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Adult Clinical Medicine > Adrenal and Pituitary Disorders > Flashcards

Adrenal and Pituitary Disorders Flashcards

1
Q

where do the adrenal glands sit

A

on kidneys

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2
Q

describe the anatomy of the adrenal gland

A

Outer to inner:

  1. adrenal cortex
  2. zona glomerulosa- aldosterone
  3. zona fasciculata- cortisol
  4. zona reticularis- androgens (testosterone)
  5. medulla- catecholamines
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3
Q

4 divisions of the adrenal gland and what they release

A
  1. zona glomerulosa- aldosterone
  2. zona fasciculata- cortisol
  3. zona reticularis- adrenal androgens (testosterone)
  4. medulla- catecholamines (aka adrenaline)

*each division essentially acts as an independent organ

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4
Q

what is so important about the zona glomerulosa

A
  1. secretes aldosterone
  2. tied to renin stimulatin
  3. important for BP control
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5
Q

what is so important about the zona fasciculata

A
  1. releases cortisol
  2. tied to ACTH
  3. effects the immune system, inflammation, BP
  4. stress hormone
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6
Q

what is so important about the medulla

A
  1. releases catecholamines
  2. stress hormone
  3. essentially a sympathetic ganglion
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7
Q

what is the hypothalamic pituitary adrenal axis?

A

Stress stimulates Hypothalamus–> releases CRH–> stimulates pituitary–> releases ACTH–> stimulates adrenal glands–> releases testosterone, aldosterone, and cortisol

-cortisol neg. feedback on pituitary and hypothalamus

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8
Q

what hormones does the anterior pituitary release and what are its target

A
  1. Adrenocorticotropic Hormone (ACTH)–> adrenal
  2. Growth Hormone–> liver
  3. Prolactin–> mammillary glands
  4. Thyroid Stimulating Hormone (TSH)–> thyroid
  5. Luteinizing Hormone (LH)–> ovaries-testicles
  6. Follicle Stimulating Hormone (FSH)–> ovaries-testicles

*FLAT PiG

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9
Q

categories of adrenal disorder

A
  1. hormone over-production
  2. hormone under-production
  3. adrenal tumors (often incidental findings)
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10
Q

types of hormone over-production adrenal disorders

A
  1. Cortisol –> Cushing’s Syndrome
  2. Catecholamines –> Pheochromocytoma
  3. Aldosterone –> Hyperaldosteronism
  4. Androgens –> Virilism, PCOS?
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11
Q

types of hormone under-production adrenal disorders

A
  1. adrenal insufficiency
    - Primary: Addison’s disease
    - Secondary: Pituitary Disease
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12
Q

what is primary adrenal insufficiency

A

-adrenal gland doesn’t make enough hormone (low testosterone, aldosterone, and cortisol) despite normal signaling from hypothalamus and pit. (elevated CRH and ACTH)

hypothalamus releases increased CRH–> stimulates ant. pituitary to release increased ACTH–> Adrenal cannot release HR**–> decrease testosterone, aldosterone, and cortisol

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13
Q

Etiology of primary adrenal insufficieny

A
  1. Autoimmune: Addison’s Disease (80%) -Think esp in setting of other autoimmune disorders (#1 cause was previously TB)
  2. Infections: TB, HIV, CMV, fungus
  3. Metastatic disease
  4. other Rare causes
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14
Q

other rare causes of primary adrenal insufficieny

A
  1. Adrenal hemorrhage, infarction
  2. Infiltrative diseases: sarcoid, amyloid, hemochromatosis
  3. Meds: enzyme inhibitors, cytotoxic agents
  4. Surgery, XRT (radiation)
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15
Q

what is secondary adrenal insufficiency

A

-adrenal gland is not getting stimulated adequately (low cortisol, normal testosterone and aldosterone) due to problem w/ hypothalamus or pit. (low CRH and low ACTH)

hypothalamus does not release CRH–> ant. pit. does not release ACTH–> decrease cortisol and Testosterone aldosterone

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16
Q

etiology of secondary adrenal insufficiency

A
  1. pituitary
    - tumors, trauma, XRT, infiltrative disease, apoplexy: hemorrhage, infarction, Sheehans
  2. hypothalamic
    - glucocorticoid therapy (most common), other drugs, tumors
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17
Q

symptoms of adrenal insufficiency

A
  1. fatigue
  2. weakness
  3. myalgias
  4. arthralgia
  5. anorexia
  6. N/V
  7. HA
  8. Abdominal pain
  9. weight loss
  10. postural dizziness*
  11. salt craving*
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18
Q

PE signs of adrenal insufficiency

A
  1. hypotension (seen less w/ secondary)
  2. tachycardia*
  3. fever
  4. vitiligo (hypo-pigmentation) (Primary only)
  5. hyperpigmenation–> bc ACTH stimulates melanin (primary only)
  6. abdominal tenderness/guarding
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19
Q

what labs for adrenal insufficiency

A
  1. hyperkalemia (primary only)
  2. hyponatremia
  3. hypoglycemia
  4. azotemia (increase BUN/Cr)
  5. anemia
  6. eosinohilia (Addison’s)
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20
Q

how do you diagnose adrenal insufficiency

A

**If you don’t have enough–> try to stimulate it

  1. Random Cortisol greater than 3 µg/dl
  2. Cosyntropin Stimulation Test (Gold Standard)
    Standard test:
    -Baseline cortisol level (ideally in AM)
    Give 250 µg cortrosyn (ACTH) IV (or IM)
    -Measure cortisol at 30, 60 minutes
    -Adrenal Insufficiency = 30/60 min Cortisol less than 20 µg/dl
  3. imaging?– not unless you suspect metastatic disease

*Cosyntropin= synthetic ACTH

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21
Q

how do you differentiate between primary vs secondary adrenal insufficiency

A

ACTH greater than 100 pg/ml in Primary adrenal insufficiency

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22
Q

Tx of acute adrenal insufficiency

A
  1. Hydrocortisone 100 mg IV q 8 hrs
    - Can also use dexamethasone if cannot wait for Cort Stim Test
  2. Hydration and BP Support: saline, pressors
  3.   Rule out and treat precipitating factors: (trauma, infection, dehydration)
  4. Taper as quickly as clinical condition allows
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23
Q

Tx of chronic primary adrenal insufficiency

A
  1. Hydrocortisone ~30 mg/d (2-3 divided doses)
  2. +/- mineralocorticoid (aldosterone effect)
  3. Consider DHEA in women
  4. pt education

*use lowest dose possible to avoid complications.(Cushing’s syndrome, osteoporosis, DM)

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24
Q

Tx of chronic secondary adrenal insufficiency

A
  1. prednisone ~5mg once daily (pure glucocorticoid– no mieralocorticoid effect)
  2. pt education

*use lowest dose possible to avoid complications.(Cushing’s syndrome, osteoporosis, DM)

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25
Q

what do you need to educate your patient on when treating for adrenal insufficiency

A
  • stress/illness dosing of steroids

- medical alert, family education

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26
Q

___ is uncommon in
traditional primary care practice, 5-8% of
patients with hypertension

A

Secondary hypertension

*high rate of false positives

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27
Q

secondary causes of HTN

A
  1. endocrine causes

2. non-endocrine causes

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28
Q

endocrine causes of secondary HTN

A
  1. Adrenal:
    - Primary Aldosteronism
    - Cushing’s Syndrome
    - Pheochromocytoma
  2. Non-Adrenal
    - Hypo- or Hyperthyroidism
    - Hyperparathyroidism
    - Acromegaly
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29
Q

non- endocrine causes of secondary HTN

A
  1. Renal Parenchymal Dz
  2. Renovascular HTN
    - Age over 55, known CVD, worsening renal function on ACE or ARB
  3. Coarctation of the Aorta
  4. Severe Obesity
  5. Insulin Resistance
  6. Sleep Apnea
  7. Alcohol Abuse
  8. Oral contraceptives
  9. Ureteral/Bladder Obstruction
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30
Q

when to screen for secondary/endocrine HTN

A

 1. Age less than 30 (esp with no risk factors)

  1. Severe/Resistant HTN
    - End organ damage
  2. Family History of Endocrine Disease
  3. “Spells”- Labile Hypertension
  4. Worsening BP after β-Blockers (suggests pheochromocytoma)
  5. Hypokalemia (on low dose diuretic)
  6. Premenopausal Osteoporosis (think of Cushing’s)
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31
Q

describe the renin angiotensin aldosterone system

A

liver secretes angiotensionogen and kidney secretes renin–> renin cuts angtiotensiongen into angiotensin I–> cut by ACE in lungs–> angiotensin II–> vasoconstriction and stimulates adrenal gland –> adrenal gland (zona glomerulosa) releases aldosterone–> Na retention and K excretion in the kidneys

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32
Q

what is primary aldosteronism

A

aka Conn’s syndrome

-Too much production of aldosterone by the adrenal glands resulting in low renin levels, vasoconstriction, Na retention/K excretion= HTN

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33
Q

what can primary aldosteronism cause

A
  • HTN
  • hypokalemia
  • metabolic alkalosis
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34
Q

main subtypes of primary aldosteronism

A
  1. aldosterone producing adenoma (APA)- 34% (curable)

2. idiopathic hyperaldosteronism- 66% (aka hyperplasia of adrenal glands)

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35
Q

who is screened for aldosteronism?

