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First Aid: Pathology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What type of shunt produces early cyanosis?

What is the usual treatment?

Causes?

A

Right-to-left shunts.

Urgent surgical correction and/or maintenance of PDA.

5 T’s:

  1. Truncus arteriosus (1 vessel)
  2. Transposition (2 switched vessels)
  3. Tricuspid atresia (3 = tri)
  4. Tetralogy of fallot (4 = tetra)
  5. TAPVR (5 letters in name)
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2
Q

Neonate presents with cyanosis at birth and dies.

Autopsy shows a single great vessel that supplies the lungs and systemic circulation. What disease was present?

A

Persistent Truncus Arteriosus.

Most patient have accompanying VSD.

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3
Q

A concerned mother brings her newborn to you because she thinks the baby is turning blue.

An echocardiogram shows the aorta leaving the right ventricle and the pulmonary trunk leaving the left ventricle.

What is that disease? What must be associated for the child to have survived to this age?

A

D-transposition of the great vessels.

Failure of the aorticopulmonary septum to spiral.

There must be a VSD or PDA, or patent foramen ovale to produce a shunt and allow mixing of blood (needed so systemic circulation can get oxygen!).

Without surgical intervention, most infants die within the first few months of life.

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4
Q

What defects are associated with tricuspid atresia?

A

Absence of tricuspid valve and hypoplastic RV.

Requires an atrial septal defect and ventricular septal defect for viability.

Early cyanosis.

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5
Q

What defects are associated with Tetralogy of Fallot?

A

PROVe

  1. Pulmonary infundibular stenosis (most important determinant for prognosis)
  2. RVH - boot shaped heart on CXR
  3. Overriding aorta
  4. VSD

Caused by anterosuperior displacement of the infundibular septum.

Most common cause of early childhood stenosis.

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6
Q

What is the etiology of cyanosis in tetrology of fallot?

How does squatting affect a patient with tetrology of fallot?

What is the treatment for this disease?

A

Cyanosis due to pulmonary stenosis forcing right-to-left flow across VSD. Causes “tet spells” and right-ventricular hypertrophy.

Squatting increases systemic vascular resistance, reduces right-to-left shunt, and improves cyanosis.

Treat with early surgical correction.

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7
Q

Neonate presents with cyanosis.

Echocardiogram discovers an ASD and that the pulmonary veins drain into the right heart circulation.

What is this disease?

A

Total anomalous pulmonary venous return (TAPVR)

Pulmonary veins will drain into the SVC, coronary sinus, etc instead of the left atrium.

Associated with ASD and sometimes PDA to allow for right-left shunting to maintain cardiac output.

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8
Q

What conditions result in late cyanosis (“blue kids”).

List in order of frequency

A

Ventricular septal defect (VSD) > Atrial septal defect (ASD) > Patent ductus arteriosus (PDA)

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9
Q

Is a VSD typically symptomatic at birth?

What is the usual course?

A

VSD usually asymptomatic at birth, manifests weeks late ror remain asymptomatic throughout life.

Most will self-resolve. Larger lesions cause LV overload and heart failure.

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10
Q

A defect in what is the most common cause of ASD?

What might you hear on auscultation?

A

Defect in the septum secundum most common cause of isolated ASD. (Defects in the septum primum associated with other anomalies).

Might hear loud S1; wide, fixed split S2.

May be asymptomatic or cause heart failure.

Different than patent foramen ovale - septae are missing rather than unfused.

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11
Q

Neonate presents with late cyanosis. You hear a “machine like murmur” on auscultation.

Pathogenesis of this disease?

A

Patent ductus arteriosus.

Fetal period, shunt is from right to left (normal) to bypass lung circulation.

In neonatal period, lung resistance decreases, shunt becomes left to right, RVH and/or LVH and heart failure occurs.

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12
Q

What can you use to close a PDA?

What could you use to maintain patency? When would you want to do that?

A

Endomethacin (indomethacin) ends patency of PDA

PGE kEEps it open - use to sustain life in conditions such as transposition of the great vessels.

(Low O2 tension also keeps PDA open)

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13
Q

A child presents with cyanosis, clubbing, and polycythemia.

Echocardiography reveals a VSD.

What is this condition?

A

Eisenmenger syndrome.

