Endocrine Pt 2 (adrenal/parathyroid Flashcards

(82 cards)

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
Cushing's Syndrome aka
hypercortisolism
26
ACTH dependent Cushings is
inapproriately high plasma ACTH stimulating the adrenal cortex to produce excessive amounts of cortisol | acute ectopic ACTH is associated with small lung cell carcinoma
27
ACTH independent Cushings is
excessive cortisol productin by abnormal adrenocortical tissue that is not regulated by CRH and ACTH
28
29
what is usually the cause of ACTH independent cushings syndome
benign or malignant adrenocorticol tumors
30
symptoms of Cushing's Syndrome
sudden weight gain, usually central with facial fat (moon) face, eccymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia ## Footnote Kahoot Q
31
diagnisos of cushings
24 hour urine demonstrating cortisol
32
Determining whether Cushing's is ACTH dependent or independent requires reliable measurements of plasma ACTH using
immunoradiometric assays
33
The high-dose dexamethasone suppression test distinguishes
Cushings from ectopic ACTH syndrome
34
treatment for Cushings
transphenoidal microdenomectomy if microadenoma can be identified and resected
35
alternetive surgical resection for hypercortisolism
resection of anterior pituitary
36
other treatment for hypercortisolism
pituitary irradiation and bilateral total adrenalectomy
37
surgical removal of adreal gland is indicated for treatment
for adrenal adenoma or carcinoma ## Footnote kahoot Q
38
preop for hypercortisolism
evaluate/treat BP, electroylte imbalance, and blood glucose consider osteroposis positioning
39
Conn Syndrome is also known as
hyperaldoseteronism
40
primary hyperaldosteronism is
excess secretion of aldosterone from a functional tumor (aldosteronoma) that acts independent of physiologic stimulus
41
Conn Syndrome is also associated with
pheochromocytoma, hyperparaythroidism, or acromegaly
42
seconday hyperaldosteronism
presents when serum renin is increased, stimualting the release of aldosterone
43
symptoms of Conns
nonspecific - some are asymptomatic HTN, hypokalemia, metabolic alkalosis
44
symptoms highly suggestive of hyper-aldosteronism
HTN and hypokalemia
45
T/F primary hyperaldo - plasma renin is suppressed T/F secondary hyperaldo - renin activity is low
T) In **primary** hyper-aldosteronism, plasma renin activity is suppressed  F) In **secondary** hyper-aldosteronism, the plasma renin activity is high
46
long term licorice can cause a syndrome that mimic the features of hyperaldosteronism such as
suppresion of RAAS hypokalemia HTN
47
treatment for Conn's Syndrome (6)
spironolactone K+ replacement Antihypertensives diuretics tumor removal possible adrenalectomy
48
HyperK+ in the absence of renal insufficicency suggests
hypoaldosteronism
49
hyperK+ can be enhanced with
hyperglycemia
50
what form of acidosis is common with hypoaldosteronism
hyperchloremic metabolic acidosis
51
what symptoms may also be present with hypoaldosteronism
heart block secondayr to HyperK+, orthostatic Hypotension and hyponatremia
52
lack of aldo secretion reflects
congentitial deficiency of aldo synthesase or hyporenimeia caused by defects at the JGA or ACE-Is
53
hyporeninemic hypoaldo occurs in patients above 45 with
CRF or DM
54
Indomethacin induced prostaglandin deficiency is a (reversible or irreversible) cause
reversible cause
55
treatment for hypoaldo includes
liberal Na+ intake and dialy fludrocortisone
56
addison's disease
adrenal glands unable to prodice enough glucocorticoid, mineralocorticoid and adrogen hormones
57
how much destruction of the glands need to be destroyed before signs appear in adrenal destruction
>90%
58
secondary adrenal insufficency
hypothalamic-pituitary disease or supression leading to failure in the production of CRH or ACTH
59
with secondary adrenal insufficiency what is the deficiency
glucocortoid
60
most cases of adrenal insufficency are iatrogenic caused by
pituitary surgery irradation, or use of synthetic glucocorticoids
61
diagnosis of adrenal insufficency
baseline cortisol < 20 mcg/dL and remain <20 mcg/dL after ACTH stimulation
62
with ACTH stimulation - positive test demonstrates
poor response to ACTH and indicates an impairment of the adrenal cortex
63
absolute adreal insufficiency is characteristics vs relative adrenal insufficiency
absolute.. low baseline cortisol levels and positive result with ACTH stimulation relative... higher baseline cortisol levels and positive result with ACTH stimulation
64
treatment for adrenal insufficiency
steroids
65
how many paraythroid glands are there
4 | located bilateral of thryoid glands - has upper and lower poles
66
hypocalcemia stimualtes the release of
PTH
67
hypercalcemia suppresses
hormonal synthesis and release
68
PTH maintains normal plasma calcium levels by promoting the movement of Ca++
across the GI tract, renal tubules, and bone
69
primary hyperparathyroidism is caused by
benign parathyroid adenoma (90%) carcinoma (<5%) parathryroid hyperplasia
70
symptoms of hyperPTH
sedation, N/V, decreased strength and sedation, polyuria, renal stones, PUD, cardiac disturbances
71
diagnosis of hyperPTH
plasma Ca++, 24 hour urinary Ca++
72
treatment of hyperPTH
surgical removal of abnormal portions of the gland
73
what is secondary hyperPTH.. and a cause
compensatory response of the PTH glands to counteract a disease process (**CRF**) causing hypocalcemia | seldomly produces hypercalcemia
74
treatment for secondary hyperPTH
control underlying disease normalize serum Phosphate concentrations with renal disease (PhosLow)
75
hypoPTH
when PTH is deficient or peripheral tissues are resistant to its effects
76
T/F hypoPTH is almost always iatrogenic
true - inadvertent removal od PTH glands as during thyroidectomy
77
what is pseudohypoparathyroidism
congenital disorder where PTH is adeqaute but the kidneys are unabel to respond to it
78
diagnosis of HypoPTH
Hypocalcemia < 4.5 mEq/L iCa++ < 2.0 mEq/L along with decreased PTH and increased phosphate
79
acute hypocalcemia with accidental removal of parathyroid during thryoidectomy may cause
inspiratory stridor = reflecting irritability of intrinsic laryngeal musculature
80
chronic hypocalcemia is associated with
fatigue, cramps, prolonged QT interval, lethargy, cataracts, SQ calcifications, thickening of skull, neuro deficits
81
common cause of hypocalcemia
chronic renal failure
82