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Step 2 UWORLD > Internal Endo/ID > Flashcards

Internal Endo/ID Flashcards

1
Q

Fever and sore throat, pt taking anti-thyroid meds

A

Agranulocytosis (not strep)

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2
Q

Which patients are most likely to develop Rhizopus/mucormycosis (Fever, necrotic invasion of orbit/palate/maxillary bones, purulent nasal discharge)

A

Diabetics

Tx infection with surgical debridgement and amphotericin b

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3
Q

Tx for asymptomatic TB vs Sx

A

No symptoms: Isoniazid, with added Pyridoxine (to prevent peripheral neuropathy)

Symptomatic: RIPE (P = pyrazinamide)

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4
Q

branching filamentous rods partially acid-fast

A

Nocardia (vs TB: strongly acid fast; vs Actinomycyes: grows on gram stains)

  • ->Pulmonary disease, may also have CNS and skin involvement
  • ->Imaging: nodular/cavitary lesions in upper lobes (so easily confused with TB)
  • ->Immunocompromised pts
  • ->Sulfonamides, i.e. Bactrim
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5
Q

After a URI, glomerulonephritis can be due to:

A 
PSGN 
IgA Nephropathy (DONT FORGET THIS ONE)
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6
Q

PSGN vs IgA Nephropathy

both have gross hematuria aka dark urine

A

PSGN: 10-21 days after URI; children; low C3; renal biopsy = c3 deposits

IgA Neph: 5 days after URI; young adults; normal complement; mesangial IgA deposits;

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7
Q

Bicarb, Chloride, Potassium in pt with vomiting

A 
Elevated Bicarb (because losing H+)
Hypochloremia, Hypokalemia (losing KCl and HCl)
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8
Q

Tx for patient with vomiting

A

Normal Saline + Potassium

vomiting = hypochloremic, hypokalemic metabolic alkalosis

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9
Q

Explain contraction alkalosis

A

Fluid depletion from vomiting –> RAAS triggered –> conserve Na and H20 –>Aldosterone retains water at the cost of excreting sodium and potassium in urine (already a hypokalemic, alkalotic state with vomiting)

–>Volume resuscitation with NS corrects this

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10
Q

HIV patient, African american, nephrotic syndrome

A

Focal Segmental. Also big for diabetics, hispanics, SCD

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11
Q

What happens to H+ and K+ in states of high aldosterone?

A

Aldosterone Saves Sodium and Pushes Potassium Out –> Metabolic Alkalosis. Also, HTN.

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12
Q

Which drug can cause cyanide toxicity?

A

Nitroprusside…given during HTN emergency. Flushing, AMS, Metabolic acidosis

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13
Q

Indications for hemodialysis

A

Acidosis
Electrolyte abnormalities (Hyper-K+)
Ingestion (alcohol, salicylate, Li, sodium valproate, carbamazepime)
Overload (Volume overload refractory to diuretics)
Uremia (sxs= eneceph, pericarditis, bleeding)

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14
Q

when should metformin not be given/held?

A

Increases risk of lactic acidosis in patients with :

  • acute renal failure
  • liver failure
  • SEPSIS
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15
Q

Urinary retention secondary to anticholinergic use (i.e. 1st gen H1 blocker) is due to:

A

detrusor hypocontractility

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16
Q

+Urinary cyanide nitroprusside test

A

Cystinuria (hereditary condition leading to hx of nephrolithiasis)

Hexagonal crystals

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17
Q

Main danger of rhabdomyolysis? (immobilization and cocaine abuse are big risk factors)

A

Acute renal failure (ATN) secondary to myoglobinuria

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18
Q

Tx for SIADH:

A

IV HYPERTONIC SALINE
Fluid Restriction
Demeclocycline
Vaptans

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19
Q

Extrahepatic manifestations of Hep C

A

Arthralgias, fatigue, Porphyria Cutaneous Tarda = photosensitive skin that develops vesciles/bullae with trauma/sun exposure

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20
Q

yeast + granulomatous skin lesion + pulmonary complications, seen in Central USA

A

Blastomycosis

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21
Q

Yeast infection that mimics sarcoidosis (non-caseating granulomas), especially in Ohio/Mississippi river, arthralgias

A

Histoplasmosis

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22
Q

Epididymitis causes

A

> 35: E coli (bladder obstruction)
<35: NG/Chlamydia

Don’t pick mumps unless theres parotiditis/prodromal viral sxs

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23
Q

TIck bite + elevated transaminases + thrombocytopenia/leukopenia + no rash

A

Ehrlichosis

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24
Q

How often should IVDU and MSM be screened for HIV?

A

Annually

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25
Q

Tx for meningococcal meningitis

A

Ceftriaxone + Vancomycin

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26
Q

Tx of choice for Lyme dz in pregnant pt

A

Can’t give doxy, so give Amoxicillin

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27
Q

Who gets PCP pneumonia?

A

HIV <200

or Chronic Glucocorticoids

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28
Q

Manifestations of vibrio vulnificus

A

Rapidly progressive, cellulitis, hemorrhagic bullae, nec fas, septicemia

  • ->marine environments/oysters
  • ->IV Ceftriaxone + Doxycycline
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29
Q

How to do you make the dx of C dif?

A

Stool toxin testing

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30
Q

Sxs of Coccioides

A

Community-acquired pneumonia, arthralgias, erythema nodosum, erythema multiforme

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31
Q

What metabolic abnormalities does hypothyroidism cause?

A

Hyperlipidemia (hypercholesterolemia +/- hypertriglyeridemia), Hyponatremia, sxs elevated transaminases and CK

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32
Q

Side effects of sulfonylureas

A

weight gain, hypoglycemia

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33
Q

Which anti-diabetic is good for weight loss and maintaining glucose control?

A

GLP-1 agonist (exenatide)

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34
Q

Side effects of TZDs (pioglitazone)

A

weight gain, CHF, edema, bone fracture, bladder cancer

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35
Q

T/F: Hashimoto thyroiditis (hypothyroid) ass with increase risk of lymphoma

A

True. Including thyroid lymphoma

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36
Q

Tx of DKA

A

Normal Saline + Insulin

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37
Q

central hypopituitarism vs primary adrenal insuff

A

Both have low T4 and Cortisol. Normal Aldosterone in central hypoP, vs decreased in adrenal insuff (b/c Aldosterone secretion regulated by RAAS, not AP)

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38
Q

Next step in patient with hypercalcemia

A

measure PTH.
High PTH = Primary hyperparathyroid, Familial Hypocalciuric hypercalcemia, Lithium

Suppressed PTH = Malignancy (PTHrP), granulomatous dz, vit D toxicity, etc

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39
Q

Toxicity of Methimazole/PTU (hyperthyroid drugs)

A

Agranulocytosis, aplastic anemia, skin rash.
PTU: hepatotoxicity
M: teratogen (aplasia cutis)

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40
Q

Criteria for Metabolic syndrome

A
  • 3/5:
    1. Abdominal obesity (Male waist>40, F waist>35)
    2. Fasting glucose >100-110
    3. BP >130/80
    4. TG > 150
    5. HDL: Men <40, Female <50
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41
Q

Key pathogenic factor in development of T2DM and metabolic syndrome

A

Insulin resistance

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42
Q

Adverse effects of radioiodine ablation for hyperthyroidism

A

Worsening eye problems, permanent hypothyroidism, radiation side effects

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43
Q

Adverse effects of surgery for hyperthyrodism

A

permanent hypothyroidism, recurrent laryngeal nerve damage, hypoparathyroidism

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44
Q

Eye problems with graves dz

A

Proptosis, swelling of periorbital tissue, diplopia, discomfort with ocular movements

–>made worse by therapeutic radioiodine ablation

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45
Q

T/F: Myopathy occurs in 1/3 of pts with hypothyroidism

A

True. Typically elevated CK, Myalgias, Muscle weakness

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46
Q

necrolytic migratory erythema, diabetes

A

Glucagonoma.

erythematous, papular/plaque/blistering rash affecting perioral region and LE

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47
Q

causes of Cushing syndrome

A

Cushings dz (ACTH-producing pit adenomas), exogenous glucocorticoid use, ectopic ACTH (small cell lung cancer)

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48
Q

Conn syndrome

A

Primary Hyperaldosteronism (Adrenal tumor): HTN, low renin, high aldosterone, high bicarb, high Na, low K

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49
Q

Hyperthyroidism + decreased radio-iodine uptake

A

means that its not from excess production of thyroid hormone (i.e. not Graves)

release of preformed thyroid hormone = painless thyroiditis

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50
Q

Steattorhea effect on PTH

A

Lose out Vitamin D cause its a fat-soluble vitamin, shit it all out. so you can’t absorb calcium and phosphate so these are low, and get reflexive increase in PTH

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51
Q

how do you test for acromegaly?

