Cardiovascular Pathology

Card Set Information

Author:
jknell
ID:
209445
Filename:
Cardiovascular Pathology
Updated:
2013-04-05 12:03:35
Tags:
Step
Folders:

Description:
Step I
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user jknell on FreezingBlue Flashcards. What would you like to do?


  1. Heart Murmurs
    • Systolic:
    • -Mitral/Tricuspid Regurgitation (MR/TR)
    • -Aortic Stenosis (AS)
    • -VSD
    • -Mitral Valve Prolapse (MVP)

    • Diastolic:
    • -Aortic Regurgitation (AR)
    • -Mitral Stenosis (MS)

    • Continuous:
    • -PDA
  2. Mitral Regurgitation
    • Reflux of blood from LV into LA during systole
    • Characteristics:
    • -Holosystolic
    • -High-pitched
    • -"Blowing"

    • Location:
    • -loudest at apex

    • Radiation:
    • -toward axilla

    • Maneuvers that Enhance:
    • -↑ TPR (squatting, hand grip)
    • -↑ LA return (expiration)

    • Etiology:
    • -often due to ischemic heart disease
    • -mitral valve prolpase
    • -LV dilation (LHF)
    • -acute rheumatic heart disease (vs. chronic → stenosis)
    • -infective endocarditis
    • -papillary muscle rupture (after MI)

    • Complications:
    • -volume overload and L-sided HF
  3. Tricuspid Regurgitation
    • Reflux of blood from RV to RA during systole
    • Characteristics:
    • -Holosystolic
    • -High-pitched
    • -"Blowing"

    • Location:
    • -loudest at tricuspid area

    • Radiation:
    • -right sternal border

    • Maneuvers that Enhance:
    • -↑ RA return (inspiration)

    • Etiology:
    • -RV dilation
    • -rheumatic fever (MR or TR)
    • -infective endocarditis (MR or TR)
  4. Aortic Stenosis
    • Narrowing of aortic valve orifice: fibrosis and calcification (<1cm2)

    • Characteristics:
    • -Systolic ejection murmur
    • -Ejection click (due to abrupt halting of valve leaflets)
    • -Crescendo-Decrescendo

    • Radiation:
    • -carotids/heart base

    • Etiology:
    • -"wear and tear" (presents in late adulthood)
    • -increased risk with bicuspid aortic valve
    • -chronic rheumatic heart disease (coexisting MS and fusion of aortic valve commissures)

    • Complications:
    • -prolonged asymptomatic stage
    • -Syncope
    • -Angina
    • -Dyspnea on exertion
    • "SAD"

    • -concentric LVH
    • -microangiopathic hemolytic anemia (schistocytes)

    • Treatment:
    • -valve replacement when complications develop
  5. VSD Murmur
    • Characteristics:
    • -Holosystolic
    • -"Harsh"

    • Location:
    • -loudest at tricuspid area

    • Maneuvers that Enhance:
    • -↑ Afterload (hand grip)
  6. Mitral Valve Prolapse
    • Ballooning of mitral valve into LA during systole
    • -Most frequent valvular lesion: seen in 2-3% of US adults

    • Characteristics:
    • -Late systolic
    • -Midsystolic click (due to sudden tensing of chordae tendinae)
    • -Crescendo murmur

    • Location:
    • -loudest over apex
    • -loudest at S2

    • Maneuvers that Enhance:
    • -↓ Venous return (Standing, Valsalva)

    • Etiology:
    • -unknown
    • -myxomatous degeneration
    • -rheumatic fever
    • -chordae rupture
    • -Marfan Syndrome
    • -Ehlers-Danlos syndrome

    • Complications:
    • -rare, usually asymptomatic
    • -predispose to infective endocarditis
    • -arrhythmia
    • -severe mitral regurgitation
  7. Aortic Regurgitation
    Backflow of blood from aorta into the LV during diastole

    • Characteristics:
    • -diastolic murmur
    • -decrescendo
    • -high-pitched
    • -"blowing"

    • Maneuvers that Enhance:
    • -↑ Afterload (Hand grip)

    • Manuevers that ↓ Intensity:
    • -Vasodilators

    • Clinical Features:
    • -wide pulse pressure
    • -bounding pulses
    • -head bobbing
    • -pulsating nail beds

    • Etiology:
    • -aortic root dilation (syphilitic aneurysm and aortic dissection)
    • -bicuspid aortic valve
    • -endocarditis (valve damage)
    • -rheumatic fever

    • Complications:
    • -LV dilation and eccentric hypertrophy
  8. Mitral Stenosis
    Narrowing of the mitral valve orifice

    • Characteristics:
    • -delayed, late diastolic
    • -follows OS (abrupt halt of leaflet motion in diastole after rapid opening due to fusion at leaflet tips)
    • -"rumbling"