A

hypertensive patients with:

  1. hypokalemia: spontaneous or provoked w/ diuretics
  2. Severe HTN ( over 160/100)
  3. resistant HTN (over 2 drugs)
  4. HTN onset less than 20-30 yrs old
  5. Adrenal incidentaloma
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36
Q

Screening tests for primary aldosteronism

A
  1. MORNING Blood Sample (seated) for:
    -Plasma Aldosterone (PA) - high
    -Plasma Renin Activity (PRA) - low
  2. Positive Screen:
    PA/PRA ratio over 20 and PA over 15 ng/dl

*PA(H) : PRA (L) ratio is key

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37
Q

screening issues for primary aldosteronism

A
  1. stop meds that affect the RAAS system
  2. supplement potassium to maintain a level of at least 0.3 mmol/L
  3. Do not restrict salt
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38
Q

what meds affect the RAAS system that need to be stopped prior to screening for primary aldosteronism

A
  1. Spironolactone, estrogens for 6 weeks
  2. ACE, ARB, diuretics, NSAIDS, β-blockers,
    nondihydropyridine CCBs for 2 weeks
  3. Hydralazine, verapamil, alpha blockers have least
    impact on PA/PRA ratio
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39
Q

confirmation tests for primary aldosteronism

A
  1. Sodium Suppression Testing
    - Oral Salt Loading (High Na Diet x 3 days)
    - IV Saline Infusion (2 L NS over 4 Hours)
  2. diagnostic results:
    - Oral Salt Loading Test (High Na Diet)- 3rd Day: 24 hr Urine Aldosterone over 12 ug
    - IV Saline Test- PA over 10 ng/dl
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40
Q

when would you need unilateral adrenalectomy (APA)

A

*Only get abdominal CT if confirmation tests are positive (endocrinologist would order these)

  1. unilateral hypodense nodule on CT greater than 1cm and less than 40 y/o
  2. unilateral hypodense nodule on CT greater than 1cm, over 40, and lateralization w/ adrenal vein sampling
  3. normal or micronodularity or bilateral mass on abdominal CT, and lateralization w/ adrenal vein sampling
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41
Q

when would you need medical management for primary aldosteronism (IHA)

A
  1. normal or micronodularity or bilateral mass on abdominal CT–> APA unlikely
  2. normal or micronodularity or bilateral mass on abdominal CT w/ likely APA, and NO lateralization w/ adrenal vein sampling
  3. unilateral hypodense nodule on CT greater than 1cm, over 40, and NO lateralization w/ adrenal vein sampling
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42
Q

how do you treat primary aldosteroneism (APA)

A

pre-op: aldosterone antagonist (spironolactone, Eplerenone)
THEN
adrenalectomy: laparoscopic open

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43
Q

how do you treat primary aldosteroneism (IHA)

A 
aldosterone antagonist  (spironolactone, eplerenone)
PLUS
hypertension meds (thiazide, CCB, ACE I, ARB)
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44
Q

causes of Cushing Syndrome

A
  1. Ectopic ACTH secreting tumor 10%
  2. ACTH secreting pit. tumor 80%
  3. cortisol secreting adrenal tumor 10%
  4. exogenous corticosteroids

*all increase cortisol release

45
Q

clinical features of Cushing Syndrome

A
  1. Central obesity
  2. Plethora
  3. “Moon” facies (compare old pics)
  4. Menstrual irregularities
  5. Hirsutism
  6. Decreased libido
  7. Hypertension
  8. Lethargy, depression
  9. Proximal muscle weakness
  10.   Purple striae (stretch marks are normally skin colored)
  11. Easy bruising
  12.   Dorsal cervical fat pad
  13. acne

*normal pulse

46
Q

Who do you screen for cushing syndrome?

A
  1. Symptoms and signs of Cushing’s
  2. Hypertension
  3. Hyperglycemia, insulin resistance
  4. Low bone density
  5. Adrenal Incidentaloma or pit. tumor
47
Q

why does someone w/ cushing syndrome have HTN

A
  • Sodium retention from cortisol
  • Increased production of mineralocorticoids
  • Hypokalemia (esp with ectopic tumors)
48
Q

screening tests for cushing syndrome

A

**Too much HR so try to suppress it!

  1. low dose dexamethasone suppression test (in AM)
  2. 24 hr urinary free cortisol
  3. late night (midnight) salivary cortisol –cortisol is lowest at midnight bc it has a diurnal release pattern (highest in AM, lowest in PM)
49
Q

what is the low dose dexamethasone suppression test

A

*screening test for cushings syndrome

  • 1 mg at 10-11 pm and measure 8 AM cortisol
  • Normal less than 1.8mg/dl
  • less than3% false negative
50
Q

pros and cons of the low dose dexamethasone suppression test

A

Pros: easy, cheap

Cons: lower specificity, false positives with obesity, depression

51
Q

what is the 24 hr urinary free cortisol test (pros and cons)

A
  • screening test for Cushing’s syndrome
  • Cushing’s Syndrome: greater than 4 x normal

Pros: high sensitivity and specificity
Cons: 24-hr urine collection, multiple collections

52
Q

effects of medicine on cortisol:

-decrease metabolism

A
  • ritonavir, fluoxetine, diltiazem, cimetidine, itraconazole

- Results in potentail false negative

53
Q

effects of medicine on cortisol:

-increase metabolsim

A
  • phenobarb, rifampin, dilantin, tegretol, pioglitazone

- Results in potential false positives

54
Q

effects of medicine on cortisol:

-increase cortisol binding globulin

A
  • estrogens, mitotane

- Results in potential false positives

55
Q

effects of medicine on cortisol:

-increase urinary free cortisol

A
  • tegretol , fenofibrate, licorice (inhibits 11OH steroid dehydrogenase)
  • Results in potential false positives
56
Q

subtypes of Cushings syndrome

A
  1. ACTH independent

2. ACTH dependent

57
Q

Cushing’s Syndrome Confirmation and Subtype Differentiation

A

repeat 24 hr urinary free cortisol –> ACTH level

  1. ACTH independent: ACTH less than 10 pg/ml
    - adrenal
    - imaging of Abd (CT or MRI)
  2. ACTH dependent: ACTH greater than 20 pg/ml
    - pituitary or ectopic
    - High dose dexaethasone suppression test
    - MRI of sella/pituitary
    - Inf petrosal sinus sampling
58
Q

Tx of Cushings Disease

A

(pituitary)

-transphenoidal surgery

59
Q

tx of Cushing syndrome from adrenal tumor

A

laproscopic surgery

60
Q

tx of Cushing syndrome from ectopic ACTH

A
  1. Surgery (carcinoid)
  2. Chemotherapy (small cell ca)
  3. Bilateral adrenalectomy
61
Q

what is pheochromatocytoma

A

rare tumor of adrenal gland tissue. It results in the release of too much catecholamies (epinephrine and norepinephrine)

*secretes catecholamines episodically so you get “spells”

62
Q

what can pheochromacytoma cause

A
  • HTN
  • HA
  • Sweating (w/ pallor NOT FLUSHING)
  • palpitations
63
Q

prevalence of phenochromocytoma is ____

A

Prevalence is Low:
1/1,000-10,000 of hypertensive patients

  • Frequently Sought, but Rarely Present:
  • 1/200 of those investigated
64
Q

what is the rule of 10’s w/ phenochromocytoma

A

10% are Malignant
10% are Familial
10% are Bilateral
10% are Extra-Adrenal

**most are benign

65
Q

who do you screen for phenochromocytoma

A
  1. Spells
    - HAs, Sweating, Palpitations
    - Not flushing
  2. Severe HTN (episodic)
  3. Resistant HTN
    - But orthostatic hypotension
  4. Shock or hypertensive crisis at surgery delivery,anesthesia
  5. Adrenal Incidentaloma
  6. Familial Syndrome
66
Q

how do you screen for phenochromocytoma

A
  1. 24-hr Urine Metanephrines
    -Positive: over 1,300 ug/24 hr
  2. 24-hr Urine Catecholamines
    Positive: over 2 fold elevated
  3. Plasma Metanephrines
    -Positive Metanephrine: over 0.5 nmol/L
    -Positive Normetanephrine: over 2 fold
  4. Chromogranin A level (rises on PPIs)
67
Q

what is the sensitivity and specificity of:

  • Urine metanephrines plus catecholamines
  • plasma metanephrines

(screening tests for pheochromocytoma)

A
  • Urine metanephrines plus catecholamines
    Sen: 90%, Spec: 98%
  • plasma metanephrines
    Sen: 97%, Spec 85%
68
Q

what things can cause a false positive when testing for pheochromocytoma

A
  1. meds
  2. alcohol
  3. renal failure
  4. sleep apnea
  5. physical stress and acute illness
69
Q

what meds can cause a false positive when testing for pheochromocytoma

A
  • Levodopa, tricyclics, buspirone (and other anti-psychotics), amphetamines, vasoconstrictors, opioids, acetaminophen* (plasma metanephrines)
  • Clonidine withdrawal
70
Q

when do you refer to an endocrinologist when evaluating pheochromacytoma

A
    • Urine catecholamines over 2x ULN
    • Urine metanephrine over 400 ug
    • Urine normetanephrine over 900 ug
    • Plasma metanephrine over 2x ULN
  2. abdominal MRI or CT
  3. refer
71
Q

what do you do if you have high clinical suspicion of pheochromocytoma and the 24 hr urine metanephrines, catecholamines, plasma: metanephrines were normal?

A

check during a spell

72
Q

tx of pheochromocytoma

A
  1. pre-operative:
    -alpha blocker (1st**), Beta blocker (2nd) or calcium channel blocker
    THEN
  2. Adrenalectomy: laproscopic open
  • Rx effects from pre-op tx:
  • vasodilation
  • volume expansion
  • rate control

*always need to start alpha blocker before beta blocker or else you will have increase alpha binding

73
Q

how do you evaluate spells

A
  1. Pheo? Boderline elevated BP; “episodes of sweats”; Flushing is not a symptom of pheo
  2. Perimenopausal? Could check an FSH
  3. Carcinoid? Could do 24-hr urine for 5-HIAA
  4. Depression/Anxiety?
74
Q

how do you evaluate fatigue

A
  1. Hypothyroidism? Check TSH
  2. Cushing’s? No clear sx or signs except fatigue, wt gain, irregular periods, depression. Could do a LDDST
  3. Poor Sleep?
  4. Depression?
75
Q

why do we care about incidental adrenal masses, and what do we do next to assess

A
  1. HR secreting?
  2. benign adenoma vs malignant?
  • screen for hormone hypersecretion (subclinical)
  • screen for malignancy
76
Q

when screening for hormone hypersecretion in an incidental adrenal mass what are you looking for?

A
  1. Cushing’s: LDDST, 24-hr UFC
  2. Pheo: 24-hr urine for metanephrines, catecholamines
  3. Aldosteronism: PA/PRA if hypertensive +/- low K+
  4. Testosterone: look for signs of virilization in women
77
Q

how do you screen for malignancy in an incidental adrenal mass

A
  1. Consider CT guided FNA if h/o of other cancer
  2. Serial CT’s (6, 12, 24 mo): consider FNA if growing

**Don’t do an FNA if concerning for a pheo bc could cause a hypertensive crisis

78
Q

tx of incidental adrenal mass

A
  1. Observation
  2. Surgery:
    - Tumor over 4-6 cm
    - Hormone Secreting
    - Concerning FNA
79
Q

what hormones does the posterior pit. release

A
  • Antidiuretic Hormone (ADH)

- Oxytoxicin

80
Q

Hormone over-production disorders of the pituitary gland

A

Tumors:

  • Prolactin (prolactinoma)
  • FSH/LH
  • Growth Hormone –> Acromegaly and Gigantism
  • ACTH –> Cushing’s Disease
  • TSH –> Hyperthyroidism (very rare!)
81
Q

Hormone under-production disorders of the pituitary gland

A
  1. Tumors (mass effect / apoplexy)
  2. Trauma
  3. Infiltrative processes
  4. Sheehan’s Syndrome
  5. Congenital disorders
82
Q

Etiology of hyperprolactinemia

A
  1. Pregnancy
  2. Prolactinoma
  3. Hypothyroidism
  4. Pituitary/Sellar Mass
  5. Drugs (psych meds)
  6. Kidney/Liver Failure
  7. Estrogen
  8. Nipple Stimulation
  9. Chest wall tumors/injury
  10. “Stress”
83
Q

