Cvs Flashcards
Diseases of blood vessels
- Congenital anomalies:
Development or berry aneurisms
Arteriovenous fistula
2.arterioschlerosis
3.atgeroschlerosis - Hypertensive vascular disease
- Aneurisms and dissections
- Diseases of veins: thrombophlebitis, varicose veins
- Diseases of lymphatics: lymphangitis, lymphedema
- Inflammatory disease: vasculitis
- Tumors or tumor like conditions
Tumors of blood vessels
A. Benign tumor
1. Hemangioma
. Capillary hemangioma
.cavernous hemangioma
.pyogenic granuloma
2.lymphangioma
.simple lymphangioma
.cavernous lymphangioma
3.glomus tumor/ glomangioma
4. Vascular ectasias
.nevus flameus
.spider telangectasias
.heriditary hemorrhagic telangectasia
5. Reactive vascular proliferations- bacillary angiomatosis
B. Intermediate grade tumor
1.kaposi sarcoma
2. Hemangioendothemioma
C. Malignant tumor
.angiosarcoma
.hemangiopericytoma
Arterioschlerosis
It is the genetic term for thickening and loss of elasticity of arterial walls
1.atheroschlerosis
2. Monckeberg medial calcific schlerosis
3. Arterioschlerosis
Atheroschlerosis
It is a pattern of vascular disease which is characterised by initial lesions called atheromas or atheromatous or fibrofatty plaques which protrude into and obstruct vascular lumens and weaken the underlying media
Sites of atheroschlerosis
In decending order
Lower abdominal aorta
Coronary artery
Popliteal artery
Internal carotid arteries
Vessels of the circle of willis
Type of artery: large / medium sized artery
Risk factors fir atheroschlerosis
Major risk factors
1.non modifyable
Increasing age
Male gender
Family history
Genetic abnormality
2.modifyable
Hyperlipidemia
Hypertension
Smoking
Diabetes
Minor risk factors
1.obesity
2.physical inactivity
3.stress
4. Lipoprotein A
5. Alcohol
6. Post menopausal estrogen deficiency
7.high carb diet
8. Hardened saturated fat intake
9. Hyperchromocystineuria
10.homocystinuria
11.metabolic syndrome
12.inflammation
13.chlamydia pneumoniae
Complications of atheroschlerosis
A. Advanced lesions undergo pathological changes
1.. Focal rupture and ulceration or erosion of intimal surface of atheromatous plaques
. Exposes the blood to highly thrombotic substances
. Thrombus formation
. Thrombus can partially or completely occlude the lumen
. Causing ischemia
2.hemorrage into the plaque due to rupture of the overlying fibrous cap or thin walled vessels in area of neovacularization. A contained hematoma may expand the plaque or induce plaque rupture
3. Atheroembolism
Plaques rupture and discharge atheroschlerotic debris into blood stream producing microemboli
4. Aneurismal dilatation
Results from atheroschlerosis induced pressure or ischemic atrophy of underlying media which causes loss of elastic tissue and weakens it causing rupture
5.other changes include:
Atheroschlerotic stenosis
Acute plaque change
Thombosis
Vasoconstriction
6. Calcification
Consequences of atheroschlerosis
Major consequences
1. Ischemic bowel disease and infarction
2.MI
3. Aortic aneurism
4.cerebral infarction
5.peripheral vascular disease
Consequences due to atheroschlerotic stenosis
1. Sudden cardiac death
2.mesenteric occlusion and bowel ischaemia
3. Chronic IHD
4. Ischemic encephalopathy
5. Intermittent claudication
Consequences due to acute plaque change
1.plaque rupture
2.plaque erosion/ ulceration
3.plaque hemorrhage
4.thrombus formation
5. Embolization
Atheroma
Atheroma or atheromatous plaque consists of a raised focal lesion initiating within the intima having a soft yellow grumous core of lipid covered by a firm white fibrous cap
0.3 - 1.5 cm in diameter
