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Hematosis - 2024 > Week 3 Anemia of Chronic Inflammation > Flashcards

Week 3 Anemia of Chronic Inflammation Flashcards

1
Q

What are the anemias of INSUFFICEINT vs INEFFECTIVE erythropoiesis

A

INSUFFICEINT
-IDA : diminished heme synthesis
-Anemia of Chronic Inflammation : Iron sequestering

INEFFECTIVE
-Sideroblastic anemia and Lead poisoning - defective protoporphyrin synthesis
-Thalassemia - Defective globin chain synthesis

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2
Q

what are examples of micro cytice anemia

A

IDA- most common cause of microcytic anemia
Anemia of chronic inflammation
Sideroblastic anemia and lead Poisoning
Thalassemia

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3
Q

what is anemia of chronic inflammation

A

-chronic inflammation common in hospital pts
-associated with chronic infections like TB, HIV, RA, Renal disease, Hodgkins

Other names
Iron reutilization anemia
Anemia of chronic infection
Anemia of chronic disease

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4
Q

What are the symptoms of ACI and what would you see in a smear

A

-patients with system diseases
-normo/normo or micro//hypo
-when you have decreased serum iron levels but with many iron stores

Symptoms
Weakness, pallor, shortness of breath

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5
Q

What causes ACI

A

increased inflammation activates macrophages that secrete cytokines which produce Acute Phase Reactants that have a negative impact on iron levels, RBC production and life

APRs- Hepcidin, Lactoferrin, Ferritin

They cause impaired ferrokinetics causing iron restricted erythropoiesis which lessens RBC life span

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6
Q

What is hepcidin

A

-helps to maintain the bodys’ iron status
-systemic iron regulatory hormone
-produced by the liver
-binds to ferroportin
-regulates intestinal iron absorption
-regulates plasma iron concentrations
-regulates tissue iron distribution

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7
Q

how does Hepcidin act when body iron levels increase

A

heptaocytes increase hepcidin production
enterocytes release LESS iron into plasma
macrophages and heptocytes retain more iron

hepcidin levels increase during inflammation regardless of body iron levels
a non specific defense against bacterial infection to ensure iron is not made available to bacteria

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8
Q

how does Hepcidin act when body iron levels decrease

A

-hepatocytes produce less hepcidin
-enterocytes release more iron into plasma
-macrophages and hepatocytes release more iron into plasma

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9
Q

when there is inflammation in the body what will we see with hepcidin levels

A

-hepcidin synthesis increased with IL acting on the liver
-iron absorption from intestine is decreased
-iron release from macrophages and hepatocytes also decrease
-now iron is not available for developing RBCs

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10
Q

what is lactoferrin

A

-part of transferrin family an iron binding glycoprotein
-found in 2ndry neut granules
-prevent bacteria from using phagocytized iron
-protects from oxidized iron during phagocytosis
-contributes to ACI but less than hepcidin acting as an APR

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11
Q

how does lactoferrin act as an APR

A

-released in plasma during inflammation as neuts die
-scavenges iron and binds it -oxidized iron is bad
-higher affinity for Iron than Transferrin
-increased hepcidin means iron cant be taken up by macrophages or hepatocytes because ferropotin is blocking it
-RBC progenitors dont have receptors for lactoferrin
-iron cannot be incorporated into developing RBC

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12
Q

What action does increased Ferritin have in inflammation

A

another APR
-primary non specific response to inflammation

-in high ferritin levels it binds functional iron
-developing RBCs dont have a ferritin receptor like lactoferrin
-iron cannot be brought into the hemoglobin
-reduced tissue release

also sequesters iron by making it unavailable to developing RBCs

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13
Q

How does impaired erythropoiesis contribute for anemia

A

-macrophages produce inflammatory cytokines that act on BM and kidney to
-impair proliferation of erythroid progenitor cells
-decrease EPO production
-reduce erythroid progenitor response to EPO
-reduce RBC lifespan with increased production of macrophages due to increased inflammation

EPO binds RBC precursors allows early release of RBC from bone marrow , prevents apoptosis, reduced BM transit time

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14
Q

what are the expected CBC results of ACI

A

HGB - normal or SD
HCT - normal or SD
MCV - Normal due to duel pop with micro (2 peaks on histo)
Ret- decreased (because erythropoiesis decreases)

starts as normo/normo but can turn into micro/hypo over time on PBF

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15
Q

What would be the results of iron studies with ACI

A

Serum iron - N or D
TIBC - N or D - reflects iron store in hepatocytes
FER - N or I
% SAT - N or D

what does it mean
if you have decrease iron with lots of iron stores - Functional Iron Def
in BM biopsy BM macrophages are stained positive for PPB and RBC precursors are more pale

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16
Q

how is ACI treated

A

EPO therapeutic administration

17
Q

comparison between IDA and ACI
why is HCT and HGB decreased in IDA but normal in ACI

A

IDA has stores that are becoming depleted and functional iron is reducing. This leaves no iron to be incorporated into heme that is why for IDA we see decreases in HCT, RBC

Whereas in ACI the stores in the macrophages are abundant but will decrease over time but you wont see the same decreases

18
Q

what is sideroblastic anemia and its symptoms

A

-when the enzyme that synthesizes or incorporates iron into protoporphyrin ring is impaired

Acquired
- primary SA refractory
-secondary caused by drugs and bone marrow toxins , metal poisoning, chloramphenicol or chemo

Inherited
-porphyria’s - X linked
Autosomal recessive

symptoms
fatigue, SOB, hepatomegaly, splenomegaly

19
Q

if incorporation of iron into protoporphyrin ring is blocked what happens

A
  • iron builds up in the BM
    -specifically in the mitochondria of developing erythroblasts- waiting to be taken into as heme
    -therefore when you do a BM biopsy and stain with PPB you see Ringed sideroblasts (hemosiderin deposits) which is a hallmark of sideroblastic anemia
20
Q

how does IDA result from VS SA

A

IDA comes from inadequate supplies of iron for hem production or lack of raw materials to product hem, RBC precursors are not defective

SA come from inadequate amounts of protoporphyrin , RBC precursors are defective but there is enough iron

unlike IDA iron is abundant in BM in SA.

21
Q

what would we see in SA with a CBC, PBF and BM

A

HGB - low
HCT- lot
MCV - N or D
Morph - dual pop with PPHB

BM biopsy
ringed sideroblast present
positive staining with PPB erythroblasts have mitochondria that is loaded with iron

22
Q

what would iron studies in SA show

A

Serum iron - N or I- abundant iron stores occur
TIBC - N or D - all spots on transferrin are occupied by iron
FER - N or I
% SAT - N or I

23
Q

How does lead poisoning cause SA
acute vs chronic

A

Heavy metal poisoning is most common cause of SA
- lead interferes with porphyrin synthesis (enzyme impairment and iron incorporation)
-affects nervous system
-anemia especially in kids

Acute exposure
normo/normo but increased RET and poly because of RBC hemolysis

Chronic exposure
Micro/hypo
-decreased RET
-Basophilic stippling
-stomatocytes

the iron studies will show abundant iron storage but the iron is not available to developing erythroblasts

24
Q

how to treat SA if inheritied vs acquired

A

Inherited
pyridoxine B6 - first step in porphyrin synthesis

Acquired
Calcium Disodium edetate or dimercaprol are used because they chelate the lead in the body so it can be excreted in the urine

25
Q

What is iron overload Primary and Secondary

A

Access Iron accumulation

Primary
inherited conditions causing too much iron to be absorbed and stored - Hereditary Hemochromatosis (where there are genes for proteins controlling iron kinetics)

Secondary
-when iron accumulates because of chronic anemias like Sickle or Thalassemia Major and the treatment of repeat transfusions

either way acquisition is greater than loss because the body conserves as much as possible

26
Q

how is excess iron stored

A

Ferritin and then hemosiderin within cells

-when the stores becomes saturated ferrous iron or free iron builds up intracellularly and forms free radicals. this causes damage to neighboring cells , pancrease, heart and skin can cause mutations

27
Q

what will iron studies show you in iron over load

A

Serum iron - variable
TIBC - N
FER - I - increased because because there is no way to excrete the increasing iron
% SAT - I

Hematosis - 2024 (11 decks)

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