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1 USMLE - Cardiovascular System > Pathology > Flashcards

Pathology Flashcards

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USMLE® Step 1 flashcards
1
Q

Physically what causes an Aortic Dissection?

A

Tear in the intima, blood then flows between the intima and media, causing a dissection. Blood can then rip though all of the walls into the adventitia as well.

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2
Q

What are the two main causes of Aortic Dissection? And where is the most common area?

A

Must have Pre-existing weakness of media*

  • Hypertension causes arteriolosclerosis of the vasa vasorum, thus reducing O2 flow to the adventitia and media weakening it. HTN is most common cause
  • inherited defect of CT - Marphans or Ellers Danlow
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3
Q

Marfan Syndrome

A

CT disease, defect of fibrillin. Lanky, tall, and thin. Can have nocturnal blindness or astigmatism. Also associated with aortic dissection.

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4
Q

Ehlers–Danlos syndrome

A

CT disease, defect in collagen. Hyperflexible joints. Risk of aortic dissection.

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5
Q

Complications of Aortic Dissection

A
  • Pericardial tamponade if dissection goes back towards heart and filled the pericardium.
  • If dissects inferiorly, can go to renal artery and occlude it (end organ ischemia of kidney)
  • Ruptures in mediastinum, resulting in fatal hemorrhage
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6
Q

What causes an aneurism? What are the two main places in the aorta that aneurisms occur? Causes.

A

Weakness in wall*

  • Thoracic aneurism - tertiary syphilis* causing arteritis, resulting atrophy of media and adventitia, thus ballooning of aorta. Tree bark appearance of aorta*
  • Abdominal - Below renal arteries and above aortic bifurcation. Cause is atherosclerosis*
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7
Q

Complication of thoracic aortic aneurism?

A
  • Dilatation of aortic root, pulling apart aortic valve causing Aortic Insufficiency.
  • Thrombosis along wall of aneurism due to turbulent flow, can cause embolism - Stroke
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8
Q

How does atherosclerosis cause an aneurism? Feared complication? Classic patient?

A

Thickening of wall creates a larger diffusion distance for O2, weakens wall causing ballooning. Classic patient is male smoker over 60. Pulsatile abdominal mass*
-AAA Rupture can be fatal - hypotension, pulsatile abdominal mass, and flank pain. Medical emergency.

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9
Q

Main cause of thoracic aortic aneurism?

A

Tertiary syphilis

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10
Q

Main cause of AAA?

A

Atherosclerosis

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11
Q

Definition of vasculitis? Symptoms.

A

Inflammation of blood vessel wall. Arteries or veins.
Etiology is usually not known.
Nonspecific symptoms (inflammation - fever, myalgia…)
Symptoms of organ ischemia (thrombosis or post inflammation healing causes fibrosis and thus lack of blood flow to organ)

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12
Q

Temporal (Giant Cell) Arteritis. Symptoms? How to diagnose? Treatment? When to treat?

A

Most common in older adults (>50 y/o female)

  • Affects aortic artery (temporal - headache*, opthalmic - visual disturbances, jaw claudication, flu-like symptoms (joint and muscle pain)
  • ESR is elevated* >100
  • Dx: Biopsy - granulomatous vasculitis - fibrosis causes narrowing of vessel lumen, giant multinucleate cells
  • Tx: Corticosteroids - treat ASAP, do not wait for biopsy results - if opthalmic artery is involved permanent vision loss can occur
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13
Q

Takayasu Arteritis. Symptoms? Diagnosis? Treatment?

A

Adult < 50 (classic is young Asian female)
Granulomatous vasculitis of Aortic Arch at branch points*
-Weak or absent pulses in upper extremities
-Visual and neurologic symptoms
-ESR is elevated
Tx: Corticosteroids

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14
Q

Polyarteritis Nodosa. Symptoms? Diagnosis? Treatment? What is it associated with?

A

Medium vessel vasculitis. Necrotizing vasculitis involving any organ EXCEPT the lungs.
-Hypertension if renal artery
-Abdominal pain with melena if mesenteric artery
-Neurologic disturbances
-Skin lesions
-Fibrinoid Necrosis (transmural inflammation) - can cause ‘String-of-Pearls’ Appearance*
Associated with serum HBsAg (hep B surface antigen)
Tx: Corticosteroids or Cyclophosphamide (fatal if untreated)

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15
Q

Mechanism of corticosteroids?

A

mech

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16
Q

Mechanism of Cyclophosphamide?

