Ischemic Heart Disease Flashcards by Iseoluwa Ojo

Ischemic heat disease

Synonym: ________________________

coronary artery disease -CAD

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Ischemic heat disease

This is the generic name used for a group of closely related syndromes resulting from _____, an imbalance between ________ and ______ of the heart for oxygenated blood
L

ischaemia

supply (perfusion) and demand

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Ischemic heat disease

Ischaemia is characterized by insufficiency of _____, reduced availability of _______ and inadequate removal of _____ .

oxygen

nutrient substrates

metabolites

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Cardiac function is strictly dependent upon the __________ of ———- through the coronary arteries, since cardiac myocytes generate energy almost exclusively through _____________

continuous flow of oxygenated blood

mitochondrial oxidative phosphorylation

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IHD
• It is a disease characterized by ____ to the heart muscles. usually due to ___________ disease.

ischaemia

coronary artery

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IHD

Its risk increases with age,smoking, hypercholesterolaemia, diabetes, and hypertension

T/F

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IHD

Its more common in (men or women?) and those who _____________________

Men

have close relatives with ischaemic heart disease

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Pathogenesis of IHD

Four factors play roles in the pathogenesis of IHD.
These are

________
__________
____________
_______________

Coronary atherosclerosis
Acute plaque changes
Thrombosis
Vasospasm

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Pathogenesis of IHD

___________ is responsible for more than 90% of the cases

Atherosclerosis

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Pathogenesis

• IHD is a consequence of inadequate ________ relative to _________

coronary perfusion

myocardial demand.

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Pathogenesis of IHD

• Imbalance occurs as a consequence of the combination of __________________ and new, __________ and/ or ______

preexisting atherosclerotic occlusion

superimposed thrombosis

vasospasm

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Fixed coronary atherosclerosis with less than ____% reduction in the cross sectional area of the coronary artery lumen is (symptomatic or asymptomatic?)

asymptomatic

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• Lesions that occlude more than _____% of vessel lumen (_____ stenosis) cause symptom ( _______ ) in the setting of increased demand. (__________ )

critical

chest pain

stable angina

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Fixed stenosis that occludes _____% or more of vascular lumen may cause symptoms even at rest

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Pathogenesis of IHD

• Onset of ischaemia may depend not only on the _____________ disease but also on __________ in the coronary ______ morphology as further reduction in coronary perfusion may result from ___________ on a fixed coronary atherosclerosis.

extent of fixed atherosclerotic

dynamic changes; plaque

superimposed thrombosis

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Pathogenesis of IHD

• The thrombosis is a consequence of _______ with _____, _____ and or vasospasm resulting in _____,______, and ________ of the plaque exposing the ________ surfaces of the vessels.

acute plaque changes

stress

tachycardia

fissuring, fractures and ulceration

thrombogenic

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Pathogenesis of IHD

• Thrombosis results in the ________ of the vessel and release of substances such as ________ which further worsens _________.

total occlusion

thromboxane

vasospasm

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Pathogenesis of IHD

• In most patients, unstable angina and infarction occur as a result of _____ followed by _________.

abrupt plaque change

thrombosis

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Ischaemic heart disease
There are four clinical syndromes of IHD namely.

List the 4

Angina pectoris
Myocardial infarction
Chronic ischaemic heart disease.
Sudden cardiac death

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Angina pectoris

This is a symptom complex of IHD characterized by _________ of _______ or _______ chest discomfort caused by (transient or extended?) (___-____) myocardial ischaemia that falls short of ___________.

paroxysmal attacks

substernal or precordial

Transient ; 5secs- 15minutes

inducing an infarct

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Angina pectoris

There are 3 types of angina pectoris

______ or _______ angina
_______ or _______ angina
_________ or _______ angina

Stable or Typical

Prinzmetal or variant

Unstable or crescendo

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Stable or typical angina

• Occurs predictably at certain level of _______.

• characterized by attacks of _____ following _______,________ leading to increase in amino acid

exertion

pain

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Stable or typical angina

• Relieved by _____, and vasodilation such as ________.

rest

nitroglycerin

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______ Or ——— angina is the Commonest form of angina.

Stable or typical

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Stable or typical angina • Associated with _____________ in ECG because ischemia is most intense in the _______ zone of the _________

ST segment depression subendocardial Left ventricle.

Stable or typical angina elevation of cardiac enzymes in blood. T/F

F No elevation of cardiac enzymes in blood.

