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UWORLD Q REVIEWS > Cardio Block Week 1 (2) > Flashcards

Cardio Block Week 1 (2) Flashcards

1
Q

Where is the SA node located?

A

At the junction of the R. atrium and the SVC

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2
Q

Retinal artery occlusion is an important cause of ?

A

Painless, monocular vision loss.

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3
Q

The most common cause of retinal artery occlusion is?

A

Thromboembolic complications of atherosclerosis in the internal carotid.

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4
Q

The retinal artery is a branch of the ____ artery?

A

Ophthalmic artery

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5
Q

What does the retinal artery travel within?

What does the retinal artery supply?

A

The retinal nerve

The inner retina and and the surface of the optic nerve.

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6
Q

Dystrophic calcification is considered to be a hallmark of ___?

A

Cell injury and death, occurring in all types of necrosis.

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7
Q

How do calcium deposits in dystrophic calcification stain?

A

dark-purple shard edged aggregates.

*With lamellated outer layers are described as psammoma bodies.

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8
Q

How do dystrophic calcifications occur?

A

Chronic hemodynamic stress -> Endothelial fibroblast death ->
Release of cellular degradation products into valvular interstitium ->calcification.

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9
Q

In HOCM, left ventricular outflow obstruction is due to ?

A

Abnormal systolic anterior motion of the anterior leaflet of the mitral vlave toward the hypertrophied interventricular septum.

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10
Q

Patients with SLE have accelerated levels of____?

This leads to an increased risk of?

A

Atherosclerosis

MI

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11
Q

Other cardiac features of SLE include?

A

SLE (verrucous endocarditis) on both surfaces of the mitral or aortic valves.

  • Pericarditis
  • Small vessel necrotizing vasculitis
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12
Q

Vegetations in SLE are made up of?

A

Sterile platelets + fibrin, immune complexes and mononuclear cells

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13
Q

Renal involvement in SLE manifests as?

A

Diffuse proliferative glomerulonephritis (necrotizing lesion with crescent formation)

**Light microscopy shows glomerular capillary walls with wire loop structures.

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14
Q

Why does increased physical activity lead to anginal symptoms in stable angina?

A

Mismatch of oxygen supply and demand.

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15
Q

Dobutamine can be used in diagnosis of ?

A

Atherosclerotic CAD via pharmacological stress testing.

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16
Q

How will a positive stress test for CAD present?

A

Transient decrease in contractility (wall motion defect) -> reduced ejection fraction.

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17
Q

How would Concentric hypertrophy px:

A

Uniformly thickened LV and a small LV cavity (impaired diastolic filling) -> HF with preserved ejection fraction.

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18
Q

Can Dilated cardiomyopathy be inherited?

Gene affected?

A

Yes - familial DCM is transmitted in an AD pattern.

TTN (codes for sarcomere protein - titin)

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19
Q

Patient with dilated Cardiomyopathy also develop this their LV?

A

Mural thrombus.

** increased risk for sudden death due to ventricular arrhythmia.

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20
Q

What liver enzymes metabolize statin?

A

CYP3A4

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21
Q

What are some adverse effects of statin use?

A

Statin myopathy

**can be triggered when levels are increased.

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22
Q

Macrolide antibiotics inhibit this liver enzyme.

A

CYP3A4

Other drugs that inhibit: ketoconazole, NOn-dihydropyridine CCB.

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23
Q

Which of the macrolides does not significantly inhibit CYP3A4 levels?

A

Azithromycin

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24
Q

What medication should be avoided in HOCM?

Why?

A

Vasodilators (decrease afterload & LV volumes) and Diuretics (decrease venous filling)

Lessened LV volume (caused by reduction in cardiac preload and/or afterload)
-> leads to greater flow obstruction due.

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25
Q

A tricuspid regurgitation will increase with?

A

Inspiration (due to increased preload).

Mitral regurge or VSD would either decrease or remain unchanged during inspiration.

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26
Q

What type of arrythmias does lidocaine treat?

Why?

A

Ischemia induced ventricular tachy.

Binds to inactivated Na channels and rapidly dissociates.

