Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PATHOLOGY > Heart > Flashcards

Heart Flashcards

(107 cards)

Start Studying
1
Q

effects of aging on myocardium

A 
 Increased mass
 Increased subepicardial fat
 Brown atrophy
 Lipofuscin deposition
 Basophilic degeneration
 Amyloid deposits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Older persons develop small filiform processes _______________ on the closure lines of aortic and mitral valves resulting from the organization of small thrombi

A

(Lambl excrescences)

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

extensive lipofuscin deposition in a small, atrophied heart; often accompanies cachexia, as seen in terminal cancer

A

Brown atrophy

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

Categories of Heart Dse

A 
 Congenital Heart Abnormalities
 Ischemic Heart Diseases
 Heart diseases caused by Hypertension
 Heart diseases caused Pulmonary diseases (cor pulmonale)
 Diseases of the Cardiac valves
 Primary cardiac diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

SIX PRINCIPLES OF PATHOLOGY

A 
Pump failure
Obstruction to flow
Regurgitant to flow
Shunted flow
Disorders of cardiac conduction
Rupture of the heart or a major vessel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Occurs when the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues

A

CARDIAC HEART FAILURE

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

Physiologic mechanisms maintain arterial pressure and perfusion of vital organs in HF

A

 Frank-Starling mechanism
 Myocardial adaptations (hypertrophy)
 Activation of neurohumoral system

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

o Occurs in response to increases in pressure
o Usually due to hypertension or aortic stenosis
o Causes a concentric increase in wall thickness

A

Pressure-overload hypertrophy

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

o Characterized by ventricular dilation
o the new sarcomeres assembled are positioned in series with existing sacromeres
o As a result, the wall thickness may be increased, normal, or less than normal
o Heart weight, rather than wall thickness, is the best measure of hypertrophy in volume overloaded hearts

A

Volume-overload hypertrophy

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

3x or 4x the normal weight of the heart

A

 aortic regurgitation

 hypertrophic cardiomyopathy

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

Causes:of LEFT-SIDED HEART FAILURE

A

o Ischemic heart disease
o Hypertension
o Aortic and Mitral valvular heart disease

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

o CO is preserved at rest, but the left ventricle is
abnormally stiff or otherwise restricted in its ability to relax during diastole
o Because the left ventricle cannot expand normally, any increase in filling pressure is immediately referred back to the pulmonary circulation

A

Systolic failure

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

o There is rapid onset pulmonary edema (aka flash

pulmonary edema)

A

Systolic failure

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

o Reduction in the ability of the left ventricle to relax

and fill

A

Diastolic failure

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

o are the hemosiderein-laden macrophages
o phagocytosed RBCs store the iron recovered from
hemoglobin

A

Heart failure cells

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

o Pure right-sided heart failure
o Associated with parenchymal diseases of the lung
o Pulmonary hypertension

A

 Cor pulmonale

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

Most common congenital heart disease

A

VSD

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

Most common genetic cause of congenital heart disease is

A

trisomy 21 (Down syndrome)

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

MAJOR CATEGORIES OF CONGENITAL HEART DISEASE

A

 Malformation causing a Left to Right Shunt
 Malformation causing a Right to Left Shunt
 Malformation causing an Obstruction

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

Causes of R–>L shunt

A
  1. Tetralogy of Fallot
  2. Transposition of the great arteries
  3. Persistent truncus arteriosus
  4. Tricuspid atresia
  5. Pulmonary venous connection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

 Most commonly encountered LRS

A
  1. ASD
  2. Patent foramen ovale
  3. VSD
  4. Patent ductus arteriosus
  5. AV septal defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

result from a
deficient or fenestrated oval fossa near the center of the
atrial septum

A

Secundum ASDs (90%)

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

occur adjacent to the

AV valves

A

Primum anomalies (5% of ASDs)

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

are located near the
entrance of the superior vena cava and may be
associated with anomalous pulmonary venous return to
the right atrium.

A

Sinus venosus defects (5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Complications of ASD?
o heart failure o paradoxical embolization o irreversible pulmonary vascular disease.
26
is an abnormal, fixed opening in the atrial septum caused | by incomplete tissue formation
ASD
27
a small hole created by an open flap of tissue in the atrial | septum at the oval fossa
PATENT FORAMEN OVALE
28
Incomplete closure of the ventricular septum, allowing free | communication of blood between the left to right ventricles
VSD
29
About 90% of VSD; involves the region of the membranous interventricular septum
Membranous VSD
30
lie below the pulmonary valve () or within | the muscular septum.
Infundibular VSD
31
VSDs in the muscular septum may be multiple and called?
“Swiss-cheese” septum
32
Harsh “machinery-like” murmur
PATENT DUCTUS ARTERIOSUS
33
results when the ductus arteriosus remains open after birth
Patent (also called persistent) ductus arteriosus (PDA)
34
preservation of ductal patency is done by administering
prostaglandin E
35
ATRIOVENTRICULAR SEPTAL DEFECT other names
COMPLETE ATRIOVENTRICULAR CANAL DEFECT | ENDOCARDIAL CUSHION DEFECT
36
results from the embryologic failure of the superior and inferior endocardial cushions of the AV canal to fuse adequately
ATRIOVENTRICULAR SEPTAL DEFECT
37
consequences of ATRIOVENTRICULAR SEPTAL DEFECT
o incomplete closure of the AV septum | o malformation of the tricuspid and mitral valves
38
Forms of ATRIOVENTRICULAR SEPTAL DEFECT
Partial AVSD | Complete AVSD
39
consisting of a primum ASD and a cleft | anterior mitral leaflet,causing mitral insufficiency
Partial AVSD
40
consisting of a large combined AV septal defect and a large common AV valve— essentially a hole in the center of the heart
Complete AVSD
41
The diseases in this group cause cyanosis early in postnatal | life (cyanotic congenital heart disease)
RIGHT TO LEFT SHUNTS
42
is the most common disease in this group
Tetralogy of Fallot
43
RIGHT TO LEFT SHUNTS
Tetralogy of Fallot persistent truncus arteriosus tricuspid atresia total anomalous pulmonary venous connection
44
TETRALOGY OF FALLOT Four cardinal features
VSD (subpulmonary stenosis) an aorta that overrides the VSD right ventricular hypertrophy
45
“boot-shaped” heart
TETRALOGY OF FALLOT
46
mild TOF: the abnormality resembles an isolated VSD, and the shunt may be left-to-right, without cyanosis
pink tetralogy
47
ventriculoarterial discordance; the aorta arises from the right ventricle, and lies anterior and to the right of the pulmonary artery, which emanates from the left ventricle
TRANSPOSITION OF THE GREAT ARTERIES
48
Right ventricular hypertrophy becomes prominent, because this chamber functions as the systemic ventricle (what dse)
TGA
49
developmental failure of separation of the embryologic truncus arteriosus into the aorta and pulmonary artery
Persistent Truncus Arteriosus
50
Complete occlusion of the tricuspid valve orifice
Tricuspid Atresia
51
pulmonary veins fail to directly join the left atrium, results embryologically when the common pulmonary vein fails to develop or becomes atretic
Total Anomalous Pulmonary Venous Connection
52
OBSTRUCTIVE CONGENITAL ANOMALIES
 COARCTATION OF AORTA  PULMONARY STENOSIS AND ATRESIA  AORTIC STENOSIS AND ATRESIA
53
form with tubular hypoplasia of the aortic arch proximal to a patent ductus arteriosus that is often symptomatic in early childhood
infantile
54
form in which there is a discrete ridgelike infolding | of the aorta, just opposite the closed ductus arteriosus (ligamentum arteriosum)distal to the arch vessels
“adult”
55
(“notching”) of the undersurfaces of the ribs –collateral circulation of the intercostal & mammary arteries assoc with what dse?
Coarctation of Aorta
56
Coarctation of aorta is associated commonly with what syndrome?
Turner syndrome
57
Congenital narrowing and obstruction of the aortic valve can | occur at three locations
Valvular Subvalvular Supravalvular
58
Syndrome of Ischemic Heart Disease/CAD: Presents as one or more of the ff:
 Myocardial infarction (MI)  Angina pectoris  Chronic IHD with heart failure  Sudden cardiac death
59
Leading cause of death worldwide for both men and women
Ischemic Heart Disease/CAD
60
The coronary artery that perfuses the | posterior third of the septum (called “dominant” coronary arteries)
Right coronary artery | Left circumflex
61
Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort
ANGINA PECTORIS
62
Three Types of Angina pectoris
Stable (Typical) Angina Prinzmetal Variant Unstable (Crescendo) Angina
63
Increase in myocardial oxygen demand that outstrip the ability of stenosed coronary arteries to increase oxygen delivery
Stable (Typical) Angina
64
Complicated by partially occlusive thrombosis and vasoconstriction  severe but transient reductions in coronary blood flow
Prinzmetal Variant
65
Cause: disruption of an atherosclerotic plaque with superimposed partial (mural) thrombosis and possibly embolization or vasospasm (or both)
Unstable (Crescendo) Angina
66
 “Heart attack” |  Death of cardiac muscle due to prolonged severe ischemia
MYOCARDIAL INFARCTION
67
initial event: sudden change in an atheromatous plaque
Coronary arterial occlusion
68
Progression of myocardial necrosis after coronary artery occlusion
MYOCARDIAL RESPONSE
69
``` Onset of: ATP depletion ________ Loss of contractility _______ ATP reduced: to 50% of normal ______ to 10% of normal ______ Irreversible cell injury _______ Microvascular injury _______ ```
Seconds | 1 hr
70
Ischemia is most pronounced in the (what zone in the heart)
subendocardium:
71
Most common infarction; Near full thickness (>60%) of the ventricular wall in the distribution of a single coronary artery o “ST elevation infarcts
Transmural – (“Q” wave infarct)
72
Inner third to half of wall type of infarct; Normally the least perfused region: most vulnerable to any reduction in coronary flow
Subendocardial (nontransmural)
73
o “Non-ST elevation infarcts”
Subendocardial (nontransmural)
74
o “ST elevation infarcts
Transmural – (“Q” wave infarct)
75
 Most effective way to “rescue” ischemic myocardium | threatened by infarction
INFARCT MODIFICATION BY REPERFUSION
76
Severe ischemia lasting _______minutes or longer leads to irreversible damage
20 to 30
77
The typical changes of coagulative necrosis become | detectable in the first _____ hours.
6 to 12
78
result from the forceful systolic tugs of the viable fibers on immediately adjacent, noncontractile dead fibers
Wavy fibers
79
areas of necrosis are stained by (MI)
triphenyltetrazolium chloride
80
most common cause of death (90% of | cases)
Post infarct arrhythmia
81
complication of MI that is due to myocardial | inflammation
Fibrinohemorrhagic pericarditis | Also called DRESSLER SYNDROME
82
COMPLICATIONS OF MI
Post infarct arrhythmia CHF – 60% Hypotension and cardiogenic shock – 10% Myocardial rupture – 1-5%
83
CHRONIC ISCHEMIC HEART DISEASE
Progressive heart failure as a result of ischemic myocardial damage
84
Unexpected death from cardiac causes early after symptom | onset (within 1hr) or without the onset of symptoms
SUDDEN CARDIAC DEATH
85
Causes pressure overload and ventricular hypertrophy; Most commonly seen in the left side of the heart
HYPERTENSIVE HEART DISEASES
86
Pulmonary HPN may cause:
o Right-sided HHD | o Aka COR PULMONALE
87
Cross section: Normal crescent shape of the RV is transformed to a dilated ovoid
Acute Cor Pulmonale
88
Due to stenosis, insufficiency (regurgitation or incompetence), or both
VALVULAR HEART DISEASE
89
 failure of a valve to open completely |  impediment of forward flow
o stenosis
90
 failure of a valve to close completely |  allowing reversed flow
o insufficiency
91
 incompetence of valve stemming from an abnormality in one of its support structures  allowing reversed flow
o functional regurgitation
92
Most common of all valvular abnormalities
CALCIFIC AORTIC STENOSIS
93
most frequent congenital CV malformation in humans
CALCIFIC STENOSIS OF CONGENTITALLY BICUSPID AORTIC VALVE
94
degenerative calcific deposits develop in the peripheral fibrous ring (annulus) of the mitral valve
MITRAL ANNULAR CALCIFICATION
95
“floppy” mitral valve
MITRAL VALVE PROLAPSE (MYXOMATOUS | DEGENERATION OF THE MITRAL VALVE)
96
Key histologic feature of MITRAL VALVE PROLAPSE
o Myxomatous degeneration
97
disease associated with mitral valve prolapse
Marfan’s Syndrome
98
Major Manifestations of Rheumatic Fever
``` o Migratory polyarthritis o Pancarditis o Subcutaneous nodule o Erythema marginatum of the skin o Sydenham Chorea ```
99
Minor Manifestations of Rheumatic Fever
o Fever o Arthralgia o ↑ blood levels of acute phase reactants
100
 Aschoff bodies o distinctive lesions in the heart o consist of:
 foci of lymphocytes (primarily T cells)  occasional plasma cells  Anitschkow cells: plump activated macrophages
101
o pathognomonic for RF
 Anitschkow cells
102
o leaflet thickening o commisural fusion and shortening o thickening and fusion of the tendinous cords
Cardinal anatomic changes of the mitral valve in chronic RHD
103
o maplike thickening of endocardiumover lesions, usually in | left atrium
MacCallum’s plaques
104
more commonly: | o following recurrent ARF
Chronic Rheumatic Heart Disease
105
Heart disease resulting from a primary abnormality in the | myocardium
CARDIOMYOPATHY
106
o diseases predominantly confined to the heart muscle
 Primary cardiomyopathies
107
o myocardial involvement as a component of a systemic or | multiorgan disorder
 Secondary cardiomyopathies

PATHOLOGY (9 decks)

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