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Flashcards in Anemia Deck (22)
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1
Q

What is Anemia

A

A deficiency in RBC or Hemoglobin

2
Q

Etiology of Anemia ?

3 General Causes

A
  • Defect erythropoiesis (Dec in Production)
  • Inc hemolysis (Defective Breakdown or Removal)
  • Inc loss (Hemorrhage)
3
Q

Basic Pathology of Anemia

A

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

→dec O2 carrying capacity→hypoxia
other complications

4
Q

The Key MNFT?

Moderate Vs Chronic

A
  • 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)
5
Q

The central Complication of Anemia

Hypoxia = ?

A

ACIDOSIS!

6
Q

Why are palpitations and Cardiac issues associated with Anemia?

A

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
Q

7 Types of Anemia

A
Iron deficiency Anemia
Vitamin B12 & Folic Acid deficiency 
Pernicious Anemia
Aplastic Anemia
Hemolytic Anemia
Hemorrhagic Anemia
Sickle Cell Anemia
8
Q

Describe Iron Deficiency

What Test will not work?
Tx?

A

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

9
Q

Describe Vitamin B12 & Folic Acid Deficiency

A

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

10
Q

Describe Pernicious Anemia

A

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

11
Q

Aplastic Anemia

A

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

12
Q

What is Hemolytic Anemia?

Possible Etiology?

A

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)

13
Q

MNFTS of Hemolytic Anemia

A
  • 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)
14
Q

Tx for Hemolytic Anemia

A
  • Underlying cause?
  • Tx symptoms of Hypoxia
  • Transfusion
  • Steroids (dampen hemolysis)
  • Tx for Renal fx (precipitate in renal tubule d.t hemolysis)
  • Splenectomy
15
Q

Describe Hemorrhagic Anemia

Acute vs Chronic

Tx?

A

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

16
Q

What is Sickle-Cell Anemia

Etiology?

A

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

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

17
Q

What is different about Hb in Sickle cell Anemia?

A

• 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

18
Q

The two consequences of sickling?

A

2 consequences:

  • chronic hemolytic anemia
  • hook in blood vessels and occlusion of vessels→ischemia→infarction
19
Q

Where do cells often become sickled?

A

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

20
Q

Vicious cycle of Sickle Cell Anemia

A

• 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)

21
Q

Extra MNFTS of Sickle cell anemia?

A
  • hemolysis (liver will not be able to cope with excess breakdown)
  • thrombosis + infarction (caused by sickle cell blocking vessels)
  • inc bilirubin (causing jaundice)
22
Q

Describe Tx for sickle cell anemia

A

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)