04.22 - Ischemic HD 2 (Nichols) Flashcards
Stunned Myocytes =
Myocytes injured by acute ischemia (look normal microscopically, need time to repair before they work normally again)
3 Different proteins that influence/ compose the mPTP
Voltage-dep anion Channel (VDAC), Adenine Nucleotide Translocator (ANT), Cyclophilin D (CypD)
5 Factors that Contribute to Reperfusion Injury:
(1) Mitochondrial Dysfunction; (2) Myocyte Hypercontracture; (3) ROS; (4) Leukocyte Aggregation; (5) Platelet and complement activation
5 Major (Jones) Criteria for Dx of Acute Rheumatic Fever
Fever, Polyarthritis, Sydenham’s Chorea, Subcutaneous Nodules, Erythema Marginatum
6 Lethal Causes of Chest pain
Acute Coronary Syndromes, Pulmonary Embolism, Aortic Dissection, Pneumothorax, Pericardial Tamponade, Mediastinitus
Angina Pectoris
Exertional chest pain due to inadequate perfusion, and is typically due to atherosclerotic disease causing greater than 70% fixed stenosis
Aschoff Bodies =
Foci of Fibrinoid Necrosis with Histiocytes and Anitschkow cells
Aschoff Body:
Microscopic lesion of fibrinoid necrosis w/ histiocytes and Anitschkow Cells
Autocoids released during ischemia that activate G proteins in preconditioning
Adenosine, Bradykinin, Opioids
Chordae in Mitral Stenosis
Thickened, Retracted, and Fused
Chronic IHD is aka
Ischemic Cardiomyopathy
Chronic Rheumatic Heart Disease is more common with
Recurrent Carditis, Severe Carditis, and Carditis at an early age
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
Clinical presentation of classical MI
Severe, Crushing substernal chest pain that can radiate to neck, jaw, epigastrium, or left arm
Clinical presentation of Fibrinohemorhagic Pericarditis
Anterior Chest Pain and Pericardial Friction Rub
Clumped chromatin resembling caterpillar
Anitschkow Cells
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
Do Ventricular Aneurysms usually rupture?
No
Epicardial manifestation of underlying myocardial inflammation
Fibrinohemorhagic Pericarditis
Fibrin + Platelet thrombi on valves and Aschoff Bodies w/ Anitschkow Cells
Microscopic pathology of Acute Rheumatic Heart Disease
Fibrinohemorhagic Pericarditis
Epicardial manifestation of underlying myocardial inflammation
Fibroblasts with multiple bodies inside them =
Metabolically active, not necessarily pathologic
Foci of Fibrinoid Necrosis with Histiocytes and Anitschkow cells
Aschoff Bodies
Gross pathology of Acute Rheumatic Heart Disease
Tiny (1-2mm) verrucous vegetations lined up on line of valve closure; Fibrinous pericarditis
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
No
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
Anterior
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