A

IGF-1 levels (can’t do GH levels because they fluctuate a lot)

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52
Q

T1DM or T2DM: DKA vs Hyperosmolar Hyperglycemic State

A

T1: DKA
T2: HHS

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53
Q

Hyperthyroid, low radio-iodine uptake, high anti-TPO. Dx and Tx?

A

Dx: Painless thyroiditis (variant of Hashimoto thyroiditis). Self limited hyper-thyroid state followed by hypothyroid and then euthyroid. Does not require methimazole or PTU!!!

Give a beta-blocker for sx mgmt

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54
Q

how to diff btwn Psychogenic polydipsia and Diabetes Insipidus?

A

PP: Low Serum Na
DI: Normal/High Serum Na

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55
Q

Types of DI

A

Central: Dec ADH rel from PP (hypernatremia due to impaired thirst)
Nephrogenic: renal ADH resistance (normal sodium b/c intact thirst mechanism)

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56
Q

Polyuria in non-hospitalized patient

A

Psychogenic Polydipsia and Diabetes Insipidus

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57
Q

causes of central Diabetes Insipidus

A

Pituitary tumor, trauma, surgery, ischemic encephalopathy

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58
Q

causes of nephrogenic Diabetes Insipidus

A

Lithium, Hereditary, 2nd to

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59
Q

weight gain, psych sxs, hirsutism, proximal mm weakness, hypertension, hyperglycemia

A

Cushings Syndrome

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60
Q

Causes of Cushings Syndrome

A

Cushings Disease (ACTH-secreting pituitary adenoma)
Exogenous glucocorticoid
Ectopic ACTH
Primary Adrenal Dz

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61
Q

Dx of Cushings Syndrome

A

2/3 positive:

  • 24 hour urinary cortisol excretion
  • late night salivary cortisol assay
  • low dose dexamethasone suppression test
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62
Q

T/F: Successful intensive glycemic index control in T2DM improves all-cause mortality

A

False. It improves microvesicular complications (retinopathy, nephropathy) but not macrovesicular complications ( MI/stroke)

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63
Q

what does ankle-brachial reflex help you assess?

A

Peripheral vascular disease

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64
Q

Which antithyroid drug can you use in pregnancy?

A

PTU in the first trimester. Can also do thyroidectomy if preg

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65
Q

non alpha/non beta pancreatic islet cell tumor

A

VIPoma

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66
Q

features of VIPoma

A

Watery diarrhea, Hypokalemia, Achlorhydria.

  • flushing, muscle cramps, lethargy, N/V
  • pancreatic tail tumor
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67
Q

When should you not use Amitriptyline for peripheral neuropathic pain?

A

It is not recommended in age >65 due to anticholinergic effects; also, not recommended in patients with pre-existing cardiac dz

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68
Q

Drugs to tx neuropathic pain (i.e. diabetic nephropathy)

A

TCA (Amitryptiline), Anticonvulsants (Gabapentin/Pregabalin), Opioids, Topical capsaicin or lidocaine

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69
Q

Plasma aldosterone/renin ratio > _____ suggests hyperaldosteronism

A

20

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70
Q

which electrolyte abnormalities can cause muscle weakness?

A

Hypokalemia, Hypomagnesemia

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71
Q

most common cause of Cushing syndrome

A

exogenous glucocorticoid

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72
Q

Primary Hyperparathyroidism (adenoma/hyperplasia) labs

A

Elevated Calcium, which normally suppresses PTH but this will show High PTH.

Phosphorous is USUALLY NORMAL SO DON’T BE A PEASANT

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73
Q

Tx for prolactinoma

A 
Dopamine agonists (Bromocriptine or Cabergoline)
-->inhibit prolactin secretion

NOT INITIAL SURGICAL RESECTION EVEN IF ITS A PITUITARY TUMOR PEASANTRY

74
Q

Relationship btwn prolactin, GnRH, dopamine

A

Prolactin inhibits GnRH

Prolactin stimulates Dopamine (which inhibits AP–>Prolactin)

75
Q

how does hypomagnesemia cause hypocalcemia?

A

inducing PTH resistance and decreased PTH secretion

not a major cause though

76
Q

Hypocalcemia + Hyperphosphatemia + increased PTH levels

A

Secondary Hyperparathyroidism secondary to Chronic Renal Failure
–>dec GFR = Phosphate retention…P binds circulating Ca and interferes with renal vit D production…= dec intestinal Ca absorption = increased PTH secretion. High P also directly stimulates PTH.

77
Q

Fever, neck pain, tender goiter following URI. Increased ESR.

A

Subacute Thyroiditis (de Quervain is associated with pain)

78
Q

low Ca, low Phosphate, high PTH, low vit D, elevated alk phos, bone pain/muscle weakness

A

Osteomalacia (caused by
malabsorption/intestinal bypass/celiac/chronic liver/chronic kidney) is “due to defective mineralization of organic bone matrix” (and not “accelerated focal bone remodeling”= Paget)

79
Q

When do you use metoclopromide?

A

Gastroparesis (diabetic or post-op). Also, anti-emetic

80
Q

What is gastroparesis?

A

Delayed emptying of the stomach…typically due to diabetic autonomic neuropathy.

81
Q

T/F: Diabetic patients can have hypoglycemia with insulin injections if they have impaired gastric emptying/delayed absorption

A

True. I.e. Gastroparesis

82
Q

Does diabetic neuropathy affect long or short axons first?

A

Long. Its a length-dependant neuropathy.

83
Q

Small fiber vs large fiber diabetic neuropathy

A

Small: Positive sxs –> pain, paresthesias, allodynia (ordinarily painless stimuli = painful)

Large: Negative sxs –> loss of MVP, numbness, loss of reflex

84
Q

Sxs that PCOS does and does not share with Cushing

A

Both: obesity, irregular menstrual periods, hyperandrogenism (acne, hirsutism, irreg menstrual)
Cushings only: skin atrophy, bruisability, muscle weakness, increased cutaneous fungal infections (tinea), hyperpigmentation, lanugo

85
Q

Does cushings have hyper or hypo androgenism?

A

Hyper (menstrual irregularities, acne, hirsutism)

  • ->due to co-secretion of Cortisol and Androgen (adrenals)
  • ->absent in iatrogenic steroid use…exogenous steroid inhibits adrenal
86
Q

Does cushings have hyper or hypo glycemia?

A

Hyper

–>due to decreased glucose tolerance (diabetes)…peripheral insulin resistance + cortisol induced gluconeogenesis

87
Q

what are the MSK effects of Cushing’s and why do they occur?

A

Proximal muscle weakness/wasting, osteoporosis, aseptic necrosis of femoral head
–>Cortisol increases protein catabolism and impairs collagen production

88
Q

How do you workup Cushing syndrome to determine presence and cause?

A
  1. Overnight low-dose dexamethasone suppression or 24 hour urinary free cortisol level
    - ->if normal, not cushings
    - ->if cortisol >5, its Cushings syndrome. now figure out etiology
  2. Measure ACTH
    - ->low: Adrenal imaging for tumor/hyperplasia
    - ->high: High Dose-Dexamethasone suppression test
    • ->ACTH suppressed: Cushings disease
    • –>ACTH not suppressed: ectopic ACTH tumor
89
Q

when would you suspect ectopic ACTH-producing tumor and what are the dx steps?

A

When High cortisol with low-dose dex + high ACTH with high-dose dex suppression tests.

Get Chest CT, Abdominal CT, Ocreotide scan

90
Q

who gets parathyroidectomy in primary hyperparathyroidism?

A
  • Symptomatic hypercalcemia (stones, bones, groans)
  • Complications: Osteoporosis, nephrolithiasis, impaired renal f(x)
  • Age <50
  • Serum calcium >1 above normal; Urine calcium >400
91
Q

T/F: Patients with HHS develop neuro complications including lethargy, blurry vision, obtundation

A

True (Hyperosmolar Hyperglycemic State…T2DM)

92
Q

T/F: DKA and HHS patients typically have normal serum and total potassium levels

A

False. Will typically have normal serum values but depleted total K (loss of insulin = all the K comes out of the cells and gives false picture of K state…also have excessive urinary loss due to osmotic diuresis)

93
Q

DHEA vs DHEAS

A

Ovaries and adrenals both produce DHEA, only adrenals produce DHEAS (and thus controlled by ACTH, whereas ovaries conducted by LH).
so Adrenal tumor: Both are up
Ovarian tumor: DHEA up, DHEAS normal

94
Q

how can blood transfusion affect calcium levels?

A

Hypocalcemia
–>citrate in transfused blood binds ionized calcium (typically seen in pts with hepatic dysf(x) because liver can normally get rid of citrate)

95
Q

What should diabetic patient between 40-75 with normal total cholesterol but high triglycerides use?

A

dont be a peasant: all diabetics btwn 40-75 get statins b/c proven decrease in cardiac events (they want you to pick fibrates)

96
Q

T/F: Hirsutism in females is always due to PCOS

A

FALSE YOU PEASANT. WHEN THEY SEE HIRSUTISM + IRREGULAR MENSTRUAL, DO NOT always AUTO JUMP PCOS.

