RBC

Question 1

methylmalonic acic –> succinyl CoA. What cofactor?

Answer 1

B12.

Question 2

What process is impaired by increased levels of methylmalonic acid?

Answer 2

Spinal cord myelinization.

Question 3

What is a pernicous anemia?

Answer 3

Autoimmune destruction of stomach parietal cells –> lack of intrincis factor, that participate in B12 absorbtion.

Question 4

In what reaction B12 is cofactor?

Answer 4

Methylmalonic acic –> succinyl CoA.

Question 5

What 3 main symptoms of macrocytic anemia regardless type?

Answer 5

RBC macrocytosis, hypersegmented neutrophils, glossitis.

Question 6

What component increases thrombosis risk in macrocytic anemiae?

Answer 6

Increased levels of homocysteine

Question 7

Why reticulocytes have bluish cytoplasm on blood smear?

Answer 7

Due to residual RNA

Question 8

Why there are symptoms of fatigue, weakness, pale skin, angina, headache in anemia?

Answer 8

Due to HYPOXIA

Question 9

Where is stored iron? (2) cells

Answer 9

Marcophages and liver

Question 10

Why gastrectomy cause IDA?

Answer 10

gastric acids maintain Fe2+ state, which is better absorbed than Fe3+.

Question 11

Why normacytic anemia stage in IDA?

Answer 11

bone marrow makes less RBC, but normal sized.

Question 12

Why microcytis anemia stage in IDA?

Answer 12

bone marrow makes less and smaller RBCs. Smaller - extra division to maintain Hb levels.

Question 13

What are 3 clinical findings in iron deficiency?

Answer 13

Anemia+koilonychia+pica.

Question 14

What supplemental iron is used in IDA treatment?

Answer 14

ferrous sulfate

Question 15

IDA, atrophic glossitis and esophageal web. Syndrome?

Answer 15

Plummer-Vinson

Question 16

Clinical presentation of Plummer-Vinson syndrome?

Answer 16

Anema, beefy-red tongue, dysphagia.

Question 17

What is the most common anemia worldwide?

Answer 17

IDA

Question 18

What is the most common anemia in hopitalized patients?

Answer 18

Anemia of chronic disease

Question 19

What hormone production is suppressed by hepcidin?

Answer 19

EPO

Question 20

What micro anemias present with increased free erythrocyte protoporfirin? (FEP)

Answer 20

IDA and anemia of chronic disease

Question 21

Hepcidin –> decr. macrophages release of iron. Where iron is normally transfered from macrophages?

Answer 21

to erythroid precursors.

Question 22

How ringed sideroblasts are formed?

Answer 22

macrophages bring Fe2+ to erythroid precursor mitochondria –> it merges to protoporphyrin –> HEME.

When protoporphyrin deficiency: Iron is trapped in mithochondria. Iron laden mitochondria form a ring around the nucleus of erythroid precursors cell.

Question 23

TB –> isoniazide treatment. What vitamin lack and that process is impaired?

Answer 23

B6, impaired succinyl-CoA to aminolevulenic acid. (rate limiting step).

Question 24

In which body part are seen ringed sideroblasts?

Answer 24

Bone marrows, because heme synthesis is in erythroid precursors nx

Question 25

in what disorder individs are protedted against plasmodium falciparum malaria?

Answer 25

thalasemia

Question 26

How is named disease when tree genes are deleted in alpha thalassemia?

Answer 26

hemoglobin H disease (HbH).

Question 27

Whan chains form tetramers in HbH?

Answer 27

Beta. Those tetramers damage RBCs.

Question 28

Whan chains form tetramers when 4 genes are deleted in alpha thalassemia?

Answer 28

Gamma. Those tetramers damage RBCs.

Question 29

How is named disease when 4 genes are deleted in alpha thalassemia?

Answer 29

Hemoglobin Barts disease. (Hb Barts)

Question 30

Target cells. What disorder?

Answer 30

beta thalassemia. Due to blebbing of RBCs membrane.

Question 31

what clinical (3) symptoms are due to increased metylmalonic acid damage?

Answer 31

Poor proprioreception+ vibratory sensation+spastic paresis

Question 32

What predisposes sickling of RBCs in kidney in sickle cell disease?

Answer 32

In renal MEDULA low Po2 --> deoxygenated sickle cells --> sickling --> oclussion--> renal papillary necrosis

Question 33

Why PNH may cause iron deficiency anemia?

Answer 33

Due to chronic hemoglobin loss in the urine

Question 34

Why PNH cause acute MYELOID leukemia?

Answer 34

Because PNH is acquired defect in MYELOID stem cells

Question 35

Why there are bite cells in G6PD deficiency?

Answer 35

Oxidative stress --> precipitates Hb as Heinz bodies --> Heinz bodies are removed from RBCs by splenic macrophages --> bite cells.

Question 36

What are the symptoms of G6PD deficiency?

Answer 36

Hemoglobinuria and back pain few days after oxidative stress

Question 37

Why back pain manifest in G6PD deficiency?

Answer 37

Because of nephrotoxicity of hemoglobin

Question 38

What component is important to prevent effect of oxidative stress?

Answer 38

Reduced glutathione (redukuotas). Jo buna sumazeje in G6PD deficiency.

Question 39

What 3 groups of drugs are contraindicated in patients with G6PD deficiency?

Answer 39

Sufa-drugs; antimalarians (primaquine); dapsone

Question 40

What screening and diagnostic methods used in G6PD deficiency? (2)

Answer 40

Screening: Heinz preparation Confirmation: Enzyme studies

Question 41

What is warm IHA? Chronic or acute? Intra or extra?

Answer 41

IgG; chronic; extravascular

Question 42

What is cold IHA? Chronic or acute? Intra or extra?

Answer 42

IgM and complement; acute; intravascular