An uncorrected left-to-right shunt (VSD, ASD, PDA) increases pulmonary blood flow which induces remodeling of the vasculature and pulmonary arterial hypertension.

Right ventricular hypertrophy occurs to compensate and shunt becomes right to left.

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14
Q

An infant with Turner syndrome presents with a systolic click and a delayed femoral pulse as compared with the brachial pulse.

A

Infantile type coarctation of the aorta.

Aorta narrowing is proximal to insertion of the ductus arteriosus (preductal). Associated with bicuspid aortic valve (systolic click) and other heart defects.

Infantile: In close to the heart.

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15
Q

An adult presents with notching of the ribs, hypertension in the upper extremities, and weak, delayed pulses in lower extremities (radiofemoral delay).

A

Adult-type Coarctation of the aorta.

Aorta narrowing is distal to ligamentum arteriosum (postductal)

Adult: Distal to ductus.

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16
Q

What congenital heart defects are associated with 22q11 syndromes?

A

Include DiGeorge, velo-cardio-facial syndrome, Shprintzen syndrome, conotruncal anomaly face syndrome, Strong syndrome, congenital thymic aplasia, and thymic hypoplasia. Due to small deletion in chromosome 22.

Truncus arteriosus, tetralogy of Fallot.

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17
Q

What congenital heart defects are associated with Down syndrome?

A

ASD, VSD, AV septal defect (endocardial cushion defect)

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18
Q

What congenital heart defects are associated with congenital rubella?

A

Septal defects, PDA, pulmonary artery stenosis.

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19
Q

What congenital heart defects are associated with Turner syndrome?

A

Bicuspid aortic valve, coarctation of aorta (preductal)

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20
Q

What congenital heart defects are associated with Marfan syndrome?

A

MVP (mitral valve prolapse), thoracic aortic aneurysm and dissection, aortic regurgitation.

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21
Q

What congenital heart defects are associated with an infant of a diabetic mother?

A

Transposition of the great vessels.

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22
Q

What values define hypertension?

Risk factors?

A

Systolic BP > 140 mmHg and/or diastolic BP > 90mmHg

Age, obesity, diabetes, smoking, genetics, black > white > Asian.

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23
Q

Young patient presents with hypertension. Angiography shows a “string of beads” appearance of the renal artery.

A

Fibromuscular Dyplasia

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24
Q

What are some causes of hypertension?

A

90% is primary (essential) and related to increased cardiac output or total peripheral resistance.

Remaining 10% mostly secondary to renal disease, including fibromuscular dysplasia in younger patients.

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25
Q

What defines hypertensive emergency?

A

Severe hypertension (> 180/120 mmHg) with evidence of acute, ongoing organ damage (e.g., papilledema, mental status changes)

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26
Q

What conditions does hypertension predispose to?

A

Atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, and aortic dissection.

Picture below shows hypertensive nephropathy - Renal artery hyalinosis by PAS stain.

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27
Q

Patient presents with yellow plaques and nodules of in the skin and eyelids.

What are these lesions called? What’s in them? What is the underlying derangement?

A

Skin - xanthomas

Eyelids - xantholasma

Composed of lipid-laden histiocytes.

Reflect underlying hyperlipidemia.

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28
Q

Patient presents with a thickened knobbly achilles tendon.

Biopsy shows lipid deposits.

A

Tendinous xanthoma

A sign of hyperlipidemia

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29
Q

Patient presents with a white corneal ring.

What is this called? What does it reflect?

A

A corneal arcus. Can be a white, gray, or blue opaque ring around the cornea.

Caused by lipid deposit in the cornea. Presents early in life with hypercholesterolemia. Common in elderly (arcus senilis).

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30
Q

Patient presents with “pipestem” arteries on x-ray.

Your attending says there is calcification in the media of the arteries.

What is this condition?

A

Monckeberg arteriosclerosis (medial calcific sclerosis)

Usually benign, does not obstruct blood flow, intima not involved.

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31
Q

What are the two types of arteriolosclerosis?

What causes each?

A

Hyaline arteriolosclerosis: Thickening of small arteries in essential hypertension or diabetes mellitus

Hyperplasic arteriolosclerosis: Seen in severe hypertension

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32
Q

Disease characterized by thickening of large-and-medium muscular arteries and elastic arteries with cholesterol deposits in the arterial wall.

