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Foundations III- Endocrine > disorders of the adrenal gland > Flashcards

Flashcards in disorders of the adrenal gland Deck (64)
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1
Q

where is the problem located in the hypothalamic-pituitary axis for: primary, secondary, and tertiary disorder

A

primary = target organ

secondary = pituitary

tertiary = hypothalamus
*more organs involved

2
Q

what is the predominant feedback loop w/in the endocrine system?

A

Negative

3
Q

example of a positive feedback loop?

A

oxytocin

4
Q

what types of hormones are produced in the 4 zones of the adrenal gland?

A

outer = Mineralocorticoids (Aldosterone)

middle = Glucocorticoids (Cortisol)

inner = Adrenal Androgens (DHEA)

medulla = Catecholamines (epi and NE)

5
Q

aldosterone causes increased reaborptionn of ____ and increased excretion of _____.

A

Na and water

K+ and H+

aldosterone controls fluid volume**

6
Q

describe cortisol secretion

A

it is pulsatile (stress), diurnal (circadian regulation), and under control of ACTH

7
Q

long term high dose glucocorticoid therapy can cause…?

A

adrenal atropohy

8
Q

primary overproduction of cortisol by adrenal glands inhibits _____.

A

ACTH secretion

9
Q

what is the role of glucocorticoids (cortisol) in the body?

A
Protects against hypoglycemia
Decrease insulin sensitivity
Anti-inflammatory
Suppression of immune responses
Maintain vascular responsiveness to NE/Epi
Inhibits bone formation
Promotes increases in GFR
10
Q

what effect can “weak” androgens have in males/females?

A

males –> limited physiological significance

females –> major source of androgens (pubic and axillary hair during early development), masculinization

11
Q

How can you measure catecholamine levels?

A

urine test bc metabolites are excreted in the urine

12
Q

what are some physiologic effects of catecholamines?

A
Increased rate and force of contraction of the heart muscle
Constriction of blood vessels
Stimulation of lipolysis in fat cells
Increased metabolic rate
Dilation of the pupils
13
Q

effects of short-term stress response in the body

A

increased HR and BP, liver converts glycogen to glucose > releases glucose to blood, incr. metabolic rate

14
Q

effects of long-term stress response in the body

A

retention of Na/H2O by kidneys, incr. blood volume and BP, proteins and fats converted to glucose or broken down, increased blood sugar, suppression of immune system

15
Q

What type of test would assess for hypofunctioning? hyperfunctioning?

A

hypo = stimulation test

hyper = suppression test

16
Q

what are adrenal lab tests?

A
Serum total cortisol
24-hour urinary free cortisol
Plasma ACTH
ACTH stimulation
Dexamethasone suppression
17
Q

when should you obtain a serum cortisol level?

A

btwn 8-9am

18
Q

what lab values would indicate adrenal insufficiency?

A

serum total cortisol:
< 3 = very likely adrenal insufficiency

btwn 3-10 = inconclusive

> 10 = unlikely adrenal insufficiency

19
Q

what is the ideal situation for using a 24-hr urinary free cortisol test?

A

suspected hypercortisolism

20
Q

where is ACTH produced?

A

pituitary

21
Q

what time of day should you measure plasma ACTH?

A

in the AM

22
Q

when would you order an ACTH stimulation test?

A

to differentiate source of adrenal insufficiency (cortisol deficiency)

23
Q

ACTH stimulation test: if cortisol level doubles where is the problem?

if it is a subnormal response where is the problem?

A

no problem. adrenal gland is functioning!

adrenal insufficiency

24
Q

what is the dexamethasone suppression test confirm?

A

Confirm abnormal excess production

25
Q

Dexamethasone Suppression Test: what result would indicate excess cortisol production

A

if cortisol level does not change

if suppressed = normal fx

26
Q

Cushing’s syndrome?

A

Collection of signs and symptoms due to prolonged exposure to elevated cortisol

MC overal is excess d/t exogenous use

27
Q

Cushing’s syndrome d/t endogenous reasons?

A

MC = Pituitary adenoma

adrenal hyperplasia
Adrenocortical tumor
Neuroendocrine tumor
Ectopic production

28
Q

clinical manifestations of cushing’s syndrome?

A

HTN, central obesity (moon face), insulin resistance, purple striae, androgen excess (hirsutism), osteoporosis

29
Q

what 3 signs would increase your suspicion for cushing’s?

A

characteristic body changes
HTN
glucose intolerance

30
Q

what tests would you order to dx cushing’s?

what are results consistent w/ cushing’s?

A

24-hour urinary free cortisol levels = Elevated

Midnight salivary cortisol level = Elevated on 2 separate nights

Dexamethasone suppression test = No change in cortisol levels

31
Q

Cortisol and ACTH levels for Adrenal hyperplasia or tumor?

A

cortisol = High

ACTH = low

*target organ problem! ACTH independent

32
Q

Cortisol and ACTH levels for ACTH producing tumor – pituitary or ectopic?

A

cortisol = high

ACTH = high

*ACTH dependent

33
Q

Management of Cushing’s syndrome?

A

excluded exogenous cortisol use?

pituitary tumor –> consider MRI

ectopic ACTH secreting tumor –> consider CXR and pelvic U/S

adrenal tumor –> palp mass? CT abd

34
Q

Tx for exogenous corticosteroids?

A

taper to lowest therapeutic dose

35
Q

Tx for pituitary adenoma in cushing’s syndrome

A

transsphenoidal resection

36
Q

tx for adrenal hyperplasia in cushing’s syndrome

A

medical management

37
Q

tx for adrenal tumor in cushing’s syndrome

A

adrenalectomy

38
Q

tx for Ectopic ACTH syndrome in cushing’s syndrome

A

targeted at source of ectopic production

39
Q

What medications can you use to tx cushing’s?

A

adrenolytic agents- mitotane

adrenal enzyme inhibitors- Ketoconazole, metyrapone

40
Q

what is adrenal insufficiency?

primary, secondary, tertiary

A

primary -> glucorticoid defiencies

secondary -> insufficient ACTH secretion (long term corticoco’s)

tertiary -> insufficient CRH secretion

41
Q

causes of primary adrenal insufficiency?

A

MC in US d/t autoimmune cortical destruction (addison’s dz), TB (worldwide), congenital deficiencies, infx, surg (s/p adrenalectomy)

42
Q

clinical manifestations of adrenal insufficiency

A

Insidious onset w/ nonspecific symptoms (weakness, fatigue, anorexia, wt. loss), GI sxs (V/D, abd pain), hypotension, hypoglycemia, salt cravings,

**hyperpigmentation - classic

severe –> extremely low levels of cortisol

43
Q

diagnostic studies assoc. w/adrenal insufficiency

A

CMP (hyperkalemia, hypercalcemia, hyponatremia)

eosinophilia

andi-adrenal antibodies

AM plasma cortisol (abn low)

plasma ACTH level

ACTH stimulation test (cortisol does NOT incr)

44
Q

when do you order a radiographic eval of the adrenals for insufficiency?

A

if the lab workup reveals autoimmune adrenalitis

CT -> infx or malignancy

45
Q

when should you order an MRI of the pituitary for adrenal insufficiency?

A

if secondary adrenal insufficiency points toward hypothalamic or pituitary source

46
Q

Tx for primary adrenal insufficiency

A

requires both glucocorticoid (hydrocortisone) & mineralocorticoid (fludrocortisone) replacement

47
Q

Tx for secondary and tertiary Adrenal insuffiency

A

only glucocorticoid replacement is necessary

48
Q

what do you need to do if pt is on meds for adrenal insufficiency and they are going through a period of increased stress?

A

increase the steroids during the period of stress

49
Q

Tx for adrenal crisis?

A
IV steroids
Correct electrolyte abnormalities
50% dextrose to correct hypoglycemia
Initiate volume resuscitation
Search for underlying cause
50
Q

Primary hyperaldosteronism

A

aka Conn’s syndrome d/t

adrenocortical adenoma or cortical hyperplasia

51
Q

presentation of primary hyperaldosteronism

A
Hypertension
Hypokalemia
Muscular weakness
Paresthesias
Headache
Polyuria &amp; polydipsia
52
Q

diagnostic workup for primary hyperaldosteronism

A

Elevated plasma and urine aldosterone
Low plasma renin levels
Ct scan of adrenals to evaluate for adrenal adenoma

53
Q

management for primary hyperaldosteronism

A

Surgical removal of adenoma

Medical = spironolactone and antihypertensive agents

54
Q

what is Pheochromocytoma

A

Rare tumor that arises from chromaffin cells that secretes catecholamines

80% to 90% located in adrenal medulla

10% are malignant

55
Q

clinical manifestations for pheochromocytoma

A
Paroxysmal Palpitations (tachycardia), Headache and Episodic sweating
Paroxysmal or sustained hypertension 

less common: pallor, N, tremor, fatigue, anxiety, hypertensive retinopathy

56
Q

describe a Pheochromocytoma “attack”

A

Usu. last 30-40 minutes

May be precipitated by displacement of abdominal contents (ie lifting, bending, deep palpation)

57
Q

when to suspect a pheo?

A

Classic paroxysmal “attacks,”
refractory HTN or onset <20 y/o, idiopathic dilated cardiomyopathy, abd mass, family hx, incidentally discovered adrenal mass

58
Q

what is the 1st line screening for dx of pheochromocytoma?

A

metanephrine (catecholamine metabolite) 24hr urine screen

59
Q

what other tests can you order to dx pheo?

A

Clonidine suppression test
MRI of abd/pelvis to locate tumors
MIBG scintigraphy

60
Q

Tx of pheochromocytoma

A

surgical resection

prior to surg

  • alpha adrenergic blocker until BP and sxs controlled
  • BB (propranalol) for tachy
61
Q

Adrenal Incidentaloma

A

Mass lesion greater than 1 cm discovered incidentally by radiologic examination

higher prevalence in obese, HTN, and DM pt’s

62
Q

workup for adrenal incidentaloma

A

Everyone gets plasma cortisol, serum ACTH, serum DHEA, plasma aldosterone

s/s of cushing’s –>
yes = 24 hr urinary free cortisol
no = 1-mg overnight dexamethasone suppression test

susp. for pheo?
24-hr urine metanephrines, catecholamines

63
Q

when is FNA/bx indicated for adrenal incidentaloma?

A

Do it –> known primary malignancy elsewhere

Do NOT –> Biochemical evidence of pheo or known widespread metastatic disease

64
Q

management of adrenal incidentaloma

A

documented pheo or carcinoma –> prompt surg.

pharmacologic to tx underlying

benign appearing on imaging:
>2cm –> consider resection
<2cm –> repeat imaging 6mo’s
repeat Dexamethasone suppr. test annually x4yrs