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Pathology 2 > 6.9 Cardiac Pathology > Flashcards

6.9 Cardiac Pathology Flashcards

1
Q

Normal Heart

A

90% of mass is cardiac muscle,
very special inexhaustible muscle,
pumps 6000 litres of blood daily,
relies on coordination contractions and functions of valves

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2
Q

Clinical presentation of heart disease

A

arrhythmias,
congestive heart failure,
chest pain,
abnormal heart sounds

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3
Q

Branches of circumflex

A

marginal M1 and M2

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4
Q

Branches of LAD

A

diagonal D1, D2, D3

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5
Q

How is coronary artery dominance determined

A

the artery that supplies the posterior decending artery.

If the PDA is supplied by the right coronary artery (RC) then the coronary circulation can be classified as “right-dominant”.

If the PDA is supplied by the circumflex artery, a branch of the left coronary arter, then the coronary circulation can be classifed as “left -dominant”

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6
Q

Branches of the Left coronary

A

LAD–> diagonal branches (D1, D2),
septal branches,
Circumflex –>Marginal branches (M1, M2)

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7
Q

Branches of the Right coronary

A

Acute marginal branch,
AV node branch,
Posterior decending artery (PDA)

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8
Q

the right coronary

A

supplys blood to the right ventricle,
the RCA supplies 25% to 35% of the left ventricle (LV),
The RCA also supplies the SA nodal artery in 60% of pts
(the other 40% of the time, the SA nodal artery is supplied by the left circumflex artery)

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9
Q

the PDA off of the right coronary (usually)

A

supplies the

inferior wall,
ventricular septum, and the
posteromedial papillary muscle.

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10
Q

Papillary muscles

A

there are 5 papillary muscles in the heart,

3 in the right ventricle and
2 in the left,

the papillary muscles attach the mitral valve and the tricuspid valve to the wall of the heart,

Right–>anterior, posterior, and septal papillary muslces each attach via chordae tendinae to the tricuspid valve;

Left –> anterior and posterior papillary muscles attach via chordae tendinae to the mitral valve

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11
Q

What is the significance of the papillary muslces

A

bc there is only 2 papillary muscles on the left side, the left will fail faster

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12
Q

If the papillary muscles are damaged it leads to

A

mitral regurgitation and tricuspid insufficiency or tricuspid regurgitation

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13
Q

supply of the anterolateral papillary muscle

A

more frequently receives two blood supplies:
left anterior descending (LAD) artery and the
left circumflex artery (LCX)
—> thus it is more frequently resistant to coronary ischemia

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14
Q

supply of the posteromedial papillary muslce

A

usually supplied only by PDA –> this makes the posteromedial papillary muscle significantly more susceptible to ischemia.
The clinical significance of this is that a myocardial infarction involving the PDA is more likely to cause mitral regurgitation.

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15
Q

MI involving the PDA is more likely to cause

A

mitral regurgitation

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16
Q

histologically what is distinct about cardiac myocytes

A

nuclei are very round and you have interdigitations. Nuclei are also more centrally located

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17
Q

What part of the tissue in the heart is most prone to ischemia

A

endocardium is the furthest away from blood supply so more prone to damage and ischemia

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18
Q

Wiring of the heart

A

SA node –> AV node –> AV bundle –> AV bundle branches –> purkinje

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19
Q

In an MI what do you damage

A

you damage the part that is supplied by the vessel that is infarcted. In the heart most of the tissue is muscular, but you also have the wiring of the heart like the SA node, AV node, etc that can be damaged too

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20
Q

Hows is the musculature of the valves arranged

A

valves – chordae tendinae – papilarry muscles – ventricular wall

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21
Q

How dies the heart respond to changes in demande

A

the heart responds to demand from the rest of the body mostly by intrinsic mechanisms like hypertrophy, hyperplasia, atrophy, anaplasia, dysplasia, and also will dialate —-but failure to adapt leads to death via apoptosis or necrosis

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22
Q

how are the muscle fibers arranged in the heart

A

you have a myosin ford with a myosin light chain and myosin heavy chain, and you have actin fibers with Troponin I, C, and C, alpha tropomyosin, and Myosin binding protein C.

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23
Q

How do you monitor heart damage in the blood

A

when you have damage to the heart, some of the proteins in the arrangement of muscle fibers will be released into the blood like Troponin C, I and T

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24
Q

Z-disc

A

only actin

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25
Q

a single muscle fiber unit is called a

A

sarcomere–from z disk to z disk

26
Q

Myosin - actin motion

A

myosin head is bound to the actin filament,
ATP binds the Myosin head and releases the actin,
ATP hydrolysis to ADP and Pi causing a confirmational change in the myosin head,
Pi released allowing for myosin head binding to actin,
ADP release allowing for conformational change causing power stroke

27
Q

Cardiac Dysfunction

A 
Pump failure, 
obstruction to flow, 
Regurgitation of flow, 
electrical conduction disturbance, 
distruption of continuity
28
Q

Types of hear disease

A 
ischemic, 
hypertensive, 
valvular, 
Primary myocardial (non ischemic), 
congenital
29
Q

Heart failure definition

A

failure to pump out all of the blood returned to the heart

30
Q

Heart failure concequences

A

back up of blood and/or decreased perfusion of tissues

31
Q

types of heart failure

A 
left failure, 
right failure, 
forward failure, 
backward failure, 
congestion and sequelae (lungs liver), 
ischemia and sequelae (kidneys)
32
Q

in Left-Sided Heart Failure, the morphologic and clinical effects of left-sided CHF primarily result from

A

progressive damming of blood within the pulmonary circulation, and the concequences of diminished peripheral blood pressure and flow

33
Q

Morphology of LHF

A

findings in the heart depend on the underlying disease,
Left ventricle is usually hypertrophied and often dialated, sometimes quite massively (except in mitral stenosis),
nonspecific changes of hypertrophy and fibrosis in the myocardium,
secondary enlargement of the left atrium with resultant atrial fibrillation,
can reduce stroke volume or lead to blood stasis and thrombus formation,
fibrillating left atrium carries a substantially increased risk of embolic stroke,
The extracardiac effects of lef-sided heart failure are manifested most prominently in the lungs

34
Q

In what circumstance of LHF do you not see a massively hypertrophied or dialated heart

A

mitral stenosis

35
Q

Virchow’s triad

A

stasis, hypercoaguability, endothelial injury –blood damming coincides with virchov’s triad and you can get thrombus formation

36
Q

What is the effect of inablity to pump out all the blood in the left ventricle in LHF

A

increased pressure in the pulmonary veines and capillaries leading to pulmonary congestion and edema. The lungs are heavy and boggy.

37
Q

Histologically what do you see in LHF

A

perivascular and interstitial transudate,
alveolar septal edema, and
intra-alveolar edema,

38
Q

In LHF what does the pulmonary capillary leak lead to

A

capillary leak leads to accumulation of erythrocytes (containing hemoglobin) that are phagocytosed by machrophages. Within macrophages, hemoglobin in converted to hemosiderin (but this takes 24hr….NOT seein in early changes), Hemosiderin-containing macrophages in the alveoli (called heart failure cells) are evidence of prior pulmonary edema.

39
Q

Clinical features of LHF

A 
Dyspnea, 
cough, 
orthopnea, 
PND, 
cardiomegaly, 
tachycardia, 
a third heart sound (S3), 
Fine rales, 
systolic murmur, 
atrial fibrillation
40
Q

Dyspnea in LHF

A

the earliest and most significant complaint of pts in left-sided heart failure

41
Q

Cough in LHF

A

is also a common accompaniment of LHF due to fluid transudation in air spaces

42
Q

Orthopnea in LHF

A

further cardiac impairment: dysnea when recumbent, this occurs bc of increased venous return from the lower extremities and by elevation of the diaphragm when in the supine position. Orthopnea is typically releved by sitting or standing, so that pts usually sleep while upright.

43
Q

PND in LHF

A

paroxymal nocturnal dyspnea –dificulty breathing in the night when you are sleeping. A particularly dramatic form of breathlessness awakening pts from sleep with attacks of extreme dyspnea bordering on suffocation. you need to get up. You are relieve bc fluid goes down but remember it goes down slowly.

44
Q

Other manifestations of LHF

A

Cardiomegaly, tachycardia, a third heart sound (S3)

45
Q

Sounds in the lungs in LHF

A

rales, crackles, ronchi at the lung bases, produced by respirations through edematous pulmonary alveoli

46
Q

in LHF with progressive ventricular dialation

A

the papillary muscles are displaced laterally, causing mitral regurgitation and a systolic murmur

47
Q

In LHF, subsequent chronic dialation of the Left atrium is often associated with

A

atrial fibriallation, manifested by an irregularly irregular heart beat that you cannot predict and the pt can die

48
Q

Lungs histology in LHF

A

fill of fluid (we tell by an increased specific gravity in exudate)

49
Q

Right sided heart failure usually occurs

A

as a concequence of left sided heart failure. Any pressure increase in the pulmonary circulatioin inevitabley produces an increased burden on the right side of the heart.

