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Block 10 Week 2 > Adrenal Pharm-Burkin > Flashcards

Adrenal Pharm-Burkin Flashcards

1
Q

What does somatostatin do?

What does dopamine inhibit?

A

inhibits GH

Prolactin

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2
Q

Hormones are released from the

anterior pituitary in a (blank) fashion. What is this regulated by?

A

pulsatile
fluctuations in neuronal activity

e.g. Growth hormone is release in a pulsatile
fashion with a diurnal rhythm.

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3
Q

Where does GH come from?

A

somatotroeps and somatommaotropes of anterior pituitary

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4
Q

What does GH do?

A 
decreased insulin sensitivity
increased lipolysis
increased IGF-1
Increased protein synthesis
increased epiphyseal (bone) growth
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5
Q

What stimulates GH?

A

GHRH, hypoglycemia, exercise, certain AAs, sleep

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6
Q

What inhibits GH?

A

somatostatin
IGF-1
Hyperglycemia

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7
Q

How do you treat a somatotrope tumor?

A

tumor removal
Somatostatin analogs
Octreotide

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8
Q

What can cause GH deficiency?

A

hypothalamic and pituitary lesions

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9
Q

What disease can you get if you have GH Deficiency early in life?

A

dwarfism

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10
Q

What will will GH deficiency cause in adults?

A

weakness, fine wrinkling and pale skin, loss of sex drive, genital atrophy, menstrual cycle cessation

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11
Q

What is Laron Dwarfs syndrome?

A

GH receptor defect in target tissues

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12
Q

What causes African Pygmies?

A

IGF-1 deficiency

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13
Q

How do you treat GH deficiency?

A

GH and IGF1 replacement

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14
Q

(blank) is a recombinant form of human GH and is used to treat patients with GH deficiency.

A

Somatrophin

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15
Q

Tx of Turners syndrome patients with (blank) leads to an increase in final adult height.

A

GH

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16
Q

What can GH treat in children?

What can it treat in adults?

A

failure to thrive due to chronic renal failure, HIV infections

AIDS associated wasting

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17
Q

(blank) is used to increase milk production in dairy cows.

A

Recombinant bovine GH

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18
Q

A synthetic version of GHRF called (blank or blank) is an alternative tx for idiopathic growth hormone deficiency

A

Sermoelin, or Geref

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19
Q

What is the source of prolactin?

What does it inhibit?

A

lactotropes and samatomammotropes of anterior pituitary

-gonadotropin actin in gonads (decreased steroidogenesis)

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20
Q

What stimulates prolactin?

A

oxytocin, TRH, VIP and estrogen

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21
Q

What is the tx for excess prolactin secretion?

A

dopamine agonist (bromocryptine/CB154/Parlodel) suppresses prolactin secretion and shrinks prolactinomas

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22
Q

What does oxytocin do?

A

stimulates release of milk during lactation and contributes to the initiation of uterine contraction during labor. IV oxytocin is used to induce or reinforce labor and as a nasal spray to induce postpartum lactation

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23
Q

(blank) is secreted in response to rising plasma tonicity or falling blood pressure. Deficiency in this causes (blank)

A

Vasopressin

Diabetes insipidous

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24
Q

(blank) is used to treat diabetes insipidus.

A

Desmopressin acetate

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25
Q

Bedtime administration of desmopressin is used to treat (blank)

A

nocturnal enuresis

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26
Q

what is this:

partial or complete loss of adrenocortical function

A

Addisons’ disease

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27
Q

What is this:

suppression in the ability of the adrenal cortex to produce corticosteroids

A

Adrenal suppression

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28
Q

What is this:

A metabolic disorder caused by excess secretion of adrenocorticoid steroids

A

Cushing’s disease

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29
Q

What is this:

a substance that activates glucocorticoid receptors

A

glucocorticoid

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30
Q

What is this:

a substance that activates mineralocorticoid receptors

A

mineralcorticoid

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31
Q

How many AAs make up ACTH?
What ones are for activation?
What ones are for binding?

A

6-10

15-18

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32
Q

What do you find in the glomerulosa?

A

angiotensin II
K+
-> causes aldosterone release

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33
Q

What is ACTH independent?

