Brainscape's Knowledge GenomeTM

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


See full index

CV II > Cardiac Path > Flashcards

Cardiac Path Flashcards

1
Q

What is the predominant coronary artery in most people?

A

90% RCA dominant

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

How many people have patent foramen oval?

A

20-25%

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

What are specialized end-end junctions of adjoining cardiac cells?

A

Intercalated discs

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

What are 6 basic causes of cardiac dysfunction?

A

1) Pump failure
2) Obstruction to Blood Flow through heart
3) Regurgitant flow
4) Shunted Flow
5) Disorders of Cardiac Conduction
6) Disruption of continuity of circulatory system

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

Cardiac hypertrophy

A

Increase in ventricular thickness

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

Cardiomegaly

A

Increase in heart size/weight

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

What is a normal heart weight?

A

Male 300-350gm

Female 250-300 gm

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

Pressure Overload Hypertrophy

A

Concentric hypertrophy with increase in wall thickness of stressed ventricle

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

Volume Overload Hypertrophy

A

Eccentric hypertrophy with chamber dilation/increased ventricular diameter
Ventricle wall normal or minimally thickened
Due to increase in chamber size overall cardiac muscle mass is increased
(Heart getting larger not thicker)

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

CHF

A

Insufficient pump rate to meet demands

Pump can only meet demands with elevated filling pressure

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

Systolic Heart Failure

A

Decreased LV contraction

Low EF

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

Diastolic Heart Failure

A

Decreased LV compliance with impaired relaxation
Normal EF at rest
S4 atrial gallop due to increased resistance to filling in late diastole
Usually accompanied by pulmonary congestion

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

When might isolated RHF occur?

A

With severe chronic pulmonary HTN = cor pulmonale

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

What level of BNP is most consistent with CHF?

A

BNP >500

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

When do congenital heart defects occur?

A

Between 3-8 weeks gestational age

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

NKX2.5 gene mutation

A

Non-Syndromic
ASD or conduction defects
Congenital Heart Disease

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

Holt-Oram Syndrome

A

TBX5

ASD, VSD, Conduction defects

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

DiGeorge Syndrome

A

TBX1 del 22q11.2
Cardiac outflow tract obstruction
ASD/VSD

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

Left to right shunt develops Pulm HTN and then…

A

Eisenmenger syndrome as the right heart has increased pressure over the left heart and the shunt reverse form right to left
Now we have RV volume and pressure hypertrophy
Cyanosis may occurs months to years after birth

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

Types of ASD

A

1) Secundum: most common a patent foramen ovale
2) Primum: adjacent to AV valve
3) Sinus venosus: near SVC

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

How often do ASD pt’s present with Pulm HTN?

A

only 10% it is generally well tolerated and pt tend to be asymptomatic

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

When does the ductus arteriosus usually close and what causes it to close?

A

Increased O2
Decreased pulmonary resistance
Decreased prostaglandin E2
Usually closes 1-2 days

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

How does a PDA present and how do you treat it?

A

Presents as a continuous harsh machine like murmur
If chronic develop pulmonary HTN and cyanosis
Tx NSAIDs to close
Sets up Left to Right shunt which is why pulmonary HTN develops

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

What population most commonly has AVSD?

A

Down Syndrome Pt >1/3

40-60% have CHD with AVSD leading the list

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

What are the four defects in Tetralogy of Fallot?

A

1) VSD
2) Subpulmonic stenosis with obstruction of right ventricular outflow
3) Aorta overrides VSD (Dextrorotated aorta with right sided aortic arch)
4) RVH

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

Supravalvular aortic stenosis

A

Elastin gene mutation with aortic dysplasia thickening often presents with Williams Beuren syndrome

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

Williams Beuren Syndrome

A

Deletion of 28 genes on chrome 8 with elastin gene
hypercalcemia
glucose intolerance
facial and cognitive defects

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

Coarctation of aorta infantile form

A

cyanosis of inferior body and weak femoral pulses

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

Coarctation of aorta adult form

A 
Increased UE BP 
Decreased SBP and pulse in LE 
Leg claudication 
Renal HTN 
Blood flow through collaterals 
Pansystolic murmur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

4 Clinical Syndromes of Ischemic Heart Disease

A

1) Sudden cardiac death
2) Angina pectoris
3) Chronic IHD with heart failure
4) MI

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

Most ischemic heart disease is due to

A

Atherosclerotic coronary arterial obstruction

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

IHD is uncommon in

A

Premenopausal women

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

How much of a fixed obstruction is required to cause Sx during exercise?

A

> 75%

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

How much of a fixed obstruction is required to cause Sx during rest?

A

> 90%

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

Acute ruptures with subsequent thrombosis occurs…

A

In vessels that are narrowed less than 50%

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

Acute plaque change usually occurs in…

A

Non-severely stenotic portions of arteries

New plaques with thin fibrous caps are most likely to rupture

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

Prinzmetal (Variant) Angina

A

Sustained vasospasm causing angina

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

Sudden Cardiac Death

A

Unexpected death from cardiac causes early after onset of symptoms (1 to 24 hours) or sudden death from cardiac cause without antecedent acute symptoms

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

Channelopathies

A

Disorders of K, Na or Ca channel structures or accessory proteins involved in channel function
Mostly autosomal dominant

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

Chronic Ischemic Heart Disease

A

Insidious/progressive CHF resulting from long term ischemic damage to myocardial tissue via MIs or angina
Due to replacement of tissue with non-contractile scar tissue which decreases the overall contractile force

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

Unstable angina

A

Acute plaque change
Progressive increase in frequency and severity of attacks
Provoked by progressively less effort and may occur at rest

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

Stable angina

A

Decreased perfusion secondary to fixed narrowing

Can be provoked by increased cardiac demand during emotion or exercise

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

Lipid risk factors account for how many MI’s?

A

50-60%

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

Transmural Infarction

A

Ischemic necrosis involves >50% of the ventricular wall thickness
Commonly associated with acute plaque change with thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Subendocardial infarction

A

Area of ischemic necrosis limited to the inner 1/3 or at most the inner 1/2
May occur as a result of acute plaque change and thrombosis
May result from prolonged and severe reduction in systemic blood pressure ,as encountered in shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

MI Pathogenesis

A
  • Initial sudden change in plaque
  • Immediate formation of initial platelet plug over plaque
  • Vasospasm from platelet adhesion (vasoactive substances from platelets)
  • Propagation of platelet plug into stable clot via extrinsic clotting system
  • Within minutes, clot occludes lumen of the involved vessel = thrombosis with coronary occlusion
47
Q

Adrenergic Stimulation of MI

A

Peak incidence btw 6am-12pm

Awakening causes intense emotional stress

48
Q

When does complete unsalvageable necrosis occur in MI?

A

6 hrs

49
Q

Which coronary artery is most commonly obstructed?

A

LAD

50
Q

What are the MI modification by reperfusionn techniques?

A

Lysis of thrombus
Balloon angioplasy
Coronary a. bypass graft

51
Q

STEMI

A

ST segment elevation MI transmural

52
Q

Non-STEMI

A

Non ST segment elevation MI subendocardial

53
Q

Cardiac tamponade

A

Pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium)
Complication of acute MI

54
Q

Systemic Hypertensive Heart Disease

A

1) LV hypertrophy in the absence of other cardio pathology that may cause it
2) Systemic HTN
May present clinically with CHF or atrial arrythmias

55
Q

Pulmonary Hypertensive Heart Disease

A

Cor Pulmonale occurs with

1) Pulmonary parenchyma disorders (COPD, diffuse interstitial lung disease)
2) Pulmonary vessel disorders (recurrent PE, Pulm HTN)
3) Chest movement disorders (kyphoscoliosis)
4) Disorders inducing pulmonary arterial constriction (Metabolic acidosis, hypoxemia)

56
Q

Functional regurgitation

A

Normal valve leaflets but problem with supporting structures

57
Q

Stenosis Pathophys

A

Almost always a primary valve cusp abnormality and virtually always a chronic disease