A

mech

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17
Q

Kawasaki Disease. Symptoms? Diagnosis? Treatment?

A

Medium vessel vasculitis. Child (Asian) under 4 years, rash on palms and soles, fever, conjunctivitis, cervical lymphadenopathy (mimics viral infection).

  • Coronary artery is usually involved: risk is thrombosis with MI or coronary aneurism with rupture
  • Tx: Aspirin (protects against thrombus/embolism) and IVIG
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18
Q

Mechanism of Aspirin? Who do you never give it to?

A

COX 1 and 2 inhibitor - decreases TXA2 (thromboxane A2) -leads to permanent inactivation of platelets - cannot aggregate and form a clot
-Never give to a child with a systemic viral infection, can cause Reyes syndrome

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19
Q

Mechanism of action of IVIG?

A

Mech

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20
Q

Reyes Syndrome

A

Encephalopathy and massive liver necrosis - a child with a viral illness who was administered Aspirin.

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21
Q

Buerger Disease. Symptoms? Diagnosis? Treatment?

A

Medium vessel vasculitis. A necrotizing vasculitis involving the digits*. Presents in a SMOKER** with ulceration, gangrene, auto-amputation of fingers and toes, and also Raynaud phenomenon.
Tx: Stop smoking

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22
Q

Raynaud Phenomenon

A

Vasospasm resulting in discoloration. In ditigts, first turn white, then become hypoxic and turn blue, then return to red once blood flow is returned.

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23
Q

Wegener Granulomatosis. Symptoms? Diagnosis? Treatment?

A

Small vessel vasculitis. Necrotizing granulomatous vasculitis involving NASOPHARYNX, LUNGS, KIDNEY*
-C disease - We’c’ener - Nose, lung, kidney
-c-ANCA
-Cyclophosphamide is tx
Sinusitis/epistaxis
Hemoptysis with bilateral lung infiltrates/nodules
Hematuria due to RPGN (rapidly progressive glomerular nephritis)

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24
Q

Hemoptysis

A

Coughing up blood.

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25
Q

Microscopic Polyangiitis. Symptoms? Diagnosis? Treatment?

A

Small vessel vasculitis. Necrotizing vasculitis involving LUNG, KIDNEY (NO nasopharyngeal involvement), and other organs (NOT granulomatous*).

  • p-ANCA disease
  • Tx: Corticosteroids and cyclophosphamide
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26
Q

Churg-Strauss Syndrome. Symptoms? Diagnosis? Treatment?

A

Small vessel vasculitis. Necrotizing granulomatous* vasculitis with eosinophils. Involves LUNGS, HEART, and other organs.
-Asthma* and peripheral eosinophilia*
-p-ANCA disease
Tx: Corticosteroids and cyclophosphamide

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27
Q

Henoch–Schönlein purpura (HSP). Symptoms? Diagnosis? Treatment?

A

Small vessel vasculitis. Vasculitis due to IgA* immune complex deposition (type III hypersensitivity)

  • Most common vasculitis in CHILDREN
  • PALPABLE purpura on button and legs*
  • GI pain and bleeding
  • Hematuria** (IgA nephropathy)
  • Usually occurs following an URI (IgA is produced to fight URI, the deposition of the IgA deposition causes the vasculitis)
  • Tx: Corticosteroids if severe
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28
Q

Systemic Hypertension. Primary vs Secondary? Risk factors?

A

Hypertension > 140/90 (normal 120/80)
25% of US population.
95% of cases classified as Primary HTN where etiology is unknown.
Risk: Age, Race, Obesity, Stress, Lack of activity, High salt diet
5% of cases classified as Secondary HTN, etiology is known

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29
Q

Blood Pressure, systolic vs diastolic

A

Systolic is determined by Stroke Volume
Diastolic is determined by TPR
-Sodium effects both of these

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30
Q

Secondary Systemic Hypertension. Cause? Clinical sign?

A

Renal artery stenosis

  • Will see an increase in plasma Renin*
  • Unilateral atrophy of the affected kidney
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31
Q

Renal Artery Stenosis. Causes (2) and mechanism.

