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94 Cards in this Set

  • Front
  • Back
What does plasma contain?
Mostly water, proteins (albumin, fibrinogen, antibodies (IgG most), soluble substances like nutrients, resp. gases, wastes
Total volume of formed elements/total volume of blood
All blood cell formation
Formation of red blood cells
Formation of white blood cells
Basic facts on erythrocytes
no mitosis
live 120 days
transfer form of iron
storage form of iron in liver
Hemoglobin structure
globin - 4 polypeptide chains (2 alpha, 2 beta)
heme - each chain has a heme group - iron.
1 hemoglobin = 4 oxygen
saturated hemoglobin, carrying 4 oxygen
Hemoglobin A
normal adult,
2 alpha, 2 beta chains
Hemoglobin F
produced during fetal life up to 3-6months
2 alpha, 2 F chains
Stimulus for erythropoeisis
Low tissue oxygen, stimulates secretion of erythropoetin, which stimulates RBC production
Polycythemia (erythrocytosis)
Too many RBC's
excess RBC's increases vessel wall pressure, causes high BP
Primary Polycythemia
rare neoplastic disease

stem cell to become RBC gets altered - RBC cancer

white males 40-60

flushed face, thrombi, hypertension.

viscous blood from too many RBC's, causes platelets to spontaneously activate, causes thrombi
Secondary polycythemia
Usually caused by prolonged hypoxia

could be normal physiologic response to:
tissue hypoxia (heart & lung)
high altitudes
heavy smoking (CO2 takes place of oxygen on hemoglobin, bonds easier)

marrow responding to kidney increasing output of EPO
Autologous transfusion blood doping
remove own blood, reinject later.

inc. risk blood clots, hypertension
Synthetic EPO blood doping
EPO taken for renal failure

stimulates more RBC production
Homologous transfusion blood doping
easiest to trace
blood from someone w/ same blood type
reduction of normal Hb in blood

may be due to:
abnormal Hb
reduced # RBC's (dec. prod, blood loss, inc. destruction)
structural abnorm. of RBC's

ALL ANEMIAS - transp. of oxygen is impaired. can't enter Kreb's, produce lactic acid.
Hemolytic Anemia
normocytic/normochromic (normal size, normal amt. Hb)

premature RBC death

liver can't keep up with excess bilirubin, builds up in connective tissue
hemolytic anemia

autosomal dominant disorder expressed when heterozygous - 50% passed to children, M or F

abnormal spectrin AND ankyrin leads to spherical RBC shape

normocytic, but wrong shape, harder to get through capillaries, clogs up spleen - spleenomegaly

RBC ruptures easily in tight curves of spleen

spleenectomy helps
Sickle cell anemia
blacks/equatorial descent

autosomal recessive disorder

genetic defect in beta Hb chains - valine in place of glutamic acid

homozygous - sickle cell disease

heterozygous - sickle cell trait
Homozygous Sickle Cell Anemia
Sickle cell disease, symptomatic

produce only HbS, no HbA
all beta chains are S chains, which combine with normal alpha chains to form HbS

cells only sickled in venous blood

sickled RBC lives 10-14 days
Heterozygous sickle cell anemia
both normal beta and S chains are synthesized

can be symptomatic in times of stress.

asymptomatic if producing at least 40% HbA
Clinical manifestations of sickle cell anemia
symptoms first noticed 6mo-1yr age (growth puts more demands for oxygen, out of HbF)

low hematocrit

sickling or hemolytic crisis may occur spontaneously, usually induced by fever, resp. disease, pregnancy, stress

peripheral tissues deprived of oxygen due to massive blockage of capillaries.

blood transfusion to treat
Complications of hemolytic anemias
pigmentary gall stones (inc. bili in bile, supersaturated, crystallizes and becomes a stone)


stroke (rbc's cause traffic jam to cerebral arteries)

neuro complications (high bili is toxic to CNS)

survival: 40-50yrs, stroke, MI
bone transplants, blood transfusions successful

hydroxyurea - med decreases painful episodes, inc prod of HbF

gene therapy, nitric oxide therapy (dilates vessels so sickled cells get through easier)
Immune Hemolytic Anemia
ex. drug induced anemia

penicillin for some people is a hapten, attaches to RBC proteins. type II sensitivity, tissue specific destruction

idiopathic (unknown cause)
Iron Deficiency Anemia
most common, more prev. in women

detrimental to dev. of NS

microcytic, hypochromic (small cells, not as much Hb)

low hematocrit

poikilocytosis (abnormal shape possible)

Causes: menstruation, bleeding ulcer, defic. iron rich foods
Pernicious anemia
malabsorption of vit. B12 due to lack of gastric intrinsic factor

vit b12 req. for normal DNA synthesis

lack of parietal cells, which produce intrinsic fact, which binds with B12 in stomach, enters small int., absorbed by epithelial cells of small int., sent into bloodstream

schilling test - measures b12 absorption w/ radioact b12
Causes of pernicious anemia
avoidance of dietary b12

atrophic gastritis complications(small parietal clls, less intrinsic factor)

gastric bypass (many parietal cells removed)

Crohn's or other malabsorption syndrome

Autoimmune - antibodies against parietal cells or intrinsic factor

Vit b12 injections directly into bloodstream for treatment
Aplastic anemia
panctyopenia (many cells affected, low numbers of RBC's, WBC's, dec. thrombocytes) shows up in lab findings

fatigue, pale, inc. infection risk, bruising, excessive blood loss
Idiopathic aplastic anemia
underlying autoimmune disease?

therapy may require bone marrow transplant
Secondary aplastic anemia
caused by cytotoxic drugs, radiation therapy or viral infection
Infectious mononucleosis
Epstein-Barr virus (B-cell lymphoma link)

infects pharyngeal epithelial cells --> adjacent lymph tissue --> B cells w/ EBV receptors --> infected B cell w/ EBV genome becomes plasma cell --> heterophil antibodies

heterophil antibodies bind to RBC proteins in sheep

4-8 week incubation period

T-cytotoxic cells destroy infected cells
Malignant lymphomas
tumors arising in the cells of lymphoid tissue

6th most common cause of cancer death in the US
Hodgkin Disease
young adults and those over 50

Reed-Sternberg cell (probably a transformed macrophage)

cure rate high w/ radiation, chemotherapy

lymph adenopathy (swollen nodes) tired - causes an anemia, increased inf. risk

produce excessive interleukin 13 which leads to proliferation of immune cells
Non-Hodgkin Lymphoma
more frequent than Hodgkin

numerous subtypes (T or B cell, mostly B) Epstein-Barr virus??
Human t-lymph virus??

Rituximab (drug) binds CD20 on B cell lymphomas and controls proliferation. CD20 NORMALLY causes cells to proliferate

SV40 virus - 40% infected with this, only prior known to inf. rhesus monkey. polio vaccine?
means "white blood"
neoplastic cell in blood and bone marrow

derived from stem cells

type of leukemia based on which stem cell failed
Causes of leukemia
most common childhood cancer

high levels of radiation
anti-tumor drugs
down's syndrome (10x more than normal)
virus (human T lymphocytic virus (HTLV) type 1 and 2)
Clinical features common to all leukemias
leukoblasts (immature WBC's) larger than WBC's

bone marrow contains malignant cells

leukostasis (WBC's thicken blood flow)

lymphadenopathy, hepatomegaly, splenomegaly

complications: anemia, recurrent infections, uncontrollable bleeding (WBC production takes all resources)
Acute Lymphoblastic Leukemia (ALL)
most common malignancy affecting children

breastfed children at dec. risk

chemotherapy successful
Acute myelogenous leukemia (AML)
myeloid stem cell leukemia, can present in many ways

many subtypes, most common: acute granulocytic leukemia (neutrophils, basophils, eosinophils)

presents after middle age

down syndrome inc. risk

clinical trials under way for vaccine
Chronic Lymphocytic Leukemia (CLL)
30% of all leuk. in US
95% of cases a malignant B cell precursor is at fault

asymptomatic at time of Dx

usually affects older adults

error: bcl-2 gene apoptosis
Chronic Myelogenous Leukemia
Philadelphia chromosome (unique)
30-50yrs old

bone marrow transplant, chemo

long arm of chrom 9 fused w/ short arm of chrom 22 which puts BCR and ABL gene next to each other, which stimulates all to proliferate and differentiate
no cholesterol plaque, just hardening of arteries
cholesterol plaque (atheroma) present, arteries hardened.

underlying disease process in most coronary artery diseases that cause MI, and arterial alterations that produce CVAs

can affect any artery in body

develops from birth, significant in 20's
top 5 arterial locations for atherosclerosis, know in order
1. abdominal aorta and iliac arteries

2. coronary arteries

3. thoracic/femoral

4. internal carotids

5. cerebral
atherosclerosis risk factors
age - men over 45, women over 55 (estrogen deters)

gender - more males than premenopausal females, equal after menopause

genetic predisposition:
familial hypercholesterolemia (mutated LDL receptor), sibling history

EBT (electron beam tomography) measures calcium deposits in arteries
primary causes: defective synthesis of apoproteins(lipid carriers), lack of receptors

secondary causes: obesity, DM, inc. cholesterol ingestion, excess calorie intake (lowers HDLs), inc. saturated fats
apoprotein + lipid
dietary lipids
lipids are insoluble in plasma

mostly triglycerides, some cholesterol, some phospholipids

transported in blood by lipoproteins. protein component = apoprotein (ex. A, B, C, E)
Classification of lipoproteins
by density (more protein = higher density)
Low density lipoproteins
chylomicrons - major triglyceride carriers, 2% protein

LDL - 10% triglyceride, 50% chol, 25% protein
high density lipoproteins
HDL - 50% protein, 20% chol., 5% triglycerides
inc. bp, norm <120/<80

prevalence inc. with age

more common in men than women, equal after menopause

more common in blacks
Primary hypertension (aka essential hypertension)
inc. BP existing in absence of another major disease

risk: FH, old age, black, obese (inc. periph resistance), type II diabetes, oral contraceptives, high salt intake
cardiac output
stroke volume x heart rate

approx. 70mL

amount ejected from each ventricle during contraction
What is arterial blood pressure related to?
Cardiac output and peripheral resistance.
homocysteine inhibits components of the anticoagulation cascade

inc. homocysteine promotes clotting

taking folate dramatically reduces risk of this, which reduces atherosclerosis and therefore MI and stroke risk
tobacco use and hypertension
smoking pack/day increases likelihood of coronary thrombosis and MI

when acute MI occurs, more likely to be fatal

tobacco damages vascular endothelium and enhances platelet aggregation

smoking lowers HDL levels

nicotine stimulates release of EP and NOREP which inc. heart rate (nicotine patches too!)
C-reactive protein
released from liver

serum marker of systemic inflammation, can be lowered with statins
pathophysiology of atherosclerosis
1. damage occurs in tunica intima where blood/arterial wall interface

2. blood platelets and lipoprotein deposit

3. platelets release growth factors that penetrate vessel wall (proliferation of smooth muscle, attracts calcium into tunica media layer)

4. monocytes adhere to the injured endothelium, engulf lipoproteins by foam cell, which leads to fatty streaks

5. proliferating smooth muscle and fibroblast surround, fatty streak --> plaque, atheroma. start depositing connective tissue to cover the fatty streak
complications of atherosclerosis
1. thrombosis and embolism - pressure of lipid soft region may cause fibrous capsule to rupture --> ulceration. contents of atheroma highly thrombogenic --> blood clot.

