RBC Disorders Flashcards

(35 cards)

1
Q

What is hemoglobin

A

Conjugated protein that serve as vehicle for transportation of o2 and co2

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2
Q

Packed red cell volume
Raised blood cells of RBC to the total blood called

A

Hematocrit

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3
Q

Anemia characteristics and features

A

Reduce in total circulating RBC
May be MCV IS micro, normo, macrocytic
MCHc is hypo or normochromic

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4
Q

Microcytic anemia disease

A

T-Thalaseemia
A-Anemia of chronic disease
I- Iron deficiency
L-Lesd poisoning

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5
Q

Macrocytic disease

A

Megaloblastic and non megaloblastic
Defective in DNA synthesis, they are
Folate deficiency
Vit B12 deficiency
Orotic aciduria
Fanconi anemia

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6
Q

Hemolytic anemia common features

A

Shortened life span
Elevated erythropoietin
Reticulocytosis
Accumulation of hemoglobin degraded products like jaundice, gallstones and hemosiderosis

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7
Q

Hereditary sperocytosis

A

It’s a dominant disorder.
Defect in cell membranes skeleton like spectrin, ankyrin, band 4.2,and band 3

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8
Q

Features of hereditary sperocytosis

A

Normocytic
Hyperchromic
Intrinsic damage and extravascular hemolysis in spleen
Anisocytosis
Spherocytes
Howen jolly bodies

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9
Q

Glucose 6 phosphate dehydrogenase deficiency

A

X linked recessive

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10
Q

Causes of hemolysis in G6PD

A

Intrinsic and episodic hemolysis
Both intra and extravascular hemolysis
In intra heinz bodies cause membrane damage
Extravascular has heinz bodies are bittenoff by spleen

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11
Q

Main features seen in G6PD deficiency

A

Heinz bodies
Bite cells or degmacytes
Protective against p. Falciparum

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12
Q

Sickle cell disease

A

Autosomal recessive
Point mutation on 6th codon of beta globin chain glutamine to valine
Extramedullary hematopoisis is seen

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13
Q

Sickle cell disease features

A

Sickle cells called drepanicytes
Target cells called codocytes
Howen jolly bodies
None marrow expansion
Anisocytosis and poikilocytosis
Vasoocculisive crisis

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14
Q

Alpha -Thalaseemia results in mutation in which chromosome

A

Ch 16 of 4 genes

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15
Q

Beta thalaseemia mutation in

A

Ch 11 of 2 genes

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16
Q

Thalaseemia main featurrs

A

Extravascular hemolysis
Anisocytosis
Microcytic, hypochromic
Poikilocytosis
Target cells
Beta thalaseemia major called as cooley anemia which has crewcut appearance on x ray

17
Q

Paraxysomal nocturnal hemoglobinuria identification

A

It’s immunohemolytic anemia
It’s identifird by negative expression of CD 55 and 59
Mutation in phosphotidylinositol glycan complementation group A gene

18
Q

PNH which type of hemolysis

A

Both intra and extravascular by complement fixation and spleen sequestration

19
Q

Large bizzare multinuckeated marcroohages seen in

A

Megaloblastic anemia

20
Q

Features of megaloblastic anemia

A

Macrocytic, normochromic
Anisocytosis, poikilocytosis
Low reticulocyte count
Hypersegmented neutrophils

21
Q

Pencil cells and plummer vinson syndrome triad is seen in

A

Iron deficiency anemia

22
Q

Microcutic, hypochromic anemia

A

Iron deficiency anemia

23
Q

Serum ferritin is high andblow in which disorders

A

Anemia of chronic inflammation and iron deficiency anemia respectively

24
Q

Aplastic anemia

A

Chronic primary hematopoietic failure and pancytopenia

25
Reticulocytopenia is the rule in in which disease
Aplastic anemia
26
Tear drop cells and leukoerythroblastosis is seen in
Myelophthisic anemia
27
Relative polycythemia of which etiology has vomiting stress etc.. Called as
Stress polycythemia and gaisbock syndrome
28
Prolonged prothrombin time (PT) results in
Deficiency or dysfunction in factor v, vii, x prothrombin and fibrinogen Measures extrinsic and common pathway of coagulation
29
Prolonged Partial thromboplastin time (Ptt) results in
Deficiency of intrinsic factors like factor v, viii, ix, x, xi, xii, prothrombin and fibrinogen
30
High platelet count seen in
Myeloproliferative neoplasm
31
Autoimmune mediated destruction of platelets seen in
Chronic immune thrombocytopenic purpura
32
Parvovirus B19 leads to
Aplastic anemia
33
Haemophilia A patients have
Factor 8 deficiency and prolonged ptt and normal pt
34
Haemophilia B
Defect in factor 9 or Christmas factor
35
Excessive activation of coagulation and formation of thrombi in microvasculature
Disseminated intravascular coagulation