Pathologies

Question 1

Heart Failure

Answer 1

Most cases of heart failure are due to systolic
dysfunction—inadequate myocardial contractile function,
characteristically a consequence of ischemic heart disease
or hypertension. Alternatively, CHF also can result from
diastolic dysfunction—inability of the heart to adequately
relax and fill, such as in massive left ventricular hypertro-
phy, myocardial fibrosis, amyloid deposition, or constric-
tive pericarditis.

Question 2

Forward and backward failure

Answer 2

In CHF, the failing heart can no longer efficiently pump
the blood delivered to it by the venous circulation. The
inc ED ventricular volume,
leading to increase ED pressures and, finally,
elevated venous pressures. So, inadequate cardiac
output—called forward failure—is accompanied by increased congestion of the venous circulation>backward failure

Question 3

Compensated Heart Failure

Answer 3

Increased end-diastolic
filling volumes dilate the heart and cause increased
cardiac myofiber stretching; these lengthened fibers con-
tract more forcibly, thereby increasing cardiac output. If
the dilated ventricle is able to maintain cardiac output, the patient is in compensated
heart failure

Question 4

DEcompensated heart failure

Answer 4

ventricular dilation because of an increased EDV comes at
the expense of increased wall tension and magnifies
the oxygen requirements of an already-compromised myocardium. failing muscle cannot fulfill its needs

Question 5

Compensatory mechanisms

Answer 5

RAAS
Norepinephrine release
Release of ANP
Ventricular Dilation

Question 6

Left Sided HF

Answer 6

causes of left-sided cardiac failure are ischemic heart
disease (IHD), systemic hypertension, mitral or aortic
valve disease, and primary diseases of the myocardium
(e.g., amyloidosis

Question 7

Symptoms of LSHF

Answer 7

Dyspnea (shortness of breath) on exertion is usually the
earliest and most significant symptom of left-sided heart
failure; cough is also
common as a consequence
of fluid
transudation into air spaces
dyspnea when recumbent (orthopnea); this
occurs because the supine position increases venous return
from the lower extremities and also elevates the diaphragm.
Orthopnea typically is relieved by sitting or standing
Paroxysmal nocturnal dyspnea

Question 8

presentations(2)

Answer 8

enlarged heart (cardiomegaly), tachycardia, a third
heart sound (S3), and fine ráles at the lung bases, caused by
the opening of edematous pulmonary alveoli.
ventricular dilation, the papillary muscles are displaced
outward, causing mitral regurgitation and a systolic
murmur
A fib
risk of thrombi

Question 9

Complications

Answer 9

A fib
worsening of pulmonary edema
prerenal azotemia
hypoxic encephalopathy

Question 10

Right sided cardiac failure

Answer 10

variety of disorders affecting the lungs; hence it is
often referred to as cor pulmonale. Besides parenchymal
lung diseases, cor pulmonale also may arise secondary
to disorders that affect the pulmonary vasculature for example primary pulmonary hypertension

Question 11

clinical features

Answer 11

systemic and portal venous congestion
hepatic and splenic enlargement
peripheral edema
pleural effusion
ascites. congestion of kidney and brain
progressive:
diminished cardiac output and inc congestion

Question 12

Congenital heart disesae

Answer 12

Rubella, diabetes in mother

trisomy 13,15,18,21

Question 13

Types

Answer 13

variety of disorders affecting the lungs; hence it is
often referred to as cor pulmonale. Besides parenchymal
lung diseases, cor pulmonale also may arise secondary
to disorders that affect the pulmonary vasculatur

Question 14

Shunt

Answer 14

Abnormal connection between chambers/vessels

Question 15

Right to left shunt

Answer 15

Dusky blueness of the skin(cyanosis) results because the pulmonary circulation is bypassed and poorly oxygenated blood collected from the venous system enters the systemic arterial circulation

Question 16

Left to right shunts

Answer 16

Right ventricular hypertrophy because the vein(pulmonary circulation) are exposed to high pressure and increased volume. Increased lung vascular resistance. Shunt reversal

Question 17

Left to right shunt

Answer 17

VSD
ASD
PDA
Consequence
RT ventricular hypertrophy
RT to left shunting(Eisenmenger syndrome)

Question 18

ASD/VSD

Answer 18

Diagnosis in adults
Pulmonary hypertension
VSD
Chronic Lto R shunting followed by pulmonary hypertension and chf

Question 19

Patent Ductus arteriosus

Answer 19

Left pulmonary artery joins just distal to the origin of the left subclavian
IU life pillmonary artery to aorta Jane Deta ha» Ductus constricts and and closes bad me surf lig arteriosum

Question 20

PDA features

Answer 20

Machinery like murmurs

Infective endocarditis predisposition

Question 21

Tetralogy of Fallot•

Answer 21

VSD • Right ventricular outf l ow tract obstruction (subpul-monic stenosis) • Overriding of the VSD by the aorta • Right ventricular hypertrophy

Question 22

Morphology

Answer 22

The heart is enlarged and “boot-shaped” as a consequence of right ventricular hypertrophy; the proximal aorta is dilated, while the pulmonary trunk is hypoplastic.