–>PCOS (most common), CAH, OVARIAN/ADRENAL TUMORS, CUSHING, ACROMEGALY, High Prolactin

97
Q

What dx steps if you think woman has androgen-secreting tumor (acute-onset hirsutism/androgenism)?

A

Its either Adrenal or Ovarian Tumor. Order Testosterone and DHEAS.

IF T and DHEAS both up: Adrenal tumor (DHEAS only adrenal)
If T up with normal DHEAS: Ovarian tumor (more common)
Note: DHEA is made by both, so need DHEA-S

98
Q

Next step if patient has high calcitonin + malignant thyroid tumor

A

=Medullary thyroid cancer. Associated with MEN 2a and b, which have Pheochromocytoma. Get plasma metanephrines.

99
Q

Sxs of pheochromocytoma

A

Pressure (BP), Pain (HA), Perspiration, Palpitation, Pallor

100
Q

Sxs of carcinoid

A

Episodic flushing, secretory diarrhea, bronchospasm, cardiac valvular abnormalties.
–> cause increased production of Serotonin from Tryptophan (req for niacin synth) = niacin def = pellagra = dermatitis, diarrhea, dementia

101
Q

T/F: If a patient with syphillis is penicillin allergic, you treat with doxycycline

A

True: don’t need to do desensitization for early syphillis.

If CNS affected, multiple tx failures with alternatives, or PREGNANT PATIENTS, then you do desensitization

102
Q

T/F: Toxoplasmosis causes fungal meningitis particularly in HIV patients

A

False. it is a PARASITE, that causes brain abscess/lesion in HIV patients

103
Q

Tx for cryptococcal meningitis

A

Amphotericin + Flucytosine, followed up with Fluconazole

104
Q

Cardiac block, erythematous rash, lightheadedness, syncope, myalgia

A

Lyme

105
Q

T/F: Acyclovir, ganciclovir, and valcyclovir all work well against CMV

A

False…only Ganciclovir

106
Q

most common cause of odynophagia/dysphagia in HIV patients

A 
Candida esophagitis
(CMV esophagitis will be if there are linear ulcers/intracytoplasmic and intranuclear inclusion bodies)
107
Q

Rheumatic fever vs Infective Endocarditis

A

RF - Strep pyo: JONES
IE - several organisms staph/strep/enterococci: Fever, Roth Spots, Osler Nodes, Murmur, Janeway lesions, Anemia, Nail-bed hemorrhage, Emboli

108
Q

causes of Infective Endocarditis

A

Staph aureus/epidermidis: prosthetic valves, intravascular catheters, pacemaker, IVDU
Enterococci: Nocosomial UTIs
Strep viridans: dental procedure

109
Q

Sxs of Pheochromo

A 
Episodic hyperadrenergic sxs: 
Pulse
Pressure
Pallor
Pain (HA)
Palpitations (Tachycardia)
110
Q

T/F: Once you discover a thyroid nodule, next step is FNA

A

False. Next step is TSH level, US, and clinical eval. FNA if US/clinical shows signs of cancer

111
Q

Patient has thyroid nodule. TSH is low. Next step?

A

Radio-iodine…if hot nodule (low risk), tx hyperthyroidism; if cold nodule (higher risk), FNA

112
Q

Patient has thyroid nodule. TSH is normal or elevated. Next step?

A

FNA

113
Q

T/F: Anti-TPO associated with misscariages

A

True. Hashimoto’s can cause miscarriage (so not always antiphospholipid)

114
Q

What is it called when a patient has abnormal thyroid function tests after a severe illness but no hx of thyroid dz?

A

Euthyroid sick syndrome (low T3 syndrome) –> normal TSH, T4, but low T3

115
Q

best markers for DKA resolution:

A
  1. Anion gap

2. beta-hydroxybutyrate (and NOT acetoacetate)

116
Q

Anorexic gets admitted and given NG feeds. what might you expect? labs and cause

A

Refeeding syndrome: Surge in INSULIN

  • ->causes uptake (DECREASE IN) PHOSPHATE, MAGNESIUM, POTASSIUM
  • ->cardiopulmonary distress/failure
117
Q

What hormones do you look at to differentiate between 3 most common causes of secondary amenorrhea?

