Cvs Written Flashcards
(15 cards)
What is atherosclerosis? (DU-22M, 18M)
Atherosclerosis is a pattern of vascular disease which is characterized by initial lesions called atheromas or atheromatous or fibro Fatty plaques, which protrude into and obstruct vascular lumens and weaken the underlying media.
What are the common sites and complications of atheromatous plaque? (DU-23N)
Sites:
In descending order-
Lower abdominal aorta
Coronary artery
Popliteal artery
Internal carotid arteries.
Vessels of the circle of Willis.
spared vessels:
Vessels of upper extremities.
Mesenteric vessel
Renal artery
-Except at their ostia.
Type of artery large / medium sized artery
Complications:
Changes in a plaque
Advanced lesions undergo pathological changes:
. focal rupture and ulceration on erosion of intimal surface of atheromatous plaques.
Exposes the blood to highly thrombogenic substances.
Thrombus Formation
Thrombus can partially or completely occlude lumen.
Lead to downward ischemia.
2.Hemorrhage into the plaque
Rupture of the overlying fibrous cap or thin walled vessels in the area of neovascularization.
A contained hematoma may expand the plaque or induce plaque rupture
3.Atheroembolism
Plaques rupture and dischange atherosclerotic debris into the blood stream, producing micro emboli, composed of lesion contents (cholesterol emboli or atheroemboli).
Superimposed thrombus, usually occurs on disrupted lesions (those with rupture, ulceration, erosion or hemorrhage) and may partially or completely occlude the lumen.
(4) Aneurysmal dilatation
Result from atherosclerosis induced pressure or ischemic atrophy of the underlying media…
Loss of elastic tissue
Weakens and rupture…
(5) Other changes
Atherosclerotic stenosis.
Acute plaque change
Thrombosis.
Vasoconstriction.
short note on: Atheromatous plaque (DU-17Nov)
Atheroma/Atherosclerotic Plaque: A Pathology Overview
Atheroma / atherosclerotic plaque: consists of a raised focal lesion initiating within the intima having a soft yellow grumous core of lipid covered with a firm white fibrous cap.
Common sites of formation of atheroma / atherosclerotic plaque: The blood vessels which are most extensively involved by atherosclerosis (in descending order) are:
Lower abdominal aorta and iliac arteries
Coronary arteries
Popliteal arteries
Internal carotid arteries
Vessels of the circle of Willis.
Morphology of an atherosclerotic plaque:
A) Macroscopic:
Colour: Yellow-tan and are raised above the surrounding vessel wall.
Size: Plaques vary in size but can coalesce to form larger masses.
Shape: Atherosclerotic lesions are patchy and rarely circumferential.
Cut section: The plaques have a central (necrotic) core covered by a subendothelial fibrous cap:
Superficial fibrous cap: Composed of smooth muscle cells and relatively dense collagen.
Necrotic core: Deep to the fibrous cap is a necrotic core containing lipid (primarily cholesterol and cholesterol esters), debris from dead cells, foam cells (lipid-laden macrophages and lipid-laden SMCs), fibrin, thrombus in varying degrees of organization, and other plasma proteins.
Periphery of the lesions: Neovascularization (proliferating small blood vessels) present.
Microscopic: Atherosclerotic plaques have four principal components:
1.Cells including variable numbers of SMCs, macrophages, and T lymphocytes
2.Extracellular matrix (ECM) including collagen, elastic fibers, and proteoglycans
3.Intracellular and extracellular lipids (mostly cholesterol & cholesterol ester)
4.Calcifications (in later stage plaques).
**3. Draw and label a typical atheroma. (DU-23N)
Write in short the pathogenesis of atherosclerosis. (DU-22M)
Atherosclerosis progresses in the following sequence:
1 Endothelial injury and dysfunction, causing increased vascular permeability, leukocyte adhesion, and thrombosis
2.Accumulation of lipoproteins in the vessel wall
3.Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells
4.Platelet adhesion
5.Factor release from activated platelets, macrophages
6.Smooth muscle cell proliferation, extracellular matrix production, and recruitment of T-cells
7.Lipid accumulation both extracellularly and within cells
8.Calcification of ECM and necrotic debris late in the pathogenesis.
