525 patho exam I
Terms
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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 ce - 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 den
-
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
- 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, - 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 hem
-
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 - 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, decrea - 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 barorecep - 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 anticoagul - 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 r - 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 - 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:
- 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 colo -
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 asymptoma - 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 in - 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, obe -
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 - manifestations, diagnosis, treatment of varicose veins
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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 necr - CHRONIC VENOUS INSUFFICIENCY
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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
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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 - COMPARTMENT SYNDROME
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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
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PRESSURE ULCERS
(Decubitus ulcers, bedsores) - JNC7
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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 - related conditions to the pathophysiology of primary (essential, idiopathic) HTN
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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
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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 - proposed mechanism of increased BP
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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
P - secondard HTN is due to a known cause
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∑ 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 pressu - PATHOPHYSIOLOGY OF HYPERTENSION
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∑ 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 - ISOLATED SYSTOLIC HYPERTENSION (ISH)
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often asymptomatic
headache, nosebleed, dizzy, tinnitus, blurred vision
target organ damage - physiological effects of HTN
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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.
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ORTHOSTATIC HYPOTENSION
(Postural Hypotension)