JH IM Board Review - SOS III Flashcards

1
Q

CKD classification (KDIGO 2012) is based on (3):

A
  1. Cause ==> Presence of systemic disease and its location in the kidney.
  2. GFR category.
  3. Albuminuria.
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2
Q

Etiology of CKD:

A
  1. DM (40%).
  2. HTN (25%).
  3. Glomerulonephritis (10%).
  4. Genetic (PKD, etc, 3%).
  5. Urologic (approx. 2%).
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3
Q

Calcific uremic arteriolopathy (calciphylaxis):

A

Skin and fat necrosis with calcification and thrombosis of small arterioles — MC in ESRD.

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4
Q

Calciphylaxis usually occurs in the setting of:

A
  1. High Ca x Ph.
  2. Violaceous, indurated skin lesions that may ulcerate.
  3. Predilection for the lower extremities and trunk.
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5
Q

ACEIs/ARBs delay CKD progression — What is their effect on Cr?

A

Rise is 20% or less — Continue therapy as there is long-term benefit in preservation of GFR.

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6
Q

Atenolol in CKD — Problem?

A

It is excreted via the kidney, therefore, use with caution or consider switching to a nonrenally cleared beta-blocker (eg metoprolol).

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7
Q

Tx of atherosclerotic RAS:

A
  1. ACEI/ARB + Statin + Aspirin (1st line).
  2. Stop smoking.
  3. Angioplasty + endovascular stenting — NOT superior to medical management except in selected cases.
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8
Q

Goal of HbA1C in CKD:

A

7% — Lower A1c is NOT a/w slower CKD progression and INCREASES RISK OF HYPOGLYCEMIA.

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9
Q

Statin therapy and N-acetylcysteine may reduce the risk of … nephropathy.

A

CONTRAST nephropathy.

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10
Q

Vaccines for CKD:

A
  1. Annual flu vaccination.
  2. HBV series.
  3. Pneumococcal ==> PCV13 (conjugate) followed by PPSV23 (polysaccharide) at least 8 weeks later.

Repeat PPSV23 in 5y.

***If previous PPSV23 vaccination ==> Administer PCV13 1y or more after last PPSV23 dose.

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11
Q

CIs to renal transplantation:

A
  1. Metastatic or untreated cancer.
  2. Recent malignancy (time varies according to cancer type).
  3. Active infection.
  4. Severe psychiatric disease.
  5. Active/unstable CAD or CHF.
  6. NON renal organ failure (liver, lung).
  7. Persistent substance abuse.
  8. Unresolved psychosocial problems.
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12
Q

…-…% of >50y have microscopic hematuria.

A

2-18%.

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13
Q

Hematuria is more than … per hpf.

A

3 RBC/hpf.

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14
Q

Urine dipstick testing is highly sensitive for microscopic hematuria but it is NOT specific.

Heme (+) testing in the absence of RBCs suggests:

(4)

A
  1. Myoglobinuria.
  2. Intravascular hemolysis.
  3. Povidone-iodine administration.
  4. Presence of oxidizing agents.
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15
Q

Exercise-induced hematuria typically resolves with …-… of rest.

A

1-3 days.

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16
Q

Papillary necrosis may be precipitated by:

Ischemic damage to renal papillae

A
  1. SCD/trait.
  2. DM.
  3. Heavy use of phenacetin or acetaminophen.
  4. NSAIDs.
  5. UT obstruction.
  6. TB.
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17
Q

3 MCC of isolated hematuria w/o significant proteinuria (<500).

A
  1. IgA nephropathy.
  2. Thin basement membrane disease.
  3. Alport syndrome.
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18
Q

Approx. …% of men and …% of women will have a symptomatic stone by age 70.

A

16%

8%.

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19
Q

Latent autoimmune diabetes of adulthood (LADA):

A

DM I that can present in adulthood.

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20
Q

Tx of necrobiosis lipoidica:

A

1st line ==> Topical and intralesional steroids.

For ulcers ==> Cyclosporine — hyperbaric O2 — Infliximab.

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21
Q

Diagnostic criteria for prediabetes:

3

A
  1. Impaired glucose tolerance — 2h plasma glucose 140-199 mg/dL during OGTT.
  2. Impaired fasting glucose — Fasting plasma glucose 100-125.
  3. Increased risk for DM II — HbA1c 5.7-6.4%.
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22
Q

Insulin is the preferable 1st line therapy in certain clinical situations:

(4)

A
  1. Pregnancy ==> Only insulin is approved for use in pregnancy.
  2. Polyuria — polydipsia ==> Indicates severe hyperglycemia that should be rapidly reversed with insulin therapy.
  3. Ketosis ==> Indicates insulinopenia.
  4. LADA.
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23
Q

IMPORTANT CI of liraglutide?

A

CANNOT BE USED IN TS W/ PERSONAL OR FHx OF MEDULLARY THYROID CANCER

OR

MEN II.

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24
Q

Factors that may increase urinary albumin excretion over baseline values include:

A
  1. Exercise within 24h.
  2. Fever.
  3. Infection.
  4. CHF.
  5. Marked hyperglycemia.
  6. Marked HTN.
  7. Pyuria.
  8. Hematuria.
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25
Q

The lower limit of normal for TSH may be LOWER THAN established in African Americans …

A

Leading to possible MISDIAGNOSIS of SUBCLINICAL HYPOTHYROIDISM in healthy individuals.

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26
Q

What is apathetic thyrotoxicosis?

A

Classic signs of thyrotoxicosis may be absent in the older individuals, except for:

  1. Weight loss.
  2. Mental status changes.
  3. A-fib.
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27
Q

What is the laboratory importance of T3/T4 ratio:

A

If it is increased ==> GRAVES.

In contrast, in thyroiditis, the serum T3/T4 ratio is normal.

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28
Q

TSH-antibodies may be useful for …? (3)

A
  1. Confirm Graves.
  2. Stratify risk of neonatal thyrotox when measured at 22wk.
  3. Prognostication in Graves EYE disease.
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29
Q

Methimazole vs PTU?

A

Methimazole is the drug of choice!

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30
Q

PTU, rarely, can cause …

A

Fulminant hepatic failure.

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31
Q

Pregnancy — MMI — PTU?

A

PTU in 1st trimester.

MMI in 2nd/3rd.

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32
Q

Iodine Tx for Graves — Antithyroid drugs must be stopped …-… days before Iodine administration.

A

3-7 days.

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33
Q

TSH is decreased in pts taking … or …

A

Dopamine or HIGH-dose glucocorticoids.

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34
Q

CIs to iodine tx:

A

Absolute ==> Pregnancy and recent breastfeeding.

Relative ==> Moderate to severe eye disease — may be worsen (may give pre-tx with glucocorticoids).

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35
Q

As said before, Iodine may do what to Graves ophthalmopathy?

A

EXACERBATION — Especially in smokers.

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36
Q

Conditions a/w an acute or subacute non thyroidal illness:

A
  1. Non thyroidal surgery.
  2. Infection.
  3. Stroke.
  4. PE.
  5. Parturition.
  6. DKA.
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37
Q

Amiodarone-induced Thyrotoxicosis — How many types?

A

2 types.

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38
Q

Amiodarone-induced thyrotoxicosis type 1 VS AIT type 2:

A

Preexisting thyroid disease ==> Yes — No.

Duration of amiodarone therapy ==> Months — Years.

Iodine uptake ==> Low — Very low.

TFTs ==> Same.

Thyroid Doppler ==> Increased parenchymal blood flow — Normal, decreased parenchymal blood flow.

Tx ==> Antithyroid drugs/Surgery — Prednisone/Surgery.

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39
Q

Slightly elevated serum TSH levels in the elderly (75-80) have been a/w …

A

SURVIVAL BENEFIT.

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40
Q

Keep in mind that a normal total Ca may actually be high if … is low.

A

ALBUMIN IS LOW.

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41
Q

Formula for correcting total calcium when albumin is LOW:

A

Corrected Ca = Total serum Ca + (0.8 x [4 — albumin]).

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42
Q

Renal manifestations of hypercalcemia:

A
  1. Polyuria and polydipsia ==> Interference w/ ADH + Inhibition of Na resorption.
  2. Azotemia ==> Dehydration + Afferent vasoconstriction (!).
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43
Q

Li causes hypercalcemia via what mechanism?

A

Changes “set point” for PTH.

44
Q

CHRONIC manifestation of hypercalcemia in the EYES:

A

BAND KERATOPATHY ==> Deposition of Ca-Ph in sun-exposed cornea.

45
Q

Role of bisphosphonates in hypercalcemia:

A

Pamidronate + Zoledronate = choice.

==> Potent and effective ==> Ca begins to decline in 2 days and hits nadir at 7 days.

46
Q

AEs of bisphosphonates:

A
  1. Mild increase in temp.
  2. Myalgias.
  3. Transient increase in Cr.
47
Q

Glucocorticoids for hypercalcemia:

A

Most useful in tx of vitD-mediated hypercal.

**also useful in certain malignancies involving cytokine release (!) — Some myelomas.

48
Q

Glucocorticoids are the MC 2o cause for osteoporosis — Small or large doses for osteoporosis to occur?

A

SMALL — 5mg prednisone/day for 3 or more months.

49
Q

In men w/ osteoporosis, consider checking …

A

TESTOSTERONE LEVEL — Hypogonadism is a fairly common cause.

50
Q

X-ray is helpful for detecting early osteoporosis?

A

NO — Osteopenia is NOT evident until approx. 30% of bone is lost.

51
Q

What are the indications for BMD measurement with DXA scan:

A
  1. All women >65y + All men >70y.
  2. <65 and <70 w/ one or more clinical risk factors ==> LBW — previous fracture — high risk meds — Comorbidities a/w bone loss.
52
Q

Osteonecrosis of the jaw w/ bisphosphonates is a risk in which pts?

A

Cancer pts.

53
Q

Long-term, uninterrupted (5y or longer) use of bisphosphonates a/w the very rare complication of …

A

Atypical fractures of the femoral shaft(subtrochanteric or diaphyseal).

54
Q

Teriparatide is used for a max of 2y. Why is that?

A

It has been found to cause OSTEOSARCOMA IN RATS.

NOT in humans (yet).

55
Q

Denosumab side effect to remember:

A

RANKL plays a role in immune function — 1% increased risk of infections.

*not opportunistic infections.

56
Q

Tx for Paget is indicated in (4):

A
  1. All sx pts.
  2. Asx pts w/ involvement of the skull — axial skeleton — weight-bearing long bones (high risk of progression to deformity).
  3. Asx pts w/ ALP 3x greater than the upper limit of normal.
  4. Pts undergoing surgery on sites of active disease — Tx will reduce the hypervascularity of the bone.
57
Q

What to give in Paget?

A
  1. Analgesics for pain.
  2. Bisphosphonates for severe disease — 1st line (higher doses than osteoporosis).
  3. Calcitonin is approved but rarely used (short-lived effect) — SIGNIFICANT BONE PAIN RELIEF.
58
Q

Paget can be monitored w/ …(2):

A
  1. ALP.

2. C-telopeptide (!).

59
Q

Ddx of pathologic SECONDARY amenorrhea consists of 4 main disease states:

A
  1. Hyperprolactinemia.
  2. Anovulatory states (MC PCOS).
  3. Androgen excess (androgen-secreting tumors).
  4. Hypothalamic amenorrhea.
60
Q

Hirsutism and virilization:

A

Hirsutism = terminal hairs in male body sites (face, chest, back, lower abdo, inner thighs).

Virilization = MORE SEVERE ANDROGEN EXCESS — Deep voice, clitoromegaly, frontal balding, enhanced musculature, hirsutism.

61
Q

Hirsutism MCC:

A

Idiopathic familial (physiologic).

62
Q

Hirsutism MC OVARIAN cause:

A

PCOS.

63
Q

Hirsutism MC adrenal cause:

A

CAH.

64
Q

MCC of 1o hypogonadism in men:

A

Klinefelter.

65
Q

Testosterone therapy — What must be kept in mind?

A
  1. Monitor possible erythrocytosis.
  2. Prostate exam + PSA in >40y.
  3. Caution with CVS risks.
66
Q

PDE-5 inhibitors should be taken … before intercourse.

Their duration is …

A

1h before.

4h duration.

67
Q

Tadalafil has a faster onset of action and longer duration (…)

A

36h!

68
Q

Warn pts about potential side effects of PDE-5 inhibitors:

3

A
  1. Color vision changes.
  2. Headaches.
  3. SUDDEN BLINDNEES from NON ischemic anterior optic neuropathy (case reports).
69
Q

45% of pituitary masses are hormone-secreting tumors — 45% are NON-secreting tumors.

10% include …

A
  1. Craniopharyngiomas.
  2. Rathke cysts.
  3. Meningiomas.
  4. Metastatic tumors.
  5. Lymphoma.
  6. Granulomatous diseases.
  7. The increasingly recognized AUTOIMMUNE LYMPHOCYTIC HYPOPHYSITIS — (either 1o or 2o to cancer immunotherapy — particularly IPILIMUMAB.
70
Q

Incidentalomas <1cm grow in less than …% of cases.

A

10%.

71
Q

Incidentalomas >1cm grow in about …% of cases.

A

35%.

72
Q

Pituitary tumors may exist as part of genetic syndromes — Carney complex:

A

AD complex:

  1. Cardiac myxomas.
  2. Spotty pigmentation of the skin.
  3. Various hyperendocrine states (!) — often including GH secretion.
73
Q

Pituitary tumors may exist as part of genetic syndromes — Familial isolated pituitary adenomas (FIPA):

(Sometimes called isolated familial acromegaly syndrome)

A
  1. AIP inactivating mutations.
  2. AD but low penetrance (20%).
  3. Tumors mostly GH-secreting + large + aggressive + typically early in life.
74
Q

Lymphocytic hypophysitis occurs in about …% of pts taking ipilimumab.

A

10%

75
Q

If prolactin is >…, prolactinoma is very likely.

A

> 200 ng/mL.

76
Q

A sellar mass in the presence of elevated serum prolactin, is NOT a definitive proof of prolactinoma.

What may be happening?

A

A large, NON-secreting adenoma may cause elevated PRL levels by COMPRESSING THE PITUITARY STALK.

==> Inhibiting hypothalamic dopaminergic regulation of PRL.

***Suspect this if macroadenoma is seen and PRL is <100 ng/mL.

77
Q

If PRL is elevated but the pt has no sx — The presence of MACRO-PROLACTINEMIA must be suspected.

What is happening now?

A

PRL molecules bind to circulating immunoglobulins — causing MARKED increased in PRL half-life (though biologically INACTIVE).

78
Q

How can we identify macroprolactinemia:

A

By repeating serum PRL measurement AFTER precipitating immunoglobulins with POLYETHYLENE GLYCOL.

79
Q

Macroprolactinemia Tx?

A

None.

80
Q

In difficult cases of differentiation of pituitary vs ectopic ACTH, what can we do?

A

Bilateral inferior petrosal sinus sampling after administration of corticotropin-releasing factor.

81
Q

Drug that inhibits ACTH secretion:

A

Pasireotide.

82
Q

With pituitary tumors/mass effect the order of the loss of hormones is:

GH ==> FSH/LH ==> TSH ==> ACTH.

Is there a case when this may not be followed?

A

Yes — with other causes of hypopituitarism.

Radiation or lymphocytic hypophysitis (!).

