E2: Hematologic disorders Flashcards
erythrocytes are what kinda cells
RBC
erythrocytes are doughnut shaped why
- increases surface are a it can carry more O2
- very flexible
- can flatten and squeeze through capps
function of erythrocytes
transports o2 via hemoglobin to the cell and carries CO2 to the lungs
what is hemoglobin
molecule in cytoplasm of RBC that the O2 attaches to
What are Leukocytes
WBC
function of leukocytes
defend against infections and remove debris
what are the two agranulocytes
- macrophages
2. Lymphocytes
what do neutrophils do
function first 2 days of inflammation (granulocytes)
normal level of neutrophils
55-70%
segmented neutrophils
mature
proliferation of cells
rapid reproduction of cells (not normal)
band neutrophils
immature neutrophils
basophils
anti-parasitic granulocytes
eosnophils
controls inflammatory/allergic responses (granulocytes)
normal level for basophils
.5-1%
eosinophils normal level
1-4%
lymphocytes
primary cells of immune response
thrombocytes
platelets
hematopoiesis
production of blood cells in the bone marrow
function of platelets
blood coagulation and control of bleeding
what is thrombocytopenia
platelet count less than 100,000
what is the lifespan for RBC
3-4 months
lifespan of leukocytes
7-21 days
thrombocyte life span
5-9 days
what forms with minor injuries that have vasoconstriction
platelet plug
how does hemostasis stop bleeding with minor injuries
- vasoconstriction
- formation of platelet plug
how does hemostasis stop bleeding with major injureis
clot formation (coagulation cascade)
what are the 3 causes of thrombocytopenia
- autoimmune disorder (IS destroys platelets)
- complication of heparin therapy (HIT)
- blood loss
clinical mani of thrombocytopenia
- Decreased platelets
- hemorrhage
- epistaxis
- petechiae
- hematuria
- bleeding gums
- ecchymosis (bruising)
disseminated intravascular coagulation (DIC)
sequence of events resulting from abnormal, diffuse activation of:
- coagulation
- fibrinolysis (clot digestion)
what causes DIC
- burns
- trauma
- shock
- cancers- termal
- emboli
6 sepsis (most common cause)
what causes DIC
- burns
- trauma
- shock
- cancers- termal
- emboli
6 sepsis/septicemia- (most common cause)
what is hemostasis
arrest of bleeding (stops bleeding)
what are the two ways that the coagulation cascade start
intrinsic pathway
extrinsic pathway
intrinsic pathway starts with what
blood vessel injury
extrinsic pathway starts with what
tissue injury
coagulation cascade patho chain
after intrensic and extrensic is activated:
aggregation of platelet at site of injury-> prothrombin converts to thrombin->thrombin makes fibrinogen which converts to fibrin-> fibrin becomes fibrin clot which is broken down by FDP
why is septicemia cause DIC
bacteria breaks down which releases endotoxins which act as procoagulants (activates DIC)
what is the patho chain of DIC
activation (usually sepsis)->release of procoags (stimulates clotting)-> overstimulation of coag system->excess fibrin formation-> disseminated (systemic) intravascular clotting->THEN increased consumption of platelets and clotting factors->decreased platelets and clotting factors->hemorrhage
->OR fibrin deposits in microcirculation “log jam”-> ischemia and infarction (widespread organ hypoperfusion)->clotting
how do they diagnose DIC
increase D-Dimer which measures the rate of fibrin clot breakdown
microvascular clinical mani of DIC
CNS- decreased LOC
Skin- Ischemia leading to gangrene
Kidney-oliguria, RF
lungs-SOB, PE
GI-acute ulcerations, necrosis
hemorrhage clinical mani of DIC
- CNS- intracranial bleeding
- skin-petechiae, echymosis
- mems- gingival bleeding
- kidney- hematuria
- Gi- bleeding
mortality rate of DIC
high, depends on cause
disorder of coagulation
DIC
multiple myeloma
malignant disorder characterized by proliferation of abnormal plasma (b lymphocytes) in the bone marrow
incidence of multiple myeloma
peaks in the 6th decade of life
etiology of multiple myeloma
UNKNOWN
- genetics
- viruses
- bacteria
- chemicals
patho chain of multiple myeloma
excess number of abnormal plasma cells (b lymphs) infiltrate the bone marrow-> develop into tumors-> destroy bone-> invade lymph nodes, liver, spleen, kidneys
abnormal plasma cells produce
myeloma (M) protein
(test for this during diagnosis)
(is a large protein=renal failure)
clinical mani of multiple myeloma
- frequent infections
- anemia/bleeding
- bone pain/fractures
- renal insufficiency/failure
lymphoma
malignant disease of the lymphoid tissues (thymus, bone marrow, lymph nodes, spleen)
where is the majority of the disease located in lymphona
90% in the lymph nodes
etiology of lymphoma
UNKNOWN
- chromosome abnormality
- virus
- immunosuppression
incidence of lymphoma
- Hodgkin’s peaks at 20-30
- non-hodgkins at 50+
patho of lymphoma
normal lymph node or tissue lymph structure is destroyed by excessive (abnormal) proliferation of lymphocytes
onset of myeloma
insidious and slow
hodgkin’s signs
reed-sternberg cells in lymph nodes
non-hodgkin’s signs
- bone marrow involvement occurs more often than hodgkins
- may different types of cells seen
clinical mani of lymphoma
- enlarged, painless, lymph nodes
- night sweats, fever, weight loss
cure rate for hodgkins
complete remission if treated in early stages one and two
cure rate for non hodgkins
varies
can be slowly developing or agressive and rapidly fatal
