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Big Ol' Patho. > Not So Sexy > Flashcards

Not So Sexy Flashcards

1
Q

Routes of STi transmission?

A 
Genitalia
Mouth
Rectum
SKin
Placenta
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2
Q

What causes STIs?

Examples of each?

A 
Viral (recurring)
- Herpes, warts, AIDS
Bacterial (eliminated)
- Syphilis, chlamydia
- Gonorrhea, chancroid

Protozoa
Fungi
Ectoparasites

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3
Q

Risks for STIs?

A 
Multiple sex partners
UNsafe/high risk sexual practices
Drug abuse
Medically under served
Prior STDs
Non compliant STD tx

No/low risk:
abstinence
monogomy

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4
Q

Which herpes types are responsible for what?

A

• Type 1 responsible for “cold sores”, type 2 responsible for genital herpes → strains 6 + 11 here (16 and 18 associated with CA)

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5
Q

Genital herpes

  • Caused by?
  • What kind of microbe is this?
  • How is it spread?
A
  • Recurrent, systemic viral infection
  • Herpes simplex virus Type II
  • Neurotropic microbe (infects neurons)
  • Spread via contact with lesions or secretions
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6
Q

Genital herpes
- Incubation?
Manifests how many days after contact?

A

Inc = 2-10days

3-7d post contact

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7
Q

S/S of genital herpes?

Curable?

A
  • Burning at site
  • Painful vesicles
  • Fever, muscle ache
  • Sublinical? (not always symptomatic; virus may lay dormant for a bit)

NO CURE
• Cannot eliminate the virus – true for both types 1 and 2 → just have to deal with symptoms

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8
Q

Why do women have larger risk of transmission of genital herpes?

Why is detection more difficult/delayed?

A
  • Larger SA in woman’s genitals (vag + cervix) = more contact surface = greater risk of tranmission
  • For men, more readily visible on penis; detection harder in women, diagnosis delayed
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9
Q

Tx of genital herpes?

What is a major problem with this condition?

A

No cure
Antivirals (used for flare-up)
Symptomatic tx

Recurrence (flare-ups) is major problem

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10
Q

What causes genital warts?
What are they?
Where are they?

Incubation?
Cure?

A

HPV (strains 6 + 11)

Benign, multiple growths
• Lesions: short stalk with irregular head on it – is a benign neoplasm

Genital or anorectal

Incubation = 1-2months
No cure

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11
Q

Tx of genital warts?

A

Remove warts

  • Topical drugs, sx, cryotherapy
  • Monitor for CA (types 16 + 18)
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12
Q

Protection from genital warts?

A

Gardasil

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13
Q

What causes Syphilis?

Spread?

Incubation?
How does microbe behave once infection?

A

• Treponema pallidum

Spread via contact with lesions + by placenta

Incubation 10-90days
- Microbe division & distributes systemically

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14
Q

outline 1st stage of syphilis infection?

A
  • Painless chancre at exposure sites ( Once bacteria establishes, develops as ulcerative non-bleeding lesion)
  • Heals in 3-12wks (b/c disspears, person may falsely believe is result of sexual activity itself and not seek tx)
  • Regional lymphadenopathy

Easily eradicated at this stage – abx

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15
Q

outline 2nd stage of syphilis infection?

A

(up to 6 months)-
- Bacteria has gone systemic
- begins 6-8wks post infection
• Maculopapular rash on soles of feet and palms of hands – reddish, tiny pimples
• Flat papules - Whitish patches on mucous membranes (ex: on tongue)
• Generalized lymphadenopathy
- Fever, malaise

• Can still eradicated the bacteria at this stage! Just a bit harder now

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16
Q

What occurs after 2nd stage of syphilis infection?

A

Can move into up to 50 year latency period! Bacteria latent but in first year can still transmit to others.

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17
Q

3rd stage of syphilis?

A

1-35yrs untreated primary infection

Irreversible damage to bone, joints, CVS, NS

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18
Q

Tx of syphilis?

What is unique about this abx treatment?

A
  • Long acting penicillin – are dealing with spirochete bacterium – spiral shaped, this bacteria have long generation time (duration required for bacterial colony to double in size)
  • Gen time for E. Coli = 30 minutes
  • This bacteria gen time = 30 HOURS…long acting drug needed because is available in circulation for much longer peiod of time (which is necessary for such a long generation time)
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19
Q

What causes chlamydia?

Incubation?

A

Clamydia trachomatis

7-21 d incubation

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20
Q

Symptoms of chlamydia.

A

Asymptomatic in most cases

Male:

  • White or clear discharge
  • Mild dysuria
  • Testicular pain

Female:

  • mucopurulent vaginal discharge
  • dysuria
  • bleeding
  • pelvic pain (D/t complication of PID)
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21
Q

What is unique about Clamydia trachomatis?

A
  • Rudimentary (simple) bacteria + is tiny → thereore difficult to isolate, culture, and therefore identify + treat
  • Is gram –ve
  • Obligate intracellular bacterium = must remain inside host cell (does what viruses do) → this also makes it very hard to isolate + detect
22
Q

Explanation of pain in testes from CHlamydia?

A

pain in scotum but not related to problem in testes itself, but rather epididymus (accessory organ attached to testes which caries sperm for ejaculation) – this becomes inflamed = epididymitis

23
Q

Tx of chlamydia

A

• Abx: preferred = doxycycline + azithromycin

24
Q

What causes Gonorrhea?

Incubation?

A

Neisseria gonorrhoeae
Bacteria

3-8d incubation

25
Q

S/S of gonorrhea?

A

Female

  • purulent vaginal discharge
  • Dysuria
  • genital irritation
  • late pelvic pain (PID)

Male

  • urethral discharge
  • dysuria

Systemic:

  • Bacteremia
  • Pharyngeal infection, conjunctivities
  • Arthritis dermatitis syndrome
26
Q

Why Pharyngeal infection, conjunctivitis from gonorrhea?

A

septicemia → can establish in other parts of the area (ex: oropharyngeal)…also can spread orally via pharyngeal infection d/t oral sex

bacteria have entered eye → could devel visual problems

27
Q

Arthritis – dermitis syndrome?

A

this is septic arthritis = arthritis d/t infection (is only arthritis we will discuss that is due to infection); infection has also moved through into skin

28
Q

Tx of gonorrhea?

A
  • 1st line: cephalosporin’s

* 2nds line: inc dose of ceph’s, and add another class of abx

29
Q

HIV = ?

AIDS = ?

A

Human Immunodeficiency Virus

Acquired IMmunodeficiency syndrome

•HIV = virus; AIDS = disease

30
Q

How does AIDS work?
What complications may result?
Acute or chronic?

A
  • targets I system
  • severely immunocompromised –> op infections, CA
  • Chronic, progressive
31
Q

Et + transmission of AIDS

A

• Have two strains: HIV1 and HIV2 → both are now occuring globally

  • Sexual (harbours well in semen)
  • contaminated blood
  • maternal (in utero across placenta, labor + delivery, lactation)
  • Occupational (health workers) ~0.3% risk
32
Q

What is a retro virus?

A

• Retro virus –
o Typically in our cells, have DNA → RNA → proteins
o Retro viruses do this in reverse: RNA → DNA, incorporate genetic material into host DNA
o Retro drug oppose this

33
Q

Outline patho of AIDS

A
  • targets Th cells (CD4)
  • Also macrophages, B cells
  • Destoyes immune system –> dec immunity + defenses –> inc new infections + via latent pathogens
  • Various organs affected
3 phases
PRIMARY INFECTION occurs
- weeks to months (?)
- window period + seroconversion
- High viral load + severe dec in CD4 count
LATENT PERIOD
- Asymptomatic? (yrs)
- Lymphatic tissue damage
• Varies greatly in length
• Affects other parts of body
• Will pick up pneumonia, TB, etc
- Current resp infections
- Fatigue

OVER AIDS
occurs about ~10yrs after infect

34
Q

Factors that come into play with needlestick HIV transmission:

A

the viral load in the blood (quantity of virus within the blood), the site of needlestick injury (is it in site that would bring about easy introduction of the virus) and depth of the injury

provided you follow universal precautions, can almost eliminiate risk; mostly d/t needlestick unjury

35
Q

what is the “window period” of aids?

A

• Window period = time required for a diagnostic test to detect the microbe – need quantity of viruses to develop first
o For HIV, set at 3 months…so “up to 3 months” as have much better tests now
• Will do monthly test after exposure (1,2,3 months)

36
Q

What is CD4?

A

cluster of differntiation…are surface receptors (CD4 and CD8)…CD4 is found in abundance on surface of Th cells

37
Q

When is HIV infection classified as AIDS?

A

• If patient exceeds 20 opporunistic infection, will cateogirze this as AIDS
(I thought it had to do with CD4 count?)

38
Q

Dx of AIDS?

A
  • Clinical progression
  • ELISA
  • Western Blot Assay
  • PCR
  • CD4 counts + viral loads
    + P24 Ag test
    + NAT
39
Q

ELISA test?

A
  • Traditionally, first test = ELISA = Enzyme Linked Immunosolvent Assay –
    o Assay = a biochemical test
    o Measures antibodies against the entire virus
    o In order to be sensitive enough, have to have sufficient number of antibodies…the window period
40
Q

Western blot assay:

A
  • TEST FOR AIDS
    o Measures abs against specific antigens on the virus
    o More specific test than ELISA → now looking at specific antigen now, which is unlikely to be found on other virses…whereas the general proteins found on whole virus are more likely to be found on others as well (those detected by ELISA)
41
Q

PCA test?

A
  • TEST FOR AIDS

= polymerase chain reaction
o Very sophisticated + expensive test
o Expand DNA sequence
o Are measuring presence of the virus itself

42
Q

CD4 counts?

A
  • TEST FOR AIDS

essentially measuring number of Th cells, by way of measuring the number of CD4 markers on those cells → typically used to detect the efficacy

43
Q

P24 Ag test

A
  • TEST FOR AIDS
    one that’s not available to most people…
    o Measuring protein in viral core (the P24 protein) → appears early on in serum of individual who is infected
    o From time of infection until sero-conversion (when you start producing antibofies against the virus?), you will find this → is good early detection test!
44
Q

NAT test?

A
  • TEST FOR AIDS

Nucleic Acid Testing
o Replaces PCR test (is faster and less expensive, serves similar purpose)
o Testing nucleic acid (genetic components) of the virus

45
Q

Manifestations of AIDS?

A
  • MANY
  • Opportunistic infections
  • Resp (TB + pneumonia)
  • GI – variety of issues, gastroenteritis, diarrhea, etc.
  • NS (dementia, encephalopathy)
  • CA (kaposi’s sarcoma, non-hodgkin’s lymphoma, cervical)
46
Q

Tx of AIDS?

A
  • THERE IS NO CURE FOR HIV/AIDS – you can control the virus + the progression of the disease, but you cannot eradicate the virus!
  • Antiretroviral agents – are many, will usually use coctail of drugs (2-3)
47
Q

TB that develops in AIDS is often ______

A

drug resistant

48
Q

why encephalopathy from AIDS?

A

from toxins from infect + HIV affecting nervous system itself

49
Q

HIV and CA – is not infection, so why is it opportunistic?

A

o The immune system is defensive against abnormal cells – CA no longer protected against
o Relationship between viruses + CA – altered DNA + mutations (may alter those that prevent proliferation)

50
Q

Kaposi’s Sarcoma?

A

arises in endothelial cells (in the blood vessel) but malignant lesions widespread → may see on skin, in mucosa of mouth, lymph nodes…

Big Ol' Patho. (17 decks)

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