Anemias Flashcards
Describe IDA (Iron deficiency Anemia)
common?
types of rbcs?
most common world wide 2% of men 5% of women
microcytic/hypochromic rbcs (due to decrease hgb/iron)
Describe causes of IDA
Increased demand (childhood/preg)
Excess loss (Menstruation/chronic bleeding)
Decreased absorption (gastrectomy/malabsorption)
Iron poor diet (milk babies/elderly)
Describe stage 1 of IDA
BM
Serum iron
Pt response
hgb/rdw
Ferritin levels
iron depletion
iron in bm decreased to absent
NO DECREASE IN SERUM IRON
pt is asymptomatic/hgb norm/RDW slightly increased
ferritin decreased
Describe stage 2 of IDA
Hgb
Hct
Serum Iron
ZPP/FEP
iron deficiency EPO
hgb decreases
hgb content of rbcs (CHr) decreased
hct normal
serum iron decreased
FEP/ZPP increased
Describe stage 3 of IDA
classic iron deficiency
serum iron/ferritin/% sat/BM Iron/MCHC/hepcidin decreased
STFR TIBC FEP/ZPP increased
Describe ACI (anemia of chronic inflammation)
what can cause it?
chronic disease, secondary to other disease/inflamm/supressive effect
ex. chronic infect
AI
infectious mono
malignancies
TRAPPED IN MACROPHAGES
What are some proposed mechanisms of ACI ?
overactivates what
Inability of rbc to access iron trapped w/in macrophages (Mediated by HEPCIDIN)
Ineffective EPO
Hemolysis overactivates RES
Briefly describe the mechanism of ACI
invasion of malignancy induces cytokines
stimulation of hepcidin/inactivates ferroportin
iron stuck in macrophages
increase DMT1 damage to rbc membrane
inhibit of EPO/no precursors
How do you distinguish between IDA and ACI?
looks similar to distinguish via TIBC and ferritin levels
Lab findings of ACI
Serum iron
ferritin
BM
TIBC
Hepcidin
%sat
serum iron DECREASED TRAPPED IN MACROS
ferritin increase
BM stores increased
TIBC decreased
HEPCIDIN INCREASED
%sat decreased
Important lab findings of ACI
Increased Hepcidin
Serum Iron Low
BM stores high
IDA Review: causes
increased demand
increased loss
decreased absorption
iron poor diet
MICRO/HYPO
ACI review:
causes
inactivates
mediated by
2nd to disease to inflammation
decreased epo
increased hemolysis
MEDIATED BY HEPCIDIN
Inactivates ferroportin
Describe Sideroblastic anemia
defect in what
Hereditary disorders (2)
defect in heme synthesis/inadequate iron utilization
Hereditary defect (rare)
1.) x linked (ALAS2)
2.) recessive Stem cell dysfunction (decreased heme/pancytopenia)
Describe the Aquired defect diseases in Sideroblastic anemia
(2)
Primary - myelodysplastic syndromes
Secondary (exposures) toxins/ LEAD poisoning etc
Briefly describe lead poisoning and the pathways it interferes with
interferes with 3 paths
5-ALA - prophobiligen
Copro III - Protop III
LEAD INHIBITS FERROCHELATASE
Describe the Lab results of Sideroblastic Anemia
HGB/HCT
RBC population
RBC inclusions
low hgb/hct
RBC: dimorphic/micro/hypo
baso stippling
PAPPENHEIMERS
target cells
What does the BM look like in Sideroblastic anemia
erythroid hyperplasia (ineffective EPO) (mainly rbcs)
RINGED SIDEROBLASTS (nrbcs)
Sideroblastic anemia
Serum Iron
TIBC
Serum ferritin
STfRs
FEP/ZPP
Hepcidin
Serum iron increased (overload)
TIBC norm/low
Serum ferritin Increased
STfRs norm/low
FEP/ZPP high
Hepcidin High
Lab results of lead poisoning
COGNATIVE IMPAIRMENT
course baso stippling
increased lead
increased urin ALA/Corpop
accum of iron/rbc proto
Describe Porphyrias
what type of diseases
signs/sympt
rare diseases (hereditary) that results in errors in heme biosynth
each disorder has specific enzyme defect in porphyrin in tissues
signs/symp vary and may result in anemia
T/F: Porphuria is the spill over in urine/deposit in tissues
true
Describe Hemochromatosis
what type of disorder(Hint I)
inappropriate
doesnt cause what
disorder in iron storage
inappropriate increase in iron absorb resulting in excess iron depletion
damages organs
doesnt cause anemia
Describe Hereditary Hemochromatosis (HH)
What ancestory
excess what
what defect
colored skin?
amount of iron
what type is most common
mutation to what
northern europe ancestory
excess iron absorption due to HEPCIDIN DEFECT
Bronze skin
2-3x iron than normal
type 1 most common
MUTATION TO HFE ALL AFFECT HEPCIDIN
Describe 2nd Hemochromatosis
(hint:aquired..)
aquired to inhereited anemia/treatment
repeated transfusions
increased Iron storage
(no mech for iron secretion)
Lab findings of Hereditary Hemochromatosis
EPO
Heme
liver enzymes
Iron studies
EPO normal
Heme no abnormalities
Increased liver enzymes
All iron studies increased (EXCEPT TIBC)
Describe Megaloblastic anemias
what do rbcs look like
Vitamin B12 def, Pernicious anemia, Folate deficiency
RBC: macro ovalocytes
hypersegmented
T/F: folate deficiencies involve drugs that interfere with DNA synth or inibit folate
true (megaloblastoid)
Describe Vitamin B 12 deficiency
functions and participates in folate metabolism
required for degradation of fatty acids
NEUROLOGICAL DAMAGE
What is intrinsic factor
secreted by the stomach, needed in order to absorb B12
What is Transcobalamin 1
picks up B12 and carries to cells
Describe Vit B12 def in terms of diet, disease of what
failure of what organ
diet of animal proteins
increased requirements
Disease of terminal ileum (chrons_
Gastric failure
Competing organisms:
Bacteria
diphylo. latum
Describe Pernicious anemia
Anti-IF anti- Pariteal AB
Describe Folate
diet/diseases(hint c)
required for DNA synth
Vit B12 required to convert folate to functional state
def due to diet
malabsorption syndrom
(celiac/tropical)
rbc Morphology in megaloblastic anemias (all 3 cell lines)
megaloblastic/asynch
Macro/Ovalo
Tear drops
baso stippling
HJ bodies
Inc MCV/RDW
What does the BM look like in megaloblastic anemia?
WBC?
PLT?
BM: erythrohyperplasia increased bilirubin
WBC: decreased/hypersegmented
PLTS: abnormal
What are some other presentations of megaloblastic anemia?
Stomatitis (Inflam of mouth)
B12/Folate levels
rbc folate levels (better than serum)
Anti-IF/Anti-Paretial (early MMA/homocystine)
Treatment of B12
Folic Acid
Pernicious anemia
Treat w folic acid, improves anemia but not neruologic problems
IM
Folic acid oral
Pernicious B12 Im
Describe Aplastic Anemia
What does the BM look like?
Cells?
damage to what cell line
failed production of Rbcs/plt/wbc due to hematopoetic Stem cell damage
BM hypocellular
Relative lymphocytosis
T/F: Aplastic anemia is idopathic or aquired: in aquired it can be caused by benzene, epstein barr virus or radiation
true
Describe the hereditary aplastic anemias (2)
leukemia/sc
fanconis - Sc chromosomes
high incidence of leukemia AML
most die in 20s
Congenital Pure red cell aplasia (diamond-black fan)
defective stem cell unable to commit to rbc precursors
may have spontaneous remission
physically norm/wbc/plt norm
Describe congenital dyserythropoetic anemia
change in what
what type of cells
types?
increased what?
key factors?
change in eryth cell nuclear membrane/chromatin
Macrocytes
3 types
RBC destroyed in BM
increased Bilirubin/ineffec EPO
Mulinuclear/nuclear bridges
Oval/macro
Describe Anemia w marrow infiltration
damage to what casues what kind of hematopoesis
BM infiltration
abn cells/tumors
crowd out normal cells
damage to stem cell
EXTRAMED HEMATOPOESIS
poik/tear drop/schisto
megakaryotes
Describe anemia of chronic renal disease
what kind of proliferation
iron?
EPO def
Hemolysis
blood loss/PLT dysfunction
Chronic inflam/Limited iron
Dialysis
HIGH SERUM CREATININE/BUN
burrs/acanthos/uremia
HYPOPROLIFERATION
Describe anemia of liver disease
no megaloblastoid changes
increased what?
what happens to spleen
hemolysis, acanthocytes
blood loss - dec coag factors
Hyperspleenism/PLT sequestered chronic bleedimg
ROUND MACROCYTES
HYPOPROLIFERATION
increase cholesterol/lipids
Describe endocrine disorder anemia
EPO not only hormone that participates
Pituitary - androgen production - hgb
Thyroid - hypothyroid disease demand for O2
Describe Anemia of Viral infections
measels has increased iron in macrophages
Parvovirus /HIV aplastic
What are the micro/Hypo anemias?
IDA, MBA, ACI
