Cvs Flashcards

Question

Ischemic heart disease

Answer 1

It represents a group of pathophysiologically related syndromes resulting from an imbalance between myocardial supply and cardiac demand of the heart for oxygenated blood

Answer 2

Angina pectoris MI Chr ihd with heart failure Sudden cardiac death

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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

Answer 7

Also known as heart attack is the death of cardiac myocytes due to prolonged severe ischaemia

Answer 8

1. Age: freq increases with increasing age 2. Race: black=white 3. Men >women 4. Predisposing factors to atheroschlerosis Ie. Htn Smoking DM Genetic hypercholestrolenemia

Answer 9

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

Answer 10

Lad: 40-50% Rca: 30-40% Lcx: 15-20%

Answer 11

1. Coronary artery occlusion 2. Myocardial response 3. Transmural vs subendocardial infarction

Answer 12

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

Answer 13

Coronary artery obstruction causes 1.Diminished blood flow to myocardium causing ischemia 2. Rapid myocardial dysfunction 3.myocyte death

Answer 14

1. 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 4. Mural thrombus 5.pericarditis 6.papillary muscle dysfunction 7.progressive late heart failure 8.Ventricular aneurism 9. Infarct expansion 10. Rt ventricular infarction

Answer 15

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

Answer 16

Wbc - neutrophilic leukocytosis Esr- raised Crp- raised and positive in MI And negative in ihd without infarction

Answer 17

Myoglobin Cardiac troponin I and T Creatinine kinase MB fraction Lactate dehydrogenase AST

Answer 18

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

Answer 19

Normally absent Begins to rise at 2-4 hrs Reaches peak at 48 hrs Again reaches normal in 7-10 days

Answer 20

Normal: 100-300 u/l Begins to rise: 12 hr Reaches peak: 2-3 days Again comes to normal:7-14 days

Answer 21

Normal level:10-30 u/l Begins to rise:8 hrs Reaches peak:16-24 hrs Comes to normal:4 days

Answer 22

Peaks at 6 hrs Returns to normal at 48 hrs

Answer 23

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. 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 8. 10-14 DAYS GROSS FEATURES Red gray depressed infarct borders LIGHT MICROSCOPE Well established granulation tissue with new blood vessels 9. 2-8 WEEKS GROSS FEATURES Gray white scar progressive from border to core of infart LIGHT MICROSCOPE Increased collagen deposition with decreased cellularity 10. >2 MONTHS GROSS FEATURES Scarring complete LIGHT MICROSCOPE Dense collagenous scar

Answer 24

It is an acute , immunologically mediated multisystem inflammatory disease that occurs a few weeks following an episode of group A beta haemolytic streptococcal pharyngitis

Answer 25

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

Answer 26

Acute rf Chronic rhd

Answer 27

65-70 % cases mitral valve 25% aortic valve Acute rf occurs mostly in children 10days to 6 weeks after an episode of pharyngitis

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

Deforming fibrotic valvular disease due to partial mitral stenosis Prominent permanent dysfunction and severe sometimes fatal cardiac problems

Answer 32

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

Answer 33

Bacteria Fungi Rickettsia Chlamydiae

Answer 34

Acute IE Sub acute IE

Answer 35

Strptcoccus viridans 50-60% Str Staphylococcus aureus 10-20% Enterococci Hacek group Hemophillus Actinobacillus Cardiobacterium Eikinella Kingella Staphylococcus epidermidis in prosthetic valves

Answer 36

1.Cardiac cause: rhd Mitral valve prolapse Biscuspid aortic valve Prosthetic valve 2. Host factors: Neutropenia Immunodeficiency Malignancy DM Alcoholism 3. Organisms

Answer 37

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

Answer 38

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

Cvs Flashcards

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