A

Zona glomerulosa

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34
Q

What is ACTH dependent?

A

Zona fasciculata
Zona Reticularis
Medulla

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35
Q

ACTH stimulates steroid synthesis via the action of (blank). What is the rate limiting step?

A

cAMP-PK

delivery of cholesterol to mitochondria via StAR

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36
Q

The steroid synthetic capacity of the adrenal gland is markedly enhanced by the action of (blank)

A

ACTH

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37
Q

What will ACTH do?

A

converts cholesterol to pregnenolone

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38
Q

What does angiotensin II do?

A

converts corticosterone to aldosterone

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39
Q

What will inhibit ACTH and CRH?

A

DHEA
Aldosterone
Cortisol

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40
Q

What is the main source of androgen in females?

A

DHEA

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41
Q

What affects kidney to regulate water and salt metabolism?

A

Aldosterone

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42
Q

What increases metabolic fuels: blood glucose, amino acids and fatty acids

A

Cortisol

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43
Q

ACTH synthesis is (blank) under the control of higher brain centers in response to (blank)

A

diurnal

light-dark cycles

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44
Q

App. (blank) mg of cortisol is released daily.

A

10

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45
Q

Cortisol circulates bound to (blank) and (blank)

A

transcortin (cortisol binding globulin) and albumin

46
Q

Does aldosterone concentrations cahnge during the day?

A

no it is consistent

47
Q

When are cortisol levels that highest?

A

during the day

48
Q

ACTH can be administered parenterally as (blank or blank) with a T 1/2 of (blank)

A

Acthar or Cosyntropin

15 minutes

49
Q

What is used as a diagnostic agent in adrenal insufficient? (i.e normal rise in cortisol rules out adrenal failure)

A

ACTH

50
Q

What are the actions of ACTH?

A
  • homeostatic hormone

- cant survive w/out it unless food, water and salt are always available and temp is consistent

51
Q

Cortisol is a (Blank) hormone: low levels of catecholamine have little effect on (blank),
But in the presence of low levels of cortisol marked activation of lipolysis is seen.

A

Permissive

lipolysis

52
Q

(blank) is the major form of glucocorticoid. It is bound to (blank) in circulation

A

Cortisol

transcortin

53
Q

Cortisol is essential for life because of its important direct effects on intermediary metabolism of (blank X 3)

A

carbs, proteins, lipids

54
Q

What does cortisol do?

A
  • stimulates protein breakdown to AAs (especially muscles)
  • facilitates lipid breakdown of adipose tissue to fatty acids and glycerol
  • promotes hepatic gluconeogenesis from AAs, glycerol, and fatty acids (via oxaloacetate)
  • make glucose available to brain by inhibiting utilization by other otissues
55
Q

What is the permissive action of cortisol?

A

-small amount required for metabolisms, especially those promoted by catecholamines (e.g lipolysis, bronchodilation)

56
Q

What is the major form of adrenal androgens but is weak (not important in males)?

A

DHEA

57
Q

What is an important source (50%) of androgen in females? What is it important for?

A

DHEA

  • enhancement of pubertal growth spurt
  • maintains secondary sex characteristics-pubic and axillary hair
  • libido
  • some conversion by aromatase to estrogen (via testosterone) in peripheral tissues
58
Q

What are the synthetic glucocorticoids that have mechanisms of actions identical to cortisol? What are their half lifes like and what do they do to sodium?

A

prednisone, prednisolone, dexamethasone, triamcinolone

-longer half lives, and reduced Na+ retention effects

59
Q

(blank) is a glucocorticoid with a low degree of protein binding. Who is it given to?

A

Bethamethasone

Pregnant women in premature labor to hasten fetal lung maturation (increase surfactant)

60
Q

(blank) has significant glucocorticoid activity, but because of its long duration of action compared to aldosterone it is favored in conditions requiring mineralocorticoid therapy (e.g. adrenalectomy)

A

fludrocortisone

61
Q

What is primary hyperaldosteronism caused by? What are the clinical findings and lab findings?

A

Hypersecreting tumor of Z. glomerulosa causing excess aldosterone.

