Anemia

Question 1

What is Anemia

Answer 1

A deficiency in RBC or Hemoglobin

Question 2

Etiology of Anemia ?

3 General Causes

Answer 2

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

Question 3

Basic Pathology of Anemia

Answer 3

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

→dec O2 carrying capacity→hypoxia
other complications

Question 4

The Key MNFT?

Moderate Vs Chronic

Answer 4

• 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)

Question 5

The central Complication of Anemia

Hypoxia = ?

Answer 5

ACIDOSIS!

Question 6

Why are palpitations and Cardiac issues associated with Anemia?

Answer 6

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.

Question 7

7 Types of Anemia

Answer 7

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

Question 8

Describe Iron Deficiency

What Test will not work?
Tx?

Answer 8

MOST COMMON

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

Question 9

Describe Vitamin B12 & Folic Acid Deficiency

Answer 9

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

Question 10

Describe Pernicious Anemia

Answer 10

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

Question 11

Aplastic Anemia

Answer 11

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

Question 12

What is Hemolytic Anemia?

Possible Etiology?

Answer 12

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)

Question 13

MNFTS of Hemolytic Anemia

Answer 13

• 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)

Question 14

Tx for Hemolytic Anemia

Answer 14

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

Question 15

Describe Hemorrhagic Anemia

Acute vs Chronic

Tx?

Answer 15

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

Question 16

What is Sickle-Cell Anemia

Etiology?

Answer 16

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

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

Question 17

What is different about Hb in Sickle cell Anemia?

Answer 17

• 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

Question 18

The two consequences of sickling?

Answer 18

2 consequences:

• chronic hemolytic anemia
• hook in blood vessels and occlusion of vessels→ischemia→infarction

Question 19

Where do cells often become sickled?

Answer 19

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

Question 20

Vicious cycle of Sickle Cell Anemia

Answer 20

• 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)

Question 21

Extra MNFTS of Sickle cell anemia?

Answer 21

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

Question 22

Describe Tx for sickle cell anemia

Answer 22

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)