What are the risk factors of atherosclerosis? (DU-22M,
Risk Factors for Atherosclerosis:
Major Risk Factors:
A) Non-modifiable –>
Increasing age.
Male gender.
Family history.
Genetic abnormality.
B) Modifiable –>
Hyperlipidemia.
Hypertension.
Smoking.
Diabetes.
Minor Risk Factors: (20% Cases)
Obesity
Physical inactivity
Stress (type-A personality)
Lipoprotein A
Alcohol
Post-menopausal estrogen deficiency.
High carbohydrate diet.
Hardened (trans) saturated fat
Hyperchomocystinemia
Homocystinuria - An inborn error of metabolism.
Metabolic syndrome.
Chlamydia pneumoniae
Inflammation
1 What are the ischaemic heart diseases? (DU-22N,20Nov/ July, 19Nov)
Ischaemic Heart Disease
Definition:
IHD represents a group of patho-physiologically related syndromes resulting from myocardial ischaemia - an imbalance between myocardial supply (perfusion) & cardiac demand of the heart for oxygenated blood.
Also known as:
Coronary Artery Disease
In 90% cases - due to obstructive atherosclerotic lesion in epicardial coronary artery.
Classification/Types/Syndromes of IHD:
Angina pectoris. (literally chest pain).
MI.
Chronic IHD & Heart failure
Sudden cardiac death (SCD).
Site:
Only 1 major coronary epicardial vessel may be affected.
Left Anterior descending artery. (LAD)
Left circumference artery. (LCA)
Right coronary artery. (RCA)
Sometimes major secondary branches are also involved.
Diagonal Branches of LAD artery.
Obtuse marginal branches of LCA.
Posterior descending branches of RCA
Mention the important cardiac markers of myocardial infarction. (DU-22N)
CK:
Normal : males: 30-200 units/l
Female: 30-150u/l
Begins to rise at 2-4 hrs
Reaches peak at 24 hrs
Again returns to normal at 72 hrs
Cardiac Troponin
Normally absent
Begins to rise at 2-4 hrs
Reaches peak at 48 hrs
Again reaches normal in 7-10 days
Ldh:
Normal: 100-300 u/l
Begins to rise: 12 hr
Reaches peak: 2-3 days
Again comes to normal:7-14 days
Ast
Normal level:10-30 u/l
Begins to rise:8 hrs
Reaches peak:16-24 hrs
Comes to normal:4 days
Myoglobin
Peaks at 6 hrs
Returns to normal at 48 hrs
Write in short the pathogenesis and complications of myocardial infarction. (DU-20Nov/ July, 19Nov)
Coronary arterial occlusion:
a) Thrombotic occlusion of coronary artery: The following sequence of events likely underlies most MIs.
An atheromatous plaque is eroded or suddenly disrupted by endothelial injury, intraplaque hemorrhage, or mechanical forces, exposing subendothelial collagen and necrotic plaque contents to the blood.
Platelets adhere, aggregate, and are activated, releasing thromboxane A2, adenosine diphosphate (ADP), and serotonin—causing further platelet aggregation and vasospasm.
Activation of coagulation by tissue factor and other mechanisms adds to the growing thrombus.
Within minutes, the thrombus can evolve to completely occlude the coronary artery lumen.
b) Non-thrombotic occlusion of coronary artery: The mechanisms include-
Vasospasm with or without coronary atherosclerosis, perhaps in association with platelet aggregation or due to drug ingestion (e.g. cocaine or ephedrine).
Emboli from the left atrium in association with atrial fibrillation, a left-sided mural thrombus, vegetations of infective endocarditis, intracardiac prosthetic material: or paradoxical emboli from the right side of the heart or the peripheral veins, traversing a patent foramen ovale and into the coronary arteries.
Uncommon causes of MI without atherothrombosis include disorders of small intramural coronary vessels (e.g. vasculitis), hematologic abnormalities (e.g. sickle cell disease), amyloid deposition in vascular walls, vascular dissection, marked hypertrophy (e.g. due to aortic stenosis), lowered systemic blood pressure (e.g. shock), or inadequate myocardial “protection” during cardiac surgery.
B) Myocardial response: Coronary arterial obstruction diminishes blood flow to a region of myocardium, causing ischemia, rapid myocardial dysfunction, and eventually—with prolonged vascular compromise—myocyte death. The anatomic region supplied by that artery is referred to as the area at risk. The outcome depends predominantly on the severity and duration of flow deprivation.
Complications
Contractile dysfunction.
Abnormalities in left ventricular function.
Left ventricular failure & hypotension.
Pulmonary edema.
Respiratory impairment.
Severe pump failure - cardiogenic shock.
Arrhythmia
Myocardial rupture.
The myocardial rupture syndrome results from the mechanical weakening that occurs in necrotic subsequently inflamed myocardium and include:
Left ventricular free wall rupture (most common)
Ventricular septum rupture.
Papillary muscle rupture
Pericarditis.
Rt. ventricular infarction.
Infarct expansion.
Mural thrombus.
Ventricular aneurysm.
Papillary muscle dysfunction.
Progressive late heart failure.
Write short note on: Angina pectoris (DU-21M)
Angina pectoris (literally chest pain) is characterized by paroxysmal and usually recurrent attacks of sub-sternal or pre-cordial chest discomfort (variously described as constricting, squeezing, choking or knife-like) - caused by transient (15 seconds to 15 minutes) myocardial ischaemia that falls short of inducing cellular/myocyte necrosis that defines ischaemia.
Types/pattern of Angina:
3 overlapping patterns of Angina pectoris:
A) Stable/typical angina.
B) Prinzmetal/Variant angina.
C) Unstable/cresendo angina.
A) Stable/Typical Angina –>
Most common and also called - typical angina pectoris.
Cause:
Reduction of coronary perfusion due to chronic stenosing coronary atherosclerosis.
Occurs:
When there is:
(i) Physical activity
(ii) Emotional excitement.
(iii) Any cause of ↑ Cardiac work
.Relieved by:
Rest
Administering nitroglycerine (a strong vasodilator) or
Ca-channel Blockier.
B) Prinzmetal Variant Angina
Uncommon pattern of episodic myocardial ischaemia or angina that occurs at rest due to coronary artery spasm.
Although these patients may have significant coronary atherosclerosis but they are unrelated to -
Physical activity.
Heart Rate.
Blood pressure.
Cause : Coronary Artery Spasm.
Relieved by :
Nitroglycerine (strong vasodilaton)
Ca-channel Blocleer.
On ECG :
Elevated ST segment - indicates transmural.
3.Unstable or Crescendo Angina:
Refers to pattern of pain, that occurs with progressive
increased Frequency of prolonged period (>20min).
Severe pain/discomfort
is precipitated with - progressively less effort.
-lower level of physical activity.
on even at rest.
and tends to be of more prolonged duration.
Cause:
Disruption of atherosclerotic plaque with superimposed partial (mural) thrombosis and embolization or vasospasm or both.
About half of the patient has evidence of MI.
Pre-infarction Angina:
Unstable angina is sometimes referred to as pre-infarction angina
Warning that an acute MI may be imminent.
Name the different cardiac enzymes related to diagnosis of MI. (DU-20Nov/
CK:
Normal : males: 30-200 units/l
Female: 30-150u/l
Begins to rise at 2-4 hrs
Reaches peak at 24 hrs
Again returns to normal at 72 hrs
Cardiac Troponin
Normally absent
Begins to rise at 2-4 hrs
Reaches peak at 48 hrs
Again reaches normal in 7-10 days
Ldh:
Normal: 100-300 u/l
Begins to rise: 12 hr
Reaches peak: 2-3 days
Again comes to normal:7-14 days
Ast
Normal level:10-30 u/l
Begins to rise:8 hrs
Reaches peak:16-24 hrs
Comes to normal:4 days
Myoglobin
Peaks at 6 hrs
Returns to normal at 48 hrs
Give pathogenesis of rheumatic fever. (DU-15Ja, 12Ju)
Group-A & hemolytic streptococcal pharyngeal infection precedes clinical manifestation of ARF by 2-6 weeks.
Body produces antibodies against Streptococci.
The antibodies cross react with human tissues because of the antigenic similarity between Streptococcus components and human connective tissue.
Human cardiac sarcolemma: Similar to S. pyogenes cell wall.
Cardiac myosin: Similar to S. pyogenes M-protein.
Heart Valve glycoprotein: Similar to S. pyogenes capsule.
Thus immunologically mediated inflammation and damage (auto-immune) to human tissue (like-heart, joint, CNS) occurs.
Type-II hypersensitivity reaction occurs causing injury to host tissues and damage to heart valves and muscles.
Probably genetic susceptibility regulates the hypersensitivity reaction.
Types of rheumatic fever and valves involved
①Acute RF.
②Chronic RHD.
Valves involved in RHD
65-70% Cases : Mitral valve
25% Cases : Aortic valve.
Age incidence For ARF
Mostly - in children.
20% - middle age.
10 days - 6 weeks after an episode of pharyngitis.
Cause
Group-A β hemolytic streptococci.
Complications of rheumatic fever
Complications:
① Carditis is likely to worsen with each recurrence.
② Embolization From mural thrombi.
③ Infective endocarditis.
④ Acute carditis
Pericardial friction ribs.
Weak heart sound.
Tachycardia
Arrhythmia (particularly atrial fibrillation)
⑤ Arthritis - migratory polyarthritis.
Most common cause of death:
Acute Rheumatic Myocarditis.
What is vegetation? Write classification and pathogenesis of infective endocarditis. Mention its complications
vegetation” refers to a mass-like growth, typically composed of bacteria, fibrin, and platelets, that forms on the heart valves or the lining of the heart chambers due to infection, usually related to infective endocarditis
Classify
Acute ie
Subacute ie
Etiopathogenesis
Cardiac cause →
@Rhd
⑥ Mitral valve prolapse.
ⓒ Degenerative calcific valvular stenosis.
ⓓ Bicuspid aortic valve - calcified or not.
ⓔ Artificial/prosthetic valve.
ⓕ Unrepaired and repaired congenital defects.
②Host factors →
@Neutropenia.
⑥ Immuno deficiency.
ⓒ Malignancy.
ⓓ Therapeutic immunosuppression.
ⓔ Alcohol/IV drug user.
ⓕ DM.
Organism involved:
@Streptococcus viridans (50-60%).
⑥ Staphylococcus aureus (10-20%).
ⓒ Enterococci.
ⓓ HACEK Group:
ⓐ Hemophillus
ⓑ Actino bacillus
ⓒ Cardio bacterium
ⓓ Eikinella.
ⓔ kingella.
f.Staph epidermidis
Portal of entry
Inf elsewhere in body
Dental or surgical procedure
Iv drug abuser
Occult source eg gut, oral cavity
Complications of IE
1.Cardiac complications:
Valvular insufficiency
Abscess of valve ring
Myocardial abscess with perforation of wall or septum
Cardiac failure
Suppurative pericarditis
2.Renal complications:
Glomerulonephritis may lead to renal failure
Embolic infarction
3.Embolic complication:
Left side
Sterile emboli cause cerebral, coronary, renal or splenic infarction
Septic emboli cause abscesses in brain, kidney and other organs
Right side
Septic emboli cause pulmonary congestion
Septic emboli cause lung abscess
Microthromboemboli manifest as splinter or subungual haemorrhage
Erythematous or haemorrhagic nontenderlesion on palm and sole: Janeway lesions
Subcutaneous nodule in pulp of the digits: Osler node
Retinal haemorrhage in the eye: Roth spot
