Brainscape's Knowledge GenomeTM

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


See full index

Health Assessment > Endocrine Pt 2 (adrenal/parathyroid > Flashcards

Endocrine Pt 2 (adrenal/parathyroid Flashcards

1
Q

adrenal gland consists of

A

cortex and medulla

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

what does the adrenal cortex synthesize

A

glucocorticoids, mineralcorticoids (aldosterone), and adrogen

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

hypothalamus sends what to the anterior pituritary

A

corticotropin releasing (CRH)

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

after the anterior pituitary is stimulated by CRH what is released

A

corticotropin (ACTH)

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

ACTH stimulates the adrenal cortex to

A

produce cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cortisol facilitates what conversion

A

NE to EPI in the adrenal medulla

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

cortisol induces what

A

hyperglycemia - refelcting gluconeogenesis and inhibiton of glucose uptak eby cells

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

together cortisol, aldosterone cause

A

Na+ retention and K+ excretion

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

what is pheochromocytoma

A

catecholamine secreting tumor that arises from chromaffin cells of the sympathoadrenal system

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

uncontrolled catecholamine release results in

A

malignant HTN, CVA, and MI

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

what is the cause of pheochromocytoma

A

precise cause unknown
90% are isolated
10% inherited

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

most pheo’s secrete what

A

NE:EPI ration 85:15 the inverse of normal adrenal secretion

some secrete higher levels of EPI, and rarely dopamine

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

how do malignant pheo’s spread

A

through venous and lymph systems

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

pheo attack triggers

A

can be spontaneous or triggered by injury, stress, or meds

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

symptoms of pheo attack

A

headache, pallor, sweating, palpitations, orthostatic Hypotension

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

what CV changes may occur with pheo

A

coronary vasoconstriction, cardiomyopathy, CHF, and EKG changes

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

diagnosis of pheos

A

24 hour urine collection for metanephrine and catecholamines
CT/MRI to localize tumor

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

preop for a pheo

A

alpha blockade to lower BP, decrease intravascular volume, prevent paroxysmal hypertenive episodes, allow sensitization of adrenergic receptors and decrease myocardial dysfunction

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

most common alpha blocker for pheo preop

A

phenoxybenzamine

noncompetitive alpha1 antag with some alpha2 properities

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

short acting, pure alpha1 blockers with less tachycardia

A

prazosin and doxazosin

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

tachycardia after alpha blockade should be treated with

A

BB

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

never give ______ BB before an alpha blocker - bc the blocking _______ receptors results in unopposed alpha agonism; leading to vasoconstriction and hypertensive crisis

A

nonselevcitve BB
B2 receptors

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

what is also used to control HTN with pheos

A

CCB

since calcium triggers catecholamine release from tumor and ecvess calcium entry into myoacrdial cells contributes to catecholamine mediated cardiomypoath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cushing’s Syndrome aka

A

hypercortisolism

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

ACTH dependent Cushings is

A

inapproriately high plasma ACTH stimulating the adrenal cortex to produce excessive amounts of cortisol

acute ectopic ACTH is associated with small lung cell carcinoma

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

ACTH independent Cushings is

A

excessive cortisol productin by abnormal adrenocortical tissue that is not regulated by CRH and ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is usually the cause of ACTH independent cushings syndome

A

benign or malignant adrenocorticol tumors

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

symptoms of Cushing’s Syndrome

A

sudden weight gain, usually central with facial fat (moon) face, eccymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia

Kahoot Q

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

diagnisos of cushings

A

24 hour urine demonstrating cortisol

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

Determining whether Cushing’s is ACTH dependent or independent requires reliable measurements of plasma ACTH using

A

immunoradiometric assays

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

The high-dose dexamethasone suppression test distinguishes

A

Cushings from ectopic ACTH syndrome

34
Q

treatment for Cushings

A

transphenoidal microdenomectomy if microadenoma can be identified and resected

35
Q

alternetive surgical resection for hypercortisolism

A

resection of anterior pituitary

36
Q

other treatment for hypercortisolism

A

pituitary irradiation and bilateral total adrenalectomy

37
Q

surgical removal of adreal gland is indicated for treatment

A

for adrenal adenoma or carcinoma

kahoot Q

38
Q

preop for hypercortisolism

A

evaluate/treat BP, electroylte imbalance, and blood glucose
consider osteroposis positioning

39
Q

Conn Syndrome is also known as

A

hyperaldoseteronism

40
Q

primary hyperaldosteronism is

A

excess secretion of aldosterone from a functional tumor (aldosteronoma) that acts independent of physiologic stimulus

41
Q

Conn Syndrome is also associated with

A

pheochromocytoma, hyperparaythroidism, or acromegaly

42
Q

seconday hyperaldosteronism

A

presents when serum renin is increased, stimualting the release of aldosterone

43
Q

symptoms of Conns

A

nonspecific - some are asymptomatic
HTN, hypokalemia, metabolic alkalosis

44
Q

symptoms highly suggestive of hyper-aldosteronism

A

HTN and hypokalemia

45
Q

T/F primary hyperaldo - plasma renin is suppressed
T/F secondary hyperaldo - renin activity is low