Risk factors?

A

Atherosclerosis

Forms atherosclerotic plaques with cholesterol crystals.

Modifiable Risk factors: Smoking, hypertension, hyperlipidemia, diabetes

Non-modifiable: Age, sex (higher in men and postmenopausal women), family history

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33
Q

What is the pathogenesis of an atherosclerotic plaque?

A

Inflammation important in pathogenesis.

Endothelial cell dysfunction -> macrophage and LDL accumulation -> foam cell formation -> fatty streaks -> smooth muscle migration (PDGF and FGF), proliferation and extracellular matrix deposition -> fibrous plaque -> complex atheromas

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34
Q

What are complications of atherosclerosis?

A

Aneurysm, ischemia, infarcts, peripheral vascular disease, thrombosis, emboli

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35
Q

What are the most common locations for atherosclerosis?

A

Abdominal aorta > coronary artery > popliteal artery > carotid artery

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36
Q

What are some symptoms of atherosclerotic plaques?

A

Angina, claudication, or asymptomatic.

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37
Q

What is an aortic aneurysm?

A

Localized pathogenic dilation of the aorta.

Pain is a sign of leakage, dissection, or imminent rupture.

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38
Q

What is associated with abdominal aortic aneurysms?

A

Atherosclerosis. More frequently in hypertensive male smokers > 50 years old.

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39
Q

What is associated with thoracic aortic aneurysms?

A

Cystic medial degeneration due to hypertension (older patients)

Marfan syndrome (younger patients)

Tertiary syphilis (obliterative endarteritis in vasa vasorum)

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40
Q

Patient presents with tearing chest poain radiating to the back and unequal blood pressure in the right and left arms.

CXR shows mediastinal widening.

CT shows this finding.

A

Aortic dissection - an intraluminal tear forming a false lumen.

Associated with hypertension, bicuspid aortic valve, and inherited connective tissue disorders (Marfan syndrome).

False lumen can be limited to ascending aorta, propagate from ascending aorta or propagate from the descending aorta.

Can result in pericardial tamponade, aortic rupture, and death.

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41
Q

Patient presents with chest pain that worsens with exertion and resolves with rest.

ST depression is seen on ECG during exertion.

A

Stable angina - usually secondary to coronary artery atherosclerosis.

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42
Q

Patient presents with chest pain that shows transient ST elevation on ECG.

He reports it sometimes happens when he smokes.

A

Varient angina (Prinzmetal) - due to coronary artery spasm.

Triggers include tobacco, cocaine, and triptans, but trigger often unknown.

Give calcium channel blockers, nitrates, and smoking cessation.

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43
Q

Patient presents with chest pain that comes and goes and sometimes affects him at rest.

ST depression is seen on ECG

A

Unstable/crescendo angina. Thrombosis with incomplete coronary artery occlusion. Increase in frequency or intensity of chest pain; any chest pain at rest.

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44
Q

What is coronary steal syndrome?

A

Distal to coronary stenosis, vessels are maximally dilated at rest.

When a vasodilator is given (dipyridamole, regadenoson), blood is shunted towards well-perfused area which decreases flow and causes ischemia in the poststenotic region.

Principle behind pharmacologic stress tests.

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45
Q

Patient presents with diaphoresis, nausea, vomiting, severe retrosternal pain, pain in the left arm and jaw, shortness of breath, and fatigue.

Lab tests show elevated troponin.

How to differentiate between variants of this disease?

Pathogenesis?

A

Myocardial infarction

Acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery and myocyte necrosis.

Transmural infarction: ECG will show ST elevation

Subendocardial: ECG may show ST depressions

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46
Q

What is the most common cause of sudden cardiac death?

Associated diseases?

A

Sudden cardiac death: Death within 1 hour of onset of symptoms.

Most often due to a lethal arrhythmia (e.g., ventricular fibrillation).

Associated with CAD, cardiomyopathy (hypertrophic, dilated), and hereditary ion channelopathies (long QT syndrome)

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47
Q

What is seen by gross examination and light microscopy from 0-4 hours after the start of an MI?

A

No changes can be identified.

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48
Q

What is seen by gross examination and light microscopy 4-12 hours after the start of an MI?

A

Gross: Infarcted area with dark mottling, pale with tetrazolium stain.