A

Causes: Renal artery atherosclerosis (elderly males) and Fibromuscular Dysplasia (young females)

  • Less blood flow to kidney, and thus the glomerulus
  • Renin release from JGA ( juxtaglomerular apparatus) as a response to decreased blood flow (senses stretch and therefore pressure)
  • Renin converts angiotensinogen to angiotensin I
  • In the LUNG angiotensin I is converted to angiotensin II (ACE)
  • Angiotensin II constricts arterial smooth muscle to increase TPR (incr. BP), also promotes adrenal release of aldosterone
  • Aldosterone goes to distal convoluted tubule and resorbs Na, therefore raising plasma volume (incr. BP)
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32
Q

Fibromuscular Dysplasia. Mechanism.

A

Developmental defect of blood vessel walls, usually medium and large arteries but in particular the renal arteries. Classically seen in YOUNG FEMALES
-The defect causes abnormal thickening and thus stenosis of the arteries and thus less blood flow.

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33
Q

Benign vs Malignant HTN

A

Benign: mild to moderate
-Usually silent, causes organ and vessel damage over time
Malignant: Severe increase (> 200/120 mmHg) causing ACUTE organ damage
-Acute renal failure
-Headache
-Papillediema
-MEDICAL EMERGENCY

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34
Q

Atherosclerosis. Define. What are the main arteries involved? Risks?

A

Thickening of INTIMA of blood vessel wall that obstructs blood flow
-Medium and Large vessels
-Plaque mainly consists of necrotic lipid core (cholesterol)
-Prone to calcification due to fibromuscular cap
Main arteries: Abdominal aorta, coronary, popliteal, internal carotid
Risk (modifiable)***: HTN, Hypercholeterolemia, Smoking Diabetes
Risk (non modifiable): Age, Male, Postmenopausal female, genetics
Mechanism: Damage to endothelium of intima, lipid enters into intima and is oxidized (fatty streak), then inflammation and healing, gives rise to lipid core and fibromuscular cap: atherosclerotic plaque

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35
Q

Arteriolosclerosis. Name the two types.

A

Narrowing of small arterioles.

  • Hyaline arteriolosclerosis
  • Hyperplastic arteriolosclerosis
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36
Q

Complications of atherosclerosis (4).

A

Stenosis of medium sized vessels supplying organs
-Popliteal: PDA (peripheral vascular disease)
-Coronary: Angina
-Mesenteric: Ischemic bowel disease
-Must have greater than 70% stenosis before symptoms arise*
Plaque rupture with thrombus
-Coronary: MI
-Middle cerebral: Stroke
-Mech: Stenosis of blood vessel, at the neck* of the vessel (leading to the organ) the plaque can rupture exposing necrotic lipid core, this activates the coagulation cascade leading to a thrombus, this can occlude the vessel leading to infarction of the organ
Plaque rupture with embolization
-Part of artherosclerotic plaque can break off, creating an emboli that can move to distal sites
-The hallmark of atherosclerotic emboli is the presence of cholesterol clefts*
Weakening of the vessel wall
-Due to thickening of the intima there is a diffusion barrier so O2 cannot get to the media and adventitia, thus weakening the vessel
-Weakening can cause dilatation of the vessel wall causing an aneurism

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37
Q

Hyalin Arteriolosclerosis. Causes (2)? Complications?

A

Thickening of wall of small blood vessels do to excess protein.
-Proteins leaking into the vessel walls - looks like pink hyalin on biopsy
Causes: Benign HTN (high pressure forces protein into the walls of the vessel) and Diabetes (non-enzymetic glycosylation of basement membrane making it leaky, thus proteins leak in)
-This results in end organ ischemia.
-Main arterioles involved are the glomerular afferent arterioles - causing glomerular scarring (arteriolonephrosclerosis) leading to RENAL FAILURE

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38
Q

Hyperplastic Arteriolosclerosis. Cause? Complication?

A

Thickening of wall of small blood vessels by hyperplasia of smooth muscle
- ‘Onion Skin Appearance’
Cause: Malignant Hypertension (the muscle tries to hypertrophy due to the high pressures.
- Thickening and thus stiffening (fibrinoid necrosis) of arterioles leads to end organ damage
-Acute Renal Failure (ARF) with ‘flea-bitten’ appearance (narrowing of glomerular afferent arterioles and thus glomerular stiffening)

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39
Q

Mönckeberg’s Medial Calcific Sclerosis

A

Calcification of the MEDIA, however, NON obstructive

  • Not clinically significant
  • Seen on X-ray or mammography (calcification can be a sign of cancer)
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40
Q

Hemangioma

A

Benign tumor comprised of blood vessels

  • Present at birth, usually regresses in childhood* so don’t remove it
  • SKIN and LIVER
  • If on the skin and you push on it it will BLANCH (blood is within the blood vessels, NOT a bleed into the skin which would not blanch)
41
Q

Angioscarcoma

A

Malignant proliferation of endothelial cells

  • Highly aggressive
  • SKIN, BREAST, LIVER
  • Associated with PVC exposure*, arsenic, or Thorotrast
42
Q

Kaposi Sarcoma. Viral association? Who gets them? Signs?

