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Unit 1 ID+LC > ID Small Groups > Flashcards

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
Q

Immune-complex mediated manifestations

A

Olser nodes
- tender purplish raised papules on digits

Roth spots - retinal flame-like hemorrhage on fundoscopy

Glomerulonephritis

26
Q

Organisms most assoc. w/

  1. Acute endocarditis
  2. Subacute endocarditis:
  3. Prosthetic valve endocarditis
A
  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
Q

HACEK group

A

Gram neg bacteria less commonly associated with endocarditis

H: Haemophilus
A: Actinobacillus
C: Cardiobacterium
E: Eikenella
K: Kingella

*candida can also cause endocarditis

28
Q

Duration of tx for IE

A

~4 weeks of bactericidal agents

29
Q

Drugs with good activity against MSSA

A
  1. Dicloxacillin
  2. Amox-clav
    Amox-sulbactam (IV)
  3. Cephalexin

*rest are PO

30
Q

Drugs with activity against MRSA

A

All PO

  1. Clindamycin
  2. TPM-SMX
  3. Doxycycline-minocycline
  4. Linezolid

IV
1. Vancomycin
(glycopeptide)

31
Q

Bactericidal

A

30S:
1. AG (30s)

Peptidoglycan synth:

  1. Vanc
  2. PCN
  3. Cephalosporin

DNA fxn:

  1. FQ
  2. Metronid
  3. Rifampin
32
Q

Bacteriostatic

A
  1. Chloramphenicol
  2. Clindamycin
  3. Linezolid
  4. Macrolides
  5. TCN
  6. Sulfonamides
  7. Trimethoprim
33
Q

Hepatically elim drugs (nonrenal)

A

CCRIMESS

  1. Clindamycin
  2. Chloramphenical
  3. Rifampin
  4. Isoniazid
  5. Metronidazole
  6. Erythromycin
  7. Sulfonamide
  8. Streptogramins
34
Q

Risks for enteric infxn while traveling abroad

A
  1. Eating uncooked, unpeeled vegetables
  2. Fresh salsa (unbottled, open, many hands, uncooked)
  3. ceviche (uncooked fish and vegies)
35
Q

Inflammatory vs Non-inflamm diarrhea

A

Inflammatory:

  • from colon
  • fever
  • fecal WBC/RBC

Non-inflammatory:

  • from upper small bowel
  • no fever
  • no fecal WBC or RBC
36
Q

3 common organisms causing inflamm and non inflamm diarrhea

A

Inflam:

  1. Campylobacter
  2. Salmonella/ Shigella
  3. EHEC

Non-Inflam:

  1. ETEC
  2. Norovirus
  3. Rotavirus
    - others: Giardia, Cryptosporidium, Vibrio cholera
37
Q

Single most important and effective intervention for controlling the morbidity and mortality of diarrheal illness in children and adults in U.S and worldwide

A

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
Q

Diarrhea

A

3/M loose or watery stools lasting >24 hours

39
Q

Most highly recommended ab to treat travelers diarrhea

A

FQ (Cipro)
- target DNA topo

Macrolide
- azithro: targets 50S

Rifaximin (rifampin analog)

40
Q

Common etiologies of viral gastroenteritis in childhood

A
  1. Rotavirus
  2. Caliciviruses (norovirus, sapovirus)
  3. Enteric adenovirus

*Gastroenteritis (presence of both vomiting and diarrhea)

41
Q

Tx of viral gastroenteritis

A

Oral rehydration

  • water, glucose, sodium
42
Q

Strategies for prevention of viral gastroenteritis

A

Derp stuff

Rotavirus: 2 types of vaccines
- do not give after 12 weeks of age

43
Q

Viral vs bacterial etiology of gastroenteritis

A

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
Q

Enterotoxin prod by rotavirus

A

NSP4: alters epithelial cell fxn and permeability contributing to secretory diarrha

45
Q

FQs and their elimination

A
  1. Ciprofloxacin
  2. Levofloxacin

Renally eliminated

can cause tendon rupture, prolonged QT, or arthropathy

46
Q

Organisms most responsible for:

  1. Cystitis:
  2. Urethritis:
  3. Cervicitis:
  4. Vaginitis:
A
  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
Q

First line tx for uncomplicated cystitis

- what if they are pregnant?

A

TMP-SMX

**Nitrofurantoin or Fosfomycin for pregnancy

48
Q

First line tx for complicated cystitis

A

FQ - cipro/levo

bactericidal
Can cover GNR and some GP

49
Q

First line tx for uncomplicated and complicated pyeloneph

A

uncomp: FQ
comp: Empiric broad spec. 3rd gen Ceph, FQ

50
Q

The majority of young sexually active pts who have genital ulcers have:

A
  1. Genital herpes (HSV)
  2. Syphilis
  3. Chancroid (H. ducreyi)
  4. LGV (C. trachomatis)
51
Q

How is acyclovir effective against HSV?

A

acyclovir is selectively PHOSPHORYLATED by HSV infected cells to acyclovir monophosphate

Unit 1 ID+LC (32 decks)

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