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Mercy CLS 6: Hematology > 12) Hemolytic anemia—nonimmune defects > Flashcards

12) Hemolytic anemia—nonimmune defects Flashcards

1
Q

2 types of extrinsic factors that can cause hemolytic anemia

A
  • immune
  • nonimmune
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2
Q

general categories of nonimmune causes of hemolysis

A
  • physical trauma to RBC (MAHA, malignant HTN, exercise, heat, heart valve)
  • antagonists (toxins, infectious agents)
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3
Q

general antagonist behind the hemolysis in HUS, TTP and DIC

A

thrombi in microcirculation

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4
Q

snake bites often cause mechanical damage to RBCs via…

A

DIC

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5
Q

general signs of traumatic injury to RBCs on PB and in chemistry

A
  • schistocytes/helmet cells
  • ↑ retics/polychromasia
  • striking poik
  • signs of IV hemolysis (hemoglobinuria, ↓ hapto, ↑ LD, ↑ unconjugated bilirubin)
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6
Q

general term indicating RBCs are lysed or damaged by microcirculatory lesions or shear forces in circulation

A

microangiopathic hemolytic anemia (MAHA)

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7
Q

explain the process of MAHA

A
  1. endothelial lining of small vessels damaged
  2. platelets & fibrin deposits form
  3. thrombus formation in vessels
  4. RBCs forced through fibrin strands in thrombus, causing fragmentation
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8
Q

MAHA hemolysis is (intravascular/extravascular)

A

depends on severity
less damage —EV
more damage —IV

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9
Q

examples of MAHA disorders

A
  • HUS
  • TTP
  • DIC
  • malignant HTN
  • disseminated cancer
  • preeclampsia/eclampsia
  • HELLP syndrome
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10
Q

triad of HUS s/s

A
  • hemolytic anemia with schistocytes
  • thrombocytopenia
  • acute nephropathy/renal failure
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11
Q

2 groups of HUS

A
  • D+HUS—diarrhea —90% cases, mostly children <5 —caused by shiga toxin
  • D=HUS —no diarrhea —atypical HUS
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12
Q

causes of D+HUS

A
  • E. coli O157:H7
  • Shigella dysenteriae serotype I
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13
Q

causes of D=HUS

A
  • postinfection (Spne, viruses)
  • immunosuppression (chemo)
  • renal/BM transplantation
  • pregnancy
  • OC
  • toxins
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14
Q

how does shiga toxin cause HUS?

A
  • enters circulation through tears in colon mucosa
  • damages endothelial cells in glomeruli
  • platelet activation & fibrin microthrombi form
  • erythrocytes are damaged & kidney loses function
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15
Q

acute onset
bloody hematuria
sudden pallor
abd pain
vomiting
bloody diarrhea

A

HUS

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16
Q

(TTP/HUS) has less severe CNS sx if present.

A

HUS

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17
Q

Hgb in HUS

A

7-9 g/dL, some requiring transfusion

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18
Q

HUS on PB

A
  • normo/normo
  • schistocytes, helmet cells
  • spherocytes
  • polychromasia
  • occasional nRBCs
  • left shift of leukocytosis
  • platelet count low to markedly low
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19
Q

HUS chemistry findings

A
  • signs of IV hemolysis
  • ↑ BUN, creatinine
  • hypokalemia, hyponatremia
  • proteinuria, hematuria, pyuria
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20
Q

HUS coag tests

A

normal to slightly elevated

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21
Q

plasma exchange may be indicated in —- HUS

A

D=

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22
Q

new tx for HUS

A

monoclonal Ab against shiga toxin

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23
Q

etiology of TTP

A
  • lack of ADAMTS13 enzyme, which cleaves vWF multimers
  • vWF multimers cause thrombi by attaching to endothelials and attracting platelets
24
Q

unusually large forms of vWF multimers

A

thrombotic thrombocytopenic purpura (TTP)

25
Q

2 causes of TTP

A
  • familial—mutation in ADAMTS13 gene
  • acquired—autoAb against gene, or precipitating factors (infections, pregnancy)
26
Q

TTP age group

27
Q

renal function in TTP vs HUS

A

TTP—renal dysfunction, mild to mod
HUS—renal failure

28
Q

TTP on PB

A
  • normo/normo
  • ↑↑ schistocytes
  • polychromasia
  • nRBCs
  • leukocytosis with left shift
29
Q

typical platelet count for TTP

A

8-40, very severe

30
Q

TTP coag tests

A

usually normal or slightly abnormal

31
Q

—– must be treated, and is 90% fatal without treatment (multiorgan failure)

32
Q

TTP tx

A
  • FFP plasma exchange
  • cryo
  • drug tx
33
Q

DIC

A

disseminated intravascular coagulation

complex bleeding & clotting condition in which normal coagulation balance is altered

34
Q

common triggers of DIC

A
  • bacterial sepsis
  • neoplasms
  • trauma/burns—release of tissue factor
  • immunologic disorders (trxn, transplant rejection)
  • misc—venom or drugs
35
Q

DIC coag tests

A

very abnormal
prolonged PT, PTT
decreased fibrinogen
positive or ↑ D-dimer

36
Q

DIC tx

A
  • pRBC and platelet transfusions
  • FFP
  • factor concentrates
  • treatment of underlying cause

important not to upset coag balance, difficult to tx

37
Q

HELLP syndrome

A

complication of pregnancy

Hemolysis
Elevated Liver enzymes
Low Platelet count

38
Q

pathogenesis of HELLP

39
Q

—— may be a severe form of preeclampsia

40
Q

↑ liver enzymes due to sinus obstruction or liver damage

41
Q

HELLP coag tests

A

usually normal

42
Q

malignant HTN is a form of ——- hemolysis with unknown mechanism

43
Q

caused by artificial heart valve damage to RBCs

A

traumatic cardiac hemolytic anemia

44
Q

in this form of MAHA, platelet count is normal

A

traumatic cardiac hemolytic anemia

45
Q

Waring Blender syndrome

A

traumatic cardiac hemolytic anemia

46
Q

prominent on PB of a burn patient

A
  • microspherocytes
  • RBC budding
  • schistocytes
  • aniso/poik
47
Q

“march hemoglobinuria”

A

excercise-induced
short term

48
Q

traumatic disruption of RBCs with no anemia and no schistocytes

A

exercise-induced hemoglobinuria

49
Q

potential complication of march hemoglobinuria

50
Q

malaria usually causes a mild —–/—— anemia, but ———– can cause a severe anemia

A

normo/normo
Plasmodium falciparum

51
Q

malaria causes (EV/IV) hemolysis

52
Q

3 life stages of malaria

A
  1. ring form
  2. schizont form
  3. gametocyte
53
Q

protozoan infection of RBCs
looks like malaria

A

babesiosis

54
Q

coccobacillus that releases proteins inducing pitting of RBC membrane

A

bartonellosis

55
Q

GI flora that can cause rapid, massive hemolysis in bloodstream

A

Clostridium perfringens

56
Q

——— venom cleaves off glycophorins, causing C-mediated lysis

A

brown recluse

Mercy CLS 6: Hematology (25 decks)

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