Anemia - CC3 Flashcards
1
Q
3 components to blood
A
- plasma -55%
2. WBC/plateles -
2
Q
3 steps to CBC review
A
- review Hb and MCV
- review WBC and DDx
- review platelet count
3
Q
what does a marrow problem look like
A
loss of all cell lines
4
Q
3 ways a single cell line can be low
A
- low prod
- destruction
- sequestration
5
Q
what is anemia
A
low RBC
- very common
- abnormalities often found before Sx
6
Q
what is too much RBC
A
polycythemia/erythrocytosis
- much less common
-
7
Q
sign and Sx of anemia
A
- faigue
- HA
- lightheaded
- nausea
- chest pain
- SOB
- tachycard.
- HF
- hypotension
8
Q
2 key part to approach to anemia
A
- cell size - MCV
2. retic count - underprod vs. destruction/sequestration
9
Q
how to ID retics
A
- inceased color
- larger
- increased central pallor
- have RNA
10
Q
DDx for microcytic
A
- Thallasemia
- Anemia of chronic disease
- Iron def
- Lead poisoning
- Sideroblastic
11
Q
how is iron moved in body
A
- absorbed in duod
- transported by transferritin
- stored by ferritin in heart and liver and in Hb
- no excretion mechanism
12
Q
how is Fe regulated
A
- taken up by ferrroportin
- ferroportin blocked by hepcidin
- ## hepcidin produced in liver
13
Q
3 measures of Fe in body
A
- ferritin - primary storage
- transferritin
- serum iron/transferritin - used to assess Fe overload
14
Q
what would be seen in Fe def. (5)
A
- low ferritin
- low MCV
also, but don;t need to measure
- low retic
- low serum Fe
- high transferritin (TIBC)
15
Q
what to do in Fe def.
A
- in male and non-mens. females, always look for blood loss
- diet, bleeds
- treat Fe def., even if not anemia in women of child bearing age
16
Q
2 types of Fe
A
- oral - may not be tolerated well
2. IV
17
Q
def. anemia of chronic disease
A
- can be micro or normo
- due to acute or chron. inflammation
- caused by cytokines increasing hepcidin
18
Q
5 things seen in anemia of chronic disesase
A
- high ferritin
- retics inapproriately low
- low serum Fe
- low TIBC
- low transferritin sat.
- low EPO
19
Q
2 treatments of anemia of chronic disease
A
- treat underlying cause
2. EPO
20
Q
what is thallasemia and 2 types
A
- abnormal prod. of Hb
- can be a or B
21
Q
2 types of macrocytic
A
- megalobalstic - cells cannot mature
2. non-megaloblastic
22
Q
4 causes of megaloblastic
A
- B12 def.
- folate def.
- cytotoxic drugs
- genetics
23
Q
what is B12
A
- cobalamin
- found in animal products
- absorbed via inrinsic factor
- needed for blood
24
Q
4 causes of B12 def.
A
- strict veganism
- unable to absorb - terminal ileum
- pernicious anemia - no intrisic factor
- Gi infection
25
4 nonmegaloblastic causes
1. myelodisplastic syndrome
2. retics bleeding or hemolysis
3. liver disease - target cells
4. hypothyroidism - uncommon
26
what do we need to check in normocytic
retics
27
2 causes of low retics
1. primary or secondary bone marrow failure
| 2. low EPO
28
what is term when RBC destroyed too soon
hemolysis
29
2 causes
1. extravascular - RBC don't make it full life and destroyed
| 2. intravascular - lose all the good stuff inside liek FE
30
4 things that happen with hemolysis
1. incr. retics
2. incr. bili
3. incr. LDH
4. dec. haptoglobin
31
2 tests for intra vs. extravascular hemolysis
1. DAT antiglobin tests
| 2. blood film spertocytes (EV) vs. schistocytes (IV)
32
3 intrinsic RBC factors causing hemolysis
1. hemoglobin - sickle cell
2. enzymes
3. cytoskeleton problem
33
5 external factors causing hemolysis
1. drug!
2. infection
3. ABs against RBC antigens
4. structural probs - mechanical valves ets
5. DIC
34
2 treatments of hemolyssi
1. underlying cause
| 2. suportive care
35
2 other causes of anemia
1. dilution
| 2. sequestration in spleen
36
when is transfusion reccomended
HB
37
what is Hct formula
Hb x 3
38
what does retic count indicate
2% excessive destruciton
39
signs of hemolysis
1. signs of anemia
2. signs of underlying disease
3. dark urine
4. jaundice
5. hepatoplenomeg, cholelith, lymphadenopathy
40
test findings in hemolysis
1. HB levels depend on degree
2. elevated retics
3. peripheral smear
- schistocytes - intravasc
- pherocytes or helmet - extravasc.
4. haptoglobin
- low - normally binds to Hb
5. high indirect bili
6. high LDH
7. direct coombs - +ve in autoimmune
41
Tx of hemolysis
1. Tx underlying cause
2. PRBCs
3. folate suppluments
42
patho of sickle cell
HbA replaced by mutant hemoglobin
| - under reduced O2 times, they sickle and obstruct
43
4 complications of SCC
1. severe, lifelong hemolytic anemia
2. occlusions Sx
3. infections
- functional asplenia
4. delayed growth and maturation
44
Sx of SCC oclusion
1. bone pain - most common
2. hand-foot syndrome - dactylitis
3. acute chest
- similar to PNA
4. repeated splenic infarcts
5. avasc. joint necrosis
- most common in hip
6. priapism
7. CVAs
8. optho infarcts
9. leg ulcers
45
Dx for SCC
1. anemia
| 2. sickle smear
46
Tx for sickle
1. avoid low O2
2. early vaccinations
3. prophylactic pen for kids
4. folic acid supplements
5. mgmt of crises
6. hydroxyurea
7. transfusions
8. marrow transplant
47
what is spherocytosis
hereditary
- defect in spherin gene
- loss of RBC membrane area without loss of volume
- get trapped and destroyed by spleen
48
Sx of spherocytosis
1. hemolytic anemia
2. jaundice
3. splenomegaly
4. gallstones
5
49
Tx
splenectomy
50
what is G6PD def.
X-linked - male
- get H2O2 that breaks down RBCs
- preciptated by certain ABx and fava beans
51
Sx of G6PD
- episodic anemia that is drug induced
| - dark urine and jaundice on Phx
52
what is seen on smear
1. bite cells
| 2. heinz bodies
53
what is autoimmune hemolytic anemia (AIHA)
- produce autoantibodies to RBCs
| - more fulminant in childs
54
2 types of AIHA
1. warm
- due to IgG which binds at 37
- extravascular hemolysis
2 cold
- due to IgM
- intravasuclar - in liver
55
Sx of AIHA
1. anemia
| 2. jaundice if sig
56
Dx of AIHA
1. direct coombs
- IgG or cpmplement
2. cold agglutinatin
57
Tx of AIHA
often none
1. warm
- steroids
2. cold
- avoid cold
- transfusions
