Brainscape's Knowledge GenomeTM

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


See full index

Appendix > Adrenals > Flashcards

Adrenals Flashcards

1
Q

Adrenals are one of the most highly perfused organs in the body;

A

2000 cc/kg/min

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

Where do adrenal cortex and medulla arise from?

A

cortex–> mesoderm

medulla–> ectoderm; neural crest origin

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

What is the blood supply of the adrenal glands?

A

superior adrenal arteries–> from inferior phrenic arteries

middle adrenal arteries–> from aorta

inferior adrenal arteries–> from renal arteries

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

What is special about the venous drainage of the adrenal glands?

A

left adrenal vein is longer; drains into inferior phrenic veins–> which drains in left renal vein–> IVC

right adrenal vein is shorter; drains directly into IVC

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

Where does right adrenal vein drain into?

A

directly into IVC

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

Left adrenal vein drains where?

A

its longer

drains into left inferior phrenic vein; then left renal vein; then into IVC

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

what are the three layers of the adrenal cortex?

A

outer zona glomerulosa;

middle zona fasciculata;

inner zona reticularis

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

Outward to inward, what are the layers of the adrenal cortex?

A

glomerulosa
fasciculata
reticularis

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

In what part of adrenal medulla do we see an interface between sympathetic NS and endocrine system?

A

adrenal medulla

sympathetic fibers synapse with chromaffin cells

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

What converts norepinephrine into epinephrine?

A

phenylethanolamine n-methyl tranferase

PNMT

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

Zona glomerulosa makes what hormone?

A

aldosterone

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

Highest levels of ACTH and thus cortisol are seen when?

A

early morning when we wake

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

What do glucocorticoids do?

A

have a net catabolic effect

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

Aldosterone released from what zone?

A

zona glomerulosa

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

How does aldosterone get released from zona glomerulosa?

A

RAAS

low Na is detected in distal convoluted kidney tubule (seen in septic shock, hypovolemia)

renin is released from JGA

renin then cleaves angiotensinogen (made in liver) to angiotensin I

Angiotensin I cleaved to AT II by ACE in lungs

ATII is a potent vasoconstrictor–> stimulates aldosterone release

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

How does K affect aldosterone release or the RAAS?

A

hypo-kalemia reduces aldosterone released by suppressing renin release

hyper-kalemia; opposite effect

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

What does aldosterone do?

A

regulates circulating fluid volume and electrolyte balance

promotes Na/Cl retention in distal convoluted tubule

K/H are secreted into urine

negative feedback occurs when too much Na is seen at distal convoluted tubule, suppressing renin release

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

Where are catecholamines synthesized in the adrenals?

A

medulla

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

Adrenal medulla makes what?

A

catecholamines

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

Synthesis of catecholamines in adrenal medulla begins with what?

A

tyrosine

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

How is epinephrine made?

A

tyrosine–> L-dopa–> Dopamine–> Norepi–>Epi

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

Norepi is converted to epinephrine by actions of phenylethanolamine n-methyl transferase, which is located where?

A

chromaffin cells of adrenal medulla

and in the organ of Zuckerkandl

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

How are catecholamines released from adrenal medulla?

A

sympathetic stimulation of adrenal medulla causes release of stored catecholamines

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

What is the net effect of adrenal medulla catecholamine release?

A

deliver blood and oxygen to brain, heart and muscle at the expense of the rest of the body

fight-or-flight response

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

What does stimulating b1 and b2 receptors do?

A

b1—> receptors in myocardium–> increase contractility and increased HR

b2–> smooth muscle of uterus, bronchus, skeletal muscle arterioles –>smooth muscle relaxation

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

What does stimulation of a1 receptors do?

A

vasoconstriction seen in skin and GI system

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

What does stimulation of a2 receptors do?

A

a2 receptors found in pre-synaptic locations in CNS

attenuate SNS outflow

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

Plasma half life of catecholamines?

A

1 min

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

Epinephrine and norepi are inactivated by what enzymes?

A

MAO (monoamine oxidase)

COMT (catechol o methyl transferase)

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

What effect do MAO and COMT have on epinephrine and norepi and how can we use this diagnostically?

A

break down nore and epi to metanephrine and noremetanephrine and final product is vanillymandelic acid (VMA)

these products have longer half lives than nore and epi and they are secreted in urine

UA can be used for diagnostic purposes

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

What is primary adrenal insufficiency?

A

Addison’s dx

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

Addison’s dx AKA?

A

primary adrenal insufficiency

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

Sx of Addison’s dx, AKA primary adrenal insufficiency?

A 
weakness
fatigue
hyperpigmentation
weight loss
electrolytes; hyponatremia, hyperK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What causes hyperpigmentation in Addison’s dx, primary adrenal insufficiency?

A

ACTH-induced melanogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What causes adrenal insufficiency in Addison’s dx (primary adrenal insufficiency)?

A

autoimmune destruction of adrenals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Waterhouse Friedrichsen syndrome and adrenal insufficiency?

A

adrenal hemorrhage usually caused by meningococcal infection

more common pediatric/asplenic pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is secondary adrenal insufficiency?

A

ACTH deficiency

usually seen in pts from steroid withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does Sheehan syndrome cause secondary adrenal insufficiency?

A

post-partum hemorrhage leads to pituitary infarction, which leads to decreased ACTH and adrenal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Adrenal insufficiency in critically ill pts?

A

some studies suggest 30% of critically ill pts may suffer from adrenal insuficiency

usually do to adrenal ACTH resistance and decreased responsiveness of target tissues to steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

This is a serious, life threatening event that occurs in pts with already marginal adrenal function that incur a significant stressor such as surgery or trauma or infection ;

A

adrenal crisis

41
Q

What are symptoms of adrenal crisis?

A

shock
abd pain
n/v
electrolyte disturbances

42
Q

Primary mechanism behind acute adrenal crisis?

A

menalcorticoid deficiency

inability to maintain Na and intra-vascular volume

43
Q

Tx for acute adrenal crisis?

A

large volume resuscitation (>2 L) w/saline

hydrocortisone 100 mg IV Q 6-8 hrs or dexamethasone 4 mg IV Q 24 hrs)

44
Q

How do we work up someone we suspect has adrenal insufficiency?

A

measure morning levels of cortisol in serum/saliva
(serum cortisol > 15.8 or saliva cortisol > 5.8 excludes adrenal insufficiency)

in pts with lower serum/saliva cortisol–> you do a high dose cosyntropin stimulation test with 250 ug of ACTH

measure cortisol levels 30-60 mins later

cortisol levels less than 18 ug/dL –> adrenal insufficiency (these pts did not respond to ACTH stimulation appropriately)

after this, a morning ACTH level is done to differentiate between primary vs secondary adrenal insufficiency

high ACTH–> primary adrenal insufficiency
low ACTH–> secondary adrenal insufficiency

45
Q

How do we treat adrenal insufficiency?

A

the goal of maintenance adrenal insufficiency is to replace physiologic cortisol and mineralcorticoids

prednisone 5 mg/day given to replace normal cortisol

fludrocortisone 0.1 mg/day given to replace mineralcorticoids

doses can be increased if pt is undergoing a stressor like surgery or infection

46
Q

What is CONN syndrome?

A

primary hyperaldosteronism

47
Q

Primary hyperaldosteronism AKA?

A

Conn syndrome

48
Q

Pts with Conn syndrome, primary hyperaldosteronism present with what?

A

resistant HTN

hypokalemia

49
Q

How do pts with Conn syndrome, primary hyperaldosteronism present?

A

usually asymptomatic, some can have muscle cramps from hypokalemia

resistant HTN (usually on 2-4 anti-hypertensive meds)

50
Q

What are the most common causes of primary hyerpaldosteronism, Conn syndrome?

A

unilateral aldosterone producing adenomas

b/l adrenal hyperplasia

51
Q

When trying to diagnose someone with primary hyperaldosteronism, Conn syndrome what do we begin with?

A

plasma aldosterone concentration/ plasma renin activity

> 30–> then you create a state of hypervolemia , Na excess by loading the pt up with IV NS or salt loading and measuring aldosterone levels

if aldosterone is not suppressed, then they probably have primary hyperaldosteronism

now you need to localize the lesion by performing adrenal CT scanning (adrenalectomy in pts with clear cut CT abnormality)

then you do adrenal venous sampling if CT equivocal–> measuring aldosterone and cortisol levels in periphery and R/L adrenal veins

52
Q

Surgical approach of choice for most aldosteronoma and most adrenal tumors?

A

laparoscopic adrenelectomy

53
Q

What;s Cushing;s syndrome?

A

clinical features that accompany steroid excess

54
Q

Most common cause of Cushing syndrome?

A

pharmacological steroid use for tx of inflammatory dx

55
Q

What is Cushing’s dx?

A

steroid excess caused by ACTH-secreting pituitary adenoma

56
Q

Cushing syndrome vs Cushing dx?

A

syndrome–> steroid excess causing plethora of symptoms

disease–> steroid excess caused by ACTH secreting pituitary adenoma

57
Q

How do we screen for Cushing syndrome?

A

start with measuring 24 hr urine cortisol; 2 samples needed

58
Q

First line antihypertensive intra-op for pheochromocytoma?

A

nitroprusside

59
Q

Why do we perform dexamethasone suppression test?

A

helps us to identify cause of cushing’s syndrome

why do we have excess cortisol, is it from exogenous source, is it from ACTH secreting tumor, is it from somewhere else

60
Q

Describe dexamethasone suppression test;

A

normal axis; hypothalamus makes CRH–> stimulates AP to make ACTH–> which stimulates adrenal make cortisol

low dose dexamethasone 1mg is given; and normal response is it will negatively feedback to brain, and adrenal and decrease CRH, ACTH and cortisol

in cases of cushing;s syndrome; where we have excess cortisol produced, the 1 mg dexamethasone suppression is not going to affect it much

so with low dose dexamethasone, if we still have high cortisol, this is suggestive of a cushing syndrome

so now we do a high dose dexamethasone suppression test with 8 mg

if we have cushing disease ( a pituitary adenoma which is makes lots of ACTH and causing adrenal to make lots of cortisol), the high dose dexamethasone will suppress the pituitary adenoma and cortisol levels will decrease

if we have an adrenal adenoma which is makes lots of cortisol, the high dose dexamethasone is not going to suppress the adrenal adenoma (but it will still suppress the CRH and ACTH, so we see low ACTH but high cortisol)

now if we have a lung cancer that is making ACTH, the dexamethasone suppression will suppress the hypothalamus and the pituitary from making CRH and ACTH, but we still have this endogenous ACTH being made that is not suppressed, so we still see high ACTH and high cortisol (the high dose dexamethasone is not able to suppress the ectopic ACTH tumor source)

61
Q

Peak age of pheochromocytomas?

A

40-50

62
Q

Classic triad of pts who present with pheochromocytomas?

A

headache

diaphoresis

palpitations

**HTN also present, can be episodic vs sustained

63
Q

Rules of 10s of pheochromocytomas?

A

10% malignant

10% bilateral

10% extra-adrenal

10% familial

64
Q

How do we diagnose pheochromocytomas?

A

detection of 24 urine for catecholamines

65
Q

Most common peri-operative changes witnessed with pheochromocytomas is?

A

intra-op; HTN
post-op; hypotension

intra-op; anesthetic induction and manipulation of tumor

post-op; due to state of hypovolemia due to excess circulating catecholamines; sudden withdrawal from this stimulus causes arteriolar vasodilation

66
Q

How can we prevent the hemodynamic changes assc with pheochromocytomas intra-op and post-op?

A

use of a-adrenergic blockade as soon as the diagnosis of pheo is made

phenoxybenzamine is used; 10 mg twice/daily; two weeks before planned surgery

67
Q

How does phenoxybenzamine work in pheo?

A

non-specific, irreversible A-adrenergic antagonist

SE: postural hypotension, nasal congestion

**b-blockers can be used after adequate a-blockade, should never be used as first line drugs

68
Q

Tx for pheo?

A

surgery is curative >90% of cases

most can be done laparoscopically

**lap contraindicated if there is local invasion

69
Q

What % of pheochromocytomas are familial?

A

20-30%

70
Q

Are pheochromocytomas malignant?

A

2-40% are

71
Q

What are incidentalomas?

A

incidentally discovered adrenal masses

are discovered thru imaging for non-adrenal causes

72
Q

How do we work up incidentalomas?

A

size criteria + hormonal evaluation

73
Q

For incidentalomas whats the size cutoff for surgical removal?

A

remove all incidentalomas >5 cm

consider strongly removal of masses 3-5 cm

**if observation chosen, imaging should be done 6-12 months

74
Q

What are suspicious imaging characteristics of incidentalomas that would warrant removal?

A

heterogenous
high attenuation
irregular margins

75
Q

Do we use FNA for adrenal masses suspected of being malignant?

A

NO

76
Q

What are some cancers that mets to adrenal glands due to their rich vascular supply?

A

LUNG

Gi tract

77
Q

Benefits of laparoscopic adrenalectomy vs open?

A

less pain
less bleeding
less hospital stay

78
Q

Conversion rate from laparoscopic to open adrenalectomy?

A

5%

79
Q

When is an adrenalectomy performed open?

A

tumor suspicious for malignancy

size > 8cm

clinical feminization

local or vascular invasion

mets

regional adenopathy

80
Q

What’s Palmer’s point?

A

mid-clavicular, 2 inch inferior to costal margin

81
Q

When do we use adjuvant mitotane for carcinoma of adrenal?

A

vascular/capsular invasion

intra-op tumor spillage

high-grade disease

82
Q

After removal of an adrenal carcinoma, what type of surveillance do we do?

A

abdomen/pelvis/chest every 3 months for 2 yrs

every 4-6 months for 5 yrs

83
Q

What ectopic lesions cause Cushing syndrome?

A

small cell lung ca

84
Q

Causes of Cushing syndrome?

A

pituitary lesions

adrenal adenoma

ectopic tissue; small cell lung Ca

85
Q

When is laparoscopic adrenalectomy not performed for adrenal lesions?

A

relative contraindication for lesions 6-8 cm

absolute contraindication is local invasion of lesion to surrounding structures

86
Q

Whats the difference between adrenocortical carcinoma stage I vs stage II?

A

related to size

whether tumor is less than or greater than 5 cm

87
Q

During intra-op manipulation of an adrenal carcinoma, you get tumor spillage, what do you do?

A

add mitotane adjuvantly

88
Q

What do the three zones of the adrenal cortex make?

A

zona glomerulosa–> mineralcorticoids (aldosterone)

zone fasciculata—> glucocorticoids (cortisol)

zona reticularis–> sex hormones

medulla–> catecholamines

89
Q

What CT findings are concerning for an adrenal ca?

A

> 20 hounsfield units

lesion has calcifications

size > 4 cm

unilateral location

heterogenous appearance on CT

90
Q

Most common cause of Cushing’s dx is?

A

iatrogenic due to exogenous steroid use

2nd most common; ACTH producing pituitary tumor

91
Q

Most common cause of Conn syndrome (primary hyperaldosteronism?)

A

b/l adrenal hyperplasia (need to localize is with thin cut adrenal ct; venous sampling if CT inconclusive)

(second most common cause is unilateral adrenal adenoma; tx is lap adrenalectomy)

b/l adrenal hyperplasia managed with aldosterone antagonists

92
Q

Most commonly use screening test for Conn syndrome; hyperaldosteronism?

A

aldosterone; renin ratio; cutoff is 30

93
Q

What is Cushing’s dx and what is the tx?

A

ACTH secreting pituitary tumor

trans-sphenoidal resection usually curative in 75%

remission rates can be improved by re-operative vs pituitary radiation

94
Q

Advantage of posterior laparoscopic retroperitoneal adrenalectomy approach?

A

good for pts that have had prior abdominal surgeries

good for pts who need b/l adrenalectomies

95
Q

Gold standard initial test when you suspect someone has Cushing syndrome (hypercortisolism)?

A

24-hr urine collection for free cortisol

> 300 mcg/day are diagnostic

once you confirm pt has cushing syndrome; gotta check an ACTH level

if ACTH is low, cortisol is high–> adrenal adenoma or hyperplasia

if ACTH is high, cortisol is high–> pituitary adenoma vs ectopic ACTH tumor (high dose dexamethasone test then done)

96
Q

When MEN2A and MEN2 disorders are involved, when do we perform thyroidectomies for pts?

A

MEN2B; thyroidectomy before 1 year old

MEN2A; thyroidectomy before 5 years old

97
Q

Most common primary tumor to mets to adrenals is?

A

lung

98
Q

MC cause of hyperaldosteronism? Conn syndrome?

A

bilateral adrenal hyperplasia

2nd most common cause is adrenal adenoma

99
Q

Nitrogen balance formula?

A

protein/ 6.25 - (UUN +4)

Appendix (39 decks)

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