ID Small Groups Flashcards

1
Q

3 Identities In dx of a tender red leg

A
  1. Noninfectious
    - DVT
    - Venous insuff
    - Fracture
    - Ruptured bakers cyst
  2. Infectious - cellulitis
  3. Infectious -
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2
Q

4 Cardinal sz of soft tissue infection

cardinal findings of inflammation

A
  1. Rubor - Redness
  2. Dolor - Pain
  3. Calor - Heat
  4. Tumor - Swelling

*bonus: functio laesa

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3
Q

Two most common pathogens that cause cellulitis

A
  1. S. pyogenes (GAS)
    - cellulitis is assoc. with more rapidly spreading, diffuse process w. lymphangitis and fever
  2. S. aureus (MRSA)
    - Cellulitis caused by MSSA or MRSA is usually associated with a focal infection, such as a furuncle, a carbuncle, a surgical wound, or an abscess.
  3. less often GBS
    - elderly patients and those with diabetes mellitus or peripheral vascular disease
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4
Q

Level of skin involvement for:

  1. Erysipelas
  2. Cellulitis
  3. Abcess
  4. Necrotizing Fasciitis
A
  1. Erysipelas
  2. Cellulitis
  3. Abcess
  4. Necrotizing Fasciitis
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5
Q

Erysipelas

A

Infectious

  1. NOT commonly seen in lower extremities (face)
  2. Sharply demarcated borders
    (cellulitis is irregular)
  3. Infects Superficial Dermal Papillae
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6
Q

Cellulitis

A

Infectious

  1. Cardinal signs of inflammation
  2. Irregular border
    (erysipelas is sharp, Nec Fasc is poorly defined)
  3. Fever +leukocytosis
  4. Unilateral
  5. Infects the dermal + Subcutaneous layer (where capillary vessels are)
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7
Q

Nectrotizing fasciitis

  • layer affected
  • Organism
  • borders
A
  1. Affects subcutaneous tissue along the surface of the connective tissue that covers muscle (fascia)
    - S. pyogenes (GAS)
  • Poorly defined erythema
    (erysip is sharp)
  • PAIN IS OUT OF PROPORTION TO EXAM due to deep tissue involvement
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8
Q

Is cellulitis almost always unilateral or bilateral?

A

Unilateral

venous insuff is often bilateral

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9
Q

How does uncontrolled diabetes mellitus interfere with treatment for bacterial infxns?

A
  1. DM interferes with neutrophil fxn
  2. Infection causes inflammation –> TNF-a –> insulin resistance and worsens diabetes control
    - Catecholamines
    - TNF
    - IL-6
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10
Q

Is culturing effective for cellulitis?

A

Yield of cultures is very low in cellulitis.
- if you get center of lesion –> 20% +
(meaning very low #bacteria cause cellulitis)

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11
Q

Treatment for MRSA (find out bc they are resistant to cephalosporin - cephalexin)

A

TMP - SMX

Bactrim

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12
Q

Which layer of skin is affected in:

  1. Erysipelas
  2. Cellulitis
  3. Nec Fasc
  4. Myositis
A
  1. Erysipelas
    - Superficial Dermal layer
  2. Cellulitis
    - Dermal + subcutaneous layer
  3. Nec Fasc
    - Subcutaneous layer along fascia of muscle (pain out of proportion)
  4. Myositis
    - Muscle
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13
Q

Clinical manifestations of Nec Fasc

A

PAIN IS OUT OF PROPORTION TO EXAM

  • due to deep tissue involvement
  • thrombosis of small vessels and destruction of superficial nerves

Initially extremely painful –> anaesthesia with nerve dmg

Elevated creatinine kinase

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14
Q

2 types of Nec Fasc and organisms involved

A
  1. Type I: caused by mixed bacterial infxns
    (often including anaerobes)
    - typically in pts with risk factors: sx, DM, periph vascular disease
  2. Type II: monomicrobial and can occur in any age group w/o any medical comorbidities
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15
Q

Gold std for dx Nec Fasc

A

Open surgical inspection, with debridement as indicated: best way to determine the extent and severity of infection and to obtain material for Gram’s staining and culture.

High mortality so surgical debridement/biopsy should not be delayed
- or CT + MRI to view subcu and fascial edema

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16
Q

Importance of type of treatment for Nec Fasc

A

Empiric IV then surgery
1. Clindamycin + Amp-Sulbactam:
cover broad spectrum of org in Type I
- Clinda suppress toxin (50S) and facilitate phagocytosis of S. pyogenes by inhib M protein

  1. Amp-Sulbactam:
    If Type II and GAS alone is cause

Surgery - thrombosis of small vessels of skin prevents antimicrobials from reaching site of infxn

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17
Q

Fast acuity and fast progression of pain and systemic toxicity in unilateral limb should alert you to?

A

Nec Fasc

  • systemic: tachy, hypotensive, hyperthermic
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18
Q

Does Nec Fasc commonly have an obvious portal of entry?

A

No - 50%

  • trauma site
  • sx
  • peri-rectal abcesses
  • decubitus ulcer/intestinal perforation
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19
Q

Sz + sx of Endocarditis

A

Any febrile syndrome where there is evidence of >1 organ system involved

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20
Q

Pre-existing cardiac lesions that predisposed Endocarditis

A

Heart murmur in 90% of cases:

Valvular lesions that lead to Hi P gradients can result in:

  1. turbulent, non-laminar bf
  2. Endothelial trauma
  3. Fibrin-platelet dep.

organisms liek strep can produce extracellular polysacc dextrans that can adher to fibrin-platelet thrombi on damaged heart valves –> vegetation

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21
Q

Attachment of bacterial species to endocardial structures

A

organisms liek strep can produce extracellular polysacc dextrans that can adher to fibrin-platelet thrombi on damaged heart valves –> vegetation

Prosthetic valve endocarditis
- Coag neg staph (S. epidermidis)

22
Q

Local destruction of endocardial structures

Local effect of IE on integrity of heart valves and surrounding cardiac tissue.

A
  1. valvular insufficiency
  2. CHF
  3. Myocardial and valve ring abcesses
  4. Pericarditis
  5. Conduction system disturbances
23
Q

Embolization

A

Emboli can be release from the valve vegetation to any organ –>

  1. embolic stroke
  2. MI
  3. Renal infarct
  4. Retinal hemorrhage from left-sided valves (mitral/aortic)
  5. Pulmonary emboli from right-sided valves (tricuspid)
24
Q

Systemic signs-fever, malaise

A

Bacteremia: cytokine mediated

  • sepsis: chills, fever, sweats, cachexia
  • Fatigue, weight loss, anemia may accompany IE
25
Immune-complex mediated manifestations
Olser nodes - tender purplish raised papules on digits Roth spots - retinal flame-like hemorrhage on fundoscopy Glomerulonephritis
26
Organisms most assoc. w/ 1. Acute endocarditis 2. Subacute endocarditis: 3. Prosthetic valve endocarditis
1. Acute endocarditis - S. aureus: fibronectin-binding protein that can invade intact endo 2. Subacute endocarditis - S. viridans - S. bovis - E. faecalis : can produce extracellular polysacc dextran to adhere to fibrin-platelet thrombi on dmged heart valves 3. Prosthetic valve endocarditis - Coag neg staph (S. epidermidis)
27
HACEK group
Gram neg bacteria less commonly associated with endocarditis ``` H: Haemophilus A: Actinobacillus C: Cardiobacterium E: Eikenella K: Kingella ``` *candida can also cause endocarditis
28
Duration of tx for IE
~4 weeks of bactericidal agents
29
Drugs with good activity against MSSA
1. Dicloxacillin 2. Amox-clav Amox-sulbactam (IV) 3. Cephalexin *rest are PO
30
Drugs with activity against MRSA
All PO 1. Clindamycin 2. TPM-SMX 3. Doxycycline-minocycline 4. Linezolid IV 1. Vancomycin (glycopeptide)
31
Bactericidal
30S: 1. AG (30s) Peptidoglycan synth: 2. Vanc 3. PCN 4. Cephalosporin DNA fxn: 5. FQ 6. Metronid 7. Rifampin
32
Bacteriostatic
1. Chloramphenicol 2. Clindamycin 3. Linezolid 4. Macrolides 5. TCN 6. Sulfonamides 7. Trimethoprim
33
Hepatically elim drugs (nonrenal)
CCRIMESS 1. Clindamycin 2. Chloramphenical 3. Rifampin 4. Isoniazid 5. Metronidazole 6. Erythromycin 7. Sulfonamide 8. Streptogramins
34
Risks for enteric infxn while traveling abroad
1. Eating uncooked, unpeeled vegetables 2. Fresh salsa (unbottled, open, many hands, uncooked) 3. ceviche (uncooked fish and vegies)
35
Inflammatory vs Non-inflamm diarrhea
Inflammatory: - from colon - fever - fecal WBC/RBC Non-inflammatory: - from upper small bowel - no fever - no fecal WBC or RBC
36
3 common organisms causing inflamm and non inflamm diarrhea
Inflam: 1. Campylobacter 2. Salmonella/ Shigella 3. EHEC Non-Inflam: 1. ETEC 2. Norovirus 3. Rotavirus - others: Giardia, Cryptosporidium, Vibrio cholera
37
Single most important and effective intervention for controlling the morbidity and mortality of diarrheal illness in children and adults in U.S and worldwide
Rotavirus: 5% of all gastroenteritis in children ... but MOST COMMON CAUSE OF SEVERE GE IN INFANTS AND YOUNG CHILDREN Primary MOT is F-O route: highly contagious
38
Diarrhea
3/M loose or watery stools lasting >24 hours
39
Most highly recommended ab to treat travelers diarrhea
FQ (Cipro) - target DNA topo Macrolide - azithro: targets 50S Rifaximin (rifampin analog)
40
Common etiologies of viral gastroenteritis in childhood
1. Rotavirus 2. Caliciviruses (norovirus, sapovirus) 3. Enteric adenovirus *Gastroenteritis (presence of both vomiting and diarrhea)
41
Tx of viral gastroenteritis
Oral rehydration - water, glucose, sodium
42
Strategies for prevention of viral gastroenteritis
Derp stuff Rotavirus: 2 types of vaccines - do not give after 12 weeks of age
43
Viral vs bacterial etiology of gastroenteritis
Viral: 80% of diarrhea in children - no mucous/blood Bacterial: less common - blood/mucous in stool - fever *but 1/3 of rotavirus will have fever
44
Enterotoxin prod by rotavirus
NSP4: alters epithelial cell fxn and permeability contributing to secretory diarrha
45
FQs and their elimination
1. Ciprofloxacin 2. Levofloxacin Renally eliminated can cause tendon rupture, prolonged QT, or arthropathy
46
Organisms most responsible for: 1. Cystitis: 2. Urethritis: 3. Cervicitis: 4. Vaginitis:
1. Cystitis: - E. coli - S. Sapro 2. Urethritis: - N. gonorrhoeae - C. trachomatis - HSV 3. Cervicitis: - N. gonorrhoeae - C. trachomatis 4. Vaginitis: - Candida - Trichomonas vaginalis
47
First line tx for uncomplicated cystitis | - what if they are pregnant?
TMP-SMX **Nitrofurantoin or Fosfomycin for pregnancy
48
First line tx for complicated cystitis
FQ - cipro/levo bactericidal Can cover GNR and some GP
49
First line tx for uncomplicated and complicated pyeloneph
uncomp: FQ comp: Empiric broad spec. 3rd gen Ceph, FQ
50
The majority of young sexually active pts who have genital ulcers have:
1. Genital herpes (HSV) 2. Syphilis 3. Chancroid (H. ducreyi) 4. LGV (C. trachomatis)
51
How is acyclovir effective against HSV?
acyclovir is selectively PHOSPHORYLATED by HSV infected cells to acyclovir monophosphate