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Organ Systems - UWorld Factoids > Heme > Flashcards

Heme Flashcards

1
Q

RBC source of energy?

A

glucose: (90% used in glycolysis, 10% used in HMP shunt)

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2
Q

vWF receptor on platelet

A

GpIb

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3
Q

fibrinogen receptor on platelet

A

GpIIb/IIIa

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4
Q

causes of eosinophilia

A 
NAACP:
Neoplasia
Asthma
Allergies
Connective tissue diseases
Parasites
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5
Q

what activates macrophages?

A

gamma-interferon

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6
Q

how do macrophages function as APC cell?

A

-MHC II

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7
Q

how do eosinophils protect against helminths?

A

major basic protein

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8
Q

how do eosinophils limit reaction following mast cell degranulation

A

histaminase

arylsulfatase

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9
Q

in what conditions are basophils elevated?

A

myleoproliferative diseases / CML

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10
Q

what are in basophilic granules?

A

1) heparin
2) histamine
3) leukotrienes

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11
Q

when are mast cells deployed?

A

1) type I hypersensitivity

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12
Q

how are mast cells reversed / inhibited?

A

cromolyn sodium prevents mast cell degranulation –> used for asthma prophylaxis

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13
Q

treatment to prevent erythroblastosis fetalis

A

-administer Rho(D) iG for mother during pregnancy –> prevent sensitization of Rh- mother to Rh antigen

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14
Q

what enzyme doe swarfarin inhibit?

A

epoxide reductase –> less reduced vitamin K –> less cofactor available to mature II, VII, IX, X, C, S

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15
Q

what is the role of vWF

A

carries / protects VIII

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16
Q

how does tPA work?

A

tpa: breaks down plasminogen to plasmin.

plasmin leads to fibrinolysis:

1) cleavage of fibrin mesh
2) destruction of coagulation factors

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17
Q

what are principal targets of antithrombin?

A

thrombin / factor XA

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18
Q

what are steps in primary hemostasis / platelet plug formation?

A

1) injury
2) adhesion
3) activation
4) aggregation

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19
Q

what happens with injury in primary hemostasis?

A

1) vWF binds to exposed collagen due to endothelial damage

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20
Q

describe adhesion of 1* hemostasis

A

platelets bind vWF via Gp1b –> release of ADP / Ca2+ (coag cascade)

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21
Q

describe activation of 1* hemostasis

A

ADP binding to receptor –> GpIIb/IIIa expression at platelet surface

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22
Q

aggregation of 1* hemostasis

A

fibrinogen binds GpIIb/IIIa receptors and links platelets

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23
Q

what are pro-aggregation factors:

A
  • TXA2 from platelets
  • dec. blood flow
  • incr. platelet aggregation
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24
Q

what are anti-aggregation factors

A
  • PGI2 / NO from endothelial cells
  • incr. blood flow
  • dec. platelet aggregation
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25
Q

how is ristocetin used?

A

ristocetin activates vWF to bind GpIB –> diagnoses vWF disease where no aggregation occurs following administration

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26
Q

ticlopidine / clopidogrel

A

inhibit ADP-induced expression of GpIIB / IIIa

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27
Q

abxicimab

A

inhibits GpIIb/IIIA directly

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28
Q

what does increased ESR mean?

A

acute-phase reactants in plasma (like fibrinogen) cause RBC aggregation –> faster sedimentation rate

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29
Q

significance of schistocyte / helmet cell

A

traumatic hemolysis / DIC / TTP ? HUS

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30
Q

ringed sideroblast

A

excess Fe in mitochondria = pathologic

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31
Q

target cell

A

HbC disease, Asplenia, Liver disease, Thalassemia

32
Q

heinz bodies

A

oxidation of hemoglobin sulfhydral groups –> denatured hemoglobin precipitation / phagocytic damage to rBC membrane

33
Q

heinz body significance

A

G6PD deficiency / alpha-thalassemia

34
Q

howell-jolly bodies

A

basophilic nuclear remnants in RBCs –> seen in functional hyposplenia / asplenia

35
Q

symptoms of 1-2 allele deletion of a-thalassemia?

A

none –> not clinically significant anemia

36
Q

4-allele deletion for a-thalassemia

A

no-alpha globin, excess gamma-globin –> forms Hb Barts (gamma4).

-hydrops fetalis –> incompatible w/ life

37
Q

beta-thalessemia molecular problem?

A

point-mutation in splice site / promoter –> dec. beta-globin synthesis

38
Q

beta-thalassemia minor heterozygote

A
  • b chain underproduced
  • asymptomatic
  • diagnosis confirmed by greater than 3.5% of HbA2 on electrophoresis
39
Q

beta-thalassemia major

A

-beta chain is absent –> severe anemia
-extramedullary hematopoesis:
+hepatosplenomegaly
+skeletal deformaties

40
Q

why do infants present with b-thal major after 6 months?

A

HbF is protective

41
Q

lead poisoning presentation?

A

Lead lines on gingivae
Encephalopathy / Erythrocyte basophilic stippling
Abdominal colic / sideroblastic Anemia
Drops: wrist / foot drop; dimercaprol

42
Q

lead poisoning enzymes

A

inhibition of ferrchelatase / ALA DEHYDRATASE–> dec. heme sythesis / incr. RBC protoporphyrin

43
Q

why is there basophilic stippling in lead poisoning?

A

inhibition of rRNA degradation –> retain aggregates of RBCs

44
Q

sideroblastic anemia deficiency?

A

delta-ALA SYNTHASE

45
Q

iron deficiency labs

A

dec. iron, incr. TIBC, dec. ferritin

46
Q

sideroblastic anemia labs

A

incr. iron, normal TIBC, inc. ferritin

47
Q

how do you differentiate folate def. from b12 def?

A

both:
-dec. folate, incr. homocystine
folate def:
-normal methylmalonic acid / no neurological deficits
b12 def:
-incr. methylmalonic acid, neuro problems

48
Q

neurologic symptoms of B12 deficiency:

A
  • peripheral neuropathy w/ sensorimotor dysfunction
  • dorsal columns 9vibration / proprioception)
  • lateral corticospinal (spasticity_
  • dementia
49
Q

orotic acid uria enzyme defect + treatment

A

UMP synthase deficiency

bypass enzyme w/ URIDINE MONOPHOSPHATE

50
Q

orotic aciduria presentation:

A

megalblastic anemia in children, unresponsive to folate / B12. no hyperammonemia

51
Q

how does ornithine transcarbamylase deficiency present?

A

incr. orotic acid w/ hyperammonemia

52
Q

findings for intravascular hemolysis

A
  • dec. haptoglobin
  • incr. LDH, schistocytes, and reticulocytes
  • incr. urobilinogen in urine
53
Q

features of extravascular hemolysis

A

-incr. LDH + incr. unconjugated bilirubin –> jaudince / hereditary spherocytosis

54
Q

labs for hereditary spherocytosis

A

osmotic fragility test

  • eosin-5-maleimide binding test for screening
  • normal to dec. MCV
55
Q

treatment for hereditary spherocytosis (E hemolysis)

A

splenectomy

56
Q

GCPD deficiency (I/E)

A

defect in G6PD –> dec. glutathione –> incr. RBC susceptibility to oxidant stress

57
Q

G6PD precipitants

A

sulfa drugs, antimalarials, infections, fava beans

58
Q

pyruvate kinase deficiency (E)

A

defect in pyruvate kinase –> dec. ATP –> rigid RBCs

Hemolytic anemia IN A NEWBORN

59
Q

what is association w/ paroxysmal nocturnal hemoglobinuria (I)?

A

acquired mutation in hematopoetic stem cell disease –> loss of protective factor from complement-mediated RBC lysis

-increased incidence of acute leukemia

60
Q

findings for paroxysmal nocturnal hemoglobinuria

A

-triad:
negative coombs hemolytic anemia
-pancytopenia
-venous thrombosis

labs: CD55/59.

61
Q

treatment of paroxysmal nocturnal hemoglobinuria

A

eculizumab

62
Q

treatment of sickle cell anemia

A

hydroxuria (incr. HbF) + bone marrow transplant

63
Q

warm agglutinin

A

IgG –> chronic anemia seen in SLE, CLL, a-methyldopa + other drugs

64
Q

what is the diff. b/w direc vs indirect coombs test?

A

direct coombs: anti-Ig antibody added to patient’s blood, will agglutinate if RBCs coated w/ Ig

indirect coombs = normal RBCs added to patient’s serum. RBCs agglutinate when anti-Ig antibodies are added

65
Q

cold agglutinin

A

IgM

66
Q

diff. b/w microangiopathic vs. macroangiopathic anemia

A

micropathic is through narrowed vessels; macroangiopathic = mechanical destruction

67
Q

whats the difference b/w ferrtin + transferrin?

A

1) transferrin transports Fe in blood

2) ferritin = storage protein for Fe in body

68
Q

porphyria

A

hereditary / acquierd defects in heme synthesis –> accumulation of heme precursors –> symptoms

69
Q

lead poisoning enzymes deficiency

A

ferrochelatase + ALA dehydratase

70
Q

lead poisoning accumulated substrate

A

protoporphyrin / delta-ALA

71
Q

acute intermittent porphyeria enzyme deficiency

A

prophobilinogen deaminase

72
Q

acute intermittent porphyria accumulated substrate

A

porphobilinogen, delta-ALA, coporphobilinogen in urine

73
Q

symptoms of acute intermittent porphyria (5)

A

1) Painful abdomen
2) Port-wine-colored urine
3) Polyneuropathy
4) Psyche
5) Precipitated by drugs, alcohol, starvation

74
Q

treatment of AIP

A

1) glucose / heme –> inhibit ALA synthase

75
Q

porphyria cutanea tarda enzyme deficiency

A

uroporphyrinogen decarboxylase

76
Q

accumulated substrate in porphyria cutanea tarda

A

uroporphyrin –> tea-colored urine

77
Q

symptoms of porphyria cutanea tarda

A

blistering cutaneous photosensitivity –> most common porphyria

Organ Systems - UWorld Factoids (8 decks)

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