Light microscope: Early coagulative necrosis, release of necrotic cell contents into blood; edema, hemorrhage, wavy fibers.

49
Q

What is seen by gross examination and light microscopy 12-24 hour after the start of an MI?

A

Gross: Infarcted area with dark mottling, pale with tetrazolium stain.

Light microscope: Neutrophil migration. Reperfusion injury causes contraction bands (free radical)

50
Q

What are complications within the first 24 hours of an MI?

A

Arrhythmia, HF, cardiogenic shock, death.

51
Q

What is seen by gross examination and light microscopy 1-3 days after an MI?

What is a complication at this time?

A

Gross: Hyperemia

Light microscope: Extensive coagulative necrosis, tissue surrounding infarct shows inflammation with necrosis

Complications: Fibrinous pericarditis

52
Q

What is seen by gross examination and light microscopy 3-14 days after an MI?

What are some complications at this state?

A

Gross; Hyperemic border; central yellow-brown softening – maximally yellow and soft by 10 days.

Light microscopy: Macrophages, then granulation tissue at margins.

Complications: Free wall rupture -> tamponade

Papillary muscle rupture -> mitral regurg

Interventricular septal rupture due to macrophage-mediated structural degradation.

LV pseudoaneurysm (mural thrombus “plugs” hole in myocardium -> “time bomb”.

53
Q

What is seen by gross examination and light microscopy 2 weeks to several months after an MI?

What are some complications at this state?

A

Gross: Recanalized artery, gray-white scar.

Light microscope: Contracted scar complete

Complications: Dressler syndrome (Autoimmune reaction resulting in fibrinous pericarditis), Heart failure, arrhythmias, true ventricular aneurysm (outward bulge during contraction, “dyskinesia”.

54
Q

What lab test is used to diagnose MI in the first 6 hours?

What’s special about Cardiac troponin I?

What is CK-MB useful for diagnosing?

A

First 6 hours - ECG is the gold standard

Cardiac troponin I rises after 4 hours, elevated for 7-10 days. Most specific maker

CK-MB: Useful for diagnosing reinfaction following acute MI because levels return to normal after 48 hours (shorter than troponin!) Found primarily in myocardium, but also released from skeletal muscle (less specific).

55
Q

Describe some characterstic ECG changes for MI

A

ST elevation (STEMI, acute transmural infarct)

ST depression (subendocardial infarct)

Pathologic Q waves (evolving or old transmural infarct)

56
Q

What is meant by a transmural myocardial infarct?

Signs on ECG?

A

Widespread cardiac necrosis that affects the entire muscular wall.

ST elevation on ECG and Q waves.

57
Q

What is meant by a subendocardial infarct?

Signs on ECG?

A

Ischemic necrosis of < 50% of ventricle wall

Subendocardium especially vulnerable to ischemia, so it can be preferentially killed

ST depression on ECG

58
Q

A patient presents with acute chest pain.

An EKG shows Q-waves in leads V1 - V4.

Where is the infarct? What artery supplies this region?

A

Anterior wall infarct.
LAD

59
Q

A patient presents with acute chest pain.

An EKG shows Q-waves in leads V1-V2

Where is the infarct?

A

Anteroseptal infarct

LAD

60
Q

A patient presents with acute chest pain.

An EKG shows Q-waves in leads V4-V6

Where is the infarct?

A

Anterolateral infarct

LAD or LCX (circumflex branch left coronary artery)

61
Q

A patient presents with acute chest pain.

An EKG shows Q-waves in leads I and aVL.

Where is the infarct?

A

Lateral wall infarct

Supplied by LCX

avL

62
Q

A patient presents with acute chest pain.

An EKG shows Q-waves in leads II, III, and aVF

Where is the infarct?

A

InFerior wall

Supplied by RCA

aVF

63
Q

When is a patient at highest risk for a ventricular free wall rupture, papillary muscle rupture, or interventricular septal rupture?

A

6-14 days post MI

Ventricular free wall rupture -> cardiac tamponade

Papillary muscle rupture -> mitral regurg

64
Q

When is a patient at highest risk for a pseudoaneurysm post MI?

What is a pseudoaneurysm?

A

About a week post-MI.

Pseudoaneurysm: A mural thrombus that “plugs” hole in myocardium. Reduces cardiac output. Risk for arrhythmia and embolus.