58
Q

Insufficiency Pathophys

A

From intrinsic disease of valve cusp or acquired structural abnormality of supporting anatomical structures

59
Q

Most frequent cause of Aortic Stenosis

A

Calcification of anatomically normal and congenitally bicuspid aortic valves

60
Q

Most frequent cause of Aortic Insufficiency

A

Dilation of ascending aorta due to HTN and aging

61
Q

Most frequent cause of Mitral Stenosis

A

Rheumatic heart disease

62
Q

Most frequent cause of Mitral Insufficiency

A

Myxomatous degeneration (mitral valve prolapse)

63
Q

Most common valvular abnormality

A

Calcific Aortic Stenosis

64
Q

Calcific Aortic Stenosis

A

Consequence of calcification due to advanced age
Nodular masses of Ca heaped up in sinuses of Valsalva
Clincial Sx present in 7th (60s) to 9th (80s) decade
LV concentric hypertrophy from flow obstruction
Tends to become ischemic leading to CHF (death w/i 2yrs) Syncope (death w/i 3yrs) Angina pectoris (death w/i 5yrs)

65
Q

Calcific Stenosis of Congenitally Bicuspid Aortic Valve

A

Two cusps not equal size
More susceptible to progressive degenerative calcification earlier
Develop clinical Sx and signs of cardiac dysfunction in 5th-6th decades, earlier than tricuspid calcification

66
Q

Mitral Annular Calcification

A

Occurs in
1) Women over 60yrs of age
2) Individuals with myxomatous mitral valves
3) Pt with elevated LV pressure (systemic HTN)
Generally doesn’t affect valvular function
Occasionally associated with arrythmias
Most diagnosed because of large Ca deposits found on CXR

67
Q

Myxomatous Degeneration of Mitral Valve

A

One or both leaflets floppy and prolapse into LA during systole
MIDSYSTOLIC CLICK +/- REGURGITANT MURMUR
Most often in young women
Seen with Marfan’s
Clinically asymptomatic

68
Q

Four Serious complications of myxomatous degeneration of mitral valve

A

1) infective endocardiits
2) mitral insufficiency
3) stroke/iscemic infarct
4) arrhythmias
5) atypical chest pain

69
Q

Pathological Changes of Myxomatous Degen of Mitral Valve

A

Intercordal ballooning of mitral valve leaflets
Leaflets are enlarged, thick and rubbery
Thinned fibrosa layer, marked thickened spongiosa layer with mucoid deposition
Dilation of annulus, fibrosis of leaflets and endocardial surface = jet lesions

70
Q

Acute Rheumatic Fever

A

Occurs 10 days- 6 weeks post strep pharyngitis
Ab against group A strep Ag (hypersensitivity rxn to M protein cross-reacting with tissue glycoproteins)
Develop fever and polyarthritis
= Acute Rheumatic carditis
Small warty verrucase along lines of closure of leaflets

71
Q

Aschoff cells

A

multinucleated forms of caterpillar cells in unique linear chromatin pattern

72
Q

Acute Rheumatic fever clinical Sx and diagnostic criteria

A

Affects 5 major systems

1) migratory polyarthritis of large joints (swollen, painful joints)
2) Acute carditis with cardiac enlargement and diminished function
3) SubQ nodules
4) Erythema marginatum of skin
5) Sydenham chorea (involuntary purposeless movements of extremities)

Jones criteria requires evidence of prior group A strep infection plus either: 2 major system findings or 1 major system finding plus 2 minor manifestations such as fever, arthralgia, or evidence of acute phase reactants (elevated see rate or elevated C-reactive protein)

73
Q

Acute Rheumatic Fever Tx

A

Pt should receive long term antibiotic PCN prophylaxis into adulthood and perhaps for life

74
Q

Rheumatic Heart Disease

Which valves are most commonly affected

A

Term used for chronic valvular disease that results

Most commonly affects the mitral and aortic valves

75
Q

Infective Endocarditis

A

Serious destructive infection of heart valves or mural endocardium by organisms
Involves left valves except in IV drug users

76
Q

Infective Endocarditis Morphologic Changes

A

Bulk friable vegetations of fibrin-platelet clot and organisms
Large irregular masses on valve cusps that can extend onto chordae
Destruction of underlying cardiac organisms especially valves
Risk of systemic microemboli leading to

77
Q

Infective Endocarditis Organisms

A

S.viridans, S. aureus, HACEK

S.epidermidis #1 in artificial valves

78
Q

Acute Bacterial Endocarditis

A

Rapidly progressive destruction of infected valve which was normal prior to infection
Highly virulent bacteria infection such as S. aureus in IV drug abusers
Even with aggressive Ab therapy 50% of pt die

79
Q

Subacute Bacterial Endocarditis

A

Insidious onset and lengthy clinical course
Deformed/defected valve prior to infection (mitral valve prolapse)
Low virulence bacterial infection (S. viridians MCC)
Pt recover with Abi therapy

80
Q

Diagnostic Criteria for Infective Endocarditis

A

GET 3 BLOOD CULTURES IN 24 HRS
New valvular regurg MURMUR and ECHO findings all MAJOR along with a + blood test
*Diagnosis by these guidelines, often called the Duke Criteria, requires either pathologic or clinical criteria; if clinical criteria are used, 2 major, 1 major + 3 minor, or 5 minor criteria are required for diagnosis.

81
Q

Tetralogoy of Fallot Morphology

A

Boot shaped heart

82
Q

Nonbacterial Thrombotic Endocarditis

A

Small 1-5mm along line of closure of valve leaflets or cusps, small bland vegetations on line of closure
Lesions are sterile & non-destructive
Major risk factor is hyper-coagulable state
May fragment and produce system emboli
“Marantic endocarditis”
Paraneoplastic syndrome

83
Q

Libman-Sacks Disease

A

= Endocarditis of SLE
Small 1-4mm sterile verrucous vegetations on any surface of Av leaflets, valvular endocardium, chord tendinae
Vegetations on either or both sides of valve leaflets or elsewhere
SLE pt with antiphoshpholipid Ab syndrome
May be due to IC deposition with inflammation

84
Q

What is the most consistent clinical sign for infective endocarditis?

A

Fever! usually of unknown origin

85
Q

Carcinoid Heart Disease

A

Result of tumor of the small intestine that has metastasized to the liver and is producing serotonin there which gains access to the hepatic vv. IVC and then right heart causing increased fibrosis which results in TV regurg and PV stenosis
Fibrous intimal thickening of endocardial surfaces of right heart
Thickening is composed of muscle proliferation and increased acid mucopolysaccharide matrix

86
Q

Cardiomyopathy

A

Heart disease resulting from primary abnormality in the myocardium
Either dilated, hypertrophic or restrictive

87
Q

Myocarditis

A

Global enlargement of heart and dilation of all chambers
Lymphocyte infiltrate with focal necrosis highly predictive of viral myocarditis
Major cause of sudden death
Presents with dyspnea, fever, chest pain, arrhythmias

88
Q

Causes of myocarditis

A 
Coxsackievirus A & B 
Borrelia burgorferi 
Rickettsiae rickettsi 
Hypersensitivity 
Tricihnella spiralis 
Trypanosoma cruzi causes Chagas Disease in South America
89
Q

What is the most common indication for cardiac transplantation?

A

Dilated Cardiomyopathy

90
Q

Dilated Cardiomyopathy

A

Insidious slowly progressive CHF w/
1) Progressive cardiac dilation
2) Contractile (Systolic) dysfunction (decrease in contractility leads to global heart enlargement)
3)Cardiomegaly with increased cardiac mass (hypertrophy)
Sx of CHF but poorly responsive to CHF treatments

91
Q

Causes of Dilated Cardiomyopathy

A

1) Myocarditis (Coxsackie B virus)
2) Alcohol
2) Peripartum cardiomyopathy
3) Iron overload
4) Familial (presents in children with autosomal dominant pattern)
5) Supraphysiologic stress

