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Medicine shelf > CF cases 1 > Flashcards

CF cases 1 Flashcards

1
Q

What is the most common cause of mitral stenosis?

A

Rheumatic heart disease

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2
Q

What is the common presentation of mitral stenosis?

A

Young woman, often in pregnancy, with shortness of breath, hemoptysis, and a diastolic murmur

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3
Q

What is the most common presentation of mitral valve prolapse?

A

Pain, palpitations, panic attack. More common in women. Different symptoms from mitral stenosis.

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4
Q

Which murmur gets better with increased blood flow?

A

Mitral valve prolapse

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5
Q

What does the murmur of MS sound like?

A

Opening diastolic snap with late diastolic decrescendo murmur (often called a rumble). Louder S1

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6
Q

Which action would worsen the murmur of MS?

A

Anything that increases venous return to the heart (Ex: leg raising)

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7
Q

What is the pathophysiology in hemoptysis in MS?

A

Increased pulmonary vein pressure causes small vessel rupture in the lungs, leading to hemoptysis

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8
Q

What is the pathophysiology in dysphagia in MS?

A

Dilation of the left atrium presses against the esophagus, which lies immediately behind the left atrium.

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9
Q

What is Kussmaul’s Sign?

A

Increase in JVP on inhalation

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10
Q

What is Kussmaul’s Sign indicative of?

A

Defective filling of the right ventricle, such as in constrictive pericarditis

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11
Q

What is pulsus paradoxus?

A

Drop in > 10mmHg in blood pressure during inhalation. Often, radial pulse is no longer palpable during inhalation

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12
Q

How does the murmur of MS change as disease worsens?

A

Opening snap occurs earlier (closer to S2) and the duration of the rumble is longer.

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13
Q

What is the treatment of choice in stable V-tach?

A

Amiodarone

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14
Q

What is the treatment of choice in unstable V-tach?

A

Cardioversion

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15
Q

Which EKG finding is associated with MS?

A

Atrial fibrillation

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16
Q

What is the most accurate test in MS? What is the best first test?

A

Most accurate is cardiac cath and direct measurement of the mitral valve opening. Best first test is transesophageal echocardiography.

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17
Q

How is cardiomegaly defined on CXR?

A

> 1/2 transthoracic diameter

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18
Q

What is the most accurate test for pleural effusion?

A

Thoracentesis

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19
Q

What are the medical treatments of choice in aortic dissection?

A

Labetalol (to decrease pulse and pressure) and nitroprusside (to decrease afterload)

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20
Q

What is the most accurate test for aortic dissection?

A

Angiogram

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21
Q

What is the best initial therapy for mitral stenosis?

A

Diuretic such as furosemide

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22
Q

What are the roles of digoxin, beta blockers, and Ca channel blockers in A-fib?

A

Slowing heart rate to allow for more time for ventricular filling

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23
Q

What is the treatment for mitral stenosis refractory to diuretics/salt restriction?

A

Manual balloon valvuloplasty

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24
Q

What is the definitive treatment for aortic stenosis?

A

Aortic valve replacement

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25
Q

What is the pathophysiology for hoarseness in mitral stenosis?

A

Compression of recurrent laryngeal nerve by a dilated left atrium

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26
Q

What patients should be screened for diabetes?

A

Asymptomatic obese patients with BP > 135/80

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27
Q

Which patients should be screened with abdominal ultrasound?

A

Males 65-75 years of age who have a history of smoking (to rule out abdominal aortic aneurysm)

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28
Q

When should patients be screened with colonoscopy?

A

Starting at age 50 at least once every 10 years.

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29
Q

What is the most appropriate screening test for diabetes?

A

2 fasting glucose measurements of >126 OR 1 random glucose over 200 OR abnormal glucose tolerance test. HA1C is NOT part of diagnostic screening.

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30
Q

What is the underlying pathophysiology of Type II DM?

A

Insufficient number of insulin receptors. Obesity is a risk factor b/c adipocytes and resting muscle MUST have insulin for glucose to enter

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31
Q

What is the mechanism of miglitol?

A

Inhibits breakdown of disaccharides and polysaccharides by alpha glucosidases so that glucose absorption in the small intestine is decreased

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32
Q

What is the best first treatment option in patients with hyperglycemia?

A

Diet and exercise. First pharm treatment is metformin b/c it doesnt cause hypoglycemia or weight gain

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33
Q

Why are sulfonylureas not first line drugs in diabetes?

A

They can cause weight gain and hypoglycemia (due to increased insulin release –> lower glucose and greater glucose uptake by adipocytes)

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34
Q

What is the mechanism of metformin?

A
  1. Decreased hepatic gluconeogenesis and 2. increased insulin sensitivity
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35
Q

What is the only commonly used drug of the biguanide class?

A

Metformin

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36
Q

What is the mechanism of pioglitazone?

A

PPAR-gamma agonist. Increases transcription of insulin sensitive genes. Increases insulin sensitivity

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37
Q

What is the adverse effect of metformin use?

A

Lactic acidosis (in patients renal insufficiency)

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38
Q

Which diabetes drug is associated with diarrhea and flatus?

A

Miglitol. It induces a lactose-intolerance-like state

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39
Q

Which diabetes drugs are associated with exacerbation of heart failure?

A

Glitazones (pioglitazone, rosiglitazone)

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40
Q

Which diabetes drugs are associated with SIADH?

A

Sulfonylureas

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41
Q

Which hypertensive drugs are first line in diabetics?

A

ACE inhibitors or angiotensin receptor blockers (NOT beta blockers or diuretics) due to renal protective effect (dilation of efferent arteriole)

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42
Q

What is the target BP in a diabetic patient or a patient with renal insufficiency?

A

Less than 130/80

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43
Q

What is the target for LDL in diabetic patients or patients with coronary artery disease?

A

<100.

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44
Q

What is the best next step in management in a diabetic patient with elevated LDL?

A

A statin drug such a simvastatin. Statins are preferred because they lower the mortality more than other options. If LDL >100, diet/exercise alone are not considered sufficient

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45
Q

Which cholesterol control agent is contraindicated in diabetes?

A

Niacin, because it can actually raise blood glucose

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46
Q

What is the most common adverse effect of statin therapy?

A

Increased LFTs. This is much more common than myositis. Thus, LFTs should be routinely checked. CPK doesn’t have to be routinely checked.

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47
Q

How long into the past does HA1c predict glucose levels?

A

Past 3 months, because of the lifespan of RBCs

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48
Q

What is the routine management of renal function in a diabetic with normal BUN/creatinine?

A

Microalbumin level (NOT dipstick b/c it is not sensitive enough). Microalbuminuria is LESS protein than trace urine on urinalysis.

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49
Q

What drug should be started in a diabetic with microalbuminuria?

A

ACE inhibitor or angiotensin receptor blocker (for renal protective effect)

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50
Q

What histological finding is unique to diabetic nephropathy?

A

Kimmelsteil-Wilson nodules

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51
Q

Which populations are at greatest risk for focal segmental glomerulonephropathy?

A

HIV and IV drug use

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52
Q

What is the normal cup to disk ratio on fundoscopic exam?

A

0.3

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53
Q

What is the fundoscopic finding in diabetic retinopathy?

A

Neovascularization into the optic disc

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54
Q

What is the treatment for diabetic retinopathy?

A

Laser photocoagulation

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55
Q

What is the fundoscopic finding in glaucoma?

A

Increased cup to disc ration

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56
Q

What is the fundoscopic finding in central retinal artery occlusion?

A

Pale retina due to lack of blood flow

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57
Q

What is the fundoscopic finding in hypertensive retinopathy?

A

AV nicking, cotton wool spots, and copper wiring

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58
Q

What is the test of choice to detect diabetes in a pregnant woman?

A

Oral glucose tolerance test. Blood glucose levels > 200 several hours after drinking the sugar solution is a positive result

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59
Q

What is the underlying cause of diabetic foot ulcers?

A

Neuropathy leading to decreased sensation –> injuries are not realized –> infection –> ulcers

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60
Q

What is the underlying cause of decreased gastric motility and bloating in diabetics?

