FSH?

A

secrete Inhibin, a heterodimer that inhibits FSH secretion

49
Q

DHT induces the urogenital sinus to form:

A

testis, penix, prostate, etc

50
Q

how is testosterone converted to estradiol?

A

aromatase in the hypothalamus

51
Q

What are the three estrogens?

A

estradiol
estriol
estrone

52
Q

In females, FSH stimulates:

A

stimulates ovarian follicle growth & mitosis of granulosa cells

53
Q

In conjunction with FSH, LH (in females) stimulates:

on its own, it stimulates:

A

estradiol production by follicles, maturation and ovulation of follicles;
maintenance of corpus luteum & progesterone production

54
Q

how do thecal and granulosa cells in the ovary interact to produce estradiol?

A

LH stimulates cholesterol&raquo_space; pregnenolone&raquo_space; DHEA» ANDROSTENEDIONE, which cross into granulosa cells, is phosphorylated by PKA&raquo_space; estrone,&raquo_space; estradiol

55
Q

When does the “window of vulnerability” occur?

A

between 7-10 days after ovulation

56
Q

Which protein must be targeted by antibodies in order to neutralize orthomyxovirus virions? Which protein cannot be targeted for neutralization but can help prevent the spread of infenction?

A

hemagglutin (HA); N-antigen antibodies prevent virions from escaping infected cells and spreading, but do not neutralize virion)

57
Q

Which enzyme enables orthomyxovirions to leave the cell?

A

Neuraminidase glycoprotein (N-antigen): cuts the sialic bond attachment to host cell

58
Q

Do orthomyxoviruses undergo hemagglutination?

A

yes; b/c of the H-antigen in the envelope of virions

59
Q

How many types of influenza viruses (human) exist? why are there multiple strains constantly evolving?

A

three; however, there are multiple strain of each. A is the most frequent. strains evolve because there are multiple pieces of cRNA for reassotment

60
Q

What is the difference between antigenic shift and drift?

A

DRIFT: minor antigenic variants&raquo_space; minor epidemic.
SHIFT: major antigenic variants&raquo_space; major pandemics. caused by genetic reassortment (ex, swine flu) or direct transmission between species

61
Q

How is influenza diagnosed in a lab?

A

look for rise of anti-hemagglutin (anti-HA) antibody by inhibition assay

62
Q

Immunity against influenza is largely dependent in Ig__ because it attacks mucosal surfaces of the respiratory tract. Immunity from prior infections is less effective because:

A

IgA; influenza does not have obligatory viremia

63
Q

Diagnosis of paramyxoviruses can be done using what kind of test? which virus is the exception to this?

A

hemagglutination; syncytial virus does not have HA protein and cannot agglutinate RBCs

64
Q

What is Croup and which viruses can cause it?

A

acute laryngo-tracheo-bronchitis; disease of first three years of life; parainfluenza viruses but others too

65
Q

What are the two classes of proteins in the interferon system? what is their function?

A
  1. interferons: proteins synthesized by virus-infected cells and antigen-stimulated T-cells
  2. virus inhibitory proteins, synthesized by uninfected cells when interferon binds. protects uninfected cells from future infection
66
Q

What are available treatments for influenza and what do they do?

A
  1. oseltamivir and zanamivir: slow release of virus and spread from cell to cell
  2. adamantanes
67
Q

How is Hepatitis A transferred? What are the options for vaccines? What is the test to diagnosis it?

A

feco-oral;
intramuscular injection of human gamma globulin (passive) or killed-vaccine;
serological test for antibody to the virus

68
Q

How is serological data for Hep A interpreted?

A

anti-HAV- IgG/IgM
-/- : not currently/not ever Hep A
+/- current is not hep A but pt had it or the vaccine in past
+/+ acute or recent infection or vaccination

69
Q

Why is the absence of needle tracks relevant for Hepatitis diagnosis?

A

absence decreases likelihood of blood-borne. helps rule out Hepatitis B or C (more likely Hepatitis A, spread by feco-oral route)

70
Q

Hepatitis A is a _____ (virus family) while Hepatitis B is a _____

A

picornovirus; B is a hepadnavirus

71
Q

What is the process for Hep B virus replication? What happens late in infection?

A

cell > nucleus > gaps in its circular double strand are filled by reverse transcriptase > genes are transcribed into mRNAs, proteins are translated
LATE in infection:
RNA polymerase copies entire genome (pregenome) and nucleocapsid surrounds it. reverse transcriptase copies RNA into DNA. DNA buds out to form new virions.

72
Q

What is the significance of the presence of Hepatitis B antigen HBeG?

A

it is strongly correlated with infectious HBV with progression to hepatic carcinoma.

73
Q

How should the neonates of mothers with Hepatitis B be immunized?

A

both passive and active immunization (immune globulin and HB-vaccine) immediately after birth

74
Q

What is the window period?

A

the interval between the time that a donor gives blood and the time that infection can be detected (W.P. varies with different tests)

75
Q

What does 5-alpha reductase do?

A

converts testosterone to DHT

76
Q

What is the intracellular signaling mechanism for ADH’s action on aquaporins?

A

G-portein adenylate cyclase > cAMP

Endocrine Physiology (2 decks)

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