65
Q

When is a patient at risk for postinfarction fibrinous pericarditis?

How will you know that it has occurred?

A

1-3 days post MI

Auscultate a friction rub.

66
Q

What is Dressler syndrome?

A

Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post-MI.

67
Q

Patient presents with heart failure and sound on S3.

CXR shows a baloon appearance of the heart.

Echocardiogram shows a enlarged chambers.

What type of disease is this?

What type of dysfunction occurs, diastolic or systolic?

What kind of hypertrophy has occurred to produce enlargement?

A

Dilated cardiomyopathy

Systolic dysfunction ensues (heart can fill fine, but it can’t pump)

Eccentric hypertrophy (sarcomeres added in series)

68
Q

What are the causes of dilated cardiomyopathy?

A

Most commonly idiopathic or congenital.

Other causes: ABCCCD

Alcohol abuse

wet Beriberi

Coxsackie B virus myocarditis

chronic Cocaine use

Chagas disease

Doxorubicin toxicity, hemochromatosis, and peripartum cardiomyopathy

69
Q

How do you treat dilated cardiomyopathy?

A

Na+ restriction, ACE inhibitors, beta-blockers, diuretics, digoxin, implantable cardioverter defibrillator (ICD), heart transplant

70
Q

You examine a young athlete and find that he has a S4 heart sound.

Later, he suddenly dies during a competition.

Autopsy shows marked ventricular hypertrophy with myofibrillar disarray and fibrosis.

What disease is this a classic scenario for?

What is the cause?

Systolic or diastolic dysfunction?

A

Hypertrophic cardiomyopathy

60-70% due to autosomal dominant mutation in β-myosin heavy-chain. Rarely associated with Friedrich ataxia. Sudden death due to ventricular arrhythmia.

Diastolic dysfunction (heart can’t fill). Myocardial ischemia causes arrhythmia.

71
Q

What are treatments for hypertrophic cardiomyopathy?

A

Cessation of high-intensity athletics.

Use of a β-blocker or non-dihydropyridine calcium channel blocker (verapamil)

ICD if patient is high risk.

72
Q

What occurs in obstructive hypertrophic cardiomyopathy?

A

Subset of disease.

Hypertrophied septum too close to anterior mitral leaflet -> outflow obstruction -> dyspnea, possible syncope.

73
Q

What are some causes of restrictive/infiltrative cardiomyopathy?

Do they cause systolic or diastolic dysfunction?

A

Sarcoidosis, amyloidosis, postradiation fibrosis, endoardial fibroelastosis (thick fibroelastic tissue in endocardium of young children).

Loffler syndrome: Endomyocardial fibrosis with a prominent eosinophilic infiltrate

Hemochromatosis (can also cause dilated cardiomyopathy)

Diastolic dysfunction ensues. Can have low-voltage ECG despite thick myocardium (especially amyloid)

74
Q

Patient presnts with dyspnea, orthopnea, and fatigue.

Rales are heard on lung auscultation.

JVD is present and there is bilateral pitting edema.

Diagnosis?

A

Congestive heart failure.

75
Q

A patient with CHF undergoes cardiac testing.

Testing shows low ejection fraction and poor contractility.

Is this systolic or diastolic failure? What’s the most common cause?

A

Systolic dysfunction.

Due to ischemic heart disease of dilated cardiomyopathy.

76
Q

A patient with CHF undergoes cardiac testing.

Testing shows normal ejection fraction and contractility but impaired relaxation and reduced compliance.

Is this systolic or diastolic failure? What’s the most common cause?

A

Diastolic dysfunction.

Hypertrophic cardiomyopathy or restrictive/infiltrative cardiomyopathy.

77
Q

Right heart failure usually results from what two causes?

A

Left heart failure

Isolated right heart failure generally due to cor pulmonale, or increased pulmonary vascular resistance.

78
Q

What drugs reduce CHF mortality?

A

ACE inhibitors, β-blockers (not during acute decompensation), angiotensin II receptor blockers, and spironolactone all reduce mortality.

Thiazide/loop diuretics: Symptom relief.

Hydralazine with nitrate therapy: Improves symptoms and mortality in select patients

79
Q

What causes cardiac dilation in CHF?

A

Greater ventricular end-diastolic volume.

80
Q

What causes dyspnea on exertion in CHF?

A

Failure of cardiac output to increase during exercise.

81
Q

What are signs of left heart failure?

A

Pulmonary edema

Orthopnea

Paroxysmal nocturnal dyspnea

82
Q

What characteristic finding can be seen in the lungs due to left heart failure?

A

Hemosiderin-laden macrophages “heart failure” cells in the lungs.

Left heart failure causes an increase in pulmonary venous pressure -> pulmonary venous dilation and transudation of fluid.

83
Q

What causes orthopnea during left heart failure?

A

When supine, venous return increases.

This exacerbates pulmonary vascular congestion.

84
Q

What is paroxysmal nocturnal dyspnea?

A

Breathless awakening from sleep, increased venous return from redistribution of blood.

85
Q

What are signs of rigth heart failure?

A

Hepatomegaly (nutmeg liver): Increased central venous pressure -> increased resistance to portal flow. “Cardiac cirrhosis” possible.

Peripheral edema: Increased venous fluid pressure, transudation.

Jugular venous distention: Increased venous pressure.

86
Q

Patient presents with fever, new murmur, round white spots on the retina surrounded by hemorrhage, tender raised lesions on the finger or toe pads, erythematous lesions on palm or sole, anemia, and splinter hemorrhages on the nail bed.

What is that disease?

What anatomical location is most frequently involved?

A

Bacterial endocarditis

Usually involves the Mitral valve

Tricuspid valve endocarditis assocaited with IV drug abuse “don’t tri drugs”

Bacteria FROM JANE:

Fever

Roth spots (white spots on retina)

Osler nodes (tender raised lesions on finger or toe pads)

Murmur

Janeway lesions (Small painless erythematous lesions on palm or sole)

Anemia

Nail-bed hemorrhage

Emboli

87
Q

What bacteria typically cause endocarditis?

What characterizes each infection?

A

Acute - Staph Aureus (high virulence). Large vegetations on previously normal valves.

Subacute: Viridans streptococci (low virulence). Small vegetations on congenitally abnormal or diseased valves. Sequelae of dental procedures. Gradual onset.

Culture negative: Coxiella burnetii and Bartonella species.

  • Streptococcus bovis* in colon cancer
  • Staphylococcus epidermidis* on prosthetic valves.
88
Q

What are complications of endocarditis?

What conditions aside from bacteria can cause endocarditis?

A

Chordae rupture, glomerulonephritis, suppurative pericarditis, emboli.

Can be secondary to malignancy, hypercoagulable state, or lupus.

89
Q

Patient presents with fever, chest pain, and a history of pharyngitis.

What disease is this? What are some possible sequelae?

What is the cause?

A

Rheumatic fever.

Consequence of infection with group A β-hemolytic streptococci.

Early deaths due to myocarditis.

Late sequelae can include rheumatic heart disease - affects mitral > aortic >> tricuspid

Mitral valve regurg -> mitral valve stenosis.

Immune mediated (type II hypersensitivty) caused by antibodies to M protein that cross-react with self antigens.

90
Q

What does the acronym FEVERSS stand for, with reference to Rheumatic Fever?

A

FEVERSS:

Fever

Erythema marginatum: pink rings on the trunk and inner surfaces of the limbs which come and go

Valvular damage (vegetation and fibrosis)

ESR increased

Red-hot joints (migratory polyarthritis)

Subcutaneous nodules

St. Vitus’ dance (Sydenham chorea)

91
Q

A patient with myocarditis undergoes biopsy.

The pathologist reports finding Aschoff Bodies (granuloma with giant cells)

and Anitschkow cells (see picture, enlarged macrophages with ovoid, wavy, rod-like nucleus)

What disease is this?

A

Rheumatic fever.

92
Q

Patient presents with sharp chest pain that is aggravated by inspiration and relieved by sitting up and leaning forward.

Auscultation reveals a friction rub.

ECG finds widespread ST-segment elevation and PR depression.

What is this disease?

What are some classes and causes?

A

Acute pericarditis.

Fibrinous: Dressler syndrome, uremia, radiation. Loud friction rub

Serous: Viral pericarditis (spontaneous resolve), Noninfectious inflammatory disorders (Rheumatoid arthritis, SLE)

Suppurative/purulent: Bacterial infections - Pneumococcus, streptococcus.