A

Autonomic neuropathy –> no perception of stretch in GI –> decreased GI motility –> gastroparesis

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61
Q

What is the best treatment for diabetic gastroparesis?

A

Metoclopramide or erythromycin

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62
Q

What is the mechanism of metoclopramide?

A

D2 receptor antagonist –> antiemesis and increased gastric motility

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63
Q

What is the most likely diagnosis in a diabetic in DKA with black lesion on the roof of the mouth?

A

Mucormycosis infection (fungus). This is a medical emergency

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64
Q

What is the treatment of choice for mucormycosis?

A

Amphotericin B

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65
Q

What is the most common side effect of amphotericin B?

A

Type I renal tubular acidosis

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66
Q

What is a side effect of ketoconazole in men?

A

Gynecomastia - antiandrogenic effect

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67
Q

What is the most important treatment of mucormycosis aside from amphotericin B?

A

Surgical debridement

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68
Q

What is glargine?

A

Glargine (Lantus) is long acting insulin. Provides stable overall insulin levels

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69
Q

What is aspart?

A

Insulin aspart (NovoLog) is a rapid acting insulin given prior to mealtime

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70
Q

What is seen on CT in malignant otitis externa?

A

Collapsed mastoid air cells

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71
Q

What is the most common organism responsible for malignant otitis externa?

A

Pseudomonas

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72
Q

Why can infection trigger DKA?

A

Infection causes insulin resistance and also increase of cortisol, which decreases uptake of glucose by tissue

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73
Q

Why is Kussmaul’s breathing seen in DKA?

A

Compensation for metabolic acidosis. Deep, rapid breaths blow off more CO2

74
Q

What is the best initial therapy in DKA?

A

Normal saline bolus and IV insulin

75
Q

What EKG finding will be seen in DKA?

A

Peaked T waves indicative of hyperkalemia (due to exchange of H+/K+ in cells in an attempt to correct the acidosis)

76
Q

What is the treatment for hyperkalemia?

A

Calcium chloride or calcium gluconate

77
Q

What happens to serum sodium levels when glucose levels increase?

A

Increase of 100 mg/dL in glucose causes a 1.6mEq/L decrease in Na+

78
Q

What is the mechanism of hypotension in DKA?

A

Osmotic diuresis

79
Q

What is the first test to order for a patient with purpura or petechiae and epistaxis?

A

Platelet count

80
Q

When is a bleeding time the best study?

A

When a patient has platelet type bleeding but a normal platelet count

81
Q

Which test is used to assess functionality of vonWillebrand factor?

A

Ristocetin. It acts as an artificial endothelial membrane that platelets should bind to.

82
Q

When is a Ristocetin cofactor assay the best study?

A

Platelet type bleeding with normal platelet count and normal quantitative vWF

83
Q

What is the primary difference between platelet type bleeding and coagulation factor type bleeding?

A

Platelet type bleeding is generally more superficial and presents as petechiae, purpura, bleeding gums, epistaxis

84
Q

What is the difference between petechiae and purpura?

A

Size. Purpura is just larger petechiae.

85
Q

Which drugs can be associated with thrombocytopenia?

A

Penicillin, sulfa drugs, allopurinol, quinidine, lamotrigine, and rifampin

86
Q

What is the presentation of ITP?

A

Isolated thrombocytopenia in a healthy person with a normal spleen

87
Q

What is the best next step in a patient with suspected ITP?

A

Initiate treatment with prednisone (NOT order diagnostic tests. Do this after treatment is initiated)

88
Q

Which disease is associated with Auer rods?

A

Acute myeloid leukemia

89
Q

What is seen in increased numbers on a peripheral smear of an ITP patient?

A

Megakaryocytes

90
Q

What is the best next step in a patient treated with prednisone for ITP and now presenting with GI bleeding?

A

IVIG (plasmapheresis does NOT work)

91
Q

When is IVIG necessary in ITP?

A

Brain or bowel bleeds constitute life threatening bleeding and require IVIG therapy

92
Q

What is the role of platelet transfusion in ITP?

A

None. ITP is a platelet destruction problem, not a production problem. Transfused platelets will be destroyed.

93
Q

What is the inheritance pattern of vonWillebrand disease?

A

X-linked recessive

94
Q

What is the typical presentation of vonWillebrand’s disease?

A

Patient with platelet type bleeding and normal platelet count but increased bleeding time and aPTT (due to decreased Factor VIII)

95
Q

Which drug can possibly precipitate vonWillebrand’s disease?

A

Aspirin

96
Q

What is the best initial test in suspected vonWillebrand’s disease?

A

Bleeding time

97
Q

What is Factor VIII antigen?

A

Factor VIII antigen = vWF

98
Q

What are the two ways one can have vonWillebrand’s disease?

A

Quantitative decrease in vWF or functional quality decrease in vWF

99
Q

What is the role of desmopressin in vonWillebrand’s disease?

A

Increases release of subendothelial stores of Factor VIII and vWF

100
Q

What is the best initial therapy in vonWillebrand’s disease?

A

Desmopressin. If this doesn’t work, give Factor VIII replacement

101
Q

What is the typical presentation of hemophilia?

A

Boy with delayed hemarthrosis. Hemophilia A is far more common than Hemophilia B

102
Q

What is the best initial test in suspected Hemophilia?

A

aPTT. If aPTT prolonged, follow it up with a mixing study

103
Q

What does a mixing study accomplish?

A

Distinguish between a factor deficiency (aPTT corrected with mixing) and an antibody inhibitor (aPTT doesn’t correct with mixing)

104
Q

What is the next test in a patient with prolonged aPTT that is corrected with mixing study?

A

Factor VIII level. Factor VIII deficiency is far more common than factor IX deficiency

105
Q

What is the best treatment for hemophilia A?

A

Recombinant Factor VIII replacement

106
Q

What is a treatment for very mild hemophilia A?

A

Desmopressin

107
Q

What type of bleeding is caused by DIC?

A

Both platelet type and coagulation factor type bleeding.

108
Q

Which tests are the most accurate in diagnosing DIC?

A

D-dimer or fibrin split products

109
Q

What is the best treatment for DIC?

A

Replace platelets and fresh frozen plasma. Heparin is NOT an option because the patient is already bleeding.

110
Q

What is acquired storage pool disorder?

A

Uremia induced platelet dysfunction. Uremia prevents platelets from degranulating –> no aggregation

111
Q

What is Glanzmann’s thrombasthenia?

A

Genetic condition in which defective GpIIb/IIIa prevents platelet to platelet adhesion, increasing bleeding time. Presents like vonWillebrand disease with normal vWF levels.

112
Q

What is Bernard-Soulier syndrome?

A

AR deficiency in the Gp1b glycoprotein receptor on the surface of the platelets. Presents like vonWillebrand disease with normal vWF levels.

113
Q

What is the best treatment for uremic induced platelet dysfunction?

A

DDAVP - releases more Factor VIII and vWF

114
Q

What is the presentation of heparin induced thrombocytopenia?

A

Dropping platelet counts after starting a patient on heparin

115
Q

What is the next step in a patient with HIT who must continue to be anticoagulated?

A

Switch to a direct thrombin inhibitor such as argatroban and hirudin

116
Q

What is the best test in suspected heparin induced thrombocytopenia?

A

Platelet factor 4 antibodies

117
Q

What is the clinical triad of HUS?

A

Hemolytic anemia, acute renal failure, and thrombocytopenia.

118
Q

What is the pathophysiology of HUS?

A

Shiga-like toxins inactivate ADAMTS13, resulting in formation of microthrombi and consumption of platelets. Narrowed blood vessels cause shearing of RBCs and ischemia to end organs (particularly kidney)

119
Q

What is the difference between TTP and HUS?

A

Very similar pathophysiology and presentation. TTP often presents with fever and neurologic symptoms

120
Q

Which organism is most associated with HUS aside from E. coli O157:H7

A

Shigella

121
Q

What is the role of ADAMTS13?

A

Dissolves vWF so that small primary platelet clots that aren’t crosslinked with fibrin get broken up

122
Q

What happens to aPTT and PT in HUS?

