cvs 2

CARDIOVASCULAR SYSTEMDr. Atifa Shuaib

Associate Professor of Pathology

Rawalpindi Medical College

CARDIOVASCULAR SYSTEM

Diseases of Blood vessels

Diseases of Heart

Diseases of blood vessels

Congenital anomalies

Arteriosclerosis

Hypertensive vascular disease

Aneurysms & Dissections

Vasculitis

Tumors


ARTERIOSCLEROSIS:

Atherosclerosis

Monckeberg medial calcific sclerosis

Arteriolosclerosis


Fatty streaks Aortas of children

Risk factors Atheroma in adults

↓ ↓

Ischaemic Heart Disease


ATHEROSCLEROSIS


RISK FACTORS:

Non Modifiable

Modifiable


NONMODIFIABLE:Age:

advancing ageSex:

males > femalespostmenopausal risk equal

Genetics:familial predisposition


MODIFIABLE:

Hyperlipidemia:

hypercholesterolemia

LDL (bad cholesterol)

HDL (good cholesterol)

↓ by exercise

↑ by obesity & smoking


Diet

↑ cholesterol egg yolk, butter, animal fat

↓ cholesterol omega 3 FA

Statins ↓ cholesterol


Hypertension:>169/95 mm Hg 5 fold ↑ risk

Smoking:200% ↑ death rate

Diabetes Mellitis:hypercholesterolemiatwice ↑ risk MIgangrene lower limbs (200% risk)


Others:homocystinuriainflammationlipoprotein a (Lp a)lack of exercisestressful lifetype A personalityobesity


Multiple 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).

PATHOGENESIS:

“response to injury hypothesis”

A disease of intima

Chronic inflammation of arterial wall in

response to injury to endothelium


Chronic endothelial injury activation Accumulation of lpoproteins (LDL) Oxidation of LP Monocyte migration macrophage

accumulation Foam cells


Platelet adhesion Chemical mediator release Smooth muscle cells migration SMCs proliferation ECM deposition Lipid accumulation


1. Endothelial injury (repetitive):endothelial dysfunction ? injuryrepetetive non denudingtoxins, chemical mediators, infectionshemodynamic disturbance sites of ostia and bifurcationposterior wall of abdominal aortahypercholesterolemia


2. Inflammation (chronic):initiation - complicationsendothelial cell adhesion moleculesVCAM-1monocyte adhesion & migrationmacrophage accumulation in intimafoam cell formationIL-1, TNFMCP-1


Macrophages toxic oxygen species oxidation of lipids GF smooth muscle cell proliferationT lymphocytes cellular & humoral

3. Lipids:cholesterol & its esters in atheromasOxidized LDL in macrophages


genetic defects hypercholesterolemia AS

MI at young age with ↑ cholesterol

DM, hypothyroidism ↑ cholesterolAS

high cholesterol diet AS

severity of AS levels of cholesterol

↓ing cholesterol levels risk of AS ↓


Mechanism :1. Chronic hyperlipidemia EC activation2. Chronic hyperlipidemia LP accumulate in intima3. Oxidized LDL macrophages foam cells

monocyte accumulation GF, cytokine release Ecs, SMCs cytotoxicity


4. Smooth muscle cells:SMCs migration proliferation & ECM deposition

↓Fatty streak fibrofatty atheromatous plaquePDGF, TGF-a, FGFFoam cellsECM (collagen) depositedSMCs apoptosis


MORPHOLOGY:

Fatty streak:

children aortas

coronaries in adolescents

multiple, flat yellow dots

coalesce to streaks

lipid laden foam cells


FATTY STREAK

Atheromatous plaque:elastic & muscular arterieslower abdominal aorta > thoracic aortaostia and branchessymptomatic AS disease

MI heart attackcerebral infarction strokeperipheral vascular gangrene


aorta > coronaries > popliteal > internal carotid > circle of willis

white – white yellow

variable size

eccentric lesions

obstruction of lumen


Mild, Moderate, Severe AS

Components:

1. Cells:

SMCs

macrophages

T lymphocytes

other leukocytes


2. ECM:

collagen

elastic fibers

proteoglycans

3. lipids:

intracellular

extracellular


Plaque change:enlargementulceration/erosionrupturethrombosisembolismhaemorrhagecalcificationaneurysmal dilation


ARTEIOLOSCLEROSIS:Small Bv, arterioles

Hyaline homogenous pink hyaline thickeningnarrowed lumenelderlyHypertensionBenign nephrosclerosis


microangiopathy of DM

Hyperplastic:

malignant HTN

onion skin

concentric, laminated thickening

SMCs & thickened BM

necrotizing arteriolitis


ANEURYSM:

Localized abnormal dilation of a blood vessel or

heart.

True aneurysm

all layers of Bv or heart

False aneurysm (pseudoaneurysm)

extravascular hematoma


Causes:AtherosclerosisCystic medial degenerationTrauma (A-V aneurysms)Congenital defects (berry aneurysms)Infections (mycotic)Vasculitis


Types:SaccularFusiform

Sites:Abdominal aortacommon iliac AArch of aortadescending thoracic aorta


Mycotic aneurysm:

septic embolus

direct extension

bacteraemia


ABDOMINAL AORTIC ANEURYSMS(AAA):Atherosclerosis> 50 yrs> malesgenetic susceptibility ↓ connective tissue

strengthMMP TIMPHTN


Morphology:

B/W bifurcation & renal arteries

saccular/fusiform

variable size

thromboemboli

occlusion of ostia


Variants:

Inflammatory AAA

dense periaortic fibrosis

inflammatory cells (lymphos, plasma cells)

Mycotic AAA

AS AAA + bacteremia

Salmonella gastroentritis


Complications:

Rupture

Obstruction adjacent BV

Embolism

Compression adjacent structures

Abdominal mass


SYPHILITIC ANEURYSM:

Leutic

Obliterative endartritis

vasa vasorum

lymphocytes & plasma cells

syphilitic aortitis


weakening of media

tree barking

aortic valve insufficiency

cor bovinum (cow’s heart)


AORTIC DISSECTION

“Dissection of blood between & along laminar planes of media”

1. HTN 40-60 yrs males

2. CT defects young age

3. Iatrogenic

4. Pregnancy


Morphology:

intimal tear

10 cm from aortic valve

transverse / oblique

sharp edges

extension

dissecting hematoma


rupture out pericardial, pleural, peritonealdouble barreled aortacystic medial degeneration cystic medial necrosis

Classification:Type A: Proximal

III

Type B: Distal


VASCULITIS:

Inflammation of vessel wall.

Infectious

direct invasion

immune mechanism

Immune mediated


PATHOGENETIC CLASSIFICATION:Direct infection:

Bacterial, Rickettsial, Spirochetal, Fungal, ViralImmunologic:

immune complex mediatedANCA mediatedDirect antibody mediatedCell mediated

Unknown


CLASSIFICATION ACCORDING TO SIZE:

Large vessel

Medium sized vessel

Small vessel


TYPES:

Granulomatous

granuloma formation

giant cells

Necrotizing

fibrinoid necrosis

fibrous thickening of wall


TUMORS OF BLOOD VESSELS:Vascular malformations

HamartomasReactive vascular proliferations

Bacillary angiomatosisBenign tumors:Blood/lymphatic filled channelsTransudateEndothelial lining without atypia


Malignant tumors :

More solid & cellular

Atypia ++

Mitotic figures

No well formed vascular channels


Benign:Hemangioma

capillarycavernouspyogenic granuloma

Lymphangiomasimplecavernous


Glomus tumor

Vascular ectasias

nevus flamus

spider telangiectasia

hereditary haemorrhagic telangiectasia

reactive vascular proliferations

bacillary angiomatosis


Intermediate grade tumors:

Kaposi sarcoma

Hemangioendothelioma

Malignant neoplasms:

Angiosarcoma

Hemangiopericytoma


HEMANGIOMA:

localized

superficial

head & neck

internal

angiomatosis

7% of benign childhood tumors


Capillary hemangioma:Gross:

skin, sub-cutaneous tissue, mucus membranesliver, spleen, kidneysvariable sizebright red – blueelevatedintact epithelium


Histologically:lobulatedunencapsulatedclosely packedthin walled capillariesflat endotheliumscanty stromathrombosed lumen


Strawberry hemangioma

newborns

grows and regresses


Cavernous hemangioma:

less common

larger

less well circumscribed

deep structures

locally destructive


Gross:red-bluespongy1-2 cm

Histologically:sharply definednot encapsulatedlarge cavernous vascular spaces


blood filled

scanty stroma

intravascular thrombosis

dystrophic calcification


GLOMUS TUMOR:Benign PainfulGlomus bodyDistal part of digitsSmall, elevated, roundRed-blue firm nodulesBranching vascular channelsAggregates/nests of glomus cells around BV

IOVCARDASCULAR SYSTEM

KAPOSI’S SARCOMA:1. Chronic/Classic/European

Kaposi in 1872older mennot associated with HIVhomosexual menmultiple red – purple skin plaques/nodulesarms & legs


gradual spread

asymptomatic & localized

visceral involvement 10%

2. Lymphadenopathic/African/Endemic:

Bantu children of SA

lymphadenopathy

aggressive


3. Transplant associated/immunosuppression associated:

months-years post transplant

aggressive

lymph node, mucosa, viscera

internal involvement fatal


4. AIDS associated:1/3rd AIDS patientswide dissemination

Morphology:3 stages: Patch

pink-red-purplesingle/multiple macules


distal lower extremitiesdilated, irregular angulated BVendothelial cell linedlymphocytes, plasma cells, macrophages

Plaqueslarger, violaceousraiseddermal dilated vascular channels


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


Nodulesneoplasticsheets of plump spindle cellsproliferate in dermis, sub-cutaneous tissueslit like spaces & small Bvhemosiderin , macrophagesmitotic figuresLN + viscera


Pathogenesis:

HHV-8/KSHV latent infection

immunosuppression ↓ apoptosis endothelial cells (p53)

↑ cell proliferation


DISEASES OF HEART:

Mechanisms of Cardiac dysfunction:

1. Pump failure

2. Outflow obstruction

3. Regurgitant flow

4. Conduction defects

5. Disruption of circulation


Genetics environment


HEART FAILURE (Congestive heart failure):Forward failure (↓ CO) orBackward failure (venous damming) orBothMyocardial hypertrophy:

permanent cellsno hyperplasiahypertrophy


CARDIAC HYPERTROPHY:

Pressure overload hypertrophy

concentric hypertrophy

HTN, aortic stenosis

thickened left vent wall ↓ chamber

sarcomere deposition parallel

cross sectional area of myocyte ↑ not length


Volume overload hypertrophy:

ventricular dilation

wall thickness chamber diameter

sarcomere deposition parallel & vertical

↑ thickness & length


“ 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.”


Molecular & cellular changes that initially mediate enhanced function later contributes to heart failure.

Physiologic hypertrophy.

Pathologic hypertrophy.


Left sided heart failure:

Causes:

IHD

HTN

Aortic, mitral valvular disease

non ischemic MC disease


Morphology:

Evidence of cause

enlarged size

↑ left vent wall thickness

secondary effects on atria


Extracardiac 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


dyspnea

orthopnea

paroxysmal nocturnal dyspnea

2. Kidneys

↓ renal perfusion

pre renal azotemia


3. Brainhypoxic encephalopathy

Right sided heart failure:Causes

left sided heart failurechronic severe pulmonary HTN

(cor pulmonale)


Morphologyengorgement of systemic & portal venous systems

1. Liver & portal system:congestive hepatomegalycentrilobular necrosiscardiac sclerosis / cardiac cirrhosiscongestive splenomegaly


2. Kidneys:severely affectedpronounced azotemia

3. Brain:venous congestion & hypoxia

4. Pleural & pericardial space:effusions

5. Subcutaneous tissues:edema (pedal)anasarca


Heart disease:

Congenital heart disease

Ischemic heart disease

Hypertensive heart disease

Valvular heart disease

Myocardial disease


ISCHEMIC HEART DISEASE (IHD):

↓ oxygen supply

↓ nutrient supply

↓ removal of waste

90% coronary atherosclerosis CAD


4 clinical manifestations of IHD:

1. Myocardial Infarction

2. Angina Pectoris

3. Chronic IHD

4. Sudden cardiac death

Acute Coronary Syndromes (1, 2, 4)


Leading cause of death

50% reduction in IHD related mortality in USA

Prevention

Early diagnosis (advanced facilities)

Therapeutic intervention (effective, safer)


PATHOGENESIS:

Demand supply

↑↑ ↓↓

↓ ISCHEMIA


AS obstruction fixed / stable obstruction

plaque change ↓

↓ ↓

ISCHEMIA

75% obstruction symptomatic on ↑ demand

90% obstruction symptomatic at rest


Role of acute plaque change:Rupture/ulcerationErosion/fissuring thrombosisHaemorrhageIntrinsic influences

structure & composition of plaqueextrinsic influences

blood pressure, Plt reactivity


Structure of plaqueVulnerable plaque

↑ foam cells↑ extracellular lipidsthin fibrous capsfew SMCsinflammatory cell clusters

Junction of fibrous cap & adjacent endothelium


Collagen deposition degradationmetalloproteinases by macrophages

Adrenergic stimulation systemic HTN & plt reactivity stress on plaques

Early morningEmotional stress


Role of inflammation:

All stages of AS

Macrophages & T lymphocytes

IL-1, IL-6, TNF, INF g

Metalloproteinses weaken plaque

Inflammation destabilizes plaque


Role of coronary thrombus:

Partial / total acute coronary syndromes

Mural branch thrombus embolize

Microinfarcts

Role of vasoconstriction:

Potentiate plaque change


ANGINA 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.”


TYPES:

Stable / typical

Unstable / crescendo

Prinzmetal / variant


STABLE ANGINA:

Chronic stenosing atherosclerosis ↓ coronary perfusion

↑ demand MC ischemia

Triggered by exercise, stress

Relieved by rest, nitroglycerine


UNSTABLE ANGINA:

Progressively ↑ing frequency

At rest

Prolonged duration

Disruption of stable atheroma thrombosis

Embolization, vasospasm


PRINZMETAL ANGINA:

Uncommon

Episodic

At rest

Coronary vasospasm

Responds to vasodilators


MYOCARDIAL INFARCTION:

“Heart attack”

Death of cardiac muscle due to ischemia.

Transmural infarction

Subendocardial infarction


CARDIOVASCULAR SYSTEMTRANSMURAL SUBENDOCARDIAL

Full thickness of MC Inner 1/3rd or half

AS plaque change thrombosis

As plaque change thrombosis recanalized

Hypotension / shock on chronic stenosing AS

Limited to area of supply Can extend beyond

Incidence & risk factors:

Any age

Risk factors of AS

Pathogenesis:

Coronary artery occlusion

Acute plaque change thrombosis VC

↑ size of thrombus complete occlusion


10% MI not associated with AS plaque change. Vasospasm Emboli (paradoxical emboli) Unexplained (vasculitis, Hg defects, amyloid)


Myocardial response:

Biochemical

Functional

Morphological


CARDIOVASCULAR SYSTEM FEATURE TIME

ATP depletion Seconds

Loss of contractility < 2 min

ATP reduced to 50%

10%

10 min

40 min

Irreversible cell injury 20 – 40 min

Microvascular injury > 1 hr

Early identificationReperfusion

30 min reversible injuryMC ischemia subendocardial zoneWavefront progression transmural Necrosis within 6 hrsGrossly visible after 12 hrs


Factors 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 SYSTEMMorphology:

Left ventricle > right ventricle

Rim of subendocardium preserved

LAD 40 – 50% Ant wall left vent, apex, ant septum

RCA 30 – 40% Inf-post wall lt vent, post septum, post right vent

LCA 15 – 20% Lat wall left vent

CARDIOVASCULAR SYSTEMTIME GROSS MICROSCOPIC

0 – ½ hr ----- myofibril relaxation, swelling of mitochondria

½ - 4 hr ----- Wavy fibers

4 – 12 h Occ dark mottling Coag necrosis, edema, hge

12-24 h Dark mottling Necrosis, pyknosis,myocyte eosinophilia, contraction bands, neutrophils

CARDIOVASCULAR SYSTEM1 -3 days Mottling + yellow

centreLoss of nuclei & striations, PMNs ++

3 – 7 days Red border, yellow tan center

Disintegration, phagocytosis

7 – 10 days

Max yellow soft center, red borders

Phagocytosis ++, granulation tissue at margins

10-14 days

Red-gray depressed

Granulation tissue ++, 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

Reperfusion injury/Myocardial stunning:

Restoration of coronary flow reperfusion

Ischemia variable effects on MC

Reperfusion salvage

damage O2 free radicals

haemorrhage

apoptosis


Persistence of biochemical & functional changes

in reperfused MC stunned MC

CARDIAC ENZYMES:

CPK (MM, MB, BB)

AST

LDH

Troponins


Complication 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


BE GENTLE WITH THE EARTH

RHEUMATIC FEVER & HEART DISEASE

“A multisystem inflammatory disease having an

acute onset with underlying immune

pathogenesis occurring few weeks after streptococcal pharyngitis.”