Components of atheroma
- Cells: smooth muscle cells, mq, other leucocytes, t lymphocytes
- Extracellular matrix; collagen fibres, elastic fibres, proteoglycan
- Intracellular and extracellular lipid: mostly cholesterol and cholesterol esters
Atheroma morphology
Microscopic:
Contains cells , extracellular matrix and intra and extracellular lipid
Macroscopically:
colour: yellow tan
Shape; eccentric/patchy
Size: variable
1. Superficial fibrous cap composed of smooth muscle cells and dense ecm
2. Beneath and sides: cellular area composed of mq, smooth muscle cells and t lymphocytes
3.necrotic core: comprising of
.disorganised mass of lipid
.left debris from dead cells
.foam cells
. Fibrin
. Other plasma proteins
. Thrombus in varying degrees of organization
In the periphery there is evidence of neovascularization
Complications of atheroma
- Focal rupture and ulceration of intimal surf of atheromatous plaques causing thromus formation and downward ischemia
- Hemorrhage into the plaque
3.atheroembolism
4.aneurismal dilatation
5.other changes( AATV) - CALCIFICATION
Hypertension
It is a complex multifactorial disease that has both genetic and environmental determinants characterized by sustained diastolic pressure >89mm hg or
Sustained systolic pressure >139 mm of hg
Types: 1.essential or primary htn
2. Secondary htn
Complications of htn
1.Increased risk of atheroschlerosis
2. Cardiac hypertrophy or heart failure
3. MI
4. Stroke
5. Sudden cardiac death
6. Renal failure
7. Hypertensive retinopathy
8. Hypertensive encephalopathy
What are the lipoproteins
Lipoprotein
Chylomicrons
Vldl
Ldl
Hdl
Lipid profile
The determination of concentration of the four major lipids of clinical importance grouped into test order is called lipid profile
1. Total cholesterol: normal upto 200 mg/dl
2. Hdl:
male:> 37mg /dl
Femlale: >40 mg/dl
High risk: <7-15 mg/dl
Damage: <7 mg /dl
3.ldl:
Normal: <130mg/dl
Risk : >130-159mg/dl
High risk: > 160mg/dl
- Triglyceride:
Normal 40-160 mg/dl in males
35-135mg /dl in females
Indications of lipid profile
Htn
Hyper and hypothyroidism
Ischemic heart disease
Diabetes mellitus
Dyslipidemia
Cerebrovascular disease
Dyslipidemia causes
- Primary cause:
Def in lipoprotein lipase activity
Familial combined hyperlipidemia
Familial hypertriglyceremia
Familial hypercholesterolemia
2.secondary causes
a.Exogenous; drugs like coticosteroids and beta blockers, alcohol, obesity
b.endocrine and metabolic :
DM, hypopituitarism, hypothyroidism
c. Strorage disease like glycogen storage disease, neimann pick disease
d. Chronic renal disease , nephrotic syndrome
E. Hepatitis
F. Burns
G. MI
Causes of hypercholestrolinemia
Nephrotic syndrome
Myxoedema
Obstructive jaundice
DM
Primary biliary corrhosis
Hypopituitarism
Chr glomerulonephritis
Causes of hyperglyceridemia
Obesity
DM
Type 1 glycogen storage diasease
Alcoholism
Nephrotic synd
Hypothyroidism
Hypoalbuminemia
Diseases of the heart
A. Congenital heart disease
1.malformations causing left to right shunt
Atrial septal defect
Ventricular septal defect
Atrio ventricular septal defect
Patent ductus arteriosis
Patent foramen ovale
2. Malformation causing rt to left shunt
Fallots tetrology(vsd, aorta overriding vsd,obs of rt ventricular outflow tract, rt ventricular hypertrophy)
Transposition of great vessels
Tricuspid atresia
3. Obstructive lesions
Coarctation of aorta
Pulmonary stenosis and atresia
Aortic stenosis and atresia
B. Acquired heart diseases
1. Ihd
2.hypertensive heart disease
Systemic and pulmonary
3. Valvular heart disease
Aortic stenosis
Aortic regurgitation
Mitral stenosis
