CARDIOVASCULAR_PATH_MS2

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soren101
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112730
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CARDIOVASCULAR_PATH_MS2
Updated:
2011-11-07 15:58:53
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CARDIOVASCULAR PATHOLOGY MS2
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CV PATH MS2
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  1. FORMS OF VEGETATIVE VALVULAR Dz
    • INFECTIOUS
    • --SUBACUTE
    • --ACUTE

    • POST INFECTIOUS
    • --RHEUMATIC FEVER

    • NON-INFECTIOUS
    • --NBTE
    • --LIBMAN-SACKS
  2. ACUTE vs. SUBACUTE ENDOCARDITIS
    • SUBACUTE
    • --AFFECTS ABN/Dz VALVES
    • --LOW VIRULENCE ORGANISMS (viridians)
    • --HOST REACTION PRESENT ON VALVES

    • ACUTE
    • --AFFECTS BOTH nL AND ABN/Dz VALVES
    • --HIGH VIRULENCE (aureus)
    • --HOST REACTION NOT PRESENT
  3. PREDISPOSING FACTORS OF INFECTIVE ENDOCARDITIS
    • STRUCTURAL
    • --VALVE Dz
    • --CHD
    • --PROSTHETIC VALVE

    • BACTEREMIA
    • --IV
    • --DENTAL
    • --INFECTION ELSEWHERE
    • --CATHETER

    IMMUNE DISFUNCTION
  4. COMPLICATIONS OF INFECTIVE ENDOCARDITIS
    • CARDIAC
    • --ABSCESS
    • --VALVE FAILURE
    • --MYOCARDIAL INJURY

    SEPTIC EMBOLI

    • IMMUNE COMPLEX
    • --RENAL
    • --SKIN
    • --ARTHRITIS
  5. ETIOLOGY AND VEGITATIONS OF NBTE

    MARANTIC ENDOCARDITIS
    ETIOLOGY

    • HYPERCOAG STATES
    • --MUCINOUS ADENOCARCINOMAS
    • --SOME NON-MUC MALIGs (promyelocytic leukemia)
    • --HYPERESTROGENIC STATES

    • ENDOCARDIAL TRAUMA
    • --INDWELLING CATHs

    • VEGITATIONS
    • --OCCUR ON nL VALVES

    --SINGLE OR MULTI SMALL 1-5mm STERILE VEGs DISTRIBUTED ON LINE OF CLOSURE OF LEAFLETS

    --MICROSCOPIC: BLAND THROMB w/o INFLAM INFILTRATE OR UNDERLYING VALVE DAMAGE. STERILE
  6. LIBMAN SACKS ENDOCARDITIS
    ASSOC w SLE

    • VAGITATIONS
    • --SINGLE OR MULTI SMALL STERILE

    • LOCATION
    • --UNDERSURFACE OF MITRAL AND TRICUSPID VALVE LEAFLETS
    • --CHORDAE TENDINAE
    • --MURAL ENDOCARDIUM

    • MICROSCOPIC
    • --FINELY GRAN AND HEMATOXYLIN BODIES
    • --UNDERLYING VALVE SHOWS INTENSE VALVULITIS w FIBRONOID NECROSIS
    • --MILD TO SEVERE DEFORMITY POSS IN LATER STAGES
  7. PATHOGENESIS AND CLINICAL FEATURES OF RHEUMATIC HEART Dz
    IMMUNE RESPONSE TO M PROT OF GAS CROSS REACTS TO SELF Ag IN HRT

    DAMAGE BY BOTH HUMORAL AND CELL-MEDIATED

    • CLINICAL FEATURES
    • MAJOR
    • --PANCARDITIS
    • --MIGRATORY ARTH OF LRG JOINTS
    • --SUBCUTE NODULES
    • --ERYTHEMA MARGINATUM OF SKIN
    • --SYDENHAM CHOREA

    • JONES CRITERIA:
    • EVIDENCE OF PREV GAS INF w EITHER:
    • --2 MAJOR
    • --1 MAJOR and 2 MINOR

    • MINOR
    • --FEVER
    • --ARTH
    • --ELEV ACUTE PHASE REACTANT
  8. JONES CRITERIA FOR RHEUMATIC HEART Dz
    • EVIDENCE OF PREV GAS INF w EITHER:
    • --2 MAJOR
    • --1 MAJOR and 2 MINOR

    • MAJOR
    • --PANCARDITIS
    • --MIGRATORY ARTH OF LRG JOINTS
    • --SUBCUTE NODULES
    • --ERYTHEMA MARGINATUM OF SKIN
    • --SYDENHAM CHOREA

    • MINOR
    • --FEVER
    • --ARTH
    • --ELEV ACUTE PHASE REACTANT
  9. MORPHOLOGY OF RHEUMATIC HEART Dz
    FOCAL INFLAM LESIONS IN TISSUES

    • DIFFUSE INFLAM IN ANY OF 3 LAYERS
    • --ENDO
    • --MYO
    • --PERI

    • ASCHOFF BODIES
    • --FOCI OF LYMPHs, PLASMA CELLS, AND ANITSCHKOW CELLS (activated macros)

    • ANITSCHKOW
    • --CATERPILLAR CELLS
    • --Dx FOR RHEUM FEVER
    • --ABUNDANT CYTO
    • --CENTRAL ROUND TO OVOID NUC
    • --CHROM IN CENTRAL "RIBBON"

    VALVES SHOW FIBRINOID NECROSIS IN CUSPS OR CHORDATE TENDINAE

    OVERLYING SMALL VEGs ON LINES OF CLOSURE
  10. CHRONIC RHEUMATIC HEART Dz
    DEFORMING FIBROTIC VALVULAR ABNs

    • MITRAL STENOSIS +/- AORTIC STENOSIS
    • --FISH MOUTH

    CHORDAE TENDINAE THICKENED, SHORTENED, AND POSS FUSED

    • MICRO
    • --ORGANIZATION OF ACUTE INFLAM
    • --DIFFUSE FIBROSIS AND NEOVASC OBLITERATING nL aVASC CUSP
    • --ASCHOFF BODIES RARELY SEEN
  11. ATHEROSCLEROSIS vs. ARTERIOSCLEROSIS
    • ATHERO
    • --LRG ELASTIC AND MEDIUM MUSC ARTERIES

    • ARTERIO
    • --HT
    • --SMALL MUSC ARTs AND ARTERIOLES
  12. 8 FUNCTIONS OF ENDOTHELIAL CELLS
    1) MAINTENANCE OF PERM BARRIER

    2) MAKE ANTI-COAG, ANTI-THROMB, AND FIBRINOLYTIC FACTORS

    3) MAKE PROTHROMB MOLs

    4) MAKE ECM (collagen, proteoglycans)

    5) MOD OF BLD FLOW AND VASC REACTIVITY

    6) REGULATE INFLAM AND IMMUNITY

    7) REGULATE CELL GROWTH

    8) AFFECTS VASOREACTIVITY OF SMOOTH MUSC CELLS
  13. STEPS LEADING TO INTIMAL THICKENING
    ENDO DYSFUNCTION OR INJURY -> STIM SM AND ECM SYNTH

    HEALING LEADS TO FORMATION OF NEOINTIMA BY ENDO CELLS MOVING TO INJURY

    SM CELLS AND PRECURSERS MOVE TO INTIMA, PROLIF, AND SYNTH ECM. DO NOT CONTRACT

    CELL PROLIF STOPS BUT INTIMAL THICK PERMANENT

    PERSISTANT INJURY LEADS TO THICK

    THICK IN nL VESSLES DURING AGING BUT w OUTWARD REMODELING
  14. 3 TYPES OF ARTERIOSCLEROSIS
    • 1) ARTERIOLOSCLEROSIS
    • --CHRON HEMODYNAMIC STRESS
    • --INC ECM SYNTH
    • --INC SM, FOCAL NECROSIS severe

    • SMALL MUSC ARTERIES AND ARTERIOLES
    • --MAY CAUSE ISCH INJ

    OCCURS IN HT AND DM

    • 2) ATHEROSCLEROSIS
    • --HIGH LIPID DIET
    • --ECCENTRIC INTIMAL LESIONS PROTRUDE INTO LUMEN
    • --THROMB FORMATION
    • --WEAKENING UNDERLYING MEDIA AND poss ANEURISM

    • 3) MONCKEBERG MEDIAL SCLEROSIS
    • --CALCIFIED DEPOTS IN Pts > 50
    • --NOT CLINICALLY SIG
  15. LIST THE MAJOR CONSTITUTIONAL AND MODIFIABLE RISK FACTORS FOR DEV OF ATHEROSCLEROSIS
    • CONSTITUTIONAL
    • --AGE > 40
    • --MALES & POSTMENOPAUSAL WOMEN
    • --GENETICS - FAM HIST

    • MODIFIABLE
    • --HIGH LIPID / CHOL IN BLD
    • --HT
    • --SMOKING
    • --DM
  16. PATHOGENESIS AND STEPS OF ATHEROSCLEROSIS
    • RESPONSE-TO-INJURY HYPOTHESIS
    • --CHRON INFLAM & HEALING RESP OF ARTERIAL WALL TO ENDO INJ

    • LOCATION AT SITES OF TURBULENT FLOW
    • --OSTIA
    • --BRANCH POINTS

    • STEPS
    • 1) ENDO DYSFUNC / INJ
    • 2) ACCUM OF LDL IN VESSEL WALL
    • 3) MONOCYTE ADHES AND MIG INTO INTIMA --> MACROs AND FOAM CELLS
    • 4) PLATELET ADHES
    • 5) PLATELETS/MACROs/ENDOs RELEASE FACTORS --> SM INTO INTIMA
    • 6) SM CELL PROLIF AND ECM PROD
    • 7) MORE LIPID ACCUM
  17. MORPHOLOGY OF ATHEROMATOUS PLAQUES
    • FATTY STREAKS
    • --EARLIEST LESION

    • PLAQUE
    • 1) WHITE-YELLOW RAISED ECCENTRIC LESION within THROMB

    2) PATCHY - NOT CIRCUMFERENTIAL

    • 3) LRG & MED ARTERIES MOSTL
    • --ABDOM AORTA >>> THORACIC
    • --CORONARY > POPLITEAL > INT CAROTID > CIRC OF WILLIS

    • 4) MICRO
    • --FIBROUS CAP
    • --CELLULAR AREA UNDER AND TO SIDE OF CAP w VASCULARIZATION
    • --NECROTIC CORE
    • --PLAQUES CHANGE/ENLRG OVER TIME
  18. CHANGES IN ATHEROMATOUS PLAQUES OVER TIME
    RUPTURE / ULCERATION / EROSION

    • HEMORRHAGE INTO PLAQUE FROM NEOVASV AREAS
    • --ATHER EMBOLISM
    • --ANEURYSM FORMATION
  19. CONSEQUENCES OF CLINICAL ATHEROSCLEROSIS
    OCCLUSION

    • STENOSIS
    • --CLINICAL AT > 70%
    • --ANGINA
    • --CHRON DIMINISHED PERFUSION
    • --COLLATERAL CIRC MAY DEVELOP OVER TIME IN SOME

    • ACUTE PLAQUE CHANGE
    • --THROMB, HEMORR
    • --ACUTE TISSUE INFARCT
    • --STABILITY AND VULNERABILITY MORE IMP THAN % OCCLUSION
    • --EXTRINSIC FACTORS. ADREN STIM INC BP, CIRCADIAN PERIODICITY OF MI, EMOTIONAL STRESS

    • EMBOLISM
    • DISTAL ISCH
  20. ACUTE PLAQUE CHANGE IN ISCHEMIC HEART Dz
    UNPREDICTABLE, ABRUPT

    SUPERIMPOSED THROMB

    PARTIALLY OR COMP OCCLUDE ARTERY

    • STEPS
    • --INTRAPLAQUE HEMOR / RUPTURE
    • --PLATELET ADHESION & AGG
    • --THROMB FORMATION
    • --OCCLUSION
  21. STABLE vs. UNSTABLE ANGINA
    • STABLE
    • --SIGNIF OBSTRUCTION
    • --DEMAND EXCEEDS SUPPLY
    • --DEV OF COLLATERAL CIRC PROTECTIVE

    • UNSTABLE
    • --CRESCENDO
    • --PARTIAL OCCL -> SEVERE TRANSIENT ISCH (15sec TO 15mins)
    • --DOES NOT CAUSE NECROSIS
    • --HARBINGER OF INFARCTION
  22. CAUSES OF MYOCARDIAL INFARCTION
    90% DUE TO ACUTE PLAQUE CHANGE

    • 10% OTHER
    • --VASOSPASM
    • --EMBOLI
    • --VASCULITIS
    • --SHOCK
    • --etc
  23. CHANGES AFTER MI IN FIRST MINUTE
    REVERSIBLE

    --DEC ATP PRODUCTION

    --INC LACTIC ACID

    --LOSS OF CONTRACTILITY wi 60 sec

    MAY LEAD TO HF BEFORE ACUTE MYOCARDOAL DEATH
  24. CHANGES IN MYOCARDIUM MINUTES AFTER MI
    STILL REVERSIBLE

    GLYCOGEN DEPLETION

    CELL SWELLING
  25. CHANGES IN MYOCARDIUM 20-30 mins AFTER MI
    IRREVERSIBLE

    • DISRUPTION OF SARCOLEMMAL MEM INTEGRITY
    • --INTRACELLULAR MACROMOLs LEAK INTO CIRC
    • --MEASURES TO DETECT INJURY

    >1 hr, MICROVASC INJURY
  26. LOCATION OF DAMAGE IN LAD OCCLUSION
    ANT LV WALL NEAR APEX

    ANT INTERVENTRICULAR SEPTUM

    CIRCUMFERENTIAL APEX
  27. LOCATION OF DAMAGE IN RCA OCCLUSION
    INF/POST LV WALL

    POST INTERVENTRICULAR SEPTUM

    INFERIOR/POSTERIOR RV FREE WALL
  28. LOCATION OF DAMAGE IN LCX OCCLUSION
    LV LATERAL WALL EXCEPT APEX
  29. GROSS AND MICRO FINDINGS 0-30mins AFTER INFARCT
    NONE
  30. GROSS & MICRO FINDINGS 1-2hrs AFTER INFARCT
    • GROSS
    • NONE

    • MICRO
    • NONE TO FEW WAVY FIBERS
  31. GROSS & MICRO FINDINGS 4-12 hrs AFTER INFARCT
    • GROSS
    • OCCASIONAL MOTTLING

    • MICRO
    • EARLY COAG NECROSIS
    • WAVY FIBERS
    • CONTRACTION BANDS
  32. GROSS AND MICRO FINDINGS 18-24 hrs AFTER INFARCT
    • GROSS
    • MOTTLING, PALE

    • MICRO
    • COAG NECROSIS
    • PYKNOTIC NUC
    • EARLY NEUT INFILTRATE

    PICS 18-72 hrs

  33. GROSS & MICRO FINDINGS 24-72 hrs AFTER INFARCT
    • GROSS
    • PALLOR

    • MICRO
    • COMPLETE COAGULATION
    • HEAVY NEUT INFILTRATE
  34. GROSS AND MICRO FINDINGS 4-7 DAYS AFTER INFARCT
    • GROSS
    • HYPEREMIC BORDER
    • YELLOW-TAN SOFT CENTER

    • MICRO
    • DISENTIGRATION OF MYOCYTES
    • EARLY PHAGOCYTOSIS

    • 3-7 DAYS
    • WEAKEST STRUCTURALLY
    • PHAGO BUT NO COLLAGEN DEPOT
    • MYOCARDIAL RUPTUTE
    • DEATH FROM CARDIAC TAMPONADE

    • PICS 4-10 DAYS
  35. GROSS & MICRO FINDINGS 10 DAYS AFTER INFARCT
    • GROSS
    • YELLOW-TAN
    • DEPRESSED MARGIN

    • MICRO
    • PHAGO
    • EARLY GRANULATION
  36. GROSS & MICRO FINDINGS 7-8 WEEKS AFTER INFARCTION
    • GROSS
    • GRAY-WHITE SCAR

    • MICRO
    • COLLAGEN DEPOSITION
    • FIBROSIS

    HEALED INFARCTS AFTER 8 WEEKS CANNOT BE DATED

    • 3.5 WEEKS

  37. MORPHOLOGY OF REPERFUSION AFTER INFARCT
    ALTERS MORPH OF IRREVERSIBLY INJURED CELLS

    USUALLY HEMORRHAGIC

    • CONTRACTION BANDS
    • --FLOODING OF SARCOLEMMA w Ca INTO PLASMA
  38. MYOGLOBIN AS LAB MARKER OF MI
    • PEAK
    • 2-3 hrs

    • ELEVATED
    • 6-8 hrs

    • RETURN TO nL
    • 18-24 hrs
  39. CK-MB AS LAB MARKER OF MI
    • PEAK
    • 3-4 hrs

    • ELEVATED
    • 24 hrs

    • RETURN TO nL
    • 72 hrs
  40. TROPONIN I & T IN LAB MARKERS FOR MI
    MOST SENSITIVE & SPECIFIC

    • PEAK
    • 4-8 hrs
    • 3-4 hrs

    • ELEVATED
    • 48 hrs

    • RETURN TO nL
    • 7-10 days
    • > 10 days
  41. COMPLICATIONS FROM MI
    CONTRACTILE DYSFUNCTION --> LV FAILURE

    ARRHYTHMIA

    MYOCARDIAL RUPTURE

    ANEURISM

    MURAL THROMBUS --> EMBOLI

    PERICARDITIS

    INFARCT EXPANSION

    PAPILLARY MUSC DYSFUNC/RUPTURE

    PROG CHRON HRT Dz
  42. PATHOGENESIS AND PREDISPOSING FACTORS FOR ANEURYSMS
    STRUCT/FUNC OF CONNECTIVE TISSUE COMPROMISED

    • POOR INTRINSIC QUALITY
    • --MARFAN
    • --EHLERS-DANLOS
    • --VIT C DEF

    • LOCAL INFLAM:
    • --ATHEROSCLEROSIS
    • --VASCULITIS

    • LOSS/DYSFUNC SMC FROM ISCHEMIA
    • --CYSTIC MEDIAL DEGENERATION (ssen in marfan, athero, ht, scurvy)
  43. ABDOMINAL AORTIC ANEURYSM
    • ASSOC w ATHEROSCLEROSIS
    • --INC METALLOPROTEINASE DEGRADES ECM
    • --MEDIAL DEGENERATION

    USUALLY BELOW RENAL ARTERIES & ABOVE BIFURCATION
  44. ETIOLOGY AND PATHOGENESIS OF AORTIC DISSECTIONS
    >90% FROM HT MALES 40-60yrs

    SMALL % YOUNGER (marfans)

    • PATHOGEN
    • --HT
    • --NARROWING VASO VASORUM (cmd)
    • --INTIMAL TEAR
  45. GIANT CELL ARTERITIS
    aka TEMPORAL ARTERITIS

    MEN > 50yrs

    • GRANULOMATOUS Dz IN MED/LRG ARTERIES
    • --PRIMARILY IN HEAD (temporal, opthal, vertebral arts)
    • --NONCONTINUOUS

    ELASTIC LAMINA FRAG

    • CLINICAL PRESENTATION
    • --HEADACHE or FACIAL PAIN
    • --OCULAR Sx

    Dx BY TEMPORAL ART BIOPSY
  46. TAKAYASU'S ARTERITIS
    PULSELESS Dz

    • YOUNG WOMEN < 50yrs
    • --giant cell arteritis = men > 50yrs

    • GRANULOMATOUS Dz OF LRG ARTERIES
    • --AORTIC ARCH and poss branches
    • --IRREG THICK --> NARROWING OR OBLITERATION

    MICRO INDISTINGUISHABLE FROM GIANT CELL

    • CLINICAL PRESENTATION:
    • --CONSTITUTIONAL -- FATIGUE, WT LOSS, FEVER
    • --ABSENT OR WEAK PULSES esp in UPPER EXTREMITIES
    • --OCULAR
    • --SYSTEMIC HT
  47. THROMBOANGIITIS OBLITERANS
    TOBACCO USE

    • YOUNG SMOKERS
    • --MEN < 35-45yrs

    • SHARPLEY SEGMENTAL VASCULITIS OF SMALL & MED ARTS
    • --TIBIAL & RADIAL ARTs

    CLAUDICATION OF FEET, LEGS, HANDS, ARMS, OR SUPERFICIAL SKIN

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