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Block 6: Microbio, ID, Derm, Heme-Onc > STDs, UTIs, Protein Synthesis Inhibitors, Intro to Eye (Week 4) > Flashcards

STDs, UTIs, Protein Synthesis Inhibitors, Intro to Eye (Week 4) Flashcards

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1
Q

Bacterial STDs

A

Most are curable!

Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum (syphilis), Klebsiella granulomatis, Haemophilus ducreyi

However, complications if untreated (PID; epididymitis; syphilis becomes chronic)

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2
Q

Reporting STDs

A

Syphilis: report and try to track down partners

Chlamydia and gonorrhea: report (?) but don’t track down partners

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3
Q

Sequelae of N. gonorrhoeae and C. trachomatis

A

Urethritis (urethral inflammation): dysuria, discharge, WBCs, leukocyte esterase positive

Cervicitis (cervical inflammation): asymptomatic; vaginal bleeding, discharge, friable cervix

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4
Q

Most common bacterial STD

A

Chlamydia trachomatis

(reportable)

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5
Q

Chlamydia

A

Requires columnar epithelial cells

Young people more prone, because have more columnal epithelial cells

Beefy red cervical mucosa, follicular changes “cobblestoning”

Women: Cervicitis, urethritis, conjunctivitis (auto-inoculation) –> PID, peri-hepatitis (Fitz-Hugh-Curtis)

Men: Urethritis, proctitis, conjunctivitis (auto-inoculation) –> epididymitis, reactive arthritis

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6
Q

Pelvic inflammatory disease (PID)

A

Can be acute or silent

A result of untreated chlamydia or gonorrhea

Infection of entometrium (endometriosis), fallopian tubes (salpingitis), pelvic peritoneum (Fitz-Hugh-Curtis syndrome w/violin strings)

Adnexal pain, easily provoked cervical bleeding, elevated ESR or CRP

Diagnose with imaging or laparoscopy

Leads to ectopic pregnancy because of scarring, infertility because of fallopian tube occlusion, chronic pelvic pain

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7
Q

Reiter’s syndrome (reactive arthritis)

A

Complication of chlamydia

Oligoarthritis (swelling and tenderness in mult joints)

Circinate balantis (scaling erythematous plaques on penis)

Autoimmune reaction associated with HLA B27

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8
Q

Lymphogranuloma venereum (LGV)

A

Serotypes L1, L2, L3 of chlamydia causes this

Enters lymphatics, replicates in macrophages –> inguinal lymphadenitis –> proctocolitis

Groove sign: enlarged inguinal and femoral nodes separated by ligament of Poupart

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9
Q

Neonatal chlamydia

A

Note: not one of “ToRCHeS” but mother can still give to child during birth

Conjunctivitis, pneumonia

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10
Q

Diagnostic tests for chlamydia

A

Chlamydia is INTRACELLULAR organism, so need to culture cells

However, now we can do nucleic acid amplification testing (NAAT) just using urine specimens: PCR, LCR, TMA, SDA

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11
Q

Treatment for chlamydia

A

Azithromycin 1g PO x 1

Doxycycline 100mg PO BID x 7 days

Patient delivered partner therapy

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12
Q

Gonorrhea

A

Facultative intracellular (can be inside or out of cells)

Infects noncornified epithelium

Formation of submucosal abscesses and accumulation of exudate in lumen

Women: cervicitis, urethritis, proctitis, pharyngitis, skene/bartholin gland infection –> PID, Fitz-Hugh-Curtis, disseminated infection

Men: urethritis, epididymitis/seminal vesiculitis, proctitis, conjunctivitis, abscess of Cowper’s/Tyson’s glands, pharyngitis –> disseminated gonococcal infection (DGI), urethral stricture, penile edema

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13
Q

Disseminated gonococcal infection (DGI)

A

Gonococcal bacteremia

Symptomatic or asymptomatic infection of pharynx, urethra, cervix

<5% of GC infected people

Complement deficiency (C7, 8, 9) means higher risk for this

“Arthritis-dermatitis syndrome” with polyarthritis and sterile tenosynovitis and skin lesions

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14
Q

Neonatal gonorrhea

A

Not one of “ToRCHeS” but vertical transmission during birth (30%) if no prophylaxis

Ophthalmia neonatorum, DGI, vaginal/rectal/pharyngeal infections

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15
Q

Diagnostic tests for gonorrhea

A

Gram stain, culture, DNA probe, NAATs using urine

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16
Q

Treatment for gonorrhea

A

Ceftriaxone IM (injection) x 1

PLUS

Azithromycin 1g PO x 1 or doxycycline 100mg PO BID x 7d (same as chlamydia, but also enhanced activity against gonorrhea!)

DON’T use fluoroquinolones (resistance) or cefixime (anaphylactic shock)

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17
Q

Epididymitis

A

Complication of gonorrhea or chlamydia in men; also from UTI

Unilateral testicular pain/swelling, usually accompanied by urethritis

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18
Q

Genital ulcer disease

A

STD causes: herpes simplex, syphilis, chancroid, lymphogranuloma venereum, granuloma inguinale

Non-STD causes: Candida balanitis, impetigo, trauma, Bechet’s syndrome, fixed drug eruption, malignancy, contact dermatitis

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19
Q

Vaginitis

A

Trichomonas vaginalis (parasite)

Related to sexual activity, but not clearly transmitted sexually

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20
Q

Tetracyclines mechanisms of resistance

A

1) Bacteria alter outer membrane porin proteins so decreased influx of drug into bacteria
2) Bacteria do active transport out of cell by pump proteins

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21
Q

Tetracycline considerations regarding food, etc

A

Do not take tetracycline with dairy (calcium) because will form chelates so cannot be absorbed

Do not give tetracycline to pregnant women (bc of effect on fetus) or children under 8 whose teeth have not formed because will stain teeth brown

Take with full glass of water because can cause gastric discomfort if stuck in esophagus

Causes phototoxicity, dizziness, liver failure

Can cause superinfection (because broad spectrum)

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22
Q

Tigecycline

A

Clycylcycline class of protein synthesis inhibitors

IV administration only

Very broad spectrum (gram +, gram -, anaerobes MRSA, VRE, MDR acinetobacter)

Good for intra-abdominal infection (Enterococci, E. coli, Klebsiella, Bacteroides fragilis)

NOT Pseudomonas aeruginosa

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23
Q

Mechanisms of resistance to aminoglycosides

A

Bacteria can:

1) Alter uptake mechanisms to decrease influx of drug into bacteria
2) Alter target (mutate 30S ribosome)
3) Enzymatic modification to phosphorylate, adenylate, acetylate the drug to make it inactive

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24
Q

Dosing of aminoglycosides

A

Exhibit concentration dependent killing: bactericidal activity proportional to peak concentration (so want peak conc as high as possible)

Have post-antibiotic effect (drug works even after levels are below MIC)

Toxicity less with once daily dosing

Give one single high dose per day

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25
Q

Pharmacokinetics and toxicities of aminoglycosides

A

Only used IV, IM or topically (poor absorption in GI)

Polar, bad CSF penetration

High levels in urine because excreted there so good for treating UTIs

Also get into blood so good for gram - septic shock

Toxicities: nephrotoxicity and ototoxicity

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28
Q

Adverse effects of macrolides

A

Epigastric distress (worst with erythromycin)

Cholestatic jaundice

Ototoxicity (rare)

QT prolongation

Adverse drug interactions because interfere with CYP450 clearance

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31
Q

Mupirocin

A

AKA Bactroban, pseudomonic acid A

Active against gram + bacteria including MRSA

Used topically only

Used before surgery to prevent MRSA into open would

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32
Q

Drugs for anaerobic infections

A

Clindamycin

Chloramphenicol

Tigecycline

Penicillins

Piperacillin/tazobactam

Ampicillin/sulbactam

Amoxicillin/clavulanate

2nd generation cephalosporins (cefoxitin, cefotetan)

Carbapenems

Moxifloxacin

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33
Q

Treatments for specific anaerobic infections

A

Anaerobic streptococci: penicillin

Oropharyngeal GI infections (head and neck abscess): clindamycin, penicillin, penicillin + beta lactamase inhibitor

Intestinal GI infections (ruptured appendix): metronidazole, cefoxitin, cefotetan, carbapenem, penicillin + beta lactamase inhibitor, clindamycin

Abscesses: metronidazole, chloramphenicol

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33
Q

Causative organisms for UTI in women

A

E. Coli

S. saprophyticus

P. mirabilis, Klebsiella, Pseudomonas, Serratia, Enterococcus, yeast

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34
Q

Uropathogenic E. coli (UPEC)

A

A few serotypes of E. coli cause UTI

Virulence factors specific/important to UPEC: adhesins (type 1 fimbriae, P fimbriae)

Contains pathogenicity-associated islands (PAIs) which contain clusters of virulence factor genes

Pathogen has to stick in order to infect you (or else you’d pee it out)

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35
Q

Type 1 Fimbriae

A

One of two adhesins important to UPEC

Rod-like polymer of FimA with one FimH on the tip which adheres to mannose-containing uroplakin proteins on bladder uroepithelial cells

Cystitis

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36
Q

P Fimbriae

A

Adhesin that helps E. coli (UPEC, specifically) bind to uroepithelial cells

Pyelonephritis-associated pilus (pap) gene cluster has 11 genes

PapG adhesin subunit at tip binds glycolipids on uroepithelial cells of kidney –> causes pyelonephritis

P fimbriae is important vaccine target

Pyelonephritis

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37
Q

Host defense mechanisms against UTI

A

Unobstructed flow of urine (flush out anything that tries to colonize)

Normal urine characteristics (osmolality, urea concentration, pH, etc)

Tamm-Horsfall glycoprotein (THP) produced by ascending loop of Henle and DCT, mannose rich residue secreted into urine

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38
Q

Host susceptibility to UTI

A

Obstruction to urine flow

Neurogenic bladder (incomplete emptying)

Renal calculi

Sexual activity

Antibiotic therapy (altered flora)

Diabetes (glucose in urine)

Low estrogen (post-menopause) makes it easier for bacteria to attach to cells

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39
Q

Urinalysis for UTI

A

10 WBC/high power field = pyuria = evidence for inflammatory response

RBCs = evidence for damage to uroepithelium

Gram stain = evidence for bacteria in urine

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40
Q

2 lab tests used together to diagnose UTI

A

Leukocyte esterase (suggests WBCs in urine)

Nitrite (suggests bacteria in urine)

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41
Q

Cystitis vs. pyelonephritis

A

Cystitis: bladder infection

Pyelonephritis: kidney pelvis infection (have abscess formation in kidney; costovertebral-angle tenderness; fevers, chills, nausea) and can lead to sepsis or death

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42
Q

What else can present with burning on urination?

A

Urethritis due to N. gonorrhoeae, chlamydia, HSV

This is NOT a UTI

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43
Q

Should you get a culture when you suspect UTI?

A

Only if you suspect pyelonephritis since that is dangerous

No need to culture for uncomplicated cystitis

44
Q

What can cause kidney stones?

A

Bacteria produces urease –> splits urea into ammonium hydroxide –> raises urinary pH –> precipitation of struvite and apatite stones in bladder and kidney –> obstruction of urine flow

Intervention to relieve pressure in order to preserve renal function

Urease +: Proteus mirabilis, S. saprophyticus, K. pneumoniae, C. urealyticum

45
Q

Asymptomatic bacteriuria

A

Positive bacterial culture from appropriately collected sample in patient with no symptoms

Only treat pregnant women (reduce risk of pyelonephritis which would be bad because hard to treat pregnant women!)

46
Q

Drugs to treat uncomplicated UTI

A

Trimethoprim-sulfamethoxazole BID x 3 days

Nitrofurantoin 100mg BID x 5 days

47
Q

Nitrofurantoin

A

AKA Macrobid 100mg

No tissue penetration, so use only for cystitis

Proteus and Klebsiella resistant

Safe in pregnancy

Can cause severe lung injury: acute presenting like allergy, or chronic interstitial fibrosis

48
Q

Fosfomycin

A

To treat uncomplicated UTIs

Activity against VRE, ESBL producing E. coli, some MDR Pseudomonas aeruginosa, few MDR Acinetobacter baumanii

49
Q

Fluoroquinolones for UTI

A

Don’t use them for uncomplicated UTIs because you need them for more serious infections (pyelonephritis)

50
Q

Risk of “collateral damage” or producing resistance by using these drugs

A

High: TMP-SMX, fluoroquinolones, beta-lactams

Low: nitrofurantoin, fosfomycin, pivmecillinam

51
Q

Inpatient treatment of pyelonephritis

A

3rd generation cephalosporin +/- aminoglycoside

Extended spectrum penicillin +/- aminoglycoside

Carbapenem +/- aminoglycoside

52
Q

Outpatient treatment of pyelonephritis

A

PO fluoroquinolone +/- IV aminoglycoside one time

Ciprofloxacin better than TMP-SMX

53
Q

How to deal with pyelonephritis

A

Get a urinalysis and culture for all patients with pyelonephritis

CT scan for anyone with history of renal colic

If fever persists after 72 hours, reculture because might be missing a pathogen and do radiological studies

54
Q

Mechanisms of resistance to fluoroquinolones

A

Mostly due to alteration in subunits of DNA gyrase or topoisomerase IV

Less commonly decreased outer membrane permeability, activation of efflux pumps

55
Q

Adverse effects of fluoroquinolones

A

GI upset is most prominent side effect

Dizziness with moxifloxacin, tendinopathy (achilles tendon rupture), hepatotoxicity, hyper/hypoglycemia

Contraindicated in pregnancy and in children due to cartilage toxicity

56
Q

Pharmacokinetics of fluoroquinolones

A

Well absorbed but don’t give with Ca2+, Fe, Mg2+ because it will inhibit absorption

Concentration in kidney and urine is high (good for UTIs!), CSF levels lower than plasma

Hepatic metabolism clears 20% and the rest excreted in urine (good for UTIs!)

57
Q

Adverse effects of methenamine

A

GI distress

Contraindicated in patients with renal dysfunction, hepatic dysfunction

Don’t give with sulfonamides because will inactivate both agents

58
Q

Daptomycin

A

Inserts K+ channel into bacterial cell membrane to disrupt electrochemical gradient –> bactericidal

Active against many gram +, MRSA, VRE

NOT active against gram -

Used for skin infection, bacteremia, right sided endocarditis; NOT for pneumonia bc inactivated by surfactant

Doesn’t break open bacteria like beta-lactams do so might use this if worried about that

59
Q

Chlamydiaecea

A

Chlamydia trachomatis

Chlamydophila pneumoniae, Chlamydophila psittaci

Obligate intracellular

Gram - but LPS does not cause cytokine storm!

No peptidoglycans of cell wall so beta lactams don’t work!

60
Q

Treatment for chlamydia

A

Azithromycin (macrolide) 1g PO x 1 day

Doxycycline (tetracycline) 100mg BID x 7 days

Quinolones x 7 days

61
Q

Chlamydophila pneumoniae

A

Pharyngitis, bronchitis

Atypical pneumonia (interstitial infiltrates, non-productive cough)

Otitis media, endocarditis (rare)

62
Q

Mycoplasma and Ureaplasma

A

M. pneumoniae, M. hominis, M. genitalium, U. urealyticum

Smallest bacteria

Lack rigid cell wall

Diagnosis: NAAT, serology, cold hemagglutinin

Treatment: tetracyclines, macrolides, quinolones (NOT cell wall agents!)

63
Q

M. hominis, M. genitalium, U. urealyticum

A

Cause of non-gonococcal urethritis

64
Q

Rickettsiae

A

Rickettsia, Orientia, Coxiella, Anaplasma

Infect vascular endothelial cells, and other cells

Arthropod vector transmission for Rickettsia, Orientia, Anaplasma

Goats, sheep etc transmission for Coxiella

65
Q

Anaplasmosis (Ehrlichiosis)

A

Tick vector

Similar to RMSF without a rash (headache and fever)

Infects leukocytes; monocytic, granulocytic; doesn’t infect vascular endothelium so no rash!

Treatment: doxycycline/chloramphenicol

66
Q

Endemic (murine) typhus

A

Rickettsia typhi

Rats with fleas are reservoir –> fleas bite humans accidentally

Abrupt onset fevers, chills, headaches, myalgias

Milder than RMSF and resolves without treatment

Treatment: doxycycline or chloramphenicol, if necessary

67
Q

Tpr membrane proteins

A

Proteins on surface of Treponema pallidum that change variable region so immune system cannot catch them!

68
Q

Stages of syphilis

A

Incubation: 21 days

Primary syphilis: 3-6 weeks; painless chancre w/raised borders

Secondary syphilis: 2-8 weeks after chancre appeared; dissemination, condyloma lata, maculopapular rash on palms and soles, meningitis, hepatitis, arthritis

Latent syphilis: early or late (1 year cutoff)

Tertiary (late) syphilis: gummas, cardiovascular (aortitis, aortic aneurysm), neurosyphilis (meningiovascular, general paresis, tabes dorsalis, Argyll Robertson pupil)

69
Q

Serodiagnosis of syphilis

A

Nonspecific (nontreponemal) tests: VDRL, RPR; used as screening, titer measures disease activity, response to therapy; antibody to cardiolipin (lipid found in normal tissues); false positive reactions in SLE

Specific (treponemal) tests: FTA-ABS, MHA-TP; antibody to specific antigens of T. pallidum; used to confirm positive VDRL or RPR

70
Q

How do you treat syphilis if patient is allergic to penicillin?

A

Desensitize to penicillin (especially if patient is pregnant)

Doxycycline, ceftriaxone, chloramphenicol

71
Q

Interaction between syphilis and HIV

A

Patients with syphilitic lesions more susceptible to acquiring HIV

Co-infected patients more likely to transmit both HIV and syphilis

Co-infected patients have more malignant course of syphilis

Syphilis relapses after adequate therapy in co-infected individuals

72
Q

Nonvenereal treponematoses

A

Yaws: T. pallidum (pertenue) in humid tropics, transmitted skin to skin, papules, gummas of bone and skin

Pinta: T. carateum in arid Americas, transmitted skin to skin, papules, achromic macules

Bejel: T. pallidum (endemicum) in arid Africa, transmitted mouth to mouth, oral lesions, gummas of bone and skin

73
Q

Borrelia vsp expression

A

vsp = variable surface protein

Moves antigenic genes around by recombination to produce different vsp proteins to evade immune response!

Borrelia recurrentis, Borrelia hermsii

74
Q

Relapsing fever

A

Borrelia recurrentis spread by lice; higher fatality

Borrelia hermsii and others spread by ticks; lower fatality

Fever, chills, headache, myalgias, sweats, febrile relapses

75
Q

OspA

A

OspA = outer surface protein

On Borrelia burgdorferi (in tick midgut)

OspA helps bacteria stay attached to tick midgut but as tick sucks blood from mouse, temperature rises and that causes OspA to be downregulated

Also increase in temperature upregulates OspC which is important for Borrelia burgdorferi life in the mouse

76
Q

Do we have a vaccine for B. burgdorferi?

A

No

Tried to give antibodies to OspA because it kills B. burgdorferi before it can get into humans and infect them, but was shown to induce autoimmune arthritis (very bad side effect!)

77
Q

Stages of Lyme disease

A

Stage 1: localized infection; erythema chronicum migrans (target) around bite location, flu-like symptoms

Stage 2: disseminated infection; secondary annular skin lesions, pain in joints, tendons, lymphocytic meningitis, cranial neuritis (Bell’s palsy), radiculoneuropathy, AV nodal block

Stage 3: persistent infection; intermittent attacks of joint swelling and pain primarily in large joints (knee; 1 or 2 joints at a time)

78
Q

Indications for testing for Lyme disease

A

Migratory pain in joints, tendons, brief attacks of arthritis

Lymphocytic meningitis, cranial neuritis (facial palsy), radiculoneuropathy

AV nodal block

All the serious symptoms…

79
Q

How do you prevent Lyme disease

A

Can wear clothing with permetherine in it

Check for ticks! Early detection and removal of tick within 24 hours can prevent disease

Prophylactic doxycycline 200mg if engorged tick is found

80
Q

Leptospira weilii

A

Spirochete wound in thin tight coil

Lives in renal tubules of host (rodent, dog, fish, bird), shed in animal urine, transmitted to humans via contaminated water (surfers get this)

First/septicemic (leptospiremic) phase: 3-7 days; bacteria invade blood and CSF; high fever, headache, malaise, myalgia, abdominal pain, conjunctival suffusion (red), photophobia

Second (immune) phase if ANICTERIC: 0-1 month; milder fever, headache, vomiting, aseptic meningitis

Second (immune) phase if ICTERIC (Weil’s Syndrome): jaundice, renal failure, hypotension, hemorrhagic pneumonitis, mortality 5-40%

81
Q

Do spirochetes have toxins?

A

No!

82
Q

Which innate immune response mechanism recognizes leptospiral LPS?

A

TLR-2

Usually LPS recognized by TLR-4, but leptospiral LPS is different!

83
Q

3 layers of tear film

A

1) Lipid layer
2) Aqueous layer (composed of proteins)
3) Glycocalyx (covers surface of cornea)

84
Q

Where do lipids come from?

A

Meibomian oil at the meibomian orifice

85
Q

Where do tears come from?

A

Lacrimal gland

Note: tears protect you because they contain immunoglobulins

86
Q

Dry eye disease

A

Most common eye disease

87
Q

Conjunctiva

A

Conjoins cornea to eyelid at the limbus

Non-keratinized stratified squamous epithelium with goblet cells (which produce mucin 5AC which goes into tear film and is very protective)

Clear so you can’t see it, but contains blood vessels that you can see

88
Q

Squamous carcinoma of the eye

A

Gelatinous layer that covers surface of cornea (so can’t see well)

Most common malignant disease

89
Q

Cornea

A

Central visual axis, must remain clear for good vision

Key refractive surface

5 layers

90
Q

5 layers of the cornea

A

1) Epithelium
2) Bowman’s layer
3) Stroma (most of the thickness of cornea)
4) Descemet’s membrane
5) Endothelium

91
Q

Infectious corneal ulcer

A

Most common disease of cornea

Most common reason for this disease is contact lens wearing

Can perforate through eye, through stroma and can lose eye if not treated rapidly

92
Q

Lens

A

Behind iris

Grows for your entire life

Lens fibers surrounded by thin capsule

Most common disease of lens is cataract

93
Q

Cataract

A

Precipitation of aggregation of lens crystalline proteins

Opaque, so can’t see through it

94
Q

Anterior chamber

A

Bounded by cornea anteriorly, iris posteriorly, scleral spur, ciliary body

Key structures for aqueous drainage: Schlemm’s canal and trabecular meshwork

95
Q

Uvea

A

Contains iris, ciliary body and choroid

Contains melanocytes to absorb scattered light and give you a good view

96
Q

Iris

A

Anterior border layer

Stroma

Constrictor muscle

Dilator muscle

Posterior pigmented epithelium

97
Q

Ciliated body

A

Produces aqueous (non-pigmented layer)

2 layers: pigmented layer and non-pigmented layer

Muscle for accommodation

Important blood vessel that can rupture during trauma

98
Q

Malignant melanoma of eye

A

Most common malignant disease of uvea

Slower growing than melanoma on the skin, but still can kill you

99
Q

Retina

A

Thin membrane that covers entire posterior compartment, contiguous with optic nerve

Joins ciliary body

Processes light, modulates, and sends to lateral geniculate ganglion

3 major cellular layers: ganglion cell layer (will form optic nerve), inter-nuclear layer (electrical modulation system), photoreceptors, retinal pigment epithelium (integrated with photoreceptors and keeps them alive)

100
Q

Macular degeneration

A

Causes decrease in central vision

Fibrous tissue grows between retina, from choroid

Doesn’t cause complete blindness

101
Q

Optic nerve

A

At posterior part of eye

Tubular structure containing numerous axons of ganglion cells and glial cells arranged in columns which are separated by fibrous sheaths

102
Q

Optic atrophy

A

Final common pathway of most optic disease

Block 6: Microbio, ID, Derm, Heme-Onc (10 decks)

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