Case 5: Post strep infection Flashcards
Poststreptococcal Glomerulonephritis:
-Caused by prior infection with specific _______ strains of _____
-nephritogenic strains of GABS
2 main nephritogenic antigens:
nephritis-associated plasmin receptor (NAPlr) & streptococcal pyogenic exotoxin B (SPE B)
Poststreptococcal Glomerulonephritis:
- Occurs mostly in _______ countries
- Risk increased in which Pt populations?
- developing
- older patients and kids 4-15
- M>F
What is the most common cause of acute nephritis in kids worldwide?
Poststreptococcal Glomerulonephritis
Pathophysiology- PSGN
- After impetigo: develops in ____ weeks
- After pharyngitis: develops in ____ weeks
- 3-6
- 1-3
PSGN:
Streptococcal nephritogenic antigens are deposited within the _______–> Immune complexes form–> _______ activated, inflammatory cells recruited.
- glomerulus
- complement
Clinical Manifestations: PSGN
-Can be asymptomatic with microscopic _______
-Can have a full nephritic syndrome presentation: (describe)
- hematuria
- red/brown urine, proteinuria, edema, hypertension, elevated serum creatinine
Clinical Manifestations: PSGN
-MC presenting Sx: ______
- Generalized edema
- Gross hematuria
- HTN
PSGN:
-Possible systemic symptoms: ______
headache, malaise, anorexia, flank pain
PSGN: Labs
- UA: _____
- BUN/Cr: _____
- Serum complement–>
- UA: RBCs, red cell casts, proteinuria
- Increased BUN/Cr
- Serum complement: LOW –> Complement system has been activated & complement components consumed
PSGN: Labs (cont)
-Serology: ______
-ASO, anti-DNAse –> evidence of a recent streptococcal infection
A streptozyme test measures __ different streptococcal antibodies
5
Complement is part of the _____ immune system
innate
Describe Complement
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
PSGN: dx
-what 2 things are needed to make the diagnosis?
-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
PSGN: tx goals
- Eradicate residual nephritogenic bacteria
- Provide supportive care
PSGN: management
- **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
PSGN: management
-IF hypertensive encephalopathy: treat ______
treat emergently to lower BP
PSGN: management
-May need dialysis: IF _____ (3 conditions)
- 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
PSGN: Admission Criteria (5 things)
Severe renal dysfunction Oliguria Severe hypertension CHF Significant volume overload
PSGN:
- do Abx alter the clinical course of the disease?
- when do some experts recommend abx?
- NO
- Some experts recommend abx ONLY if there’s proven active strep infection at time of diagnosis
Others recommend treating patients with PSGN as if they have an active strep infection:
-drug of choice=
- **penicillin
- Alternate 1st line therapy: amoxicillin
- PCN allergy (mild): cephalexin (Keflex)
- If can’t take cephalosporins: azithromycin
PSGN: course/prognosis
-Most Pts (esp. kids) have _____
a complete recovery
PSGN: course/prognosis
-But some develop _____
HTN, recurrent proteinuria, and renal insufficiency long term
PSGN:
- Creatinine usually back to baseline by _____ weeks
- Usually begin diuresing in __ week
- 3-4
- 1
PSGN:
- Hematuria resolves in ____
- Proteinuria decreases, but much _____
- Children fare better than the _____
- 3-6 months
- slower
- elderly
Rheumatic Fever is a multisystem disease that results from:
an autoimmune reaction to infection with GAS
What is the MC cause of heart disease in kids in developing countries?
Rheumatic fever
Rheumatic Fever:
is mainly a disease of _____ age
children, 5-14 yo
Rheumatic fever- s/s:
-MC presentation pattern is 1 of the following:
-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
Rheumatic fever- other s/s
- 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
Jones Criteria:
-Need ___ major or __ major + ___ minor (and evidence of strep infection)
-2 major
OR
-1 major, 2 minor
Jones Criteria:
List Major
Carditis & valvulitis Arthritis CNS involvement (usu. chorea) Subcutaneous nodules Erythema marginatum
Jones Criteria:
List Minor
Arthralgia
Fever
Elevated acute phase reactants
Prolonged PR on EKG
CARDIAC/EKG findings
- 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
Treatment- Acute Rheumatic Fever
-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
Hypersensitivity Reaction:
-Type II: Acute Rheumatic Fever
- 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
Hypersensitivity Reaction:
Type III: Poststreptococcal glomerulonephritis
- Immune complexes (Ab & Ag) promote tissue damage through complement activation (alternate pathway)
- Complexes deposited in tissues