2. acute arterial occlusion - occurs at bifurcations: aorta, iliac and femoral, popliteal... pulse pressure decreases downstream of occlusion
cardiovascular disease
#1 cause of death in US

1 in 3 MI die within hour

coronary artery disease leads to myocardial ischemia leads to myocardial infarction
male MI symptoms
left side pain jaw - right arm


crushing pain
female MI symptoms
chronic atherosclerosis
more time for alternate blood vessel pathways to form

leads to stable angina or silent MI
acute atherosclerosis
no time for alternate blood vessel pathways to form

leads to MI, unstable angina
angina pectoris
clinical manifestation of myocardial ischemia

intense pain, buildup of lactic acid and/or irritation of myocardial nerve fibers

stable, unstable, variant
stable angina
narrowing of lumen due to fixed plaque

relieved by rest or nitroglycerin (vasodilator)
unstable angina
cannot be predicted

attacks increase w/ frequency

caused by vasospasms and atherosclerotic lesions

treat w/ heparin (blood thinner)
variant angina
attacks almost always while at rest

vasospasm of 1 or more of the major coronary arteries
blockage in left coronary artery
affects left atrium
blockage in right coronary artery
affects right ventricle, right atrium
blockage in posterior descending branch of right coronary artery
affects right and left ventricle
blockage in left coronary artery, circumflex branch
affects left atrium, left ventricle
blockage in left coronary artery, anterior descending branch
affects left ventricle, right ventricle
extent of MI depends on
1. location of occlusion
2. degree of blockage
3. collateral circulation
therapy for myocardial ischemia
nitrates (vasodilator)

anti-platelet drugs (aspirin, platelet receptor antagonist so it prevents clotting)

block beta-adrenergic receptors- found in cardiac cells, binds epinephrine

calcium channel blockers - lower contractile force of cardiac cell

coronary artery bypass graft - alternate route around occlusion (usually saphenous vein or internal mammary artery)

percutaneous coronary intervention (+ stent) - balloon catheter, squishes plaque, stent keeps bv open
temporary ischemia
<20 minutes

leads to angina + reversible cell injury
prolonged ischemia
>20 minutes

leads to MI + irreversible cell injury --> scar tissue
Leading locations of MI
1. blockage in anterior descending

2. blockage in rt. coronary artery
CK-MB - creatinane kinase - MB, shows up 4-8 hrs post MI. enzyme in myocardial cells involved in ATP prod. if found in blood, MI occured and dead cells were lysed

Myoglobin - oxygen carrying molecule in muscle cells, increases about 1hr post MI (any muscle)

troponin levels - inc. within 3 hours of MI

CRP - c reactive protein, inc. prior to or following MI
sequelae of acute MI
1. arrythmias - most serious is ventricular fibrillation

2. cardiogenic shock - decline in cardiac output when 40% of LV myocardium has died

3. thromboemboli
4. healing of infarcted tissue
5. aneurysm
6. rupture (survive? cardiac tamponade - pericardium full of fluid, pushes on heart, makes contraction difficult)
Right sided congestive heart failure manifestations
peripheral tissue congestion

congested liver w/ impaired liver function --> dec. clotting factors, dec. albumin --> edema. event. jaundice

edema, ascites

GI congestion - anorexia, wt. loss, GI distress
Left sided congestive heart failure manifestations
dec. cardiac output --> activity intolerance --> dec. tissue perfusion

pulmonary congestion --> impaired gas exchange, pulmonary edema, cough, dyspnea, cyanosis and signs of hypoxia
Acute pericarditis
chest pain that worsens w/ resp.

inc. capillary permeability --> fibrous deposits

friction rub

anti-inflammatory agents to treat
Dilated cardiomyopathy
ventricular dilation leads to dec. stroke volume, inc. end-diastolic volumes


dyspnea, fatigue, sometimes inc. BP

treatment: vasodilators and diuretics
Valvular Dysfunction
endocardium disorder

aortic stenosis (narrowing)

causes: rheumatic disease (strep bact)
congenital defect

diminished stroke volume
Mitral stenosis
causes: acute rheumatic fever, bacterial endocarditis

increased atrial pressure, atrial hypertrophy, atrial dilation

pulmonary congestion, rt. ventricular failure
aortic regurgitation
causes: rheumatic fever, Marfan syndrome (mutated fibrilin) and hypertension

heart murmur

large stroke volume

Mitral regurgitation
causes: mitral valve prolapse, rheumatic heart disease

atrial dilation

pulmonary hypertension
mitral valve prolapse
thickened mitral cusps

long chordae tendinae

end result, the valve doesn't close as well, causes mitral regurgitation