A

Low grade malignant proliferation of endothelial* cells
-HHV8**
-Purple patches, plaques, or nodules on skin - DOES NOT blanch when you push on it (tumor of endothelial cells, not vessels)
-May involve visceral organs
Who: Older Eastern European Males - surgical removal
AIDS patients can get HHV8 infection of endothelial cells resulting in Kaposi Sarcoma - give anti retroviral agents
Transplant Patients - involves skin, treatment is to decrease immunosuppression then immune system can fight the virus

43
Q

Stable Angina

A

Chest pain on exertion or stress, NOT at rest.
-Caused by atherosclerosis of coronary arteries (only if occlusion is >70%)
-Demand of myocardium is greater than supply
-REVERSIBLE injury to myocytes, CP lasts LESS than 20 minutes
-ST segment depression (coronary arteries supply the epicardium, then myocardium, and finally the endocardium) so SUBENDOCARDIAL ischemia occurs
Tx: Rest or Nitroglycerine

44
Q

Nitroglycerine Mechanism

A

Vasodilator of both arteries and VEINS
-Decreases amount of blood returning to heart which thus decreases preload and thus the work the heart has to do. This decreases oxygen consumption of the myocardium, reducing the CP.

45
Q

Unstable Angina

A

Chest pain that occurs AT REST

  • Rupture of atherosclerotic plaque at the neck of plaque, exposing lipid core, activation of coagulation, and thrombosis, however, only produces INCOMPLETE occlusion of coronary artery
  • Reversible, subendocardial ischemia lasting LESS than 20 minutes, shows ST segment depression
  • Relieved by nitroglycerine
  • HIGH risk for progression to MI
46
Q

Prinzmetal Angina

A

Chest pain due to vasospasm of coronary artery

  • Complete occlusion of coronary artery
  • EPISODIC chest pain UNRELATED to exertion
  • Reversible injury to myocytes, however shows ST segment ELEVATION - blood is cut to entire wall of ventricle - TRANSMURAL ischemia lasting less than 20 mins
  • Relieved by nitroglycerine or Class IV drugs
47
Q

Class IV drugs: Mechanism, Use

A

Calcium channel blockers

  • Verapamil
  • Diltiazem
  • Dihydropuridines (-pine)
48
Q

Myocardial Infarction

A

Necrosis of cardiac myocytes

  • Rupture of atherosclerotic plaque with COMPLETE occlusion of coronary artery lasting longer than 20 minutes
  • Can also be caused by coronary vasospasm, emboli lodged in coronary, vasculitis (Kawasaki’s)
  • Severe crushing chest pain for more than 20 minutes, diaphoresis, dyspnea (pulmonary congestion and edema)
  • NOT relieved by nitroglycerine
49
Q

What arteries are involved in MI? What is most common? What parts of the heart to they supply?

A
  • LAD (off LCA) is most common, supplies the anterior portion of LV and anterior portion of intraventricular septum
  • Right Coronary Artery (RCA), supplies posterior portion of LV and posterior intraventricular septum
  • Circumflex Coronary Artery (off of LCA), supplies lateral portion of LV
50
Q

Progression of MI

A

Initial phase: Subendocardial infarct ( < 50% of myocardial thickness), ST segment DEPRESSION
-Coronary arteries flow from epicardium to endocardium so the farthest away, the endocardium and inner myocardium, are the first to develop necroses
Later phase: Continued ischemia results in trasmural necrosis and entire wall will be damaged, causing ST segment ELEVATION

51
Q

Serum markers of MI

A

Troponin I - Most sensitive and specific
-Rises 2-4 hours post MI, peaks at 24, and returns to normal at 7-10 days
CK-MB - Useful for detecting a REinfarction days after the first
-Rises 4-6 hours after MI, Peaks at 24, but returns to normal after 72 hours

52
Q

MI treatment. What are two risks with one of the treatments?

A

Aspirin/Heparin - eliminate the thrombosis
Supplemental O2
Nitrates
Beta blockers (Slow HR, reduce arrhythmia)
ACE Inhibitors (Reduce LV dilatation (decrease blood volume - aldosterone), decrease after load (reduce peripheral resistance)
Fibrinolysis/Angioplasty* - Reperfusion*
-Risk: Contraction band necrosis and reperfusion injury

53
Q

Reperfusion Injury

A

When you return blood, you also return O2. This can create free radicals which can cause more injury to the myocardium. Serum markers will continue to rise.

54
Q

Contraction Band Necrosis

A

Returning blood to dead myocytes (remember no nucleus) also returns Ca. Ca causes contraction of the dead muscle cells, contraction causes dense pink bands in the dead cells that can be seen on biopsy.

55
Q

What are the microscopic and gross changes in the myocardium following MI? Name the 3 main stages.
At 4 hours? At 4-24 hours? 1-3 days? 4-7 days? 1-3 weeks? Months?

A

1 day Coagulative necrosis, 1 week inflammation, and 1 month healing to scar.

< 4 hours - No changes - Cardiogenic shock, CHF, Arrhythmia
4 - 24 hours - Dark - Coagulative Necrosis - Arrhythmia
1 - 3 days - Yellow (WBC’s) - Neutrophils - fibrinous pericarditis (some exudate enters pericardium - can ONLY HAPPEN if transmural - if subendocardial infarct, neutrophils would ONLY be in inner myocardium)
4 - 7 days - Yellow (WBC’s) - Macrophages - risk of rupture*
- cardiac tamponade, septal shunt, papillary rupture (mitral insufficiency - only with RCA* occlusion (papillary muscles are fed through RCA))
1 - 3 weeks - Red boarder - Healing - Granulation, fibroblasts, collagen, blood vessels
Months - White Scar (type I collagen) - Fibrosis - Aneurism, mural thrombosis, Dressler Syndrome

56
Q

Dressler Syndrome

A

If transmural infarction, will have a inflammatory response, potentially exposing the pericardial antigens. The immune system could potentially create antibodies against the pericardial antigens, mounting an immune response, autoimmune pericarditis 6 to 8 weeks post MI

57
Q

Sudden Cardiac Death. Causes?

A

Unexpected death due to cardiac disease
-Asymptomatic or within ONE hour of symptoms
-Usually due to fatal VENTRICULAR ARRYTHMIA
Causes: 90% due to ACUTE Ischemia, mitral valve prolapse, cardiomyopathy, cocaine abuse

58
Q

Chronic Ischemic Heart Disease

A

Chronic ischemia that slowly damages myocardium (with or without infarction)

  • Causes poor myocardial infarction
  • Progresses to CHF
59
Q

Causes of left-sided Heart Failure (5)?

A

Ischemia (decrease blood flow and damage myocardium)
Hypertension (concentric LVH, more difficult to oxygenate myocardium)
Dilated Cardiomyopathy (4 chamber dilatation of the heart, stretched muscle cannot contract as well)
Myocardial Infarction (if myocardium is infarcted it will not function properly)
Restrictive Cardiomyopathy (cannot fill heart and therefore cannot pump adequate blood flow)

60
Q

Signs of Left-sided Heart Failure? Tx?

A
  • Pulmonary Congestion: pulmonary edema, dyspnea, paroxsysmal nocturnal dyspnea, orthopnea, crackles
  • Heart Failure cells (hemociderin laden macrophages): due to rupture of pulmonary capillaries, blood flows into alveolar air sac, macrophages take up excess iron)
  • Decreased foreword perfusion: activation of Renin - Angiotensin system (raises blood pressure, serum renin incr.) - mainstay treatment of CHF are ACE INHIBITORS*
61
Q

Right-sided heart failure. Causes?

A
  • Most common cause is left-sided HF
  • Left to Right shunt: causes increase SV of RV and thus pulmonary hypertension, leading to RV hypertrophy and right-sided HF
  • Chronic Lung Disease (Cor Pulmonale): hypoxia causes blood vessel constriction in lungs, causes pulmonary hypertension, RVH, and right sided HF
62
Q

Signs of Right-sided Heart Failure?

A
  • JVD
  • Painful hepatosplenomegaly, can lead to cirrhosis (NUTMEG liver)
  • Dependent pitting edema
63
Q

VSD. Association? Tx?

A

Left to right shunt through the ventricular septum
-Number one congenital heart defect
-Associated with fetal alcohol syndrome*
-Asymptomatic if small
-If large, increase in blood volume in pulmonary circuit, pulmonary hypertension occurs, eventually the pulmonary system becomes higher pressure than the systemic system and the shunt reverses - right to left shunt resulting in cyanosis (Eisenmenger syndrome)
Tx: Surgical closure

64
Q

Eisenmenger Syndrome

A

Reversal of left to right shunt due to increasing pulmonary hypertension over time

  • Cyanosis
  • Pulmonary hypertension
  • RVH
  • Polycythemia (excessive RBC production, elevated hematocrit - hypoxemia causes EPO release and therefore RBC production)
  • Clubbing
65
Q

ASD. Types? Rare complication?

A

Left to right shunt due to defect in atrial septum

  • Ostium secundom is most common
  • Ostium primum also, associated with Down Syndrome
  • ‘Fixed-Split’ S2* pulmonary hypertension causes closure of pulmonic valve after aortic
  • Rare complication, DVT releases emboli that flows through ASD and up to brain - Paradoxical Embolism*
66
Q

Patent Ductus Arteriosus. Association? Signs? Tx?

A

Left to right shunt caused by failure of ductus arteriosus to close after birth
-Associated with fetal RUBELLA*
-Holosystolic ‘MACHINE-LIKE’ murmur
-Blood from aorta is shunted to the pulmonary artery causing pulmonary hypertension
-Eisenmenger syndrome can occur later in life - causes cyanosis in LOWER EXTREMITIES (PDA arises after main branches of aortic arch)
Tx: Indomethacin, decreases PGE*. PGE kEEps the PDA open.

67
Q

Tetralogy of Fallot

A

Right to left shunt due to: Stenosis of RV outflow tract, RVH, VSD, Aorta that overrides the VSD

  • Blood is shunted from RV to aorta, some blue blood flows to extremities, this causes cyanosis at birth. Depending on the DEGREE of STENOSIS, child may be more asymptomatic until exertion, then, on exertion the child will learn to squat down when fatigued, this increases aortic pressure and less blood is shunted into it, more through the pulmonary circuit and cyanosis will resolve.
  • BOOT SHAPED heart on CXR
68
Q

Transposition of the Great Arteries

A

Right to left shunt due to transposition, RV to aorta, and LV to pulmonary circuit: causes 2 separate circuits

  • Tx is to give PGE to kEEp PDA open: thus connecting the two circuits. Surgical repair is needed later in life*
  • Associated with MATERNAL DIABETES*
69
Q

Truncus Arteriosus

A

One large trunk arising from both ventricles

  • Deoxygenated and oxygenated blood mix
  • Early cyanosis
70
Q

Tricusped Atresia

A

Tricuspid valve orifice fails to develop

  • No blood from RA to RV
  • RV becomes hypplastic
  • Associated with ASD or baby would not survive
71
Q

Coarctation of the Aorta. Infantile vs Adult.

A

Infantile
-Narrowing of the aorta
-Associated with PDA
-Coarctation occurs DISTAL to the aortic arch but PROXIMAL to the PDA
- LOWER EXTREMITY cyanosis (blue blood through PDA to lower extreme, while red blood in aortic arch is normal
-Associated with TURNER syndrome
Adult
-Narrowing of aorta NOT associated with PDA
-Coarctation lies distal to aortic arch
-Extra blood flows to upper extremities, and causes hypotension and weak pulses in lower extremities*
-Associated with BICUSPID Aortic valve
-Collateral circulation develops across intercostal arteries to make up for the poor lower extremity circulation
-RIB NOTCHING*

72
Q

Acute Rheumatic Fever. Cause?

A

Complication of group A beta-hemolic strep (pyogenes) pharyngitis

  • Usually in a child 2-3 weeks after strep throat
  • Caused by type II hypersensitivity reaction (Molecular Mimicry*): bacterial M protein resembles antigens in endocardium of heart valves
  • Need presence of Jones Criteria
  • Heart problems are worst (pancarditis)
  • Endocarditis results in vegitations on valves, in particular MITRAL valve, also the AORTIC but ALWAYS mitral - leads to mitral regurgitation)
  • Myocarditis causes Aschoff* bodies which contain Anitschkow* cells (caterpillar nucleus): Myocarditis is the MOST COMMON cause of DEATH in FIRST PHASE of acute rheumatic fever**
  • Pericarditis causes a friction rub on auscultation
73
Q

Jones Criteria

A

Evidence of prior group A beta-hemolytic strep pyogenes infection (Anti-Streptolycin O (ASO) or anti-DNase B titer positive)
-Minor criteria (fever and elevated ESR)
-Major criteria (JONES)
JOINT problems (migratory poly arthritis)
CARDITIS: endocarditis, myocarditis, pericarditis
NODULES in skin
ERYTHEMA Marginatum
SYDENHAM’S chorea

74
Q

Chronic Rheumatic Valve Disease

A

Valve scarring that results from chronic rheumatic fever

  • Results in MITRAL valve stenosis
  • Occasionally Aortic valve stenosis (fusion of commisures*)
  • ENDOCARDITIS is a complication due to a Strep Viridans infection
75
Q

Aortic Stenosis. Cause? Complications? Treatment?

A

Narrowing of Aortic valve orifice
-Usually due to fibrosis and calcification (‘wear and tear’
-Presents in late adulthood
-Bicuspid Aortic valve increases risk*
-Clinically a SYSTOLIC ejection click followed by crescendo/decrescendo murmur is heard
-Can also be caused by chronic rheumatic valve disease (BUT MUST ALSO HAVE MITRAL STENOSIS, and NO fusion of commisures wear and tear damage is different)
Complications: LVH, Angina, Syncope, Microangiopathic hemolytic anemia
Tx: Valve replacement AFTER onset of complications

76
Q

Microangiopathic Hemolytic Anemia

A

Ruptured blood cells caused by turbulent and high velocity flow across a stenotic Aortic valve

77
Q

Aortic Regurgitation. Cause? Complications? Treatment?

A

Backflow of blood from Aorta into the LV during diastole
Cause: Isolated dilation of aortic root, pulling valves apart
-Can also be caused by a syphilitic aneurism
-Valve cusp damage from bacterial endocarditis
Clinically: Blowing DIASTOLIC murmur
-HYPERDYNAMIC circulation - very large pulse pressure: bounding pulses, pulsatile nail bed, head bobbing
-LV dilatation, LVH
Tx: Valve replacement when LV DYSFUNCTION develops

78
Q

Mitral Valve Prolapse. Cause? Complications? Treatment?

A

Balooning of mitral valve into LA during systole
Cause: Mixoid degeneration of valve, could be associated with CT diseases but usually etiology is unknown
Clinically: Mid systolic click followed by regurgitation murmur
Complications: Rare IE, Arrhythmia, Severe mitral regurgitation
Tx: Valve Replacement

79
Q

Mitral Regurgitation. Cause? Complications? Treatment?

A

Reflux of blood form LV to LA during systole
Clinically: Holosystolic ‘blowing’ murmur, louder with squatting or expiration (increases aortic pressure, on expiration more blood enters LA)
Cause: Complication of mitral valve prolapse, LV dialation (pulls apart valve leaflets), IE, ACUTE Rheumatic Heart Disease, papillary muscle rupture post MI
Tx: Valve replacement

80
Q

Mitral Stenosis

A

Narrowing of mitral valve orifice
Cause: CHRONIC Rheumatic Heart Disease
Clinically: Opening snap followed by diastolic rumble
-Overload of blood in LA leading to pulmonary congestion (causes edema and heart failure cells), pulmonary HTN (can lead to RHF), Atrial fibrillation (conducting system abnormalities due to stretching of atrium, also have risk of mural thrombus and stroke)

81
Q

Endocarditis

A

Inflammation of endocardium that lines the surface of cardiac valves
-Main cause is bacterial infection

82
Q

Most common cause of bacterial endocarditis

A

Strep Viridans

  • Low virulence so can only infect PREVIOUSLY DAMAGED valves
  • Damaged endocardial surface developed thrombotic vegitations made of platelets and fibrin, bacteremia can be trapped, causing IE
  • SUBACUTE IE
  • Dental procedures should be treated PROPHYLACTICALLY if have a heart murmur/valve damage
83
Q

Endocarditis in IV drug user cause?

A

Staph Aureus

  • High virulence, infects NORMAL valves
  • Results in large vegitations that destroy the valve
  • ACUTE IE
  • Usually effects the TRICUSPID valve (IV drug use - S Aureus gets into vein - goes to RA and RV and hits tricuspid valve first)
84
Q

Endocarditis of prosthetic valves?

A

Staph Epidermidis

-Infects PROSTHETIC valves

85
Q

Staph Bovis infections endocarditis, what do you always need to look for?

A

Colorectal Carcinoma**

-Order an endoscopy

86
Q

HACEK organisms

A 
Hemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella
-They will cause endocarditis with NEGATIVE blood cultures
87
Q

Clinical features of Infective endocarditis

A

Fever
Murmur
Janeway Lesions (septic emboli - NON TENDER)
Osler Nodes (type III hypersensitivity - PAINFUL)
Splinter Hemorrhages
Anemia of chronic disease (due to chronic inflammation)

88
Q

Laboratory features in Infective endocarditis

A

Positive Blood cultures
Anemia or chronic disease (generally microcytic anemia: Low Hbg, Low MCV, Elevated Hepcidin (traps iron in storage cells), High ferritin (storage form or iron), Low TIBC), Low Serum Iron, Low Percent saturation of iron)
Trans-Esophageal Echocardiogram - Most Specific and Sensitive test for endocarditis.

89
Q

Non-bacterial Thrombotic Endocarditis

A

Sterile vegitations that arise with hyper coagulable state or underlying adenocarcinoma
-Vegitations arise on MITRAL valve along lines of closure resulting in regurgitation

90
Q

Libman-Sacks Endocarditis

A

Sterile vegitations associated with SLE

  • MITRAL valve vegitations on BOTH sides of valve
  • Mitral regurgitation
91
Q

Dilated Cardiomyopathy. Symptoms? Causes? Treatment?

A

Dilatation of ALL four chambers of the heart
-Most common type of cardiomyopathy
-Results in SYSTOLIC dysfunction: stretching leads to reduced ability to contract and therefore less SV and CO
-Leads to biventricular CHF
-Can also cause mitral and tricuspid regurgitation and cardiac arrhythmia
Causes: Usually idiopathic, genetic mutations (Autosomal dominant), Myocarditis (Coxsackie virus), Alcohol abuse, Drugs (doxorubicin, cocaine), Pregnancy (late in 3rd trimester or after birth)
Tx: Heart replacement

92
Q

Hypertrophic Cardiomyopathy. Symptoms? Causes? Biopsy?

A

Massive hypertrophy of the LV
Cause: Genetic mutations in the SARCOMERE proteins, autosomal dominant
Sx: Decreased CO (loss of LV compliance: heart wall is so thick it can’t fill)
Sudden Death due to arrhythmias (most common cause of death in young athletes)
Syncope with exercise (creates a block like aortic stenosis)
Biopsy: Myocyte hypertrophy with disarray**

93
Q

Restrictive Cardiomyopathy. Symptoms? Causes?

A

Loss of compliance of LV endomyocardium: restricts filling during DIASTOLE
-Amyloidosis (amyloid in wall of heart)
-Sarcoidosis (granulomas in wall of heart)
-Hemochromatosis (iron in wall of heart)
-Edocardial fibroelastosis* (in CHILDREN*: dense layer of fibrosis and thickened with elastic tissue in endocardium)
-Loeffler Syndrome (eosinophilic infiltrate with inflammation within the wall of the heart, endocardium and myocardium)
Symptoms: CHF, low voltage EKG with diminished QRS amplitudes

94
Q

Mixoma

A

Benign mesenchymal proliferation of with a gelatinous appearance (abundant ground substance)

  • Most common primary cardiac tumor in adults
  • Affects the LA
  • Myocytes are PERMANENT cells so will not get tumors of heart cells
  • Symptoms of mitral valve stenosis including SYNCOPE*
95
Q

Rhabdomyoma

A

Benign hamartoma of cardiac muscle

  • Most common primary cardiac tumor in CHILDREN*
  • Associated with tuberous sclerosis
  • Usually ventricular
96
Q

Cardiac Metastasis

A

More common than primary tumors

  • Breast and lung carcinoma, melanoma, and lymphoma
  • Most commonly involves the PERICARDIUM, resulting in pericardial effusion
97
Q

Systemic Lupus Erythematosus

A 
Systemic autoimmune disease
-Type II and Type III hypersensitivity Reaction
Patient must meet 4 of 11 criteria
-Malar Rash
-Photosensitivity
-Anemia
-Hematologic disorders
-Arthritis
98
Q

Turner’s Syndrome. Signs? Associated cardiac birth defect.

A

Wide neck and cystic hygroma (translucent clear fluid filled neck mass), webbed neck, lymphedema of extremities, broad ‘shield’ chest, high arched stature, high arched palate, gonadal dysgenesis, hypothyroidism, infertility
-Associated with coarctation of the aorta

1 USMLE - Cardiovascular System (3 decks)

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