04.22 - Ischemic HD 2 (Nichols) Flashcards by Ryan Lee

Stunned Myocytes =

Myocytes injured by acute ischemia (look normal microscopically, need time to repair before they work normally again)

How well did you know this?

Not at all

Perfectly

3 Different proteins that influence/ compose the mPTP

Voltage-dep anion Channel (VDAC), Adenine Nucleotide Translocator (ANT), Cyclophilin D (CypD)

How well did you know this?

Not at all

Perfectly

5 Factors that Contribute to Reperfusion Injury:

(1) Mitochondrial Dysfunction; (2) Myocyte Hypercontracture; (3) ROS; (4) Leukocyte Aggregation; (5) Platelet and complement activation

How well did you know this?

Not at all

Perfectly

5 Major (Jones) Criteria for Dx of Acute Rheumatic Fever

Fever, Polyarthritis, Sydenham’s Chorea, Subcutaneous Nodules, Erythema Marginatum

How well did you know this?

Not at all

Perfectly

6 Lethal Causes of Chest pain

Acute Coronary Syndromes, Pulmonary Embolism, Aortic Dissection, Pneumothorax, Pericardial Tamponade, Mediastinitus

How well did you know this?

Not at all

Perfectly

Angina Pectoris

Exertional chest pain due to inadequate perfusion, and is typically due to atherosclerotic disease causing greater than 70% fixed stenosis

How well did you know this?

Not at all

Perfectly

Aschoff Bodies =

Foci of Fibrinoid Necrosis with Histiocytes and Anitschkow cells

How well did you know this?

Not at all

Perfectly

Aschoff Body:

Microscopic lesion of fibrinoid necrosis w/ histiocytes and Anitschkow Cells

How well did you know this?

Not at all

Perfectly

Autocoids released during ischemia that activate G proteins in preconditioning

Adenosine, Bradykinin, Opioids

How well did you know this?

Not at all

Perfectly

Chordae in Mitral Stenosis

Thickened, Retracted, and Fused

How well did you know this?

Not at all

Perfectly

Chronic IHD is aka

Ischemic Cardiomyopathy

How well did you know this?

Not at all

Perfectly

Chronic Rheumatic Heart Disease is more common with

Recurrent Carditis, Severe Carditis, and Carditis at an early age

How well did you know this?

Not at all

Perfectly

Chronically Ischemic Myocytes, which have cleared cytoplasm due to catabolism of their contractile proteins and need time to regenerate their contractile proteins before they work normally again

Hibernating Myocytes

How well did you know this?

Not at all

Perfectly

Clinical presentation of classical MI

Severe, Crushing substernal chest pain that can radiate to neck, jaw, epigastrium, or left arm

How well did you know this?

Not at all

Perfectly

Clinical presentation of Fibrinohemorhagic Pericarditis

Anterior Chest Pain and Pericardial Friction Rub

How well did you know this?

Not at all

Perfectly

Clumped chromatin resembling caterpillar

Anitschkow Cells

How well did you know this?

Not at all

Perfectly

Contraction band necrosis

Intense eosinophilic bands of hypercontracted sarcomeres are created by an influx of calcium across plasma membranes that enhances action-myosin interactions; In absence of ATP, sarcomeres cannot relax and get stuck in an agonal tetanic state

How well did you know this?

Not at all

Perfectly

Do Ventricular Aneurysms usually rupture?

How well did you know this?

Not at all

Perfectly

Epicardial manifestation of underlying myocardial inflammation

Fibrinohemorhagic Pericarditis

How well did you know this?

Not at all

Perfectly

Fibrin + Platelet thrombi on valves and Aschoff Bodies w/ Anitschkow Cells

Microscopic pathology of Acute Rheumatic Heart Disease

How well did you know this?

Not at all

Perfectly

Fibrinohemorhagic Pericarditis

Epicardial manifestation of underlying myocardial inflammation

How well did you know this?

Not at all

Perfectly

Fibroblasts with multiple bodies inside them =

Metabolically active, not necessarily pathologic

How well did you know this?

Not at all

Perfectly

Foci of Fibrinoid Necrosis with Histiocytes and Anitschkow cells

Aschoff Bodies

How well did you know this?

Not at all

Perfectly

Gross pathology of Acute Rheumatic Heart Disease

Tiny (1-2mm) verrucous vegetations lined up on line of valve closure; Fibrinous pericarditis

How well did you know this?

Not at all

Perfectly

Hibernating Myocytes

Chronically Ischemic Myocytes; Cleared cytoplasm due to catabolism of contractile proteins; Need time to regenerate those proteins

How common is Myocardial rupture as a complication of MI

1-5%, but frequently fatal if occurs

How do leukocytes contribute to ischemia reperfusion injury

May occlude microvasculature; Elaborate proteases and elastases

How does complement activation contribute to ischemia reperfusion injury

No-reflow phenomenon

How does mitochondrial dysfunction contribute to ischemic injury

Alters permeability, apoptotic mediators released from mito

How long before Stunned Myocytes work normally again

Several days at least

How often do isolated Right Ventricular Infarcts occur relative to all

1-3%

In the vast majority of cases, cardiac ischemia is due to

Coronary Artery Atherosclerosis

In whom are silent infarcts more likely

DM, Elderly

Is classic MI chest pain relieved by Nitroglycerin

Ischemic Preconditioning

Resistance to mild-moderate ischemia due to induction of protective proteins by brief episodes of ischemia

Light Microscopic appearance of Hibernating Myocytes

Myocytolysis

Marantic Endocarditis =

Nonbacterial Thrombotic Endocarditis

Marantic Endocarditis is common with

Cancer, DIC, Hypercoagulable states, Long-term venous catheterization

Microscopic findings in Chronic IHD

Myocardial hypertrophy, Diffuse Subendocardial Myocyte Vacuolization, and Fibrosis from previous infarction

Microscopic lesion of fibrinoid necrosis w/ histiocytes and Anitschkow Cells

Aschoff Body:

Microscopic pathology of Acute Rheumatic Heart Disease

Fibrin + Platelet thrombi on valves and Aschoff Bodies w/ Anitschkow Cells

Microscopically, irreversibly damaged myocytes subject to reperfusion show

Contraction band necrosis

Mitral stenosis is almost all

Rheumatic, Marked femal predominance

Myocardial ischemia leads to loss of myocyte function within

1-2 minutes, but causes necrosis only after 20-40 minutes

Nonbacterial Thrombotic Endocarditis

Marantic Endocarditis =

Opening of what is prevented in Ischemic Preconditioning

mPTP

Overall death rate in first year after MI

30%, then 3-4% annually

Pathology of Marantic Endocarditis

Small (1-5mm) fibrin + platelet thrombi

Pathology of Mitral Stenosis

Slitlike fishmouth; or Round Buttonhole Stenosis w/ fibrous thickening and rigidity of valve

Patients with Anterior Transmural MI's are at greatest risk for

Free Wall Rupture, Expansion, Formation of Mural Thrombi, and Aneurysm Formation

Patients with Chronic IHD typically exhibit

LV dilation and hypertrophy

Patients with Posterior Transmural MI's are at greatest risk for

Serious conduction blocks, RV involvement

Presence of Fibroblasts indicates about what age

6 days old

Primary mechanism of Ischemic Preconditioning

Preservation of Mitochondrial function and ATP production

Prime target of excess oxygen radicals and calcium is

Mitochondrial Permeability Transition Pore (mPTP)

Slitlike fishmouth; or Round Buttonhole Stenosis w/ fibrous thickening and rigidity of valve

Pathology of Mitral Stenosis

Sudden cardiac death usually results from

A fatal arrhythmia, typically without significant acute myocardial damage

Time course of CK-MB in MI

Begins 2-4 hours; Peaks 24-48 hours; normal within 72 hours

Time course of Troponin

Begins 2-4 hours; Elevated for 7-10 days

Tiny (1-2mm) verrucous vegetations lined up on line of valve closure; Fibrinous pericarditis

Gross pathology of Acute Rheumatic Heart Disease

Unstable Angina Results from

Small fissure or rupture of atherosclerotic plaque triggering platelet agg, vasoconstriction, and formation of mural thrombus

What accounts for the vast majority of MI-related deaths before hospitalization

Lethal Arrhythmias

What causes mycocyte hypercontracture in ischemia

Ca increased; After reperfusion, contraction is uncontrolled and causes damage

What is result of ROS and Ca binding mPTP

Opening --> Collapsing mitochondrial function

What is the mPTP

Mitochondrial Permeability Transition Pore: V-dependent channel regulated by Ca and Oxidative stress

What is the precursor for infective endocarditis

Marantic Endocarditis

What large influx occurs in Reperfusion injury

Calcium

What layers are inflamed in Acute Rheumatic Heart Disease

All

What percent of MI's result in rhythm disturbance

90% (higher in stemis vs non-stemis)

What percent of ventricle must be affected in MI to cause cardiogenic shock

40%

When does myocardial rupture occur?

3-7 days after infarction

When does pericarditis occur in timeline after MI

2-3 days, then usually gradually resolves

When does Ventricular Aneurysm occur in timline after MI

Late

When is serious arrhythmia risk highest in timeline of MI

In first hour then declines

Where is Marantic Endocarditis most common:

First: Atrial Side of Mitral Valve; Ventricular side of Aortic Vavle

Which has worse prognosis: anterior or posterior infarct

Which is more sensitive in early stages of MI: CK-MB or Troponin?

Equal

Why are Anitschkow Cells also called caterpillar cells

Clumped chromatin resembling a caterpillar

Why can large infarct cause hemiparalysis and when does it usually occur

Embolus from Mural Thrombus, day 7

Why do myocardial ruptures occur 3-7 days after infraction

Time in healing process when lysis of myocardial CT is maximal, and when much of infarct has been converted to soft, friable granulation tissue

04.22 - Ischemic HD 2 (Nichols) Flashcards

(80 cards)