Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 10 Week 2 > Burkin: Adrenal Pharmacology > Flashcards

Burkin: Adrenal Pharmacology Flashcards

1
Q

Describe the feedback regulation of the anterior pituitary hormones

A

Hormone regulation can be ultra-short-loop, short-loop, or long-loop.
Ultra-short loop regulation occurs when hypothalamic hormones regulate the release of hormones from the hypothalamus itself.
Short-loop regulation occurs when pituitary hormones regulate the release of hormones from the hypothalamus. Long-term regulation occurs when hormones released from the target tissue feed back on the hypothalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

6 hormones released from the hypothalamus, and their effects on the pituitary

A

corticotropin-releasing hormone –> increases ACTH
thyroptropin-releasing hormone –> increases TSH & prolactin
gonadotropin-releasing hormone –> increases LH/FSH
growth hormone-releasing hormone –> increases GH
somatostatin –> decreases GH
dopamine –> decreases prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the pattern of release of growth hormone from the anterior pituitary

A

low pulsatile pattern throughout the day, large increase in GH at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does growth hormone do to the following?

insulin sensitivity
lipolysis
IGF-1
protein synthesis
epiphyseal (bone) growth
A 
decreases insulin sensitivity
increases lipolysis
increased IGF-1
increased protein synthesis
increased epiphyseal bone growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What things stimulate growth hormone synthesis?

A 
GHRH
hypoglycemia
exercise
certain amino acids
sleep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What things inhibit growth hormone synthesis?

A

somatostatin
IGF-1 via negative feedback
hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens when you have excess growth hormone?

A

gigantism (if early in life)

acromegaly (excess soft tissue hyperplasia after body growth has stopped)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do you treat excess growth hormone?

A

remove tumor

give somatostain analog like octreotide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Things that can lead to primary GH deficiency?

A

hypothalamic (GHRH) or pituitary lesions

**can cause dwarfism (if occurs early in life) or adult hypopituitarism (weakness, pale skin, no sex drive, genital atrophy, menstrual cycle cessation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some reasons for retarded growth when GH levels are normal?

A

GH receptor defect

IGF-1 deficiency (African pygmies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

somatrophin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What conditions is growth hormone used to treat?

A

Turners syndrome –> increases final adult height
Children with FTT due to chronic renal failure or HIV infection
Adults with AIDS-associated wasting

**recombinant bovine GH can be used to increase milk production in dairy cows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Discuss the feedback of growth hormone secretion

A

GHRH causes release of GH from the pituitary - increases body growth, lipolysis, and decreases glucose uptake, also acts on liver to produce IGF-1

Somatostatin decreases GH secretion from pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What cells produce prolactin?

A

lactotropes & somatomammotropes of the anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the actions of prolactin?

A

milk production
increased maternal behavior
antagonizes gonadotropin action in the gonads –> decreased steroidogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are prolactin levels controlled?

A

inhibited by hypothalamic dopamine

stimulated by oxytocin, TRH, VIP & estrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some causes of excess prolactin? How can you treat this?

A

microadenoma of lactotropes
dopamine receptor blockers (antipsychotics)
stress
vigorous exercise

treat with dopamine agonist (Bromocryptine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does increased prolactin cause in males? In females?

A

in males: inferility

in women: amenorrhea, galactorrhea, infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Stimulates release of milk during lactation and contributes to the initiation of uterine contraction during labor; used intravenously to induce or reinforce labor and as a nasal spray to induce postpartum lactation

A

oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Secreted in response to rising plasma tonicity or falling blood pressure. Deficiency causes diabetes insipidus.

A

vasopressin (ADH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

(blank) is used to treat diabetes insipidus. Bedtime administration is also used to treat nocturnal enuresis.

A

desmopressin acetate (ADH analog)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Partial or complete loss of adrenocortical function

A

Addison’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Suppression in the ability of the adrenal cortex to produce corticosteroids

A

Adrenal suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

A metabolic disorder caused by excess secretion of adrenocorticoid steroids

A

Cushing’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

POMC is cleaved to form which endocrine peptides?

A

ACTH
melanocyte stimulating hormone (MSH)
beta-endorphin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Three layers of the adrenal cortex & what do they produce?

A

Zona glomerulosa –> aldosterone
Zona fasciculata –> cortisol
Zona reticularis –> androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The adrenal medulla is made up of chromaffin cells & produces (blank)

A

catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which zone of the adrenal cortex is ACTH independent and is sensitive to Ang II? Which zones are ACTH dependent?

A

glomerulosa is ACTH independent

reticularis/fasciculata are ACTH dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does ACTH increase the production of steroid hormones in the zona fasciculata? What is the rate limiting step in this process?

A

ACTH binds to Gs –> increases cAMP –> activates a protein kinase –> cholesterol is then delivered to the mitochrondrial matrix via the StAR protein –> increased synthesis of steroid hormones (takes hours)

**rate limiting step is the delivery of cholesterol to the mito via StAR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the mineralocorticoid pathway from cholesterol to aldosterone

A

cholesterol –> pregnenolone (via ACTH)–> progesterone –> 11-deoxycorticosterone –> corticosterone –> 18-hydroxycorticosterone (via AngII) –> aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

(blank) has a large affect on the production of aldosterone

A

Ang II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What enzyme catalyzes the transformation of cortciosterone to 18-hydroxycorticosterone (which is converted to aldosterone)?

A

Ang II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How much cortisol is released daily?

A

10mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

When is cortisol secreted?

A

first thing in the morning (high levels)

**corresponds to light-dark cycles

35
Q

Cortisol circulates bound to (blank) and (blank)

A

transcortin (cortisol binding globulin); albumin

36
Q

Parenterally administered form of ACTH, with a T1/2 of 15 minutes

A

Cosyntropin

Acthar

37
Q

Used as a diagnostic agent in adrenal insufficiency

normal rise in cortisol rules out adrenal failure

A

Cosyntropin (ACTH synthetic peptide)

38
Q

Cortisol is a permissive hormone. What does this mean?

A

low levels of catecholamine have little effect on lipolysis, but in the presence of cortisol, there is marked activation of lipolysis

39
Q

(blank) is the major form of glucocorticoid; it is bound to (blank) in the circulation

A

cortisol; transcortin

40
Q

Cortisol is essential to life. What does cortisol do in regards to metabolism of carbohydrates, proteins & lipids?

A

stimulates protein breakdown to amino acids (especially muscles)
facilitates lipid breakdown in adipose tissue to fatty acids & glycerol
promotes hepatic gluconeogenesis from amino acids, glycerol, & fatty acids
makes glucose available to the brain by inhibition utilization by other tissues

41
Q

This is a major form of adrenal androgens

A weak androgen that is not important in males, but is an important source of androgen in females

A

DHEA

42
Q

What does DHEA do in females?

A

enhances pubertal growth spurt
maintains secondary sex characteristics - pubic & axillary hair
libido

**there is some conversion of DHEA to estrogen in peripheral tissues

43
Q

A glucocorticoid with a low degree of protein binding, is given to pregnant women in premature labor to hasten fetal lung maturation (increase surfactant)

A

Betamethasone

44
Q

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

45
Q

Mineralocorticoids and glucocorticoids work in essentially the same manner. Specificity relies on the (blank) and the association of response elements in specific genes.

A

target cell

mineralocorticoids act on renal tubule vs glucocorticoids in the tissues

46
Q

What is it called when you have aldosterone excess?

A

Conn’s syndrome (primary)

or

secondary hyperaldosteronism

47
Q

What causes aldosterone excess?

A

hypersecreting tumor of Z. glomerulosa (primary)

high renin-angiotensin (secondary)

48
Q

Symptoms of excess aldosterone?

A

hypernatremia –> HTN

hypokalemia

49
Q

What is it called when you have excess cortisol?

A

Cushing’s syndrome

50
Q

What can cause excess cortisol?

A

excess CRH/ACTH (hypothal disorder vs pituitary tumor)
adrenal tumor
ectopic ACTH (lung cancer)

51
Q

What are the symptoms of excess cortisol?

A

hyperglycemia
excess protein breakdown –> muscle weakness
abnormal fat distribution
insulin resistance
decreased immune response & inflammatory response

52
Q

What is it called when you have androgen excess?

A

congenital adrenal hyperplasia

53
Q

What can cause androgen excess?

A

genetic deficiencies in cortisol synthesizing enzymes

21- and 11-OH

54
Q

What are the symptoms of excess androgens?

A

inappropriate masculinization –>
pseudohermaphroditism in females
precocious puberty in males

55
Q

What is it called when you have cortisol & aldosterone deficiency?

A

primary adrenal insufficiency (Addison’s disease)

56
Q

What can cause primary adrenal insufficiency?

A

destruction or atrophy of the adrenal cortex

57
Q

What are the symptoms of primary adrenal insufficiency (Addison’s disease)?

A

related to cortisol deficiency –>
poor response to stress
hypoglycemia
low metabolic activities

58
Q

What is it called when you just have a cortisol deficiency? What causes this?

A

secondary adrenal insufficiency;

insufficient ACTH due to hypothalamus/pituitary failure

59
Q

What are these signs & symptoms of?

myopathy, central obesity, Moon face, Acne, hirsutism, bruising and capillary fragility, hypertension, glucose intolerance, hypokalemia, arteriosclerosis, infections, oestoporosis, hypogonadism

A

Cushings syndrome

60
Q

Most cases of Cushings syndrome are (blank) dependent

A

ACTH

**~80% are ACTH dependent (either pituitary tumors or lung cancers), while 20% are ACTH independent (benign adrenal adenomas or malignant adrenal carcinomas)

61
Q

To confirm Cushings disease (blank) can be ordered. Treatment with (blank) causes a reduction in cortisol in normal patients. In Cushings patients cortisol will remain the same or even elevated.

A

dexamethasone suppression test; dexamethasone

62
Q

How do corticosteroids affect carbohydrate & protein metabolism?

A

stimulate formation of glucose

diminish peripheral utilization of glucose & promote the storage of glucose as glycogen

63
Q

How do corticosteroids affects lipid metabolism?

A

redistribute body fat in the hypercorticoid state

**buffalo hump, moon face, thin extremities

64
Q

What affects do corticosteroids have on the CNS?

A

Addison’s patients are apathetic, depressed and irritable some displaying frank psychosis
Administration of corticosteroids to normal patients induces a feeling of well being

65
Q

What affects do corticosteroids have on the blood?

A

increase red cell hemoglobin & red cell content of blood –> people with Cushings get polycythemia & people with Addison’s get normochromic normocytic anemia

increase neutrophils
decrease lymphocytes, eosinophils, basophils, & monocytes

66
Q

What are the anti-inflammatory effects of glucocorticoids?

A

decrease circulating lymphocytes & suppress cytokines
suppress inflammation to all stimuli
block early & late events in the inflammatory process

67
Q

Glucocorticoids are extremely useful as (blank) agents in numerous clinical settings, such as transplantation

A

anti-inflammatory

68
Q

Glucocorticoids cause decreased synthesis of pro-inflammatory (blank) by decreasing the effectiveness of transcription factors like AP-1. In this way, they reduce (blank).

A

cytokines; inflammation

69
Q

Corticosteroid can be administered in the following ways

A 
inhaled
oral
topical
injectible
enema
70
Q

What happens when you withdraw from corticosteroids after being on a high dose?

A

adrenal insufficiency

fever, myalgia (muscle pain), joint pain & malaise

71
Q

How should you withdraw from a high dose steroid treatment after weeks to months?

A

delayed return of adrenal function

**must slowly reduce the dose over 1-2 weeks

72
Q

What are the side effects of high dose corticosteroid use?

A 
hypokalemia alkalosis & edema
increased susceptibility to infection
peptic ulceration (with H pylori infection)
myopathy
behavioral disturbance
cataracts
osteoporosis
growth arrest in children
73
Q

(blank) act on the distal tubules of the kidney to enhance reabsorption of Na+

A

mineralocorticoids

74
Q

In hypercorticoid state, what happens to Na+, water, and K+?

A

too much Na+, higher extracellular fluid volume, hypokalemia

75
Q

What are the four inhibitors of adrenal steroid biosynthesis?

A

aminoglutethamide
ketoconazole
trilostane
metyrapone

76
Q

Inhibits the first step in steroid biosynthesis (P450scc) from cholesterol interrupting production of both cortisol and aldosterone
Useful in decreasing hypersecretion of cortisol from autonomously functioning adrenal tumors and hyper-secretion due to overproduction of ACTH
Is employed in the treatment of Cushing’s disease, cortisol and mineralocorticoid supplements can be added to manage the induced insufficiency

A

Aminoglutethimide

77
Q

How does aminoglutethimide work? When is it used?

A

inhibits the first step in steroid biosynthesis from cholesterol –> interrupts the production of both cortisol & aldosterone

used in Cushing’s disease

78
Q

Anti-fungal drug

Inhibits P450 17a enzymes required for cortisol synthesis

Inhibits P450scc enzyme at high concentrations

Is used to in a number of conditions to inhibit steroid synthesis: adrenal carcinoma, hirsutism, breast and prostate cancer

A

Ketoconazole

79
Q

Inhibits 3-beta-hydroxy steroid dehydrogenase
blocks formation of cortisol and aldosterone and causes increased excretion of 17-keto steroids
Can be used in the treatment of Cushing’s disease
Benefit over aminoglutethamide is not clear and drug has not received extensive use

A

Trilostane

80
Q

Blocks 11-beta-hydroxylation terminating synthesis at 11-desoxycortisol and resulting in renal excretion of 17-OH-steroids
11-desoxycortisol is a weak inhibitor of ACTH production
Result is an increase in ACTH production permitting assessment of the pituitary release of ACTH and adrenal response in the form of 17-OH-steroid in the urine

A

Metyrapone

81
Q

Which enzymes does ketoconazole block?

A

P450 17 alpha (for cortisol synthesis) & P450 at high concentration

82
Q

What enzyme does trilostane inhibit? What does it block?

A

3-beta-hydroxy steroid dehydrogenase;

blocks formation of cortisol & aldosterone –> increases 17-keto steroids

83
Q

What enzyme does metyrapone block?

A

11-beta-hydroxylase

84
Q

What can metyrapone be used for?

A

for the assessment of Cushing’s disease –> when administered, it results in an increase in ACTH production & increased steroid precursors. If no increase in 11-deoxycortisol –> indicates adrenal insufficiency

Block 10 Week 2 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions