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    Cvs 2 Cvs 2 Presentation Transcript

    • CARDIOVASCULARSYSTEMDr. Atifa ShuaibAssociate Professor of PathologyRawalpindi Medical College
    • CARDIOVASCULAR SYSTEM Diseases of Blood vessels Diseases of Heart
    • CARDIOVASCULAR SYSTEMDiseases of blood vessels Congenital anomalies Arteriosclerosis Hypertensive vascular disease Aneurysms & Dissections Vasculitis Tumors
    • CARDIOVASCULAR SYSTEMARTERIOSCLEROSIS: Atherosclerosis Monckeberg medial calcific sclerosis Arteriolosclerosis
    • CARDIOVASCULAR SYSTEM Fatty streaks  Aortas of children Risk factors  Atheroma in adults ↓↓ Ischaemic Heart Disease
    • CARDIOVASCULAR SYSTEMATHEROSCLEROSIS
    • CARDIOVASCULAR SYSTEMRISK FACTORS: Non Modifiable Modifiable
    • CARDIOVASCULAR SYSTEMNONMODIFIABLE: Age: advancing age Sex: males > females postmenopausal risk equal Genetics: familial predisposition
    • CARDIOVASCULAR SYSTEMMODIFIABLE: Hyperlipidemia: hypercholesterolemia LDL (bad cholesterol) HDL (good cholesterol) ↓ by exercise ↑ by obesity & smoking
    • CARDIOVASCULAR SYSTEM Diet ↑ cholesterol  egg yolk, butter, animal fat ↓ cholesterol  omega 3 FA Statins ↓ cholesterol
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEM Hypertension: >169/95 mm Hg 5 fold ↑ risk Smoking: 200% ↑ death rate Diabetes Mellitis: hypercholesterolemia twice ↑ risk MI gangrene lower limbs (200% risk)
    • CARDIOVASCULAR SYSTEM Others: homocystinuria inflammation lipoprotein a (Lp a) lack of exercise stressful life type A personality obesity
    • CARDIOVASCULAR SYSTEMMultiple risk factors  Multiplicative effect
    • participants had increases in HDL cholesterol averaging about 2.5 mg/dL. This increase in HDL cholesterol was only modest, but was statistically significant. Furthermore, since cardiac risk is thought to drop by two to three percent for each 1 mg/dL increase in HDL, a 2.5 mg/dL rise in HDL amounts to a substantial reduction in risk.
    • Exercise is involved in increasing the production and action of several enzymes that function to enhance the reverse cholesterol transport system (Durstine & Haskell 1994). The precise mechanisms are unclear, but evidence indicates that other factors including diet, body fat, weight loss, and hormone and enzyme activity interact with exercise to alter the rates of synthesis, transport and clearance of cholesterol from the blood (Durstine & Haskell 1994).
    • CARDIOVASCULAR SYSTEMPATHOGENESIS:“response to injury hypothesis”A disease of intimaChronic inflammation of arterial wall inresponse to injury to endothelium
    • CARDIOVASCULAR SYSTEM Chronic endothelial injury  activation Accumulation of lpoproteins (LDL) Oxidation of LP Monocyte migration  macrophage accumulation Foam cells
    • CARDIOVASCULAR SYSTEM Platelet adhesion Chemical mediator release Smooth muscle cells migration SMCs proliferation ECM deposition Lipid accumulation
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEM1. Endothelial injury (repetitive): endothelial dysfunction ? injury repetetive non denuding toxins, chemical mediators, infections hemodynamic disturbance  sites of ostia and bifurcation posterior wall of abdominal aorta hypercholesterolemia
    • CARDIOVASCULAR SYSTEM2. Inflammation (chronic): initiation - complications endothelial cell adhesion molecules VCAM-1 monocyte adhesion & migration macrophage accumulation in intima foam cell formation IL-1, TNF MCP-1
    • CARDIOVASCULAR SYSTEMMacrophages toxic oxygen species  oxidation of lipids GF  smooth muscle cell proliferationT lymphocytes  cellular & humoral3. Lipids: cholesterol & its esters in atheromas Oxidized LDL in macrophages
    • CARDIOVASCULAR SYSTEM genetic defects  hypercholesterolemia  AS MI at young age with ↑ cholesterol DM, hypothyroidism  ↑ cholesterolAS high cholesterol diet  AS severity of AS  levels of cholesterol ↓ing cholesterol levels  risk of AS ↓
    • CARDIOVASCULAR SYSTEMMechanism :1. Chronic hyperlipidemia  EC activation2. Chronic hyperlipidemia  LP accumulate in intima3. Oxidized LDL  macrophages  foam cells  monocyte accumulation  GF, cytokine release  Ecs, SMCs cytotoxicity
    • CARDIOVASCULAR SYSTEM4. Smooth muscle cells:SMCs migration proliferation & ECM deposition ↓Fatty streak  fibrofatty atheromatous plaquePDGF, TGF-a, FGFFoam cellsECM (collagen) depositedSMCs apoptosis
    • CARDIOVASCULAR SYSTEMMORPHOLOGY:Fatty streak: children aortas coronaries in adolescents multiple, flat yellow dots coalesce to streaks lipid laden foam cells
    • FATTY STREA K
    • CARDIOVASCULAR SYSTEMAtheromatous plaque: elastic & muscular arteries lower abdominal aorta > thoracic aorta ostia and branches symptomatic AS disease MI  heart attack cerebral infarction  stroke peripheral vascular  gangrene
    • CARDIOVASCULAR SYSTEM aorta > coronaries > popliteal > internal carotid > circle of willis white – white yellow variable size eccentric lesions obstruction of lumen
    •  Mild, Moderate, Severe AS
    • CARDIOVASCULAR SYSTEMComponents:1. Cells: SMCs macrophages T lymphocytes other leukocytes
    • CARDIOVASCULAR SYSTEM2. ECM: collagen elastic fibers proteoglycans3. lipids: intracellular extracellular
    • CARDIOVASCULAR SYSTEMPlaque change: enlargement ulceration/erosion rupture thrombosis embolism haemorrhage calcification aneurysmal dilation
    • CARDIOVASCULAR SYSTEMARTEIOLOSCLEROSIS:Small Bv, arterioles Hyaline homogenous pink hyaline thickening narrowed lumen elderly Hypertension Benign nephrosclerosis
    • CARDIOVASCULAR SYSTEM microangiopathy of DM Hyperplastic: malignant HTN onion skin concentric, laminated thickening SMCs & thickened BM necrotizing arteriolitis
    • CARDIOVASCULAR SYSTEMANEURYSM:Localized abnormal dilation of a blood vessel orheart. True aneurysm all layers of Bv or heart False aneurysm (pseudoaneurysm) extravascular hematoma
    • CARDIOVASCULAR SYSTEMCauses: Atherosclerosis Cystic medial degeneration Trauma (A-V aneurysms) Congenital defects (berry aneurysms) Infections (mycotic) Vasculitis
    • CARDIOVASCULAR SYSTEMTypes: Saccular FusiformSites: Abdominal aorta common iliac A Arch of aorta descending thoracic aorta
    • CARDIOVASCULAR SYSTEMMycotic aneurysm: septic embolus direct extension bacteraemia
    • CARDIOVASCULAR SYSTEMABDOMINAL AORTIC ANEURYSMS(AAA): Atherosclerosis > 50 yrs > males genetic susceptibility  ↓ connective tissue strength MMP  TIMP HTN
    • CARDIOVASCULAR SYSTEMMorphology: B/W bifurcation & renal arteries saccular/fusiform variable size thromboemboli occlusion of ostia
    • CARDIOVASCULAR SYSTEMVariants: Inflammatory AAA dense periaortic fibrosis inflammatory cells (lymphos, plasma cells) Mycotic AAA AS AAA + bacteremia Salmonella gastroentritis
    • CARDIOVASCULAR SYSTEMComplications: Rupture Obstruction adjacent BV Embolism Compression adjacent structures Abdominal mass
    • CARDIOVASCULAR SYSTEMSYPHILITIC ANEURYSM: Leutic Obliterative endartritis vasa vasorum lymphocytes & plasma cells syphilitic aortitis
    • CARDIOVASCULAR SYSTEM weakening of media tree barking aortic valve insufficiency cor bovinum (cow’s heart)
    • CARDIOVASCULAR SYSTEMAORTIC DISSECTION “Dissection of blood between & along laminar planes of media”1. HTN  40-60 yrs males2. CT defects  young age3. Iatrogenic4. Pregnancy
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMMorphology: intimal tear 10 cm from aortic valve transverse / oblique sharp edges extension  dissecting hematoma
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEM rupture out  pericardial, pleural, peritoneal double barreled aorta cystic medial degeneration  cystic medial necrosisClassification:Type A: Proximal I IIType B: Distal
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMVASCULITIS:Inflammation of vessel wall. Infectious direct invasion immune mechanism Immune mediated
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMPATHOGENETIC CLASSIFICATION:Direct infection: Bacterial, Rickettsial, Spirochetal, Fungal, ViralImmunologic: immune complex mediated ANCA mediated Direct antibody mediated Cell mediatedUnknown
    • CARDIOVASCULAR SYSTEMCLASSIFICATION ACCORDING TO SIZE:Large vesselMedium sized vesselSmall vessel
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMTYPES: Granulomatous granuloma formation giant cells Necrotizing fibrinoid necrosis fibrous thickening of wall
    • CARDIOVASCULAR SYSTEMTUMORS OF BLOOD VESSELS:Vascular malformations HamartomasReactive vascular proliferations Bacillary angiomatosisBenign tumors:Blood/lymphatic filled channelsTransudateEndothelial lining without atypia
    • CARDIOVASCULAR SYSTEMMalignant tumors :More solid & cellularAtypia ++Mitotic figuresNo well formed vascular channels
    • CARDIOVASCULAR SYSTEMBenign: Hemangioma capillary cavernous pyogenic granuloma Lymphangioma simple cavernous
    • CARDIOVASCULAR SYSTEM Glomus tumor Vascular ectasias nevus flamus spider telangiectasia hereditary haemorrhagic telangiectasia reactive vascular proliferations bacillary angiomatosis
    • CARDIOVASCULAR SYSTEMIntermediate grade tumors: Kaposi sarcoma HemangioendotheliomaMalignant neoplasms: Angiosarcoma Hemangiopericytoma
    • CARDIOVASCULAR SYSTEMHEMANGIOMA: localized superficial head & neck internal angiomatosis7% of benign childhood tumors
    • CARDIOVASCULAR SYSTEMCapillary hemangioma:Gross: skin, sub-cutaneous tissue, mucus membranes liver, spleen, kidneys variable size bright red – blue elevated intact epithelium
    • CARDIOVASCULAR SYSTEM Histologically: lobulated unencapsulated closely packed thin walled capillaries flat endothelium scanty stroma thrombosed lumen
    • CARDIOVASCULAR SYSTEMStrawberry hemangioma newborns grows and regresses
    • CARDIOVASCULAR SYSTEMCavernous hemangioma: less common larger less well circumscribed deep structures locally destructive
    • CARDIOVASCULAR SYSTEMGross: red-blue spongy 1-2 cmHistologically: sharply defined not encapsulated large cavernous vascular spaces
    • CARDIOVASCULAR SYSTEM blood filled scanty stroma intravascular thrombosis dystrophic calcification
    • IOVCARDASCULAR SYSTEMGLOMUS TUMOR:BenignPainfulGlomus bodyDistal part of digitsSmall, elevated, roundRed-blue firm nodulesBranching vascular channelsAggregates/nests of glomus cells around BV
    • CARDIOVASCULAR SYSTEMKAPOSI’S SARCOMA:1. Chronic/Classic/European Kaposi in 1872 older men not associated with HIV homosexual men multiple red – purple skin plaques/nodules arms & legs