Ischemic myocardium has higher than normal membrane potential which delays voltage dependant recovery of sodium channels from inactivated resting state.

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27
Q

What is beta blocker withdrawal syndrome?

A

Px will px with tachy, palpitations, and anginal pain.

Due to upregulation of B-receptor after long time use of B-blockers (increasing sensitivity). Abrupt cessation of B-blockers -> Increased HR & contractility.

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28
Q

How can paroxysmal supraventricular tachy px?

A

anxiety provoked episodes of sudden onset palpitation asx with SOB & lightheadness.

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29
Q

What organ does Polyateritis Nodosa spare?

A

Lungs

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30
Q

What artery involvement is often prominent in PAN?

A

Renal Artery

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31
Q

What is a relatively uncommon cause of cardiomyopathy in postpartum women?

What type of cardiomyopathy is this?

What is it due to?

A

Peripartum cardiomyopathy.

Dilated

Impaired function of angiogenic growth factors during peripartum period.

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32
Q

What features would you see in a 3rd degree AV block?

A

Atrium and ventricle beat independently of each other. P-P (SA node) and R-R (His bundle) distances are regular.

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33
Q

What can cause AV 3rd degree block.

A 
AV node dysfunction
Ischemia
Infiltrative dz (sarcoidosis)
Lyme dz
Age related fibrosis with cellular degeneration
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34
Q

How does sodium nitroprusside work?

A

Decreases LV preload and afterload but unchanged stroke volume via direct release of NO in vascular smooth muscle.

(Balanced vasodilation - this is what allows for maintenance of stroke volume).

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35
Q

What are the 2 medications that can help in hypertensive emergency?

A

Nitroprusside

Fenoldopam

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36
Q

What is the subclavian steal syndrome?

A

Due to hemodynamically significant stenosis of the subclavian artery proximal to the origin of the vertebral artery -> reversal of flow from contra Vertebral artery to the ipsi artery

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37
Q

How will patients with subclavian steal syndrome present?

A

Arm ischemia in the affected extremity

Vertebrobasilar insufficiency (dizziness, vertigo, drop attacks).

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38
Q

What would you see in physical examination for Subclavian Steal syndrome?

How would you diagnose it?

A

Significant difference in systolic BP between arms.

Doppler US

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39
Q

How does cardiogenic pulmonary edema present in the lungs?

A

Alveolar capillaries become engorged and there is transudation of fluid plasma across the alveolar capillary membrane, which shows up as pink, acellular material within the alveoli.

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40
Q

What are the medications that lower BP by reducing systemic vascular resistance?

A

Hydralazine

Minoxidil

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41
Q

What are the adverse effects Hydralazine and minoxidil?

A

Stimulate baroreceptor -> reflex sympathetic activation -> Increase HR, contractility and CO -> activation of RAAS -> Na and water retention.

*This limits their long term use

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42
Q

To counteract their effects, what is typically given along with direct arteriolar vasodilators?

A

Diuretics and sympatholytics.

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43
Q

In unilateral renal artery stenosis, the hyper-perfused kidney will show?

A

Arteriolar wall thickening due to hyaline of hyperplastic arteriosclerosis.

**due to High BP

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44
Q

How does ischemic damage in the kidney present?

A

Cortical thinning, Tubular atrophy, interstitial ischemia/fibrosis, glomerular crowding.

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45
Q

Vascular endothelium synthesizes NO from what amino acid?

A

Arginine

**enzyme is Nitric oxide synthase

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46
Q

What is the MOA of NO released from vascular endothelium?

A

NO release -> activated guanylyl cyclase -> increase formation of cyclic GMP -> activation of protein kinase G -> reduction of cytosolic calcium levels -> relaxation of smooth m.

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47
Q

How can pulmonary HTN be recognized on physical examination?

A

Loud pulmonic component (P2) of S2 (forceful pulmonic closure) & accentuated palpable impulse at the L. sternal border (*due to R. ventricular heave).

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48
Q

How would you differentiate Pulm HTN and Pulmonic stenosis on PE?

A

Pulm HTN will have a loud pulmonic component of S2 while in pulm stenosis, there will be a delayed P2.

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49
Q

S. bovis is associated which condition?

A

Colon cancer

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50
Q

What type of infection does S. bovis cause?

A

Subacute bacterial endocarditis

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51
Q

What role does cortisol play in vasculature?

What is this phenomenon called?

A

Cortisol has no direct vasoactive properties. But it augments the vasoconstrictive effects of catecholamines and angiotensin II.

This is called permissiveness.

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52
Q

When is this cortisol role in vasculature most prominent?

A

In adrenal insufficiency, low cortisol levels contribute to hypotensive crisis by decreasing vascular responsiveness to NE & angiotensin II.

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53
Q

In which other locations, does cortisol exert its permissive effect?

A

Glucagon to increase glucose release from liver.

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54
Q

Where do nitrates primarily act on?

A

Nitrates are primarily venodilators that increase peripheral venous capacitance.

They also have a modest effect on arteriolar dilation. (decrease in systemic vascular resistance).

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55
Q

Staph. Epidermis has a _____ catalase test and ____ coagulase test?

A

+ve catalase

-ve coagulase

**Catalase test separates Strepto (-ve catalase) from staph.

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56
Q

S. epidermis is susceptible to_____?

A

Novobiocin

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57
Q

Alpha 1 uses ____ as its second messenger?

A

IP3

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58
Q

What receptors does NE stimulate?

A

B1 adrenoreceptors - ↑cAMP

A1 adrenoreceptors via ↑IP3

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59
Q

What is the preferred treatment for septic shock?

A

Norepinephrine

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60
Q

When do you hear the 3rd heart sound?

A

During passive filling of ventricles in diastole. Sudden cessation of filling as ventricles reaches its elastic limit.

61
Q

When is the 3rd heart sound normal?

A

Age <40

Pregnancy

62
Q

What are some of the conditions associated with S3?

A

Systolic HF
Mitral regurge
High output states

63
Q

When do you hear the fourth heart sound?

A

Heard immediately after atrial contraction as the blood is forced into a still ventricle.

64
Q

When is the 4th heart sound normal?

A

Healthy older adults

65
Q

What are some conditions that are associated with the fourth heart sound?

A

Abnormal in younger adults, children.

Diastolic dysfunction

66
Q

How do you best hear s3 and s4?

A

With the bell of the stethoscope over the cardiac apex.

67
Q

What is the MOA for Statins?

A

Lower LDL cholesterol by inhibiting HMG -COA.

68
Q

What are the most effective lipid lowering drugs for primary and secondary prevention of CV events regardless of baseline levels?

A

Statins

69
Q

What effect will an AV fistula have on preload and afterload?

A

Increase preload -> increase the rate and volume of flow back to the heart.

↓afterload because shunts avoid arterioles (the highest resistance vessel)

** high volume AV shunts can eventually lead to high output cardiac failure.

70
Q

How do AV shunts form?

A

AV shunts can be congenital or acquired (dialysis or penetrating injuries).

71
Q

What is the MOA for prostacyclin?

A

Secreted by vascular endothelial cells.
Inhibit platelet aggregation and causes vasodilation to oppose the functions of thromboxane A2 and maintain vascular homeostasis.

72
Q

Function of the coronary sinus?

Where does it insert?

Why is its insertion important?

A

Brings deoxygenated blood to the RA

It inserts in between the IVC & tricuspid valve. It runs transversely in the L. AV groove on the posterior aspect of the heart.

Will become dilated secondary to any factor that ↑ RH pressure (most common is pulm htn)

73
Q

What is the PDA a derivative of?

What else is a derivative of this structure?

A

Six aortic arch

Pulmonary artery

74
Q

What vessels are typically affected with a Subdural hematoma?

How does this hematoma present?

In what population does this often occur in?

How does this px?

A

Rupture of cortical bridging veins

Crescent shaped

Elderly patients due to increased age-related brain atrophy.

Gradual onset of HA and confusion.

75
Q

What vessels are affected in Hypertensive strokes?

A

Lenticulate striate arteries.

**Branch of the middle cerebral arteries.

76
Q

Rupture of what vessels cause epidural hemorrhage?

A

Middle meningeal artery.

77
Q

Pericardial inflammation (peri infarction pericarditis) in an MI is due to?

A

Inflammation overlying the necrotic segment of myocardium

78
Q

What are some causes of acute pericarditis?

A

Viral or idiopathic
Autoimmune disease.e.g SLE
Uremia
Post MI (early and Dressler syndrome)

79
Q

What is Dressler Syndrome?

A

An autoimmune mediated pericarditis provoked by antigens exposed or created by infarction and necrosis of the cardiac muscle.

80
Q

What are the two formulas for calculating cardiac output?

A

CO = SV x HR

CO= rate of O2 consumption/ arteriovenous O2 content difference (aka arterial O2 - venous O2)

81
Q

What inactivates Atrial Natriuretic Peptide and Brain Natriuretic Peptide?

A

Neprilysn

82
Q

What is the MOA of ANP and BNP?

A

Released by myocytes in response to myocardial stretching induced by hypervolemia. They bind too natriuretic peptide receptors to activate guanylate cyclase -> form cGMP -> diuresis and peripheral vasodilation.

**they inhibit the RAAS system.

83
Q

What causes swelling in transient myocardial ischemia?

A

When blood flow decreases, cardiac myocytes transition to anaerobic metabolism. W/o ATP, pumps fail -> Increase in intracellular NA & CA -> attract free water -> swelling

84
Q

Where can the great saphenous vein be accessed for use in cardio bypass grafts?

A

Just inferolateral to the pubic tubercle.

85
Q

MOA for fibrates?

A

Fibrates activate peroxisome proliferator-activated alpha (PPAR-alpha) -> decreased hepatic VLDL & increased LPL activity.

86
Q

histologic finding seen in aortic dissection?

A

Cystic medial degeneration -> weaken aortic wall and allows tear to propagate.

*elastic tissue fragmentation is in a basket weave pattern. Cystic collections are of muccopolysaccraride.

87
Q

What is the initial process involved in the pathogenesis of infective endocarditis?

A

Valvular lesions -> focal adherence of fibrin, and platelets forming a sterile fibrin platelet nidus. -> in bacteremia, microorganism colonize this nidus -> further cativation fo the coagulation system.

*Staph aureus - can attach to normal valves.

88
Q

Histopathology of pulmonary artery hypertension?

Histopathology of pulmonary edema?

A

Hypertrophy of the pulmonary vascular smooth muscle.

Alveolar capillaries become engorged -> transudation of fluid plasma across alveolar capillaries appearing as pink, acellular material within the alveoli.

89
Q

How does coarctation of the aorta px?

What is the pathognomonic sign for a large PDA?

A

BP discrepancy and pulse delay between UE and LE.

Differential clubbing and cyanosis w/o bp or pulse discrepancy.

90
Q

How does brachiocephalic vein obstruction px?

A

Obstruction of right brachiocephalic vein. Px like SVC syndrome but only on one side of the body.

91
Q

How does atrial fibrillation present?

Ventricular response in AF is due to what?

A

Irregular irregular RR interval, absent P waves and narrow QRS complexes.

Transmission of abnormal atrial impulses through the AV node.

** The AV node refractory period regulates the # of atrial impulses that reach the ventricle.

92
Q

What is transthyretin and what type of cardiomyopathy does it cause?

A

Transthyretin (TTR) produced by the liver (transports vitamin A and thyroxine) -> mutations can cause misfolding -> produces amyloid protein that infiltrates the myocardium.

93
Q

Loss of cardiomyocyte contractility occurs within how long of the onset of total ischemia?

How long after ischemia is muscle contractile function reversible?

A

60 seconds

30 minutes

94
Q

Left heart murmurs can be enhanced with this scenario?

A

At the end of expiration with the patient leaning forward (minimized lung volume with heart closer to the chest wall).

95
Q

How does distributive shock affect venous o2 saturation?

A

High flow (from compensatory increase in sympathetic drive) -> leads to incomplete oxygen extraction in the tissues -> high mixed venous oxygen saturation.

96
Q

What is the presently the first line medication for the treatment of essential hypertension in the general population?

A

Hydrochlorothiazide

97
Q

What is the best test to monitor the anticoagulation of warfarin?

Why give heparin before Warfarin?

How do you monitor unfractionated heparin?

A

Prothrombin Time
** other test - INR

Heparin bridge. To prevent hypercoagulative state (due to decreased anticoagulant C & S)

aPTT - Activated partial thromboplastin time.

98
Q

In chronic aortic regurge, how does the LV compensate?

A

Eccentric hypertrophy -> increase in SV to maintain CO.

99
Q

How does Takayasu arteritis px?

A

Large artery (aorta and its branches) vasculitis (granulomatous inflammation of vascular media). Px with constitutional sx. Arterio-occlusive (claudication, BP discrepancies, pulse deficits). Age <40.

100
Q

Possible drug causes of QT prolongation?

A 
Macrolides + fluoroquinolones. 
Antiemetics (ondansetron). 
Azoles 
Antipsychotics, TCAs &amp; methadone. 
Class IA &amp; Class III antiarrhythmic.
101
Q

Names of the congenital long Qt syndromes?

A

Romano-Ward - (AD)

Jervell & Lange-Nielson (AR)

102
Q

What are the clinical features for cardiac tamponade?

Potential causes?

A

Becks triad: JVD, hypotension & diminished heart sounds. Also pulsus paradoxus.

Malignancy/radiation therapy. Infection (viral, Tb, HIV). Drugs (hydralazine, isoniazid) CTD (SLE, RA).

103
Q

What is the most common cause of renal infarction?

How does it px?

A

Systemic thromboembolism from the LA or LV.

Flank pain, hematuria, elevated Lactate dehydrogenase and wedge shaped kidney lesion on CT scan.

*The brain and kidney are more likely to suffer embolic infarction because they are perfused at a higher rate.

104
Q

WHat is acute myocarditis most commonly caused by?

Common complications?

A

Viral infection (coxsackie virus, adenovirus, influenza).

Decompensated HF or sudden cardiac death due to Ventricular arrhythmia.

105
Q

What decreases the murmur in aortic stenosis?

Why?

A

Increased afterload

Decreases pressure gradient across the aortic valve.

106
Q

What do patients with aortic stenosis px in regards to pulses?

A

(Pulsus parvus et tardus) Small pulse amplitude with a delayed peak and slower upstroke of arterial pulse due to diminished stroke volume and prolonged ejection time.

107
Q

When do you start to see changes in myocyte pathology after an acute MI?

4-12 hours?

12-24 hrs?

A

After 4 hours.

**Cardiac specific enzymes can be detected.

Wavy fivers with narrow, elongated myocytes

Myocyte hypereosinophilia

108
Q

What is the MOA of Cilostazol?

When is it mostly used?

A

Reduces platelet activation by inhibiting platelet phosphodiesterase, Enzyme responsible for cAMP.

ls also a direct vasodilator.

**PAD (peripheral artery dz). Net effect- decrease in claudication sx.

109
Q

MOA of nitrates?

A

NO activated guanylate cyIase -> increase cGMP -> decreased calcium -> myosin light chain phosphorylation -> smooth muscle relaxation.

110
Q

What is costosternal syndrome?

aka costochondritis/ant chest wall syndrome

A

This occurs after repetitive activity, involves the upper costal cartilage and the costochondral or costosternal junction. The pain is typically reproduced with palpation and worsened with movement/changes in position.

111
Q

How would you most likely increase the ratio of forward flow to regurgitant flow in a rguritation?

A

Decrease systemic vascular resistance (so that there is more forward than backward flow).

112
Q

MOA statins?

Side effects of statins?

With what additional medication is the risk for this side effect increased?

A

1st line therapy for hypercholesteremia. Inhibit HMG CoA-reductase (responsible for rate-limiting step in cholesterol synthesis). Statins lower cholesterol, LDL, and Triglyceride levels.

Hepatitis & myopathy. Statin-associated myopathy - mild muscular pain that resolves with med discontinuation.

Risk is increased when given with fibrates (impair hepatic clearance).

113
Q

What are some changes expected in an aging heart?

A

Decreased LV size
Sigmoid shaped ventricular septum.
Atrophy -> increased collagen deposition.
Accumulation of brown lipofuscin pigment (wear and tear pigment).

114
Q

How does carcinoid syndrome present?

How do you diagnose carcinoid syndrome?

A

Episodic flushing, secretory diarrhea & wheezing.
Can lead to pathognomic plaque like deposits of fibrous tissue on the R side endocardium -> RHF.

Dx: Urinary 5 hydroxyindoleacetic acid (5HIAA).

115
Q

How is carcinoid symptoms treated?

A

Somatostatin analog -> Octreotide, SUrgery.

116
Q

What are the 6P signs that present with acute limb ischemia?

A

Pain, palor, poikilothermia (coolness to touch), paresthesia, paralysis and reduced or absent pulses.

117
Q

MOA for Sirolimus?

Which other drug has a similar MOA?

A

Blocks IL-2. Used to reduced acute kidney transplant rejection by preventing cell cycle progression and lymphocyte proliferation kidney SIRvives).

**Binds to FKBP (FK binding protein) -> forms complex that binds and inhibits mTOR -> blocks IL-2 signal transduction.

Calcineurine inhibitors. Cyclosporine & tacrolimus.

118
Q

Which DNA replication enzyme utilizes uracil?

A

DNA primase

119
Q

Type B aortic dissection occurs close to what structure?

Type A dissections?

A

L. subclavian artery

Sinotubular junction.

120
Q

What are some of the pE signs found in constrictive pericarditis?

A

JVD, pericardial knock (sudden arrest of ventricular filling), pulsus paradoxus and paradoxical rise in JVP with inspiration.

121
Q

Carotid baroreceptors afferent?
efferent?

Aortic arch baroreceptor.
afferents?

A

Glossopharyngeal n.
Vagus N.
*located on internal carotid artery above bifurcation.

Vagus N.

Both travel to the solitary nucleus of the medulla.

122
Q

How does PTH affect vitamin D?

A

PTH stimulates calcitriol production by stimulating kidney 1Alpha hydroxylase.

123
Q

Treatment of choice for diabetic ketoacidosis?

Diabetic ketoacidosis also leads to this mineral abnormality.

A

IV normal saline and insulin.

Hyperkalemia ( osmotic diuresis -> urinary loss of Na -> hyperkalemia) & lipolysis -> keto genesis -> metabolic acidosis -> K+ shift out of cell.

**insulin also drives K= into cells.

124
Q

The most highly oxygenated blood in the fetus is found in?

A

The umbilical vein which directly empties into the IVC

125
Q

What predisposing factor would be most likely responsible for a lung abcess with Peptostreptococcus and fuseobacterium?

A

Aspiration of oral bacteria.

RF for lung abscesses: conditions that increase aspiration risk -> alcoholism, drug abuse, seizure disorder, previous stroke and dementia, anatomic abnormalities (esophageal strictures/diverticula)

** these are anaerobes

126
Q

What lab study features would you see in hypovolemia?

A

Increased BUN/Creatinine ratio. Low urinary sodium. Low fractional excretion of sodium.

127
Q

Dimorphic Fungal species and diagnosis and px:

Coccidioides immitis?

Histoplasma capsulatum?

Blastomyces dermatitidis?

A

Thick walled spherules. Flu like illness (lungs). Disseminated form: skin, bones and lungs

Oval yeast within macrophages. Pulm: similar to TB (lung granuloma with calcifications)

Doubly refractile wall and single broad based bud. Pulm: Pneumonia.

128
Q

What is an adverse effect of loop diuretics?

Worse when in combination with these drugs?

A

Ototoxicity.

Aminoglycosides, salicylates & cisplatin

129
Q

What is the histopathology of Buerger disease?

A

Segmental, inflammatory vasculitis that affect small/medium arteries. Also has vein and nerve involvement.

130
Q

Classic sputum findings for asthma are?

A

Eosinophils and Charcot leyden crystals (breakdown of eosinophils in sputum).

131
Q

In atopic (extrinsic) asthma, what cytokine helps to recruit and activate eosinophils?

What secretes this cytokine?

A

IL-5

Th2 type T cells.

**atopic asthma occurs due to an excessive Th2 mediated reaction to environmental allergen.

132
Q

In atopic asthma, what cytokines are responsible for mast cell priming?

A

IL-4 & IL-13.

Th2 -> IL4 & 13 -> B cell activation & class switching to IgE production -> mast cell priming

133
Q

What vitamin maintains orderly differentiation of specialized epithelia (including mucus secreting, resp and urinary tracts, pancreatic ducts etc)?

A

Vitamin A

134
Q

Severe CF can cause these symptoms?

A

Total obstruction followed by fibrotic atrophy of exocrine glands -> Problem with absorbing fat soluble vitamins.

135
Q

Ciliated epithelium persists up to what level in the respiratory tract?

A

Respiratory bronchioles.

136
Q

Acidosis stimulates this in the kidney?

What is the starting product for this process?

A

Renal ammoniagenesis

Glutamine is convereted to glutamate -> releasing ammonia _. binds to H+

137
Q

RCC is associated with this gene?

A

VHL at chromosome 3p

VHL gene is a tumor suppressor that inhibits hypoxia inducible factor

Mutation -> overexpression of multiple angiogenic growth factors (VEG-F & PDF-F)

** tumors with VHL mutations are highly sensitive to angiogenesis inhibitors.

138
Q

Serpentine cords on TB indicate the ____ of TB?

A

Virulence. Cords (cord factor) help prevent TB from macrophage mediated destruction -> drives formation of caseating granuloma.

139
Q

Sevelamer reduces serum phosphorus levels why which mechanism?

What can lead to high phosphate levels?

A

Sevelamer is a phosphate binder. It is a non absorbable anion exchange resin that binds intestinal phosphate to reduce systemic absorption.

Chronic Kidney disease (impaired ability of kidney to excrete phosphorus)

140
Q

Which nephritic syndrome is associated with normal complement levels?

What is the typical presentation of a pt with this syndrome?

A

IgA nephropathy

Recurrent hematuria that occurs spontaneously or within 5-7 of a GI or respiratory tract infection.

141
Q

What does the presence of C. albicans in a sputum culture indicate?

A

Oral contamination. Not true pulmonary infection.

142
Q

Impairment of respiratory control center in the brainstem causes?

MG (myasthenia gravis) can often affect these muscle lead to ?

A

Hypoventilation during sleep.

Respiratory muscle -> hypoventilation

143
Q

Flank pain radiating to the groin with a ballotable flank mass that develops within a week of pelvic surgery suggests?

A

Ureteric obstruction

**ureters are vulnerable during pelvic surgery (run close to pelvic lymph nodes). (ureters run ant. to iliac vessels and post. to gonadal artery). Unintentional ureteric ligations -> obstruction

144
Q

Depletion of what ion is important in the pathophysiology of metabolic alkalosis?

A

CL

**Cl impairs renal excretion of HCO3-

145
Q

Renal damage in multiple myeloma is due due to ?

A

Light chain deposition in kidney. Appears as waxy eosinophilic casts composed of Bence Jones Proteins.

146
Q

Infants exposed to second-hand smoke can develop ___?

A

SIDs (sudden infant death syndrome).

*Half of SIDs are due to tobacco exposure. Due to ‘impaired arousal and abnormal CV response to stimuli.

147
Q

Other risks of second hand smoke?

A

Prematurity (low birth weight)
Middle ear dz (otitis media)
Asthma
Respiratory tract infections (bronchitis, pneumonia)

148
Q

Aortocavitary fistulas are an uncommon complication of?

A

Bacterial endocarditis

149
Q

Pathophy of asbestosis?

How can you differentiate asbestos bodies from other ferruginous bodies?

A

Interstitial fibrosis in lower lungs, ferruginous asbestos bodies (translucent fibers coated with iron containing material) & pleural disease (effusions, plaques) are common.

They have a translucent fiber core.

UWORLD Q REVIEWS (13 decks)

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