Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Blood patho > RBC > Flashcards

RBC Flashcards

1
Q

methylmalonic acic –> succinyl CoA. What cofactor?

A

B12.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What process is impaired by increased levels of methylmalonic acid?

A

Spinal cord myelinization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a pernicous anemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

In what reaction B12 is cofactor?

A

Methylmalonic acic –> succinyl CoA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What 3 main symptoms of macrocytic anemia regardless type?

A

RBC macrocytosis, hypersegmented neutrophils, glossitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What component increases thrombosis risk in macrocytic anemiae?

A

Increased levels of homocysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why reticulocytes have bluish cytoplasm on blood smear?

A

Due to residual RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Due to HYPOXIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is stored iron? (2) cells

A

Marcophages and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why gastrectomy cause IDA?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why normacytic anemia stage in IDA?

A

bone marrow makes less RBC, but normal sized.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why microcytis anemia stage in IDA?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are 3 clinical findings in iron deficiency?

A

Anemia+koilonychia+pica.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What supplemental iron is used in IDA treatment?

A

ferrous sulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IDA, atrophic glossitis and esophageal web. Syndrome?

A

Plummer-Vinson

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical presentation of Plummer-Vinson syndrome?

A

Anema, beefy-red tongue, dysphagia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the most common anemia worldwide?

A

IDA

18
Q

What is the most common anemia in hopitalized patients?

A

Anemia of chronic disease

19
Q

What hormone production is suppressed by hepcidin?

A

EPO

20
Q

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

A

IDA and anemia of chronic disease

21
Q

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

A

to erythroid precursors.

22
Q

How ringed sideroblasts are formed?

A

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.

23
Q

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

A

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

24
Q

In which body part are seen ringed sideroblasts?

A

Bone marrows, because heme synthesis is in erythroid precursors nx

25
Q

in what disorder individs are protedted against plasmodium falciparum malaria?

A

thalasemia

26
Q

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

A

hemoglobin H disease (HbH).

27
Q

Whan chains form tetramers in HbH?

A

Beta. Those tetramers damage RBCs.

28
Q

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

A

Gamma. Those tetramers damage RBCs.

29
Q

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

A

Hemoglobin Barts disease. (Hb Barts)

30
Q

Target cells. What disorder?

A

beta thalassemia. Due to blebbing of RBCs membrane.

31
Q

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

A

Poor proprioreception+ vibratory sensation+spastic paresis

32
Q

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

A

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

33
Q

Why PNH may cause iron deficiency anemia?

A

Due to chronic hemoglobin loss in the urine

34
Q

Why PNH cause acute MYELOID leukemia?

A

Because PNH is acquired defect in MYELOID stem cells

35
Q

Why there are bite cells in G6PD deficiency?

A

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

36
Q

What are the symptoms of G6PD deficiency?

A

Hemoglobinuria and back pain few days after oxidative stress

37
Q

Why back pain manifest in G6PD deficiency?

A

Because of nephrotoxicity of hemoglobin

38
Q

What component is important to prevent effect of oxidative stress?

A

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

39
Q

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

A

Sufa-drugs; antimalarians (primaquine); dapsone

40
Q

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

A

Screening: Heinz preparation
Confirmation: Enzyme studies

41
Q

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

A

IgG; chronic; extravascular

42
Q

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

A

IgM and complement; acute; intravascular

Blood patho (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions