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CMLFInal Sem2 > Poststrep Glomerulonephritis > Flashcards

Poststrep Glomerulonephritis Flashcards

1
Q

What is the most common cause of acute nephritis in kids worldwide?

A

Poststreptococcal glomerulonephritis

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2
Q

PSGN develops in 3-6 weeks after ________

A

impetigo

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3
Q

A patient comes into clinic with honey colored crust on face nose and mouth. If PSGN were to occur, how many weeks would it occur in?

A

3-6 wks

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4
Q

PSGN develops 1-3 weeks after _______

A

pharyngitis

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5
Q

strep nephritogenic antigens deposit where in the glomerulus which causes problems?

A

basement membrane

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6
Q

What is the presentation of nephritic syndrome?

A
  1. Hematuria
  2. Proteinuria
  3. Edema
  4. Hypertension
  5. Elevated serum Cr
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7
Q

What are the three most common presenting symptoms of PSGN?

A
  1. Generalized edema
  2. Gross hematuria
  3. HTN
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8
Q

Possible systemic symptoms of PSGN?

A

HA, malaise, anorexia, flank pain

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9
Q

What is present on UA for PSGN?

A

RBCs, red cell casts, proteinuria

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10
Q

In PSGN, there will be an __________ BUN/Cr ratio and a _____ serum complement

A

increased, low

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11
Q

ASO, anti-DNAse is present due to evidence of what?

A

evidence of a recent strep infection

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12
Q

If a patient comes in with PSGN but might not have a current infection should we perform a throat culture?

A

NO- perform a streptozyme test which measures 5 different streptococcal antibodies and we do this because most of the infectiction has passed the time of current infection

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13
Q

T/F: a renal biopsy is performed in most PSGN pts

A

FALSE- renal biopsy not performed in most patients

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14
Q

How to make the PSGN dx?

A

Clinical findings of acute nephritis PLUS demonstration of a recent GAS infection (positive throat of skin culture or serologic tests)

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15
Q

Treatment goals for PSGN?

A
  • Eradicate the residual nephritogenic bacteria

- Provide supportive care

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16
Q

Is there a specific therapy for PSGN?

A

No specific therapy: treat the clinical manifestations, esp volume overload

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17
Q

What is preferred over diuretics in kids with PSGN?

A

Sodium and water restriction

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18
Q

How should we reduce BP and edema in a patient with PSGN?

A

Furosemide

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19
Q

What should we do if a patient has hypertensive encephalopathy and PSGN?

A

Treat emergently to lower BP

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20
Q

What are three reasons someone with PSGN would need dialysis?

A
  • Life threatening fluid overload (pulmonary edema, heart failure, HTN) refractory to medical tx
  • Hyperkalemia (>6.5 unresponsive to medical tx)
  • Uremia with BUN b/t 89-100 (normal ~10)
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21
Q

What are the admissions criteria for PSGN?

A

SOSCS!

  • Severe renal dysfunction
  • Oliguria (not urinating enough)
  • CHF
  • Significant volume overload
22
Q

What is the drug of choice for PSGN?

A

Penicillin

23
Q

What is an alternate 1st line tx for PSGN for kids that tastes better?

A

Amoxicillin

24
Q

If a patient has a MILD allergy to PCN what is the tx for PSGN?

A

Cephalexin (Keflex)

25
Q

If pt can’t take cephalosporins, what is the PSGN tx?

A

Azithromycin

26
Q

When does Cr go back to baseline after PSGN?

A

3-4 wks

27
Q

How long after PSGN do patients begin diuresing?

A

1 wk

28
Q

How long does it take for hematuria to resolve after PSGN?

A

3-6 months

29
Q

What is the last thing to resolve in PSGN? Which sometimes takes 10 yrs?

A

Proteinuria

30
Q

This is a multisystem disease that results from an autoimmune reaction to infection with GAS?

A

Rheumatic fever

31
Q

This is the most common cause of heart disease in kids in developing countries and mainly a disease of children age 5-14?

A

Rheumatic fever

32
Q

Rheumatic fever starts ___ days to several weeks after GAS infecition

A

10

33
Q

What are two common presentation patterns in a patient with rheumatic fever?

A
  • Acute febrile illness with joint manifestations and/or carditis
  • Neurologic and behavioral manifestations with chorea
34
Q

T/F: Fever is present in all cases of rheumatic fever?

A

False >90%

35
Q

With RF and _______ a patient may have dyspnea, orthopnea, CP, palpitations

A

carditis

36
Q

With RF and _______ a patient will have generally large joints, migratory, dramatic response to NSAIDs/salicylates

A

joint pain

37
Q

What helps leg/joint pain in pts with RF?

A

NSAIDs

38
Q

With RF and _______ a patient will have uncontrolled jerky movements limbs, face, tongue, usually worse on one side, stop while sleeping, often associated with emotional lability

A

chorea

39
Q

With RF and _______ a patient will have painless, resolve 1-2 weeks

A

Nodular SQ lesions

40
Q

With RF and _______ a patient will have nonpruritic, nonpainful, evanescent, usually on trunk. May have central pallor

A

rash (erythema marginatum)

41
Q

What is the jones criteria?

A

-Need 2 major or 1 major and 2 minor PLUS evidence of a strep infection

42
Q

What are the major jones criteria?

A
  • Carditis & valvulitis
  • Arthritis
  • CNS involvement (usually chorea)
  • Subq nodules
  • Erythema marginatum
43
Q

What are the minor jones criteria?

A
  • Arthralgia
  • Fever
  • Elevated ESRs
  • Prolonged PR on EKG
44
Q

Does this meet the jones criteria? Evidence of GAS, carditis and chorea?

A

Yes

45
Q

What is the difference between arthritis and arthralgias?

A

Arthritis: large joint migratory arthritis from joint to joint
Arthralgias: joint discomfort/pain involving several joints

46
Q

What is a common EKG findings in RF?

A

PR prolongation

47
Q

Which valve is mostly affected in a a patient with RF? And what finding is associated with it?

A

Mitral valve and mitral regurg

48
Q

What is the tx for arthritis and how long should you take it for?

A

NSAID (Aspirin or Naproxen) and until the joint symptoms have resolved

49
Q

Is there prophylaxis for RF? If so, what is it?

A

Yes patients who have one attack of RF are at high risk for getting it again and WORSE every time.

Prophylaxis: PCN or Clinda

50
Q
  • Antibody directed against antigen on cells or extracellular materials (ie: basement membrane)
  • Ab-Ag complexes activate complement via classic pathway –> cell lysis or extracellular tissue damage
A

Type II Acute Rheumatic Fever

51
Q
  • Immune complexes (Ab & Ag) promote tissue damage through complement activation (alternate pathway)
  • Complexes deposited in tissues
A

Type III PSGN

CMLFInal Sem2 (10 decks)

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