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Heme/Onc Final Details Flashcards

1
Q

2 metabolism pathways in RBCs

A

Glycolysis and HMP shunt

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2
Q

Purpose of the HMP shunt in RBCs

A

Produce NADPH to reduce glutathione

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3
Q

Rate limiting step of the HMP shunt in RBCs

A

Glucose-6-phosephate dehydrogenase

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4
Q

Two divisions of leukocytes

A

Granulocytes (basophils, neutrophils, and eosinophils)

Mononeuclear cells (lypmphocytes and monocytes)

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5
Q

Embryo shapped nucleus with “frosted glass” cytoplasm

A

Monocytes

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6
Q

What cytokine from what cell activates macrophages

What other cytokine is produced by these cells

A

INF-y from TH1 cells

TH1 cells also produce IL-2–> induces proliferation of T cells

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7
Q

CD14 and CD40 cell surface markers

A

Marcophages

“Macro-fourges”

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8
Q

Clock face chromatin

What dyscrasia is associated with these cells?

A

Plasma cells

Multiple Myeloma

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9
Q

Which T lymphocytes recognized MHC I and which recognizes MHC II

A

MHC I–> CD8 cells (because they destroy self cells presenting forein antigen or foriengn cells presenting foreign antigen)

MHC II–> CD4 cells (mediate the responce to antigen presenting cells)

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10
Q

Vit K dependant coagulation factors

A

I, VII, IX, X

Protein C and Protein S

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11
Q

Intrinsic coagulation pathway factors and measurement

A

XII–> XI–> IX–> VIII

VIIIa then activates X–>Xa which is the rate limiting step

Measured with the aPTT

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12
Q

Factors and measurement of the extrinsic pathway

A

VII–>VIIa

VIIa converts X–>Xa which again is the rate limiting step

measured with the PT/INR

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13
Q

Common pathway factors

A

V–>Va by IIa

Va converts II–>IIa (prothrombin–>thrombin)

IIa(thrombin) cleaves fibrinogen to fibrin and crosslinks fibrin mesh

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14
Q

What factor inactivates Va and therefore suppresses the common pathway?

In what disease is this an issue?

A

Protein C cleaves Va–> Factor V Leiden (mutated) cannot be inactivated by protein C

Most common cause of inherited hypercoagulability in whites

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15
Q

Heparin inactivates what coag factor?

A

IIa

Thrombin inhbitor

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16
Q

Protein C activated by

A

thrombomodulin

“modulates platelet plug formation”

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17
Q

Two situations in which howell-jolly bodies are seen

A

Asplenia (autoinfarction or removal)

and

Napthalene poinsoning (moth balls)

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18
Q

Pt eating dirt, rocks, excessive ice chips (common)

A

Pica–> iron deficiency anemia

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19
Q

Plummer-vinson syndrome

A

Iron deficiency anemia

Esophageal webs

Atrophic glossitis

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20
Q

Two forms of deletions seen in a-thalassemia

Which is more severe?

A

Cis and trans

Cis–> problematic because both deletions can be passed down on the one chromosome (Cis occurs in asains)

Trans occurs in africans

21
Q

HbH disease:

A

3 gene deletion of the alpha chain

Excessive formation of Beta chain tetramers (HbH)

Clinically significan anemia

22
Q

Hb Barts:

A

y-chain tetramers seen in 4 gene deletion alpha thalassemia

Hydrops fetalis–> incompatible with life

23
Q

Type of thalassemia present in mediterranian populations

A

B-thalassemia

24
Q

Increased HbA2 and underproduced B-chain

A

B-thalassemia minor (heterozygote)

25
Q

B-chain absent

Increased HbF

A

B-thalassemia major

26
Q

Tx, complications and classical appearence of B-thalassemia

A

Transufusions–> 2’ hemochromotosis’

Chipmunk facies–>crew cut skull d/t extrameduallary hematopoeisis

27
Q

What is HbA2

A

alpha2delta2

28
Q

Enzymes inhibited by lead posioning

A

Ferrochelatase

ALA-dehydratase

Inhibits rRNA degrdation in RBD leading to basophilic stipling

29
Q

Signs and Sx of lead poinsoning

A

Lead lines on gingiva and metaphysis of long bones

Encephalopathy and erythrocyte basophilic stipling

Abdominal colic and anemia (sideroblastic)

Foot and writst drop

30
Q

Tx of lead poisoning in adults? Kids?

A

Adults: EDTA and dimercaperol

Kids: Succimer

31
Q

Major difference between folate and B12 deficiency

How do you tell the difference chemically?

A

**No neuro signs **with folate deficiencty

Folate deficiency: elevated homocysteine and normal MMA

B12 deficiency: elevated homocysteine and elevated MMA

32
Q

megaloblastic anemia refractory to b12 and folate

A

Orotic adiuria

Tx: uridine monophosphate

33
Q

free haoptoglobin is decreased in this type of anemia

A

invascular hymolysis (haptoglobin is binding free heme)

–> PNH, autoimmuno hemolytic anemia, mechanical causes

34
Q

elevated unconjugated bilirubin in thise type of hemolysis

A

Extravascular (spleen breaking it down)

–>G6PD def, Sickel cell, Hereditary spherocytosis, pyruvate kinase def, Hemeglobin C disease

35
Q

Underlying problem in paroxysmal nacturnal hemoglobinuria

A

Decay accelerating factor protects again hemolysis by complement (c3 convertase)

DAF secured by GPI anchoring protein

Lack of GPI causes a lack of DAF and completment mediated lysis

Occurs at night because mild acidosis activates complement

36
Q

Cell marker indicative of PNH

A

Absence of CD55 (DAF) or 59

37
Q

Hams test

A

RBC lysis at low pH–> + PNH

38
Q

Tx for sickle cell

A

hydroxyurea–> increases HbF

39
Q

Autoimmune hymolytic anemia is caused by two antibodies

A

IgG (warm, methyldopa)

IgM (cold, m. pnemonia)

40
Q

Painful abdomen, dark urine, polyneuropathy, and psycholigic disturbance

A

Acute intermittant porphyria

41
Q

enzyme deficient in acute intermittant porphyria

A

Porphobilinogen deaminase

42
Q

TTP cause and Sx

A

Defect in ADAMTS13–> accumilation of vWF multimers

FATRN

Fever, Anemia, Thrombocytopenia, Renal dysfucntion/failure, Neurologic deficits

43
Q

Fried egg plasma cells

A

Multiple myeloma

44
Q

Roleaux formation and bence-jones proteinuria (IgG light chains in urine)

Mprotein spike

A

Multiple myeloma

45
Q

Auer rods

A

AML

t(15;17)

46
Q

Tx for AML

A

All trans retioic acid

(15-17 is vitamin A receptor mutation)

47
Q

Smudge cells

A

SLL and CLL

48
Q

Trap +

A

Hairy cell leukemia

TRAP (+), trapped in bone marrow, dry tap on bone marrow biopsy

49
Q

Birbeck granules and S100+

A

Langerhans cell histiocytosis

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