Scarlet Fever/Post-Strept Glomerulonephritis/ARF Flashcards Preview

Rheum/Musculoskeletal/Derm Week 3 > Scarlet Fever/Post-Strept Glomerulonephritis/ARF > Flashcards

Flashcards in Scarlet Fever/Post-Strept Glomerulonephritis/ARF Deck (24):
1

What is scarlet fever?

A complication of GAS infection that most commonly affects children between five and fifteen years of age and typically occurs in association with pharyngitis (considered a complication)

2

What are the symptoms of scarlet fever?

-Sore throat

-Fever

-Bright red tongue with a "strawberry" appearance (below)

-A characteristic rash,

-hallucinations, paranoia 

 

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3

Describe the rash of scarlet fever

is fine, red, and rough-textured,

blanches upon pressure,

appears 12–72 hours after the fever starts and begins to fade three to four days after onset, upon which desquamation (peeling) begins. "This phase begins with flakes peeling from the face. Peeling from the palms and around the fingers occurs about a week later." Peeling also occurs in the axilla, the groin, and the tips of fingers and toes

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4

What is this?

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Pastia's lines- skin rash of scarlet fever that is worse in the skin folds where the rash runs together in the armpits and groin, appears and can persist after the rash is gone

5

Note about the characteristic face rash of scarlet fever

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red cheeks with a characteristic pale area around the mouth (circumoral pallor),

6

What is the primary mediator of scarlet fever?

•Erythrogenic toxin

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7

What is post-streptococcal glomerulonephritis?

A sequelae of GAS caused by nephritogenic strains of GAS that occurs primarily (97% of cases) in regions of the world with poor socioeconomic status and primarily in children aged 2-12 

8

What are the nephritogenic strains of GAS?

pyodermatitis with group A streptococci M protein types 2, 47, 49, 55, 60, and 57 and

throat infection with streptococci M types 1, 2, 4, 3, 12, 25, and 49.

9

What is the believed mechanism of PSGN?

APSGN is believed to be an immune-mediated disease, in which an immune complex containing a streptococcal antigen is deposited in the affected glomeruli.

10

Why is PSGN more common in children than adults?

The size of glomerular basement membrane (GBM) pores and the molecular size of the streptococcus-Ig complex are also important determinants. The molecular size of the streptococcus-Ig complex is about 15 nm (10 nm for streptococcus group A and 5 nm for immunoglobulin). The GBM pore sizes in children and adults are 2-3 nm and 4-4.5 nm, respectively. Therefore, the immune complex molecule can be more easily rodded into the glomerulus in children than in adults and, thus, may explain the increased frequency of APSGN in children compared to that in adults.

11

What are the two suspected antigens from GAS that promote PSGN?

-cationic cysteine protease streptococcal pyrogenic exotoxin B and

-nephritis-associated streptococcal plasmin receptor, which is a plasmin-binding protein with glyceraldehyde phosphate dehydrogenase (also known as presorbing antigen or PA-Ag)

 

These fractions have an affinity for glomeruli and have been shown to induce specific, long-lasting antibody responses in biopsy specimens from patients with APSGN.

12

Which compliment pathway is highly upregulated in PSGN patients? Why?

Alternative pathway - PA-Ag is also known to activate the alternate pathway of the complement cascade. The observation that some patients may only have C3 deposition may relate to this mechanism.

13

Is PSGN more likely to follow pharyngitis or skin related GAS?

skin-impetigo

14

What has to happen before PSGN occurs?

There is almost invariably a previous GAS infection 

15

What is the latency period between GAS infection and PSGN?

A latent period ALWAYS occurs between the streptococcal infection and the onset of signs and symptoms of acute glomerulonephritis. In general, the latent period is 1-2 weeks after a throat infection and 3-6 weeks after a skin infection

16

Note on DDx of PSGN

The onset of signs and symptoms at the same time as pharyngitis (also called synpharyngitic nephritis) is more likely to be immunoglobulin A (IgA) nephropathy rather than APSGN.

17

How does PSGN present?

-Dark urine (brown-, tea-, or cola-colored) is often the first clinical manifestation of APSGN. Caused by hemolysis of red blood cells

-HTN

-Periorbital edema is typical. It is usually prominent upon awakening and, if the patient is active, tends to subside at the end of the day.

-In some cases, generalized edema and other features of circulatory congestion, such as dyspnea, may be present. Edema is a result of a defect in renal excretion of salt and water. The severity of edema is often disproportionate to the degree of renal impairment.

-weakness, fatigue, N/V

18

What is acute rheumatic fever?

a sequela of streptococcal infection—typically following two to three weeks after group A streptococcal pharyngitis—that occurs most commonly in children

19

What causes ARF?

Poststreptococcal acute rheumatic fever is probably caused by antistreptococcal M protein antibodies and T cells that cross-react with cardiac proteins.

20

What are the symptoms of ARF?

Syndeham chorea, carditis, subcutaneous nodules, erythema marginatum, and migratory polyarthritis.

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21

What is the typical first sign of ARF?

The earliest and most common feature is a painful migratory arthritis, which is present in approximately 80% of patients. Large joints such as knees, ankles, elbows, or shoulders are typically affected

22

Erythema marginatum in ARF

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Subcutaneous nodules of ARF

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23

How is ARF treated?

•Treatment:  even though GAS infection was weeks earlier, full course of antibiotic therapy recommended to eradicate any residual GAS.  THEN…

•Prevent strep infections with prophylaxis in patients with history of RF (PCN IM monthly x many years)

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