A

Normal

123
Q

What does haptoglobin do?

A

Scavenges free hemoglobin (from hemolysis) and binds to it in order to recycle it.

124
Q

What happens to haptoglobin levels in hemolysis?

A

Decreased b/c they get bound to free hemoglobin

125
Q

What happens to LDH levels in hemolysis?

A

RBC have lots of LDH so hemolysis raises the serum LDH levels

126
Q

What is the best treatment for TTP/HUS?

A

Plasmapheresis or fresh frozen plasma (replaces the ADAMTS13). Do NOT give antibiotics or platelets

127
Q

Which drugs can cause HUS?

A

Clopidogrel and ticlopidine. The reason is unclear

128
Q

What is the next best step in a patient presenting with pulmonary edema?

A

Oxygen and preload reduction (furosemide)

129
Q

What are the steps in management of suspected pleural effusion?

A

Decubitus CXR’s (fluid should move around) then thoracentesis

130
Q

What are the expected findings of a CXR in pulmonary edema?

A

Congestion of the pulmonary vessels, especially at the top of the lung (cephalization of flow)

131
Q

When should an arrhythmia be cardioverted?

A

If there is hemodynamic instability (chest pain, shortness of breath, hypotension, confusion)

132
Q

What is the definitive treatment for WPW syndrome?

A

Radiocatheter ablation

133
Q

What should be done if an arrhythmia is deemed the cause of pulmonary edema?

A

Emergent cardioversion

134
Q

What is seen on Swan Ganz catheter in CHF?

A

Increased wedge pressure and decreased cardiac output

135
Q

What is the best preload reducing agent in acute pulmonary edema?

A

Furosemide

136
Q

What is the mechanism by which morphine helps in acute pulmonary edema?

A

Vasodilation of pulmonary veins decreases hydrostatic pressure in the lung

137
Q

What is nesiritide?

A

A synthetic ANP. Not shown to have any benefit over nitrates.

138
Q

Which test can be used to rule out CHF?

A

BNP. If levels are low, CHF can be ruled out. However, elevated BNP is fairly nonspecific and can be a result of numerous causes

139
Q

What is the most accurate test to determine ejection fraction?

A

MUGA (nuclear ventriculography)

140
Q

What are the types of drugs shown to decrease mortality in CHF?

A

ACE inhibitors, beta blockers, and spironolactone

141
Q

What can be used in the treatment of acute pulmonary edema that does not improve with oxygen, furosemide, nitrates, and morphine?

A

Dobutamine IV.

142
Q

What is the mechanism of dobutamine in pulmonary edema?

A

Increases inotropy of the heart and decreases afterload (some vasodilation)

143
Q

How do beta blockers affect the RAAS?

A

Decreased renin release in the nephron

144
Q

What happens to mortality benefit of beta blockers with decreasing ejection fraction?

A

Increased mortality benefit of beta blockers with decreased ejection fraction. The sicker the heart the more benefit beta blockers have

145
Q

What is the most common cause of death in CHF?

A

Ischemic ventricular arrhythmias

146
Q

What is the main mechanism of mortality benefit in beta blockers?

A

Decreased heart rate allows for decreased O2 consumption as well as increased coronary filling time –> decreases risk for ischemic arrhythmia

147
Q

What are the indications for biventricular pacemaker?

A

Decreased EF as well as wide QRS

148
Q

What is the most dangerous lesion in a pregnant woman?

A

Eisenmenger’s shunt

149
Q

Which type of restrictive cardiomyopathy is associated with speckled septum on echo?

A

Amyloid

150
Q

What is the difference in management between ischemic dilated cardiomyopathy and drug-related dilated cardiomyopathy?

A

CABG and aspirin will not help. All other mortality reducing drugs (beta blocker, ACE-I, spironolactone) are still indicated

151
Q

What will worsen the murmur of HOCM?

A

Anything that decreases LV blood volume such as standing or valsalva

152
Q

What will improve the murmur of HOCM?

A

Anything that increases LV blood volume such as squatting (increased preload) or hand grip (increased afterload)

153
Q

Where is the murmur of HOCM best heard?

A

At the lower left sternal border (the same place you would hear tricuspid stenosis)

154
Q

What is the treatment with best mortality reduction in a HOCM patient who has had syncopal episodes?

A

Implantable cardiac defibrillator or catheter septoplasty. Metoprolol should also be used but is not the immediate best option if there is a history of syncope

155
Q

What is the best option for a patient on ACE-I with a dry cough?

A

Switch the ACE-I to an angiotensin receptor blocker

156
Q

What therapy should be used for a patient who cannot tolerate ACE-I or ARBs?

A

Hydralazine (arterial vasodilation) and nitrates (dilates coronaries)

157
Q

What is a frequent side effect of nitrates?

A

Throbbing headache (migraines).

158
Q

When are triptans contraindicated for headache?

A

Patients with history of MI or CHF

159
Q

What can therapeutic digoxin present as on EKG?

A

ST depression - often difficult to distinguish from ischemia

160
Q

What is the most common risk factor for coronary artery disease?

A

Hypertension

161
Q

What is the worst risk factor for CAD?

A

Diabetes. In fact, diabetics are at equal risk for MI’s as those with coronary artery disease

162
Q

The presence of what symptoms excludes coronary artery disease?

A

Chest wall tenderness (95% sensitivity), changes with position, or changes with respiration

163
Q

What is always the next best step in a patient with any type of chest pain?

A

EKG, even if you are sure it will be normal

164
Q

What is the upper limit of a normal PR interval?

A

0.2 seconds

165
Q

What is a pathologic Q wave?

A

Greater than 1 box wide and 1 box deep and at least 1/4 of total QRS height

166
Q

What is the next step in a patient with on and off chest pain who has ST depression at baseline?

A

Stress echo (detects abnormal wall motion) or stress thallium

167
Q

What is the next best step in a patient with on and off chest pain but normal EKG?

A

Stress test and EKG

168
Q

What is the next best step in a patient with chest pain if a stress test shows ischemia?

A

Give aspirin and beta blockers. Diagnostic tests such as angiograms should be done after giving aspirin

169
Q

What is the most likely etiology of chest pain in a young, menstruating female with no risk factors for CAD?

A

Prinzmetal’s angina (vasospasm)

170
Q

What does ergonovine do?

A

Causes vasospasm of the coronary arteries. Can be used to test for Prinzmetal’s angina

171
Q

What is the upper limit of a normal QRS complex?

A

0.12 seconds (3 small boxes)

172
Q

What is the best next step in a patient with chest pain and an EKG showing STEMI?

A

Give chewable aspirin (morphine, nitrates, and oxygen do NOT lower mortality)

173
Q

What is the parasite responsible for Chagas disease?

A

Trypanosoma cruzi. It is spread by the bite of the Reduviid bug.

174
Q

What can Chagas disease do to the heart?

A

Cause dilated cardiomyopathy

175
Q

What should the target LDL be for a patient with diabetes AND coronary disease?

A

Under 70

176
Q

Which cardiac enzyme will go up first in a patient with acute STEMI?

A

Myoglobin (goes up in 1 hour). CK-MB and troponins goes up starting at 4-6 hours.

177
Q

What is the next best step in a patient with acute STEMI after aspirin is given?

A

Angioplasty

178
Q

What is the strongest indication for thrombolytics?

A

ST elevation or new LBBB within 12 hours of onset of chest pain (assuming angioplasty is not available). NOT indicated in ST depression

179
Q

What is the best test to diagnose WPW syndrome?

A

Electrophysiology study

180
Q

What is the most likely cause of erectile dysfunction post-MI?

A

Anxiety (usually NOT a drug reaction). If it must be due to a medication, think beta blockers

181
Q

What is the best next step for a patient with chest pain and an EKG with ST depression?

A

Aspirin followed by either catheterization or low molecular weight heparin. Heparin prevents the clot that would progress to STEMI.

182
Q

What drugs are used in conjunction with aspirin in NSTEMI’s when catheterization is indicated?

A

Clopidogrel or tirofiban (block platelet activation). They decrease risk of re-stenosis of the coronary artery

Medicine shelf (5 decks)

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