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1
Q

What are the 2 types of autoimmune hemolytic anemia?

A
  1. Warm aggultinin AIHA

2. Cold agglutinin AIHA

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2
Q

Compare the etiologies of warm vs. cold agglutinin AIHA.

A

Warm - drugs (eg, penicillin), viral infections, AI (eg, SLE), immunodeficiency states, lymphoproliferative diseases (eg, CLL)

Cold - infections (eg, M. pneumoniae, mononucleosis), lymphoproliferative diseases

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3
Q

Compare the clinical presentation of warm vs. cold agglutinin AIHA.

A

Warm - asymptomatic to life-threatening anemia

Cold - symptoms of anemia, livedo reticularis and acral cyanosis with cold exposure that disappears with warming

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4
Q

Compare the Coombs’ test results in warm vs. cold agglutinin AIHA.

A

Warm - Direct Coombs’ positive with anti-IgG, anti-C3, or both

Cold - Direct Coombs’ positive with anti-C3 or anti-IgM, but usually NOT IgG

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5
Q

Treatment of warm agglutinin AIHA?

A

High dose corticosteroids

Splenectomy for refractory disease

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6
Q

Treatment of cold agglutinin AIHA?

A

Avoidance of cold temperatures

Rituximab +/- fludarabine

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7
Q

Compare the complications of warm vs. cold agglutinin AIHA.

A

Warm - VTE, lymphoproliferative disorders

Cold - ischemia and peripheral gangrene, lymphoproliferative disorders

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8
Q

Presentation of warm AIHA?

A

Normocytic anemia
Evidence of hemolysis (jaundice, elevated indirect bilirubin, increased serum LDH, decreased serum haptoglobin)
Splenomegaly (erythrocyte entrapment)
Reticulocytosis (BM response)

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9
Q

Peripheral smear appearance in warm AIHA?

A

Spherocytes, microspherocytes, elliptocytes, or increased number of polychromatophilic cells

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10
Q

Diagnose warm AIHA?

A

Direct antiglobulin (Coombs) test showing autoantibodies (usually anti-IgG) or complement components (eg, anti-C3) bound to the surface of the patient’s RBCs

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11
Q

What is the next step in management of progressive pain in a patient with prostate cancer and bony metastases after androgen ablation (orchiectomy)?

A

Radiation therapy (focal external beam therapy to sites of mets)

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12
Q

MOA - flutamide?

A

Non-steroidal anti-androgen via competitive binding to dihydrotestosterone receptors

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13
Q

List the 4 major classes of anticoagulants.

A
  1. Heparin
  2. Vitamin K antagonists
  3. Direct thrombin inhibitors (argatroban, bivalirudin, dabigatran)
  4. Factor Xa inhibitors (direct - rivaroxaban and apixaban, indirect - fondaparinux)
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14
Q

MOA - heparins?

A

Inhibit Xa and IIa (thrombin)

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15
Q

MOA - vitamin K antagonists?

A

Inhibit synthesis of II, VII, IX, X (vitamin K-dependent clotting factors) and proteins C and S (vitamin-K dependent ANTICOAGULANT proteins)

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16
Q

Why is it important to know that warfarin can lead to decreased protein S?

A

May lead to an incorrect diagnosis of an inherited protein S deficiency (if possible, discontinue warfarin for 2 weeks prior to evaluating protein S levels)

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17
Q

MOA - aspirin?

A

Antiplatelet agent, inhibits COX-1 -> inhibits thromboxane A2 synthesis

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18
Q

MOA - clopidogrel?

A

Antiplatelet agent, prevents platelet activation by blocking adenosine diphosphate receptors on the surface of platelets

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19
Q

MOA - heparin?

A

Activates antithrombin III, which inactivates factor IIa, IXa, and Xa

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20
Q

MOA - simvastatin?

A

Lipid-lowering agent, inhibits 3-hydroxy-3-methylglutaryl-coenzyme reductase

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21
Q

List the 4 hereditary thrombophilias.

A
  1. Factor V Leiden
  2. Prothrombin mutation
  3. Antithrombin deficiency
  4. Protein C or S deficiency
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22
Q

Typical inheritance pattern of hereditary thrombophilias?

A

AD with variable penetrance

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23
Q

Presentation of PE that began as a DVT?

A

SOB, leg swelling, sinus tachycardia, elevated D-dimer

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24
Q

In a young patient with no obvious risk factor for a DVT/PE, what should be considered?

A

Hypercoagulable disorder

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25
Q

Who should be tested for a hypercoagulable disorder?