    • CARDIOVASCULAR SYSTEM gradual spread asymptomatic & localized visceral involvement 10%2. Lymphadenopathic/African/Endemic: Bantu children of SA lymphadenopathy aggressive
    • CARDIOVASCULAR SYSTEM3. Transplant associated/immunosuppression associated: months-years post transplant aggressive lymph node, mucosa, viscera internal involvement  fatal
    • CARDIOVASCULAR SYSTEM4. AIDS associated: 1/3rd AIDS patients wide disseminationMorphology:3 stages: Patch pink-red-purple single/multiple macules
    • CARDIOVASCULAR SYSTEM distal lower extremities dilated, irregular angulated BV endothelial cell lined lymphocytes, plasma cells, macrophages Plaques larger, violaceous raised dermal dilated vascular channels
    • CARDIOVASCULAR SYSTEM plump spindle cell lining perivascular aggregates of spindle cells red cells hemosiderin laden macrophages lymphocytes, plasma cells pink hyaline globules in spindle cells mitotic figures
    • CARDIOVASCULAR SYSTEM Nodules neoplastic sheets of plump spindle cells proliferate in dermis, sub-cutaneous tissue slit like spaces & small Bv hemosiderin , macrophages mitotic figures LN + viscera
    • CARDIOVASCULAR SYSTEMPathogenesis: HHV-8/KSHV  latent infection immunosuppression  ↓ apoptosis endothelial cells (p53)  ↑ cell proliferation
    • CARDIOVASCULAR SYSTEMDISEASES OF HEART:Mechanisms of Cardiac dysfunction:1. Pump failure2. Outflow obstruction3. Regurgitant flow4. Conduction defects5. Disruption of circulation
    • CARDIOVASCULAR SYSTEM Genetics  environment
    • CARDIOVASCULAR SYSTEMHEART FAILURE (Congestive heart failure):Forward failure (↓ CO) orBackward failure (venous damming) orBothMyocardial hypertrophy: permanent cells no hyperplasia hypertrophy
    • CARDIOVASCULAR SYSTEMCARDIAC HYPERTROPHY:Pressure overload hypertrophy concentric hypertrophy HTN, aortic stenosis thickened left vent wall  ↓ chamber sarcomere deposition parallel cross sectional area of myocyte ↑ not length
    • CARDIOVASCULAR SYSTEMVolume overload hypertrophy: ventricular dilation wall thickness  chamber diameter sarcomere deposition parallel & vertical ↑ thickness & length
    • CARDIOVASCULAR SYSTEM“ Structure of hypertrophied heart is not normal. It is a tight balance between adaptation and deleterious alterations ( ↓ capillary-to- myocyte ratio, ↑ fibrous tissue & synthesis of abnormal proteins). Thus sustained cardiac hypertrophy evolves into cardiac failure.”
    • CARDIOVASCULAR SYSTEMMolecular & cellular changes that initially mediate enhanced function later contributes to heart failure.Physiologic hypertrophy.Pathologic hypertrophy.
    • CARDIOVASCULAR SYSTEMLeft sided heart failure:Causes: IHD HTN Aortic, mitral valvular disease non ischemic MC disease
    • CARDIOVASCULAR SYSTEMMorphology: Evidence of cause enlarged size ↑ left vent wall thickness secondary effects on atria
    • CARDIOVASCULAR SYSTEMExtracardiac effects:1. Pulmonary congestion & edema heavy, wet lungs interstitial transudate  Kerly’s B lines widening of alveolar septa edema in alveolar spaces heart failure cells
    • CARDIOVASCULAR SYSTEM dyspnea orthopnea paroxysmal nocturnal dyspnea2. Kidneys ↓ renal perfusion pre renal azotemia
    • CARDIOVASCULAR SYSTEM3. Brain hypoxic encephalopathyRight sided heart failure:Causes left sided heart failure chronic severe pulmonary HTN (cor pulmonale)
    • CARDIOVASCULAR SYSTEMMorphology engorgement of systemic & portal venous systems1. Liver & portal system: congestive hepatomegaly centrilobular necrosis cardiac sclerosis / cardiac cirrhosis congestive splenomegaly
