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PHAR 230 > M4 L1: Adrenal Steroids > Flashcards

M4 L1: Adrenal Steroids Flashcards

1
Q

what are the adrenal glands

A

located on top of each kidney
divided into outer cortex and inner medulla

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2
Q

what is the adrenal medulla

A
  • modified sympathetic ganglion
  • innervated by preganglionic SNS nerve fibres
  • secretes NE and E
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3
Q

what is the effect of catecholamines

A

SNS response!

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4
Q

3 regions of the adrenal cortex

A
  1. zona glomerulosa (outermost)
  2. zona fasciculata (middle)
  3. zona reticularis (innermost)
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5
Q

what does the zona glomerulosa secrete

A

mineralocorticoids

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6
Q

what does the zona fasciculata secrete

A

glucocorticosteroids

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7
Q

what does the zona reticularis secrete

A

sex hormones

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8
Q

all steroid hormones are derived from a fat which one?

A

cholesterol

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9
Q

what does aldosterone stim

A

the renal tubules
(retention of Na+ and H2O, as well as excretion of K+)

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10
Q

what does aldosterone act on

A
  • DCT (distal convoluted tubule)
  • CD (collecting ducts)
    of the kidney
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11
Q

what does an excretion of K+ in the renal tubules cause

A

increased Na and decreased K in the blood

increased blood volume and bp

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12
Q

factors that stim aldosterone secretion

A
  • hyperkalemia
  • hypo (natremia, volemia, tension)
    this would be achieved by stim of the RAAS sys
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13
Q

glucocorticoid regulation of secretion

A

corticotropin (CRH) releasing hormone causes an increase in adrenocorticotropic hormone (ACTH) and causes an increase in glucocorticoids

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14
Q

what does ACTH stimulate

A
  • synthesis and secretion of glucocorticoids
  • growth of adrenal gland
  • there would be a -‘ve feedback for inhibition
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15
Q

“tropic” hormones do…

A

stim enlargement of the gland, and make the hormone

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16
Q

are steroid hormones water soluble

A

are not water soluble

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17
Q

how do glucocorticoids work? (also works for other steroids)

A
  • they are fat soluble
  • cross cell membrane by diffusion
  • bind to receptors in cytoplasm or nucleus
  • alter DNA transcription in nucleus
  • affect metabolic activity and structure of target cell
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18
Q

protein metabolic affects of the glucocorticosteroids

A
  • increase mobilization of proteins and amino acids
  • increase protein catabolism**
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18
Q

carbohydrate metabolic affects of the glucocorticosteroids

A
  • increase blood glucose level**

do this thru gluconeogenesis in liver, and decrease glucose uptake and utilization by cells

  • anti-insulin action
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19
Q

lipid metabolic affects of the glucocorticosteroids

A
  • increased mobilization of peripheral fat
  • redistribution of fat** from limbs to face and trunk
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20
Q

anti-inflammatory and immunosuppressive effects of glucocorticoids

A
  • decrease # and/or activities of WBC and other parts of immune sys
  • stabilize lysosomal membranes
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21
Q

glucocorticoid effect on blood cells

A
  • increase # of RBC’s and neutrophils
  • decrease # of lymphocytes and eosinophils
22
Q

mineralocorticoids-like action of glucocorticoids

A
  • retains Na+ and water, excretes K+
  • increased blood volume and bp
23
Q

glucocorticoids decreased bone formation can cause…

A

osteoporosis

24
Q

glucocorticoids effect on GIT

A

mucosal ulceration

25
Q

glucocorticoids increase CNS excitability which can cause…

A

mood changes

26
Q

glucocorticoid therapeutic indications

A
  • adrenal hypofunction (replacement therapy)
  • bronchial asthma
  • allergic reactions (eczema, anaphylaxis, etc)
  • autoimmune diseases (rheumatoid arthritis, SLE)
  • organ transplantation (immunosuppressive to inhibit rejection)
  • malignancies (chemotherapy)
  • diff inflammatory conditions (inflammatory bowel disease, renal disease, facial palsy)
27
Q

equivalent concentration for cortisone

A

25 mg

28
Q

equivalent concentration for hydrocortisone **

A

20 mg

29
Q

equivalent concentration for prednisolone **

A

5 mg

30
Q

equivalent concentration for methylprednisolone

A

4 mg

31
Q

equivalent concentration for traimacinolone

A

4 mg

32
Q

equivalent concentration for betamethasone**

A

750 mcg

33
Q

equivalent concentration for dexamethasone **

A

750 mcg

34
Q

what are route of admin for glucocorticoids

A

topical, oral, inhalation, injection (IM, IV, SC), intralesional, intra-articular

35
Q

what is a disease caused from adrenocortical hypofunction

A

addison’s disease

36
Q

what diseases come from adrenocortical hyperfunction

A
  • conn’s syndrome
  • cushing’s syndrome
  • congenital adrenal hyperplasia
37
Q

what is addison’s disease?

A
  • hypofunction of all zones of adrenal cortex

causes:
1. primary (adrenal gland disorder mostly autoimmune mediated destruction
2. secondary (pituitary gland disorder

38
Q

causes primary addison’s disease

A

adrenal gland disorder
- autoimmune-mediated destruction (80%)**
- TB (20%)

39
Q

causes of secondary addison’s disease

A

primary gland disorder
- caused by inadequate secretion of ACTH
- destruction of pituitary gland
- sudden withdrawal of prolonged steroid therapy

40
Q

clinical manifestations of addison’s disease

A
  • hypotension* (starts w orthostatic)
  • anorexia
  • weight loss
  • hyperpigmentation
  • mental depression
  • addisonian crisis
41
Q

treatment for addison’s disease

A
  • cortisol deficiency: oral hydrocortisone
  • aldosterone deficiency: oral fludrocortisone
42
Q

what is conn’s syndrome

A

increased aldosterone secretion without activation of RAAS

43
Q

what causes conn’s syndrome

A
  • adrenal hyperplasia
  • adrenal tumors: adenoma, carcinoma
44
Q

main sympt of conn’s syndrome

A
  • hypertension
  • hypokalemia
  • decreased renin level
  • alkalosis
45
Q

what is the treatment of conn’s syndrome

A

surgical and/or medical

46
Q

what is cushing’s syndrome

A

increase glucocorticoids secretion

47
Q

causes of cushing’s syndrome

A
  1. iatrogenic (most common)
    - glucocorticoids or ACTH therapy
  2. spontaneous
    - adrenal: hyperplasia or tumor
    - pituitary: adenoma -> excess ACTH secretion
    - ectopic ACTH/CRH secretion: ex tumors
48
Q

clinical manifestations of cushing’s syndrome

A
  • obesity
  • myopathy
  • hypertension
  • hyperglycemia
  • recurrent infections
  • thin atrophic skin w bruises
  • osteoporosis
  • psychosis
49
Q

cushing’s syndrome treatment

A

of the cause
ex: take the tumor out, find the origin of the cause, etc

50
Q

manifestations of cushing’s syndrome

A

“BIG”
B - bp (hypertension), bone (osteoporosis
I - immunosuppression (infection)
G - glucose (diabetes mellitus)

Obesity - fat distribution - edema

51
Q

what is congenital adrenal hyperplasia

A
  • congenital metabolic disorder (autosomal recessive)
  • due to enzymatic defect most commonly of 21-hydroxylase enzyme deficiency
52
Q

congenital adrenal hyperplasia effects

A
  • increase adrenal androgens
  • decrease cortisol and aldosterone
53
Q

congenital adrenal hyperplasia manifestations

A
  • female babies will go through masculinization sympt
  • male babies will go through precocious puberty

PHAR 230 (31 decks)

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