Question 23

Clinical features

Answer 23

right-to-left shunting, decreased pulmonary blood fl ow, and increased aortic volumes. The clinical severity largely depends on the degree of the pulmonary outf l ow obstruction; even untreated, some patients can survive into adult life.
pulmonary hyper-tension does not develop, and right ventricular failure is rare. Nevertheless, patients develop the typical sequelae of cyanotic heart disease, such as hypertrophic osteoarthrop-athy and polycythemia (due to hypoxia)

Question 24

Transposition

Answer 24

Transposition of the great arteries is a discordant connec-tion of the ventricles to their vascular outf l ow. The embryologic defect is an abnormal formation of the truncal and aortopulmonary septa so that the aorta arises from the right ventricle and the pulmonary artery emanates from the left ventricle
VSD is necessary and occurred in 1/3rd of these cases

Question 25

Clinical features

Answer 25

cyanosis, with the progno-sis depending on the magnitude of shunting, the degree of tissue hypoxia, and the ability of the right ventricle to maintain systemic pressures. Without surgery (even with stable shunting), most patie

Question 26

Coarctation of aorta

Answer 26

Coarctation (narrowing, or constriction) of the aorta is a common form of obstructive congenital heart disease Males are affected twice as often as females, although females with Turner syndrome frequently have coarctation. • An “infantile” preductal form featuring hypoplasia of the aortic arch proximal to a PDA • An “adult” postductal form consisting of a discrete ridgelike infolding of the aorta, adjacent to the ligamen-tum arteriosum

Question 27

Preductal coarctation with a PDA usually presents early in life, classically as cyanosis localized to the lower half of the body; without intervention, most affected infants die in the neonatal period.

Answer 27

the disease may remain unrecognized well into adult life. Classically, there is upper-extremity hypertension paired with weak pulses and relative hypotension in the lower extremities, associated with symptoms of claudication and coldness. Exuberant col-lateral circulation “around” the coarctation often devel-ops through markedly enlarged intercostal and internal mammary arte

Question 28

Ischemic heart disease

Answer 28

an imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nutri-tional requirements. Since cardiac myocytes generate energy almost exclusively through mitochondrial oxida-tive phosphorylation, cardiac function is strictly dependent upon the continuous fl ow of oxygenated blood through the coronary arteries.

Question 29

Manifest

Answer 29

• Angina pectoris Ischemia induces pain but is insufficient to cause myocyte death. Angina can be stable (occurring predictably at certain levels of exertion), can be caused by vessel spasm (Prinzmetal angina), or can be unstable (occurring with progressively less exertion or even at rest). • Myocardial infarction (MI). This occurs when the severity or duration of ischemia is sufficient to cause cardiomyo-cyte death. • Chronic IHD with CHF. This progressive cardiac decom-pensation, which occurs after acute MI or secondary to accumulated small ischemic insults, eventually precipi-tates mechanical pump failure. • Sudden cardiac death (SCD). This can occur as a conse-quence of tissue damage from MI, but most commonly results from a lethal arrhythmia without myocyte necrosis

Question 30

Coronary arteriosclerosis factors

Answer 30

Inflammation Interaction of endothelial cells and circulating leukocytes,resulting in T cell resulting in T-cell and macro-phage recruitment and activation. These cells drive sub-sequent smooth muscle cell accumulation and proliferation, with associated matrix production, super-imposed on an atheromatous core of lipid, cholesterol, calcif i cation, and necrotic debris. At later stages, desta-bilization of atherosclerotic plaque can occur through macrophage metalloproteinase secretion

Question 31

Thrombosis

Answer 31

Thrombosis associated with an eroded or ruptured plaque triggers the acute coronary syndromes. Partial vascular occlusion by a newly formed thrombus on a disrupted atherosclerotic plaque can wax and wane with time and lead to unstable angina or sudden death; alternatively, even partial luminal occlusion by a thrombus can com-promise blood fl ow suff i ciently to cause a infarction of the innermost zone of the myocardium (subendocardial infarct). Organizing thrombi produce potent activators of smooth muscle proliferation, which can contribute to the growth of atherosclerotic lesions. Mural thrombi in a coronary artery can also embolize; indeed, small emboli can be found in the distal intramyocardial circu-lation (along with associated microinfarcts) at autopsy of patients with unstable angina. In the most serious case, completely obstructive thrombus over a disrupted plaque can cause massive MI.