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ClinMed Lab II > Case 5: Post strep infection > Flashcards

Case 5: Post strep infection Flashcards

1
Q

Poststreptococcal Glomerulonephritis:

-Caused by prior infection with specific _______ strains of _____

A

-nephritogenic strains of GABS

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2
Q

2 main nephritogenic antigens:

A

nephritis-associated plasmin receptor (NAPlr) & streptococcal pyogenic exotoxin B (SPE B)

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3
Q

Poststreptococcal Glomerulonephritis:

  • Occurs mostly in _______ countries
  • Risk increased in which Pt populations?
A
  • developing
  • older patients and kids 4-15
  • M>F
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4
Q

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

A

Poststreptococcal Glomerulonephritis

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5
Q

Pathophysiology- PSGN

  • After impetigo: develops in ____ weeks
  • After pharyngitis: develops in ____ weeks
A
  • 3-6

- 1-3

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6
Q

PSGN:
Streptococcal nephritogenic antigens are deposited within the _______–> Immune complexes form–> _______ activated, inflammatory cells recruited.

A
  • glomerulus

- complement

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7
Q

Clinical Manifestations: PSGN
-Can be asymptomatic with microscopic _______

-Can have a full nephritic syndrome presentation: (describe)

A
  • hematuria

- red/brown urine, proteinuria, edema, hypertension, elevated serum creatinine

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8
Q

Clinical Manifestations: PSGN

-MC presenting Sx: ______

A
  • Generalized edema
  • Gross hematuria
  • HTN
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9
Q

PSGN:

-Possible systemic symptoms: ______

A

headache, malaise, anorexia, flank pain

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10
Q

PSGN: Labs

  • UA: _____
  • BUN/Cr: _____
  • Serum complement–>
A
  • UA: RBCs, red cell casts, proteinuria
  • Increased BUN/Cr
  • Serum complement: LOW –> Complement system has been activated & complement components consumed
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11
Q

PSGN: Labs (cont)

-Serology: ______

A

-ASO, anti-DNAse –> evidence of a recent streptococcal infection

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12
Q

A streptozyme test measures __ different streptococcal antibodies

A

5

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13
Q

Complement is part of the _____ immune system

A

innate

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14
Q

Describe Complement

A

Made up of inactive proteins in the blood–> cleaved to release cytokines–> complement activation–> phagocytes stimulated –> lysis, activation of inflammatory responses, clearance of circulating immune complexes

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15
Q

PSGN: dx

-what 2 things are needed to make the diagnosis?

A

-Clinical findings of acute nephritis –PLUS-
Demonstration of a recent GAS infection
-Positive throat or skin culture or serologic tests

–Renal biopsy not performed in most patients

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16
Q

PSGN: tx goals

A
  • Eradicate residual nephritogenic bacteria

- Provide supportive care

17
Q

PSGN: management

A
  • **No specific therapy: treat the clinical manifestations, especially volume overload
  • Abx treatment for the streptococcal infection
  • Sodium & water restriction
  • Loop diuretics (usually furosemide) reduce BP and edema
18
Q

PSGN: management

-IF hypertensive encephalopathy: treat ______

A

treat emergently to lower BP

19
Q

PSGN: management

-May need dialysis: IF _____ (3 conditions)

A
  • Life-threatening fluid overload (pulmonary edema, heart failure, and HTN) refractory to medical tx
  • Hyperkalemia (>6.5) unresponsive to medical tx
  • Uremia with BUN between 89-100
20
Q

PSGN: Admission Criteria (5 things)

A 
Severe renal dysfunction
Oliguria
Severe hypertension
CHF
Significant volume overload
21
Q

PSGN:

  • do Abx alter the clinical course of the disease?
  • when do some experts recommend abx?
A
  • NO

- Some experts recommend abx ONLY if there’s proven active strep infection at time of diagnosis

22
Q

Others recommend treating patients with PSGN as if they have an active strep infection:
-drug of choice=

A
  • **penicillin
  • Alternate 1st line therapy: amoxicillin
  • PCN allergy (mild): cephalexin (Keflex)
  • If can’t take cephalosporins: azithromycin
23
Q

PSGN: course/prognosis

-Most Pts (esp. kids) have _____

A

a complete recovery

24
Q

PSGN: course/prognosis

-But some develop _____

A

HTN, recurrent proteinuria, and renal insufficiency long term

25
Q

PSGN:

  • Creatinine usually back to baseline by _____ weeks
  • Usually begin diuresing in __ week
A
  • 3-4

- 1

26
Q

PSGN:

  • Hematuria resolves in ____
  • Proteinuria decreases, but much _____
  • Children fare better than the _____
A
  • 3-6 months
  • slower
  • elderly
27
Q

Rheumatic Fever is a multisystem disease that results from:

A

an autoimmune reaction to infection with GAS

28
Q

What is the MC cause of heart disease in kids in developing countries?

A

Rheumatic fever

29
Q

Rheumatic Fever:

is mainly a disease of _____ age

A

children, 5-14 yo

30
Q

Rheumatic fever- s/s:

-MC presentation pattern is 1 of the following:

A

-Start 10 days-several weeks after GAS infection

  • MC presentation pattern is one of the following:
  • -Acute febrile illness with joint manifestations and/or carditis
  • -Neurologic and behavioral manifestations with chorea
31
Q

Rheumatic fever- other s/s

A
  • Fever >90% of cases
  • Carditis: may have dyspnea, orthopnea, CP, palpitations
  • Joint pain: generally large joints, migratory, dramatic response to NSAIDs/salicylates
  • Chorea: uncontrolled jerky movements limbs, face, tongue, usually worse on one side, stop while sleeping, often associated with emotional lability
  • Nodular SQ lesions: painless, resolve 1-2 weeks
  • Rash (erythema marginatum): nonpruritic, nonpainful, evanescent, usually on trunk. May have central pallor
32
Q

Jones Criteria:

-Need ___ major or __ major + ___ minor (and evidence of strep infection)

A

-2 major
OR
-1 major, 2 minor

33
Q

Jones Criteria:

List Major

A 
Carditis & valvulitis
Arthritis
CNS involvement (usu. chorea)
Subcutaneous nodules
Erythema marginatum
34
Q

Jones Criteria:

List Minor

A

Arthralgia
Fever
Elevated acute phase reactants
Prolonged PR on EKG

35
Q

CARDIAC/EKG findings

A
  • PR prolongation (AV block) from myocardial inflammation affecting electrical conduction pathways
  • Mitral valve MC affected
  • Mitral regurgitation MC finding
  • S3: indicates failing LV in CHF/ increased volume
  • Hyperdynamic cardiac impulse: MR
  • A2 accentuated over P2: MR and pulmonary HTN can cause
  • Cardiomegaly: on EKG and/or CXR, LVH may be seen
  • Tachycardia
36
Q

Treatment- Acute Rheumatic Fever

A

-Abx tx for Streptococcal infection

  • NSAIDs for arthritis –> continue until all joint symptoms resolved
  • -Aspirin has been the traditional 1st-line therapy
  • -Naproxen also good choice
  • Carditis management: manage heart failure
  • Prophylaxis
37
Q

Hypersensitivity Reaction:

-Type II: Acute Rheumatic Fever

A
  • 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
38
Q

Hypersensitivity Reaction:

Type III: Poststreptococcal glomerulonephritis

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

ClinMed Lab II (12 decks)

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