A

Young (<45 years) patients with a first-time unprovoked DVT/PE, patients with recurrent DVT/PE, patients with unusual sites of thrombi (cerebral, mesentery, portal veins, etc.)

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26
Q

Most commonly found hereditary thrombophilia, especially in Caucasians?

A

Factor V Leiden (FVL)

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27
Q

Pathogenesis of Factor V Leiden?

A

AD point mutation in the gene for factor V that makes it unable to respond to activated protein C, an innate anticoagulant (activated protein C resistance) -> slowed degradation of procoagulant active factor V -> continued thrombin formation, slowed degradation of active factor VIII

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28
Q

PT and aPTT in Factor V Leiden?

A

Can be normal, as the major procoagulant effects are due to continued thrombin formation; elements of the coagulation cascade that can be assessed by these tests are less likely to be predominantly affected

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29
Q

Second most common hereditary thrombophilias in Caucasians?

A

Prothrombin mutation

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30
Q

Pathogenesis - prothrombin mutation?

A

Increased prothombin levels

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31
Q

Inherited form of antithrombin deficiency is rare - what are 3 acquired causes?

A

DIC, cirrhosis, nephrotic syndrome

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32
Q

Mechanism of protein C or S deficiency?

A

Decreased inactivation of factors Va and VIIIa

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33
Q

Etiology of primary hyperparathyroidism?

A
  1. Parathyroid adenoma (most common)
  2. Hyperplasia
  3. Carcinoma
  4. Increased risk in MEN 1 and 2A
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34
Q

Symptoms of primary hyperparathyroidism?

A

Asymptomatic (most common)
Mild, nonspecific symptoms (eg, fatigue, constipation)
Abdominal pain, renal stones, bone pain, neuropsychiatric symptoms

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35
Q

Diagnostic findings of primary hyperparathyroidism?

A

Hypercalcemia, hypophosphatemia
Elevated or inappropriately normal PTH
Elevated 24-hour urinary calcium excretion

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36
Q

Indications for parathyroidectomy?

A

Age <50
Symptomatic hypercalcemia
Complications or elevated risk of complications

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37
Q

Complications of primary hyperparathyroidism?

A

Osteoporosis (T-score

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38
Q

Elevated risk of complications of primary hyperparathyroidism?

A

Calcium 1+ mg/dL above normal, urinary calcium excretion > 400 mg/day

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39
Q

Pathophysiology of primary hyperparathyroidism?

A

Increased reabsorption of calcium from the distal tubule

Net urinary clacium excretion is increased due to excess resorption of calcium from bones

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40
Q

Diagnostic features of familial hypocalciuric hypercalcemia?

A

Hypercalcemia, elevated PTH, low urinary calcium excretion (often <100 mg/24 hours)

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41
Q

What is the purpose of parathyroid imaging in PHPT?

A

Optimize the surgical approach by potentially determining the affected side and evaluating for the possibility of a minimally invasive surgery

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42
Q

Parathyroidectomy is the treatment of choice for PHPT - what should be done for patients who decline surgery or have osteopenia or osteoporosis?

A

Bisphosphonate therapy

43
Q

When would extended CT imaging be indicated in the setting of hypercalcemia?

A

For suspected hypercalcemia of malignancy, which typically presents with severe, symptomatic hypercalcemia, low PTH, and elevated PTH-related protein

44
Q

When is continued observation appropriate in PTPH?

A

Older asymptomatic patients with near-normal calcium levels and normal bone density

45
Q

General clinical manifestations of Graves Disease?

A

Heat intolerance, weight loss, sweating

46
Q

Ocular clinical manifestations of Graves Disease?

A

Lid lag, proptosis, diplopia

47
Q

Dermatologic clinical manifestations of Graves disease?

A

Hair loss, infiltrative dermopathy (pretibial myxedema)

48
Q

CV clinical manifestations of Graves disease?

A

Tachycardia, HTN, AFib

49
Q

Nail manifestations of Graves disease?

A

Onycholysis, clubbing (acropachy)

50
Q

Endocrine manifestations of Graves disease?

A

Hyperglycemia, hypercalcemia, bone loss, menstrual irregularities

51
Q

GI manifestations of Graves disease?

A

Diarrhea

52
Q

Neuro manifestations of Graves disease?

A

Tremors, hyperreflexia, proximal muscle weakness

53
Q

Presentation of Graves ophthalmoplegia?

A

Features of hyperthryoidism with proptosis and impaired EOM (decreased convergence, diplopia)

Irritation (gritty/sandy sensation), redness, photophobia, tearing

54
Q

Risk factors for Graves Disease ophthalmoplegia?

A

Female sex, advanced age, smoking

55
Q

Pathophysiology of Graves disease?

