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Flashcards in Anemia Deck (22):

What is Anemia

A deficiency in RBC or Hemoglobin


Etiology of Anemia ?

3 General Causes

• Defect erythropoiesis (Dec in Production)
• Inc hemolysis (Defective Breakdown or Removal)
• Inc loss (Hemorrhage)


Basic Pathology of Anemia

Abnormal cell number OR structure of cell OR Fx of cell =

→dec O2 carrying capacity→hypoxia
other complications


The Key MNFT?

Moderate Vs Chronic

• Hypoxia! (underlies all other mnfst)

• Moderate- Dyspnea, palpitations, chronic fatigue (dec O2→dec ATP→dec energy)

• Sever- Chronic exhaustion, inc palpitations (complex etiology), Pallor, profound weakness, dizziness, headache, sensitivity to cold (dec metb→less ATP made→less heat made/given off)


The central Complication of Anemia

Hypoxia = ?



Why are palpitations and Cardiac issues associated with Anemia?

Compensatory mechanisms related to Dec in 02. Tachycardia and sympathetic response. Ventricular hypertrophy and high output heart failure associated. Murmur may be associated with dec blood thickness.


7 Types of Anemia

Iron deficiency Anemia
Vitamin B12 & Folic Acid deficiency
Pernicious Anemia
Aplastic Anemia
Hemolytic Anemia
Hemorrhagic Anemia
Sickle Cell Anemia


Describe Iron Deficiency

What Test will not work?


o Inadequate intake or loss of iron-> impaired synthesis of Hb -> Impaired 02
o CBC not test of choice (Hb is normal, Fe is low)
o TX
• Underlying cause (intake?)
• Fe p.o for 4-6m


Describe Vitamin B12 & Folic Acid Deficiency

o Both involved in cell division
o Abnormal DNA synth and cell division -> impaired RBC, WBC and platelets

o TX
• P.O B12, Folic acid


Describe Pernicious Anemia

o Intrinsic factor produced in stomach, helps you absorb B12. Damaged gastric mucosa (stomach) -> no intrinsic factor (required for B12 absorption) -> poor or no vit b12 absorption

o RBC production impaired

o TX
• `High dose vit b12 p.o.
• Passive absorption is possible at high doses
• IM only if neuropathic symptoms present, P.O isn't working


Aplastic Anemia

o Primary Bone Marrow failures
(Dec production despite All req components present)

o All bloods cells affected
o 1/3 autoimmunity and 2/3 are idiopathic

o Tx
• Underlying cause
• Transfusions?
• Marrow transplant is severe cases


What is Hemolytic Anemia?

Possible Etiology?

o Excessive break down of RBC OR Premature breakdown of RBC

o Acquired (via autoimmunity, drgus)
o Genetic (eg in thalassemia defective synthesis off hemoglobin)

NOTE: Hemolytic also used as a broad term for describing anemias that retain components of Hb in the body (i.e not blood loss)


MNFTS of Hemolytic Anemia

• Jaundice (spleen/liver overwhelmed with RBC break down, bilirubin build up, deposited tissues in body)
• Splenomegaly (enlarged spleen d/t hemolysis workload)
• Hepatomegaly (liver enlargement)


Tx for Hemolytic Anemia

• Underlying cause?
• Tx symptoms of Hypoxia
• Transfusion
• Steroids (dampen hemolysis)
• Tx for Renal fx (precipitate in renal tubule d.t hemolysis)
• Splenectomy


Describe Hemorrhagic Anemia

Acute vs Chronic


o Acute
• Rapid loss of blood (RBC & Hb)
• Severity depends on site, rate and vol lost

o Chronic
• Gradual and ongoing bleeding
• ET-
 prolonged or heavy menstrual period menses
 bleeding paeptic ulcer
 CA lesions in Gastrointestinal tract
 Hemorrhoids

Tx- Treat underlying cause


What is Sickle-Cell Anemia


RBC's assume an abnormal, rigid, sickle-like shape

o Genetic
• Recessive homozygous trait
• If heterozygous- sickle cell trait (not a major issue)


What is different about Hb in Sickle cell Anemia?

• Hb gene Is mutated
• HB S instead of Hb A (adult)
 One amino acid difference
• Valine (Hb S) instead of glutamic acid (Hb A) in Beta chain
• Hb S l is able to load and offloads normally.

Hb S chrystalizes on dissociation at low PO2 and deforms RBC→ RBC sickles


The two consequences of sickling?

2 consequences:
- chronic hemolytic anemia
- hook in blood vessels and occlusion of vessels→ischemia→infarction


Where do cells often become sickled?

occurs in capillaries/tissues (after 02 dissociation)-> vessel occlusion (sickle shape) -> ischemia -> infarction


Vicious cycle of Sickle Cell Anemia

• Obstructed cappilaries -> hypoxia -> more sickling
• Inc in viscosity -> impairs circulations -> occlusion and further hypoxia -> more RBC sickle -> vicious cycle
... Hb S is 50 times less soluble then Hb A (this is why it sickles)


Extra MNFTS of Sickle cell anemia?

- hemolysis (liver will not be able to cope with excess breakdown)
- thrombosis + infarction (caused by sickle cell blocking vessels)
- inc bilirubin (causing jaundice)


Describe Tx for sickle cell anemia

very difficult because you can’t change genetics
- Can do supportive Tx, (rest, O2, analgesics (to treat ischemia/pain), IV fluids and electrolytes d/t kidney overload)
- Hypertransfusion (more than 50% donor blood), in inc risk (eg/ surgery or pregnancy)
- Hydroxyurea drug that enhances the production of fetal Hb (fetal Hb has a higher affinity for O2) →inhibits breakdown of sickle cells
- Antineoplastic drug (anti-CA) but it has major side effects (causes toxicity to liver and bone marrow, causes CA)
- Marrow transplant (new stem cells)