    • Maneuvers that Enhance:
    • -↑ LA return (expiration)

    • Etiology:
    • -chronic rheumatic valve disease

    • Complications:
    • -chronic MS can result in LA dilation
    • -Pulmonary congestion (edema and alveolar hemorrhage)
    • -Pulmonary HTN (w/ eventual RHF)-Atrial fibrillation (increased risk for mural thrombi)
  9. PDA Murmur


    • Characteristics:
    • -continuous
    • -"machine-like"
    • -loudest at S2

    • Location:
    • -best heard at left infraclavicular area

    • Etiology:
    • -congenital rubella
    • -prematurity
  10. Atrial Natriuretic Peptide
    Released from atrial myocytes in response to ↑ blood volume and atrial pressure

    • Function:
    • -causes generalized vascular relaxation and ↓ Na+ reabsorption at medullary collecting tubule
    • -constricts efferent renal arterioles
    • -dilates afferent renal arterioles (cGMP mediated)
    • -promotes diuresis and contributes to "escape from aldosterone" mechanism
  11. Hypertension
    BP ≥ 140/90 mmHg

    • Risk Factors:
    • -age
    • -obesity
    • -diabetes
    • -smoking
    • -genetics
    • -black > white > Asian

    • Primary HTN:
    • -unknown etiology
    • -90% of HTN
    • -related to increased CO or TPR
    • -risk factors listed above

    • Secondary HTN:
    • -due to an identifiable etiology
    • -5-10% of HTN
    • -most common cause is renal artery stenosis (JGA activation of RAAS → ATII vasoconstriction and Aldo Na/H2O retention)
    • -elevated plasma renin
    • -unilateral atrophy (due to low blood flow)
    • -due to atherosclerosis (elderly men) and fibromuscular dysplasia (young females)

    • Malignant HTN:
    • -severe (>180/120) and rapidly progressing
    • -most cases of HTN are benign, 5% are malignant
    • -presents with acute end-organ damage (AKI, HA, Papilledema)
    • -medical emergency

    • Predisposes To:
    • -athersclerosis
    • -LVH
    • -stroke
    • -CHF-renal failure
    • -retinopathy
    • -aortic dissection
  12. Hyperlipidemia Signs
    • Atheromas
    • -plaques in blood vessel walls

    • Xanthomas
    • -plaques or nodules composed of lipid-laden histiocytes in the skin
    • -especially the eyelids (Xanthelasma)

    • Tendinous Xanthoma
    • -lipid deposit in tendon
    • -esp Achilles

    • Corneal Arcus
    • -lipid deposit in cornea, nonspecific (arcus senilis)
  13. Arteriosclerosis
    • "Hard arteries"
    • -due to thickening of blood vessel wall

    • 3 Types
    • -Monckeberg
    • -Arteriolosclerosis
    • -Atherosclerosis
  14. Arteriosclerosis: Monckeberg
    • Calcification in the media of the arteries
    • -especially radial and ulnar
    • -usually benign
    • -Does not obstruct blood flow
    • -Intima not involved

    "pipe stem" arteries
  15. Arteriosclerosis: Arteriolosclerosis
    • Hyaline:
    • -thickening of small arteries in essential HTN or DM
    • -caused by proteins leaking into the vessel wall → vascular thickening
    • -Complications: classically produces glomerular scarring that progresses to renal failure

    • Hyperplastic:
    • -onion skinning
    • -consequence of malignant HTN
    • -may lead to fibrinoid necrosis
    • -classically causes acute renal failure (flea-bitten appearance)
  16. Arteriosclerosis: Atherosclerosis
    Fibrous plaques and atheromas form in intima of arteries
  17. Atherosclerosis
    Disease of elastic arteries and large and medium sized muscular arteries

    • Modifiable Risk Factors:
    • -smoking
    • -HTN
    • -Hyperlipidemia
    • -DM

    • Non-Modifiable Risk Factors:
    • -age
    • -gender (↑ in men and postmenopausal women)
    • -positive FHx

    • Plaque:
    • -necrotic lipid core with fibromuscular cap

    • Progression:
    • -Inflammation is important in pathogenesis
    • 1. Endothelial cell dysfunction with LDL accumulation in intima
    • 2. LDL is oxidized and consumed by MPs
    • 3. Foam cell formation
    • 4. Fatty streaks (present in most teenagers)
    • 5. SM cell migration (involved PDGF and FGF), proliferation and ECM deposition
    • 6. Fibrous plaque
    • 7. Complex atheroma

    • Complications:
    • *account for > 50% of disease in the western world
    • -Aneurysms
    • -Ischemia
    • -Infarcts
    • -Peripheral vascular disease
    • -Thrombus
    • -Emboli

    • Location:
    • -Abdominal aorta > coronary artery > popliteal artery > carotid artery

