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Internal Medicine > Endocrinology & Metabolism > Flashcards

Endocrinology & Metabolism Flashcards

1
Q

Most common signs/sx of hyperthyroidism

A
  1. nervousness/emotional lability (99%)
  2. increased sweating (91%)
  3. heat intolerance (89%)
  4. palpitations (89%)
  5. fatigue (88%)
  6. weight loss (85%)
    - ——
  7. tachycardia/afib (100%)
  8. goiter (99%)
  9. tremor (97%)
  10. proptosis (40%)
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2
Q

Most common signs/sx of hypothyroidism

A
  1. sluggish affect/depression (91%)
  2. fatigue (87%)
  3. cold intolerance (70%)
  4. constipation (70%)
  5. weight gain (56%)
    - ————
  6. dry, coarse skin or hair (75%)
  7. periorbital puffiness (75%)
  8. bradycardia (55%)
  9. slow movements/speech (53%)
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3
Q

Indications for TSH screening w/out sx

A
  • relative with hashimoto or graves
  • other autoimmune disease (e.g. DM1)
  • hx prior thyroid dysfxn
  • pts on amiodarone or lithium
  • pts living in iodine-deficient region
  • obese pts (BMI >30)
  • women pregnant or anticipating pregnancy
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4
Q

Lab tests for autoimmune thyroid dz

A
  1. TPO-ab: good indicator of hashimoto dz (hypothyroidism)
  2. TSH-receptor ab: option when RAIU is contraindicated for detecting graves dz, but lacks sensitivity and specificity for graves
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5
Q

thyrotoxicosis =

A

excess thyroid hormone (exogenous or endogenous)

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6
Q

steps in evaluating thyrotoxicosis

A
  1. TSH: elevated => ?pituitary tumor
  2. if TSH low => free T4/3: normal = subclinical thyrotoxicosis
  3. if free T4/3 elevated => RAIU scan
  4. RAIU elevated => graves; RAIU focal => Tox Nod Goit; RAIU low => thyroiditis
  5. Thyroiditis + painful thyroid = subacute thyroiditis; painless + normal/high TG=postpartum vs. lymphocytic thyroiditis; painless + low TG=factitious thyrotoxicosis
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7
Q

Complications of graves/thyrotoxicosis

A
  1. cardiac/arrhythmias
  2. osteoporosis
  3. hypermetabolic state
  4. graves opthalmopathy (proptosis, eom. dysfxn, optic neuropathy)
  5. pretibial myxedema = infiltrative dermopathy w/nonpitting scaly thickening and induration of skin
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8
Q

subclinical hypothyroidism

A
  • mildly elevated TSH (5-10) and normal free T4

- requires no tx w/out sx or w/out pregnancy

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9
Q

Tx of thyrotoxicosis

A
  • b-blockers for tachy
  • antithyroid drugs (methimazole or propylthiouracil)
  • radioiodine therapy
  • pharma > RI tx in patients w/severe graves optho/thyroid storm
  • thyroidectomy
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10
Q

Thyroid disease and pregnancy

A
  • more thyroid hormone req. in pregnancy; low levels increase risk for maternal/fetal hypothyroidism
  • tx @ TSH>2.5
  • increase baseline levothyroxine dose by 30% as soon as pregnancy confirmed
  • measure thyroid fxn q4weeks
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11
Q

DDx of hypothyroidism

A
  • hashimoto (+TPO, fhx)
  • iodine def.
  • postpartum thyroiditis(TSH low, high, norm over 2-4 mo, ult. elevated TSH)
  • silent thyroiditis
  • subacute (painful thyroid, ESR elevated)
  • drug-induced (amiodarone, Li, interferon)
  • pit/hypothalamic mass (TSH low)
  • pit/hypo radiation hx (TSH low)
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12
Q

Thyroid storm

A
  • exaggerated s/sx of thyrotoxicosis + systemic decompensation
  • often 2/2 rapid release of thyroid hormone (s/p large iodine load, w/draw of antithyroid drugs, tx w/radioactive iodine) or surgery, infection, trauma
  • s/sx: tachy, hyperpyrexia, AMS, GI sx
  • tx = reduce thyroid hormone + supportive
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13
Q

Myxedema coma

A
  • caused by severe hypothyroidism
  • AMS + hypothermia
  • hypoxemia, hypercapnia, hyponatremia
  • tx = ppx steroid tx (prevent adrenal crisis) before thyroid hormone + supportive
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14
Q

Thyroid cancers (most => least common)

A
  1. papillary carcinoma (80-85%)
  2. follicular carcinoma (10-15%)
  3. medullary thyroid carcinoma (<5%) [MEN II]
  4. anaplastic carcinoma (<1%)
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15
Q

Layers of adrenal cortex

A
  • “GFR = salt, sugar, sex”
  • zona glomerulosa = mineralcorticoids (“salt”) <=RAAS
  • zona fasciculata = glucocorticoids/cortisol (“sugar”) <=ACTH
  • zona reticularis = androgens (“sex) <=FSH/LH
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16
Q

Causes of primary adrenal insufficiency

A
  1. autoimmune adrenalitis
  2. infection (TB, mycosis, bacterial, HIV)
  3. metastatic cancer
  4. adrenal hemorrhage
  5. medication (etomidate, ketoconazole)
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17
Q

Causes of secondary (central) adrenal insufficiency

A
  1. exogenous GC
  2. hypothalamic/pituitary diseases or surgery
  3. cranial irradiation
  4. drugs (e.g. megestrol => gc activity)
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18
Q

Indication for GC tapering

A

-tx w/GC for >3 weeks requires tapering

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19
Q

Sx of adrenal insufficiency

A
  • weight loss
  • anorexia
  • weakness
  • nausea, abd. pain
  • arthralgias
  • fatigue/malaise
  • skin hyperpigmentation @ primary insufficiency (2/2 elevated ACTH)
  • orthostatic hypotension, salt craving 2/2 volume depletion from aldosterone deficiency
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20
Q

Lab dx of adrenal insufficiency

A
  • cosyntropin stimulation test: ACTH/cortisol measured at 0,30,60 minutes s/p cosyntropin admin; rise of >18 cortisol rules out adrenal insufficiency
  • also measure free cortisol in critically ill patients
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21
Q

Tx of acute adrenal crisis

A
  1. ACTH/cortisol immediately
  2. high-dose IV GC (dexamethasone) and large-vol IV saline
  3. fludrocortisone @ primary (not secondary) insufficiency
22
Q

Common causes of hypercortisolism

A
  • exogenous GC
  • central ACTH-secreting tumor (Cushing disease)
  • adrenocortical tumor
  • ectopic ACTH-secreting tumor
23
Q

Sx of hypercortisolism

A
  • weight gain
  • recurrent/chronic infections
  • worsening DM control
  • change in menses
  • fractures
24
Q

Presentations associated with hyperaldosteronism

A
  • difficult-to-control/worsening HTN despite multiple therapies
  • spontaneous hypokalemia after low-dose diuretic
  • HTN at young age
25
Q

Lab dx of hyperaldosteronism

A
  • midmorning abulatory plasma aldosterone

- if elevated => adrenal CT

26
Q

Tx of hyperaldosteronism

A
  • adrenalectomy if aldosteronoma

- spironolactone (vs. eplerenone) + dietary sodium restriction

27
Q

Pheochromocytoma “rule of 10s”

A

10% malignant
10% recur
10% asymptomatic

28
Q

Sx of pheo

A
  • moderate/severe hypertension

- episodes w/severe h/a, diaphoresis, palpitations

29
Q

Evaluation of pheo

A
  • plasma free metanephrine level
  • 24hr urine catecholamine/metanephrine excretion
  • if elevated => CT vs. MRI
30
Q

Tx of pheo

A
  • surgical resection
  • alpha-blockers PRIOR to surgery (to avoid hypertensive emergency during surgery) => phenoxybenzamine (long-acting irrev. nonselective alpha-blocker)
31
Q

selective a1-adrenergic antagonists

A
  • terazosin
  • prazosin
  • dozazosin
32
Q

Indication for surgery for incidental adrenal nodule

A

nodule > 6cm (risk of malignancy = 25%)

33
Q

uncontrolled DM s/sx

A
  • weight loss
  • polyuria
  • frequent infections
  • erectile dysfxn
  • acanthosis nigricans
  • peripheral neuropathy
  • recurrent vaginal yeast infections
  • proliferative retinopathy
34
Q

Dx of DM

A
  • 2 positive tests OR 1 positive test + sx
  • fasting gluc > 126
  • 2hr (75g gluc) > 200
  • HbA1c > 6.5
  • random > 200
35
Q

Testing following initial dx of DM

A
  • HbA1c
  • fasting lipids
  • electrolytes
  • urinalysis + microalbuminuria
  • EKG
36
Q

macrovascular complications of DM

A
  • CAD
  • PAD
  • stroke
37
Q

microvascular complications of DM

A
  • peripheral neuropathy => amputations
  • retinopathy
  • nephropathy
  • cardiovascular autonomic neuropathy => exercise intolerance, orthostatic hypotension, cardiovascular lability
  • GI neuropahty => gastroparesis
  • erectile dysfxn
38
Q

BG control in critically ill hospitalized patients

A
  • tx at bg > 200

- goal: 140-200

39
Q

BG control for non-critically ill hospitalized patients

A

premeal < 140

random <180

40
Q

insulin types

A
  • basal
  • regular
  • NPH
  • short acting…
41
Q

Overview of physiology of DKA

A
  • insulin def + glucagon => severe hyperglycemia + excess hepatic glucose production
  • hyperglycemia => osmotic diuresis + hypovolemia
  • glucose metabolized to fatty acides => ketoacidosis, ketonuria, and electrolyte abnormalities
  • typically complications of T1DM
42
Q

Characteristics of hyperglycemic hyperosmolar syndrome

A

-complication of T2DM, without ketosis/acidosis

43
Q

Precipitating factors of DKA/HHS

A
  • infection
  • silent MI/CVA
  • omitting insulin => DKA
  • pancreatitis, trauma, EtOH, illicit drug use
  • drugs: GCs, thiazide, sympathomimetic, 2nd gen anti-psych
44
Q

Presentations of DKA/HHS that may mask precipitating factors

A
  • often normo/hypothermic even w/infxn 2/2 peripheral vasodilitation
  • (if infection susp => CXR, urine, blood cultures, CSF)
  • AMS may present w/DKA/HHS, but rarely occurs in HHS w/serum osm <320, so consider CVA
45
Q

Presentation of DKA

A
  • rapid onset (hours)
  • polyuria, polydipsia
  • blurred vision
  • N/V
  • abdominal pain
  • AMS
  • PE: signs of hypovolemia (tachycardia, hypotension, dry mucous membranes, poor skin turgor); kussmaul respiration (deep/frequent breaths), fruity breath
46
Q

Dx of DKA

A
  • hyperglycemia (BG>250)
  • increased anion gap metabolic acidosis (ph<7.3; HCO3<15)
  • positive serum/urine ketones
  • serum sodium low
  • serum potassium elevated (b/c acidosis shifts K+ into serum, but total body potassium low)
47
Q

Presentation of HHS

A
  • insidious (days-weeks) @T2DM
  • AMS
  • signs of hypovolemia
48
Q

Dx of HHS

A
  • glucose > 600
  • pH>7.3, HCO3>15
  • serum osm >320
  • absent serum/urine ketones
49
Q

Goals of DKA treatment

A
  • acidosis correction
  • volume repletion
  • correction of electrolytes
50
Q

DKA treatment

A
  1. IV normal (0.9%) saline+ regular insulin immediately
    - IV bolus regular insulin + continuous IV infusion of 0.1U/kg/hr ==> glucose target reduction: 50-100/hr
    - @BG=250 ==> IV w/1/2NS + 5-10% dextrose
    - insulin continues until AG is normalizes =>subq insulin
  2. IV potassium
51
Q

HHS treatment

A
  1. rehydration: 1LNS before initiating insulin
    - replace half fluid deficit over 24hrs, remainder over 2-3 days
  2. IV insulin: bolus 0.1U/kg then 0.1U/kg/hr => bg target reduction: 50-100/hr ==> bg<200 and patient is eating => subq
  3. monitor potassium and serum osm

Internal Medicine (4 decks)

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