A

Thyrotropin (TSH) receptor autoantibodies (TRAB) stimulate thyroid hormone production, resulting in hyperthyroidism

56
Q

Pathophysiology of Graves ophthalmoplegia?

A

T-cell activation and stimulation of orbital fibroblasts and adipocytes by TRAB, resulting in orbital tissue expansion and lymphocytic infiltration

(Thyroid hormone increases sensitivity to catecholamines and thyrotoxicosis of any etiology may cause lid lag and retraction due to sympathetic activation and contraction of the superior tarsal muscle, but this is not true exophthalmos)

57
Q

Compare the presentation of MG, LEMS, and Graves ophthalmoplegia.

A

MG - fluctuating diplopia and ptosis
LEMS - diplopia, ocular involvement less common than proximal limb muscle involvement

Neither would cause ocular irritation, pain movement, or proptosis

58
Q

General categories of male hypogonadism?

A

Primary (testicular disease) vs. Secondary (pituitary/hypothalamic disease)

59
Q

Compare the findings in primary vs. secondary testicular disease.

A

Both: decreased energy, libido, body hair

Primary: gynecomastia more likely
Secondary: gynecomastia less likely

Primary: increased LH/FSH
Secondary: decreased/normal LH/FSH

Primary: very decreased testosterone, sperm count
Secondary: decreased

60
Q

Congenital causes of primary male hypogonadism?

A

Klinefelter syndrome

Varicocele

61
Q

Acquired causes of primary male hypogonadism?

A 
Radiation
Infection (eg, mumps)
Trauma
Medications (eg, alkylating agents, glucocorticoids)
Chronic disease
62
Q

Congenital causes of secondary male hypogonadism?

A

Kallman syndrome

63
Q

Causes of secondary male hypogonadism due to gonadotropin suppression?

A
  1. Hyperprolactinemia

2. Glucocorticoids/opiates

64
Q

Causes of secondary male hypogonadism due to gonadotroph cell damage?

A

Benign/malignant tumors
Pituitary apoplexy
Infiltration (eg, hemochromatosis)
Systemic disease

65
Q

Evaluation of primary male hypogonadism?

A

Karyotype

Others based on clinic suspicion

66
Q

Evaluation fo secondary male hypogonadism?

A

Prolactin and other pituitary hormone deficiencies
Transferrin
+/-MRI (indicated with elevated Prl, mass-effect symptoms, very low <150 ng/dL testosterone, or disruptions in other pituitary hormones)

67
Q

Preferred treatment for prolactinoma?

A

Dopaminergic agonists

68
Q

Inheritance pattern of MEN1?

A

AD

69
Q

3 primary tumor types in MEN1?

A
  1. Parathyroid adenomas/hyperplasia
  2. Pancreatic/GI endocrine tumors (gastrinomas)
  3. Pituitary adenomas
70
Q

Clinical manifestation of pituitary adenoma in MEN1?

A
  • Secretion of prolactin, GH, ACTH (can be “nonfunctioning”)

- Mass effect (headache, visual field defects, etc.)

71
Q

Clinical manifestations of parathyroid adenoma/hyperplasia in MEN1?

A
  • Primary hyperparathyroidism

- Hypercalcemia (eg, polyuria, kidney stones, decreased bone density, constipation, possible abdominal pain)

72
Q

Clinical manifestations of pancreatic/GI neuroendocrine tumors in MEN1?

A

Gastrinoma - recurrent peptic ulcers
Insulinoma - hypoglycemia
VIPoma - secretory diarrhea, hypokalemia, hypochlorhydria
Glucagonoma - weight loss, necrolytic migratory erythema, hyperglycemia

73
Q

PHPT is present in >___% of patients with MEN1, usually occurs by age ___, and results form multiglandular parathyroid adenomas or parathyroid hyperplasia.

A

90; 40

74
Q

Burning upper abdominal pain that is only partially responsive to ranitidine and antacids and associated with occult GI bleeding is concerning for ___, characterized by severe and refractory PUD due to gastrinomas.

A

Zollinger-Ellison syndrome

75
Q

Features of milk-alkali syndrome?

A

Hypercalcemia, renal insufficiency, and metabolic alkalosis

76
Q

Cause of hypercalcemia in sarcoidosis?

A

Increased conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D

77
Q

What medication class slows the progression of diabetic nephropathy and why?

A

ACEIs - reduces blood pressure and intraglomerular pressure, reduces urinary albumin excretion

Recommended in patients with microalbuminuria even if their blood pressure is normal, as this is a sensitive marker of renal microvascular damage

78
Q

Pronator drift is a physical exam finding that is relatively sensitive and specific for what kind of disease?

