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Nelson - Nephrology > HUS > Flashcards

Flashcards in HUS Deck (37):
1

Triad of HUS

1) Microangiopathic hemolytic anemia 2) Thrombocytopenia 3) Renal insufficiency

2

MC HUS is caused by

Toxin-producing E. coli producing diarrhea-associated HUS

3

MC E. coli serotype that causes HUS in Europe and the Americas

O157:H7

4

Toxin of this organism is causative of HUS in Asia and southern Africa

Shigella dysenteriae type I

5

Toxin of this organism is causative of HUS in Western countries

STEC

6

Reservoir of STEC

Intestinal tract of domestic animals, usually cows

7

HUS is commonly transmitted by

Undercooked meat or unpasteurized (raw) milk and apple cider

8

HUS develops during acute infection with this organism, typically manifesting with pneumonia and empyema

Neuraminidase-producing S. pneumoniae

9

Pathology of HUS nephritis

Capillary and endothelial injury leading to localized thrombosis, particularly in the glomeruli, causing a direct decrease in GFR; consumptive thrombocytopenia; microangiopathic hemolytic anemia from mechanical damage to RBCs as they pass through damaged thrombotic vasculature

10

HUS is MC in what age group

Preschool and school-aged children

11

Timing of nephritis in HUS caused by E. coli

Few days after onset of AGE

12

Diarrhea in HUS is characteristically bloody

F, not necessarily

13

T/F No presenting features reliably predict the severity of HUS in any given patient

T

14

Significant life-threatening electrolyte abnormality in HUS nephritis

Hyperkalemia (from ARF and hemolysis)

15

HUS: CNS involvement occurs in ___% of cases

20

16

T/F Majority of patients with HUS have some CNS involvement

T

17

Severe CNS involvement in HUS results from

Focal ischemia sec to microvascular CNS thrombosis

18

T/F In HUS, large strokes and ICH are common

F, rare

19

Cell type that can be seen on PBS of patients with HUS

Schistocytes from hemolysis

20

T/F PT/PTT in HUS is usually derranged

F, usually normal

21

T/F Coombs' test in HUS is usually positive

F, usually (-) and T if HUS is pneumococci-induced

22

T/F The presence or absence of toxigenic organisms on stool culture has little role in making the diagnosis of diarrhea-associated, enteropathic HUS

T

23

T/F Stool culture is often negative in patients who have diarrhea-associated HUS

T

24

HUS may take place without diarrheal nor pneumococcal prodrome

T, as in genetic HUS

25

Patients with this type of HUS are more prone to recurrence and has a more severe prognosis

Genetic

26

T/F Most patients with HUS nephritis recover renal function completely

T

27

T/F Prognosis for HUS not associated with diarrhea is more severe

T

28

T/F Early intravenous volume expansion before the onset of oligo anuria may be nephroprotective in diarrhea-associated HUS

T

29

T/F Red cell transfusions are not required in HUS since hemolysis is part of it's pathophysiology

F, usually required as hemolysis can be brisk and recurrent until the active phase of the disease has resolved

30

Why is it critical that any administered red cells to HUS patients be washed before transfusion?

To remove residual plasma since endogenous IgM directed against revealed T antigen can play a role in accelerating the pathogenesis of the disease.

31

T/F In HUS, platelets should generally not be administered

T, because they are rapidly consumed by the active coagulation and theoretically can worsen the clinical course

32

T/F Despite low platelet counts, serious bleeding is very rare in patients with HUS

T

33

Antibiotic therapy to clear enteric toxigenic organisms (STEC) is not recommended in HUS because

It can result in increased toxin release, potentially exacerbating the disease, specifically in O157-H7-associated HUS

34

T/F Antibiotic therapy against pneumococci -associated HUS is not indicated

F, prompt therapy is important

35

Plasma infusion or plasmapheresis is contraindicated in which type of HUS

Pneumococcal-associated HUS as it could exacerbate the disease

36

Treatment for HUS which is an anti-C5 antibody that inhibits complement activation, a pathway that contributes to active disease in some forms of atypical familial HUS

Eculizumab

37

T/F Most patients with diarrhea-associated HUS recover completely with little risk of long-term sequelae

T