    • Symptoms:
    • -angina
    • -claudication
    • -MAY BE ASYMPTOMATIC
  18. Abdominal Aortic Aneurysms
    • Epidemiology:
    • -occurs more frequently in hypertensive male smokers > 50 years old

    • Pathophysiology:
    • -usually arises below the renal arteries but above the aortic bifurcation
    • -primarily due to atherosclerosis (weakens vessel wall)

    • Presentation:
    • -pulsatile abdominal mass
    • -grows over time

    • Complications:
    • -rupture!!! (esp when > 5cm in diameter)
    • -compression of local structures
    • -thrombosis/embolism
  19. Thoracic Aortic Aneurysm
    • Etiology:
    • -tertiary syphilis (endarteritis of vasa vasorum results in luminal narrowing, decreased flow and atrophy of vessel wall; Tree bark appearance)
    • -cystic medial necrosis = weakness of CT in the media (Marfan's Syndrome)
    • -HTN

    • Complications:
    • -dilation of aortic valve root → aortic insufficiency
    • -compression
    • -thrombosis/embolism
  20. Aortic Dissection
    • Pathophysiology:
    • -longitudinal tear in the intima
    • -blood flow through media of aortic wall
    • -false lumen can be limited to the ascending aorta, propagate from the ascending aorta or propagate from the descending aorta
    • -occurs in the proximal 10 cm of the aorta (high stress region) with preexisting weakness of the media

    • Etiology:
    • -most commonly HTN (hyaline arteriolosclerosis of vasa vasorum →weakens media)
    • -Marfan Syndrome (defect in fibrillin, foundation for elastin fibers)
    • -Ehlers-Danlos Syndrome (defective formation of collagen)
    • -cystic medial necrosis
    • -bicuspid aortic valve

    • Presentation:
    • -tearing chest pain radiating to the back
    • -CXR: mediastinal widening

    • Complications:
    • -pericardial tamponade (most common cause of death)
    • -rupture with fatal hemorrhage
    • -obstruction of branching arteries (ie: coronary or renal)
  21. Ischemic Heart Disease Manifestations
    • Angina
    • -CAD narrowing, no myocyte necrosis
    • -Types: stable, unstable, Prinzmetal variant

    Coronary Steal Syndrome

    Myocardial Infarction

    Sudden Cardiac Death

    Chronic Ischemic Heart Disease
  22. Coronary Steal Syndrome
    Vasodilator my aggravate ischemia by shunting blood from area of critical stenosis to an area of higher perfusion
  23. Sudden Cardiac Death
    • -unexpected death due to cardiac disease
    • -occurs without sx or within 1 hour of onset of sx

    • Etiology:
    • -most commonly due to fatal ventricular arrhythmia
    • -up to 70% of cases associated with CAD
    • -mitral valve prolapse
    • -cardiomyopathy
    • -cocaine abuse
  24. Chronic Ischemic Heart Disease
    Progressive onset of CHF over many years due to chronic ischemic myocardial damage
  25. Stable Angina
    • Presentation:
    • -chest pain that arises with exertion or emotional stress
    • -lasts < 20 minutes (no necrosis)
    • -radiate to L arm or jaw
    • -diaphoresis
    • -SOB

    • Pathophysiology
    • -mostly due to atherosclerosis
    • ->70% stenosis required for sx
    • -decreased blood flow not able to meet  demands of myocardium during exertion
    • -reversible injury to myocytes

    • EKG:
    • -ST depression (subendocardial ischemia: most susceptible)
    • Relieved by:
    • -Rest
    • -Nitroglycerin (vasodilation decreases VR, decreases preload)
  26. Unstable Angina
    • Presentation:
    • -chest pain that occurs at rest

    • Pathophysiology:
    • -usually due to rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery
    • -reversible injury to myocytes

    • EKG:
    • -ST depression (subendocardial ischemia)

    • Relieved by:
    • -Nitroglycerin

    **very high risk of progression to MI
  27. Prinzmetal Angina
    • Presentation:
    • -episodic chest pain unrelated to exertion

    • Pathophysiology:
    • -due to coronary artery vasospasm
    • -reversible injury to myocytes (no necrosis)

    • EKG:
    • -ST elevation (transmural ischemia: cut off blood supply to entire wall)

    • Relieved by:
    • -Nitroglycerin
    • -CCB (relieves spasms)
  28. Myocardial Infarction
    Necrosis of cardiac myocytes

    • Pathophysiology:
    • -usually due to rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery
    • -other causes: vasospasm (Prinzmetal angina/cocaine), emboli, vasculitis (Kawasaki)

    • Presentation:
    • -severe, crushing chest pain (>20 min)
    • -radiates to L arm or jaw
    • -diaphoresis
    • -fatigue
    • -dyspnea (pulmonary edema)
    • -nausea/vomiting
    • -NOT relieved by nitroglycerin

    • EKG:
    • -initially shows ST depression (subendocardial necrosis)
    • -continued or severe ischemia leads to ST elevation (transmural necrosis)

    • Labs:
    • -Troponin I
    • -CK-MB

    • Affected Vessels:
    • 1. LAD
    • -most common (45%)
    • -infarction of anterior wall and anterior septum of LV

    • 2. RCA
    • -second most commonly affected vessel
    • -infarction of posterior wall, posterior septum and papillary muscle of LV

    • 3. LCx
    • -infraction of lateral wall of LV
  29. Evolution of MI: 0-4 hours
    • Gross Changes:
    • -none

    • Microscopic Changes:
    • -none

    • Complications:
    • -Arrhythmia
    • -CHF exacerbation (↓ EF)
    • -Cardiogenic shock (no perfusion of vital organs)
  30. Evolution of MI: 4-12 hours
    • Gross Changes:
    • -dark mottling
    • -pale with tetrazolium stain

    • Microscopic Changes:
    • -early coagulative necrosis
    • -edema
    • -hemorrhage
    • -wavy fibers

    • Complications:
    • -Arrhythmia
  31. Evolution of MI: 12-24 hours
    • Gross Changes:
    • -dark mottling
    • -pale with tetrazolium stain
    • *same as 4-12 hours

    • Microscopic Changes:
    • -contraction bands (reperfusion injury: increased Ca2+ leads to hypercontraction of myofibrlis)
    • -release of necrotic cell content into blood

    • Complications:
    • -Arrhythmia
  32. Evolution of MI: 1-3 days
    • Gross Changes:
    • -hyperemia

    • Microscopic Changes:
    • -extensive coagulation necrosis
    • -acute inflammation around infarct
    • -NP migration

    • Complications:
    • -Fibrinous pericarditis (if transmural infarction)
  33. MI Evolution: 3-14 days
    • Gross Changes:
    • -hyperemic border
    • -central yellow-brown softening (max by 10 days)

    • Microscopic Changes:
    • -macrophage infiltration
    • -granulation tissue at margins

    • Complications:
    • -free wall rupture → cardiac tamponade
    • -papillary muscle rupture
    • -ventricular aneurysm
    • -interventricular septum rupture
    • *due to degradation by MPs
  34. MI Evolution: 2 weeks to several months
    • Gross Changes:
    • -gray-white scar

    • Microscopic Changes:
    • -contracted scar complete (fibrosis)

    • Complications:
    • -Aneurysm
    • -mural thrombus
    • -Dressler Syndrome (pericardial inflammation leads to antibody formation against pericardium → autoimmune pericarditis)
  35. Diagnosis of MI
    • EKG
    • -gold standard for first 6 hours
    • -ST depression (subendocardial infarct)
    • -ST elevation (transmural infarct)
    • -Pathologic Q waves (transmural infarct)

    • Troponin I
    • -most sensitive and specific blood test
    • -rises after 4 hours
    • -elevated for 7-10 days

    • CK-MB
    • -predominantly found in myocardium but can be released from skeletal muscle
    • -useful in diagnosing reinfarction following acute MI
    • -rises at 4-6 hours
    • -returns to normal after 48 hours

  36. Types of Infarcts
    • Transmural Infarcts:
    • -↑ necrosis
    • -affects entire wall
    • -ST elevation and pathologic Q waves on EKG

    • Subendocardial Infarcts:
    • -ischemic necrosis of < 50% of ventricular wall
    • -subendocardium is especially vulnerable to ischemia
    • -ST depression on EKG
  37. EKG Diagnosis of MI
    • Anterior Wall Infarct
    • -LAD
    • -Q waves in V1-V4

    • Anteroseptal Infarct
    • -LAD
    • -Q waves in V1-V2

    • Anterolateral Infarct
    • -LCx
    • -Q waves in V4-V6

    • Lateral Wall Infarct
    • -LCx
    • -Q waves in I, aVL

    • Inferior Wall Infarct (posterior LV)
    • -RCA
    • -Q waves in II, III, aVF
  38. MI Complications
    • Cardiac Arrhythmia
    • -important cause of death before reaching the hospital
    • -common in first few days

    LV failure and pulmonary edema

    • Cardiogenic shock
    • -large infarct has a high risk of mortality
    • -failure of CO: no organ perfusion

    • Ventricular Free Wall Rupture
    • -cardiac tamponade

    • Papillary Muscle Rupture
    • -severe mitral regurg

    • Interventricular Septum Rupture
    • -VSD

    • Ventricular Aneurysm
    • -decreased CO
    • -risk of arrhythmia
    • -embolus from mural thrombus
    • -greatest risk approximately 1 week post MI

    • Postinfarction Fibrinous Pericarditis
    • -friction rub
    • -1-3 days post MI

    • Dressler's Syndrome
    • -autoimmune phenomenon resulting in fibrinous pericarditis
    • -several weeks post- MI
  39. Cardiomyopathies
    • 1. Dilated (congestive)
    • 2. Hypertrophic
    • 3. Restrictive (obliterative)
  40. Dilated (congestive) Cardiomyopathy
    • Epidemiology:
    • -most common cardiomyopathy (90%)

    • Etiologies:
    • -often idiopathic
    • -up to 50% familial
    • -chronic Alcohol abuse
    • -wet Beriberi
    • -Coxsackie B virus myocarditis
    • -chronic Cocaine use
    • -Chaga's disease
    • -Doxorubicin toxicity
    • -hemochromatosis
    • -peripartum cardiomyopathy (pregnancy)

    "ABCCCD"

    • Pathophysiology:
    • -all four chambers of heart are dilated
    • -systolic dysfunction
    • -eccentric hypertrophy (sarcomeres added in series)
    • -biventricular CHF

    • Findings:
    • -S3
    • -dilated heart on U/S
    • -balloon appearance on X-ray

    • Treatment:
    • -Na+ restriction
    • -ACEI
    • -diuretics
    • -digoxin
    • -heart transplant
  41. Hypertrophic Cardiomyopathy
    • Etiology:
    • -60-70% of cases are familial, AD (commonly mutation in β-myosin heavy chain)
    • -associated with Friedreich's ataxia

    • Pathophysiology:
    • -massive hypertrophy of left ventricle
    • -asymmetric concentric hypertrophy (sarcomeres added in parallel)
    • -diastolic dysfunction (can't fill hypertrophied LV → ↓CO)
    • -hypertrophied interventricular septum obstructions outflow through mitral valve (causes murmur and syncope)

    • Histology:
    • -disorganized, tangled, hypertrophied myocardial fibers

    • Presentation:
    • -Decreased CO
    • -Sudden death (major cause in young athletes)
    • -syncope (mitral valve obstruction)

    • Findings:
    • -normal sized heart
    • -S4
    • -apical impulses
    • -systolic murmur (mitral obstruction)

    • Treatment:
    • -β-blocker
    • -non-DHP CCB (Verapamil)
  42. Restrictive (Obliterative) Cardiomyopathy
    • Etiology:
    • -sarcoidosis
    • -amyloidosis
    • -postradiation fibrosis
    • -endocardial fibroelastosis (children)
    • -Loffler's Syndrome
    • -hemochromatosis

    • Endocardial Fibroelastosis:
    • -thick fibroelastic tissue in endocardium
    • -young children

    • Loffler's Syndrome:
    • -endomyocardial fibrosis with a prominent eosinophilic infiltrate

    • Pathophysiology:
    • -diastolic dysfunction

    • Presentation:
    • -CHF
    • -low-voltage EKG with diminished QRS amplitude
  43. Left Sided CHF
    • Causes:
    • -ischemia
    • -HTN
    • -MI
    • -dilated cardiomyopathy (causes greater ventricular end-diastolic volume)
    • -restrictive cardiomyopathy

    • Pathophysiology:
    • -pulmonary congestion (pulmonary edema)
    • -decreased forward perfusion (kidneys)
    • -decreased kidney perfusion leads to activation of RAAS (vasoconstriction and Na+/H2O retention)
    • -exacerbates CHF


    • Pulmonary Edema:
    • -↑ pulmonary venous pressure → pulmonary venous distention and transundation of fluid
    • -hemorrhage leads to hemosiderin-laden MPs (Heart Failure cells)

    • Clinical Presentation:
    • -dyspnea
    • -paroxysmal nocturnal dyspnea (increased VR when laying flat)
    • -orthopnea (increased VR when laying flat, exacerbates pulmonary vascular congestion)
    • -crackles
    • -hemosiderin laden MP in lungs (HF cells)

    • Treatment:
    • -ACEI (mainstay)
    • -β-Blockers (except in acute decompensated HF)
    • -ARBs and Spironolactone: reduce mortality
    • -Thiazide/Loop diuretics: mostly for sx relief
    • -Hydralazine with nitrate tx: improves sx and mortality in select patients
  44. Pathophysiology of LHF



    • Decreased LV contractility leads to pulmonary venous congestion
    • -this causes pulmonary edema and decreased RV output, leading to peripheral edema

    • Decreased LV contractility also decreases CO
    • -activates RAAS: increased Na+/H2O reabsorption
    • -increases sympathetic activity: increases RAAS
    • -increased Na+/H2O retention increases systemic venous pressure

    • Increase systemic venous pressure leads to:
    • -peripheral edema
    • -increased preload, increased CO (compensation!)
  45. Right Side CHF
    • Causes:
    • -usually due to LHF
    • -isolated RHF usually due to cor pulmonale (chronic lung disease)
    • -L→R shunt

    • Pathophysiology:
    • -systemic congestion

    • Clinical Presentation:
    • -elevated JVP
    • -painful hepatosplenomegaly ("nutmeg liver", may lead to cardiac cirrhosis)
    • -dependent pitting edema

    • Treatment:
    • -ACEI (mainstay)
    • -β-Blockers (except in acute decompensated HF)
    • -ARBs and Spironolactone: reduce mortality
    • -Thiazide/Loop diuretics: mostly for sx relief
    • -Hydralazine with nitrate tx: improves sx and mortality in select patients
  46. Bacterial Endocarditis
    • Epidemiology:
    • -most commonly caused by S. viridans
    • -mitral valve most frequently involved
    • -IV drugs associated with Tricuspid valve endocarditis (S. aureus, Pseudomonas and Candida)
    • "IV drugs abuse (don't tri drugs)"

    • Acute:
    • -S. aureus
    • -high virulence
    • -large vegetations on previously normal valves
    • -rapid onset

    • Subacute:
    • -viridans strep
    • -low virulence
    • -smaller vegetations
    • -congenitally abnormal or diseased valves
    • *sequelae of dental procedures
    • -more insidious onset

    • Other Causes:
    • -S. epidermidis (prosthetic valves)
    • -S. bovis (associated with colon cancer)
    • -HACEK (Haemophilus, Actinobacillus, Cardiobacerium, Eikenella, Kingella) (negative blood cultures)

    • Pathophysiology:
    • -damaged endocardial surface develops thrombotic vegetations (platelets and fibrin)
    • -transient bacteremia leads to trapping of bacteria in the vegetations

    • Clinical Features:
    • -Fever
    • -Roth's Spots (round white spots on retina surrounded by hemorrhage)
    • -Osler's nodes (tender lesions on fingers and toes due to septic emboli)
    • -Murmur (new)
    • -Janeway lesions (painless erythematous lesions on palm or sole due to septic emboli)
    • -Anemia of chronic disease
    • -Nail-bed hemorrhage (splinter hemorrhage due to septic emboli)
    • -Emboli

    "FROM JANE"

    • Complications:
    • -chordae rupture
    • -glomerulonephritis
    • -suppurative pericarditis
    • -emboli
  47. Non-Bacterial Endocarditis
    • Etiology:
    • -malignancy
    • -hypercoagulable state
    • -lupus

    • Libmann-Sacks Endocarditis:
    • -sterile vegetations
    • -present on surface and under-surface of mitral valve (mitral regurg)
  48. Rheumatic Fever
    • Pathophysiology:
    • -systemic complication of pharyngitis due to group A β-hemolytic strep
    • -antibodies to M protein cross react with human tissue (molecular mimcry)
    • -Type II hypersensitivity (not a direct effect of bacteria)

    • Acute Rheumatic Fever:
    • -2-3 weeks after strep throat
    • -early deaths due to myocarditis
    • -mitral regurgitation
    • -repeat infections may lead to chronic rheumatic heart disease

    Presentation: Two Mnemonics

    • FEVERSS:
    • -Fever
    • -Erytema marginatum
    • -Valvular damage (vegetation and fibrosis)
    • -ESR elevated
    • -Red hot joints (migratory polyarthritis)
    • -Subcutaneous nodules
    • -St. Vitus' dance (Sydenham's chorea)

    • JNES
    • -Joints (migratory polyarthritis)
    • - Pancarditis
    • -Nodules
    • -Erythema marginatum
    • -Sydenham's Chorea

    • Pancarditis:
    • 1. Endocarditis:
    • -mitral > aortic >> tricuspid (high pressure valves affected most)

    • 2. Myocarditis:
    • -Aschoff bodies (granulma with giant cells)
    • -Anitschkow's cells (histiocytes with wavy nuclei)
    • -most common cause of death in acute phase

    • 3. Pericarditis
    • -friction rub and chest pain

    • Findings:
    • -murmur
    • -elevated ESR
    • -elevated ASO titres

    • Chronic Rheumatic Heart Disease:
    • -valve scarring as a result of rheumatic fever
    • -results in mitral stenosis (fish mouth appearance)
    • -complications: infectious endocarditis
  49. Acute Pericarditis
    • Presentation:
    • -sharp pain
    • -aggravated by inspiration
    • -relieved by sitting up and leaning forward
    • -friction rub
    • -EKG: widespread ST elevation and/or PR depression

    • Fibrinous
    • -Dressler's syndrome
    • -uremia
    • -radiation
    • -loud friction rub

    • Serous
    • -viral pericarditis (often resolves spontaneously)
    • -non-infectious inflammatory diseases (RA, SLE)

    • Suppurative/purulent
    • -usually caused by bacterial infections (pneumococcus, streptococcus)
    • -rare now with antibiotics
  50. Cardiac Tamponade
    • Pathophysiology:
    • -compression of heart by fluid (eg: blood, effusions) in pericardium
    • -prevents heart from relaxing and expanding between beats
    • -leads to decreased CO
    • -equilibration of diastolic pressures in all 4 chambers (elevated and equal to pericardial pressure)
    • -compressed chambers can't accommodate normal venous return causing an increase in systemic and pulmonary venous pressure

    • Common Causes:
    • -neoplasm
    • -post-viral
    • -uremic
    • -trauma

    • Presentation:
    • -hypotension
    • -increased venous pressure (JVD)
    • -distant heart sounds
    • -increase HR-pulsus paradoxus
  51. Pulsus Paradoxus
    -decrease in amplitude of systolic blood pressure by ≥ 10 mmHg during inspiration

    • Seen in:
    • -severe cardiac tamponade
    • -asthma
    • -OSA
    • -pericarditis
    • -croup
  52. Syphilitic Heart Disease
    • Pathophysiology:
    • -3° syphilis disrupts the vasa vasorum of the aorta with atrophy of the vessel wall and dilation of the aorta and valve ring

    • Pathology:
    • -calcifications at aortic root and ascending aortic arch
    • -tree bark appearance

    • Complications:
    • -can result in aneurysm of the ascending aorta or aortic arch → aortic insufficiency
  53. Myxoma
    • Epidemiology:
    • -most common primary cardiac tumor in adults (still more rare than mets)

    • Pathophysiology:
    • -90% occur in the atria (mostly LA)
    • -benign mesenchymal tumor
    • -pedunculated mass in LA can obstruct mitral valve

    • Presentation:
    • -multiple syncopal episodes due to mitral obstruction

    • Pathology:
    • -gelatinous appearance
    • -abundant ground substance
  54. Rhabdomyomas
    • Epidemiology:
    • -most common primary cardiac tumor in children
    • -associated with tuberous sclerosis

    • Pathophysiology:
    • -benign hamartoma of cardiac muscle
    • -usually arises in the ventricle
  55. Metastasis
    • Epidemiology:
    • -most common heart tumor
    • -from breast carcinoma, lung carcinoma, melanoma and lymphoma

    • Pathophysiology:
    • -most commonly involves the pericardium → pericardial effusion
  56. Kussmaul's Sign
    Increase in JVP on inspiration instead of a normal decrease

    • Pathophysiology:
    • -Inspiration → negative intrathoracic pressure not transmitted to heart → impaired filling of right ventricle → blood backs up into venae cavae → JVD

    • Seen with:
    • -constrictive pericarditis
    • -restrictive cardiomyopathies
    • -R atrial or ventricular tumors
    • -cardiac tamponade
  57. Raynaud's Phenomenon
    • Pathophysiology:
    • -decreased blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress
    • -most often in fingers and toes
    • -affects small vessels

    • Etiology:
    • -Primary idiopathic (Raynaud's disease)
    • -Secondary (Raynaud's syndrome: mixed CT disease, SLE or CREST)
  58. Large Vessel Vasculitis
    • Temporal (Giant Cell) Arteritis
    • Takayasu Arteritis
  59. Medium Vessel Vasculitis
    • Polyarteritis Nodosa
    • Kawasaki Disease
    • Buerger Disease
  60. Small Vessel Vasculitis
    • Wegener Granulomatosis
    • Microscopic Polyangitis
    • Churg Strauss Syndrome
    • Henoch-Schonlein Purpura
  61. Temporal (Giant Cell) Arteritis
    Granulomatous vasculitis that involves branches of the carotid artery, segmental lesions

    • Epidemiology:
    • -female, > 50 years

    • Presentation:
    • -Unilateral HA
    • -Jaw claudication
    • -Vision problems (Blindness)
    • -associated with polymyalgia rheumatica

    • Lab Findings:
    • -elevated ESR (>100)
    • -bx: giant cells and intimal fibrosis
    • -negative bx does not rule out!!!

    • Treatment:
    • -Corticosteroids (empiric)
  62. Takayasu Arteritis
    Granulomatous vasculitis that involves aortic arch and branch points

    • Epidemiology:
    • -Young Asian females

    • Presentation:
    • -pulseless disease
    • -fever
    • -night sweats
    • -arthritis
    • -myalgias
    • -skin nodules
    • -visual and neurologic symptoms

    • Lab Findings:
    • -elevated ESR

    • Treatment:
    • -corticosteroids
  63. Polyarteritis Nodosa
    Necrotizing vasculitis involving multiple organs, sparing the lungs

    • Epidemiology:
    • -young adults
    • -associated with Hepatitis B seropositivity

    • Presentation:
    • -hypertension (renal artery involvement)
    • -abdominal pain with melena
    • -neurologic dysfunction
    • -cutaneous eruptions

    • Lab Findings:
    • -transmural fibrinoid necrosis
    • -lesions of different ages
    • -string of pearls (aneurysms and constrictions)

    • Treatment:
    • -Corticosteroids
    • -Cyclophosphamide
  64. Kawasaki Disease
    • Epidemiology:
    • -Asian children, < 4 years

    • Presentation:
    • -fever
    • -conjunctivitis
    • -enlarged cervical LNs
    • -Strawberry tongue
    • -hand-foot erythema
    • "Kid on a Kawasaki motorcycle: palm and sole rash, heart racing"

    • Complications:
    • -coronary aneurysms, thrombosis (MI)

    • Treatment:
    • -IVIg
    • -ASA
  65. Buerger Disease
    Necrotizing vasculitis involving digits

    • Epidemiology:
    • -heavy smokers
    • -males, <40

    • Presentation:
    • -gangrene
    • -autoamputation of digits
    • -superficial nodular phlebitis
    • -Raynaud's (neural involvement)

    • Treatment:
    • -smoking cessation
  66. Wegener Granulomatosis
    Necrotizing granulomatous vasculitis involving nasopharynx, lungs and kidneys

    • Epidemiology:
    • -middle aged men

    • Presentation:
    • -nasopharyngeal ulceration, otitis media, chronic sinusitis, mastoiditis
    • -hemoptysis, cough, dyspnea
    • -hematuria

    • Lab Findings:
    • -c-ANCA
    • -CXR: large nodular densities

    • Treatment:
    • -Cyclophosphamide
    • -Corticosteroids
  67. Microscopic Polyangiitis
    Necrotizing vasculitis involving especially lung and kidney

    • Presentation:
    • -palpable purpura
    • -similar to Wegener
    • -but NO nasopharyngeal involvement

    • Lab Findings:
    • -NO granulomas
    • -p-ANCA

    • Treatment:
    • -corticosteroids
    • -cyclophosphamide
  68. Churg-Strauss Syndrome
    Necrotizing granulomatous inflammation with eosinophils affecting especially lung and heart

    • Presentation:
    • -asthma
    • -sinusitis
    • -palpable purpura
    • -peripheral neuropathy

    • Lab Findings:
    • -granulomatous vasculitis with eosinophilia
    • -p-ANCA

    ***distinguish from Microscopic Polyangiitis (asthma, granulomas, eosinophilia)
  69. Henoch-Schonlein Purpura
    Epidemiology: most common form of childhood systemic vasculitis

    • Pathophysiology:
    • -IgA immune complex deposition usually following URI

    • Presentation (Triad):
    • -palpable purpura on buttocks and legs
    • -GI pain and melena
    • -Arthralgia

    -often associated with IgA nephropathy

    • Treatment:
    • -often self limited-Steroids
  70. Sturge-Weber Disease
    • Pathophysiology:
    • -congenital disorder that affects capillaries

    • Presentation:
    • -port-wine stain (nevus flemmeus) on face
    • -ipsilaterial leptomeningeal angiomatosis
    • -seizures
    • -early onset glaucoma
  71. Vascular Tumors
    • Strawberry hemangioma
    • Cherry hemangioma
    • Pyogenic granuloma
    • Cystic hygroma
    • Glomus tumor
    • Bacillary angiomatosis
    • Angiosarcoma
    • Lymphangiosarcoma
    • Kaposi's Sarcoma
  72. Strawberry Hemangioma
    Benign capillary hemangioma of infancy

    Appears in first few weeks of lifegrows rapidly and regresses spontaneously around 5-8yrs

    blanchable
  73. Cherry Hemangioma
    Benign capillary hematoma of the elderly

    Does NOT regress

    Increased frequency with age
  74. Pyogenic granuloma
    Polypoid capillary hemangioma

    May ulcerate and bleed

    Associated with trauma and pregnancy
  75. Cystic hygroma
    Cavernous lymphangioma of the neck

    Associated with Turner Syndrome
  76. Glomus Tumor
    Benign, painful, red-blue tumor under fingernails

    Arises from modified smooth muscle cells of glomus body
  77. Bacillary angiomatosis
    Benign capillary skin papules found in AIDS patients

    Caused by Bartonella henselae

    Don't confuse with Kaposi Sarcoma
  78. Angiosarcoma
    Malignant proliferation of endothelial cells

    Highly lethal malignancy of liver

    Associated with Polyvinyl chloride (PVC), arsenic and thorotrast exposure
  79. Lymphangiosarcoma
    Lymphatic malignancy associated with persistent lymphedema

    ie: post radical mastectomy
  80. Kaposi's Sarcoma
    Low grade malignant proliferation of endothelial cells

    Associated with HHV-8 infection

    • Seen in:
    • -old, eastern european males
    • -AIDS
    • -transplant recipients

    NOT blanchable

    Don't mistake for bacillary angiomatosis

What would you like to do?

Home > Flashcards > Print Preview