  • hypernatremia
  • hypokalemia
  • HTN
62
Q

What is secondary hyperaldosteronism caused by? What are the clinical and lab findings?

A

high renin-angiotensin

  • hypernatremia
  • hypokalemia
  • HTN
63
Q

What is cushings disease caused by?

What are the clinical findings and lab findings

A

excess CRH/ACTH

Hyperglycemia
excess protein breakdown
abnormal fat distribution
insuling resistance
-decreased immune response
-decreased inflammatory response
64
Q

What are all the causes of cortisol excess?

A
  • excess CRH/ACTH
  • Adrenal tumor
  • ectopic ACTH (e.g lung cancer)
65
Q

What are the conditions that cause androgen excess?

A

congenital adrenal hyperplasia (CAH, adrenogenital syndrome in females)

66
Q

What causes congenital adrenal hyperplasia?

A

genetic deficiency in cortisol synthetic enzymes (21 and 11 OH)

67
Q

What are the symptoms of androgen excess?

A
  • inappropriate masculinization
  • pseudohermaphroditism
  • Virilization in females
  • pseduopuberty in boys
68
Q

What is the condition that has cortisol and aldosterone deficiency?
What is the cause?

A

Primary adrenal insufficiency (Addison’s disease)

Destruction or atrophy of adrenal cortex

69
Q

What are symptoms of primar adrenal insufficiency (addison’s disease)?

A

related to cortisol deficiency

  • poor response to stress
  • hypoglycemia
  • low metabolic activities
70
Q

What is the condition associated with cortisol deficiency?

What is the cause?

A

secondary adrenal insufficiency

-Insufficient ACTH-hypoth/pituitary failure

71
Q

What are the symptoms of cortisol deficiency?

A

Relating to aldosterone deficiency

  • hyperkalemia
  • hyponatremia
  • hypotension
72
Q

What are the signs and symptoms of Cushings syndrome?

A
  • myopathy
  • central obesity
  • moon face
  • Acne
  • Hirsuitism
  • Bruising and capillary fragility
  • HTN
  • Glucose intolerance
  • hypokalemia
  • arteriosclerosis
  • infections
  • osteoporosis
  • hypogonadism
73
Q

What percentage of cushings’ syndromes are ACTH dependent?

A

80%

  • 60% are pituitary tumors
  • 20% are due to lung cancers
74
Q

What percentage of cushings syndromes are ACTH independent?

A

20%

  • Benign adrenal tumors (adenomas)-25%
  • Malignant adrenal tumors (adrenal cell carcinoma) 10%
75
Q

How do you confirm Cushings disease?

A

dexamethasone suppression test.

NOTE: Tx w/ dexamethasone causes a reduction in cortisol in normal patiens. In Cushings patients cortisol will remain the same or even elevated

76
Q

What are the effects of corticosteroids on carbohydrate and protein metabolism?

A
  • Stimulates formation of glucose
  • Diminishes peripheral utilization of glucose
  • Promotes the storage of glucose as glycogen.
77
Q

What are the effects of corticosteroids on lipid metabolism?

A

-redistribution of body fat in the hypercorticoid state
-permissive effect on the actions of other agents that promotes lipolysis in adipocytes
NOTE: cushings patients have buffalo hump and moon face and thinning in the extremities

78
Q

(Blank) patients are apathetic, depressed, and irritable, some displaying frank psychosis

A

Addison’s

79
Q

Admin of corticosteroids to normal patients induces a feeling of (blank)

A

well being

80
Q

What do glucocorticoids do to the blood?

A
  • increase red cell hemoglobin and red cell content of blood
  • increase neutrophils
  • decreased lymphocytes, eosinophils, basophils and monocytes
81
Q

What will your blood look like in Cushings?

A

polycythemia

82
Q

What will your blood look like in Addisons?

A

normochromic normocytic anemia in Addisons

83
Q

What are the anti-inflammatory and immunosuppressive actions of glucocorticoids?

A
  • decrease circulating lymphocytes and suppress release of cytokines
  • suppress inflammation to all stimuli
84
Q

How do glucocorticoids prevent inflammation?

A

bind to transcription factors and inhibits them so that inflammatory cytokines cannot be created

85
Q

Cortisol will block both (blank and blank) events in the inflammatory process and effect both (blank and blank) pathways

A

early and late

cellular and humoral

86
Q

How do glucocorticoids effect macrophages and monocytes?

A
  • inhibits arachidonic acid w/ lipocortin (blocks phospholipase A)
  • inhibits cytokine synthesis
87
Q

How do glucocorticoids effect basophils?

A

blocks IgE mediated release of Histamine and leukotriene C4 release

88
Q

How does glucocorticoids effect fibroblasts?

A

inhibits arachidonic acid by lipocortin and suppresses growth factor-induced DNA synthesis and fibroblast proliferation

89
Q

How does glucocorticoids effect lymphocytes?

A

blocks cytokine release

90
Q

What are the 6 types of adrenocortical steroids and how do you use them?

A
  • Becloethasone diproprionate (inhalation)
  • Betamethason valerate (topical)
  • Cortisol (topical, suppositories, rectal foam, injectable, oral)
91
Q

Use of high dose steroid tx for weeks to months may result in (blank)

A

delayed return of adrenal function

92
Q

How should you end corticosteroid tx?

A

A slow reduction in the dose over 1-2 weeks to end treatment is recommended

93
Q

What can high dose chronic use of corticosteroids cause?

A 
Hypokalemic alkalosis and edema
Increased susceptibility to infection
Peptic ulceration (H. pylori)
Myopathy
Behavioral disturbance
Cataracts
Osteoporosis & vertebral compression fractures
Growth arrest in children
94
Q

Mineralcorticoids work where in the kidney?

A

distal tubule to enhance reabsorption of Na+

95
Q

In hypercorticism what happens?

A 
hypernatremia
hypokalemia 
alkalosis
edema
increase ECF
96
Q

In cortical insufficiency there is a renal wasting of (bank)

A

sodium

97
Q

What are the inhibitors of adrenal steroid biosynthesis?

A

Aminoglutethamide
Ketoconazole
Trilostane
Metyrapone

98
Q

How does aminoglutethamide work?.

A

blocks the conversion of cholesterol into pregnenolone

99
Q

How does ketoconazole work?.

A

blocks the 17-hydroxylase preventing creation of 17a-hydroxypregnenolone and 17 a-hydroxyprogresterone

100
Q

How does trilostane work.

A

blocks 3HSD so you wont have conversion of prenenolone to progesterone or conversion of 17a hydroxyprenenolone to 17 a hydroxyprogesterone

101
Q

How does metyrapone work?.

A

blocks 11-OHase so that you cannot convert 11-deoxycortisol to cortisol

102
Q

(blank) inhibits the first step in biosynthesis (P450 scc) from cholesterol interrupting production of both cortisol and aldosterone.

A

Aminoglutethimide

103
Q

What do you use aminoglutethimide for.?

A
  • Cushngs disease (if too much suppression give cortisol and mineralcorticoids)
  • adrenal tumors and overproduction of ACTH
104
Q

What is ketoconazole and what does it do?

A

antifungal drug that blocks P450 17 a enzyme required for cortisol and inhibits P450 scc enzyme at high concentrations

105
Q

What do you use ketoconzole in?

A
  • adrenal carcinoma
  • hirsuitism
  • breast and prostate cancer
106
Q

What does trilostane do?

A

inhibits 3b OH steroid dehydrogenase which blocks formation of cortisol and aldosterone and increases excretion of 17-keto steroids

107
Q

What do you use trilostane for?

A

Cushing disease

NOTE: drug not realy used, would use aminoglutethemide more often)

108
Q

What does metyrapone do?

A

blocks 11-b hydroxylation and increases 11-desoxycortisol and results in renal secretion of 17-OH steroids
Increases ACTH due to feedback (DOC is a very weak inhibitor of ACTH so ACTH is still increased)

109
Q

What is 11-deoxyotisol (DOC)?

A

a weak inhibitor of ACTH production

110
Q

Metyrapone results in an increase in ACTH production permitting assessment of the pituitary release of ACTH and adrenal response in the form of (blank) in the urine

A

17-OH steroid in the urine

Block 10 Week 2 (7 decks)

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