E2: Hematologic disorders Flashcards
(61 cards)
1
Q
erythrocytes are what kinda cells
A
RBC
2
Q
erythrocytes are doughnut shaped why
A
- increases surface are a it can carry more O2
- very flexible
- can flatten and squeeze through capps
3
Q
function of erythrocytes
A
transports o2 via hemoglobin to the cell and carries CO2 to the lungs
4
Q
what is hemoglobin
A
molecule in cytoplasm of RBC that the O2 attaches to
5
Q
What are Leukocytes
A
WBC
6
Q
function of leukocytes
A
defend against infections and remove debris
7
Q
what are the two agranulocytes
A
- macrophages
2. Lymphocytes
8
Q
what do neutrophils do
A
function first 2 days of inflammation (granulocytes)
9
Q
normal level of neutrophils
A
55-70%
10
Q
segmented neutrophils
A
mature
11
Q
proliferation of cells
A
rapid reproduction of cells (not normal)
12
Q
band neutrophils
A
immature neutrophils
13
Q
basophils
A
anti-parasitic granulocytes
14
Q
eosnophils
A
controls inflammatory/allergic responses (granulocytes)
15
Q
normal level for basophils
A
.5-1%
16
Q
eosinophils normal level
A
1-4%
17
Q
lymphocytes
A
primary cells of immune response
18
Q
thrombocytes
A
platelets
19
Q
hematopoiesis
A
production of blood cells in the bone marrow
20
Q
function of platelets
A
blood coagulation and control of bleeding
21
Q
what is thrombocytopenia
A
platelet count less than 100,000
22
Q
what is the lifespan for RBC
A
3-4 months
23
Q
lifespan of leukocytes
A
7-21 days
24
Q
thrombocyte life span
A
5-9 days
25
what forms with minor injuries that have vasoconstriction
platelet plug
26
how does hemostasis stop bleeding with minor injuries
- vasoconstriction
| - formation of platelet plug
27
how does hemostasis stop bleeding with major injureis
clot formation (coagulation cascade)
28
what are the 3 causes of thrombocytopenia
1. autoimmune disorder (IS destroys platelets)
2. complication of heparin therapy (HIT)
3. blood loss
29
clinical mani of thrombocytopenia
1. Decreased platelets
2. hemorrhage
- epistaxis
- petechiae
- hematuria
- bleeding gums
- ecchymosis (bruising)
30
disseminated intravascular coagulation (DIC)
sequence of events resulting from abnormal, diffuse activation of:
1. coagulation
2. fibrinolysis (clot digestion)
31
what causes DIC
1. burns
2. trauma
3. shock
4. cancers- termal
5. emboli
6 sepsis (most common cause)
32
what causes DIC
1. burns
2. trauma
3. shock
4. cancers- termal
5. emboli
6 sepsis/septicemia- (most common cause)
33
what is hemostasis
arrest of bleeding (stops bleeding)
34
what are the two ways that the coagulation cascade start
intrinsic pathway
| extrinsic pathway
35
intrinsic pathway starts with what
blood vessel injury
36
extrinsic pathway starts with what
tissue injury
37
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
38
why is septicemia cause DIC
bacteria breaks down which releases endotoxins which act as procoagulants (activates DIC)
39
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
40
how do they diagnose DIC
increase D-Dimer which measures the rate of fibrin clot breakdown
41
microvascular clinical mani of DIC
CNS- decreased LOC
Skin- Ischemia leading to gangrene
Kidney-oliguria, RF
lungs-SOB, PE
GI-acute ulcerations, necrosis
42
hemorrhage clinical mani of DIC
1. CNS- intracranial bleeding
2. skin-petechiae, echymosis
3. mems- gingival bleeding
4. kidney- hematuria
5. Gi- bleeding
43
mortality rate of DIC
high, depends on cause
44
disorder of coagulation
DIC
45
multiple myeloma
malignant disorder characterized by proliferation of abnormal plasma (b lymphocytes) in the bone marrow
46
incidence of multiple myeloma
peaks in the 6th decade of life
47
etiology of multiple myeloma
UNKNOWN
- genetics
- viruses
- bacteria
- chemicals
48
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
49
abnormal plasma cells produce
myeloma (M) protein
(test for this during diagnosis)
(is a large protein=renal failure)
50
clinical mani of multiple myeloma
1. frequent infections
2. anemia/bleeding
3. bone pain/fractures
4. renal insufficiency/failure
51
lymphoma
malignant disease of the lymphoid tissues (thymus, bone marrow, lymph nodes, spleen)
52
where is the majority of the disease located in lymphona
90% in the lymph nodes
53
etiology of lymphoma
UNKNOWN
- chromosome abnormality
- virus
- immunosuppression
54
incidence of lymphoma
- Hodgkin's peaks at 20-30
| - non-hodgkins at 50+
55
patho of lymphoma
normal lymph node or tissue lymph structure is destroyed by excessive (abnormal) proliferation of lymphocytes
56
onset of myeloma
insidious and slow
57
hodgkin's signs
reed-sternberg cells in lymph nodes
58
non-hodgkin's signs
- bone marrow involvement occurs more often than hodgkins
| - may different types of cells seen
59
clinical mani of lymphoma
- enlarged, painless, lymph nodes
| - night sweats, fever, weight loss
60
cure rate for hodgkins
complete remission if treated in early stages one and two
61
cure rate for non hodgkins
varies
| can be slowly developing or agressive and rapidly fatal
