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Microbiology > Micro, USMLE Part 2 > Flashcards

Micro, USMLE Part 2 Flashcards

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1
Q

Levels as HIV infxn progresses: CD4+ lymphocytes? Anti-p24 Abs? Anti-gp120 Abs? Virus, p24 Ag?

A

CD4+ T-cells have an early dip, stabilize, and fall during stages 3-4 (years after infxn) Anti-p24 and Anti-gp120 Abs rise starting ~1 mo. post-infxn, stabilize @ 3 mos (at end of acute infxn). Virus, p24 Ag: spike early (w/ start of acute Sx’s), drop to low level until stages 3-4 (years later), when they take off

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2
Q

Organ system affected in AIDS: Brain (what is the infxn/dz associated?)

A

Infxn/dz associated w/ AIDS: Crytococcal meningitis Toxoplasmosis CMV encephalopathy AIDS dementia PML (JC virus)

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3
Q

Organ system affected in AIDS: Eyes (what is the infxn/dz associated?)

A

Infxn/dz associated w/ AIDS: CMV retinitis

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4
Q

Organ system affected in AIDS: Mouth and throat (what is the infxn/dz associated?)

A

Infxn/dz associated w/ AIDS: Thrush (Candida albicans) HSV CMV Oral hairy leukoplakia (EBV)

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5
Q

Organ system affected in AIDS: Lungs (what is the infxn/dz associated?)

A

Infxn/dz associated w/ AIDS: Pneumocystis jiroveci pneumonia (PJP) TB histoplasmosis

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6
Q

Organ system affected in AIDS: GI (what is the infxn/dz associated?)

A

Infxn/dz associated w/ AIDS: Cryptosporidiosis Mycobacterium avium-intracellulare complex CMV colitis Non-Hodgkin’s lymphoma (EBV) Isopora belli

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7
Q

Organ system affected in AIDS: Skin (what is the infxn/dz associated?)

A

Infxn/dz associated w/ AIDS: Shingles (VZV) Kaposi’s sarcoma (HHV-8)

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8
Q

Organ system affected in AIDS: Genitals (what is the infxn/dz associated?)

A

Infxn/dz associated w/ AIDS: Genital herpes warts cervical cancer (HPV)

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9
Q

HIV-assicated infxns that increase in risk at CD4+ count:

A

Infxn: Oral thrush Tinea pedis (athlete’s foot) Reactivation VZV Reactivation tuberculosis Other bacterial infxns (e.g., H. influenzae, S. pneumoniae, Salmonella)

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10
Q

HIV-assicated infxns that increase in risk at CD4+ count:

A

Infxn: Reactivation HSV cryptosporidosis Isopora Disseminated coccidioidomycosis Pneumocystis pneumonia

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11
Q

HIV-assicated infxns that increase in risk at CD4+ count:

A

Infxn: Candidal esophagitis Toxoplamosis histoplasmosis

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12
Q

HIV-assicated infxns that increase in risk at CD4+ count:

A

Infxn: CMV retinitis and esophagitis Disseminated M. avium-intracellulare Cryptococcal meningitis

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13
Q

Neoplasms associated w/ HIV

A

Kaposi’s sarcoma (HHV-8) Invasive cervical carcinoma (HPV) Primary CNS lymphoma non-Hodgkin’s lymphoma

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14
Q

HIV encephalitis

A

Occurs late in the course of HIV infxn. Virus gains CNS access via infected Macrophages. Microglial nodules w/ multinucleated giant cells.

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15
Q

Prions What are they? What dz’s do they cause? Normal vs. pathologic prions?

A

Infectious agents that do not contain RNA or DNA (consist only of proteins); encoded by cellular genes. Dz’s: Creutzfeldt-Jakob dz (CJD – rapidly progressive dementia), kuru, srapie (sheep), mad cow dz Associated w/ spongiform encephalopathy . Normal prions have alpha-helix conformation; pathologic prions (like CJD) are beta-pleated sheets. Pathologic conformation accumulates b/c it is resistant to proteinase digestion.

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16
Q

Dominant normal flora of the: Skin

A

Staphylococcus epidermis

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17
Q

Dominant normal flora of the: Nose

A

S. epidermis; colonized by S. aureus

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18
Q

Dominant normal flora of the: Oropharynx

A

Viridans group streptococci

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19
Q

Dominant normal flora of the: Dental plaque

A

Streptococcus mutans

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20
Q

Dominant normal flora of the: Colon

A

Bacteroides fragilis > E. coli

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21
Q

Dominant normal flora of the: Vagina

A

Lactobacillus, colonized by E. coli and GBS

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22
Q

Neonates and normal flora

A

Neonates delivered by cesarean section havve no flora, but are rapidly colonized after birth.

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23
Q

Food poisoning from: Vibrio parahemolyticus and V. vulnificus

A

Food: Contaminated seafood (V. vulnificus can also cause wound infxn from contact w/ contaminated water or shellfish)

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24
Q

Food poisoning from: Bacillus cereus

A

Food: reheated rice. (Food poisoning from reheated rice? Be Serious! [B. cereus])

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25
Q

Food poisoning from: S. aureus

A

Food: Meats, mayonnaise, custard (pre-formed toxin)

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26
Q

Food poisoning from: Clostridium perfringens

A

Food: reheated meat dishes

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27
Q

Food poisoning from: Clostridium botulinum

A

Food: improperly canned foods (bulging cans)

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28
Q

Food poisoning from: E. coli O157:H7

A

Food: Undercooked meat

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29
Q

Food poisoning from: Salmonella

A

Food: poultry, meat, and eggs.

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30
Q

What are two bacteria that cause a food poisoning that starts quickly and ends quickly?

A

S. aureus and B. cereus

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31
Q

Bugs that cause diarrhea: Campylobacter Type of diarrhea? Findings?

A

Bloody diarrhea. Comma- or S-shaped organisms; growth at 42C; Oxidase (+) [bugs that cause diarrhea: type of diarrhea and findings]

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32
Q

Bloody diarrhea. Comma- or S-shaped organisms; growth at 42C; Oxidase (+) [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Campylobacter

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33
Q

Bugs that cause diarrhea: Salmonella Type of diarrhea? Findings?

A

bloody diarrhea. Lactose (-); Flagellar motility [bugs that cause diarrhea: type of diarrhea and findings]

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34
Q

bloody diarrhea. Lactose (-); Flagellar motility [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Salmonella

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35
Q

Bugs that cause diarrhea: Shigella Type of diarrhea? Findings?

A

Bloody diarrhea Lactose (-) Very low ID50 Produces Shiga toxin [bugs that cause diarrhea: type of diarrhea and findings]

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36
Q

Bloody diarrhea Lactose (-) Very low ID50 Produces Shiga toxin [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Shigella

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37
Q

Bugs that cause diarrhea: Enterohemorrhagic E. coli (EHEC) Type of diarrhea? Findings?

A

Bloody diarrhea O157:H7 Can cause HUS Makes Shiga-like toxin [bugs that cause diarrhea: type of diarrhea and findings]

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38
Q

Bloody diarrhea O157:H7 Can cause HUS Makes Shiga-like toxin [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Enterohemorrhagic E. coli (EHEC)

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39
Q

Bugs that cause diarrhea: Enteroinvasive E. coli (EIEC) Type of diarrhea? Findings?

A

Bloody diarrhea. Invades colonic mucosa. [bugs that cause diarrhea: type of diarrhea and findings]

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40
Q

Bloody diarrhea. Invades colonic mucosa. [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Enteroinvasive E. coli (EIEC)

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41
Q

Bugs that cause diarrhea: Yersinia enterocolitica Type of diarrhea? Findings?

A

Bloody diarrhea Day-care outbreaks Pseudoappendicitis [bugs that cause diarrhea: type of diarrhea and findings]

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42
Q

Bloody diarrhea Day-care outbreaks Pseudoappendicitis [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Yersinia enterocolitica

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43
Q

Bugs that cause diarrhea: C. difficile Type of diarrhea? Findings?

A

Can cause both watery and bloody diarrhea. Pseudomembranous colitis. [bugs that cause diarrhea: type of diarrhea and findings]

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44
Q

Can cause both watery and bloody diarrhea. Pseudomembranous colitis. [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: C. difficile

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45
Q

Bugs that cause diarrhea: Entamoeba histolytica Type of diarrhea? Findings?

A

Bloody diarrhea. Protozoan. [bugs that cause diarrhea: type of diarrhea and findings]

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46
Q

Bloody diarrhea. Protozoan. [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Entamoeba histolytica

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47
Q

Bugs that cause diarrhea: Enterotoxigenic E. coli (ETEC) Type of diarrhea? Findings?

A

Watery diarrhea. Traveler’s diarrhea Produces ST and LT toxins [bugs that cause diarrhea: type of diarrhea and findings]

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48
Q

Watery diarrhea. Traveler’s diarrhea Produces ST and LT toxins [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Enterotoxigenic E. coli (ETEC)

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49
Q

Bugs that cause diarrhea: Vibrio cholerae Type of diarrhea? Findings?

A

Watery diarrhea. Comma-shaped organisms Rice-water diarrhea. [bugs that cause diarrhea: type of diarrhea and findings]

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50
Q

Watery diarrhea. Comma-shaped organisms Rice-water diarrhea. [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Vibrio cholerae

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51
Q

Bugs that cause diarrhea: C. perfringens Type of diarrhea? Findings?

A

Watery diarrhea. Also causes gas gangrene. [bugs that cause diarrhea: type of diarrhea and findings]

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52
Q

Watery diarrhea. Also causes gas gangrene. [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: C. perfringens

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53
Q

Bugs that cause diarrhea: Protozoa Type of diarrhea? Findings?

A

Watery diarrhea Giardia, Cryptosporidium (in immunocompromised) [bugs that cause diarrhea: type of diarrhea and findings]

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54
Q

Watery diarrhea Giardia, Cryptosporidium (in immunocompromised) [bugs that cause diarrhea: type of diarrhea and findings]

A

Bugs that cause diarrhea: Protozoa

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55
Q

Bugs that cause diarrhea: Viruses Type of diarrhea? Findings?

A

Watery diarrhea. Rotavirus, adenovirus, Norwalk virus (norovirus). [bugs that cause diarrhea: type of diarrhea and findings]

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56
Q

Common causes of pneumonia in neonates (

A

Group B streptococci E. coli

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57
Q

Common causes of pneumonia in children (4wks - 18yrs)

A

Viruses (R SV) M ycoplasma C hlamydia pneumoniae S treptococcus pneumoniae (R unts M ay C ough S putum)

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58
Q

Common causes of pneumonia in adults (18-40yrs)

A

Mycoplasma Chlamydia pneumoniae Streptococcus pneumoniae

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59
Q

Common causes of pneumonia in Adults (40-65yrs)

A

Streptococcus pneumoniae H. influenzae Anaerobes Viruses Mycoplasma

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60
Q

Common causes of pneumonia in the elderly (>65)

A

Streptococcus pneumoniae Viruses Anaerobes H. influenzae Gram (-) rods

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61
Q

Common causes of nosocomial (hospital-acquired) pneumonia

A

Staphylococcus Enteric Gram (-) rods

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62
Q

Common causes of pneumonia in the immunocompromised

A

Staphylococcus Enteric Gram (-) rods Fungi Viruses Pneumocystis jiroveci (w/ HIV)

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63
Q

Common cause of pneumonia w/ aspiration

A

Anaerobes

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64
Q

Common cause of pneumonia in alcoholics/IV drug users

A

Streptococcus pneumoniae Klebsiella Staphylococcus

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65
Q

Common causes of pneumonia in CF

A

Pseudomonas

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66
Q

Common causes of post-viral pneumonia

A

Staphylococcus H. influenzae

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67
Q

Common causes of atypical pneumonia

A

Mycoplasma Legionella Chlamydia

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68
Q

Common causes of meningitis in newborn (0-6 months

A

Group B streptococci E. coli Listeria

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69
Q

Common causes of meningitis in children (6mos - 6yrs)

A

Streptococcus pneumoniae Neisseria meningitidis Haemophilus influenzae type B Enteroviruses

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70
Q

Common causes of meningitis (6-60yrs)

A

N. miningitidis Enteroviruses S. pneumoniae HSV

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71
Q

Common causes of meningitis in 60+ year-olds

A

Streptococcus pneumoniae Gram (-) rods Listeria

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72
Q

Viral causes of meningitis

A

Enteroviruses (esp. coxsackievirus) HSV HIV West Nile virus VZV

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73
Q

Common causes of meningitis in HIV

A

Cryptococcus CMV Toxoplasmosis (brain abscess) JC virus (PML)

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74
Q

Incidence of H. influenzae meningitis?

A

Has decreased greatly w/ introduction of H. influenzae vaccine in last 10-15 years.

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75
Q

CSF findings in meningitis: Bacterial [Pressure? Cell type? Protein? Sugars?]

A

Increased pressure Increased PMNs Increased protein Decreased sugar

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76
Q

Increased pressure Increased PMNs Increased protein Decreased sugar [CSF findings in meningitis – what is the bug?]

A

Bacterial

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77
Q

CSF findings in meningitis: Fungal/TB [Pressure? Cell type? Protein? Sugars?]

A

Increased pressure Increased lymphocytes Increased proein Decreased sugar

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78
Q

Increased pressure Increased lymphocytes Increased proein Decreased sugar [CSF findings in meningitis – what is the bug?]

A

Fungal/TB

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79
Q

CSF findings in meningitis: Viral [Pressure? Cell type? Protein? Sugars?]

A

Normal/increased pressure Increased lymphocytes Normal/increased protein Normal sugar

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80
Q

Normal/increased pressure Increased lymphocytes Normal/increased protein Normal sugar [CSF findings in meningitis – what is the bug?]

A

Viral

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81
Q

Osteomyelitis in most ppl is due to…? Who gets most osteomyelitis?

A

Staph aureus in most ppl. Most osteomyelitis occurs in children.

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82
Q

Elevated CRP and ESR in osteomyelitis?

A

Classic findings, but nonspecific

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83
Q

Osteomyelitis in sexually active pt

A

Neisseria gonorrhoeae (rare) Septic arthritis more common

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84
Q

Osteomyelitis in diabetics and drug addicts

A

Pseudomonas aeruginosa

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85
Q

Osteomyelitis in Sickle cell

A

Salmonella

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86
Q

Osteomyelitis in prosthetic replacement

A

S. aureus and S. epidermis

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87
Q

Osteomyelitis in vertebra

A

Mycobacterium tuberculosis (Pott’s dz)

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88
Q

Osteomyelitis with cat and dog bites/scratches

A

Pasteurella multocida

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89
Q

3 Most common causes of ambulatory UTI

A

1.) E. coli (50-80%) 2.) Staphylococcus saprophyticus (10-30%): 2nd most common cause of UTI in young, sexually active, ambulatory women 3.) Klebsiella (8-10%)

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90
Q

Common causes of UTI in a hospital setting

A

E. coli Proteus Klebsiella Serratia Pseudomonas

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91
Q

Gender and epidemiology of UTIs

A

10:1 women to men (b/c of short urethra colonized by fecal flora)

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92
Q

Predisposing factors to UTIs

A

Flow obstruction Kidney surgery Catheterization Gynecologic abnormalities Diabetes Pregnancy

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93
Q

Mechanisms of UTI infxn

A

Mostly caused by ascending infxns. In males: babies w/ congenital defects, elderly w/ enlarged prostates

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94
Q

Sx of UTI

A

Dysuria Frequency Urgency Suprapubic pain

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95
Q

Sx of Pyelonephritis

A

Fever Chills Flank pain CVA tenderness (costovertebral angle – tender above kidneys on back)

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96
Q

UTI bugs: Serratia maracescens Features?

A

Some strains produce a red pigment; often nosocomial and drug-resistant.

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97
Q

Features: Some strains produce a red pigment; often nosocomial and drug-resistant. Which UTI bug is this?

A

Serratia maracescens

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98
Q

UTI bugs: Staphylococcus saprophyticus Features?

A

2nd leading cause of community-acquired UTI in sexually active women.

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99
Q

Features: 2nd leading cause of community-acquired UTI in sexually active women. Which UTI bug is this?

A

Staphylococcus saprophyticus

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100
Q

UTI bugs: Escherichia coli Features?

A

Leading cause of UTI. Colonies show metallic sheen on EMB agar.

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101
Q

Features: Leading cause of UTI. Colonies show metallic sheen on EMB agar. Which UTI bug is this?

A

Escherichia coli

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102
Q

UTI bugs: Enterobacter cloacae Features?

A

Often nosocomial and drug resistant.

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103
Q

Features: Often nosocomial and drug resistant. Which UTI bug is this?

A

Enterobacter cloacae

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104
Q

UTI bugs: Klebsiella pneumoniae Features?

A

Large mucoid capsule and viscous colonies

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105
Q

Features: Large mucoid capsule and viscous colonies Which UTI bug is this?

A

Klebsiella pneumoniae

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106
Q

UTI bugs: Proteus mirabilis Features?

A

Motility cuases swarming on agar. Produces urease; associated w/ struvite stones.

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107
Q

Features: Motility cuases swarming on agar. Produces urease; associated w/ struvite stones. Which UTI bug is this?

A

Proteus mirabilis

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108
Q

UTI bugs: Pseudomonas aeruginosa Features?

A

Blue-green pigment and fuity odor. Usually nosocomial and drug-resistant.

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109
Q

Features: Blue-green pigment and fuity odor. Usually nosocomial and drug-resistant. Which UTI bug is this?

A

Pseudomonas aeruginosa

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110
Q

List of UTI bugs

A

SSEEK PP S erratia marcescens S taphylococcus saprophyticus E scherichia coli E nterobacter cloacae K lebsiella pneumoniae P roteus mirabilis P seudomonas aeruginosa

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111
Q

Diagnostic markers of UTI

A

Leukocyte esterase: (+) = bacterial Nitrite test: (+) = Gram(-) organism

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112
Q

ToRCHeS infxns What are they? List?

A

These important infxns are transmitted in utero or during vaginal birth: T oxoplasma gondii o R ubella C MV H IV H SV-2 e S yphilis

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113
Q

Other important congenital infxns that do not fit into ToRCHeS

A

Listeria E. coli Group B streptococci All can be acquired placentally or from birth canal.

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114
Q

ToRCHeS infxns, organism: Toxoplasma gondii Major clinical manifestations?

A

Classic triad of chorionitis, intracranial calcifications, and hydrocephalus. May be asymptomatic at birth.

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115
Q

Major clinical manifestations: Classic triad of chorionitis, intracranial calcifications, and hydrocephalus. May be asymptomatic at birth. Which ToRCHeS organism is this?

A

Toxoplasma gondii

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116
Q

ToRCHeS infxns, organism: Rubella Major clinical manifestations?

A

Deafness Cataracts Heart defects (PDA, pulmonary artery stenosis) Microcephaly Mental retardation Blueberry muffin baby due to rash

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117
Q

Major clinical manifestations: Deafness Cataracts Heart defects (PDA, pulmonary artery stenosis) Microcephaly Mental retardation Blueberry muffin baby due to rash Which ToRCHeS organism is this?

A

Rubella

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118
Q

ToRCHeS infxns, organism: CMV Major clinical manifestations?

A

Petechial rash Intracranial calcifications Mental retardation Hepatosplenomegaly Microcephaly Jaundice 90% are asymptomatic at birth.

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119
Q

Major clinical manifestations: Petechial rash Intracranial calcifications Mental retardation Hepatosplenomegaly Microcephaly Jaundice 90% are asymptomatic at birth. Which ToRCHeS organism is this?

A

CMV

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120
Q

ToRCHeS infxns, organism: HIV Major clinical manifestations?

A

Hepatosplenomegaly Neurologic abnormalities Frequent infxns

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121
Q

Major clinical manifestations: Hepatosplenomegaly Neurologic abnormalities Frequent infxns Which ToRCHeS organism is this?

A

HIV

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122
Q

ToRCHeS infxns, organism: HSV-2 Major clinical manifestations?

A

Encephalitis Conjuntivitis Vesicular skin lesions Often asymptomatic at birth Most infxns are transmitted during birth thru an infected maternal genital tract.

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123
Q

Major clinical manifestations: Encephalitis Conjuntivitis Vesicular skin lesions Often asymptomatic at birth Most infxns are transmitted during birth thru an infected maternal genital tract. Which ToRCHeS organism is this?

A

HSV-2

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124
Q

ToRCHeS infxns, organism: Syphilis Major clinical manifestations?

A

Cutaneous lesions Hepatosplenomegaly Jaundice Saddle nose Saber shins Hutchinson teeth CN VIII deafness Rhinitis (snuffles)

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125
Q

Major clinical manifestations: Cutaneous lesions Hepatosplenomegaly Jaundice Saddle nose Saber shins Hutchinson teeth CN VIII deafness Rhinitis (snuffles) Which ToRCHeS organism is this?

A

Syphilis

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126
Q

Red rashes of childhood

A

Measles Rubella HHV-6 (roseola) Scarlet fever (group A streptococcus) Parvovirus B19 (slapped cheek rash)

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127
Q

STD’s: Gonorrhea Organism? Clinical features?

A

Neisseria gonorrhoeae Urethritis, cervicitis, PID, prostatitis, epididymitis, arthritis, creamy purulent discharge

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128
Q

Neisseria gonorrhoeae Urethritis, cervicitis, PID, prostatitis, epididymitis, arthritis, creamy purulent discharge Disease?

A

Gonorrhea

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129
Q

STD’s: Primary syphilis Organism? Clinical features?

A

Treponema pallidum Painless chancre

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130
Q

Treponema pallidum Painless chancre Disease?

A

Primary syphilis

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131
Q

STD’s: Secondary syphilis Organism? Clinical features?

A

Treponema pallidum Fever, lymphadenopathy, skin rashes, condylomata lata

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132
Q

Treponema pallidum Fever, lymphadenopathy, skin rashes, condylomata lata Disease?

A

Secondary syphilis

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133
Q

STD’s: Tertiary syphilis Organism? Clinical features?

A

Treponema pallidum Gummas (a non-cancerous growth, a form of granuloma) Tabes dorsalis General paresis Aortitis Argyll Robertson pupil

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134
Q

Treponema pallidum Gummas (a non-cancerous growth, a form of granuloma) Tabes dorsalis General paresis Aortitis Argyll Robertson pupil Disease?

A

Tertiary syphilis

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135
Q

STD’s: Genital herpes Organism? Clinical features?

A

HSV-2 Painful penile, vulvar, or cervical ulcers; can cause systemic Sx such as: fever, HA, myalgia

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136
Q

HSV-2 Painful penile, vulvar, or cervical ulcers; can cause systemic Sx such as: fever, HA, myalgia Disease?

A

Genital herpes

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137
Q

STD’s: Chlamydia Organism? Clinical features?

A

Chlamydia trachomatis (D-K) Urethritis, cervicitis, conjunctivitis, Reiter’s syndrome, PID

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138
Q

Chlamydia trachomatis (D-K) Urethritis, cervicitis, conjunctivitis, Reiter’s syndrome, PID Disease?

A

Chlamydia

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139
Q

STD’s: Lymphogranuloma venereum Organism? Clinical features?

A

Chlamydia trachomatis (L1-L3) Ulcers, lymphadenopathy, rectal strictures.

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140
Q

Chlamydia trachomatis (L1-L3) Ulcers, lymphadenopathy, rectal strictures. Disease?

A

Lymphogranuloma venereum

141
Q

STD’s: Trichomoniasis Organism? Clinical features?

A

Trichomonas vaginalis Vaginitis Strawberry-colored mucosa

142
Q

Trichomonas vaginalis Vaginitis Strawberry-colored mucosa Disease?

A

Trichomoniasis

143
Q

STD’s: AIDS Organism? Clinical features?

A

HIV Opportunistic infxns, Kaposi’s sarcoma, lymphoma

144
Q

HIV Opportunistic infxns, Kaposi’s sarcoma, lymphoma Disease?

A

AIDS

145
Q

STD’s: Condylomata accumulata Organism? Clinical features?

A

HPV 6 and 11 Genital warts, koilocytes

146
Q

HPV 6 and 11 Genital warts, koilocytes Disease?

A

Condylomata accumulata

147
Q

STD’s: Hepatitis B Organism? Clinical features?

A

HBV Jaundice

148
Q

HBV Jaundice Disease?

A

Hepatitis B

149
Q

STD’s: Chancroid Organism? Clinical features?

A

Haemophilus ducreyi (it’s so painful, you do cry ) Painful genital ulcer, inguinal adenopathy.

150
Q

Haemophilus ducreyi (it’s so painful, you do cry ) Painful genital ulcer, inguinal adenopathy. Disease?

A

Chancroid

151
Q

STD’s: Bacterial vaginosis Organism? Clinical features?

A

Garnderella vaginalis Noninflammatory, malodorous discharge (fishy smell) Positive whiff test Clue cells

152
Q

Garnderella vaginalis Noninflammatory, malodorous discharge (fishy smell) Positive whiff test Clue cells Disease?

A

Bacterial vaginosis

153
Q

Top bugs that cause Pelvic inflammatory dz

A

Chlamydia trachomatis (subacute, often undiagnosed) Neisseria gonorrhoeae (acute, high fever) Chlamydia trachomatis (the most common STD in the USA: 3-4milliion cases/year)

154
Q

Signs and Sx’s of Pelvic inflammatory dz

A

Cervical motion tenderness (chandelier sign) Purulent cervical discharge. May include: Salpingitis, endometritis, hydrosalpinx, and tubo-ovarian abscess.

155
Q

Pelvic inflammatory dz can lead to… ?

A

Fitz-Hugh-Curtis Syndrome: infxn of the liver capsule and violin string adhesions of parietal peritoneum to liver.

156
Q

What is salpingitis a risk factor for?

A

Ectopic pregnancy Infertility Chronic pelvic pain Adhesions

157
Q

Other STD’s that cause PID

A

Garnderella (clue cells) Trichomonas (corkscrew motility on wet prep)

158
Q

Nosocomial pathogen: CMV, RSV Risk factor?

A

Newborn nursery

159
Q

Risk factor for a nosocomial pathogen: Newborn nursery

A

What is the pathogen? CMV, RSV

160
Q

Nosocomial pathogen: E. coli, Proteus mirabilis Risk factor?

A

Urinary catheterization

161
Q

Risk factor for a nosocomial pathogen: Urinary catheterization What is the pathogen?

A

E. coli, Proteus mirabilis

162
Q

Nosocomial pathogen: Pseudomonas aeurginosa Risk factor?

A

Respiratory therapy equipment

163
Q

Risk factor for a nosocomial pathogen: Respiratory therapy equipment What is the pathogen?

A

Pseudomonas aeurginosa

164
Q

Nosocomial pathogen: HBV Risk factor?

A

Work in renal dialysis unit

165
Q

Risk factor for a nosocomial pathogen: Work in renal dialysis unit What is the pathogen?

A

HBV

166
Q

Nosocomial pathogen: Candida albicans Risk factor?

A

Hyperalimentation

167
Q

Risk factor for a nosocomial pathogen: Hyperalimentation What is the pathogen?

A

Candida albicans

168
Q

Nosocomial pathogen: Legionella Risk factor?

A

Water aerosols

169
Q

Risk factor for a nosocomial pathogen: Water aerosols What is the pathogen?

A

Legionella

170
Q

The 2 most common causes of nosocomial infxns?

A

E. coli (UTI) S. aureus (wound infxn)

171
Q

Presume Pseudomonas aeruginosa as the cause of a nosocomial infxn when…?

A

Presume Pseudomonas AIR uginosa when AIR or burns are involved.

172
Q

When do you suspect Legionella as a cause of nosocomial infxn?

A

Suspect Legionella when a water source is involved.

173
Q

Bug hints (if all else fails):Pus, empyema (collection of pus in pre-existing anatomical cavity), abscess What is the bug?

A

S. aureus

174
Q

Bug hints (if all else fails):Pediatric infxn What is the bug?

A

haemophilus influenzae (including epiglottitis)

175
Q

Bug hints (if all else fails):Pneumonia in CF, burn infxn What is the bug?

A

Pseudomonas aeruginosa

176
Q

Bug hints (if all else fails):Branching rods in oral infxn What is the bug?

A

Actinomyces israellii

177
Q

Bug hints (if all else fails):Traumatic open wound What is the bug?

A

Clostridium perfringens

178
Q

Bug hints (if all else fails):Surgical wound What is the bug?

A

S. aureus

179
Q

Bug hints (if all else fails):Dog or cat bite What is the bug?

A

Pasteurella multocida

180
Q

Bug hints (if all else fails):Currant jelly sputum What is the bug?

A

Klebsiella

181
Q

Bug hints (if all else fails):Sepsis/meningitis in newborn What is the bug?

A

group B strep

182
Q

Antimicrobials by mechanism of action: Block cell wall synthesis by inhibition of peptidoglycan cross-linking

A

Drugs? Penicillin, ampicillin, ticarcillin, piperacillin, imipenem, aztreonam, cephalosporins [#1 below]

183
Q

Antimicrobials by mechanism of action: Block peptidoglycan synthesis Drugs?

A

Bacitracin, Vancomycin [#2 below]

184
Q

Antimicrobials by mechanism of action: Disrupt bacterial cell wall membranes Drugs?

A

Polymyxins [#3 below]

185
Q

Antimicrobials by mechanism of action: Block nucleotide synthesis Drugs?

A

Sulfonamides, Trimethoprim [#4 below]

186
Q

Antimicrobials by mechanism of action: Block DNA topoisomerases Drugs?

A

Quinolones [#5 below]

187
Q

Antimicrobials by mechanism of action: Block mRNA synthesis Drugs?

A

Rifampin [#6 below]

188
Q

Antimicrobials by mechanism of action: Block protein synthesis at 50S ribosomal subunit Drugs?

A

Chloramphenicol, macrolides, clindamycin, streptogramins (quinipristin, dalfopristin), linezolid [#7]

189
Q

Antimicrobials by mechanism of action: Block protein synthesis at the 30S ribosomal subunit Drugs?

A

Aminoglycosides, tetracyclines [#8 below]

190
Q

Bacterostatic antibiotics

A

E rythromycin C lindamycin S ulfamethoxazole T rimethoprim T etracylcines C hloramphenicol (We’re ECST aT iC about bacteriostatics )

191
Q

Bacteriocidal antibiotics

A

V ancomycin F luoroquinolones P enicillin A minoglycosides C ephalosporins M etronidazole V ery F inely P roficient A t C ell M urder

192
Q

Forms of Penicillin

A

Penicillin G (IV form), Penicillin V (oral form). Prototype Beta-lactam antibiotics.

193
Q

Mechanism of penicillin

A

1.) Bind penicillin-binding proteins 2.) Block transpeptidase cross-linking of cell wall 3.) Activate autolytic enzymes

194
Q

Mechanism of penicillinase-resistant penicillins: Methicillin, nafcillin, dicoxacillin

A

Same as penicillin*. Narrow speectrum; penicillinase resistant b/c of bulkier R group. * mechanism of PCN: 1.) Bind penicillin-binding proteins 2.) Block transpeptidase cross-linking of cell wall 3.) Activate autolytic enzymes

195
Q

Mechanism of aminopenicillins: Ampicillin, amoxicillin

A

Same as penicillin*. Wider spectrum; Penicillinase sensitive. Also combine w/ clavulanic acid (a penicillinase inhibitor) to enhance spectrum. AmO xicillin has greater O ral bioavailability than ampicillin. *Mechanism of PCN: 1.) Bind penicillin-binding proteins 2.) Block transpeptidase cross-linking of cell wall 3.) Activate autolytic enzymes

196
Q

Mechanism of antipseudomonals: Ticarcillin, carbenicillin, piperacillin

A

Same as penicillin*. Extended spectrum. *Mechanism of penicillin: 1.) Bind penicillin-binding proteins 2.) Block transpeptidase cross-linking of cell wall 3.) Activate autolytic enzymes

197
Q

Clinical use of penicillin

A

Bactericidal for Gram(+) cocci, Gram(+) rods, Gram(-) cocci, and spirochetes. Not penicillinase resistant.

198
Q

Toxicity of penicillin

A

Hypersensitivity rxtns. Methicillin: interstitial nephritis.

199
Q

Clinical use of aminopenicillins (ampicillin, amoxicillin)

A

Extended spectrum penicillin*: certain gram(+) bacteria and gram(-) rods: H aemophilus influenzae, E . coli, L isteria monocytogenes, P roteus mirabilis, S almonella, enterococci (Ampicillin/amoxicillin HELPS kill enterococci) *Think of amp icillin/amoxicillin as AMP ed up penicillin

200
Q

Toxicity of aminopenicillins (ampicillin, amoxicillin)

A

Hypersensitivity rxtns; Ampicillin rash; Pseudomembranous colitis.

201
Q

Clinical use of: Ticarcillin, carbenicillin, piperacillin

A

(antipseudomonals – TCP : T ake C are of P seudomonas) Used for Pseudomonas spp. and gram(-) rods; susceptible to penicillinase; Use w/ clavulinic acid (Beta-lactamase inhibitor).

202
Q

Toxicity of antipseudomonals (Ticarcillin, carbenicillin, piperacillin)

A

Hypersensitivity rxtns.

203
Q

Mechanism of cephalosporins

A

Beta-lactam drugs that inhibit cell wall synthesis, but are less susceptible to penicillinases. Bactericidal.

204
Q

Clinical use of 1st generation cephalosporins (Cefazolin, cephalexin)

A

Gram(+) cocci, P roteus mirabilis, E . c oli, K lebsiella pneumoniae (1st gen = PEcK )

205
Q

Clinical use of 2nd generation cephalosporins (cefoxitin, cefaclor, cefuroxime)

A

Gram(+) cocci, H aemophilus influenzae, E nterobacter aerogenes, N eisseria spp. P roteus mirabilis, E. c oli, K lebsiella pneumoniae, S erratia marcescens (2nd Gen = HEN PEcKS )

206
Q

Clinical use of 3rd generation cephalosporins (ceftriaxone, cefotaxime, ceftazidime)

A

Serious gram(-) infxns resistant to other beta-lactams; meningitis (most penetrate the BBB). Examples: Ceftazidime for Pseudomonas Ceftriaxone for gonorrhea

207
Q

Clinical use of 4th generation cephalosporins (Cefepime)

A

Increased activity against Pseudomonas and gram(+) organisms.

208
Q

Toxicity of cephalosporins

A

Hypersensitivity rxtn. Cross-hypersensitivvity w/ penicillins occurs in 5-10% of pts. Increased nephrotoxicity of aminoglycosides; disulfiram-like rxtn w/ ethanol (in cephalosporins w/ methylthitetrazole group, e.g., cefamandole)

209
Q

Mechanism of aztreonam

A

A monobactam resistant to beta-lactamases. Inhibits cell wall synthesis (binds to PBP3). Synergistic w/ aminoglycosides. No cross-allergenicity w/ penicillins.

210
Q

Clinical use of aztreonam

A

Gram(-) rods - Klebsiella spp., Pseudomonas spp., Serratia spp. No activity against gram(+)’s or anaerobes. For penicillin-allergic pts and those w/ renal insufficiency who cannot tolerate aminoglycosides.

211
Q

Toxcity of Aztreonam

A

Usually nontoxic; occasional GI upset. No cross-sensitivity w/ penicillins or cephalosporins.

212
Q

Mechanism of Imipenem/cilastatin, meropenem

A

Imipenem is a broad-spectrum, beta-lactamase-resistant carbapenem. Always administer w/ cilastatin (inhibitor of renal dihydropeptidase I) to decrease inactivation in renal tubules. (With imipenem, the kill is LASTIN’ with ciLASTATIN )

213
Q

Clinical use of imipenem/cilastatin, meropenem

A

Gram(+) cocci, gram(-) rods, and anaerobes. DOC for Enterobacter. The significant side effects limit use to life-threatening infxns, or after other drugs have failed. Meropenem, howevver, has a reduced risk of seizures and is stable to dihydropeptidase I.

214
Q

Toxicity of Imipenem/cilastatin, meropenem

A

GI distress, skin rash, and CNS toxicity (seizures) @ high plasma levels

215
Q

Mechanism of vancomycin

A

Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Resistance occurs w/ AA change of D-ala D-ala to D-ala D-lac

216
Q

Clinical use of vancomycin

A

Used for serious, gram(+) multidrug-resistant organisms, including S. aureus and Clostridium difficile (pseudomembranous colitis)

217
Q

Toxicity of vancomycin

A

N ephrotoxicity, O totoxicity, T hromophlebitis, diffuse flushing - red man syndrome (can largely prevent by pretreatment w/ antihistamines and slow infusion rate) Well toleraterd in general – does NOT have many problems.

218
Q

Protein synthesis inhibitors: 30S inhibitors

A

A = A minoglycosides (streptomycin, gentamycin, tobramycin, amikacin) [bacteriostatic] T = T etracyclines [bacteriostatic] (But AT 30 , CCELL (sell) at 50) [*note different specific sites of action of Aminoglycosides and TCNs below]

219
Q

Protein Synthesis Inhibitors: 50S inhibitors

A

C = C hloramphenicol, C lindamycin [bacteriostatic] E = E rythromycin [bacteriostatic] L = L incomycin [bacteriostatic] L = L inezolid [variable] (But AT 30, CCELL (sell) at 50 ) [note different specific sites of action below]

220
Q

Aminoglycosides (list)

A

G entamycin N eomycin A mikacin T obramycin S treptomycin (Mean GNATS [mean = amin oglycosides)

221
Q

Mechanism of aminoglycosides (gentamycin, neomycin, amikacin, tobramycin, streptomycin)

A

Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes. (Mean GNATS canNOT kill anaerobes)

222
Q

Clinical use of aminogyclosides (gentamycin, neomycin, amikacin, tobramycin, streptomycin)

A

Severe gram (-) rod infxns. Synergistic w/ beta-lactam ABX. Neomycin for bowel surgery.

223
Q

Toxicity of aminoglycosides (gentamycin, neomycin, amikacin, tobramycin, streptomycin)

A

N ephrotoxicity (especially when used w/ cephalosporins) O totoxicity (especially when used w/ loop diuretics) T eratogen. (Mean GNATS canNOT kill anaerobes)

224
Q

Tetracyclines (list)

A

Tetracylcine Doxycycline Demeclocycline Minocycline

225
Q

Mechanism of tetracyclines (tetracycline, doxycycline, demeclocyclline, minocycline)

A

Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA. Limited CNS penetration. Doxycyline is fecally eliminated and can be used in pts w/ renal failure. Must NOT take w/ milk, antacids, or iron-containing preparations b/c divalent cations inhibit absorption in gut. D emeclocycline is an ADH antagonist (acts as a D iuretic in SIADH)

226
Q

Clinical use of tetracyclines (tetracycline, doxycycline, demeclocyclline, minocycline)

A

V ibrio cholerae A cne C hlamydia U reaplasma U realyticum M ycoplasma pneumoniae T ularemia H . pylori B orrelia burgdorferi (Lyme dz) R ickettsia (VACUUM TH e B edR oom)

227
Q

Toxicity of tetracyclines (tetracycline, doxycycline, demeclocyclline, minocycline)

A

GI distress Discoloration of teeth and inhibition of bone growth in children Photosensitivity Contraindicated in pregnancy.

228
Q

Macrolides (list)

A

Erythromycin, azithromycin, clarithromycin

229
Q

Mechanism of macrolides (Erythromycin, azithromycin, clarithromycin)

A

Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.

230
Q

Clinical use of macrolides (Erythromycin, azithromycin, clarithromycin)

A

URIs, pneumonias STDs – gram(+) cocci (streptococcal infxns in pts allergic to penicillin) Mycoplasma Legionella Chlamydia Neisseria

231
Q

Toxicity of macrolides (Erythromycin, azithromycin, clarithromycin)

A

GI discomfort (most common cause of noncompliance) Acute cholestatic hepatitis Eosinophilia Skin rashes Increases serum concentration of theophyllines, oral anticoagulants.

232
Q

Mechanism of chloramphenicol

A

Inhibits 50S peptidyltransferase activity. Bacteriostatic.

233
Q

Clinical use of chloramphenicol

A

Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) Conservative use, owing to toxicities.

234
Q

Toxicity of chloramphenicol

A

Anemia (dose dependent) Aplastic anemia (dose independent) Gray baby syndrome (in premature infants b/c they lack liver UDP-glucuronyl transferase)

235
Q

Mechanism of clindamycin

A

Blocks peptide bond formation at 50S ribosomal subunit. Bacteriostatic.

236
Q

Clinical use of clindamycin

A

Tx anaerobic infxns (e.g., Bacteroides fragilis, Clostridium perfringens) (Treats anaerobes above the diaphragm)

237
Q

Toxicity of clindamycin

A

Pseudomembranous colitis (C. difficile overgrowth) Fever Diarrhea

238
Q

Sulfonamides (list)

A

Sulfamethoxazole (SMX) Sulfisoxazole Sulfadiazine

239
Q

Mechanism of sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine)

A

PABA antimetabolites inhibit dihydropteroate synthetase [see below]. Bacteriostatic.

240
Q

Clinical use of of sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine)

A

Gram(+), gram(-), Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.

241
Q

Toxicity of sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine)

A

Hypersensitivity rxtns Hemolysis if G6PD deficient Nephrotoxicity (tubulointerstitial nephritis) Photosensitivity Kernicterus in infants Displace other drugs from albumin (e.g., warfarin)

242
Q

Mechanism of trimethoprim (TMP)

A

Inhibits bacterial dihydrofolate reductase. Bacteriostatic.

243
Q

Clinical use of trimethoprim (TMP)

A

Used in combination w/ sulfonamides (trimethoprim-sulfamethoxazole [TMP-SMX]), causing sequential block of folate synthesis. Combination used for recurrent UTIs, Shigella, Salmonella, Pneumocystis jiroveci pneumonia.

244
Q

Toxicity of trimethoprim (TMP)

A

Megaloblastic anemia Leukopenia Granulocytopenia (may alleviate w/ supplemental folinic acid) (Trimethoprim = TMP : T reats M arrow P oorly)

245
Q

Sulfa drug allergies – what do you need to avoid?

A

Pts who do not tolerate sulfa drugs should not be given sulfonamides or other sulf drugs such as: Sulfasalazine Sulfonylureas Thiazide diuretics Acetazolamide Furosemide

246
Q

Fluoroquinolones (list)

A

Ciprofloxacin Norfloxacin Ofloxacin Sparfloxacin Moxifloxacin Gatifloxacin Enoxacin [above are fluoroquinolones] Nalidixic acid [a quinolone]

247
Q

Mechanism of fluoroquinolones

A

Inhibit DNA gyrase (topoisomerase II). Bactericidal. Must not be taken w/ antacids.

248
Q

Clinical use of fluoroquinolones

A

Gram(-) rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram(+) organisms

249
Q

Toxicity of fluoroquinolones

A

GI upset, superinfections, skin rashes, HA, dizziness. Contraindicated in pregnant women and in children b/c animal studies show damage to cartilage. Tendonitis and tendon rupture in adults; leg cramps and myalgias in kids. (FlouroquinoLONES hur the attachments to your BONES )

250
Q

Mechanism of metronidazole

A

Forms toxic metabolites in the bacterial cell that damage DNA. Bactericidal, antiprotozoal.

251
Q

Clinical use of metronidazole

A

Treats: G iardia E ntamoeba T richomonas G ardnerella vaginalis A naerobes (Bacteroides, Clostridium) Used w/ bismuth and amoxicillin (or TCN) for triple therapy against H. P ylori (GET GAP on the METRO !) Treats anaerobic infxns below the diaphragm.

252
Q

Toxicity of metronidazole

A

Disulfiram-like rxtn w/ alcohol Headache Metallic taste

253
Q

Polymyxins (list)

A

Polymyxin B Polymyxin E

254
Q

Mechanism of polymyxins

A

Bind to cell membranes of baccteria and disrupt their osmotic properties. Polymyxins are cationic, basic proteins that act like detergents. (MYXins MIX up membranes)

255
Q

Clinical use of polymyxins

A

resistant gram(-) infxns

256
Q

Toxicity of polymyxins

A

Neurotoxicity, acute renal tubular necrosis

257
Q

Antimycobacterial drugs: for M. tuberculosis

A

Prophylaxis: Isoniazid Tx: R ifampin I soniazid P yrazinamide E thambutol (RIPE for treatment)

258
Q

Antimycobacterial drugs: for M. avium-intracellulare

A

Prophylaxis: Azithromycin Tx: Azithromycin Rifampin Ethambutol Streptomycin

259
Q

Antimycobacterial drugs for M. leprae

A

Tx: Dapsone Rifampin Clofazimine

260
Q

Anti-TB drugs

A

S treptomycin, P yrazinamide, I soniazid (INH ), R ifampin, E thambutol (INH-SPIRE [inspire]) Cycloserine (2nd-line therapy)

261
Q

Side effects of anti-TB drugs

A

Important SE of ethambutol: optic neuropathy (red-green color blindness) For other drugs: hepatotoxicity.

262
Q

Mechanism of isoniazid (INH)

A

Decreases synthesis of mycolic acids. *note that there are different INH half-lives in fast vs. slow acetylators.

263
Q

Clinical use of isoniazid (INH)

A

Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB.

264
Q

Toxicity of isoniazid (INH)

A

Neurotoxicity, hepatotoxicity. Pyridoxine (Vitamin B6) can prevent neurotoxicity. (INH I njures N eurons and H epatocytes)

265
Q

Mechanism of rifampin

A

Inhibits DNA-dependent RNA polymerase

266
Q

Clinical use of rifampin

A

Mycobacterium tuberculosis. Delays resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children w/ Haemophilus influenzae type B.

267
Q

Toxicity of rifampin

A

Minor hepatotoxicity and drug interactions (induces P-450) Orange body fluids (nonhazardous side effect)

268
Q

Rifampin’s 4 R’s

A

R NA polymerase inhibitor R evs up microsomal P-450 R ed/orange body fluids R apid resistance if used alone

269
Q

Most common resistance mechanism for: Penicillins/cephalosporins

A

Beta-lactamase cleavage of beta-lactam ring, or altered PBP in cases of MRSA or penicillin-resistant S. pneumoniae.

270
Q

The following is the most common mechanism of resistance for what drug? Beta-lactamase cleavage of beta-lactam ring, or altered PBP in cases of MRSA or penicillin-resistant S. pneumoniae.

A

Penicillins/cephalosporins

271
Q

Most common resistance mechanism for: Aminoglycosides

A

Modification via acetylation, adenylation, or phosphorylation.

272
Q

The following is the most common mechanism of resistance for what drug? Modification via acetylation, adenylation, or phosphorylation.

A

Aminoglycosides

273
Q

Most common resistance mechanism for: Vancomycin

A

Terminal D-ala of cell wall component replaced with D-lac, decreased affinity.

274
Q

The following is the most common mechanism of resistance for what drug? Terminal D-ala of cell wall component replaced with D-lac, decreased affinity.

A

Vancomycin

275
Q

Most common resistance mechanism for: Chloramphenicol

A

Modification via acetylation

276
Q

The following is the most common mechanism of resistance for what drug? Modification via acetylation

A

Chloramphenicol

277
Q

Most common resistance mechanism for: Macrolides

A

methylation of rRNA near erythromycin’s ribosome-binding site

278
Q

The following is the most common mechanism of resistance for what drug? methylation of rRNA near erythromycin’s ribosome-binding site

A

Macrolides

279
Q

Most common resistance mechanism for: Tetracycline

A

Decreased uptake or increased transport out of cell.

280
Q

The following is the most common mechanism of resistance for what drug? Decreased uptake or increased transport out of cell.

A

Tetracycline

281
Q

Most common resistance mechanism for: Sulfonamides

A

Altered enzyme (bacterial dihydropteroate synthetase), decreased uptake, or increased PABA synthesis.

282
Q

The following is the most common mechanism of resistance for what drug? Altered enzyme (bacterial dihydropteroate synthetase), decreased uptake, or increased PABA synthesis.

A

Sulfonamides

283
Q

Most common resistance mechanism for: Quinolones

A

Altered gyrase or reduced uptake.

284
Q

The following is the most common mechanism of resistance for what drug? Altered gyrase or reduced uptake.

A

Quinolones

285
Q

Nonsurgical antimicrobial prophylaxis of: meningococcal infxn

A

Rifampin (DOC), minocycline

286
Q

Nonsurgical antimicrobial prophylaxis of: gonorrhea

A

Ceftriaxone

287
Q

Nonsurgical antimicrobial prophylaxis of: syphilis

A

Benzathine penicillin G

288
Q

Nonsurgical antimicrobial prophylaxis of: Hx of recurrent UTIs

A

TMP-SMX

289
Q

Nonsurgical antimicrobial prophylaxis of: Pneumocystis jiroveci pneumonia

A

TMP-SMX (DOC), aerosolized pentamidine.

290
Q

Nonsurgical antimicrobial prophylaxis of: endocarditis w/ surgical or dental procedures

A

Penicillins.

291
Q

Tx of highly resistant bacteria

A

MRSA: vancomycin

292
Q

Mechanism of Amphotericin B

A

Binds ergosterol (unique to fungi); Forms membrane pores that allow leakage of electrolytes. (Amphotear acin ‘tears’ holes in fungal membranes by forming pores) [on left, below]

293
Q

Clinical use of Amphotericin B

A

Use for wide spectrum of systemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross BBB.

294
Q

Toxicity of Amphotericin B

A

Fever/chills (shake and bake), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (amphotericin = amphoterrible). Hydration reduces nephrotoxicity. Liposomal amphotericin reduces toxicity.

295
Q

Mechanism of Nystatin

A

Binds to ergosterol, disrupting fungal membranes. Too toxic for systemic use. [on left w/ amphotericin, below]

296
Q

Clinical use of nystatin

A

Swish and swallow for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis.

297
Q

Azoles (list)

A

Fluconazole

298
Q

Mechanism of azoles

A

Inhibit fungal sterol (ergosterol) synthesis [below, top/middle]

299
Q

Clinical use of azoles

A

Systemic mycoses. Fluconazole for cyptococcal meningitis in AIDS pts (b/c it can cross the BBB) and candidal infxns of all types (i.e., yeast infxns). Ketoconazole for Balstomyces, Coccidioides, Histoplasma, Candida albicans, hypercortisolism. Clotrimazole and miconazole for topical fungal infxns.

300
Q

Toxicity of azoles

A

Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills

301
Q

Flucytosine mechanism

A

Inhibits DNA synthesis by conversion to 5-fluorouracil [below, middle]

302
Q

Clinical use of flucytosine

A

Used in systemic fungal infxns (e.g., Candida, Cryptococcus) in combination w/ amphotericin B

303
Q

Toxicity of flucytosine

A

Nausea, vomiting, diarrhea, bone marrow suppression

304
Q

Mechanism of Caspofungin

A

Inhibits cell wall synthesis by inhibiting synthesis of beta-glucan. [not included in image of anti-fungal mechanisms]

305
Q

Clinical use of caspofungin

A

Invasive aspergillosis

306
Q

Toxicity of caspofungin

A

GI upset, flushing.

307
Q

Mechanism of terbinafine

A

Inhibits the fungal enzyme squalene epoxidase. [below, top/right]

308
Q

Clinical use of terbinafine

A

Used to Tx dermatophytoses (especially onychomycosis)

309
Q

Mechanism of griseofulvin

A

Interferes w/ microtubule fxn; disrupts mitosis. Deposits keratin-containing tissues (e.g., nails). [below, bottom/right]

310
Q

Clinical use of griseofulvin

A

Oral Tx of superficial infxns; inhibits growth of dermatophytes (tinea, ringworm)

311
Q

Toxicity of griseofulvin

A

Teratogenic, ccarcinogenic, confusion, HA, induces P-450 (increasing warfarin metabolism).

312
Q

Mechanism of amantadine

A

Blocks viral penetration/uncoating (M2 protein); may buffer pH of endosome. (A man to dine [amantadine] takes of his coat .) Also causes the release of dopamine from intact nerve terminals. [below, top/right]

313
Q

Clinical use of amantadine

A

Prophylaxis and Tx for influenza A; Parkinson’s Dz. (A mantadine blocks influenza A and rubellA , and causes problems w/ the cerebellA )

314
Q

Toxicity of amantadine

A

Ataxia, dizziness, slurred speech. (A mantadine blocks influenza A and rubellA , and causes problems w/ the cerebellA ) Rimantidine is a derivative w/ fewer CNS side effects (does not cross BBB)

315
Q

Mechanism of resistance to amantadine

A

Mutated M2 protein. 90% of all influenza A strains are resistant to amantadine, so not used.

316
Q

Mechanism of: Zanamivir, oseltamivir

A

Inhibit influenza neuraminidase, decreasing the release of progeny virus. [below, bottom/left: Neuraminidase inhibitors]

317
Q

Clinical use of Zanamivir, oseltamivir

A

Both influenza A and B

318
Q

Mechanism of ribavirin

A

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase. [not included in figure, but acts at point of NA synthesis, bottom/right]

319
Q

Clinical use of ribavirin

A

RSV Chronic hepatitis C

320
Q

Toxicity of ribavirin

A

Hemolytic anemia. Severe teratogen.

321
Q

Mechanism of acyclovir

A

Monophosphorylated by HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination. [fits w/ NA analogs below, bottom/right]

322
Q

Clnicial use of acyclovir

A

HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised pts. For herpes zoster, use a related agent (famciclovir). No effect on latent forms of HSV and VZV.

323
Q

Toxicity of acyclovir

A

Generally well-tolerated.

324
Q

Mechanism of resistance to acyclovir

A

Lack of thymidine kinase

325
Q

Mechanism of ganciclovir

A

5’-monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase. [fits in w/ NA analogs below, bottom/right]

326
Q

Clinical use of ganciclovir

A

CMV, especially in immunocompromised pts

327
Q

Toxicity of ganciclovir

A

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

328
Q

Mechanism of resistance to ganciclovir

A

Mutated CMV DNA polymerase or lack of viral kinse.

329
Q

Mechanism of foscarnet

A

Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase. (FOS carnet = pyroFOS phate analog) [would fit into DNA synthesis on bottom/right]

330
Q

Clinical use of foscarnet

A

CMV retinitis in immunocompromised pts when ganciclovir fails; acyclovir-resistant HSV.

331
Q

Toxicity of foscarnet

A

Nephrotoxicity.

332
Q

Mechanism of resistance to foscarnet

A

Mutated DNA polymerase.

333
Q

HIV therapy: Protease inhibitors (list)

A

Saquinavir Ritonavir Indinavir Nelfinavir Amprenavir [all protease inhibitors end in -avir ] (NAVIR (never) TEASE a proTEASE )

334
Q

HIV therapy: Mechanism of protease inhibitors

A

Inhibit maturation of new virus by blocking protease in progeny of virus.

335
Q

HIV therapy: Toxicity of protease inhibitors

A

GI intolerance (nausea, diarrhea) Hyperglycemia Lipodystrophy Thrombocytopenia (indinavir)

336
Q

HIV therapy: Reverse transcriptase inhibitors –> nucleosides (list)

A

Zidovudine (ZDV, formerly AZT) Didanosine (ddI) Zalcitabine (ddC) Stavudine (d4T) Lamivudine (3TC) Abacavir (Have you dined (vudine ) with my nuclear (nucleosides ) family?)

337
Q

HIV therapy: Reverse transcriptase inhibitors –> non-nucleosides (list)

A

N evirapine, E favirenz, D elaviridine (N ever E ver D eliver nucleosides.)

338
Q

HIV therapy: Mechanism of reverse transcriptase inhibitors

A

Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of DNA copy of viral genome into host DNA. [below, bottom/right]

339
Q

HIV therapy: Toxicity of reverse transcriptase inhibitors

A

Bone marrow suppression* (neutropenia, anemia) Peripheral neuropathy Lactic acidosis (nucleosides) Rash (non-nucleosides) Megaloblastic anemia (ZDV) *GM-CSF and erythropoietin can be used to reduce BM suppression.

340
Q

HIV therapy: Clinical use of reverse transcriptase inhibitors

A

Highly active antiretroviral therapy (HAART) generally entails combination Tx w/ protease inhibitors and reverse transcriptase inhibitors. Initiated when pts have low CD4 counts (

341
Q

HIV therapy: Fusion inhibitor (there’s one – what is it?)

A

Enfuvirtide

342
Q

HIV therapy: Mechanism of fusion inhibitors (enfuvirtide)

A

Bind viral gp41 subunit; inhibit conformational change required for fusion w/ CD4 cells. Therefore block entry and susequent replication.

343
Q

HIV therapy: Toxicity of fusion inhibitors (enfuvirtide)

A

Hypersensitivity rxtns Rxtns at subcutaneous injection site Increased risk of bacterial pneumonia

344
Q

HIV therapy: Clinical use of fusion inhibitors (enfuvirtide)

A

In pts w/ persistent viral replication in spite of antiretroviral Tx. Used in combination w/ other drugs.

345
Q

Mechanism of interferons (as antimicrobials)

A

Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis. Induce ribonuclease that degrades viral mRNA.

346
Q

Clinical use of interferons

A

IFN-alpha: chronic hepatitis B and C, Kaposi’s sarcoma IFN-beta: MS IFN-gamma: NADPH oxidase deficiency

347
Q

Toxicity of interferons

A

Neutropenia

348
Q

Antibiotics to avoid in pregnancy (list – what are they, and why for each one?)

A

S ulfonamides – kernicterus

Microbiology (4 decks)

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