92
Q

Morphology of DCM

A 
Increased size (2-3x) 
Large and flabby 
Dilation of all chambers 
Ventricular wall thickness may be normal, thin or thick 
Mural thrombi common 
Normal valves and aa. free of narrowing
93
Q

Arrythmogenic RV Cardiomyopathy

A

Right sided heart failure and rhythm disturbances
Causes of unexpected death
RV severely thinned with myocytes being replaced with adipocytes and interstitial fibrous tissue
Autosomal dominant mutation in plakoglobin, desmoplakin genes
Naxos syndrome

94
Q

Naxos Syndrome

A

Palmoplantar keratoderma with arrythmogenic RV cardiomyopathy and wooly hair (recessive plakoglobin mutation)

95
Q

Carvajal Syndrome

A

Palmoplantar keratoderma with arrythmogenic LV cardiomyopathy and wooly hair (recessive desmoplakin mutation)

96
Q

What is the most common mutation in HCM?

A

Mutation of B-myosin heavy chain gene on Chr. 14

97
Q

Hypertrophic Cardiomyopathy

A

Features myocardial hypertrophy, abnormal diastolic filling, intermittent ventricular outflow obstruction with systolic ejection murmur

98
Q

HCM Clinical Features

A

Major cause of SCD in young people including basketball and football athletes
Most pt have stable non-progrssive course
Major Sx: exertional dyspnea
May exhibit Afib

99
Q

HCM vs. DCM
Ventricle/Force/Dysfunction
/Clinical/Mutations

A

HCM: firm small lumen with thick wall due to hypertrophic IVS
Hypercontracting, Distolic dysfunction, Exertional dyspnea, Sarcomere protein mutation

DCM: dilated and flabby, hypocontracting, systolic dysfunction, CHF, cytoskeleton protein mutation

100
Q

Restrictive Cardiomyopathy

A

Mild increase in heart size/mass without increase in volume of LV
Characterized by decreased ventricular compliance resulting in impaired filling during diastole
Bilateral atrial enlargement
Associated with amyloidosis, endomycoardial fibrosis, loeffler endomyocardiits, endocardial fibroelastosis

101
Q

Endomyocardial fibrosis

A

endocardial and subendocardial fibrosis with mural thrombi, occurs in African children/young adults and in other tropical areas (most common worldwide)

102
Q

Loeffler endomyocarditis

A

endomyocardial fibrosis with large mural thrombi that occurs worldwide and is associated with eosinophilic leukemia [some have platelet derived growth factor receptor abnormalities (Rx tyrosine kinase inhibitor imatinib) or may be secondary to basic protein release]

103
Q

Endoardial fibroelastosis

A

Multifactoral LV endocardial fibrosis that usually occurs in first 2 years of life

104
Q

Amyloidosis

A

Interstitial deposition of amyloid protein results in restrictive cardiomyopathy complicated by arrhythmias
Amyloidosis primariliy in heart in systemic senile in pt >60
Amyloid composed of transthyretin product and more common in AA due to transthyretin mutation

105
Q

Direct Cardiac Toxicity: Adriamycin

A

Lipid peroxidation of myocyte membranes

106
Q

Direct Cardiac Toxicity: Cyclophosphamide

A

Vascular lesion with myocardial hemorrhage

107
Q

Direct Cardiac Toxicity: High dose Catechoalmines

A

Vasopressors toxicity via calcium overload or vasoconstriction and increased cardiac load

108
Q

Direct Cardiac Toxicity: Iron-Overload

A

Interferes with metal dependent enzyme systems

109
Q

Myxoma

A

Can cause fever and malaise via interleukin 6
Carney complex includes myxomas, pigmented skin lesions and overactive endocrine organs
Large pedunculated lesion arising from fossa ovalis

110
Q

Rhabdomyoma

A

1 in children and 50% associated with tuberous sclerosis (TSC1/TSC2 genes)

111
Q

Chylous Pericardial effusion

A

Lymphatic obstruction

112
Q

Serosanginous pericardial effusion

A

Malignancy, trauma, rupture MI, aortic dissection

113
Q

Serous pericardial effusion

A

CHF, hypoalbuminemia

CV II (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions