Path Flashcards

1
Q

LAD

A

Anterior/anteroseptal wall of LV

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2
Q

LCx

A

Lateral wall LV

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3
Q

LAD+RCA

A

Septal wall

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4
Q

RCA

A

Posterior wall/posterior 1/3 of interventicular septum** SA node so infarct here can result in arrhythmia

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5
Q

Gross Changes Post MI0-12 h12-1824-721 wk2-3wk4-6wk

A

0-12 Hours – No changes 12-18 Hours – Pallor 24-72 Hours – White Infarct with Hyperemic Borders1 Week – Loss of Hyperemia 2-3 Weeks – Soft Gelatinous4-6 Weeks – Scarring/Fibrosis

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6
Q

Systolic Murmurs

A

Aortic StenosisPulmonic StenosisMitral Regurgitation/ProlapseTricuspid RegurgitationVentricular Septal DefectHypertrophic Cardiomyopathy

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7
Q

Histologic Time Sequence Post MI3-6 hr12-24 hr24 hr5-7d8-10d10-14d2-4wk4-6wk

A

3-6 Hours – Wavy fibers (non-contracting ischemic myocytes 12-24 Hours – Coagulation necrosis, hypereosinophilic myocytes24 Hours – Neutrophil infiltration peaking at 3-5 days5-7 Days – Macrophage infiltration and neutrophils regress 8-10 Days – Lipofuscin (wear and tear pigment)10-14 Days – Granulation tissue at infarct borders 2-4 Weeks – Fibroblasts depositing collagen4-6 Weeks+ - Mature Scar

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8
Q

Diastolic Murmurs

A

Aortic RegurgitationPulmonic RegurgitationMitral Stenosis Tricuspid Stenosis

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9
Q

Best to hear Aortic Valve

A

2nd-3rd R interspace

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10
Q

best to hear pulmonic valve

A

2nd-3rd L interspace

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11
Q

best to hear tricuspid valve

A

L sternal border

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12
Q

best to hear mitral valve

A

apex

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13
Q

Type I Atherosclerosis: Thickening of Intima

A

smooth muscle cells (HHF-35 positive) – you have more of these come inno macrophages (CD68 negative) and no lipids (oil-red-O negative)

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14
Q

Type II Atherosclerosis: Intimal Xanthoma

A

Progressive thickening with macrophagesCD68 positive and Oil-red-O positiveThis is when you have the formation of FOAMY CELLS (macrophages filled with lipids)

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15
Q

Type III Atherosclerosis: Pathologic Intimal Thickening

A

small cells of extracellular liquidNo symptoms at this point, because of positive remodeling Diameter of the artery changes, but the diameter of the lumen doesn’t changeThis is when you start to get worried, but this is not pathologic yet

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16
Q

Type IV Atherosclerosis: Fibroatheroma

A

core of extra-cellular lipid starts to formstart to get symptoms because lumen starts to be narrowed

17
Q

Type V Atherosclerosis: Thin-cap fibroatheroma

A

Fibrous thickening of cap. Completion of formation of fibroatheroma. Fibroatheroma = well-formed lipid necrotic core surrounded by macrophages and lymphocytes with an overlying fibrous cap rich in SMCsThin-Cap Fibroatheroma = vulnerable plaque (i.e. vulnerable to disruption, leading to coronary thrombosis), since it has a thin fibrous cap infiltrated by macrophages (CD 68+) Cap – made of fibrin and smooth muscle cells, will start getting thin or thick, important to know if it is thin or thickLipid necrotic core

18
Q

Type VI Atherosclerosis: Thrombus

A

Thrombus formation after surface defectOccurs either by plaque rupture or plaque erosion

19
Q

6 Stages of Atherosclerosis

A

Thickening of IntimaIntimal XanthomaPathological Intimal ThickeningFibroatheromaThin-cap fibroatheromaThrombus

20
Q

Most Common cause of death post-MI

A
21
Q

Congenital Diseases predisposing to aneurysm

A

Marfan Syndrome: Fibrillin-1, elastinEhler’s Danlos Syndrome: mutation in collagen, procollagen Type III

22
Q

Libman-Sacks endocarditis

A

Non-infectiousUndersurface of valvesAssoc w/ SLESmall, sterile emboli break offTricuspid, mitral

23
Q

Aortic stenosis auscultation

A

Normal S1Ejection clickSystolic C-D murmurNormal S2Diastolic D murmur

24
Q

Aortic regurg auscultation

A

Softer S1Ejection clickBrief, early systolic murmurSingle, softer S2S3 gallop*diastolic D murmur (low pitch = severe)

25
Q

Mitral stenosis auscultation

A

Louder S1Opening snapPulmonic component S2 gets louderDiastolic murmur

26
Q

Mitral regurg ausculatation

A

S1 normal or diminished*holosystolic, steady murmurS2 sound splitting increasedDiastolic murmur possibleSoft S3 gallop