Anemias Flashcards

1
Q

Describe IDA (Iron deficiency Anemia)
common?
types of rbcs?

A

most common world wide 2% of men 5% of women
microcytic/hypochromic rbcs (due to decrease hgb/iron)

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1
Q

Describe causes of IDA

A

Increased demand (childhood/preg)
Excess loss (Menstruation/chronic bleeding)
Decreased absorption (gastrectomy/malabsorption)
Iron poor diet (milk babies/elderly)

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2
Q

Describe stage 1 of IDA
BM
Serum iron
Pt response
hgb/rdw
Ferritin levels

A

iron depletion
iron in bm decreased to absent
NO DECREASE IN SERUM IRON
pt is asymptomatic/hgb norm/RDW slightly increased
ferritin decreased

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3
Q

Describe stage 2 of IDA
Hgb
Hct
Serum Iron
ZPP/FEP

A

iron deficiency EPO
hgb decreases
hgb content of rbcs (CHr) decreased
hct normal
serum iron decreased
FEP/ZPP increased

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4
Q

Describe stage 3 of IDA

A

classic iron deficiency
serum iron/ferritin/% sat/BM Iron/MCHC/hepcidin decreased

STFR TIBC FEP/ZPP increased

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5
Q

Describe ACI (anemia of chronic inflammation)
what can cause it?

A

chronic disease, secondary to other disease/inflamm/supressive effect
ex. chronic infect
AI
infectious mono
malignancies
TRAPPED IN MACROPHAGES

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6
Q

What are some proposed mechanisms of ACI ?
overactivates what

A

Inability of rbc to access iron trapped w/in macrophages (Mediated by HEPCIDIN)
Ineffective EPO
Hemolysis overactivates RES

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7
Q

Briefly describe the mechanism of ACI

A

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

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8
Q

How do you distinguish between IDA and ACI?

A

looks similar to distinguish via TIBC and ferritin levels

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9
Q

Lab findings of ACI
Serum iron
ferritin
BM
TIBC
Hepcidin
%sat

A

serum iron DECREASED TRAPPED IN MACROS
ferritin increase
BM stores increased
TIBC decreased
HEPCIDIN INCREASED
%sat decreased

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10
Q

Important lab findings of ACI

A

Increased Hepcidin
Serum Iron Low
BM stores high

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11
Q

IDA Review: causes

A

increased demand
increased loss
decreased absorption
iron poor diet

MICRO/HYPO

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12
Q

ACI review:
causes
inactivates
mediated by

A

2nd to disease to inflammation
decreased epo
increased hemolysis
MEDIATED BY HEPCIDIN
Inactivates ferroportin

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13
Q

Describe Sideroblastic anemia
defect in what
Hereditary disorders (2)

A

defect in heme synthesis/inadequate iron utilization
Hereditary defect (rare)
1.) x linked (ALAS2)
2.) recessive Stem cell dysfunction (decreased heme/pancytopenia)

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14
Q

Describe the Aquired defect diseases in Sideroblastic anemia
(2)

A

Primary - myelodysplastic syndromes
Secondary (exposures) toxins/ LEAD poisoning etc

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15
Q

Briefly describe lead poisoning and the pathways it interferes with

A

interferes with 3 paths
5-ALA - prophobiligen
Copro III - Protop III
LEAD INHIBITS FERROCHELATASE

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16
Q

Describe the Lab results of Sideroblastic Anemia
HGB/HCT
RBC population
RBC inclusions

A

low hgb/hct
RBC: dimorphic/micro/hypo
baso stippling
PAPPENHEIMERS
target cells

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17
Q

What does the BM look like in Sideroblastic anemia

A

erythroid hyperplasia (ineffective EPO) (mainly rbcs)
RINGED SIDEROBLASTS (nrbcs)

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18
Q

Sideroblastic anemia
Serum Iron
TIBC
Serum ferritin
STfRs
FEP/ZPP
Hepcidin

A

Serum iron increased (overload)
TIBC norm/low
Serum ferritin Increased
STfRs norm/low
FEP/ZPP high
Hepcidin High

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19
Q

Lab results of lead poisoning

A

COGNATIVE IMPAIRMENT
course baso stippling
increased lead
increased urin ALA/Corpop
accum of iron/rbc proto

20
Q

Describe Porphyrias
what type of diseases
signs/sympt

A

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

21
Q

T/F: Porphuria is the spill over in urine/deposit in tissues

A

true

22
Q

Describe Hemochromatosis
what type of disorder(Hint I)
inappropriate
doesnt cause what

A

disorder in iron storage
inappropriate increase in iron absorb resulting in excess iron depletion
damages organs
doesnt cause anemia

23
Q

Describe Hereditary Hemochromatosis (HH)
What ancestory
excess what
what defect
colored skin?
amount of iron
what type is most common
mutation to what

A

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

24
Q

Describe 2nd Hemochromatosis
(hint:aquired..)

A

aquired to inhereited anemia/treatment
repeated transfusions
increased Iron storage
(no mech for iron secretion)

25
Q

Lab findings of Hereditary Hemochromatosis
EPO
Heme
liver enzymes
Iron studies

A

EPO normal
Heme no abnormalities
Increased liver enzymes
All iron studies increased (EXCEPT TIBC)

26
Q

Describe Megaloblastic anemias
what do rbcs look like

A

Vitamin B12 def, Pernicious anemia, Folate deficiency
RBC: macro ovalocytes
hypersegmented

27
Q

T/F: folate deficiencies involve drugs that interfere with DNA synth or inibit folate

A

true (megaloblastoid)

28
Q

Describe Vitamin B 12 deficiency

A

functions and participates in folate metabolism
required for degradation of fatty acids
NEUROLOGICAL DAMAGE

29
Q

What is intrinsic factor

A

secreted by the stomach, needed in order to absorb B12

30
Q

What is Transcobalamin 1

A

picks up B12 and carries to cells

31
Q

Describe Vit B12 def in terms of diet, disease of what
failure of what organ

A

diet of animal proteins
increased requirements
Disease of terminal ileum (chrons_
Gastric failure
Competing organisms:
Bacteria
diphylo. latum

32
Q

Describe Pernicious anemia

A

Anti-IF anti- Pariteal AB

33
Q

Describe Folate
diet/diseases(hint c)

A

required for DNA synth
Vit B12 required to convert folate to functional state
def due to diet
malabsorption syndrom
(celiac/tropical)

34
Q

rbc Morphology in megaloblastic anemias (all 3 cell lines)

A

megaloblastic/asynch
Macro/Ovalo
Tear drops
baso stippling
HJ bodies
Inc MCV/RDW

35
Q

What does the BM look like in megaloblastic anemia?
WBC?
PLT?

A

BM: erythrohyperplasia increased bilirubin
WBC: decreased/hypersegmented
PLTS: abnormal

36
Q

What are some other presentations of megaloblastic anemia?

A

Stomatitis (Inflam of mouth)
B12/Folate levels
rbc folate levels (better than serum)
Anti-IF/Anti-Paretial (early MMA/homocystine)

37
Q

Treatment of B12

Folic Acid

Pernicious anemia

A

Treat w folic acid, improves anemia but not neruologic problems
IM

Folic acid oral

Pernicious B12 Im

38
Q

Describe Aplastic Anemia

What does the BM look like?

Cells?
damage to what cell line

A

failed production of Rbcs/plt/wbc due to hematopoetic Stem cell damage

BM hypocellular

Relative lymphocytosis

39
Q

T/F: Aplastic anemia is idopathic or aquired: in aquired it can be caused by benzene, epstein barr virus or radiation

A

true

40
Q

Describe the hereditary aplastic anemias (2)
leukemia/sc

A

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

41
Q

Describe congenital dyserythropoetic anemia
change in what
what type of cells
types?
increased what?
key factors?

A

change in eryth cell nuclear membrane/chromatin
Macrocytes
3 types
RBC destroyed in BM
increased Bilirubin/ineffec EPO
Mulinuclear/nuclear bridges
Oval/macro

42
Q

Describe Anemia w marrow infiltration
damage to what casues what kind of hematopoesis

A

BM infiltration
abn cells/tumors
crowd out normal cells
damage to stem cell
EXTRAMED HEMATOPOESIS
poik/tear drop/schisto
megakaryotes

43
Q

Describe anemia of chronic renal disease
what kind of proliferation
iron?

A

EPO def
Hemolysis
blood loss/PLT dysfunction
Chronic inflam/Limited iron
Dialysis
HIGH SERUM CREATININE/BUN
burrs/acanthos/uremia
HYPOPROLIFERATION

44
Q

Describe anemia of liver disease
no megaloblastoid changes
increased what?
what happens to spleen

A

hemolysis, acanthocytes
blood loss - dec coag factors
Hyperspleenism/PLT sequestered chronic bleedimg
ROUND MACROCYTES
HYPOPROLIFERATION
increase cholesterol/lipids

45
Q

Describe endocrine disorder anemia

A

EPO not only hormone that participates
Pituitary - androgen production - hgb
Thyroid - hypothyroid disease demand for O2

46
Q

Describe Anemia of Viral infections

A

measels has increased iron in macrophages
Parvovirus /HIV aplastic

47
Q

What are the micro/Hypo anemias?

A

IDA, MBA, ACI