Mitral regurgitation
4. Cardiomyopathies
Hypertrophic
Arrhythmogenic
Restrictive
Dilated
5. Pericardial diseases
Pericarditis
Pericardial effusion
7. Arrhythmia
8.heart failure
9. Tumors
Tumors of the heart
A. Primary cardiac tumors
1.benign: myxoma, fibroma, lipoma, pappilary fibroelastoma, rhabdomyoma
2.malignant: sarcoma eg angiosarcoma
B. Secondary or metastatic neoplasms
1.from lung and breast carcinomas
Also from melanomas leukemias and lymphomas
Ischemic heart disease
It represents a group of pathophysiologically related syndromes resulting from an imbalance between myocardial supply and cardiac demand of the heart for oxygenated blood
Classify ihd
Angina pectoris
MI
Chr ihd with heart failure
Sudden cardiac death
Site of ihd
Left anterior descending artery
Left circumference artery
Right coronary artery
Sometimes
Diagonal branches of lad artery
Obtuse marginal branches of lca
Posterior descending branches of rca
Pathogenesis of ihd
1.coronary atheroschlerosis
2. Variable degrees of superimposed acute plaque change ie.
Superficial erosion
Ulceration
Rupture
Fissuring
Deep hemorrhage
3. Non atheroschlerotic changes
Vasospasm
Embolism
Stenosis of coronary ostia
Thrombotic diseases
Trauma to coronary arteries
Aneurism
Compression of coronary artery from outside
Angina pectoris
Angina pectoris is characterised by paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort (variously described as squeezing, constricting choking or knife like ) caused by transient myocardial ischaemia that falls short of cellular or myocyte necrosis that defines ischaemia
Patterns of angina
1.Stable or typical angina
Cause: decreased coronary perfusion
physical activity
Emotional excitement
Any cause of inc cardiac workload
Treatment: rest, nitroglyecerine vasodilator, ca channel blocker
2.Prinzmetal or variant angina
On ecg : elevated st segment indicating transmural ischaemia
Cause: coronary artery spasm
Unrelated to physical activity, heart rate and blood pressure.
Relieved by
Nitroglycerine vasodilator
Ca channel blocker
3.Unstable or crescendo angina
Refers to pattern of pain that occurs with progressively increased frequency for prolonged period ie >20 mins
Precipitated with
Progressively less effort
Lower level of physical activity
Or even at rest
Cause : disrusption of atheroschlerotic plaque with siperimposed partial thrombosis and embolization or vasospasm or both
Its also known as preinfarction angina so it is most dangerous
Myocardial infarction
Also known as heart attack is the death of cardiac myocytes due to prolonged severe ischaemia
Risk factors of MI
- Age: freq increases with increasing age
- Race: black=white
- Men >women
- Predisposing factors to atheroschlerosis
Ie. Htn
Smoking
DM
Genetic hypercholestrolenemia
Patterns of MI
Transmural
Ischemic necrosis involving full or nearly full thickness of ventricular wall in distribution of single coronary artery
Subendocardial;
Ischemic necrosis involves inner 1/3rd to 1/2 of ventricular wall
Sites of myocardial lesions
Lad: 40-50%
Rca: 30-40%
Lcx: 15-20%
Pathogenesis of MI
- Coronary artery occlusion
- Myocardial response
- Transmural vs subendocardial infarction
Coronary artery occlusion
1.thrombotic occlusion
Plaque may consist of
Hemorrhage into plaque
Erosion or ulceration
Rupture or fissuring
It is then exposed to sub endothelial collagen and necrotic plaque contents
Platelets adhere, aggregate and are activated. They release their granule contents txa2, serotonin etc causing further platelet aggregation to form micro thrombi
Vasospasm is stimulated by mediators released from platelets
Tissue factor activates coagulation pathway adding to bulk of thrombus
Thrombus occludes the vessel
B. NON thrombotic occlusion of coronary artery
1. Vasospasm
2. Emboli
3. Ischemia without detectable coronary atheroschlerosis and thrombosis
Caused by disorders like
Vasculitis
Hematological abnormality
Lowered systemic bp
Myocardial response
Coronary artery obstruction causes
1.Diminished blood flow to myocardium causing ischemia
2. Rapid myocardial dysfunction
3.myocyte death
Complications of MI
- Contractile dysfunction
.abnormalities in left ventricular function
.left ventricular failure with hypotension
.pulmonary edema
.respiratory impairment
2.arrhythmia
3.myocardial rupture-
.left ventricular free wall rupture
.papillary muscle rupture - Mural thrombus
5.pericarditis
6.papillary muscle dysfunction
7.progressive late heart failure
8.Ventricular aneurism - Infarct expansion
- Rt ventricular infarction
Diagnosis of MI
1.History
2.clinical featured:
Prolonged central chest pain
Nausea and vomitting
Rapid weak pulse
Profuse sweating
Breathlessness
Hypotension
3.Lab diagnosis :
Hematological test
Biochemical evidence
Ecg
Echo
Mri
Radionucleotide angiography
Perfusion scintiography
Hematological investigation
Wbc - neutrophilic leukocytosis
Esr- raised
Crp- raised and positive in MI
And negative in ihd without infarction
Biochemical evidence
Myoglobin
Cardiac troponin I and T
Creatinine kinase MB fraction
Lactate dehydrogenase
AST
Creatinine kinase
Normal : males: 30-200 units/l
Female: 30-150u/l
Begins to rise at 2-4 hrs
Reaches peak at 24 hrs
Again returns to normal at 72 hrs
troponin
Normally absent
Begins to rise at 2-4 hrs
Reaches peak at 48 hrs
Again reaches normal in 7-10 days
LDH
Normal: 100-300 u/l
Begins to rise: 12 hr
Reaches peak: 2-3 days
Again comes to normal:7-14 days
AST
Normal level:10-30 u/l
Begins to rise:8 hrs
Reaches peak:16-24 hrs
Comes to normal:4 days
Myoglobin
Peaks at 6 hrs
Returns to normal at 48 hrs
Morphological changes in MI
A.REVERSIBLE INJURY
1. 0-1/2 HRS
GROSS FEATURES none
LIGHT MICROSCOPE none
ELECTRON MICROSCOPE
Relaxation of myofibrils
Glycogen loss and mitochondrial swelling
B.IRREVERSIBLE INJURY
1. 1/2-4 HRS
GROSS FEATURES
None
LIGHT MICROSCOPE
Usually none
ELECTRON MICROSCOPE
Sarcolemma disruption
Mitochondrial amorphous densities
2. 4-12 HRS
GROSS FEATURES
Dark mottling
LIGHT MICROSCOPE
Early coagulative necrosis , edema and hemorrhage
3. 12-24HRS
GROSS FEATURES
Dark Mottlling
LIGHT MICROSCOPE
Ongoing coagulative necrosis , pyknosis of nuclei, early neutrophilic infiltrate
5. 1-3 DAYS
GROSS FEATURES
Mottling with yellow tan centre
LIGHT MICROSCOPE
Coagulative necrosis with loss of nucleus and striations and brisk interstetial infiltrate of neutrophils
6. 3-7 DAYS
GROSS FEATURES
Hyperemic border
Central yellow tan softening
LIGHT MICROSCOPE
Beginning disintegration of dead myofibers with dying neutrophils
Early phagocytosis of dead cells by mq
- 7-10 DAYS
GROSS FEATURES
Maximally yellow tan and soft with depressed red tan margins
LIGHT MICROSCOPE
Well developed phagocytosis of dead cells by mq
Granulation tissue at margins - 10-14 DAYS
GROSS FEATURES
Red gray depressed infarct borders
LIGHT MICROSCOPE
Well established granulation tissue with new blood vessels - 2-8 WEEKS
GROSS FEATURES
Gray white scar progressive from border to core of infart
LIGHT MICROSCOPE
Increased collagen deposition with decreased cellularity - > 2 MONTHS
GROSS FEATURES
Scarring complete
LIGHT MICROSCOPE
Dense collagenous scar
Rheumatic fever
