Module 3 Complex ID and Immune Response Flashcards
Redness that does NOT blanch, swelling, warmth, TENDERNESS, may be purulent, lymphangitis → appears like lymph streaking (advanced cases), may be raised in abscess formation or erysipelas (superficial skin infection), can also have constitutional sx
Typically a larger affected area
Classic Cellulitis
Redness that does NOT blanch, swelling, warmth, TENDERNESS
Classic Cellulitis
Skin discoloration from excess Ca; more brown like venous stasis
Calciphylaxis
Skin redness from venous stasis
Stasis Dermatitis
Where is DVT typically seen?
calf
ecchymosis, palpable hematoma, hx trauma
Hematoma
central erythema, not tender or warm, hx tick bite?
Erythema migrans
erythematous, edematous JOINT that is painful, circumferential erythema typical
Septic Knee
point tenderness, over MTP, erythema (can be hard to differentiate)
Gout
fluctuant mass where bursa is filled with fluid; NOT tender or warm; should have good ROM of elbow
Olecranon Bursitis
Tx for mild non-purulent cellulitis
Oral abx: Cephalexin, Dicloxacillin, Penicillin VK, Amoxi/Clav.
if true pcn allergy= clindamycin
Tx for moderate non-purulent cellulitis : SIRS 1
Oral abx: Cephalexin, Dicloxacillin, Penicillin VK, Amoxi/Clav.
if true pcn allergy= clindamycin
SIRS criteria for cellulitis
temp >38C (100.4), HR >90, RR >20, WBC >12
Tx for moderate non-purulent cellulitis : SIRS > or = 2 (treatment failure)
IV antibiotics: Cefazolin, Ceftriaxone, penicillin G,
If PCN allergy= Clindamycin
Tx for severe non-purulent cellulitis: SIRS > or + 2 (w/ hypotension, immune compromise, or rapid disease progression)
Broad coverage IV antibiotics
- Vanc + piperacillin/ tazobactam, imipenem, or meropenem
consider surgical assessment
Tx for severe non-purulent cellulitis: probable S pyogenes infection and/ or suspected MSSA
Iv:
Cefazolin, Cefotaxime, Cefriaxone, PCN G,
If allergy- Clindamycin
Tx for severe non-purulent cellulitis: suspected or known MRSA (previous tx failure)
IV: Vanc, CLina, Linexolia, daptomycin, ceftaroline…
Tx for severe non-purulent cellulitis: suspected or known MRSA (previous tx failure)
IV: Vanc, CLina, Linexolia, daptomycin, ceftaroline…
what are most likely pathogens for cellulitis
Group A Strep and Staph Aureus
I&D indications for purulent cellulitis
fluctuance, drainage, tx failure
Abscess I&D 1st line tx
Consult surgery based on site and severity
small abscesses <1cm can be observed and tx with abx and warm compresses
treating purulent MSSA
Cephalexin, Dicloxacillin, PCN, Aug; PCN allergy- clindamycin
treating purulent MRSA
Bactrim, doxycycline, minocycline
When to refer cellulitis to ED/Hospitalization
Predictors of outpt tx failure
fever , chronic ulcers, chronic edema/lymphedema, prior cellulitis of same site, cellulitis at wound site
Greater than or equal to 2 SIRS criteria, immunocompromised, rapid dx progression
Life-threatening (drug related or mycoplasma pneumonia) detachment of the epidermis from the dermis that manifests on the skin as blisters and erosions
develops w/in 8 weeks of drug initiation. Fever, oral and ocular symptoms often precede cutaneous reaction by several days. Malaise, sore throat, arthralgias, and stinging eyes.
SJS/TEN
Central and facial dermatitis begins and spreads peripherally
SJS/TEN
Skin tender to touch and shears easily
(Nikolsky sign)
SJS/TEN
Dx and Tx of SJS/TEN
clinical presentation. Skin punch biopsy shows dermal inflammation and epidermal necrosis
Tx: admission to burn unit for skin care and hemodynamic support
DRESS
drug reaction with eosinophilia and systemic symptoms
Dermatologic and systemic manifestations develop 2-8 weeks after drug exposure. a/w reactivation of herpes virus-6
Anticonvulsants, allopurinol, dapsone, and sulfonamides
-Facial edema** , fever, malaise, lymphadenopathy, and arthralgia. Eosinophilia and leukocytosis.
DRESS (drug reaction with eosinophilia and systemic symptoms)
TX for DRESS (drug reaction with eosinophilia and systemic symptoms)
hospitalization, topical and systemic corticosteroids. Relapse may occur without reexposure which makes identifying offending medication difficult.
dark colored urine and clay-colored stools may precede presentation of jaundice by 1-5 days. Hepatomegaly and splenomegaly. ½ pts are asymptomatic
Hepatitis
Hepatitis diagnostics labs
CBC LFTs (↑AST & ALT are often first sign) total bilirubin prolonged PT if severe (marker of prognosis) low PLT and albumin if cirrhosis
fecal-oral route, blood, person-person contact, ingestion of contaminated food (shellfish) and water. Can survive for months in fresh or salt water
Most infectious in the late incubation period. Contagious when asymptomatic and until 1 week after jaundice occurs. Newborns are infectious for months.
Hep A
Incubation, Vaccination and Inactivation of Hep A
Incubation: 2-6 weeks. Viral load peaks at 2 weeks. Vaccination: 2 injections 6-12 months apart; provides immunity for 20 years
Inactivated by: boiling for 1 minute, exposure to formaldehyde, chlorine, or UV rays
sexual contact and IV drug use
Blood, tears, CSF, breast milk, saliva, vaginal secretions, and seminal fluid
Asia and Africa: vertical transmission from mother during birth
Viral load peaks at 7-8 weeks
asymptomatic or liver failure. Ongoing replication leads to cirrhosis, HCC, or both.
Hep B
Vaccinations for Hep B
at birth, then in 1-2 months, then 12 months (3-dose series)
HBsAg-positive, anti-HBc-positive IgM, anti-Hbc negative, and anti-HBS-negative
Chronic Hep B
causes cirrhosis, hepatocellular carcinoma, and liver transplantation. USPSTF: 1 time screening for all adults born b/t 1945-1965
: blood-borne (IV drug use)
High rate of replication and mutation. Difficult to treat and leads to chronic disease.
RF: blood transfusion received before July 1992, chronic hemodialysis, IV drug use, tattoos, manicures/pedicures, body piercings.
Hep C
Dx and Tx Hep C?
Diag: if HCV Ab present, test using PCR
Tx: specialist if chronic. Tx often cost prohibitive
Stop drinking, vax (A and B), adherence to tx regimen
Vasculitis occurring in children 6 wks - 12yrs; peak at 1-2 y/o; etiology unclear
If untreated → coronary artery abnormalities
Kawasaki Disease (KD)