    • CARDIOVASCULAR SYSTEM2. Kidneys: severely affected pronounced azotemia3. Brain: venous congestion & hypoxia4. Pleural & pericardial space: effusions5. Subcutaneous tissues: edema (pedal) anasarca
    • CARDIOVASCULAR SYSTEMHeart disease: Congenital heart disease Ischemic heart disease Hypertensive heart disease Valvular heart disease Myocardial disease
    • CARDIOVASCULAR SYSTEMISCHEMIC HEART DISEASE (IHD):↓ oxygen supply↓ nutrient supply↓ removal of waste90% coronary atherosclerosis  CAD
    • CARDIOVASCULAR SYSTEM4 clinical manifestations of IHD:1. Myocardial Infarction2. Angina Pectoris3. Chronic IHD4. Sudden cardiac deathAcute Coronary Syndromes (1, 2, 4)
    • CARDIOVASCULAR SYSTEMLeading cause of death50% reduction in IHD related mortality in USA Prevention Early diagnosis (advanced facilities) Therapeutic intervention (effective, safer)
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMPATHOGENESIS: Demand  supply ↑↑  ↓↓ ↓ ISCHEMIA
    • CARDIOVASCULAR SYSTEMAS  obstruction  fixed / stable obstruction  plaque change ↓ ↓ ↓ ISCHEMIA75% obstruction  symptomatic on ↑ demand90% obstruction  symptomatic at rest
    • CARDIOVASCULAR SYSTEMRole of acute plaque change:Rupture/ulcerationErosion/fissuring  thrombosisHaemorrhageIntrinsic influences structure & composition of plaqueextrinsic influences blood pressure, Plt reactivity
    • CARDIOVASCULAR SYSTEMStructure of plaque Vulnerable plaque ↑ foam cells ↑ extracellular lipids thin fibrous caps few SMCs inflammatory cell clustersJunction of fibrous cap & adjacent endothelium
    • CARDIOVASCULAR SYSTEMCollagen deposition  degradationmetalloproteinases by macrophagesAdrenergic stimulation  systemic HTN & plt reactivity  stress on plaquesEarly morningEmotional stress
    • CARDIOVASCULAR SYSTEMRole of inflammation:All stages of ASMacrophages & T lymphocytesIL-1, IL-6, TNF, INF gMetalloproteinses  weaken plaqueInflammation destabilizes plaque
    • CARDIOVASCULAR SYSTEMRole of coronary thrombus:Partial / total  acute coronary syndromesMural branch thrombus  embolize MicroinfarctsRole of vasoconstriction:Potentiate plaque change
    • CARDIOVASCULAR SYSTEMANGINA PECTORIS:“A symptom complex of IHD cahracaterized by recurrent attacks of substernal/precordial chest discomfort caused by transient MC ischemia that falls short of inducing infarction.”
    • CARDIOVASCULAR SYSTEMTYPES:Stable / typicalUnstable / crescendoPrinzmetal / variant
    • CARDIOVASCULAR SYSTEMSTABLE ANGINA:Chronic stenosing atherosclerosis  ↓ coronary perfusion↑ demand  MC ischemiaTriggered by exercise, stressRelieved by rest, nitroglycerine
    • CARDIOVASCULAR SYSTEMUNSTABLE ANGINA:Progressively ↑ing frequencyAt restProlonged durationDisruption of stable atheroma  thrombosisEmbolization, vasospasm
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMPRINZMETAL ANGINA:UncommonEpisodicAt restCoronary vasospasmResponds to vasodilators
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMMYOCARDIAL INFARCTION: “Heart attack”Death of cardiac muscle due to ischemia.Transmural infarctionSubendocardial infarction
    • CARDIOVASCULAR SYSTEMTRANSMURAL SUBENDOCARDIALFull thickness of MC Inner 1/3rd or halfAS  plaque change  As  plaque change thrombosis thrombosis  recanalized Hypotension / shock on chronic stenosing ASLimited to area of supply Can extend beyond
    • CARDIOVASCULAR SYSTEMIncidence & risk factors:Any ageRisk factors of ASPathogenesis:Coronary artery occlusionAcute plaque change  thrombosis  VC ↑ size of thrombus  complete occlusion
