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189 Cards in this Set

  • Front
  • Back
cell injury results when..
limits of adaptive response are exceeded
when cell is exposed to an injurious agent or stress
reversible cell injury
cell injury that does not necessarily result in cell death
irreversible cell injury
if stimulus persists or is severe enough to lead to ultimate cell death
type of cell death that occurs after abnormal stresses (as ischemia or chemical injury) always pathologic
types of necrosis
fat necrosis
occurs when a cell dies through activation of an internally controlled suicide program (-eliminates unwanted cells in dvpt, physio processes, -occurs in certain pathological condiitons when cells are damaged beyond repair (esp. their dna))
loss of BLOOD SUPPLY from impeded arterial flow or reduced venous damage
compromised supply of BOTH:
oxygen and metabolic substrates
just deficiency of oxygen
(vs. ischemia= loss of blood supply (deficiency in oxygen and nutrients)
abnormal accumulations of TGs in parenchymal cells
often seen in LIVER (major organ of fat metabolism) also occurs in heart, muscle kidney
condition in which hemosiderin is deposisted in many organs and tissues (whenever there are causes for systemic overload of iron: increased absorption, impaired use, hemolytic anemias, transfusions)
death of muscle resulting from ischemia
hallmarks of reversible cell injury
reduced ox/phos
ATP depletion
cellular swelling
change in ion concentrations and H2O flux
morphological changes associated with cell death
severe mitochondrial damage
loss of membrane permiability
2 types of cell death
Necrosis involves:
-severe membrane damage
-lysosomal enzymes that enter and digest the cell
-cell contents leak out
Apoptosis involves (on a cellular level) involves...
-nuclear dissolution (w/o complete loss of membrane integrity)
-caused by some noxious stimuly, esp. those that damage DNA
(occurs under both pathological and normal conditions)
Causes of Cell Injury
-oxygen deprivation
-physical agents
-chemical agents
-infectious agents
-immunologic reactions
-genetic derangements
-nutritional imbalances
cellular response to injurious stimuli depends on:
-type of injury
-duration of injurious stimulus
-severity of injurious stimulus
consequences of cell injury depend on:
-type of cell injured
-state of cell injured (nutritional/hormonal)
-adaptability of cell injured (metabolic needs/vulnerability to ischemia/genetic variants)
most important targets of injurious stimuli (in cell injury)
1) Aerobic respiration
2) Integrity of cell membranes
3) protein synthesis
4) cytoskeleton
5) integrity of genetic apparatus of cell
Effect of ATP depletion in cell injury
loss of energy-dpdt cellular fxns:
synthetic/degradative processes:
-membrane transport
-protein synthesis
-re/deacylation rxns (protein turnover)
-Na/K+ ATPase activity (Na+ accumulates in cell, K+ leaks out... cells well, ER dilates)
Effect of Membrane Damage in cell injury due to oxidative stress, disruption in protein synthesis
MITOCHONDRIA: increased permeability, destroys PMF, cyt c leakage may trigger apoptosis
LYSOSOMES: enzymatic digestion of cellular components
PLASMA MEMBRANE: loss of cellular components
Effect of increase in intracellular [Ca2+]
causes nonspecific increase in membrane permeability

and results in accumulation of ROS

both lead to protein breakdown and DNA damage
Reversible Injury can be recognized by LM as:
cellular swelling (fxn of energy-dependent membrane ion pumps lost)
Fatty Change (small and large lipid vaculoes appear in cytoplasm, seen principally in cells depedent on fat metab: hepatocytes, myocardial cells)
usually 1st manifestation of cell injury
whole organ: -some pallor, -increased turgor, -increased weight -small vacuoles in cyto
Examples of Ultrastructural Changes of Reversible Cell Injury
1) PM alterations
2) Mito changes
3) Dilation of ER
4) Nuclear Alterations
gross and histological correlate of cell death
NECROSIS (occuring in the setting of irreversible exogenous injury)
characteristics of Necrotic cells
-unable to maintain membrane integrity
-contents often leak out
-may elicit inflammation in surrounding tissue
histological appearange of necrotic cells
-increased eosinophilia (loss of RNA in cyto and increased binding of eosin to denatured cyto proteins)
-more glassy/homogenous appearance (loss of glycogen)
-vacuolated cytoplasm (enzymatic digest. of organelles)
-myelin figures (phospholipid masses) may ultimately replace dead cells
myelin figures
phospholipid masses that may ultimately replace dead cells in necrotic tissue
coagulative necrosis
when DENATURATION is primary pattern
(general architecture preserved, except in brain)
liquefaactive necrosis
when ENZYMATIC DIGESTION is dominant (liquified viscous mass)
typical in brain
casseous necrosis
form of coagulative necrosis
at foci of TB infection
formation of cheesy granuloma
fat necrosis
focal areas of fat destruction
usually involves release of activated pancreated lipases:
liquify fat cell membranes and split TGs releasing FAs that combine with Ca
In ischemic cell injury what happens if oxygen is restored:
a) before irreversible injury?
b) after irreversible injury?
a) disturbances are reversible

b) reperfusion can actually increase Ca2+ influx, causing further death (mainly by necrosis, but apoptosis may also play role)
in ischemic cell injury amorphous densities in mitochondrial matrix are indicative of:
irreversible injury/necrosis
what is an important clinical indicator of cell death (esp. myocardial cells in ischemic injury)
leakage of intracellular enzymes
how is apoptosis different from necrosis?
induced by tightly regulated cellular program
-cells destined to die activate enzymes that degrade their own DNA
-cells PM remains intact, but structure altered, to make them target for phagocytosis
-dead cells rapidly cleared, before contents leak (does NOT illicit inflammatory response)
Physiologic situations involving of apoptosis:
-hormone dependent involution
-cell deltion in proliferating cell populations
-death of host cells that have served purpose
-elimination of potentially harmful self-reactive lymphocytes
-cell death induced by cytotoxic T cells
Pathologic conditions involving apoptosis
cell death produced by injurious stimuli (DNA damage, ER stress (due to accumulation of unfolded proteins)
-certain viral diseases (hepatitis)
-pathologic atrophy in parencymal organs after duct obstruction
-cell death in tumors
morphology of apoptosis
cell shrinkage
chromatin condensation
formation of cytoplasmic blebs/ apoptotic bodies
phagocytosis of apoptotic cells or cell bodies by MOs
biochemical features of apoptosis
protein cleavage
DNA breakdown
phagocytic recognition- phospholipids flipped out, permit recognition by MOs
Apoptosis can be initiated by either:
Extrinsic Pathway (receptor mediated)
Intrinsic Pathway (mitochondrial)
Mechanisms of Apoptosis
Both Intrisic and Extrintic Pathways = INITIATION PHASE that culminates in activation of caspases

EXECUTION PHASE- caspases cause cell death
What initiates EXTRINSTIC PATHWAY apoptosis
Receptor-Ligand Interactions
(FAS/TNF receptor, adapter proteins form FADD, allows activation of INITIATOR CASPASE, activating EXECUTIONER CASPASE) --> endonuclease activation, breakdown of cytoskeleton
Causes of TG accumulation in the liver
ALCOHOL = hepatotoxin
KWASHIOKOR & CCl4 (decrease apoprotein synthesis)
ANOXIA (inhibits FA oxidation)
STARVATION (increases FA mobilization from peripheral stores)
morphology of fatty change in liver
clear vacuoles w/in parenchymal cells
occassionally contiguous cells rupture and fat globules coalesce --> fatty cysts
morphology of fatty change in heart
lipid found in small droplets
in moderate hypoxia: intracellular deposits of fat, bands of yellowed alternating with unaffected red/brown myocardium_
-Profound Hypoxia: more uniformly affected myocytes
iron appears as course, golden granular pigment w/in cell's cytoplasm
first seen in phagocytes (local if due to localized RBC breakdown, in liver, bone marrow, sleen and nodes if systemic)
iron can be visualized with what stain?
prussian blue
usual affect of iron on cells and organ function
usually does not damage cells or impair organ function
associated with liver, heart failure and DM
description or study of cause
biologically active chemical that is NOT "us" (eg chemicals, can cause cell injury and death)

but NOT all xenobiotics are poisons
a toxic chemical from the environment which causes cell injury
(if origin is exogenous to the individual = xenobiotic)
usually produced by microorganisms
agents with variety of biocehm activities which are TOXIC TO OTHER MICRO ORGANISMS (esp. bacteria and fungi and often to mammalian cells)
penicillin was first made by what?
a fungus
poisons that function because they are ABNORMAL ANALOGS of molecules normally active in cellular metabolism
-may block a biochemical pathway
-shift the equilibrium of a reaction
Antimetabolites are only Toxic to cells in which...
the involved pathway is vital
(e.g. Nucleic Acid syntehsis in growing/dividing cell populations)
What kind of therapeutic applications do antimetabolites have?
-anti cancer drugs (eg Fluorouracil)
-some function as antibiotics

by inhibiting nucleic acid synthesis in rapidly dividing cancer cells
Lipid Peroxidation
oxidative degradation of Lipids by Free Radicals (free rads steal electrons from lipids in cell membranes, usually via free rad chain rxn)
damages Plasma and Organellar Membranes
how is lipid peroxidation initiated?
initiated by attack on double bonds of unsaturated FAs by oxygen derived Free Rads (esp. OH)
lipid/free radical interactions yield peroxides (unstable and reactive) leading to autocatalytic chain reaction
what can scavenge free radicals?
Vitamin E
Reactive Oxygen Species
partially reduced reactive oxygen forms
produced by products of mitochondrial respiration
(O2-', H2O2, OH'
can damage: lipids, proteins and nucleic acids
Free Radicals
chemical species that have a single, unpaired electron in an outer orbit
-energy of unstable configuration is released via rxns w/ adjacent molecules (proteins, lipids, carbs -esp. in membranes and amino acids)
-initiate autocatalytic rxns
how might free radicals be initiated?
-absorption of radiant energy (UV light, xrays)
-enzymatic metabolism of exogenous chemicals or drugs (eg. CCl4--> CCl3)
-Redox Rxns that occur normally
-Transition metals (can catalyze free rad formation)
-NO-important chemical mediator generated by endothelial cells
decrease in size of a cell, tissue, organ or part
increase in size of organ or part, above normal, due to increase in cell size (physiologic vs. pathologic though)
increase in size of organ or part, above normal, due to increase in cell number
(physiologic vs. pathologic)
absence of growth
change of cell PHENOTYPE

(i.e. a change from one differentiated phenotype to another)
failure to differentiate completely
development of an "adult" cellular phenotype
Differentiation at cellular level
development of cytoplasmic organelles and products
Differentiation at Tissue level
organization of cells as well as individual cell phenotype
the characteristic differentiated FUNCTIONAL cells of an organ (e.g. hepatocytes)
the connective tissue and vascular framework of a tissue
Signals or stimuli that control adaptive alteration responses of "normal" cells:
Trophic hormones
Growth Factors (peptides)
Growth inhibitor hormones & peptides
Work load
Blood supply and basic nutrients
the precesnce of excessive fluid in the tissues and body cavities
fluids in cavities are usually known as
very severe generalized edema, especially of subcutaneous tissue
dependent edema
distribution by gravity
pitting edema
finger pressure leaves a depression
fluid of low protein content
fluid of high protein content
excessive peritoneal fluid
excessive pleural fluid
excessive joint fluid
Causes of generalized edema
-Insufficient Serum Protein (Kwashiorkor, Renal disease)
-Increased hydrostatic Pressure in capillaries (CHF)
Causes of Localized edema
-Increased hydrostatic pressure in blood caps (venous diseases)
-Obstruction of Lymphatics (cancer, surgery)
-Increased permeability of blood caps (inflammation)
Common sites of Edema
1) Subcutaneous tissues
2) Ankles
3) Lung
4) Brain
morphology of edema
separation of tissue elements by eosinophilic material
increased blood volume in the vascular space of the organ involved
active hyperemia
(caused by)
increased INFLOW
passive hyperemia
(caused by)
decreased OUTFLOW
morphology of hyperemia
vascular engorgement
flow of blood out of the vascular compartment
minute hemorrhages in the skin, mucus membranes or serosal surfaces (1-2 mm)
slightly larger hemorrhages on surfaces >3mm
large hemorrhages of surfaces (1-2cm, bruise)
pool of extravascular blood trapped in the tissues (under nail for example)
coughing up blood (arising from larynx, trachea, bronchi or lung)
vomiting blood (GI origin)
evacuation of tar-like stools of altered blood (indicative of lower GI blled)
hemorrhages in those spaces
causes of hemorrhage:
1) Local:
2) General:
1) trauma, infectious, degenerative, neoplasia
2) hemorrhagic diathesis (coagulation or vascular defects)
clinical significance of hemorrhage is determined by:
1) Amount
2) Rate
3) Site
Morphology of Hemorrhage
tissues suffused with blood
reduction in number and/or volume of erythrocytes per unit volume of blood
causes of anemia
-decreased production/loss of RBCs
-slow blood loss, rapid blood loss DOES NOT (until later)
effects if anemia
reduced oxygen transport
partial to complete reduction of blood supply, resulting in hypoxia (reduced oxygen) or anoxia (no oxygen) of tissue
a focus of necrosis, usually coagulative necrosis, resulting from ischemia so severe that tissue can't survive
factors affecting development of ischemia
1) supply of blood and oxygen
2) vascular pattern
3) rate of decrease of blood flow
4) tissue vulnerability
types of infarct
1) Solid organs-- anemic, white, pale
2) Soft organs -- "red"
morphology of infarct (heart example)
1) muscle necrosis
2) neutrophil inflammation
3) MOs
4) Fibroblasts and capillaries
5) Collagen
reperfusion injury
Toxic oxygen species
Heart failure
failure of pump function of heart
Pathophysiology of heart failure
myocardium, unable to contract sufficiently to empty the ventricle completely
"backward" heart failure
failure to pump out veins (Right-failure)
"forward" failure"
failure to pump enough blood to meet needs of body (Left failure)
Right-sided heart failure
reight ventricle fails to empty systemic veins, residual blood in RV in diastole, increased RA pressure, increased SVP, increased Systemic Cap Pressure
[dilated RV, systemic edema, effusions]
Left-sided heart failure
LV fails to empty pulmonic veins
[dilated left ventricle, pulmonary edema]
both sided heart failure can cause
activation of mechanisms for water and sodium retention

pleural effusions
the result of activation of the clotting mechanism within the cardiovascular system in a living person
-Physiologically, important mechanism (fibrin/platelets) for sealing leaks and maintaining homeostasis
-Pathologically, can be inappropriate bc thrombi may obstruct flow
Virchow's triad
(the 3 causes of thrombosis)
1) Injury to vessel wall
2) Increased blood coagulability
3) Decreased blood flow (stasis)
clotting cascade can be activated by what type of factors?
INTRINSIC FACTORS (in the blood, including factors from platelets)
EXTRINSTIC FACTORS (in the tissue)
the clotting cascade is activated to produce what?
thrombin: aggregates and activates platelets-> attach to vascular surface (pale or platelet thrombus)
clump on fibrin grows on this nidus (w/ R and WBCs caught in interstices) = red or coagulation thrombus
pale or platelet thrombus
activated platelet aggregates attached to vascular surface
red or coagulation thrombus
a clumb of fibrin growing on a platelet thrombus, with RBCs and WBCs caught in interstices
outcomes of Thrombi
1. Lysis (dissolution)
2. Organization (replaced by granulation tissue)
3. Propagation
4. Embolization
3 contexts of vessel wall injury appearing primary to thrombosis
a. inflammation: arteritis, phlebitis
b. anatomic alterations: atherosclerotic plaques, disrupt endothelium and cause turbulence
c. trauma
increased coagulability appears primarily when...
1. platelets are increased in #
2. platelets are more sticky (postoperative state or hyperlipidemia)
3. clotting cascade is more labile (septicemia and shock)
stasis (decreased blood flow) appears primary in what type of thrombosis?
factors contributing to stasis?
venous thrombosis
-phlebothrombosis (stasis of blood in uninflamed veins)
a. bed-ridden
b. thrombosis in dilated chabers or vessels (e.g. mural thrombi in walls of enlarged atria)
c. eddies associated with vascular or cardiac abnormalities
Ventricular Mural Thrombosis
due to both endothelial (endocardial) injury and/or decreased flow following an MI
Thombosis of heart valves
*due to endothelial injury
a) by bacteria (infective endocarditis)
b) by antibodies or immune complexes (rheumatic endocarditis)
c) by trauma of instrumentation (e.g. catheter)

*due to hypercoagulable platelets and clotting factors (non-bacterial thrombotic endocarditis)
Venous thrombosis (what are the two types?)
A) Phlebothrombosis (stasis)
B) Thrombophlebitis (venous thrombosis, in which inflammation of vein wall plays primary role)
factors contributing to phlebothrombosis
-immobilization/decreased flow
-could result from minimal injury to vessel wall
-hypercogulability (after trauma, in tumor patients)
-stasis: systemic (decreased CO or impaired venous return) or local (lack of muscular pumping efects, incompetent venous valves, external tissue pressure)
most common clinically significant form of thrombosis
most common site of phlebothrombosis
leg, deep veins in calf, popliteal fossa, main tributaries of inferior vena cava
most common gross appearance of phlebothrombosis
firmly anchored head of clumped platelets and layered platelet/fibrin thrombus; loosely anchored tail of propagated (mostly fibrin w/ trapped blood cells) thrombus
most common complications of phlebothrombosis
pulmonary emboism
edema of distal extremities
venous thrombosis in which inflammation of vein wall plays primary role
STERILE: due to trauma, radiation or chemicals
SEPTIC: due to bacteria (significant complication: septic emboli)
Thrombosis in microcirculation is known as
DIC (disseminated intravascular coagulation)

not a primary disease, but a complication of any condition associated with widespread activation of thrombin
mechanism of DIC
sudden or insidious onset of widespread fibrin thrombi in the microcirculation which causes a DIFFUSE CIRCULATORY INSUFFICIENCY (particularly in brain, lung, heart and kidney), consuming platelets and coagulation proteins, and the fibrinolitic mechanisms are activated at the same time.. can cause SERIOUS BLEEDING disorder
a blood clot, any tissue or foreign substance, carried in the bloodstream obstructing an artery
most common kinds of emboli
Pulmonary thromboemboli
form in systemic veins, travel to pulmonary arteries
embolus in large pulmonary artery, results in cardio pulmonary decompensation: repiratory and/or cardiac arrest, cardiogenic shock, collapse
result of embolus in med-sized pulmonary artery
wedge-shaped inarct may appear distal to obstruction, depending on extent of intersitial back pressure and other factors.
small pulmonary artery obstruction results in:
nothing, unless
a) embolus is spectic (where it may be a nidus of infection, eg hematogenous pneumonia) or
b) the emboli are multiple; sufficient numbers can produce pulmonary hypertension
potential fates of a thromboembolus
1. lysis
2. organization into a fibrous plug
3. organization of 1 and 2 leaving a fibrous band or web
systemic thromboemboli often come from
an intracardiac thrombus
1) in an enlarged Left Atrium (e.g. due to mitral stenosis)
2) on a mitral or aortic valve (eg endocarditis) or
3) on the wall of a dyskinetic portion of the left ventricle (following myocardial infarction)
Bland emboli do what?
obstruct vessels in which they lodge and may cause ischemia and/or infarction
Septic emboli do what?
become secondary sources of infection (e.g. systemic manifestations of subacute bacterial endocarditis)
atheromatous emboli are from what?
what might they cause?
from plaques in the aorta
may cause cerebral ischemia/infarcts, or infarcts of other vicsera or renal insufficiency
Fat and bone marrow emboli are usually consequences of what?
Tumor embolism are from what?
from malignant neoplasms (consequence of one of the characteristics of malignant neoplasms: the ability of malignant cells to invade blood vessels)
Air emboli are consequences of...
opening of veins to air or of a rapid decrease in environmental pressure
inadequate perfusion of cells and tissues,
leads to impairment and eventual failure of cellular metabolism. can occur in the presence of either a low or a high CO. the hisopathologic changes seen in shock refect cell injury (edema, ischemic chances and infarction)
3 factors that determine O2 and nutrient supply (altered by shock)
1. CO (decreased in cardiogenic shock)
2. Amt of Hb (decreased in hypovolemic shock)
3. Arterial O2 saturation (decreased in both cardiogenic and hypovolemic shock)
Primary consequences of shock (hypovolemic)
decreased blood vol., low BP, low CO, low CVP, low cardiac filling pressure
Secondary consequences of shock
(+) pulse rate, peripheral vasoconstriction, (-) perfusion of all organs except heat and brain, (+) A-VO2 difference, (+) blood lactate, (+) viscosity
Tertiary consequences of shock
decreased urine flow, etc..
Cardiogenic shock differs in some respects from hypovolemic shock
1. Low CO, despite adequate volume, low BP, (+) CVP, (+) cardiac filling pressure
2. variable pulse rate, (-) arterial pO2, (+) AV O2 difference, (+) arterial blood lactate
3. decreased urine flow, etc..
causes of cardiogenic shock
1. myocardial infarction (decreased contractility)
2. arrhythmias (inefficient contraction)
3. cardiac tamponade (inadequate filling of chambers of heart)
septic shock is called hyperdynamic because:
INCREASED: pulse rate, CO, ventilation & CVP

associated with HYPERVENTILATION (alkalosis), Increased CO (low resistance), Oliguria (?Warm, dry, extremities)
pathophysiologic mechanism of septic shock includes:
peripheral vasodilation
increased CO
peripheral circulation appear to be a compensatory attempt to supply more O2 to cell that, as the lactate in the blood indicates, are forced to utilize anaerobic metabolism
septic shock is often caused by....
gram-negative bacteria
atherosclerosis is a type of
"hardening of the arteries" is a generic term for thickening and loss of elasticity of arterial walls
3 patters of ateriosclerosis
2) Mönkeberg medial calcific sclerosis
3) Arteriolosclerosis
Monkeberg medial calcific sclerosis
characterized by calcific deposits in the muscular arteries in persons older than age 50. These deposits do not encroach the vessel lumen
affects small arteries and arterioles.
Consequence - thickening of the vessel with narrowing of the lumen and possible downstream ischemia
Most common in hypertension, DM

a chronic inflammatory disease of the large arteries that affects every human being and that progresses with age. It remains asymptomatic until a certain stage.

Consequences - contributes to more mortality and serious morbidity in the Western world than any other disorder.
Percentages of deaths caused by atherosclerosis
more than 50%!
Key Processes of Atherosclerosis
Charateristic Lesions of Atherosclerosis
ATHEROMA (athermatous plaques of fibrofatty plaques)
-raised focal lesions
-initiate into the intima
-protrude into and obstruct the vascular lumen
-weaken the underlying tunica media
-soft grumous core of lipids (cholesterol)
-covered by a fibrous cap
Fatty Dot
Type I (initial atherosclerotic lesion) isolated MO foam cells (lipid laden MOs)
Fatty Streak
Type II atherosclerotic lesion
foam cells, lipid-laden MOs, reversible, but probably precursor of Atheroma.

children of all populations, most prominent in root of aorta
active platelets
PGI2 and PAF, enhance vascular permeability P
Type IV (atheroma) lesion
fat accumulation + proliferation of myointimal cells
extends to involve media
as it enlarges, center tends to undergo necrosis, usually asymptomatic
Type V lesion
atheroma + production of collagen = fibrofatty plaque
Complicated plaques
Type VI (complicated) lesion
1) Calcification
2) Ulceration
3) Thrombosis
4) Hemorrhage into plaque
severe destruction may lead to aneurysm (atheroemboli)
3 ways atherosclerosis causes clinical manifestations:
A. Stenosis of vessel
B. Occlusion of vessel (thrombosis superimposed on plaque, hemorrhage into plaque, atheroembolus)
C. Aneurysm formation
Pathogenesis of Atherosclerosis
1. Chronic Endothelial stress/dysfunction with expression of selectins and integrins
-Monocyte adherence, invasion and prduction of mediators
-Platelet adherence
-Liberation of platelet factors
-Plasma LDL gains access to SM cells
-HDL works to remove CE from foam cells
-LDLs oxidized, taken up my MOs (cause endothelial/SM injury)
Mediators produced by monocytes in atherosclerosis:
Chemotactic Factors
Growth Factors
Factors that stimulate lipid uptake by artery SM cells
damaging Oxygen radicals and digestive enzymes
Role of Growth factors in pathogenesis of atherosclerosis
-stimulate artery wall SM cells to multiply and move into the intima
-stimulate fibroblast multiplication
-stimulate both cell types to make collagen
-stimulate endothelial cells to multiply and make new blood vessels
Platelet factors
thromboxane A2 (TXA2)
factors which stimulate proliferation of SM cells and fibroblasts
factors which stimulate collagen production
factors which enhance endothelial permeability
Risk factors for atherosclerosis
A. HYPERLIPIDEMIA (hypercholesterolemia, low ratio of HDL to LDL)
D. HYPERTENSION (endothelial damage, thickening of vasovasorum, leads to diminised blood flow to artery wall, SM proliferation)
E. SMOKING (nicotine = vasoconstrictor, inhibits prostacyclin synthesis, carboxyhemoglobin)
F. SEX (hormonal factors)
J. LIFESTYLE (stress)