83
Q

Most cases of pituitary apoplexy happen in pts w/ …

A

Previously undiagnosed pituitary tumors (2/3 of cases).

84
Q

What is the most dangerous consequence of pituitary apoplexy?

A

Acute lack of ACTH ==> Adrenal insufficiency.

85
Q

What is the clinical presentation of GH deficiency in ADULTS?

A
  1. Decrease sense of well-being.
  2. Decreased muscle mass.
  3. Increased fat.
  4. Osteopenia.
  5. Abnormal lipid profile (increased total and LDL cholesterol).
86
Q

Tx of central hypothyroidism — if we don’t follow the TSH, what do we do?

A

Repletion with T4 — Tx is ADJUSTED TO SYMPTOMS + Measure serum free T4 levels.

87
Q

What should be kept firmly in mind when treating pts with central hypothyroidism?

A

Never replace thyroid hormone before assessing ADRENAL FUNCTION.

==> DANGER ==> Pharmacologically-induced euthyroidism.

***thyroid hormones accelerate cortisol catabolism.

88
Q

Kallmann syndrome may lead to what eye problems?

A

Red-green color blindness.

89
Q

2 electrolyte disturbances that may lead to NEPHROGENIC DI:

A

HYPOkalemia

HYPERcalcemia

90
Q

Most adrenal incidentalomas (67-94%) are secretory or non secretory?

A

NON secretory.

91
Q

What determines the management of incidentaloma?

A

MASS SIZE — If >4cm ==> REMOVE.

***Biopsy CANNOT differentiate between benign and malignant.

92
Q

When FNA is appropriate management for an incidentaloma?

A

If metastases to the adrenals is suspected and pheochromocytoma has been r/o.

93
Q

Lack of hypokalemia does or does not exclude aldo excess?

A

Does not — may be unveiled by the use of diuretics.

94
Q

K should be normalized BEFORE evaluating for hyperaldo, because …

A

Hypokalemia suppresses aldo secretion.

95
Q

Initial screening for hyperaldo?

A

With serum aldo-plasma renin ratio.

If <20 ==> HYPERALDO IS RULED OUT.

96
Q

If aldo/renin ratio is >20, the next step is to …

A

Demonstrate nonsuppressible levels of aldo in presence of Na load.

Give 2L NS over 4h.

If aldo is not suppressed to <8ng/dL ==> HYPERALDO IS PRESENT.

97
Q

In pts >40y, what is recommended in order to determine the SOURCE of excessive aldo?

(given higher prevalence of bil hyperplasia and adrenal incidentalomas)

A

ADRENAL VEIN SAMPLING.

98
Q

MCC of hyperaldo is bil hyperplasia or adenoma?

A

Bil hyperplasia.

99
Q

Adrenal androgen excess — Men are typically …

A

Asx.

100
Q

Adrenal androgen excess — Women present with:

A
  1. Hirsutism.
  2. Virilization.
  3. Oligomenorrhea — amenorrhea — infertility.
  4. Acne.
101
Q

Rare mutation that may cause pheochromocytoma:

A

Succinyl dehydrogenase gene mutations — Familial paraganglioma syndromes — FPGL.

102
Q

Hyponatremia is seen less commonly with 2o adrenal insufficiency — If that is the case, then think of …

A

Central hypothyroidism.

103
Q

Gold-standard test of adrenal function is …

A

INSULIN-INDUCED HYPOGLYCEMIA or INSULIN TOLERANCE TEST.

104
Q

Insulin tolerance test is CI in:

A
  1. CAD.
  2. Seizures.
  3. > 60y.
105
Q

MC used test for adrenal function assessment is …

A

ACTH stimulation test.

Give ACTH ==> Measure cortisol before and 60min following injection.

106
Q

Other causes of hyporenimic hypoaldosteronism besides DM?

A
  1. ACEIs.
  2. NSAIDs.
  3. Cyclosporine.
  4. Heparin (!).
  5. AIDS (!).