93
Q

Patient presents with hypotension, distended neck veins, and distant heart sounds.

Systolic blood pressure appears to decrease during inspiration.

ECG shows low voltage QRS and electrical alternans

What disease is this?

A

Cardiac tamponade - compression of the heart by fluid in the pericardium.

This reduces cardiac output and diastolic pressures in all four chambers equalize.

Beck triad (hypotension, distended neck veins, distant heart sounds)

Increased heart rate

Pulsus paradoxis (reduction in systolic blood pressure during inspiration). Also seen in asthma, obstructive sleep apnea, pericarditis, and croup.

Kussmaul sign

ECG shows low voltage QRS and electrical alternans (“swinging” motion of heart in large effusion).

94
Q

A patient dies suddenly.

Autopsy shows an aneurysm of the aortic arch and “tree bark” appearance of the aorta.

What disease did this man have?

A

Syphilis.

Tertiary syphilis disrupts vasa vasorum of the aorta with atrophy of the vessel wall and dilation of the aorta and valve ring. Calcification of aortic root and ascending aortic arch may occur -> tree bark appearance.

Can result in aneurysm of the ascending aorta or aortic arch and aortic insufficiency,

95
Q

What is the most common heart tumor?

A

Metastasis (melanoma, lymphoma)

96
Q

An adult presents with recurrent syncopal episodes.

CT finds a “ball valve” obstruction of the left atrium.

Diagnosis?

A

Cardiac Myxoma - most common primary cardiac tumor in adults.

90% in atria.

97
Q

A child presents with a primary cardiac tumor.

Most likely diagnosis?

A

Rhabdomyoma.

Associated with tuberous sclerosis (multi-system non-malignant tumor syndrome)

98
Q

What is a Kussmaul sign?

What disorders may produce it?

A

During Kussmaul sign, JVP increases during inspiration (normally it should decrease).

Inspiration -> negative intrathoracic pressure not transmitted to the heat -> impaired filling of right ventricle -> blood backs up into venae cavae -> JVD

May be seen with constrictive pericarditis, restrictive cardiomyopathies, or right atrial or ventricular tumors.

99
Q

Patient presents with cyanosis in her fingertips in response to cold temperature and emotional stress.

What is the name of this symptom?
Causes?

A

Raynaud phenomenon.

Raynaud disease when idiopathic (primary)

Raynaud syndrome when secondary to disease process: Mixed connective tissue disease, SLE, or CREST syndromes.

100
Q

An infant presents with a rapidly growing red elevation of the skin.

Diagnosis? Natural history?

A

Strawberry hemangioma - a capillary hemangioma of infancy.

Grows rapidly and then regresses spontaneously at 5-8 years.

101
Q

An elderly patient presents with a red papule on the skin.

Diagnosis? Natural history?

A

Cherry hemangioma. Benign capillary hemangioma of the elderly. Does not regress, frequency increases with age.

102
Q

Patient presents with a polyploid red lesion after skin trauma.

Diagnosis?

A

Pyogenic granuloma - polypoid capillary hemangioma that can ulcerate and bleed.

Associated with trauma and pregnancy.

103
Q

A patient with turner’s syndrome presents with an enlarging mass in the neck.

Biopsy shows a cavernous lymphangioma.

A

Cystic hygroma - cavernous lymphagnioma of the neck.

Associated with Turner’s.

104
Q

Patient presents with painful red-blue mass under fingernails.

Diagnosis? What is it made of?

A

Glomus tumor.

Benign, painful. Arises from modified smooth muscle cells of glomus body.

105
Q

A patient with AIDS presents with multiple skin papules.

Diagnosis? Cause?

A

Bacillary Angiomatosis

Caused by Bartonella henselae infections in immunocompromised.

106
Q

An elderly patient develops an enlarging red mass after radiation therapy.

Diagnosis?

A

Angiosarcoma - blood vessel malignancy. Usually head/neck/breast. Sun-exposed areas, radiation therapy, and arsenic exposure.

Aggressive and difficult to resect due to delay in diagnosis.

107
Q

A patient with a history of radical mastectomy and subsequent lymphedema presents with a growing nodule in her axilla.

A

Lymphangiosarcoma - lymphoid malignancy associated with persistent lymphedema.

108
Q

A patient with AIDS presents with several red-purple masses.

Diagnosis? Underlying cause?

A

Kaposi sarcoma.

Endothelial malignancy most commonly affecting skin. Can also affect mouth, GI tract, and respiratory tract.

Associated with HHV-8 and HIV. Can be mistaken for bacillary angiomatosis.

109
Q

An elderly female presents with unilateral headache, jaw claudication, and vision disturbance.

Diagnosis? Treatment?

A

Temporal (giant cell) arteritis. A large vessel vasculitis.

Give high-dose corticosteroids corticosteroids.

May lead to irreversible blindness due to ophthalmic artery occlusion.

Tends to affect branches of carotid artery.

Focal granulomatous inflammation.

Increased erythrocyte sedimentaiton rate.

110
Q

A 20-year-old Asian female presents with fever, night sweats, arthritis, myalgias, skin nodules, and ocular disturbance.

You find that she has weak upper extremity pulses with normal lower extremity pulses.

Diagnosis? Treatment?

A

Takayasu arteritis - a large vessel vasculitis.

Granulomatous thickening and narrowing of aortic arch and proximal great vessels.
“Pulseless disease”

Increased ESR

Treat with corticosteroids.

111
Q

A young adult with a history of Hepatitis B presents with fever, weight loss, malaise, headache, hypertension, and neurologic dysfunction.

Biopsy of the kidney shows transmural inflammation of arterial wall with fibrinoid necrosis.

Diagnosis? Treatment?

A

Polyarteritis nodosa - a medium vessel vasculitis.

Typically invovles renal and visceral vessels. Immune complex mediated (Hep B).

Transmural inflammation of arterial wall with fibrinoid necrosis. Microaneurysms and spasm on arteriogram.

Give corticosteroids and cyclophosphamide.

112
Q

An Asian child presents with “strawberry tongue”, fever, cervical lymphadenitis, conjunctival injection, hand-foot erythema, and desquamating rash.

Diagnosis? Complications?

What’s the unusual treatment?

A

Kawasaki disease - medium vessel vasculitis. May develop coronary artery aneurysms, thrombosis -> MI, rupture.

Treat with IV immunoglobulin and Aspirin. Aspirin is usually not given to children due to fear of Reye syndrome!

113
Q

A male smoker presents with gangrene of the digits.

Diagnosis?

A

Buerger disease (thromboangiitis obliterans), a medium-vessel vasculitis.

Highly associated with smoking. Segmental thrombosing vasculitis. Intermittant claudication -> gangrene, autoamputation of digits, superficial nodular phlebitis.
Raynaud phenomenon often present.

114
Q

Patient presents with chronic sinusitis, hemoptysis, and hematuria.

Biopsy of the lung shows necrotizing granulomas.

Lab testing shows positive c-ANCA.

Diagnosis? Treatment?

A

Granulomatosis with polyangiitis (Wegener). Small vessel vasculitis.

C-disease (nose, lung, kindey) with c-ANCA. (aka PR3-ANCA (anti proteinase 3)).

CXR = large nodular densities.

Give cyclophosphamide and corticosteroids.

115
Q

Patient presents with necrotizing vasculitis affecting the lung, kidneys, and skin.

No granulomas are present.

p-ANCA is positive.

Diagnosis?

A

Microscopic polyangiitis - a small vessel vasculitis.

MPO-ANCA (p-ANCA) = anti-myeloperoxidase.

Treat with cyclophosphamide and corticosteroids.

116
Q

Patient presents with asthma, sinusitis, palpable purpura, and peripheral neuropathy.

Biopsy of the lung shows granulomatous necrotizing vasculitis with eosinophilia.

p-ANCA is positive.

A

Churg-Strauss syndrome.

anti-Myeloperoxidase (MPO-ANCA/p-ANCA)

Can also involve heart, kidneys (pauci-immune glomerulonephritis)

117
Q

A child with recent history of an upper respiratory infection presents with palpable purpura on the buttocks and legs, arthralgias, and abdominal pain with melena.

Biopsy of skin lesions are positive for IgA.

A

Henoch-Schonlein purpura.

Vasculitis secondary to IgA complex deposition.

Associated with IgA nephropathy.

118
Q
A

First Aid: Pathology (10 decks)

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