Acute Rheumatic carditis Rheumatic heart disease


Children (5-15 yrs)

10 days – 6 weeks

Arthritis & carditis

Relapsing course

Chronic Rheumatic Carditis


PATHOGENESIS:

Group A Streptococcal throat infection

↓

Antibodies M component streptococci

↓

Cross react glycoprotein antigens

Heart, joints, skin, brain


RF characterized by:

Migratory polyarthritis

Carditis

Subcutaneous nodules

Erythema marginatum

Sydenham chorea


MORPHOLOGY:Acute RF Focal inflammatory lesions Aschoff bodies

swollen eosinophilic collagenT lymphocytes, plasma cellsmacrophages Anitschkow cells

abundant cytoplasmcentral round/oval nucleuscentral slender chromatin caterpillar cellsAschoff giant cells


Pancarditis

Bread & Butter Pericarditis

Myocarditis Perivascular Aschoff nodules

Verrucae/vegetations on valves

fibrinoid necrosis

MacCallum Plaques (left atrium)


Chronic Rheumatic Heart Disease:Organization of acute inflammationLeaflet thickeningCommissural fusionThickened, short & fused cordae tendinaeProgressive fibrosisButtonhole deformityFish mouth appearance


Mitral stenosis:

99% cases due to RHD

RHD 65% - 70 % alone

with aortic valve 25%

Atrial dilation mural thrombosis

Pulmonary vascular changes


INFECTIVE ENDOCARDITIS:Severe infection of endocardium and heart

valvesVegetations (thrombotic debris &

microorganisms)Clinical classification:

AcuteSubacute


CARDIOVASCULAR SYSTEM ACUTE IE SUBACUTE IE

Healthy valves Diseased/prosthesis

Highly virulent organisms Low virulence

Acute & severe Insidious

50% mortality Recovery common

Destructive necrotizing Less destructive

PATHOGENESIS:Valvular diseases (RHD, prolapse, degenerative

calcific stenosis)Immune compromised statesAetiology:

Strep viridans (50-60%) defective valvesStaph Aureus (10-20%) healthy.defective

I/V drug abusers


HACEK group

Staph epidermidis prosthetic valve IE

gram –ive bacilli

fungi

culture negative


MORPHOLOGY:

Bulky, Friable, Destructive vegetations

Single/multiple

Fibrin & inflammatory cells

Aortic & mitral valves

Ring abscess


Fungal Endocarditis

larger vegetations

Systemic emboli Septic infarcts

SIE granulation tissue at base

LIBMAN-SACKS ENDOCARDITIS:

Endocarditis of SLE


Dukes Diagnostic Criteria for IE:Pathologic:

+ culturesvegetation histologyintracardiac abscess

Clinical:Major:

+ blood cultureEchocardiographic findings, valvular defects


Minor:

predisposing heart lesion

vascular lesions

immunologic phenomena

cultures

echocardiographic


CARDIOMYOPATHIES:

Intrinsic disease of myocardium:

Myocarditis

Immunologic

Systemic metabolic

Muscular dystrophies

Genetic abnormalities


Heart disease resulting from a primary

abnormality in the myocardium Cardiomyopathy

Dilated cardiomyopathy (DCM) Hypertrophic cardiomyopathy (HCM) Restrictive cardiomyopathy (RCM)


CARDIOVASCULAR SYSTEMDCM HCM RCM

Commonest 90% Least common

Systolic dysfunction

Diastolic dysfunction

Diastolic dysfunction

Dilated heart obstructive CM Compliance ↓

Hypertrophied Hypertrophy ++ Normal

Hypocontracting hypercontracting Normal

Heavy, large, flabby

Banana-like cavity left vent

-----

Thin walls Thick septum++ ----------


Dilated No dilation -----

Thrombosis Mural palque ------

Hypertrophied cells/attenuated

Hypertrophy ++

Myofiberdisarray

------

fibrosis Fibrosis Patchy/diffuse fibrosis +

Causes:

Idiopathic

Genetic abnormalities in MC metabolism

Myocarditis

Alcohol

Pregnancy associated

Genetic influences


DCM HCMGenetic(30-40%) 100% genetic

↓ Non genetic ↓↓ ↓ ↓

Force generation ↓ force generation ↓ DCM phenotype HCM phenotype

↓ ↓heart failure, sudden death, atrial fib, stroke


MYOCARDITIS:Infections:

Viruses (coxsackie, ECHO, influenza, HIV)ChlamydiaRickettsiaeBacteriaFungiProtozoaHelminths


Immune mediatedpost viralpost streptococcal (RF)SLEDrugsTransplant rejection

Unknownsarcoidosisgiant cell myeloma


Morphology:

Hypertrophy, dilated, flabby

Diffuse/patchy

Mottled

Mural thrombi

Interstitial inflammatory infiltrate (mononuclear)

Focal necrosis


Hypersensitivty MC perivascular lymphocytes

Macrophages, eosinophils

Giant cell myocarditis giant cells, lympho, eos

plasma cells, macrophages


PERICARDITIS:

Acute

Serous

Fibrinous

Purulent

Haemorrhagic

Caseous


Chronic:Adhesive mediatinopericarditisConstrictive pericarditis

CAUSES:Infectious (viruses, bacteria, TB, fungi)Immunologic (RF, SLE, scleroderma, post MI,(dresslers syndrome) drugsMiscellaneous (MI, uremia, cardiac surgery, neoplasia,

trauma, radiation)


TUMORS OF HEART:Primary (rare)Secondary/metastatic (5% dying patients)Benign:

MyxomaFibromaLipomaPapillary fibroelastomaRhabdomyomas

Malignant:Angiosarcoma & other SAs


MYXOMA:Commonest primary tumor90% in atria Atrial MyxomaLeft : right = 4 : 1SingleNear fossa ovalis<1 – 10 cmSessile / pedunculated wrecking ball effect embolize


Hard – soft gelatinous

Stellate cells (lepidic cells)

Endothelial cells

SMCs

Undifferentiated cells

Mucopolysaccharide ground substance ++

Endothelial covering


HYPERTENSIVE HEART DISEASE (HHD)

An adaptive response

Systemic HTN left HHD

Pulmonary HTN right HHD

Systemic HHD:

1. Left ventricular hypertrophy

2. Evidence of HTN


Pressure overload = afterload concentricHypertrophy↑ weightDefective diastolic fillingLeft atrial dilation↑ transverse diameter of myocyteVariation in cell sizeInterstitial fibrosis


Pulmonary HHD:

COR PULMONALE

Right vent hypertrophy & dilation

Acute/chronic

Massive pulmonary embolism acute PHHD

Prolonged pulmonary overload chronic PHHD


Acute:

Ventricle dilated ++

NO HYPERTROPHY

Ovoid shaped vent cavity

Chronic:

hypertrophy


CONGENITAL HEART DISEASE:Ventricular septal defectsAtrial septal defectsPulmonary stenosisPatent ductus arteriosisCoarctation of aortaAV septal defectsTransposition of great arteriesTruncus arteriosisTricuspid atresia


TETROLOGY OF FALLOT:

1. VSD

2. Sub-pulmonary stenosis

3. Overriding aorta over pulmonary stenosis

4. Right ventricular hypertrophy


HYPERTENSIVE VASCULAR DISEASE:

HTN carries potential risk of

cardiac hypertrophy heart failure

coronary artery disease IHD

CVA

Genetic

Environmental factors


CAUSES:Essential HTNSecondary HTN:

RenalAGNCRDpolycystic diseaserenal artery stenosisrenal vasculitisRenin producing tumors


Endocrine:Adrenocortical hyperfunctionexogenous hoemonespheochromocytomaacromegalyhypothyroidismhyperthyroidismpregnancy induced


Cardiovascular:

coarctation aorta

polyartritis nodosa

↑ intravascular volume

↑ CO

rigidity of aorta


Neurologic:

psychogenic

↑ intracranial pressure

sleep apnea

acute stress


PATHOGENESIS:

BP = CO x PR


CARDIOVASCULAR SYSTEMThe mediocre teacher tells.The good teacher explains.

The superior teacher demonstrates.The great teacher inspires.

(William Arthur Ward)

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