Lecture 2 Flashcards
ANEMIA OF CHRONIC DISEASE
Normocytic normochromic
Anemia of chronic disease is seen
Collagen disease
Chronic kidney disease
Chronic liver disease
Chron’s
Ulcerative colitis
Systemic lupus
Malignancy(leukemia and lymphoma) by infiltration of bone marrow
Pathophysiology of anemia of Chronic inflammation
Inflammation>cytokinesrelease>hepcidin increase>decrease erythropoeitin>decreases usage of iron>decrease life span of RbCs
HEMOLYTIC ANEMIA
RBCS get broken down before 120 days
It could be due to acquired or congenital disease
It could be extravascular or intravascular
SEVERE HEMOLYTIC ANEMIA
Rbcs live for 20 days
Mild hemolytic anemia
40 days
HEMOLYTIC ANEMIA gets classified according to
LIFE SPAN (MILD,MODERATE,SEVERE)
RBCs when broken down intravascularly release
Hemoglobin that either binds to haptoglobin then release haemoglobinemia
Or binds to hempoxin in kidney and gets filterated there to give hemoglobinemia
Output in hemolysis
Hemoglobin ±uria
+ emia
+haptoglobin decreases
+ hemosideuria (when hemoglobin goes to cell it gives hemosiderin deposit)
HOW TO know HEMOLYTIC ANEMIA ?
Reticulocytosis are high (more than 2%)
INDIRECT/UNCONJUGATED BILIRUBIN IS HIGH
HEMOGLOBINEMIA
HEMOGLOBINURIA
HEMOSIDEROSIS
HDH increases
NORMOCHROMIC NORMOCYTIC (except thalassemia)
HAPTOGLOBIN OR HEMOPEXIN IS LOW
2 types of hemolysis
Intravascular
Or extravascular
(Macrophage takes Rbcs out and accumulates it in liver,spleen, and gall stones so they become enlarged and there will be repeated gall stone)
HEMOLYTIC crisis
Patient with sickle cell anemia travelled and got exposed to hypoxia (abdominal pain,nausea,Vomiting,haematuria,bone pain)
Or patient with favism G6PD deficiency who took drug that got him to crisis
Patient with folic acid and b12 deficiency got into megaloblastic crisis
Or immunocompromised so gets viral infection=APLASTIC crisis
Sickle anemia causes obstruction
To diagnose hemolytic anemia
1) Normochromic normocytic(Except thalasemia)
2) Reticulocytosis more than 2%
3)white blood cells/platelets may increase
4)BONE marrow erythrocyte is high (normoblastic except incase of vitb12 deficiency or megaloblastic anemia)
5)Bilirubin is indirect
6)Haptoglobin decreases and hemopexin decreases
7)LDH increases
8)Blood film(Spherocytosis or thalassemia or sicklecellanemia or unspecific paroxysmal nocturnal hemoglobinuria or autoimmune hemolytic anemia)
Intracorpscular causes of hemolytic anemia
1) inherited (Paroxysmal nocturnal hemoglobinuria)
2)Defect in membrane (spherocytosis/nocturnal hemoglobinuria)
3)defect in globin(thalassemia or sickle cell anemia)
4)defect in enzymes G6PD
Extrinsic
Acquired or
autoimmune or
mechanical :(soilder who stands for 12 hours)
:people who have artifical valves
Or infections like malaria
Or chemicals (organophosphorus/snake or Scorpio bite)
HEREDITARY SPHEROCYTOSIS
*due to loss of spectrin no na/k Atp pump so salt water get retained in rbc so it doesn’t live
*it is familial
*anemia symptoms
*Repeated gallstones
*test osmotic fragility test
*early hemolysis
*treated by splenectomy
Major thalassemia
Severe anemia
Hemoglobin F or A2 (delta)
Depends on blood transfusion for survival
Minor thalasemia
Mild anemia
Hemoglobin 7 or 8 or 9
Spleenomegaly
Hemoglobin F or A2
Doesn’t always need blood transfusion
Intermediate thalassemia
Moderate anemia
Needs blood transfusion in certain situations such as surgery or stress or pregnancy
2 sheets of alpha affected
Hyochromic anemia
3 sheets affected
HEMOGLOBIN H
Spleenomegaly and blood transfusion in stressful situations
4 sheets affected
Parrot hemoglobin=death
Thalassemia complain
Jaundice even after 6 months from birth
THALASSEMIA hemoglobin
F