A

T) In primary hyper-aldosteronism, plasma renin activity is suppressed
F) In secondary hyper-aldosteronism, the plasma renin activity is high

46
Q

long term licorice can cause a syndrome that mimic the features of hyperaldosteronism such as

A

suppresion of RAAS
hypokalemia
HTN

47
Q

treatment for Conn’s Syndrome (6)

A

spironolactone
K+ replacement
Antihypertensives
diuretics
tumor removal
possible adrenalectomy

48
Q

HyperK+ in the absence of renal insufficicency suggests

A

hypoaldosteronism

49
Q

hyperK+ can be enhanced with

A

hyperglycemia

50
Q

what form of acidosis is common with hypoaldosteronism

A

hyperchloremic metabolic acidosis

51
Q

what symptoms may also be present with hypoaldosteronism

A

heart block secondayr to HyperK+, orthostatic Hypotension and hyponatremia

52
Q

lack of aldo secretion reflects

A

congentitial deficiency of aldo synthesase or hyporenimeia caused by defects at the JGA or ACE-Is

53
Q

hyporeninemic hypoaldo occurs in patients above 45 with

A

CRF or DM

54
Q

Indomethacin induced prostaglandin deficiency is a (reversible or irreversible) cause

A

reversible cause

55
Q

treatment for hypoaldo includes

A

liberal Na+ intake and dialy fludrocortisone

56
Q

addison’s disease

A

adrenal glands unable to prodice enough glucocorticoid, mineralocorticoid and adrogen hormones

57
Q

how much destruction of the glands need to be destroyed before signs appear in adrenal destruction

A

> 90%

58
Q

secondary adrenal insufficency

A

hypothalamic-pituitary disease or supression leading to failure in the production of CRH or ACTH

59
Q

with secondary adrenal insufficiency what is the deficiency

A

glucocortoid

60
Q

most cases of adrenal insufficency are iatrogenic caused by

A

pituitary surgery irradation, or use of synthetic glucocorticoids

61
Q

diagnosis of adrenal insufficency

A

baseline cortisol < 20 mcg/dL and remain <20 mcg/dL after ACTH stimulation

62
Q

with ACTH stimulation - positive test demonstrates

A

poor response to ACTH and indicates an impairment of the adrenal cortex

63
Q

absolute adreal insufficiency is characteristics vs relative adrenal insufficiency

A

absolute.. low baseline cortisol levels and positive result with ACTH stimulation
relative… higher baseline cortisol levels and positive result with ACTH stimulation

64
Q

treatment for adrenal insufficiency

A

steroids

65
Q

how many paraythroid glands are there

A

4

located bilateral of thryoid glands - has upper and lower poles

66
Q

hypocalcemia stimualtes the release of

A

PTH

67
Q

hypercalcemia suppresses

A

hormonal synthesis and release

68
Q

PTH maintains normal plasma calcium levels by promoting the movement of Ca++

A

across the GI tract, renal tubules, and bone

69
Q

primary hyperparathyroidism is caused by

A

benign parathyroid adenoma (90%)
carcinoma (<5%)
parathryroid hyperplasia

70
Q

symptoms of hyperPTH

A

sedation, N/V, decreased strength and sedation, polyuria, renal stones, PUD, cardiac disturbances

71
Q

diagnosis of hyperPTH

A

plasma Ca++, 24 hour urinary Ca++

72
Q

treatment of hyperPTH

A

surgical removal of abnormal portions of the gland

73
Q

what is secondary hyperPTH.. and a cause

A

compensatory response of the PTH glands to counteract a disease process (CRF) causing hypocalcemia

seldomly produces hypercalcemia

74
Q

treatment for secondary hyperPTH

A

control underlying disease
normalize serum Phosphate concentrations with renal disease (PhosLow)

75
Q

hypoPTH

A

when PTH is deficient or peripheral tissues are resistant to its effects

76
Q

T/F hypoPTH is almost always iatrogenic

A

true - inadvertent removal od PTH glands as during thyroidectomy

77
Q

what is pseudohypoparathyroidism

A

congenital disorder where PTH is adeqaute but the kidneys are unabel to respond to it

78
Q

diagnosis of HypoPTH

A

Hypocalcemia < 4.5 mEq/L
iCa++ < 2.0 mEq/L
along with decreased PTH and increased phosphate

79
Q

acute hypocalcemia with accidental removal of parathyroid during thryoidectomy may cause

A

inspiratory stridor = reflecting irritability of intrinsic laryngeal musculature

80
Q

chronic hypocalcemia is associated with

A

fatigue, cramps, prolonged QT interval, lethargy, cataracts, SQ calcifications, thickening of skull, neuro deficits

81
Q

common cause of hypocalcemia

A

chronic renal failure

82
Q
A

Health Assessment (16 decks)

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