50
Q

Isolated right sided heart failure

A

is less common and it occurs in pts with
intrinsic disease of lung parenchyma and/or
pulmonary vasculature that result in chronic pulmonary hypertension (cor pulmonale)

—heart fails from lung diease but then you get pulmonary hypertension as a result;

can also occur with pulmonic or tricuspid valve disease;

congenital heart diseases with right-to-left shunt can cause isolated right-sided heart failure as well

51
Q

Morphological changes in isolated RHF

A

hypertrophy and dilation are generally confined to the right ventricle and atrium,
bulging of the ventricular septum to the left can cause dysfunction of the left ventricle,
the major morphologic and clinical effects are engorgemtn of the systemic and prtal venous systems ( you don’t see any or see minimal pulmonary congestion)
– you’ll see pitting edema and ascities

52
Q

When you see hypertrophy in the heart what do you know

A

you are working against an increased end diastolic volume (EDV) and you’ll have a high ejection fraction

53
Q

liver has 3 zones

A

1–periportal,
2–midzona,
3–centrilobular (this one is more prone to ischemia bc it is furthest away from blood supply)

54
Q

Microscopic architecture of liver parenchyma

A

both a lobule and an acinus are represented. The calssical hexagonal lobule is centered around a central vein, also known as terminal hepatic venule, and has portal tracts at three of its apices. Regions of the lobule are generally referred to as “periporta:, “midzonal”, and “centrilobular”, according to their proximity to protal spaces and central vein. Using blood supply as a source of reference, a triangular acini can be recognized. On the basis of distance from the blood supply, the acinus is divided into zones 1 (closest to blood source), 2 and 3 (farthest from blood source)

55
Q

Morphology Liver and Portal System in RHF

A

the liver usually increases in size and weight – congestive hepatomegaly. Cut section displays prominent passive congestion, a pattern referred to as nutmeg liver. Congested red centers of the liver lobules are surrounded by paler, sometimes fatty, peripheral regions. In some instances, especially when left-sided heart failure is also present, severe central hypoxia produces centrilobular necrosis along with the sinusoidal congestion. With long-standing severe right sided heart failure, the central areas can become fibrotic, creating so-called cardiac cirrhosis.

56
Q

Nutmeg appearance of the liver in RHF

A

heterogeneous appearance of light and dark patches. There is an area of hypoxia that undergoes necrosis, that area is light. Dark spot has blood or congested sinusoids. In the light spots you find that you’ll see that within the first 6 hours. Fatty change in the first 6 hours damaging lipid metabolism creating a white spot that undergoes necrosis giving nutmeg changes in the liver.

57
Q

other changes seen in RHF

A

congestion of the spleen (it will be large and congested)

58
Q

anatomy of the venous drainage

A

GI drains into portal vein (a large part of the blood supply to the liver along with the hepatic arteries) and the portal vein breaks down into the sinusoids, the sinusoids reconverge to the central vein, and the central vein combine to form the hepatic vein that join the venacava

59
Q

Morphology of Liver and Portal system in RHF

A

RHF also leads to elevated pressure in the portal vein and its tributaries, congestion produces a tense, enlarged spleen (congestive splenomegaly), with long standing congestion, the enlarged spleen can achieve weights of 300 to 500gm (normal < 150gm)

60
Q

Microscopic changes in liver and portal system due to RHF

A

there can be marked sinusoidal dilation, chronic edema of the bowel wall may interfere with absorption of nutrients, accumulations of transudate in the peritoneal cavity can cause ascites

61
Q

Clinical features of Congestive heart failure

A

while the symptoms of left-sided heart failure are largely due to pulmonary congestion and edema, pure right-sided heart failure typically causes very few respiratory symptoms. Instead, there is systemic and portal venous congestion, with hepatic and splenic enlargement, peripheral edema, pleural effusion, and ascites. In most cases of chronic cardiac decompensation, pts present with biventricular CHF, encompassing the clinical syndromes of both right-sided and left-sided heart failure. As CHF progresses, pts can become frankly cyanotic and acidotic, as a result of decreased tissue perfusion

Pathology 2 (15 decks)

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