Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

House AMP > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Ischemic heat disease

Synonym: ________________________

A

coronary artery disease -CAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

ischaemia

supply (perfusion) and demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ischemic heat disease

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

A

oxygen

nutrient substrates

metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

continuous flow of oxygenated blood

mitochondrial oxidative phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

ischaemia

coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

IHD

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

T/F

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

IHD

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

A

Men

have close relatives with ischaemic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathogenesis of IHD

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

________
__________
____________
_______________

A

Coronary atherosclerosis
Acute plaque changes
Thrombosis
Vasospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathogenesis of IHD

___________ is responsible for more than 90% of the cases

A

Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pathogenesis

• IHD is a consequence of inadequate ________ relative to _________

A

coronary perfusion

myocardial demand.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pathogenesis of IHD

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

A

preexisting atherosclerotic occlusion

superimposed thrombosis

vasospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

70

asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

70

critical

chest pain

stable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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.

A

extent of fixed atherosclerotic

dynamic changes; plaque

superimposed thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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.

A

acute plaque changes

stress

tachycardia

fissuring, fractures and ulceration

thrombogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathogenesis of IHD

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

A

total occlusion

thromboxane

vasospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pathogenesis of IHD

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

A

abrupt plaque change

thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

List the 4

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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 ___________.

A

paroxysmal attacks

substernal or precordial

Transient ; 5secs- 15minutes

inducing an infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Angina pectoris

There are 3 types of angina pectoris

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

A

Stable or Typical

Prinzmetal or variant

Unstable or crescendo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Stable or typical angina

• Occurs predictably at certain level of _______.

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

A

exertion

pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Stable or typical angina

• Relieved by _____, and vasodilation such as ________.

A

rest

nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

Stable or typical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Stable or typical angina

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

A

ST segment depression

subendocardial

Left ventricle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Stable or typical angina

elevation of cardiac enzymes in blood.

T/F

A

F

No elevation of cardiac enzymes in blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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

A

Chronic

inadequate perfusion

workload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Prinzmetal (variant) angina.

Episodic pain

T/F

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Prinzmetal (variant) angina.

pain that does not occur at rest.

T/F

A

F. It does

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Prinzmetal (variant) angina.

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

A

coronary spasms

Unrelated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Prinzmetal (variant) angina.

• Vasospasm may follow release of humoral factors in the blood (_______,_______)

• There is ______________ on ECG, indicative of a _______ ischemia.

A

Thromboxane A2, endothelin-1

an elevation of the ST segment

transmural

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Prinzmetal (variant) angina.

• Responds to vasodilators

•Doesn’t Respond to calcium channel blockers

T/F

A

T
F( it does )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Unstable or crescendo angina.

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

A

less

at rest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Unstable or crescendo angina.

• Pain is with progressively increasing ______ and prolonged _______

A

frequency; duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Unstable or crescendo angina.

• It is induced by _____,______, or ______ of ______ with superimposed ______,_______, or ________

A

fissuring, ulceration , or rupture

an AS plaque

partial mural thrombosis, vasospasm or both.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Unstable or crescendo angina.

• ______ infarcts may occur and it forewarns ______

A

Micro

an MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Unstable or crescendo angina.

• It is also known as ______ angina or acute ___________

A

pre-infarct

coronary insufficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Myocardial infarction(heart attack)

• The severity or duration of _______ is sufficient to cause cardiomyocyte death

A

ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

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

T/F

A

F

Developed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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: _______,_______,______,______

A

artherosclerosis

obesity, physical inactivity, stress, oral contraceptives.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A

an occlusive intra coronary thrombus

an ulcerated or fissured AS plaque

blood pressure, tachycardia,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

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 _________.

A

sub endothelial collagen

thromboxane A2; coagulation

extrinsic pathway

thromboplastin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pathogenesis of MI

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

A

10

Vasospasm or Emboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

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

A

Transmural

subendocardial

micro

45
Q

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%.

A

entire thickness of the ventricular wall from endocardium to epicardium

LV anterior free wall and posterior free wall

septum

46
Q

• Isolated transmural infarcts of RV and right atrium are common

T/F

A

F

Extremely rare

47
Q

Transmural infarction

STEMI or NSTEMI ?

___ waves on the ECG

A

STEMI- ST-elevation MI)

Q

48
Q

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

A

multifocal

Inner

49
Q

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

A

Subendocardial

50
Q

Subendocardial infarctions -

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

A

partially; epicardial

Transient

51
Q

Subendocardial infarctions -
• STEMI or NSTEMI?

• Do or do not show Q waves

A

NSTEMI

No Q waves

52
Q

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 ______)

A

small

vasculitis

elevated cathecholamines

phaechromocytoma, extreme stress

cocaine

53
Q

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

A

40-50

30-40

15-20

54
Q

Vessels and infarcted areas.

Left anterior descending.
• Affects
• _________________ of ________ near ______
• ___________ of _________

A

Anterior wall of left ventricle near the apex

Anterior two thirds of interventricular septum

55
Q

Vessels and infarcted areas.

• Right coronary artery
• Affects
•___________/________ of ______

•____________ of ________

•_____________________

A

Inferior/posterior wall of left ventricle.

Posterior one third of interventricular septum

Posterior right ventricular free wall

56
Q

Vessels and infarcted areas.

• Left circumflex coronary artery
• Affects
• _________ of ________

A

Lateral wall of left ventricle

57
Q

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

A

survival of the patients post MI

4 hrs

12 hours

58
Q

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.

A

triphenyl tetrazolium chloride

brick red ; dehydrogenase

59
Q

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

A

unstained pale

leakage of dehydrogenase enzymes

60
Q

Time from Onset: Gross Morphology

18 - 24 Hours

24 - 72 Hours

3 - 7 Days

10 - 21 Days

7 weeks

A

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

61
Q

Time from Onset: micro Morphology

18 - 24 Hours

24 - 72 Hours

3 - 7 Days

10 - 21 Days

7 weeks

A

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

62
Q

Time from Onset: Gross Morphology

1 - 3 Hours

2 - 3 Hours

4 - 12 Hours

A

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

63
Q

Clinical features of MI

• Pain- ______, crushing, stabbing,____, prolonged, ______ or _____ in location. Radiates to the _____,______, and ______.

•_______ or ______ discomfort “______” with nausea and vomiting
• Apprehension
• shock

A

sudden; severe

substernal or precordial

arms, neck and back

Epigastric or retrosternal; heart burn

64
Q

Pain of MI is relieved by rest or nitroglycerine

T/F

A

F

Not relieved by rest or nitroglycerine

65
Q

Polyuria is a clinical feature of MI

T/F

A

F

Oliguria

66
Q

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

A

Low

Acute ; pulmonary; contractility

left ventricular

67
Q

ECG changes of myocardial infarction

• ST segment _____
• T wave ______
•______ Q waves

A

elevation

inversion

Deep

68
Q

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

_________
_______
__________
_________

A

Creatinine kinase
• Troponin
• Myoglobulin
• Lactate dehydrogenase

69
Q

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

A

Simple

Inexpensive

70
Q

an elevation in total CK is specific for myocardial injury

T/F

With reason

A

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.

71
Q

Creatinine kinase

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

A

MM, MB, and BB.

72
Q

Creatinine kinase

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

A

Both cardiac and skeletal muscle

cardiac

73
Q

Creatinine kinase

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

A

15 to 40

2

74
Q

Creatinine kinase

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

A

brain, bowel, and bladder

75
Q

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 ____________

A

acute myocardial

2 to 8 hours

acute myocardial infarction.

76
Q

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.

A

2 to 4 hours

9 to 12 hours

77
Q

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.

A

reinfarction or extensive

it begins to fall after a day

1 to 3

78
Q

Troponin.

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

A

I and T

myocardial injury

79
Q

Troponin.

Troponin I and T are found in the blood normally

T/F

A

F

Not found in the blood normally

80
Q

Troponin I and T

help to exclude elevations of CK with ________ trauma.

A

skeletal muscle

81
Q

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.

A

3 to 12 hours

CK-MB

rate of rise

82
Q

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

T/F

A

T

83
Q

cTnT levels peak –________

• cTnI levels peak – ______

A

12-48 hours

24 hours

84
Q

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

A

5 to 9 days

2 weeks

85
Q

Troponins will remain elevated shorter than CK

T/F

A

F

longer

86
Q

Troponin

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

A

diagnose reinfarction or extension of infarction

has already suffered an initial MI.

87
Q

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

A

T

skeletal myopathies and with renal failure.

88
Q

Myoglobin

Myoglobin is a protein found in ________ muscle which binds oxygen.

It is a very sensitive indicator of ————-

A

skeletal and cardiac

muscle injury.

89
Q

Myoglobin

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

A

size

90
Q

Myoglobin

A negative myoglobin can help to _________________

A

rule out myocardial infarction.

91
Q

Myoglobin

•It is specific for cardiac muscle

• can be elevated with any form of injury to skeletal muscle.

A

F( not)

T

92
Q

CK-MB is elevated even
before myoglobin

T/F

A

F

Myoglobin is elevated even
before CK-MB.

93
Q

Lactate Dehydrogenase

Lacks cardiac specificity

T/F

A

T

94
Q

Lactate Dehydrogenase

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

A

12 to 24 hours

2 to 3 days

5 to 14 days

95
Q

Lactate Dehydrogenase

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

A

greater specificity

96
Q

The LDH has been supplanted by other tests.

T/F

A

T

97
Q

LDH
• There are ____ isoenzymes (_________).

• LDH ___ – more myocardial specific

A

5

1 through 5

1

98
Q

LDH

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

A

2

1

1
2

99
Q

LDH

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

A

5

liver

centrilobular

congestive heart failure

100
Q

Complications of MI

•_______ and ______ defects, with possible “sudden death”

•_______ of infarction, or ___-infarction

•__________ failure (______ edema)

A

Arrhythmias; conduction

Extension; re

Congestive heart; pulmonary

101
Q

Complications of MI

•_______ shock

• ______itis

• Mural ______, with possible _______

A

Cardiogenic

Pericard

thrombosis; embolization

102
Q

Complications

• Myocardial wall ______, with possible _____

•_____ muscle rupture with possible ______

•________________ formation

A

rupture; tamponade

Papillary; valvular insufficiency

Ventricular aneurysm

103
Q

Chronic Ischemic Heart Disease
• This refers to _________ occurring usually in the _____ as a complication of ____________

• Previous history of _____ or a remote MI.

A

congestive heart failure

elderly

ischaemic cardiac disease.

angina

104
Q

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

T/F

A

T

105
Q

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 ________.

A

pericardial

Moderate to severe

Scars

patchy fibrous thickenings

atrophy; vacuolization

106
Q

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 ______

A

one hour ; without

IHD

107
Q

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

A

T

108
Q

Sudden Cardiac death

• Death is usually from _______

A

lethal arrhythmias

House AMP (64 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions