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232 Cards in this Set

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a form of fluid loss, "blood where it doesn't belong", a name is give in reference to the site or organ affected
hemorrhage

ex: cardiac hemorrhage, cerebral hemorrhage, arterial hemorrhage
"too much blood"
hyperemia
dilation of arterioles, usually a neural reflex
ex: blushing
active hyperemia
results from congestion, more sinister
ex: increase venous backflow
ex: inflammation (erythema)
passive hyperemia
one sign of this disease is passive hyperemia, when blood backs up into distensible organs like the liver and spleen
severe right-sided heart failure
one sign of this disease is active hyperemia when blood backs up into the lung capillaries
severe left-sided heart failure
congested liver from passive hyperemia due to right-sided heart failure
nutmeg liver
the ability to preserved blood as a fluid and when necessary to form a clot (thrombus)
normal hemostasis
in blood, the transformation of a liquid to a solid to prevent leakage through vessels
thrombus (clot) formation
10 steps:
1.injury to endothelium of blood vessel
2.transient vasoconstriction via a neural reflex
3.release of endothelin (a vasoconstrictor) from damaged endothelial cells
4.release of von Willebrand factor by damaged endothelial cells so platelets will adhere to exposed basement membrane of injured site
5.von W. also mediates plat.-plat. adherence
6.platelets change shape and also release ADP and thromboxane A2 granules to stimulate more adherence
7.form a platelet plug
8.circulating prothrombin --> thrombin
9.thrombin polymerizes fibrinogen --> fibrin
10.form a secondary hemostatic plug
10 steps to how blood vessels prevent or stop a leak
what deactivates thromboxane A2
aspirin
this prevents widespread thrombus formation after endothelial injury
plasminogen factor (t-PA)
Healthy endothelium at the edge of the hemostatic plug releases tissue plasminogen factor (t-PA) to block coagulation cascade
this is used to prevent further damage from occlusion in CHD and stroke
(t-PA) tissue plasminogen factor
where von Willbrand factor is stored
Weibel-Palade bodies in endothelial cells
the most common inherited bleeding disorder in humans; characterized by spontaneous bleeding from mucous membranes, excessive bleeding from wounds, prolonged bleeding times in the presence of a normal platelet count; usually seen with the first major dental procedure
von Willebrand disease
from defective or absent von Willebrand factor
in blood, the ability to transform from a liquid to a solid; fibrin forms a meshwork that cements blood cells together
coagulation
slow process where blood is transformed into a solid, a cascade of clotting factors
intrinsic system (pathway) of blood coagulation
fast process of blood being transformed into a solid, initiated by trauma to a blood vessel or surrounding tissue which causes a cascade of clotting factors to form a secondary hemostatic plug
extrinsic system (pathway)
what clotting factor is common to both the intrinsic and extrinsic system?
Factor Xa
*at the point where factor X is converted into Xa, the intrinsic and extrinsic pathways merge and the rest of the steps are the same
1.Factor X --> Factor Xa
2.prothrombin --> thrombin
3.fibrinogen --> fibrin
final steps common to both the intrinsic and extrinsic pathways of secondary hemostatic plug formation
which plasma factor is unstable and must be bound to vWF?
Factor VIII
-activated factor VIII activates thrombin and accelerates coagulation
1/2 life of VIII is 2.4 hrs, but when bound to vWF it is 12 hrs (lasts much longer to cause effect)
what causes hemophilia A?
deficiency or lack of factor VIII
ionic calcium (aka factor IV)
vitamin K
agents that promote coagulation
this removes Ca from the blood
chelator EDTA
where are many of the coagulation factors produced?
in the liver; vitamin K is often required
warfarin (coumadin)
heparin
antithrombin III
agents that inhibit coagulation
this coagulation inhibitor acts by decreasing prothrombin concetration and alters the availability of vitamin K
warfarin (coumadin)
-by altering vitamin K, it impairs production of clotting factors
-rat poison
this coagulation inhibitor acts by binding to antithrombin III to accelerate the deactivation of thrombin
heparin
this coagulation inhibitor binds to thrombin and deactivates it
antithrombin III
process by which a clot is dissolved; starts shortly after clot is formed.
fibrin activates plasminogen --> plasmin which dissolves the clot
clot dissolution
*dissolution and formation is balanced
hemostasis in an exaggerated form; predisposes to thrombis formation
hypercoagulability
1. increased platelet function
2. increased clotting activity
2 forms of hypercoagulability
this results when distubances in blood flow occur, increasing endothelial damage, and increasing platelet sensitivity.
(from atherosclerosis, diabetes mellitus, smoking, elevated blood lipids and cholesterol, increased platelet levels)
increased platelet function (a form of hypercoagulability)
results from the stasis of blood flow, increases in coagulation factors, and/or decreases in anticoagulation factors.
conditions:
pregnancy-increased clotting factors
immobility-stasis
oral contraceptives-enhance clotting factors
smoking-enhances clotting factors
malignancy-cancer cells release factors that stimulate production of clotting factors
increased clotting activity (a form of hypercoagulability)
these can form anywhere and are named in relation to location or distinctive appearance
thrombi
intramural thrombi-heart, valvular thrombi-valves, arterial thrombi, venous thrombi
also:
red thrombi, white(or layered) thrombi
thrombi that form in small veins, contain RBCs. Due to stasis. "currant jelly"

ex: pulmonary embolism from DVT formation
Red thrombi
thrombi that form in arteries or in the wall of the heart (mural thrombi); from sedimentation
White (layered) thrombi
1.small ones can be lysed
2.narrow the lumen and reduces flow (causes ischemia and impedes organ function)
3.occlude the lumen; results in infarction
4.serve as the source of an embolism
4 fates of thrombi
a freely movable intravascular mass that is carried from one anatomical site to another in the blood
embolism
1.thromboemboli
2.liquid emboli
3.gaseous emobli
4.solid particle emboli
4 types of embolism
clinically the most important form of embolism; color will tell you where it originated
thromboembolism
forms in amniotic fluid
liquid emboli
forms from a needle stick
gaseous emboli
forms from bone marrow or tumor cells in blood
solid particle emboli
what is the net effect of an emboli?
infarction
-color of thromboembolism will tell you where it originated
where are small emboli cleared from circulation?
the lungs (with some enzymes)
common cause of death in middle-age, overweight women
pulmonary embolism from DVT in legs
insufficiency of blood supply of sudden onset that results in an area of ischemic necrosis; 2 colors-white and red
infarction
these infarcts are due to venous obstruction
red infarcts
shows up in organs with single venous drainage ex: testes, ovaries - something on a long stalk which can get twisted
these infarcts are due to arterial obstruction
white infarcts
(blood can't get into organ, organ turns "white")
what infarction does to post mitotic tissue
permanent tissue damage
ex: scar formation in the heart
what infarction does to mitotic or facultative mitotic tissue
can heal with little permanent damage
ex: liver
(but chronic state will cause scar formation anyway - like cirrhosis)
1.transportation
2.regulation
3.protection
3 functions of blood (5-6L in adults)
1.oxygen, nutrients to tissue
2.wastes, from tissue
3.hormones
what the blood transports
1.heat (via vasoconstriction/dilation)
2.pH
3.acid/base balance (buffering)
what the blood regulates
immune functions
how the blood provide protection to the body
1.albumin
2.immunoglobulins
3.fibrinogen
4.thrombin
Major proteins of blood
1.erythrocytes
2.leukocytes
3.neutrophils, basophils, eosinophils, monocytes, lymphocytes
4.platelets
what are the blood cells?
1.transport lipids, metals, acid/base balance, coagulation
2.provide capillary oncotic pressure (to bring fluid back into capillary)
what plasma proteins do
this is where almost all plasma proteins are synthesized (except immunoglobulins)
Liver

(ex: people w/liver damage having bleeding problems from no coagulation factors getting produced)
production of blood cells
hematopoeisis
-in red marrow
theory that stem cells divide into myelocyte stem cell line (which will populated the marrow) and lymphoid stem cell line
stem cell theory
this organ belongs to the reticuloendothelial system (with lymph nodes,liver) and is composes of red and white pulp
spleen
1.red pulp-where RBCs are removed from blood and destroyed
2.white pulp-where lymphocytes are produced
3.removal of bacteria and viruses
what the spleen does
formation of RBCs
erythropoeisis
1.vitamin B12
2.folic acid
3.iron
3 dietary factors required for erythropoeisis
hormone that regulates RBC production by stimulating marrow to produce more RBCs; secreted into blood by capillary endothelial cells in the kidney in response to low arterial O2 pressure
erythropoietin
the source is ferritin which is stored in the liver until needed, then it is transported to bone marrow via transporter protein (transferrin), where it moves into bone marrow cells
iron
this condition results from a lack of iron
microcytic anemia (small erythrocytes)
vitamin found in green leafy vegetables, yeast, liver; it is essential for the formation of thymine
folic acid
this results from a lack of folic acid
-maturation failure anemia (aka megaloblastic anemia) - large immature RBCs
-neural tube defects in fetus
this is found only in animal products and is necessary for the action of folic acid; it is also required for normal myelin formation in the nervous system
vitamin B12
this results from a lack of vitamin B12
pernicious anemia (another form of megaloblastic anemia) - spherical cells can't transport as much O2
this is required by the intestines for absorption of vitamin B12
intrinsic factor secreted by stomach cells
term for too many RBCs
polycythemia
conditions that stimulate release of erythropoeitin
high altitude living
kidney tumor
COPD (hypoxia)
athletes
what is the arterial blood partial pressure of O2?
PO2 100 mmHg (corresponds to 95% saturation of hemoglobin)
what is the venous blood partial pressure of O2?
PO2 40 mmHg (corresponds to 70% saturation of hemoglobin)
*true everywhere except heart, which extracts 70% of O2 from hemoglobin; little reserve capacity
CO2 diffuses into erythrocytes:
1.25% gets bound to hemoglobin
2.75% of CO2 combines with water in the cell and forms carbonic acid --> carbonic acid dissociates into bicarbonate ion and hydrogen
a.bicarbonate ion diffuses into plasma, gets replaced by chloride ion in the cell to maintain electrical neutrality
b.H+ binds to hemoglobin (acts as buffer)
*Reactions reversed in the lungs and CO2 is lost
How CO2 is transported
what is the way RBCs produce ATP?
glycolysis
why do RBCs need ATP?
to produce enzymes, for Na/K pump
*ability wears out at about 120 days
what happens to old RBCs?
cleared by phagocytes in the spleen and liver
if RBC ruptures in plasma it releases hemoglobin and binds to this circulating plasma protein:
haptoglobin (which prevents renal excretion so it is preserved in the body);
hemoglobin-haptoglobin complex is taken up by phagocytes in the liver and hemoglobin is recycled
an increase in erythrocytes secondary to a known stimulus, such as renal cell cancer, or high altitude living; hypoxia causes overproduction of erythropoeitin
erythrocytosis
increase in #of circulatig RBCs from a primary myeloproliferative disorder (in bone marrow) from an unknown stimulus; symptoms include light-headedness, visual disturbances, headaches, enlarged liver & spleen r/t increased blood volume, increased hematocrit, increased viscosity, increased cardiac workload, & thrombosis
polycythemia vera
*not from overproduction of erythropoeitin!
1.not enough RBCs
2.not enough hemoglobin
3.both
the 3 causes of anemia
results from reduced bone marrow function from genetic failure or trauma to stem cells; causes weakness, dyspnea, headaches, impaired immune function & bleeding
Tx: bone marrow transplant, discontinue use of causative agent
aplastic anemia
1.radiation
2.chemitherapy
3.antimicrobials
4.anticonvulsants
5.anti-inflammatories
agents that can cause trauma to bone marrow stem cells, resulting in aplastic anemia
this results in shortened RBC life-span from:
1.abnormalities of cell membrane and shape
2.hemoglobinopathies
3.physical injury
hemolytic anemia
abnormality of RBC membrane that results in premature lysis of cell; inherited autosomal dominant (need 1 copy from 1 parent to express, not x-linked); molecular defect on membrane
Sx:jaundice, splenomegaly, anemia
hereditary spherocytosis
destruction of RBCs by immune system - IgG or complement fixed to surface of RBC-->cell gets opsonized-->phagocytized
*a type 2 hypersensitivity rxn
Dx: positive Coombs test
associated with lymphoma, lupus, certain drug rxns
acquired immune hemolysis
caused by blood transfusion rxns, incompatibility of the ABO system
-IgM binds causing lysis and removal of RBCs
secondary immune hemolysis
a type of hemoglobinopathy: an inherited disorder with structural defects of hemoglobin globin beta protein chains
sickle cell trait and disease
cell sickling is brought on by severe hypoxia; these people are heterozygous
sickle cell trait
sickling of cells is much worse; homozygous individuals
sickle cell disease (nearly all hemglobin is HbS)
at what age will sickle cell become evident?
at 6 months: when fetal Hb changes to adult Hb
10% african americans have trait with 0.2% expressing the disease
a type of hemolytic anemia hemoglobinopathy:
this is a group of disorders that results in lack of or defective globin protein
alpha, beta thalassemia
total lack of the 2 beta proteins or they are defective; autosomal codominant disorder (2 different genes, both have to express themselves); more common and more severe
beta thalassemia
heterzygotes - asymptomatic or mild
homozygotes - severe hemolytic anemia (thalassemia major) appears a 6 mos. of age-->need repeated blood transfusions or bone marrow transplant
relevant features of alpha and beta thalassemia
extended trauma
turbulent blood flow
prolonged exercise
artificial cardiac valves
extracorporeal circulation devices
hemolytic anemia resulting from direct physical trauma to RBCs
monocytes are released into blood from bone marrow and migrate into tissues (36 hrs) to become these
macrophages
(live for many years)
lymphocytes differentiate and mature here; they live for hrs to years
lymphoid tissue
which cell lives longer, T-lymphocytes or B-lymphocytes?
T-lymphocytes
(and they circulate about every 10 hours)

B-lymphocytes don't circulate, plasma cells live 2-3 days
where eosinophils are seen
inflammatory and allergic reactions
histamine
heparin
bradykinin
serotonin
receptors for IgE
- may give rise to mast cells
what basophils contain

*type I hypersensitivity?
this system is composed of fixed and mobiles phagocytes present in the liver, spleen, GI tract and lymph nodes; function to remove and recycle substances from the blood such as antigen-antibody complexes, iron, worn out RBCs
mononuclear phagocyte system (reticuloendothelial system)

*type III hypersensitivity?
>7500 per mcl blood - neutrophilia
<2500 per mcl blood - neutropenia
neutrophil disorders
the appearance of increased numbers of immature neutrophils indicates what?
acute infection ("shift to the left")
toxic granulations of neutrophils indicate this
acute bacterial infection
what tissue factors released by the inflammatory process stimulate bone marrow to release addition neutrophils?
cytokines
a lymphocyte disorder; lymphocytes are proliferating
Sx: cervial lymphadenopathy, fever, sore throat, splenomegaly, fatigue, malaise
Caused by epstein-barr virus
*may have more elevated risk for Hodgkins disease later
infectious mononucleosis
-qualitative and quantitative alterations in circulating leukocytes
-classified according to course & duration &/or the abnormal type of cells/tissues
malignant WBC disorders - Leukemia
rare leukemia with rapid onset, massive #of immature leukocytes, rapid progression,
too many leukocytes, low RBCs and platelets
bone pain
seen in children
acute leukemia
50% of all leukemia cases, adults and elderly, slow progression
granulocytic
lymphocytic
-bone marrow is infiltrated with malignant cells
caused by genes & chemical/physical agents
chronic leukemia
in chronic granulocytic (myeloid) leukemia, 90% of all cases have this
Philadelphia chromosome
solid neoplasms that contain cells of lymphoreticular origin
malignant lymphoma
white males 20-30 yrs., and again over 50 most prone to this disease; presence of giant multinucleated Reed-Sternberg cells
malignant lymphoma - Hodgkin's disease
like Hodgkin's but more diffuse and diagnosed later with poor prognosis
Non-Hodgkin's lymphoma
plasma cell myeloma, damages bone marrow and skeletal structuresm tumors arise from a single clone of plasma cells
multiple myeloma
blood traveling from right heart --> pulmonary artery --> pulmonary capillaries --> pulmonary veins --> left heart
pulmonary circulation
blood traveling from left heart --> aorta --> capillaries --> systemic veins --> vena cava --> right heart
systemic circulation
if output of left heart < right heart, where does blood accumulate?
pulmonary circulation
if output of right heart < than left heart where does blood accumulate?
systemic circulation
the physical principles governing pressure, flow, and resistance as they relate to the cardiovascular system
hemodynamics
64% of blood is found where?
in the veins and venules
16% of blood is found where?
in arteries and arterials
what do arteries have that veins don't?
smooth muscle
what do veins have that arteries don't?
"check" valves to prevent backflow
period of ventricular contraction and ejection of blood
Systole
period of ventricular relaxation in order to fill with blood (atria contract and push blood into ventricles at this time)
diastole
this sound is heard when atrioventricular valves close (tricuspid, mitral)
1st (Lub) sound
this sound is heard when semilunar valves close (pulmonic, aortic)
2nd (Dub)

3rd & 4th sounds are not heard in health adults
an electrical measurement of the action of the heart
ECG Electrocardiogram
Stroke volume X Heart Rate =
cardiac output
the maximum percentage of increase in CO possible beyond the normal resting level
cardiac reserve
the volume of blood heart must pump out of ventricles with each beat determined by venous return and muscular stretch
(before contraction)
preload
increased stretch (from increased end diastolic volume) causes increased force of contraction
Frank-Starling law
pressure the heart needs to push blood into the aorta, AFTER the contraction
afterload
this increases with Congestive Heart Failure
Preload
this increases with Hypertension
afterload
contractility; heart can change its force of contraction while maintaining the resting (diastolic) myocardial muscle length (it adjusts at the molecular level)
inotropic
heart rate; how many beats per minute; frequency ejection
chronotropic
reflects changes in the radius of arterioles and the viscosity of the blood
total peripheral resistance
1. slow contraction rate
2. high contractile forces for long time
3. low energy requirement
characteristics of vascular smoot muscle
calmodulin instead of troponin
less SR for storage
influx of Ca for depolarization
differences between cardiac and skeletal muscle
alpha adrenergic receptors are excitatory and cause Ca channels to open, resulting in
vasoconstriction
beta adrenergic receptors are inhibitory and cause Ca channels to close, resulting in
vasodilation
what is commonly used for HTN and arrthmia management?
Ca channel blockers
what is the relationship?

F=Flow
P=Pressure difference between 2 ends
R=Resistance
F=P/R

*flow decreases further from the heart
SVR
systemic vascular resistance
-the total resistance of systemic circulation; relates to afterload=total resistance
PVR
peripheral vascular resistance
-the total resistance of systemic circulation; relates to afterload=total resistance
TPR
total peripheral resistance
-the total resistance of systemic circulation; relates to afterload=total resistance
P wave – deplorization of atria
(atria push blood into ventricles)

Space – delay in AV node

QRS – depolarization ventricles
(larger wave, ventricles push blood out)

T repolarization ventricles
(wipes out repolarization of resting atrium)
basics of an ECG
What is the relationship where
P=difference between aortic or mean arterial pressure and the right atrial pressure
CO=cardiac output
SVR=systemic vascular resistance
SVR=P/CO
the smaller the vessel, the slower the
velocity
why is velocity flow slower in capillaries than other vessels?
to allow for exchange of gas and nutrient
blood flows through vessels in "layers" with plasm next to endothelium to reduce the imact of molecule or particle resistance
laminar flow
blood moving crosswise and lengthwise in blood vessels with conditions of high velocity, changes of vessel diameter, and low blood viscosity
turbulant flow
*risk of clot with platelets and other molecules contact endothelium
force in vessel wal opposing distending pressure of fluid
vessel wall tension
what is the relationship when
T=wall tension
r=vessel radius
P=intraluminal pressure
P=T/r
LAPLACE'S LAW

*wall tension is inversely proportional to wall thickness (like a balloon)
What is the relationship where
C=compliance
V=change in volume
P=change in distending pressure
C=V/P

Compliance is the total quantity of blood stored in a given portion of circulation for each mmHg rise in pressure
ability of a vessel to accomodate an increase in blood volume
distensibility
blood pressure from the periodic ejection of left ventricular blood into aorta at systole
atrial pulse pressure
What is the relationship where
BP=blood pressure
CO=cardiac output
TPR=total peripheral resistance
BP=CO x TPR
Height of pulse pressure
About 120 mmHg
Function of stroke volume and stretch of aorta
Systolic pressure
Lowest pulse pressure
About 80 mmHg
Function of the stored energy (systolic stretch) and rest tension that resists the “runoff” of blood from aorta without causing an increase in P
diastolic pressure
Difference between systolic and diastolic P
About 40 mmHg
Increases with increased volume ventricular ejection into arterial circ.

Decreases with decreased resistance to outflow
Decreases in shock (decrease in Stroke vol, decrease in syst BP) even with compensatory increase in TPR
pulse pressure
Average pressure in the arterial systemic circulation during ventricular contraction and relaxation
About 90-100 mmHg
MABP=CO/PVR
Estimate by:
(Diastolic BP)+ (Pulse Pressure/3) = MABP
Mean Arterial Pressure
Forced expiration against closed glottis leads to increased preload and afterload
Intrathoracic pressure increase can cause decrease venous return - triggers baroreceptor reflex. Upon release of pressure, venous return occurs on top of the baroreceptor triggered increase HR and arterial resistance. This leads to transient vagal slowing of heart. (heart attack on the toilet)
Valsalva's maneuver
baroreceptors in carotids and aorta (close to heart) --> to brain --> adjust BP
autonomic nervous system regulation of BP - short term
renin (from kidney):so kidney is a sensor of pressure and RBC count
angiotensin: blood (lungs)
aldosterone (from pituitary): regulate fluid retention and salt balance
humoral regulation of blood pressure - RAA system - short and long term
1. renal-body fluid system
2. increase in fluid volume
long-term regulation of blood pressure
tissue vasodilators
histamine
kinins
prostaglandins
serotonin from platelets
nitric oxide
prostacyclin
vasodilators
predominant innervation of coronary arteries is
sympathetic

alpha receptors - constrict
beta receptors - dilate

*parasympathetic role is very minor
predominant innervation of veins is
sympathetic

alpha - constrict
beta - dilate
alpha receptors are
postsynaptic
beta receptors are
presynaptic
Complex of apoproteins, cholesterol esters, triglycerides, phosopholipids, nonesterified cholesterol esters
lipoprotein
intestinal biosynthesis – transport dietary lipids to fat and muscle
Classes of lipoproteins: Chylomicrons
transport endogenous liver triglycerides to fat and muscle
Classes of lipoproteins: VLDL
very low density lipoproteins
source of LDL
Classes of lipoproteins: IDL
intermediate density lipoproteins
liver, carries cholesterol from tissues (also atheromatous plaques) to liver
Classes of lipoproteins: HDL
high density lipoproteins
main carrier of cholesterol, receptor mediated endocytosis, or nonreceptor uptake. A problem if arterial wall macrophages takes up LDL.
Classes of lipoproteins: LDL
low density lipoproteins
abnormal lipids in the blood (excess of some lipid)
DYSLIPIDEMIA
what causes dyslipidemia in genetic forms?
defects with enzymes or receptors can cause dyslipidemia
process of forming atheromas in arteries, anywhere, not just heart
ATHEROSCLEROSIS
Hyperlipidemia (cholesterol)
Genetics: multifactorial, inherited
Men>45 yrs
Women>55 yrs, premature menopause
Hypertension
Diabetes mellitus
HDL<40 mg/dL
Smoking
stress emotional
weight
diet
dependent risk factos for atherosclerosis
excess C-reactive Protein (CRP)-a marker of systemic inflammation
Homocysteine
Serum lipoprotein (a)
Infections
independent risk factors for atherosclerosis (not associated with genes or environment)
Acute inflammatory phase protein that interacts with complement to increase
inflammation
marker of atherosclerosis
marker of inflammation
indicator of CV risk (3-4X increase risk)
C-Reactive Protein
Breakdown metabolite of the amino acid methionine
Methionine breakdown requires folate, B6, B12, riboflavin(insufficient vitamins increase homocysteine)
>15 µmol/L Homocysteine is dose-dependent risk factor
Inhibits parts of anticoagulation cascade
Trigger of endothelial damage
homocysteine
Similar structure to LDL
Mechanism in atherogenesis not clear
SERUM LIPOPROTEIN (a)
Chlamydia pneumoniae
Herpes hominis
Cytomegalovirus
infections that are risk factors for atherosclerosis
NCEP ATP III guidelines

ideal LDL:?
too-low HDL:?
Ideal triglycerides:?
NCEP ATP III guidelines

ideal LDL:<100 mg/dl
too-low HDL:<40 mg/dl
Ideal triglycerides:<150 mg/dl
Still controversial whether these lead to atherosclerotic lesions
In the lumina
Thin and yellow
Contain macrophages
Contain distended smooth muscle cells of lipid – foam cells
fatty streaks
1.Endothelial injury
2.Lipid infiltration
3.Inflammation
4.Smooth muscle proliferation
steps to atherosclerotic lesion formation
1. Injury to endothelial cells (triggers of inflammation)
2a. Platelets respond to injury and are recruited to area
2b. Injury recruits monocytes (macrophage) adhere and stimulate growth of SM and cause cell damage
2c. C-reactive protein released from endothelial cells
3. LDL deposit (trapped) on the damaged site
3b. macrophages fill with oxidized LDL - foam cells
4. Smooth muscle proliferation triggered by various factors as a result of above.
5. Atheroma forms (bump with hardened fibrous cap)
6. Weak arterial wall
7. Calcification of atheroma (dystrophic) and possible necrosis
detailed hypothesis of atheroma formation
Leaks or rupture of SM wall - hemorrhage
Thrombosis
Occlusion
Sudden obstruction due to plaque hemorrhage or rupture
platelet aggregation
abnormal vasoconstriction
heart attack, stroke
possible outcomes of atheroma formation
Collateral circulation to maintain blood flow
Compensatory Mechanisms

like development anastomoses
Inflammatory injury and necrosis of blood vessel wall from:
Direct injury to vessel
Infectious agent
Secondary to another disease process
Cold – e.g. frostbite
Irradiation – e.g. sunburn
Mechanical injury
toxins
Vasculitis
Sudden interruption of blood flow to tissue or organ
Usually from thrombus or embolus

Dx:Signs of impaired blood flow
Visual, palpation, instrument measure blood flow
Acute Arterial Occlusion
ATHEROSCLEROTIC OCCLUSIVE DISEASE OF LOWER EXTREMITY
Common location: superficial femoral and popliteal arteries
Risk factors same as for atherosclerosis
manifestations:
pain (lack of oxygen, interferes w/krebs, lactic acid, triggers nerve pain)
coldness or sensitivity
impaired arterial pulsations
color changes
ulceration and gangrene
edema
sexual dysfunction
superficial thrombophlebitis (nonvaricose veins)
Ateriosclerosis obliterans
Inflammatory arterial disorder that causes thrombus

Medium size arteries: plantar and digital vessels foot and lower leg; arm and hand

Etiology not sure: associated with cigarette smoking in men

Common Manifestations:
Ischemic Pain
Sensitivity to cold
Peripheral pulses decrease or absent
Coloration
Skin- thin, shiny, altered hair and nutrition
Nails- could be thick if ischemia is severe
Thromboangiitis obliterans (Buerger’s disease)
“functional disorder” – intense vasospasm of arteries and arterioles to fingers and sometimes toes. These body parts have only sympathetic vasoconstrictor vessels.

Triggers:
cold
stress

Manifestations:
Skin color:palor to cyanosis
Cold
numb, tingle
Rebound hyperemia
Could lead to ulceration or gangrene

Dx: history

Tx: prevention, vasodilator med. (Ca channel blockers, or alpha blockers), surgery (sympathectomy)
Raynaud’s Disease and Phenomenon

Phenomenon is secondary to other disease such as:
Previous vessel injury
Collagen diseases
Neurologic disorders
Chronic arterial occlusive disorders
Localized abnormal dilation of a vessel
Can occur in arteries and veins, MORE COMMON in arteries
CLASSIFIED according to cause, location, anatomic features
aneurysm
Small, spherical at a bifurcation
Often- circle of Willis in cerebral circulation
Berry aneurysm
Entire circumference with gradual and progressive dilation
Could be large in thoracic and abdominal aortas
Fusiform aneurysm
Part of circumference with saclike appearance
Saccular aneurysm
False aneurysm
Tear in inner wall, with blood separating the layers to form cavity
Dissecting aneurysm
Vessel wall weakness
Congenital defects
Trauma
Infections
Atherosclerosis

Tension = pressure x radius
Causes of aneurysms
Rupture
Pressure on adjacent tissue
Block adjacent vessel blood flow
manifestations of aneurysms
Location: any part of aorta (ascending, descending, aortic arch, thoracoabdominal, abdominal)

Common Causes:Atherosclerosis, Degeneration of vessel media

Usually after 50 yrs; men > women

Manifestations:Often asymptomatic, Depend on location

Thoracic:Pain of substernal, back and neck; Dyspnea, stridor, brassy cough from trachea pressure; Hoarseness from pressure on laryngeal nerve; Difficulty swallow from esophageal pressure

Abdominal aorta:Often asymptomatic, Pulsating mass, Possible pain mid-abdominal or lumbar
aortic aneurysm
Acute and life threatening
Anywhere along aorta length

Caused by conditions that lead to vessel wall weakness or degeneration
Hypertension
Degeneration of medial layer vessel wall
Connective tissue disease
Pregnancy induced chemical changes

MANIFESTATIONS: (depend on location)
Abrupt and severe pain
Change in BP
Interruption blood flow to extremities
Syncope
hemiplagia
paralysis of lower extremeties
DISSECTING ANEURYSMS
1.Superficial veins collect and drain to deep venous channels; Thin walled, easily distensible

2.Return blood flow
Valves prevent retrograde flow
Require skeletal muscle contraction
Low pressure system
anatomy and physiology of veins
Distended veins usually lower extremities

Primary- superficial saphenous veins > 50 yrs, obese, hereditary?

Secondary- deep venous channels due to obstruction ( e.g. DVT, tumor, defect, pregnancy)
varicose veins
Prolonged standing

Increased intra-abdominal pressure: The valves in external iliac or femoral need to support (prevent retrograde) blood flow.

Example of situations: after pregnancy, heavy lifting, prolonged increase pressure, obesity effects on superficial fascia and tissues
mechanisms of primary varicose veins
(faulty valves)
Mx:Appearance, Ache, Edema, Venous insufficiency, Once stretched, not reversible on own

Dx:Physical inspection, Techniques to assess extent, Trendelengburg’s test, Doppler ultrasound, Contrast angiography

Tx: Avoid activities that aggravate, Elastic support stockings, Scleotherapy, Surgery for deep venous channels
manifestations, diagnosis, treatment of varicose veins
Consequence of:DVT, Valvular incompetence

MANIFESTATIONS
Impaired blood flow and associated signs and symptoms(if arterial flow in place, the oxygenation occurs)
Tissue edema
Impaired tissue nutrition
Subcutaneous fat necrosis
RBC breakdown hemosiderin deposits (brown pigment)
Secondary lymphatic insufficiency (backs up because lymph drains into veins)

Severe:Stasis dermatitis, Venous ulcers
CHRONIC VENOUS INSUFFICIENCY
Thrombus in Vein with inflammation of in vessel wall
Superficial veins or deep veins

An example of acute vessel obstruction: (DVT) most common lower extremity

Virchow triad
Stasis blood
Increase blood coagulability
Vessel wall injury
VENOUS THROMBOSIS
(Thrombophlebitis)
(tissue acts as a tourniquet ex:snakebite)

Localized pressure increase in “surrounding tissues” that restricts blood flow and can lead to ischemia
Usually in the muscle compartment
Normal P is 6 mmHg
Elevated to cause damage is 30-40 mmHg

MANIFESTATIONS:Tissue circulation decreased, Necrosis of tissue and nerves, Loss of limb function

Time/location are factors
COMPARTMENT SYNDROME
External pressure that impairs blood and lymph flow to tissue (skin and underlying) can lead to ischemic lesions.

Often over bony prominence
Prolonged lack of movement

MECHANISMS
External pressure to compress vessels
2 hours is possible
Shearing that tears and injures vessels
Sliding of one tissue layer over another with angulation of blood vessels to cause injury and thrombosis e.g. elevation head of bed to cause torso to slide

PREVENTION: Identify persons at risk, Keep tissue healthy to improve tolerance to pressure, Protect against external forces
PRESSURE ULCERS
(Decubitus ulcers, bedsores)
JNC7
Diagnostic and Treatment Guidelines from The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)
Printed by the National Heart Lung and Blood Institute (NHLBI) of the National Institutes of Health (NIH).
HTN

Normal:?
PreHTN:?
HTN1:?
HTN2:?
HTN

Normal:<120
PreHTN:120-139
HTN1:140-149
HTN2:160 and up

*Diabetes Mellitus: goal <130/80
obesity
hypercholesterolemia
atherosclerosis
high sodium diet
diabetes
hyperinsulinemia (associated insulin resistance)
stress
Type A personality
familial history (race -Blacks)
smoking
lack of exercise
Excess alcohol consumption
Decreased Intake K, Ca, Mg
Oral contraceptives
related conditions to the pathophysiology of primary (essential, idiopathic) HTN
SNS activity increase
RAA system activity increase
ANP activity increase
Nitric Oxide decrease
Pressure Natriuresis
Neural and Hormonal control of kidney
low Mg, K, Ca
Insulin resistance
Genes
what causes increase peripheral resistance and/or blood volume
Activation of Sympathetic nervous system – effects CO and TPR, renal sodium retention
Insulin stimulated vascular SM growth –increase TPR
Kidney salt and water retention
Changes in Na and Ca cell membrane transport- sensitization of blood vessels to vasopressor stimuli
proposed mechanism of increased BP
Renovascular hypertension - atherosclerotic or fibrous dypslastic stenosis of renal artery(ies)
Renal parenchymal disease - renin or sodium dependent failure
Cushing's disease (adrenal)- increase adrenocorticotropic hormone, increase vol
Primary aldosteronism (adrenal) - increase aldosterone, increase vol
Pheochromocytoma (adrenal medulla) - increase sympathetic tone
Coarctation of the aorta - congenital constriction of aorta
Estrogen-induced hypertension
Sleep Apnea
Drug induced/related
Thyroid/parathyroid disease
secondard HTN is due to a known cause
∑ elevated systolic increases risk of stroke and heart disease
∑ elevated diastolic increases risk of stroke and heart disease
∑ systolic pressure puts greatest stress on blood vessels and heart
∑ both systolic and diastolic pressures matter, but systolic matters more
∑ not normal for systolic pressure to increase with age
- elevated systolic pressure in elderly indicated arterial damage has begun
PATHOPHYSIOLOGY OF HYPERTENSION
∑ high systolic with normal diastolic reading
∑ most common form of hypertension in >65yr
∑ incidence increases with age
∑ treatment has been shown to reduce risk stroke and heart disease
∑ Decreased elastic properties of the arteries
∑ CV complications associated with increased Systolic BP
∑ CV complications associated with increased pulse pressure
ISOLATED SYSTOLIC HYPERTENSION (ISH)
often asymptomatic

headache, nosebleed, dizzy, tinnitus, blurred vision

target organ damage
physiological effects of HTN
increased afterload * heart
compensatory systems try to regulate (RAA, SNS, etc.)
damage small arterioles (single cell layer thick)
target organ dysfunction (TOD)
primarily: brain, eyes, kidneys, heart
Pathologic sequelae: series of events in steps of physiological effects of HTN
Upon standing, a sudden and abnormal drop in BP that does not adequately correct with compensatory mechanisms.
ORTHOSTATIC HYPOTENSION
(Postural Hypotension)