A

UMN or pyramidal/corticospinal tract disease

79
Q

How is the pronator drift test performed?

A

Patient outstretches arms with palms up and eyes closed so that only proprioception is used to maintain arm position

80
Q

What is a positive pronator drift test and why does it happen?

A

Affected arm drifts downward and the palm pronates toward the floor - UMN lesions cause more weakness in the supinator muscles compared to the pronator muscles of the upper limb

81
Q

A young woman with neurologic deficits disseminated in space and time (eg, hand clumsiness, ataxia, vertigo) most likely has ___.

A

MS (inflammatory demyelinating disorder characterized by white matter lesions in the CNS)

82
Q

___ dysfunction typically results in extrapyramidal signs, such as resting tremor, rigidity, bradykinesia, and choreiform movements.

A

Basal ganglia

83
Q

___ dysfunction usually causes ataxia, intention tremor, and impaired rapid alternating movements. Pyramidal tract signs are not observed.

A

Cerebellar

84
Q

How is proprioception evaluated?

A

By passively moving the distal phalange of a digit up and down and having the patients identify the direction of movement with their eyes closed + Romberg test

85
Q

Predisposing risk factors for delirium?

A 
Dementia
Parkinson disease
Prior stroke
Advanced age
Sensory impairment
86
Q

List some precipitating factors of delirium.

A

Drugs (narcotics, sedative, antihistamines, muscle relaxers, polypharmacy)
Infections (pneumonia, UTI, meningitis)
Electrolyte disturbances (hyponatremia, hypercalcemia)
Metabolic derangements (volume depletion, B12 deficiency, hyperglycemia)
Systemic illnesses (CHF, hepatic failure, malignancy)
CNS conditions (seizure, stroke, head injury, subdural hematoma)

87
Q

Initial evaluation of delirium?

A 
Focused H&amp;P (including pulse ox)
Review all medications
CBC
Serum electrolytes
UA
88
Q

What is relative risk (RR)?

A

Probability of the outcome of interest occurring in the exposed group compared to the probability of it occurring in the non-exposed group. Null vale = 1.0

89
Q

A p value < 0.05 corresponds to a ___ confidence interval that does not contain the ___ value.

A

95%; null

90
Q

A p value < 0.01 corresponds to a ___ confidence interval that does not contain the null value.

A

99%

91
Q

If the null value is within a given confidence interval, then the p value = ?

A

> or = to the equivalent confidence interval

92
Q

What is a hazard rate?

A

Change of an event occurring in one of the study groups during a set period

93
Q

What is a hazard ratio?

A

Chance of an event occurring in the treatment group compared to the chance of that event occurring in the control group during a set period

94
Q

What does a hazard ratio <1 indicate?

A

That an event is more likely to occur in the control group

95
Q

What does a hazard ratio >1 indicate?

A

Event is more likely to occur in the treatment group

96
Q

What does a hazard ratio = 1 indicate?

A

No difference between the 2 groups

97
Q

In any randomized clinical study, the goal of successful randomization is to eliminate bias in treatment assignments. An ideal randomization process does what?

A
  • Minimizes selection bias
  • Results in near-equal treatment and control group sizes
  • Achieves a low probability of having confounding variables
98
Q

Pathophysiology of acute asthma exacerbation leading to respiratory failure?

A

Exacerbation causes increased respiratory drive and hyperventilation, leading to decreased partial pressure of PaCO2

99
Q

Signs of impending respiratory failure?

A 
Elevated or even normal PaCO2 in a patient with hyperventilation (should have decreased) suggest an inability to meet increased respiratory demands
Markedly decreased breath sounds
Absent wheezing
Decreased mental status
Marked hypoxia with cyanosis
100
Q

Management of impending respiratory arrest?

A

Admission to ICU with endotracheal intubation to maintain adequate oxygenation and ventilation

101
Q

Management of mild to moderate asthma exacerbation?

A

Oxygen and inhaled short-acting beta-2 agonists to effectively reverse airflow obstruction; no response -> systemic corticosteroids

102
Q

Management of severe asthma exacerbation?

A

SABAs, ipratropium nebulizer, systemic corticosteroids; no improvement after 1 hour of therapy -> additional bronchodilation wihth a one-time infusion of IV magnesium sulfate

Adding ipratropium to SABAs may cause greater bronchodilation than either alone and is recommended during emergency care of severe exacerbations

103
Q

When is systemic epinephrine indicated in treating acute asthma?

A

Only in severe exacerbation when inhaled therapy cannot be given; no proven benefit over aerosol therapy

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