A

Prolactin (hyperprolactinemia)
TSH (hypothyroidism)
FSH (premature ovarian failure. young lady 20s-30s, increased FSH and LH, low estrogen)

(could do hysteroscopy if prior uterine procedure/infx and worried about an Ashermans)

118
Q

Dx of metabolic syndrome

A

3/5:

  1. Abdominal obesity (M: waist>40in. F: wait>35)
  2. Fasting glucose >100-110
  3. BP >130/80
  4. Triglyceride>150
  5. HDL (M: <40. F: <50)
119
Q

____ ____ plays a central role in metabolic syndrome

A

Insulin Resistance

120
Q

T/F: Subacute (de quervian) thyroiditis is a postviral inflammatory illness associated with pain and hypothyroidism

A

False, everything true but its HYPERthyroidism

121
Q

T/F: “Thyroiditis” is always hyperthyroid state

A

False.

  • Subacute thyroiditis (-TPO) and painless thyroiditis (+TPO) = hyperthyroid
  • Hashimoto thyroiditis (+TPO) = hypothyroidism
122
Q

What is chronic lymphocytic thyroiditis?

A

aka Hashimoto’s habibti

123
Q

T/F: Tx of subacute thyroiditis is reassurance

A

Nah, give beta blockers (thyrotoxic sxs) and nsaids (pain )

124
Q

Think of hypercalcemia as : (1) or (2)

A

PTH dependent: high PTH (Primary; familial hypocalciuric; lithium)

PTH independent: low PTH (malignancy i.e. PTHrP, VIt D, Granuloma, thiazides, milk-alkali)

125
Q

Hyperosmolar Hyperglycemic state = high glucose/osmolarity due to insulin _____ and _____ counterregulatory hormones (cortisol/glucogon/GH/catecholamines)

A

insulin def

elevated counter-reg

126
Q

What precipitates HHS in T2DM?

A

Infection (most common)
Meds (STEROIDS, thiazides, atypical antipsychotics)
Trauma/MI/stroke

127
Q

dif btwn euthyroid sick syndrome and subclinical hypothyroidism

A

Euthryoid: “Low t3 syndrome” in a patient thats sick (t4, tsh normal)

Subclinical: elevated TSH, normal T4 and T3 (t3 can dec late)

128
Q

Patient with hypertension has hypernatremia and hypokalemia. What are you suspecting and what’s the workup?

A

Hyper-aldosteronism.
1. MEASURE free Renin:Aldosterone RATIO. >20 = likely
2. if likely, Adrenal suppression testing (salt loading). +test = inabiity to suppress
3. next, get CT to decide if its hyperplasia or adenoma
(if CT doesn’t diff, do adrenal vein sampling). Resect adenoma, medical for hyperplasia

129
Q

T/F: Patient w/hypertension, hypernatremia and hypokalemia. Suspecting hyper-aldosteronism so get dexamethasoen supp test

A

False. You have to get Renin:aldosterone ratio (look for >20) and salt (adrenal) suppression testing

130
Q

T/F: DKA is characterized by osmotic diuresis that reduces total body K even though serum K may be elevated

A

TRUE!

  • ->osmotic diuresis = losing shit ton of K through kidneys
  • ->acidosis and low insulin causes extracellular shift of K
131
Q

why does infection precipitate DKA?

A

systemic release of counter-regulatory hormones (cortisol, catecholamines, glucagon)….resultant excess glucagon = hyperglycemia, ketonemia, osmotic diuresis

132
Q

what is the state of hepatic gluconeogenesis in DKA?

A

its actually increased even though glucose levels are high af.

  • ->high glucagon (counter-reg hormone), cortisol, catecholamines
  • ->low insulin
133
Q

most common cause of central adrenal insufficiency?

A

Exogenous steroids!! i.e. PMR or autoimmune pt.

–>suppress CRH from hypothal and ACTH from AP

134
Q

Labs in central (exogenous steroids) vs peripheral adrenal (autoimmune) insufficiency

A

Central: Low ACTH, Low cortisol; normal aldosterone
Peripheral: High ACTH, low cortisol, low aldosterone

135
Q

clinical features of central vs peripheral adrenal insuff

A

Peripheral (primary): Much worse…hyperpigmentation, hyperkalemia, hyponatremia, hypotension

Central: mild…no hyperpig or hyperkalemia

136
Q

how do you differentiate follicular thyroid carcinoma from benign follicular adenoma (both have follicular cells in similar organization i.e. clusters/clumps)

A

Follicular cancer: invasion of tumor capsule/blood vessels. Mets via hematogenous spread.

137
Q

what are the cardiac manifestations of carcinoid?

A

right-sided valvular lesions…i.e. tricuspid regurg

138
Q

T/F: Carcinoid can cause paraneoplastic ACTH secretion just like small cell (and lead to Cushings)

A

True

139
Q

How do you interpret RAIU scan in hyperthyroid patients (wouldn’t need if signs of graves present i.e. exopthalmos and goiter)?

A

LOW: measure THYROGLOBULIN.

  • ->Low: Exogenous hormone
  • ->High: Thyroiditis; Iodide exposure

HIGH: look at uptake pattern

  • ->Diffuse: Graves
  • ->Nodular: Toxic adenoma; Multinodular goiter
140
Q

why is fetal hyperthyroidism seen in graves patients?

A

TSH receptor antibody crosses placenta

141
Q

Risk of untreated hyperthyroidism?

A

Bone loss/osteoporosis

142
Q

management of hypothyroidism patient during pregnancy?

A

increase levothyroxine ONCE THE pregnancy is detected

143
Q

Total T4, free T4, TSH levels during pregnancy

A

Total T4 Increased, Free T4 unchanged/inc, TSH dec.

  • ->b-hCG stimulates Thyroid hormone in 1st sem (so dec TSH)
  • ->Estrogen stim TBG, and thus thyroid gland has to make more to keep free t4 levels steady ( so total increases)
144
Q

hyperthyroidism with diffuse, nontender enlargement of thyroid gland

A

= goiter + hyperthyroidism = GRAVES GRAVES GRAVES

145
Q

Sxs of thyroid (thyrotoxic crisis) storm (seen in patients with un-dx/poorly controlled hyperthyroidism)

A

fever, hemodynamic instability, cardiac instability, CHF, seizures

146
Q

precipitants of thyroid storm (in pt w/un-dx or poorly controlled hyperthyroidism)

A

Surgery, infection, trauma, iodine contrast (i.e. CT w/contrast), childbirth etc

147
Q

what labs would you expect in a patient with hyperosmolar hyperglycemic state?

A

pH: normal
anion gap: normal
Glucose>1000
serum osmolality>320 ((2xNa) + (plasma glucose/18))

148
Q

most important step in tx of HS

A

FLUIDS (normal saline). and then, IV Insulin (not subq)

149
Q

hemodynamic effects of thyroid storm

A

systolic htn (increase contractility), widened pulse pressure, increase CO, decrease systemic vascular resistance, increase myocardial O2 demand

150
Q

how does hyper prolactinemia lead to hypogonadism?

A

Suppression of GnRH (so get low FSH, LH and T)

151
Q

myalgias, progressive proximal mm weakness, elevated CK-MB, normal ESR, fatigue, delayed reflexes (“sluggish ankle jerks bilaterally”)

A

Hypothyroid myopathy

152
Q

T/F: Hot nodules are almost always benign and can be treated like hyperthyroidism

A

True. “Hot” = increased isotope uptake/hyperfunctioning

153
Q

Insensitivity of FSH and LH receptors, so have low testosterone but high FSH and LH.

A

Klinefelter. Also have testicular atrophy, 47 XXY, infertility, eunuchoid body shape. Tx with testosterone

154
Q

low GnRH, low FSH LH, low testosterone. Anosmia

A

Kallmans

155
Q

how do you differentiate btwn Gonadotropin-dependent and gonadotropin-independent precocious puberty?
(workup for kid with advanced bone age and low basal level of LH)

A

Dependent (central): GnRH stimulation test = high LH (may have high basal LH with advanced bone age)
–>80% = idiopathic precocious puberty (only females). premature HPA axis activation

Independent (peripheral): GnRH stim test = low LH
–>late-onset (nonclassical) CAH (severe acne, course pubic/axillary hair)
–>exogenous testosterone
–>Leydig cell tumor (unilateral enlargement)
etc

156
Q

complicated delivery + lactation failure, hypotension, anorexia, hypotension

A

Sheehan (ischemic necrosis AP)

157
Q

effect of ACE-I on renin

A

Increases!!

–>So not converting AG1->AG2. Aldosterone is decreased so renin is reflexively increased

158
Q

Why isnt clinically significant hypernatremia and edema seen in primary hyperaldosteronism?

A

Aldosterone escape
–>HTN caused by initial increase in aldosterone causes reflexive increased in renal blood flow and GFR and increasing Na excretion, mitigating the effects

159
Q

_____ may present with androgenic alopecia in females

A

PCOS

160
Q

PCOS patients should be screened for:

A

Diabetes with oral glucose tolerance test

161
Q

In the tx of PCOS, _____ are for controlling menstrual irregularities; _____ is for inducing ovulation

A

OCP

Clomiphene citrate

162
Q

In females with precocious puberty, source of premature adrenarche vs thelarce

A

Adrenarche (hair/acne): Adrenals (androgens)
Thelarche (boobs): Ovaries
–>although ovaries make some testosterone (esp in PCOS), you would expect thelarche with ovarian excess

163
Q

Diabetes meds:

  • wt gain
  • wt neutral
  • wt loss
A

Gain: sulfonylureas, TZD (pioglitazone)
Neutral: metformin, DPP4,
Loss: GLP-1 agonist (exenatide)

164
Q

prolactinoma vs pituitary adenoma

A

Prolactinoma: primary prolactin secreting tumor, levels >200 are diagnostic

Adenoma: nonfunctional, sxs from mass effect. mild increase in prolactin but not that high. central hypogonadism and hypothyroidism (look for dude with libido and tired probs)

165
Q

who gets diuretic-induced hypokalemia?

A

Primary hyperaldosteronism patients. may not have a lot at rest but withdiuretic sig hypokalemia

166
Q

ddx: htn and hypokalemia; increased renin, increased aldosterone

A
  • diuretic
  • cirrhosis, chf
  • renovascular htn
  • Renin secreting tumor
  • malignant htn
  • coarctation aorta
167
Q

ddx: htn and hypokalemia; decreased renin, increased aldosterone

A

primary hyperaldosteronism. get adrenal CT

168
Q

ddx: htn and hypokalemia; decreased renin, decreased aldosterone

A
  • CAH
  • Cushings
  • glucocorticoid resistance
  • exogenous mineralocorticoid
169
Q

polyuria in a non-hospitalized patient

A
  • DM
  • DI
  • PP
170
Q

how do sodium values differentiate PP and DI in a patient with polyuria

A

<135 –>PP

>145 –>DI

171
Q

Thyroid changes of pregnancy

A

Estrogen: increases thyroid-binding globulin = increase total t4
hCG: stimulates TSH receptors causing increase in free T4, T3

so on the hyperthyroid side of things (lab wise not sx)

172
Q

Patient undergoes surgery and is fucked up after. How do you differentiate malignant hyperthermia from thyroid storm?

A

MH: hypercarbia, sinus tachy, MUSCLE RIGIDITY, elevated Creatine Kinase, HYPERKALEMIA, hyperthermia

TS: tachycardia, hypertension, high fever, tremor, cardiac arrythmias (i.e. afib), altered mentation, LID LAG

173
Q

tx thyroid storm

A

beta blocker (dec adrenergic sxs)
PTU with iodine solution (dec T4 synth)
steroids (dec peripheral T4–>T3 conversion)
(all)

174
Q

how to tx Graves?

A

Options:

  1. Antithyroid drugs (PTU/M): old people! pregnancy! mild dz
  2. Radioactive iodine: moderate-severe
  3. Thyroidectomy: large goiter, possible cancer, also hyper parathyroid, severe opthalmopathy,
175
Q

T/F: Failure to suppress GH with glucose admin r/o Acromegaly

A

false, this makes the dx of Acromegaly

so suppression of GH by glucose r/o acro

176
Q

Tx of acromegaly

A

surgical resection (pituitary)

  • octreotide
  • pegvisomant (GH receptor antagonist)
  • cabergoline/bromocriptine
177
Q

cause of death in acromegaly

A

cardiac

–>concentric myocardial hypertrophy, diastolic dysfx, global hypokinesis

178
Q

why do alcoholics have hypocalcemia?

A

due to hypomagnesemia (dec release and sensitivity of pth)

179
Q

best markers indicating resolution/improved DKA

A

serum anion gap and beta-hydroxybutyrate levels

180
Q

pt has signs of hyperthyroidism. RAIU shows uptake <5% and anti-TPO present in high titers. dz and tx

A

Silent (painless) thyroiditis. will have nontender enlarged goiter also.
SO because not uptaking a lot, youre not making increase thyroid hormone so dont use anti-thyroid drugs or radioactive iodine.
The TPO antibodies (normally hashimoto) tell you youre just releasing pre-formed hormone, will ultimately become hypothyroid and then euthyroid. give beta blockers rn

181
Q

Despite normal/elevated serum levels, patients with which disease have total K deficit due to excessive urinary loss

A

DKA or HHS. Cause by glucose induced osmotic diuresis

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