It is an acute , immunologically mediated multisystem inflammatory disease that occurs a few weeks following an episode of group A beta haemolytic streptococcal pharyngitis
Rheumatic heart disease
Acute rheumatic carditis is a common manifestation of active rheumatic fever and may progress over time to chronic rheumatic heart disease which is characterised principally by deforming fibrotic valvular disease particularly involving the mitral valve
Types of rheumatic heart disease
Acute rf
Chronic rhd
Valves involved
65-70 % cases mitral valve
25% aortic valve
Acute rf occurs mostly in children
10days to 6 weeks after an episode of pharyngitis
Diagnostic criteria of rf
Major criteria
1. Migratory polyarthritis
2.pancarditis ie. Myocarditis
Pericarditis endocarditis
3. Subcutaneous nodules
4. Erythema marginatum
5. Sydenhams chorea
Minor criteria
1. Fever
2. Arthalgia
3.Higher acute phase reactants.. crp,complements, coagulation proteins
4.raised esr
5.peolonged pr interval on ecg showing first degree av block
Morphology of rhd
During acute rheumatic fever Focal inflammatory lesions are found in various tissues most distinctive within heart called ashkoff bodies. they consist of a foci of swollen eosenophilic collagen surrounded by lymphocytes ,occasional plasma cells and plump activated macrophages called antischoff cells and occasional multi nuclear giant cells ashkoff cells or ashkoff giant cells
Antischoff cells are pathogenic of rheumatic fever
Tgese cells have abundant cytoplasm
Central round to ovoid nuclei in which chromatin is like slender wavy ribbon
Caterpillar cell
Aschoff giant cells
Some of the larger mq become multinucleated
Complications of rheumatic fever
Mitral stenosis
Cardiac hypertrophy
Cardiac dilation
Heart failure
Embolization from mural thrombi
Infective endocarditis
Migratory polyarthritis
Acute carditis. It has pericardial friction ribs, weak heart sound and tachcardia
Consequences of rf
Deforming fibrotic valvular disease due to partial mitral stenosis
Prominent permanent dysfunction and severe sometimes fatal cardiac problems
Infective endocarditis
It is defined as colonisation or invasion of heart valves or mural edocardium by microbe that leads to the formation of vegetations composed of thrombotic debris and organisms often associated with destruction of underlying cardiac tissue
Causes of IE
Bacteria
Fungi
Rickettsia
Chlamydiae
IE classify
Acute IE
Sub acute IE
Organisms involved in IE
Strptcoccus viridans 50-60%
Str
Staphylococcus aureus 10-20%
Enterococci
Hacek group
Hemophillus
Actinobacillus
Cardiobacterium
Eikinella
Kingella
Staphylococcus epidermidis in prosthetic valves
Eitiology of iE
1.Cardiac cause: rhd
Mitral valve prolapse
Biscuspid aortic valve
Prosthetic valve
2. Host factors:
Neutropenia
Immunodeficiency
Malignancy
DM
Alcoholism
3. Organisms
Diff between acute and subacute endocarditis
Acute infective endocarditis
Is caused by highly virulent org.
Sub acute is caused by low virulence org
Acute ie occurs in previously normal heart valve
Sub acute ie occurs in deformed heart valves
Acute is difficult to treat with antibiotics and req surgery
Subacute is cured by antibiotic
Does not req surgery
Acute has destructive and necrotizing lesions
Subacute lesions are less destructive
Complications of iE
Cardiac complications
1. Valvular insufficiency
2.abscess of valve ring
3.cardiac failure
4.suppurative pericarditis
Renal complications
1. Glomerulonephritis
2. Embolic infarction
Janeway lesions : these are non tender lesions on palm and sole
Subcutaneous nodules in pulp of digits called oslers nodes
Retinal hemorrhage in eye called roth spots