Signs and Sx of hyperprolactinemia

A
  1. Hypogonadsim
    - Amenorrhea
    - Impotence/ED
  2. Infertility
  3. Galactorrhea*
  4. Headaches
  5. Visual field defects

*often detected earlier in females due to amenorrhea

84
Q

Work up of hyperprolactinemia

A
  1. full H and P (pay attention to meds)
  2. Labs
    - Pregnancy test** (#1 test)
    - TSH
    - CMP
    - Estradiol/Testosterone
    - LH/FSH (low)
    - Consider other pituitary related labs: GH, IGF-1, cortisol, TSH/FT4
  3. imaging- MRI
85
Q

goals of prolactinoma tx

A
  1. Restoration of gonadal function
    - Estrogen for women
    - Testosterone for men
  2. Fertility
  3. Mass effect
86
Q

tx for prolactinoma

A
  1. Medical therapy: Dopamine agonists: bromocriptine, cabergoline
    - HRT: OCPs in premenopausal women testosterone in men
  2. surgery
87
Q

why do we care about incidental pituitary masses, and what do we do next to assess

A
  1. Hormone secreting?
  2. hypopituitarism?
  3. Mass effect?
  • screen for hormone dysfunction (subclinical)
  • screen for mass effect– visual field testing
88
Q

when screening for hormone dysfunction in an incidental pituitary mass what are you looking for?

A
  1. Cortisol: LDDST/24-hr UFC (vs Cort Stim)
  2. Acromegaly: GH, IGF-1
  3. Prolactinoma: PRL
  4. Sex Steroids: LH, FSH, Estradiol/Testosterone
  5. Thyroid: T4
  6. Non-Secreting: alpha-subunit
  7. Diabetes Insipidus
89
Q

tx for hormone hypersecretion with an incidental pituitary mass

A

Appropriate medical (prolactinoma) vs. surgical therapy

90
Q

tx for hypopituitarism with an incidental pituitary mass

A

hormone replacement +/- sugery

91
Q

tx for mass effect with an incidental pituitary mass

A

consider surgery (unless prolactinoma)

92
Q

tx for an incidental pituitary mass w/ no hormone dysfunction or mass effect

A
  • Observation

- Consider repeat imaging in 6-12 months

93
Q

hormone replacement therapy for hypogonadism

A
  • Testosterone in men

- Estrogen +/- progesterone in women

94
Q

panhypopituitarism conditions

A
  1. hypogonadism
  2. hypothyroidims
  3. adrenal insufficiency
  4. growth hormone deficiency
  5. diabetes inspidus
95
Q

hormone replacement therapy for hypothyroidism

A
  • Levothyroxine

- Follow FT4 not TSH, aim for high-normal FT4

96
Q

hormone replacement therapy for adrenal insufficiency

A

prednisone 4-5mg daily

97
Q

hormone replacement therapy for growth hormone deficiency

A

daily injection, very expensive

98
Q

hormone replacement therapy for diabetes inspidius

A

ddAVP intranasally as needed to control polyuria

99
Q

Labs for primary adrenal insufficiency

A 
K high
Na low
BUN/Cr high
CRH high
ACTH high
Testosterone, aldosterone and cortisol low
100
Q

ddx for adrenal insuffiecieny

A

infection/spesis

polynephritis

101
Q

what is sheehan’s syndrome

A

postpartum hypopituitarism or postpartum pituitary gland necrosis, is hypopituitarism (decreased functioning of the pituitary gland), caused by ischemic necrosis due to blood loss and hypovolemic shock during and after childbirth

*often causes secondary adrenal insufficiency

102
Q

symptoms of sheehan’s syndrome

A
  • difficulty breastfeeding
  • hypotension
  • fatigue
  • irregular heart beat
  • no period

*often causes secondary AI

103
Q

how long does it take to develop Cushing’s syndrome

A

-typically months to years unless its an ectopic ACTH secreting tumor

104
Q

classic triad of sx for pheochromocytoma

A

HA, sweating (w/o flushing), palpitations

*probably hypertensive during these spells

105
Q

what do ACE meds (ex. lisinopril) do to K+?

A

boost it a little

*so someone with borderline low K+ (3.8) on lisinopril might actually have lower K

106
Q

FNA of a pheo could cause what

A

hypertensive crisis

107
Q

what is the “master” gland

A

pituitary gland

108
Q

ddx of hyperprolactinemia

A

pregnancy

hypothyroidism

109
Q

what hormone do you not replace w/ panhypopituitarism

A

prolactin

Adult Clinical Medicine (26 decks)

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