# Cardiovascular System for NEET PG Pathology: Atherosclerosis, Aneurysm, MI, Rheumatic Fever, Endocarditis, Cardiomyopathy, Congenital Heart Disease

Source: https://tracknation.in/story/cardiovascular-system-for-neet-pg-pathology-atherosclerosis-aneurysm-mi-rheumatic-fever-endocarditis-cardiomyopathy-congenital-heart-disease (TrackNation — free UPSC notes with PYQs)

> NEET PG Pathology: arteriosclerosis and atherosclerosis, AAA and aortic dissection, myocardial infarct timeline and TTC staining, rheumatic fever and Aschoff bodies, infective, Libman-Sacks and marantic endocarditis, cardiomyopathies, pericarditis, myxoma and rhabdomyoma, and congenital heart disease, with a diagram, hooks, vignette MCQs and cards.

## Start Here

🎯 **Exam priority: High.** *Expect: infarct age from the histology, TTC staining, Aschoff bodies and the Jones criteria,
Osler vs Janeway, Libman-Sacks vs marantic vegetations, HCM genetics and disarray, the commonest cardiac tumour, and TOF/VSD/ASD/PDA/coarctation clues.*

CBME mapping: **PA 26.1–26.10**. Haemodynamics (thrombosis, embolism, infarction in general) is in article 3; amyloid heart in article 6.

*Infarct timeline, valve vegetations, vessels, cardiomyopathy, tumours and congenital heart disease. Drawn by TrackNation.*

## Arteries and Aneurysms

- **Arteriosclerosis** = arterial wall thickening with lost elasticity. Three forms: **atherosclerosis** (intimal
plaques in large and medium arteries), **arteriolosclerosis** (small arteries and arterioles thickened by cell proliferation or hyaline
deposition) and **Mönckeberg medial calcific sclerosis** (calcified media of muscular arteries).

- **Atheroma**: monocytes become macrophages, take up lipoprotein through scavenger receptors and turn into **foam
cells** — the hallmark of the early plaque. A mature plaque has a lipid core under a **fibrous cap** of smooth muscle and collagen.
A *vulnerable* plaque has a thin cap and a big lipid core and is the one that ruptures.

- **Abdominal aortic aneurysm**: diameter ≥ 3 cm, usually infrarenal. Smoking is the strongest risk factor. Repair when
> 5.5 cm in men or > 5 cm in women. **Mycotic** (infected) aneurysm: *S. aureus* first, then *Salmonella*.

- **Aortic dissection**: blood surges through an intimal tear and splits intima from media, making a false lumen.
Hypertension is a key contributor. Peak age 50–65 in general but 20–40 in Marfan or Ehlers-Danlos. **Stanford A** involves the ascending
aorta; **B** is confined to the descending aorta beyond the left subclavian.

- Primary (essential) hypertension is about 85% of cases; the rest are secondary (for example primary aldosteronism, renal disease).

## Ischaemic Heart Disease

- **Spectrum**: unstable angina (ischaemia, troponin below the 99th percentile) → NSTEMI (subendocardial; troponin up, no ST
elevation) → STEMI. MI = troponin rise above the 99th percentile plus ischaemic symptoms, ECG change or imaging evidence.

- **Type 1 MI**: plaque rupture, erosion or fissuring with thrombus. **Type 2**: supply-demand mismatch (for
example coronary spasm or a demand surge). **Transmural** infarcts span epicardium to endocardium.

- **Infarct age on histology** (autopsy series): < 4 h wavy fibres with a few neutrophils; 4–12 h coagulative necrosis;
7–10 days granulation tissue at the edge; > 6 weeks fibrous scar. Gross changes need 24–48 h, so very early infarcts are found with
**TTC stain**: living muscle turns brick red (dehydrogenase activity); the infarct stays pale.

- **Site clues**: right ventricular infarction usually means proximal right coronary artery occlusion. Papillary muscle
dysfunction gives a soft apical murmur of mitral regurgitation; a friction rub on days 2–3 after STEMI is common.

## Rheumatic Fever and Endocarditis

- **Rheumatic fever**: a non-suppurative complication of group A streptococcal *pharyngitis* — arthritis, carditis,
subcutaneous nodules, erythema marginatum, chorea (modified Jones criteria). Evidence of preceding infection: throat culture/antigen or ASO > 320 U.

- **Aschoff bodies** (granulomatous collections of leukocytes, myocytes and collagen) form in the myocardium. Carditis is a
pancarditis, but **valvulitis** is its most consistent feature. Acute: mitral regurgitation; chronic rheumatic heart disease: **mitral
stenosis**, then aortic disease. Sydenham chorea reflects basal ganglia involvement.

- **Infective endocarditis**: *S. aureus* attacks even normal valves; viridans streptococci follow dental bacteraemia (even
toothbrushing with gingivitis). Mostly left-sided; 5–10% right-sided (tricuspid, pulmonary), much commoner in IV drug users. HACEK organisms are a
minority. Signs: Roth spots (retina), **Osler nodes** (painful, finger tips), **Janeway lesions** (painless, palms and soles),
splinter haemorrhages.

| **Valve lesion**

 | **Vegetations**

 | **Setting / clue**

 |
| Rheumatic

 | Valvulitis with Aschoff bodies in the myocardium

 | Group A streptococcal throat infection; mitral, then aortic valve

 |
| Infective

 | Infected, friable; destroy valves, cause emboli

 | S. aureus (even normal valves), viridans streptococci after dental bacteraemia

 |
| Libman-Sacks

 | Sterile platelet-fibrin, along the leaflet closure line

 | SLE (circulating immune complexes)

 |
| Marantic (non-bacterial thrombotic)

 | Sterile, embolise

 | Mucin-producing cancers (lung, stomach, pancreas), wasting disease, DIC

 |

## Myocardium, Pericardium and Tumours

- **Dilated cardiomyopathy**: genetic, or acquired — coxsackievirus B, *Trypanosoma cruzi*, alcohol, cardiotoxic
chemotherapy. The commonest cardiomyopathy of childhood.

- **Hypertrophic cardiomyopathy**: usually a **sarcomere gene** mutation. Asymmetric hypertrophy of the basal septum;
histology shows myocyte hypertrophy, **myocyte disarray** and fibrosis. Systolic murmur louder with Valsalva; syncope and sudden death.

- **Restrictive cardiomyopathy**: stiff walls that impede filling with near-normal systolic function — amyloidosis, sarcoidosis,
haemochromatosis, Fabry, and endomyocardial fibrosis (children and young adults in the tropics).

- **Pericarditis**: mostly viral or idiopathic in the West, **TB** where TB is endemic; also uraemia, MI, cancer.
Constrictive pericarditis = fibrous scarring fuses both layers. Tamponade = compression by fluid or blood.

- **Cardiac tumours**: metastases are far commoner than primaries. **Myxoma** is the commonest primary, usually in the
**left atrium**; about 15% of pedunculated ones give a "tumour plop". **Rhabdomyoma** is the commonest in children — up to 90%
have tuberous sclerosis.

## Congenital Heart Disease

- The commonest congenital anomaly, in almost 1% of live births.

- **VSD**: about 20% of defects; loud harsh holosystolic murmur at the lower left sternal border. A large shunt raises pulmonary
resistance until flow reverses — **Eisenmenger syndrome**.

- **ASD (secundum**, at the fossa ovalis): wide, fixed splitting of S2; paradoxical emboli later. **PDA**:
continuous murmur and bounding pulses; a COX inhibitor (ibuprofen or indomethacin) may close it in preterm babies.

- **Tetralogy of Fallot** — the commonest cyanotic lesion (twice TGA): large VSD, RV outflow obstruction, RV hypertrophy, overriding
aorta. Boot-shaped heart; right aortic arch in 25%. **TGA**: egg-on-a-string shadow with a narrow mediastinum.

- **Coarctation**: in 10–20% of Turner syndrome; arm hypertension with weak, delayed femoral pulses; collateral intercostal arteries
notch ribs 3–8 (rarely before age 5).

## Traps the Examiner Sets

- Osler = Ouch (painful); Janeway = painless.

- Libman-Sacks (SLE) and marantic vegetations are sterile; infective ones are not.

- Acute rheumatic carditis → mitral *regurgitation*; chronic → mitral *stenosis*.

- TTC: pale = dead; brick red = alive.

- Commonest primary cardiac tumour: myxoma (adult, left atrium); in children: rhabdomyoma (tuberous sclerosis).

## Memory Hooks & Shortcuts

*Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.*

- 🧠 **Osler = Ouch; Janeway = painless (J for 'just a spot')** — IE skin signs

- 🧠 **Wavy at 4, Necrosis by 12, Granulation at 10 days, Scar at 6 weeks** — infarct dating

- 🧠 **TTC: Tissue That's Caput stays pale** — TTC staining

- 🧠 **Libman-Sacks = Lupus; Marantic = Malignancy (mucin)** — sterile vegetations

- 🧠 **Myxoma Mostly in the left atriuM** — myxoma

- 🧠 **Rhabdo for babies with tubers (tuberous sclerosis)** — rhabdomyoma

- 🧠 **Turner turns the aorta tight (coarctation)** — coarctation

## Rapid-Revision Cards

- Small arteries/arterioles: hyaline or cell proliferation.

- Calcified media of muscular arteries.

- Foam cells (lipid-laden macrophages).

- Thin fibrous cap, big lipid core.

- ≥ 3 cm, infrarenal; smoking; repair > 5.5 cm (men).

- S. aureus, then Salmonella.

- A = ascending aorta; B = descending only.

- Wavy fibres, few neutrophils.

- Coagulative necrosis.

- Granulation tissue at the edge.

- Fibrous scar.

- Brick red = alive; pale = infarct.

- 1 = plaque rupture; 2 = supply-demand.

- Rheumatic carditis; myocardium.

- Acute MR; chronic mitral stenosis.

- > 320 U.

- Osler painful finger tips; Janeway painless palms/soles.

- Right-sided (tricuspid).

- SLE; sterile; closure line.

- Mucin-producing cancer; sterile; embolise.

- Sarcomere genes; septum; disarray; Valsalva ↑ murmur.

- Amyloid, sarcoid, haemochromatosis, EMF.

- Commonest primary; left atrium; tumour plop.

- Children; tuberous sclerosis.

- VSD, RVOT block, RVH, overriding aorta; boot heart.

- Wide fixed split S2.

- Turner; weak femorals; rib notching.

## Sources

*Facts in this article were checked against these documents.*

- MSD Manual Professional: Atherosclerosis; Abdominal Aortic Aneurysms; Aortic Dissection; Hypertension; Heart Failure — Merck & Co. (MSD Manuals), reviewed 2024–26 (link)

- MSD Manual Professional: Acute Coronary Syndromes; Acute Myocardial Infarction; Infective and Noninfective Endocarditis; Rheumatic Fever; Dilated, Hypertrophic and Restrictive Cardiomyopathy; Pericarditis; Cardiac Tumors — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

- MSD Manual Professional: Congenital Cardiovascular Anomalies (overview, VSD, ASD, PDA, Tetralogy of Fallot, TGA, Coarctation) — Merck & Co. (MSD Manuals), reviewed 2023–26 (link)

- Standard Treatment Workflow: Acute Rheumatic Fever — ICMR, 2022

- Medical Subject Headings (scope notes) — US National Library of Medicine, 2026 (link)

- Varun KB et al. Comparison of histopathological and triphenyl tetrazolium chloride test in diagnosing myocardial infarction: an autopsy study. F1000Research (CC BY 4.0) — F1000Research, 2024 (link)

- Competency Based Undergraduate Curriculum, Pathology (PA 26) — National Medical Commission, 2024

## Test Yourself: Practice Questions

Thirty-four questions in NEET PG style, most of them clinical vignettes.

## Practice Questions (NEET PG pattern)

*Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer
was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.*

**Q1.** A kidney biopsy shows small arteries and arterioles whose walls are thickened by hyaline deposition. This lesion is

- (a) fibromuscular dysplasia

- (b) arteriolosclerosis

- (c) Mönckeberg medial calcific sclerosis

- (d) atherosclerosis

**Answer: (b)** — Arteriolosclerosis thickens small vessels by hyaline deposition or cell proliferation.

**Q2.** Sections of a muscular artery show calcification confined to the tunica media, with the intima spared. The condition is

- (a) Buerger disease

- (b) atherosclerosis

- (c) arteriolosclerosis

- (d) Mönckeberg medial calcific sclerosis

**Answer: (d)** — Calcification of the tunica media of muscular arteries.

**Q3.** The cell that is the hallmark of the early atherosclerotic plaque is the

- (a) plasma cell

- (b) Langhans giant cell

- (c) eosinophil

- (d) foam cell (lipid-laden macrophage)

**Answer: (d)** — Macrophages ingest lipoprotein through scavenger receptors.

**Q4.** Which plaque is most likely to rupture and cause an acute coronary event?

- (a) a fatty dot without a core

- (b) heavily calcified small plaque

- (c) thick fibrous cap with a small lipid core

- (d) thin fibrous cap with a large lipid core

**Answer: (d)** — Matrix breakdown thins and weakens the cap.

**Q5.** A 72-year-old smoker has a pulsatile abdominal mass. Ultrasound shows an infrarenal aortic diameter of 3.8 cm. The single strongest risk factor for this lesion is

- (a) syphilis

- (b) diabetes

- (c) female sex

- (d) smoking

**Answer: (d)** — AAA = aortic diameter ≥ 3 cm.

**Q6.** The organism most often responsible for a mycotic (infected) aortic aneurysm is

- (a) Candida

- (b) Staphylococcus aureus

- (c) Streptococcus pyogenes

- (d) Treponema pallidum

**Answer: (b)** — Salmonella is second.

**Q7.** A 30-year-old with Marfan syndrome has abrupt tearing chest pain. Imaging shows an intimal flap and double lumen involving the ascending aorta. This is

- (a) Stanford type A aortic dissection

- (b) abdominal aortic aneurysm

- (c) Stanford type B dissection

- (d) pulmonary embolism

**Answer: (a)** — Type A involves the ascending aorta; connective tissue disorders lower the age of onset.

**Q8.** The basic lesion of aortic dissection is

- (a) a saccular outpouching of all three layers

- (b) an intimal tear with blood splitting intima from media (false lumen)

- (c) a full-thickness wall rupture

- (d) medial calcification

**Answer: (b)** — Hypertension is an important contributor.

**Q9.** A man with severe chest pain dies within 3 hours. The most likely microscopic finding in the infarcted myocardium is

- (a) wavy fibres with a few neutrophils

- (b) dense fibrous scar

- (c) granulation tissue

- (d) macrophages full of haemosiderin only

**Answer: (a)** — Coagulative necrosis is obvious from about 4–12 hours.

**Q10.** At autopsy, the margin of a myocardial infarct shows well-formed granulation tissue. The infarct is most likely about

- (a) 2 hours old

- (b) 7–10 days old

- (c) 12 hours old

- (d) 6 months old

**Answer: (b)** — A scar is seen after 6 weeks.

**Q11.** A heart slice is immersed in triphenyl tetrazolium chloride (TTC). A pale unstained area against brick-red muscle means

- (a) normal myocardium

- (b) fatty infiltration

- (c) infarcted myocardium that has lost dehydrogenase activity

- (d) fixation artefact

**Answer: (c)** — Useful because gross infarct changes need 24–48 hours.

**Q12.** An MI caused by coronary plaque rupture with thrombosis is classified as

- (a) type 3

- (b) type 2

- (c) type 5

- (d) type 1

**Answer: (d)** — Type 2 is supply-demand mismatch.

**Q13.** A patient has rest angina for 30 minutes; ECG has no ST elevation and troponin stays below the 99th percentile. The diagnosis is

- (a) unstable angina

- (b) STEMI

- (c) NSTEMI

- (d) type 2 MI

**Answer: (a)** — No necrosis means no troponin rise.

**Q14.** An infarct of the right ventricle most often results from occlusion of the

- (a) left anterior descending artery

- (b) left main coronary artery

- (c) diagonal branch

- (d) proximal right coronary artery

**Answer: (d)** — Raised RV filling pressure, often with tricuspid regurgitation.

**Q15.** Two to three weeks after a sore throat, a child develops migratory polyarthritis and an apical pansystolic murmur. Which antibody titre supports preceding streptococcal infection?

- (a) anti-dsDNA

- (b) anti-CCP

- (c) ANCA

- (d) ASO above 320 units

**Answer: (d)** — Or a positive throat culture or rapid antigen test.

**Q16.** Heart tissue from a child who died of acute rheumatic carditis shows granulomatous collections of leukocytes, myocytes and collagen. These are

- (a) Aschoff bodies

- (b) Anitschkow cells alone

- (c) Mallory bodies

- (d) Langhans giant cells

**Answer: (a)** — They develop in the myocardium and other parts of the heart.

**Q17.** The commonest valve lesion of chronic rheumatic heart disease is

- (a) mitral stenosis

- (b) tricuspid stenosis alone

- (c) pulmonary stenosis

- (d) aortic coarctation

**Answer: (a)** — Acute carditis more often gives mitral regurgitation.

**Q18.** The most consistent feature of rheumatic carditis, without which the diagnosis should be reconsidered, is

- (a) valvulitis

- (b) myocardial abscess

- (c) heart block

- (d) pericardial effusion

**Answer: (a)** — Although it is a pancarditis.

**Q19.** A patient with fever and a murmur has painful red nodules on the finger pads. These are

- (a) Osler nodes

- (b) splinter haemorrhages

- (c) Janeway lesions

- (d) Roth spots

**Answer: (a)** — Janeway lesions are painless and on palms and soles.

**Q20.** A person who injects drugs has septic pulmonary emboli. The valve most likely involved by endocarditis is the

- (a) tricuspid valve

- (b) mitral valve

- (c) a prosthetic mitral valve

- (d) aortic valve

**Answer: (a)** — Right-sided disease is much commoner in IV drug users.

**Q21.** An organism able to cause endocarditis on a previously normal valve is

- (a) Staphylococcus aureus

- (b) Lactobacillus

- (c) Staphylococcus epidermidis on a native valve

- (d) Corynebacterium diphtheriae

**Answer: (a)** — Massive bacteraemia or virulent organisms.

**Q22.** A woman with SLE has small sterile vegetations along the closure line of the mitral leaflets. These are

- (a) Libman-Sacks lesions

- (b) marantic vegetations

- (c) Lambl excrescences

- (d) infective vegetations

**Answer: (a)** — Immune complexes cause platelet-fibrin vegetations.

**Q23.** A man with metastatic pancreatic adenocarcinoma has a systemic arterial embolus; echo shows valve vegetations and blood cultures are negative. The lesion is

- (a) Libman-Sacks endocarditis

- (b) rheumatic valvulitis

- (c) carcinoid heart disease

- (d) marantic (non-bacterial thrombotic) endocarditis

**Answer: (d)** — Mucin-producing carcinomas of lung, stomach or pancreas.

**Q24.** A young athlete collapses and dies. Autopsy shows asymmetric thickening of the basal interventricular septum and microscopic myocyte disarray. The usual cause is

- (a) a sarcomere protein gene mutation

- (b) amyloid deposition

- (c) alcohol

- (d) coxsackievirus myocarditis

**Answer: (a)** — Hypertrophic cardiomyopathy; murmur louder with Valsalva.

**Q25.** Which of these is a recognised infectious cause of dilated cardiomyopathy?

- (a) Mycobacterium leprae

- (b) Treponema pallidum

- (c) Trypanosoma cruzi

- (d) Entamoeba histolytica

**Answer: (c)** — Also coxsackievirus B; alcohol and chemotherapy are toxic causes.

**Q26.** Restrictive cardiomyopathy with stiff ventricles and near-normal systolic function is classically caused by

- (a) sarcomere gene mutation

- (b) coxsackievirus B

- (c) chronic alcohol use

- (d) amyloidosis

**Answer: (d)** — Also sarcoidosis, haemochromatosis, Fabry disease.

**Q27.** In a country where tuberculosis is endemic, the commonest cause of pericarditis is

- (a) tuberculosis

- (b) uraemia

- (c) radiation

- (d) viral infection

**Answer: (a)** — In the West it is mostly viral or idiopathic.

**Q28.** A woman has a murmur like mitral stenosis whose loudness varies with body position; echo shows a pedunculated left atrial mass. The likely tumour is

- (a) rhabdomyoma

- (b) fibroma

- (c) myxoma

- (d) angiosarcoma

**Answer: (c)** — The commonest primary cardiac tumour; most arise in the left atrium.

**Q29.** An infant with multiple cardiac tumours in the ventricular walls is most likely to have which underlying syndrome?

- (a) tuberous sclerosis

- (b) Down syndrome

- (c) Marfan syndrome

- (d) Turner syndrome

**Answer: (a)** — Rhabdomyoma, the commonest cardiac tumour of children.

**Q30.** A cyanotic infant's chest X-ray shows a boot-shaped heart with reduced pulmonary markings. The four components of the lesion are

- (a) ASD, PDA, LVH, coarctation

- (b) VSD, ASD, PDA, TGA

- (c) mitral stenosis, AR, TR, PS

- (d) VSD, RV outflow obstruction, RV hypertrophy, overriding aorta

**Answer: (d)** — Tetralogy of Fallot, the commonest cyanotic congenital heart disease.

**Q31.** A child with an uncorrected large VSD later becomes cyanosed as pulmonary resistance rises and the shunt reverses. This is

- (a) Eisenmenger syndrome

- (b) Ebstein anomaly

- (c) tetralogy of Fallot

- (d) transposition

**Answer: (a)** — Right-to-left shunting.

**Q32.** Wide and fixed splitting of the second heart sound is typical of

- (a) patent ductus arteriosus

- (b) ventricular septal defect

- (c) coarctation

- (d) atrial septal defect

**Answer: (d)** — Secundum ASD lies at the fossa ovalis.

**Q33.** A preterm infant has bounding pulses and a continuous murmur at the upper left sternal border. Medical closure is attempted with

- (a) a cyclo-oxygenase inhibitor such as ibuprofen or indomethacin

- (b) a beta-blocker

- (c) digoxin

- (d) prostaglandin E1

**Answer: (a)** — Patent ductus arteriosus; after birth, falling prostaglandin normally closes the duct.

**Q34.** A girl with Turner syndrome has hypertension in the arms with weak, delayed femoral pulses. The likely cardiovascular lesion is

- (a) coarctation of the aorta

- (b) Ebstein anomaly

- (c) tetralogy of Fallot

- (d) patent ductus arteriosus

**Answer: (a)** — Occurs in 10–20% of Turner syndrome; rib notching may appear later.

### Active Recall

From memory: distinguish the three forms of arteriosclerosis; describe the atheroma and vulnerable plaque; define AAA and dissection; date an infarct from histology and explain TTC staining; describe rheumatic fever, Aschoff bodies and its valve lesions; compare infective, Libman-Sacks and marantic vegetations; summarise DCM, HCM and RCM; name the commonest cardiac tumours; and give the clues for VSD, ASD, PDA, TOF and coarctation.