Pathophysiology of Myocardial Infarction, COPD, BPH

Predisposing factors: Precipitating Factors

age - 89 y.o. sedentary lifetyle
gender - male hypertension
History of CHF - jan.2010 diet
CAD - jan. 2010

injury on endothelium from plaque deposits

increased permeability adhesion of molecules

monocyte, platelet adherence, lipid accumulation (2-5-10) (2-7-10) (2-9-10)

Hematocrit 35.5 35.5 39.1
aggregation of monocytes and macrophage Platelet Count 124 109 145
Neutrophils 69.2 84.9 58.9
progressive thickening of lumen Lymphocytes 20.6 10.9 30.5
Monocytes 6.5 9.7 8.2
narrowing of artery

occlusion in blood flow

`
decreased coronary blood flow

inadequate supply of oxygen to heart muscles

ischemia, increased cellular hypoxia ST segment depression and T-wave inversion – indicates pattern of ischemia

anearobic metabolism and increase in lactic acid production release of metabolites (e.g. K ions, lactic acid, carbon dioxide, adenosine)

damage to cardiac cells

necrosis Q wave present – tissue necrosis

 Myocardial infarction presence of S3 and S4 heart sounds

failure of cardiac compensatory mechanism

decreased myocardial contractility

decreased cardiac output

decreased arterial pressure

stimulation of baroreceptors

stimulation of sympathetic receptors

increase peripheral vasoconstriction increased myocardial contractility hypertrophy of cardiac muscle

increased afterload and cardiac output increased heart rate

X-RAY REPORT (2-4-10)
decreased diastolic filling Heart is enlarged with CT ratio of .78.
Impression:
decreased myocardial tissue perfusion Cardiomegaly LV and LA form.
Atheromatous thoracic aorta. Consider Pneumonia, righ
diastolic failure

impairment of left venticle to fill up with blood

increased pressure in left atrium and pulmonary vasculature

increase in left atrial and left ventricular end diastolic pressures

congestion of pulmonary circulation

X-RAY REPORT (2-4-10)
accumulation of fluid in the lungs Minimal haziness in the right base.
 obstruction of airflow from fluid accumulation and mucus production

loss of elasticity of lung fibers

impaired expiratory flowrate

increased air trapping

airway collapse

destruction of alveolar tissue

decreased surface for gas exchange

COPD dyspnea

activity intolerance

constipation
of ischemia

chest pain
 decreased circulation
CT scan (2-1-10)
plaqued and narrowed blood vessels present > The middle cerebral arteries are calcified.

Distribution of of
Distribution cerebral bloodflow
cerebral blood flow (CBF)
(CBF) decrease
decrease

Decrease blood
Decrease flowflow
blood to to
middle
middle cerebral artery
carrotid artery

HypoxiaHypoxia
of the of
left
thehemisphere
left hemisphere

Ischemia Ischemia

Disturbance of the
Disturbance cellular
of cellular metabolism
metabolism

Use of anaerobic metabolism

Use of anaerobic metabolism Decrease Decrease
ATP production
ATP production

neumonia, right base Accumulation of lactic

Accumulation of acid
lactic acid Induction of excitotoxicity
Induction of excitotoxicity

Decrease cellular
DecreasepHcellular pH Increase concentration of glutamate and
aspartate in the extracellular space

Opening ofOpening
Ca channel ??????????
of Ca channels

Persistent depolarization
(influx of Ca, Na, Cl ions, efflux of K)

CaCa
activated relase of
activated release ofdestructive
distructive enzymes
enzymes (proteases,
lipases,
(proteases, lipases, endonucleaseas)
?????????
(proteases, lipases,ordonucleases)
 Release of cytokines
Release of cytokines CT SCAN REPORT (2-1-10)

Loss of cellular
Loss ofintegrity
cellular integrity > There are punctuate hypodensities in the peri ventricu
There is a 2.2 cm hypodense focus in the left mi
Cell death Cell death
Consider small vessel ischemic changes both peri ventri
Necrosis Necrosis Consider an infarct, left mid peri ventricular white matt

Infarction

Right sided weakness Lessions formed

slurring of speech

facial asymmetry

decreased mentation

dysphagia
 peri ventricular white matter.
n the left mid peri ventricular white matter.

oth peri ventricular white matter..

ar white matter likely old.

Course of diseasse
signs and symptoms
laboratory results
diagnosis

direct realtion
possible outcome