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146 Cards in this Set

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red bone marroe in long bones >
1-RBC
2-WBC
3-platelets
hemocytoblasts
Red bone marrow precursor cells
hemocytoblasts >
formed elements
megakaryocytes >
platelets
red bone marrow in
cancellous/spongy bone
yellow bone marrow
fat storage
platelets role
hemostasis
granulocytes
neb

neutrophil
eosinophil
basophil
agranulocytes
monocytes
lymphocytes
hematocrit
45% in males

proportion of erythrocytes
least abundant leukocytes
basophils
blood =
- 8% of body weight
- 4-6 L
LEUKOCYTES:

neutrophils
70%
LEUKOCYTES:

lymphocytes
30%
LEUKOCYTES:

monocytes
2-6%
plasma %
55% of volume
formed elements volume
45% of volume
% of H2O in plasma
90%
portion of blood not plasma
formed elements
formed elements =
erythrocytes
leukocytes
platelets
serum =
blood plasma -
fibrinogen
portion of plasma that is protein
7%
proteins in plasma =
albumin 55%
globulin 38%
fibrinogen 7%
cytoplasmic fragments of cells =
platelets
platelet life span
5-9 days
megakaryocytes > platelets
thrombopoietin
secretory vesicles are located in
platelets
directly promotes platelet aggregation
thromboxane A
platelets adhere to collagen and release
ADP
increased RBC
polycythemia vera
opposite anemia
polycythemia vera
erythrocytosis
leukocytosis
thrombocytosis
splenomegaly
polycythemia vera
decrease in erythropoietin
polycythemia vera
chronic hypoxia
high altitudes
heavy smoking
adult polycystic kidney
secondary polycythemia
high altitudes
osker dx
fibrous tissue replace precursor cells that make RBC in bone marrow
myelofibrosis
cancerous
abnormal granulocyte
CML
myeloid stem cells>
produce blood cells
increase in basophils
serum uric acid
splenomegaly
myeloproliferative
myeloid stem cells dev and reproduce abnormally
myeloproliferative
pernicious anemia
lack of intrinsic factor
abnormal hemoglobin
low levels of erthyrocytes
thalassemia
imbalance in production of 1/4 chains in AA that make up hemoglobin
thalassemia
inhibition/destruction of red bone marrow
aplastic anemia
radiation
toxins
meds >
aplastic anemia
inadequate production of erythrocytes
aplastic anemia
megaloblastic anemia
pernicious anemia
prone gastric carcinoma
pernicious anemia
-obstructive venous return
-increased back pressure from CHF
passive congestion
localized arteriolar dilation
active congestion
blushing
inflammation
active congestion
passive congestion 2 forms
acute
chronic
acute>
shock
right sided heart
chronic>
lung=left sided heart

liver=right sided heart
wear out HTN
cardiac failure
blow out HTN
cerbrovascular accident
run out HTN
renal failure
ABCDE
secondary HTN
A-
B
C
D
E
common cause of secondary HTN
kidney disease
HTN
no identifiable cause
90-95%
essential HTN
increased RBC destruction
hemolytic anemia
erythroblastosis fetalis

sicle cell anemia

thalasemias
hereditary sperocytosis
hemolytic anemia
circulating RBC greater than normal
macrocytic anemia
chronic blood loss
nutritional anemia
microcytic anemia
def of folic acid
def of vit B12
macrocytic anemia
def B12
def folic acid
megaloblastic anemia
oral anticoagulant
dicumarol
dicumarol
interferes with
vit k
inhibits formation of prothrombin in liver
dicumarol
dicumarol=
warfarin
delay clotting of blood
warfarin
delayed blood clotting
-heparin
-leukemia
-cirrhosis
thrombocytopenia= decreasedplatelets
-von willebrand
-aspirin
-bernard soulier dx
platelet adhesion disorder
bernard soulier
cylooxygenase inhibitor
aspirin
impaired platelet adhesion
von willebrand dx
prothrombin
made/stored in liver
antithrombin
heparin
erythroblastosis fetalis
sickle cell anemia
thalassemia
hemolytic anemia
increase of bilirubin
hemolytic anemia
released from dying RBC
bilirubin
accumulation of unconjugated bilirubin

in brain and spinal cord
kernicterus
low platelet count of blood

thrombosis in terminal arterioles
TTP
thrombotic
thrombocytopenic
purpuraq
reduced # platlets
thrombocytopenia
most common bleeding disorders
thrombocytopenia
arteriosclerosis
aorta
coronary arteries
hardening of arteries
arteriosclerosis
consequences of
atherosclorosis
ischemic heart disease

stroke

aneurysm
coronary artery dx=
ischemic heart dx
degenerative changes in walls of arteries
atherosclerosis
hepatocellular damage
carbon tetrachloride
renal tubular necrosis
mercury chloride
blindness
methyl alcohol
basophilic stippling of RBC
lead
cherry red discoloration of
skin
mucosa
tissue
acute carbon monoxide
generalized swelling
edema
anasarca
excess fluid in peritoneal cavity
ascites
noninflammatory edema fluid
due to
altered
-intravacular hydrostatic or osmotic pressure
transudate
result of inflammation>
edema from increased vascular permeability
exudate
peripheral edemA
right sided CHF
pulmonary edema=
left sided CHF
finger against swollen area (5 sec)

then indentaion is left that fills slowly
pitting edema
finger against swollen area (5 sec)

no indentation is left
nonpitting edema
blood clot inside
-BV
-cavity of heart
thrombus
blood clot that moves thru bloodstream until it lodges
embolus
develops in
is attached to BV wall
embolus
common source of pulmonary embolism>
thrombophelebitis
inflammation of vein
phlebitis
accumulatin of excessive blood within BV
congestion
not getting enough blood flow>
shock
shock that results from injury to CNS
neurogenic
shock that occurs with severe allergic rxn
anaphylactic
main factor in all types of shock
reduced cardiac output
shock that occurs with severe allergic rxn
anaohylactic
contributor to arterial thrombosis
atherosclerosis
thrombus composed of blood platelets
white thrombus
formed by coagulation of stagnatig blood
red thrombus
thrombus composed of RBC
not platelets
red thrombus
doesnt occlude vessel
fibrin thrombus
damage of ventricular endocardium
mural thrombosis
MI>left ventricle
mural thrombosis
heart failure
extensive tissue damage
bed rest
pregnancy
oral contraceptives
age
obesity
venous thrombosis
formed by enchanced endo injury
thrombus
alteration in blood flow
thrombus
hypercoagulability
thrombus
alternating red and white laminations
lines of zahn=

arterial thrombus
unifomly red
venous thrombi
progressive stage of shock
progressive stage
advanced stage of shock>
excess acid produced
increased HR
increased periph resistance
non progressive stage
metabolic acidosis
progressive stage
compensatory mxns no longer adequate
progressive stage
organ damage
survival not possible
irreversible
main factor in all types of shock
reduced cardiac output
occurs after large MI
cardiac tamponade
most serious complication of pericarditis
cardiac tamponade
inflammation causes fluid /blood products into pericardial space
acute pericarditis
postinflamm thickening/scarring of pericardium>

constriction of cardiac chambers
constrictive pericarditis
caused by TB
constricive pericarditis
aortic rupture in pericardial sac
>
fatal cardiac tamponade
dissecting aneurysm
heart cant pump
CHF
chronic long term condition
heart failure
left ventricle fails 1st
heart failure
systemic venous congestion
periph edema
right sided CHF
earliest /common signs of CHF
paroxysamal nocturnal dyspnea
swollen edema
peripheral edema -CHF
life complication of left heart CHF=
pulmonary edema