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Download PG Medical 2nd Year Pathology CVS Handwritten Notes

Download PG Medical ( Post Graduate Medical degree) 2nd Year Pathology CVS Handwritten Notes

This post was last modified on 02 August 2021

NEET PG Last 15 Years 2012-2025 Previous Question Papers with Answers (Solved Question Papers)


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Adventitia

Lumen

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Media (smooth muscles)

Intima

One/2 layers of endothelial cells

Neo-intima endothelial cells + New smooth muscle cells

during injury, inflammation, grafting.

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Atherosclerosis - Intimal based plaques...

Risk factors

Modifiable

-Obesity

-DM

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-HTN.

Infections-

CMV + Herpes + Chlamydia

Non-modifiable

age

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male

stress (Type-A)

Hyperhomocystinuria

Widely accepted Hypothesis - Endothelial injury

Intimal

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cytokines

Recruit Smooth muscles Inflammation (macrophages)

Oxidized LDL + macrophages ? Foam cells

Smooth muscles

Fibrous plaque

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Fatty streak (earliest feature visible)

m/c site - Abdominal aorta Least/c site - Cardiac willing

Aneurysm - Dilatation of Blood wall Heartucale

a) True aneurysm. All layers of Blood vessel wall

b) Pseudo Aneurysm - only one wall (intimal) Tear

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extravascular Hematoma

m/c Cause - Post myocardial .cardiac wall ruptures

c) Mycotic aneurysm - m/c a/w Staphylococcus

m/c site - Femoral Artery

Luetic aneurysm - Syphilis (Tertiary stage)

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Intimal wrinkling - Tree Bark appearance

m/c site - Ascending aorta (Root)

AR ? enlarged Heart chamber Cor bovinum

Ascending A

Arch

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Hypertension

Atherosclerosis

Descending

Aortic dissection- 40-60 years.

Dissection into T.media

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M/C Cause aortic dissection ? HTN

m/c Histology - cystic medial degeneration: (Marfan's, ORTA, EDS)

Vasculitis

Large

1) Giant cell arteritis

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2) Takayasu

Medium

1) PAN

NO ANCA

all stages of inflammation in all vessels

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Small

Wegener's

microscopic polyangitis

Churg-Strauss

Medium

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Giant cell arteritis

Kawasaki

Segmental Biopsy

granulationmatous

Fragmentation of internal elastic lamina

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anti endothelial Ab

Small

Churg-Strauss

eosinophilic granuloma

P-ANCA

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M/C Cause of vasculitis:

a) Pediatric - Henoch Schonlein purpura.

b) Adult - Giant cell arteritis.

c) m/c COD in ped - Kawasaki

II Takayasu arteritis - m/c site - Subclavian arteritis.

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m/c Cause of mononeuritis multiplex

Diabetes mellitus (Ind/world)

amongst Vasculitis- PAN.

Hairy cell leukemia - PAN.

Anti endothelial antibodies-Kawasaki.

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Coronary Artery disease

Significant Obstruction >75%

Risk factors

1) hs-CRP.

2) Total cholesterol

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HDL

3) ApoB/ApoA.

4) LDL

5) HDL.

m/c site

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Left anterior descending artery

MI (LV)

Gross - up to 12 Hrs no

fading/occasional microscopy

TTCAssay- Triphenyl Tetrazolium chloride assay

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Normal TTC

LDH

+

TTC

Dark red Colour

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Normal.

MI

all LDH Released into Serum.

(no LDH to combine)

Pale colour

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M.I

earliest myoglobin

m. sensitive/specific - Troponin I>T.

?2-4hrs-7-10 days.

Re-infarction- CK-MB.

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Flipping of LDH - Normal LDH2>1

Gross

12Hrs Occasional dark mottling

established dark mottling

1-3 days- yellow-tan-infarct

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3-7 days- Hyperaemic Borders

2 months- Scarring complete.

Jeep pattern. LDH1>2.

Microscopy

4Hrs-waviness of fibres.

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12-24Hrs- Coagulation necrosis. early neutrophilic infiltrate

1-3 days-max Neutrophilic infilt

7-10 days- early granulation tissue

10-14 days- max. granulation tissue

EM

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1st/2how-mitochondrial Swelling

1/2how-Large flocculent amorphous densities.

GABH: 1, 3, 5, 6, 18

Pharyngitis 3+ RHD

valve m/c mitral

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4c-pulmonary

Aschoff Bodies

Swollen Collagen

Plasma cells

Histiocytes. Caterpillar like nuclear chromatin

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Anitschow cells

No epitheloid cells

No Langhans giant cells

Diagnostic of RHD

Aschoff Bodies - myocardium (m/c)-Perivascular areas.

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Pericardium

endocardium

Acute RHD:

m/c - mitral Regurgitation.

Overall- mitral stenosis

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Chronic

mitral stenosis

Atrium posterior wall

Subendocardial patches Mac Callum plaques

Aschoff Bodies

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Commonly seen in Chronic RHD

Chronic RHD- myocarditis

Overall - myocarditis

RHD

Small

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sterile

along line of closure of wall

(Coagulase)

NBTE (malignancy, estrogen) LSE I.E)

Small NBTE>RHD

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more prone for embolisation.

sterile.

along lined of closure of wall

medium Large

Verrucous.

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flat

Sterile

either side of wall.

Lower Surface up. upper>

pocket fucalls.

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Non-sterile.

Both surfaces

layer

One liners-

Destructive. max embolization,

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most destructive

Related Cardiomyopathy- a/w Largest Fibrin (30,000).

wall

Arrhythmogenic @ventricular Cardiomyopathy.

ake plakoglobin protein mutation.

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Lv Hypertrophy: osteoglycan (CGN).

HOCM: m/c cause of Sudden death in athletes HOCM

m/c mutation - BmHcgene (myosin heavy chain) in...

- Banana like cavity

MED

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Disarray of myofibers

Helter Skelter disarray)

Myocarditis - Viral infections

m/c- Parvovirus-B19+ Herpes Coxsackie

Parasite-m/c - Trichinella Spiralis.

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m/c Cause of Hemorrhagic pericarditis malignancy

m/c Cause-Lung Ca.

m/c Bpleen tumor Benign Cavernous Hemangioma,

Rest all malignancies.

m/c Tumor of Heart metastasis

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m/c - lung

m/c site-pericardium

Cardiac tumors

Pediatric

m/c malignancy

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Rhabdomyosarcoma?

1° Benign Rhabdomyoma.

Adults

m/c malignancy

Angiosarcoma.

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m/c Benign - Cardiac

myxoma.



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