XI - The Heart Flashcards
The left ventricle is hypertrophied and dilated, with secondary left atrial dilation. The lungs are heavy and boggy, with perivascular and interstitial transudate, alveolar septal edema, and intra-alveolar edema. Hemosiderin-laden macrophages are present. SEE SLIDE 11.1.
Left-sided heart failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Hemosiderin laden macrophages are also called _______
Heart failure cells. SEE SLIDE 11.1. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Earliest and most significant complaint of patients with left-sided heart failure
Dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Most common cause of right sided HF.
Left-sided HF(TOPNOTCH)
This is a particularly dramatic form of breathlessness, awakening patients from sleep with attacks of extreme dyspnea bordering on suffocation.
Paroxysmal nocturnal dyspnea (PND) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Isolated right sided HF occuring in patients with intrinsic lung disease that result in chronic pulmonary hypertension.
Cor Pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition.
Cardiac cirrhosis(TOPNOTCH)
Term used when the liver has congested centrilobular areas (due to back up of blood) surrounded by paler peripheral regions. SEE SLIDE 11.2.
Nutmeg liver (CPC of the liver)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Hallmark of right sided HF.
Pedal and pretibial edema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
Most congenital heart disease arises from faulty embryogenesis during what AOG?
3 - 8 weeks AOG(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
An abnormal communication between chambers of the heart or blood vessels.
Shunt(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
Smooth-walled defect near the foramen ovale, usually without associated cardiac abnormalities. It comprises 90% of ASDs.
Ostium secundum ASD(TOPNOTCH) Robbins Basic Pathology, 9th Ed., p 371
Chamber abnormalities seen in ASD.
Accompanied by right atrial and ventricular dilation, right ventricular hypertrophy, and dilation of the pulmonary artery– reflecting chronic right-sided volume overload. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p 371
Reversal of blood flow through a prolonged left-to-right shunt due to pulmonary hypertension, yielding a right-to-left shunt. This causes unoxygenated blood to go into circulation, causing cyanosis.
Eisenmenger syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
These occur at the lowest part of the atrial septum and can extend to the mitral (anterior leaflet) and tricuspid valves (septal leaflet).
Ostium primum ASD. SEE SLIDE 11.3. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 384
Incomplete closure of the ventricular septum leading to left-to-right shunting. The right ventricle is hypertrophied and often dilated. Diameter of pulmonary artery is increased because of the increased volume by the right ventricle.
Ventricular Septal Defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
This arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery.
Ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
The most common cause of cyanotic congenital heart disease. Heart is large and “boot-shaped” as a result of right ventricular hypertrophy.
Tetralogy of Fallot. SEE SLIDE 11.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
Components of Tetralogy of Fallot.
Pulmonary valve stenosis, Overriding of aorta, Right ventricular hypertrophy, Ventricular septal defect. SEE SLIDE 11.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
It is a discordant connection of the ventricles to their vascular outflow. The defect is an abnormal formation of the truncal and aortopulmonary septa.
Transposition of the Great Arteries. SEE 11.5 (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
Predominant manifestation of TGA?
Early cyanosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
Characterized by circumferential narrowing of the aortic segment between the LEFT SUBCLAVIAN ARTERY and the ductus arteriosus. DA is usually patent and is the main source of blood to the distal aorta. RV is hypertrophied and dilated, pulmonary trunk is also dilated.
Preductal “infantile” coarctation of the aorta. SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
Aorta is sharply constricted by a ridge of tissue at or just distal to the NONPATENT ligamentum arteriosum. Constricted segment is made of smooth muscle and elastic fibers that are continuous with the aortic media, and lined by thickened intima. Ductus arteriosus is closed. Proximally, the aortic arch and its vessels are dilated, LV is hypertrophic.
Postductal “adult” coarctation of the aorta. SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
There is upper extremity hypertension, due to poor perfusion of the kidneys, but weak pulses and low blood pressure in the lower extremities. Claudication and coldness of the lower extremities also present. Enlarged intercostal and internal mammary arteries due to collateral circulation, seen as rib “notching” on xray.
Postductal coarctation of the aorta (without a PDA). SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Atrial septal defect
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?TOF
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?VSD
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Eisenmenger syndrome
Right-to-Left (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Transposition of great arteries
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein the severity or duration of ischemia is enough to cause cardiac muscle death.
Acute Myocardial Infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This refers to progressive cardiac decompensation (heart failure) following myocardial infarction.
Chronic Ischemic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This can result from a lethal arrythmia following myocardial ischemia.
Sudden Cardiac Death(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic, in the setting of increased demand?
More than 70% (critical stenosis)(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 375
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic at rest (unstable angina)?
90%(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 375
Episodic chest pain associated with exertion or some other form of increased myocardial oxygen demand. Pain described as crushing or squeezing substernal sensation which can radiate to left arm. Relieved by rest or vasodilators.
Stable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Increasing frequency of pain, precipitated by progressively less exertion, episodes tend to be more intense and longer lasting.
Unstable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Angina occuring at rest due to coronary artery spasm.
Variant or Prinzmetal angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Infarct involving >= 50% of the myocardial wall thickness.
Transmural infarcts(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 391
Most common blood vessel involved in myocardial infarction?
Left anterior descending artery (40-50%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 392
Electron microscope findings 30 minutes after an ischemic event.
Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)
An infarct can be readily identified by a reddish blue discoloration after how many hours after MI?
12-24 hours(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 393
Coagulation necrosis ensues how many hours after MI?
4-12 hrs after an irreversible injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Injury to infarcts mediated in part by oxygen free radicals generated by increased number of infiltrating leukocytes facilitated by reperfusion.
Reperfusion injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Cardiac enzymes that become detectable 2-4 hours post-infarct peaks at 48 hours and remains elevated for 7-10 days.
Troponin I and Troponin T(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
This cardiac enzyme is detectable in the blood within 2-4 hrs of MI, peaks at 24-48 hrs and returns to normal within approximately 72 hrs.
CKMB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
Myocardial rupture may occur how many days after MI?
3-7 days after infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This occurs within 2-3 days of a transmural infarct and typically resolves within time. It is the epicardial manifestation of the underlying myocardial inflammation.
Pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
A late complication of MI, most commonly results from a large transmural anteroseptal infarct that heals with formation of a thin scar tissue.
Ventricular aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This type of hypertrophy develops in pressure-overloaded ventricles, with an increase in wall thickness, and reduced cavity diameter.
Concentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
Type of hypertrophybthat develops in patients with volume overload such as aortic valve insufficiency. Characterized by hypertrophy associated with ventricular dilation.
Eccentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
Normal weight of heart and normal LV wall thickness
320-360 grams, 1.2-1.4 cm (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 387
In this disease, the left ventricle may exceed 2.0 cm in thickness and the heart may weigh >500 grams (Left ventricular hypertrophy). Microscopically, myocyte diameter increases, associated with irregular nuclear enlargement and hyperchromasia (“box-car nuclei”), and increased interstitial fibrosis.
Sytemic Hypertensive heart disease(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 387
It is the failure of a valve to open completely, obstructing forward flow.
Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This results from failure of a valve to close completely, thereby allowing reversed flow.
Insufficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
The hallmark of this disease is heaped-up calcified masses on the outflow side of the cusps, which protrude intonthe sinuses of Valsalva and mechanically impede valve opening. Cusps may become secondarily fibrosed and thickened.
Calcific aortic stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This is characterized by ballooning or hooding of the mitral leaflets. Affected leaflets are enlarged, redundant, thick and rubbery. The tendinous cords are elongated, thinned and occasionally ruptured. Histologically, there is thinning of the fibrosa layer of the valve, accompanied by expansion of the middle spongiosa layer with increased deposition of mucoid material.
Myxomatous degeneration of the mitral valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Patients with this disease may complain of palpitations, dyspnea or atypical chest pain. Auscultation shows a midsystolic click associated with a regurgitant murmur.
Mitral valve prolapse(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402