    • CARDIOVASCULAR SYSTEM10% MI not associated with AS plaque change. Vasospasm Emboli (paradoxical emboli) Unexplained (vasculitis, Hg defects, amyloid)
    • CARDIOVASCULAR SYSTEMMyocardial response:BiochemicalFunctionalMorphological
    • CARDIOVASCULAR SYSTEM FEATURE TIMEATP depletion SecondsLoss of contractility < 2 minATP reduced to 50% 10 min 10% 40 minIrreversible cell injury 20 – 40 minMicrovascular injury > 1 hr
    • CARDIOVASCULAR SYSTEMEarly identificationReperfusion30 min reversible injuryMC ischemia  subendocardial zoneWavefront progression  transmuralNecrosis within 6 hrsGrossly visible after 12 hrs
    • CARDIOVASCULAR SYSTEMFactors influencing MI:1. Site, size, rate of development of AS2. Size of vascular bed3. Duration4. Mc demands5. Collateral circulation6. Coronary artery spasm7. BP, HR, cardiac rhythm
    • CARDIOVASCULAR SYSTEM Morphology: Left ventricle > right ventricle Rim of subendocardium preservedLAD 40 – 50% Ant wall left vent, apex, ant septumRCA 30 – 40% Inf-post wall lt vent, post septum, post right ventLCA 15 – 20% Lat wall left vent
    • CARDIOVASCULAR SYSTEMTIME GROSS MICROSCOPIC0 – ½ hr ----- myofibril relaxation, swelling of mitochondria½ - 4 hr ----- Wavy fibers4 – 12 h Occ dark mottling Coag necrosis, edema, hge12-24 h Dark mottling Necrosis, pyknosis,myocyte eosinophilia, contraction bands, neutrophils
    • CARDIOVASCULAR SYSTEM1 -3 days Mottling + yellow Loss of nuclei & striations, centre PMNs ++3 – 7 days Red border, Disintegration, phagocytosis yellow tan center7 – 10 Max yellow soft Phagocytosis ++, granulationdays center, red borders tissue at margins10-14 Red-gray Granulation tissue ++,days depressed collagen +2 – 8 wks Grey white scar ↑ collagen, ↓ cellularity> 2 month Complete scar Dense collagenous scar
    • 1 day MI showing contraction band
    • 1-2 days
    • 3-4 day
    • 1-2 wks
    • Healing infarct
    • CARDIOVASCULAR SYSTEMReperfusion injury/Myocardial stunning:Restoration of coronary flow  reperfusionIschemia  variable effects on MCReperfusion  salvage  damage  O2 free radicals  haemorrhage  apoptosis
    • CARDIOVASCULAR SYSTEMPersistence of biochemical & functional changesin reperfused MC  stunned MCCARDIAC ENZYMES:CPK (MM, MB, BB)ASTLDHTroponins
    • CARDIOVASCULAR SYSTEMComplication of MI:1. Contractile dysfunction  crdiogenic shock2. Arrhythmias3. MC rupture  cardiac rupture syndrome4. Pericarditis5. Right ventricular infarction6. Extension7. Mural thrombosis8. Ventricular aneurysm9. Papillary muscle dysfunction10. Progressive late heart failure
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEM
    • BE GENTLE WITH THE EARTH
    • CARDIOVASCULAR SYSTEMRHEUMATIC FEVER & HEART DISEASE“A multisystem inflammatory disease having anacute onset with underlying immunepathogenesis occurring few weeks after streptococcal pharyngitis.”Acute Rheumatic carditis  Rheumatic heart disease
    • CARDIOVASCULAR SYSTEMChildren (5-15 yrs)10 days – 6 weeksArthritis & carditisRelapsing courseChronic Rheumatic Carditis
    • CARDIOVASCULAR SYSTEMPATHOGENESIS: Group A Streptococcal throat infection ↓ Antibodies M component streptococci ↓ Cross react glycoprotein antigens Heart, joints, skin, brain
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMRF characterized by:Migratory polyarthritisCarditisSubcutaneous nodulesErythema marginatumSydenham chorea
    • CARDIOVASCULAR SYSTEM
    • CARDIOVASCULAR SYSTEMMORPHOLOGY:Acute RF  Focal inflammatory lesions Aschoff bodies swollen eosinophilic collagen T lymphocytes, plasma cells macrophages  Anitschkow cells abundant cytoplasm central round/oval nucleus central slender chromatin  caterpillar cells Aschoff giant cells
    • CARDIOVASCULAR SYSTEMPancarditis Bread & Butter Pericarditis Myocarditis  Perivascular Aschoff nodules Verrucae/vegetations on valves fibrinoid necrosis MacCallum Plaques (left atrium)
    • CARDIOVASCULAR SYSTEMChronic Rheumatic Heart Disease:Organization of acute inflammationLeaflet thickeningCommissural fusionThickened, short & fused cordae tendinaeProgressive fibrosisButtonhole deformityFish mouth appearance
    • CARDIOVASCULAR SYSTEMMitral stenosis: 99% cases due to RHD RHD  65% - 70 % alone with aortic valve 25%Atrial dilation  mural thrombosisPulmonary vascular changes
    • CARDIOVASCULAR SYSTEMINFECTIVE ENDOCARDITIS:Severe infection of endocardium and heart valvesVegetations (thrombotic debris & microorganisms)Clinical classification: Acute Subacute
    • CARDIOVASCULAR SYSTEM ACUTE IE SUBACUTE IEHealthy valves Diseased/prosthesisHighly virulent organisms Low virulenceAcute & severe Insidious50% mortality Recovery commonDestructive necrotizing Less destructive
    • CARDIOVASCULAR SYSTEMPATHOGENESIS:Valvular diseases (RHD, prolapse, degenerative calcific stenosis)Immune compromised statesAetiology: Strep viridans (50-60%)  defective valves Staph Aureus (10-20%)  healthy.defective I/V drug abusers
    • CARDIOVASCULAR SYSTEM HACEK group Staph epidermidis  prosthetic valve IE gram –ive bacilli fungi culture negative
    • CARDIOVASCULAR SYSTEMMORPHOLOGY:Bulky, Friable, Destructive vegetationsSingle/multipleFibrin & inflammatory cellsAortic & mitral valvesRing abscess
    • CARDIOVASCULAR SYSTEMFungal Endocarditis larger vegetationsSystemic emboli  Septic infarctsSIE  granulation tissue at baseLIBMAN-SACKS ENDOCARDITIS: Endocarditis of SLE
    • CARDIOVASCULAR SYSTEMDukes Diagnostic Criteria for IE:Pathologic: + cultures vegetation histology intracardiac abscessClinical:Major: + blood culture Echocardiographic findings, valvular defects
    • CARDIOVASCULAR SYSTEMMinor: predisposing heart lesion vascular lesions immunologic phenomena cultures echocardiographic
    • CARDIOVASCULAR SYSTEMCARDIOMYOPATHIES:Intrinsic disease of myocardium:MyocarditisImmunologicSystemic metabolicMuscular dystrophiesGenetic abnormalities
    • CARDIOVASCULAR SYSTEMHeart disease resulting from a primaryabnormality in the myocardium Cardiomyopathy Dilated cardiomyopathy (DCM) Hypertrophic cardiomyopathy (HCM) Restrictive cardiomyopathy (RCM)
    • CARDIOVASCULAR SYSTEMDCM HCM RCMCommonest 90% Least commonSystolic Diastolic Diastolicdysfunction dysfunction dysfunctionDilated heart obstructive CM Compliance ↓Hypertrophied Hypertrophy ++ NormalHypocontracting hypercontracting NormalHeavy, large, Banana-like -----flabby cavity left ventThin walls Thick septum++ ----------
    • CARDIOVASCULAR SYSTEMDilated No dilation -----Thrombosis Mural palque ------Hypertrophied Hypertrophy ++ ------cells/attenuated Myofiberdisarrayfibrosis Fibrosis Patchy/diffuse fibrosis +
    • CARDIOVASCULAR SYSTEMCauses:IdiopathicGenetic abnormalities in MC metabolismMyocarditisAlcoholPregnancy associatedGenetic influences
    • CARDIOVASCULAR SYSTEMDCM HCMGenetic(30-40%) 100% genetic ↓ Non genetic ↓ ↓ ↓ ↓Force generation ↓ force generation ↓ DCM phenotype HCM phenotype ↓ ↓ heart failure, sudden death, atrial fib, stroke
    • CARDIOVASCULAR SYSTEMMYOCARDITIS:Infections: Viruses (coxsackie, ECHO, influenza, HIV) Chlamydia Rickettsiae Bacteria Fungi Protozoa Helminths
    • CARDIOVASCULAR SYSTEMImmune mediated post viral post streptococcal (RF) SLE Drugs Transplant rejectionUnknown sarcoidosis giant cell myeloma
    • CARDIOVASCULAR SYSTEMMorphology:Hypertrophy, dilated, flabbyDiffuse/patchyMottledMural thrombiInterstitial inflammatory infiltrate (mononuclear)Focal necrosis
    • CARDIOVASCULAR SYSTEMHypersensitivty MC perivascular lymphocytesMacrophages, eosinophilsGiant cell myocarditis giant cells, lympho, eosplasma cells, macrophages
    • CARDIOVASCULAR SYSTEMPERICARDITIS:Acute Serous Fibrinous Purulent Haemorrhagic Caseous
    • CARDIOVASCULAR SYSTEMChronic: Adhesive mediatinopericarditis Constrictive pericarditisCAUSES:Infectious (viruses, bacteria, TB, fungi)Immunologic (RF, SLE, scleroderma, post MI,(dresslers syndrome) drugsMiscellaneous (MI, uremia, cardiac surgery, neoplasia, trauma, radiation)
    • CARDIOVASCULAR SYSTEMTUMORS OF HEART:Primary (rare)Secondary/metastatic (5% dying patients)Benign: Myxoma Fibroma Lipoma Papillary fibroelastoma RhabdomyomasMalignant: Angiosarcoma & other SAs
    • CARDIOVASCULAR SYSTEMMYXOMA:Commonest primary tumor90% in atria  Atrial MyxomaLeft : right = 4 : 1SingleNear fossa ovalis<1 – 10 cmSessile / pedunculated  wrecking ball effect embolize
    • CARDIOVASCULAR SYSTEMHard – soft gelatinousStellate cells (lepidic cells)Endothelial cellsSMCsUndifferentiated cellsMucopolysaccharide ground substance ++Endothelial covering
    • CARDIOVASCULAR SYSTEMHYPERTENSIVE HEART DISEASE (HHD)An adaptive responseSystemic HTN  left HHDPulmonary HTN  right HHDSystemic HHD:1. Left ventricular hypertrophy2. Evidence of HTN
    • CARDIOVASCULAR SYSTEMPressure overload = afterload  concentricHypertrophy↑ weightDefective diastolic fillingLeft atrial dilation↑ transverse diameter of myocyteVariation in cell sizeInterstitial fibrosis
    • CARDIOVASCULAR SYSTEMPulmonary HHD:COR PULMONALERight vent hypertrophy & dilationAcute/chronicMassive pulmonary embolism  acute PHHDProlonged pulmonary overload  chronic PHHD
    • CARDIOVASCULAR SYSTEMAcute: Ventricle dilated ++ NO HYPERTROPHY Ovoid shaped vent cavityChronic: hypertrophy
    • CARDIOVASCULAR SYSTEMCONGENITAL HEART DISEASE:Ventricular septal defectsAtrial septal defectsPulmonary stenosisPatent ductus arteriosisCoarctation of aortaAV septal defectsTransposition of great arteriesTruncus arteriosisTricuspid atresia
    • CARDIOVASCULAR SYSTEMTETROLOGY OF FALLOT:1. VSD2. Sub-pulmonary stenosis3. Overriding aorta over pulmonary stenosis4. Right ventricular hypertrophy
    • CARDIOVASCULAR SYSTEMHYPERTENSIVE VASCULAR DISEASE:HTN carries potential risk of cardiac hypertrophy  heart failure coronary artery disease  IHD CVAGeneticEnvironmental factors
    • CARDIOVASCULAR SYSTEMCAUSES:Essential HTNSecondary HTN: Renal AGN CRD polycystic disease renal artery stenosis renal vasculitis Renin producing tumors
    • CARDIOVASCULAR SYSTEM Endocrine: Adrenocortical hyperfunction exogenous hoemones pheochromocytoma acromegaly hypothyroidism hyperthyroidism pregnancy induced
    • CARDIOVASCULAR SYSTEM Cardiovascular: coarctation aorta polyartritis nodosa ↑ intravascular volume ↑ CO rigidity of aorta
    • CARDIOVASCULAR SYSTEM Neurologic: psychogenic ↑ intracranial pressure sleep apnea acute stress
    • CARDIOVASCULAR SYSTEMPATHOGENESIS: BP = CO x PR
    • The mediocre teacher tells. The good teacher explains.The superior teacher demonstrates. SYSTEM CARDIOVASCULAR The great teacher inspires. (William Arthur Ward)