Stable or typical angina • The pathogenesis lies in (acute or chronic?) stenosing coronary atherosclerosis that leads to __________ of the myocardium when the _____ on the heart increases

Chronic inadequate perfusion workload

Prinzmetal (variant) angina. Episodic pain T/F

Prinzmetal (variant) angina. pain that does not occur at rest. T/F

F. It does

Prinzmetal (variant) angina. • Associated with ______ and (related or unrelated?) to physical activity, heart rate or blood pressure.

coronary spasms Unrelated

Prinzmetal (variant) angina. • Vasospasm may follow release of humoral factors in the blood (_______,_______) • There is ______________ on ECG, indicative of a _______ ischemia.

Thromboxane A2, endothelin-1 an elevation of the ST segment transmural

Prinzmetal (variant) angina. • Responds to vasodilators •Doesn’t Respond to calcium channel blockers T/F

T F( it does )

Unstable or crescendo angina. • Precipitated with progressively (more or less?) exertion and can occur even _____

less at rest.

Unstable or crescendo angina. • Pain is with progressively increasing ______ and prolonged _______

frequency; duration

Unstable or crescendo angina. • It is induced by _____,______, or ______ of ______ with superimposed ______,_______, or ________

fissuring, ulceration , or rupture an AS plaque partial mural thrombosis, vasospasm or both.

Unstable or crescendo angina. • ______ infarcts may occur and it forewarns ______

Micro an MI

Unstable or crescendo angina. • It is also known as ______ angina or acute ___________

pre-infarct coronary insufficiency.

Myocardial infarction(heart attack) • The severity or duration of _______ is sufficient to cause cardiomyocyte death

ischemia

Myocardial infarction(heart attack) is the leading cause of death in the developing world. T/F

F Developed

Myocardial infarction(heart attack) • The risk factors for MI are those for \________. • Major :Genetic abnormalities, Family Hx, increasing age, male gender, hyperlipidemia, hypertension, cigarette smoking, DM, inflammation • Minor: _______,_______,______,______

artherosclerosis obesity, physical inactivity, stress, oral contraceptives.

Pathogenesis of MI • 90% of transmural acute myocardial infarcts are caused by _____________ overlying ______________.The ischemia is worsened by factors such as a fall in ___________,________

an occlusive intra coronary thrombus an ulcerated or fissured AS plaque blood pressure, tachycardia,

Pathogenesis of MI • The exposure of the ___________ results in platelet adhesion, aggregation, activation release of aggregators • The activated platelets release ______, platelet factors 3 and 4 which predispose to _____ and cause _______ • Also there is activation of the ———— of coagulation due to the release of tissue _________.

sub endothelial collagen thromboxane A2; coagulation extrinsic pathway thromboplastin

Pathogenesis of MI In ____% of MI cases there is no evidence of Atherosclerosis. Infarct results from •________ or _________ -

10 Vasospasm or Emboli

Gross morphology of MI:Patterns of infarction include: •_______ infarctions •_________infarctions •______ infarction

Transmural subendocardial micro

Gross morphology : Patterns of infarction include: • Transmural infarctions - involving the _______________ of the _________, from ______ to _______, usually the _________ as ________ and ____ with extension into the RV wall in 15-30%.

entire thickness of the ventricular wall from endocardium to epicardium LV anterior free wall and posterior free wall septum

• Isolated transmural infarcts of RV and right atrium are common T/F

F Extremely rare

Transmural infarction STEMI or NSTEMI ? ___ waves on the ECG

STEMI- ST-elevation MI) Q

Subendocardial infarctions -______ areas of necrosis confined to the (inner or outer ?) third of the myocardium.

multifocal Inner

•_____________ region of the myocardium is most vulnerable to hypoperfusion and hypoxia

Subendocardial

Subendocardial infarctions - • Seen in (partially or completely?) occluded _______ artery, (transient or rapid?) decreases in oxygen delivery (hypotension, anaemia, pneumonia)

partially; epicardial Transient

Subendocardial infarctions - • STEMI or NSTEMI? • Do or do not show Q waves

NSTEMI No Q waves

Microscopic infarcts • Microscopic infarcts can occur in the setting of _____ vessel occlusions eg ____, embolisation, thrombi, or vessel spasm due to _______ either endogenous ( _______,________) or exogenous( eg ______)

small vasculitis elevated cathecholamines phaechromocytoma, extreme stress cocaine

Vessels and infarcted areas. • Left anterior descending. ______% of infarcts • Right coronary artery ______% • Left circumflex coronary artery _____%

40-50 30-40 15-20

Vessels and infarcted areas. Left anterior descending. • Affects • _________________ of ________ near ______ • ___________ of _________

Anterior wall of left ventricle near the apex Anterior two thirds of interventricular septum

Vessels and infarcted areas. • Right coronary artery • Affects •___________/________ of ______ •____________ of ________ •_____________________

Inferior/posterior wall of left ventricle. Posterior one third of interventricular septum Posterior right ventricular free wall

Vessels and infarcted areas. • Left circumflex coronary artery • Affects • _________ of ________

Lateral wall of left ventricle

Morphologic changes in MI • Development of Gross and Microscopic features depends on the __________ • Microscopic changes are not significant until ______ • MI fewer than _________ old are inapparent on gross examination

survival of the patients post MI 4 hrs 12 hours

If infarct has occurred 2 to 3 hrs before death :immersion of tissue slides in a solution of ______________ imparts to the intact non infarcted myocardium ________ colour, where _______ activity is preserved.

triphenyl tetrazolium chloride brick red ; dehydrogenase

• Infarcted area is revealed as an ___________ zone due to the _______________

unstained pale leakage of dehydrogenase enzymes

Time from Onset: Gross Morphology 18 - 24 Hours 24 - 72 Hours 3 - 7 Days 10 - 21 Days 7 weeks

Red blue discoloration of myocardium Pallor with some hyperaemia Hyperaemic border with central yellowing Maximally yellow and soft with vascular margins. Granulation tissue enters from edge of infarct White fibrosis

Time from Onset: micro Morphology 18 - 24 Hours 24 - 72 Hours 3 - 7 Days 10 - 21 Days 7 weeks

Continuing coagulation necrosis, pyknosis of nuclei, and marginal contraction band necrosis Total loss of nuclei and striations along with heavy neutrophilic infiltrate Macrophage and mononuclear infiltration begins, fibrovascular response begins Fibrovascular response with prominent granulation tissue Fibrosis

Time from Onset: Gross Morphology 1 - 3 Hours 2 - 3 Hours 4 - 12 Hours

Wavy myocardial fibers Staining defect with tetrazolium or basic fuchsin dye Early coagulation necrosis with loss of cross striations, edema, hemorrhage, and early neutrophilic infiltrate

Clinical features of MI • Pain- ______, crushing, stabbing,____, prolonged, ______ or _____ in location. Radiates to the _____,______, and ______. •_______ or ______ discomfort “______” with nausea and vomiting • Apprehension • shock

sudden; severe substernal or precordial arms, neck and back Epigastric or retrosternal; heart burn

Pain of MI is relieved by rest or nitroglycerine T/F

F Not relieved by rest or nitroglycerine

Polyuria is a clinical feature of MI T/F

F Oliguria

clinical feature of MI • (Low or high ?) grade fever • (Acute or chronic ?) _____ oedema due to impaired ____ of the ischaemic myocardium and ________ failure: dyspnoea, orthopnoea, suffocation

Low Acute ; pulmonary; contractility left ventricular

ECG changes of myocardial infarction • ST segment _____ • T wave ______ •______ Q waves

elevation inversion Deep

Serum cardiac markers • Assessment of blood levels of proteins that have leaked out of the dead myocytes _________ _______ __________ _________

Creatinine kinase • Troponin • Myoglobulin • Lactate dehydrogenase

Creatinine kinase • The total CK is a (simple or complex?) and (expensive or inexpensive?) test that is readily available using many laboratory instruments.

Simple Inexpensive

an elevation in total CK is specific for myocardial injury T/F With reason

F an elevation in total CK is not specific for myocardial injury, because most CK is located in skeletal muscle, and elevations are possible from a variety of non-cardiac conditions.

Creatinine kinase • Creatinine kinase can be further subdivided into three isoenzymes:____,____, and ____

MM, MB, and BB.

Creatinine kinase • The MM fraction is present in ___________, but the MB fraction is much more specific for______ muscle:

Both cardiac and skeletal muscle cardiac

Creatinine kinase • About ______% of CK in cardiac muscle is MB, while less than ___% in skeletal muscle is MB.

15 to 40 2

Creatinine kinase • The BB fraction (found in ____,_____, and _____) is not routinely measured.

brain, bowel, and bladder

Creatine Kinase - MB Fraction: CK-MB is a very good marker for ________ injury, because of its excellent specificity, and it rises in serum within _______ of onset of ____________

acute myocardial 2 to 8 hours acute myocardial infarction.

Creatine Kinase - MB Fraction: Serial measurements every ________ for a period of _______ after the patient is first seen will provide a pattern to determine whether the CK-MB is rising, indicative of myocardial injury.

2 to 4 hours 9 to 12 hours

Creatine Kinase - MB Fraction: The CK-MB is also useful for diagnosis of ________ or _______ nature of an MI because __________, dissipating in _____ days, so subsequent elevations are indicative of another event.

reinfarction or extensive it begins to fall after a day 1 to 3

Troponin. Troponin __ and ___ are structural components of cardiac muscle. They are released into the bloodstream with _______.

I and T myocardial injury

Troponin. Troponin I and T are found in the blood normally T/F

F Not found in the blood normally

Troponin I and T help to exclude elevations of CK with ________ trauma.

skeletal muscle

Troponins will begin to increase following MI within _________, about the same time frame as _____. However, the _______ for early infarction may not be as dramatic as for CK-MB.

3 to 12 hours CK-MB rate of rise

Troponin I and T are specific for myocardial injury more so than CK-MB T/F

cTnT levels peak –________ • cTnI levels peak – ______

12-48 hours 24 hours

Troponins will remain elevated up to ______ for troponin I and up to _____ for troponin T

5 to 9 days 2 weeks

Troponins will remain elevated shorter than CK T/F

F longer

Troponin • However, this continued elevation has the disadvantage of making it more difficult to _________________________ in a patient who ___________________

diagnose reinfarction or extension of infarction has already suffered an initial MI.

Troponin ___ lacks some specificity because elevations can appear with __________ and with __________

T skeletal myopathies and with renal failure.

Myoglobin Myoglobin is a protein found in ________ muscle which binds oxygen. It is a very sensitive indicator of ————-

skeletal and cardiac muscle injury.

Myoglobin The rise in myoglobin can help to determine the ____ of an infarction.

size

Myoglobin A negative myoglobin can help to _________________

rule out myocardial infarction.

Myoglobin •It is specific for cardiac muscle • can be elevated with any form of injury to skeletal muscle.

F( not) T

CK-MB is elevated even before myoglobin T/F

F Myoglobin is elevated even before CK-MB.

Lactate Dehydrogenase Lacks cardiac specificity T/F

Lactate Dehydrogenase It begins to rise in ___________ following MI, and peaks in ________, gradually dissipating in ________.

12 to 24 hours 2 to 3 days 5 to 14 days

Lactate Dehydrogenase Measurement of LDH isoenzymes is necessary for _________ for cardiac injury.

greater specificity

The LDH has been supplanted by other tests. T/F

LDH • There are ____ isoenzymes (_________). • LDH ___ – more myocardial specific

5 1 through 5 1

LDH Ordinarily, isoenzyme ___ is greater than __, but with myocardial injury, this pattern is "flipped" and ___ is higher than ___

2 1 1 2

LDH LDH-__ from _____ may be increased with ________ necrosis from passive congestion with _________ and following ischemic myocardial injury

5 liver centrilobular congestive heart failure

Complications of MI •_______ and ______ defects, with possible "sudden death" •_______ of infarction, or ___-infarction •__________ failure (______ edema)

Arrhythmias; conduction Extension; re Congestive heart; pulmonary

Complications of MI •_______ shock • ______itis • Mural ______, with possible _______

Cardiogenic Pericard thrombosis; embolization

Complications • Myocardial wall ______, with possible _____ •_____ muscle rupture with possible ______ •________________ formation

rupture; tamponade Papillary; valvular insufficiency Ventricular aneurysm

Chronic Ischemic Heart Disease • This refers to _________ occurring usually in the _____ as a complication of ____________ • Previous history of _____ or a remote MI.

congestive heart failure elderly ischaemic cardiac disease. angina

Sometimes the myocardial damage is silent and the first indication of IHD is CIHD. T/F

Morphology of Chronic Ischemic Heart Disease • Adhesions on ______ surface • _______ to ______ stenosing atherosclerosis of the coronary arteries •_____ of previous infarcts • Normal endocardium or with areas of ____________ • Diffuse myocardial ____ and sub endocardial ________.

pericardial Moderate to severe Scars patchy fibrous thickenings atrophy; vacuolization

Sudden Cardiac death • Definition. This is an unexpected death from cardiac causes within ______ after or _______ the onset of symptoms. • In most cases SCD is a complication of ______

one hour ; without IHD

Sudden Cardiac death • SCD may be due to congenital structural abnormalities, aortic valve stenosis, cardiac conduction defects, Mitral valve prolapse, idiopathic or hypertrophied cardiomyopathy T/F

Sudden Cardiac death • Death is usually from _______

lethal arrhythmias

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Ischemic Heart Disease Flashcards

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