Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pathophysiology > lecture 8 - Communicable disease > Flashcards

lecture 8 - Communicable disease Flashcards

1
Q

communicable disease

A

disease transmitted fro person to person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

endemic

A

communicable disease in which a small number of cases are continually present in population (covid may become this)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

epidemic

A

communicable disease concurrently affecting large numbers of people in a population (contained to a defined geographical area)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pandemic

A

global, world-wide outbreak across several countries or continents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

methods of transmission: direct

A
  • direct physical contact (casual, sex)
  • droplet spread (coughing, sneezing)
  • fluids/ blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

methods of transmission: indirect (through an intermediary mechanism)

A
  • contaminated food or water
  • insects (vector)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

methods of control: direct transmission

A
  • immunization (personal vs population (herd), reduction in number of susceptible individuals)
  • active (vaccination - waking up your own immunity) vs passive (plasma containing Ab/ maternal transmission)
  • if large enough proportion are vaccinated, disease will die out as there are increasingly scarce opportunities for transmission (small pox)
  • effective relates to vaccine uptake, vaccine effectiveness, pathogen infectivity, previous exposures (protection)
    (want 50-75% vaccinated to eradicate pathogen - herd immunity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

methods of control

A

identification, isolation, and treatment (when immunization is not available)
- control transmission (masks, less contact)
- use indicators of disease (fever)
- effectiveness depends on transmissibility and symptomatic disease onset
(ebola transmissible when GI symptoms start vs rabies = mortality at symptom onset)

diagnostic testing (reliant on test availability and effectiveness) - specificity/ sens
- isolation (prevents contact with susceptible persons and stops spread)
- use diagnostic if symptomatic/ visual methods don’t work

diseases difficult to control (not obvious/ recognizable) - TB, STIs, etc…
- nonspecific, delayed symptoms, signs of immune response and not directly caused by pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

methods of control; indirect transmission

A

controlling indirect transmission of contaminated food or water
- CHLORINATION of water supplies
- effective SEWAGE treatment facilities
- standards for handling, manufacturing, and distributing commercially prepared FOODS
- eradication and/or control of ANIMAL sources and VECTORS
- physical BARRIERS - nets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

requirements for effective control

A
  • must know cause of disease and methods of transmission

bubonic plaque (swollen lymph nodes/ black colour septicemia) - 70% death rate
- one of deadliest diseases (14th century - 50m) in human history (second to smallpox)
- people did not know disease carried by rodents and bacterium (Yersinia pestis), transmitted to people by flea bites
- starts with fever, weakness, headache 1-7 days
- resulted in widespread and misguided attempts to control disease spread
- can be a spread via droplets causing pneumonic plague or fatal pulmonary infection

NOW, we know the cause, have effective tests and treatment (vaccines/ abx), and the disease still has sporadic outbreaks that are easily treated and controlled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

STIs other than HIV (4 major) - and what is the spread?

A

spread: primarily intimate contact between sexual partners
4 major STIs:
- syphilis (Treponema pallidum) - primary, secondary, tertiary
- gonorrhea (Neisseria gonorrhoeae)
- herpes (herpesvirus)
- chlamydia (chlamydia trachomatis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Syphilis (Treponema pallidum) : major clinical manifestations

A

penetrates mucous membranes of genital tract, oral cavity, rectal mucosa, or through break in skin (multiplies rapidly)

primary: chancre (small ulcer at site of inoculation)
- penis, vulva, vaginal, oral cavity, rectum
- swarming with treponemas, highly infectious
- 4-6 weeks then HEALS W/O TREATMENT (but treponemas still multiply)

secondary: systemic infection with skin rash and enlarged LN
- develops after 4-10 weeks, lasts 2-3 years
- begins several months after chancre healed
- fever, lymphadenopathy, skin rash, shallow ulcers on mucous membranes of oral
cavity and genital tract
- persists for several weeks then SUBSIDES W/O TREATMENT, recurrences subside
spontaneously
- latent phase can last many years

tertiary (latent): late destructive lesions in internal organs
- 3-15 years, develops in 15-40%
- appear up to 20 years after infection, not usually communicable
- organisms remain active causing irrepairable organ damage due to chronic
inflammation (scarring of aortic valve: degeneration of fiber tracts in spinal
cord, mental deterioration, paralysis)
- many organ systems can be effected including neuro and ocular syphilis

*latent phase can go on for a very long time –> can lead to tertiary, now sitting in organ, not contagious at this point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Syphilis (Treponema pallidum) : tests for diagnosis

A

demonstration of treponemas in chancre (microscopic exam) - swabbing sore
- establishes diagnosis several weeks before a blood test becomes positive

serologic tests (antigen-Ab rxn) - blood test looking for Ab
- turns positive soon after chancre appears, remains positive for years
- useful for diagnosing disease in asymptomatic, and in cases where chancre is inaccessible or escapes detection (most cases)
- some tests remain positive forever (reinfection more complicated to detect) - use combination testing with 3 tests and must be interpreted in combination with clinical history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Syphilis (Treponema pallidum) : major complications and treatment

A

damage to cardiovascular system in tertiary syphilis
may be fatal

tx: abx (long acting benzathine penicillin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

congenital syphilis

A

transmission of disease from mother to child
- may cause death of fetus
treatment early in pregnancy so treponemas are less likely to pass through placenta during first few weeks of pregnancy
- during early stage pregnancy, placental villi are covered by a double layer of epithelium and contain more connective tissue that is less permeable (thicker barrier to get through)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gonorrhea (Gonococcus) - Neisseria gonorrhoeae): major clinical manifestations

A

primarily infects mucosal surfaces:
- urethritis
- cervicitis (genital tract)
- pharyngitis
- infection of rectal mucosa (proctitis)

symptoms appear week after exposure
clinical manifestations differ between men and women…

men:
- acute inflammation of mucosa of anterior urethra
- purulent urethral discharge
- pain on urination
-less likely to be asymptomatic

women:
-infects mucosa, uterine cervix, and urethral mucosa
- spread to Bartholin glands (beside vaginal orifice)
- cervical infection: profuse vaginal DISCHARGE
- urethral involvement: PAIN, burning on urination
- some asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

extragenital gonorrhea

A

(outside of genitals)
- rectum: pain and tenderness, purulent blood mucoid discharge
-from anal intercourse or contamination of rectal mucosa for infected vaginal
secretions
- pharynx and tonsils: oral-genital sex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

disseminated gonococcal infection

A

(spread)
- organisms gain access into bloodstream and spread throughout body
- fever, joint pain, multiple small skin abscesses, infections of the joints, tendons, heart valves, meninges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Gonorrhea (Gonococcus) - Neisseria gonorrhoeae): tests for diagnosis

A

culture of organisms from sites of infection (swab site of interest)
- sites: urethra, cervix, rectum, phaynx

nonculture tests (NAAT- nucleic acid amplification test)
- based on identification of nucleic acids in organism (urine sample or other bodily fluid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Gonorrhea (Gonococcus) - Neisseria gonorrhoeae): major complications and treatment

A

disseminated bloodstream infection
tubal infection with impaired fertility
spread of infection to prostate and epididymides

WOMEN:
- could spread to fallopian (tubal infection) - SALPINGITIS
- abscess formation in tubes
- tubal scarring and STERILITY (can impede ovum transport with pregnancy in fallopian tubes - ECTOPIC pregnancy)
- lower abdominal pain and tenderness, fever, leukocytosis

MEN:
- spread to posterior urethra, prostate, seminal vesicles, vasa differentia, and epididymis, STERILITY

tx: abx (ceftriaxone/ doxycycline)
- penicillin-resistant strains due to penicillinase enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Herpes (Herpes virus): major clinical manifestations

A

(herpes simplex virus infection) - once you have it, you always have it
- superficial vesicles and ulcers on external genitalia and in genital tract (following sexual exposure)
- regional LN enlarged and tender

Type 1: infects oral mucous membrane
- blisters, childhood, most adults have Ab (cold sores)
- may cause genital infections

Type 2: infects genital tract
- after puberty, 80% of infection (higher recurrence), 20% from type 1 due to oral-genital sex
- may infect oropharyngeal mucous membranes

MEN:
- glans or shaft of penis

WOMEN:
- vulva: painful
-vagina, cervix: little discomfort

vesicles: small painful blisters on external genitalia and genital tract, rupture and form shallow ulcers that coalesce
- contain large quantities of virus and are infectious to sexual partners

regional LN enlarged and tender:
- virus persists in infected epithelial tissues (latent phase in neural ganglia) causing recurrent infections over time (stays in ganglia until reemergence/ stimulation)
- in herpes, immune system is trying to suppress virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Herpes (Herpes virus): tests for diagnosis

A
  • demonstration of intranuclear inclusions in infected cells
  • virus cultures (from vesicles or ulcers - most reliable test)
  • serologic tests in some cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Herpes (Herpes virus): major complications and treatment

A

spread from mother to infant
- through active herpetic lesions in mother’s genital tract
- herpes Encephalitis - trigeminal nerve (inflammation of brain)
- delivery should be C-section in presence of active lesions so it doesn’t spread to baby through direct contact

tx: ANTIVIRAL (acyclovir) drug shortens infection but not curative (orally, IV, or topically)
- cold compress and pain relievers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Chlamydia (Chamydia trachomatis): major clinical manifestations

A

MOST COMMON STD
- cervicitis
- urethritis

  • similar to gonorrhea (can spread to fallopian tubes and have similar effects)
  • many asymptomatic

WOMEN:
- cervicitis
- urethritis

MEN:
- urethritis, acute urethral inflammation with frequency and burning on urination

25
Q

Chlamydia (Chamydia trachomatis): tests for diagnosis

A
  • detection of chlamydial antigens in cervical/ urethral secretions
  • fluorescence microscopy
  • cultures (swabs)
  • nonculture tests also available (NAAT: based on chlamydial nucleic acids, swiping areas for nucleic acids) - only one we really do
    - urine or other bodily fluids
    - sires of infection and swabbed and sent off
26
Q

Chlamydia (Chamydia trachomatis): major complications and treatment

A

tubal infection with impaired fertility
epididymitis

complications: involves uterine cervix, urethra, moderate vaginal dischargae
WOMEN:
- STERILITY
MEN:
- epididymitis
- STERILITY?

tx: abx (azithromycin/ doxycycline)

27
Q

other STDs: common but less serious

A

Condylomata: anal and genital warts - HPV (can cause cervical or anal cancer, can freeze, burn off with acid, cauterize)
Trichomonal vaginitis: Trichonomas vaginalis infection (protozoan parasite)
Scabies and crabs (microscopic mites)

28
Q

HIV (human immunodeficiency virus)

A
  • attacks immune system (destroys CD4)
  • as the disease progresses, immune functions are progressively suppressed
  • leads to AIDS
  • increased susceptibility to pathogens and opportunistic infections
  • immune functional deficits occur in both infected and uninfected cells

(not autoimmune)

29
Q

data about HIV

A

1 transcript, multiple genes, over 40 different mRNA can be produced (alternative splicing)

  • core surrounded by a double-layered lipid envelope acquired from the cell membrane of the infected cell when the virus buds out from the cell

9kb genome
ssRNA retrovirus (+ve)
codes for 9 proteins
2 structural proteins Gag and Env
1 enzymatic protein (Pol)
6 regulatory proteins (Tat, Rev, Nef, Vif, Vpr, Vpu)

30
Q

HIV transmission

A

enter body
- sexual contact
- blood and body fluids (seminal, vaginal)
- mother to infant

by blood/ blood products
- DIRECT INOCULATION (sexual contact, mucosal trauma from rectal intercourse)
- TRANSFUSION (contamination, need routine testing)
- sharing contaminated INJECTION needles
- TRANSPLACENTAL or POSTPARTUM transmission via cervical or blood contact at delivery and in breast milk

NOT through causal household or social contacts (it is hard to get!!)

31
Q

steps of HIV infection

A
  1. can’t multiply alone, must be inside a cell
  2. when HIV infects cell, it hijacks its machinery
  3. in host cell, HIV makes copies
  4. newly created virus particles can go infect other cells

*w/o treatment, HIV can make up to 10 BILLION VIRUS particles every day

32
Q

HIV life cycle

A

(this makes it hard to control)
1. virus binds CD4 and enters cell
2. reverse transcriptase converts (+) RNA into DNA (opposite from what we do - DNA-RNA)
3. extremely error prone and mutations may occur here
4. DNA transported into nucleus
5. integration of viral DNA into host cell’s genome by INTEGRASE
6. after integration, virus can remain dormant in cellular genome as provirus
7. upon cellular activation, genes are TRANSCRIBED and viral RNA is transported to cytoplasm
8. viral proteins are TRANSLATED and cleaved by PROTEASE
9. viral particles are assembled at the membrane where virions are released (viral envelope composed from host lipid bi layer)
10. activation of T-cells supports infection and production of virus
- patients with other infections/ inflammation are more susceptible to HIV infection and viral production
- in vitro, only activated T cells can be infected

  • it incorporates its viral DNA into its own cell so it can make more DNA (cut and integrated and glued in)
  • now it’s in DNA body and it’s hard to detect
  • replicates with CD4 cell and spits out more virus since it’s now in the DNA
33
Q

importance of coreceptor in HIV

A

-CD4 is the primary interaction with HIV (but CD4 alone is insufficient for virus entry into cell)

CD4 BINDING –> CORECEPTOR BINDING –> VIRUS:CELL FUSION

CXCR4: on T-CELLS (SDF1-chemokine receptor)
CCR5: on MACROPHAGES
!!BOTH are required to effect conformational change in gp120/41 and initiates virus: membrane fusion

(patients with CCR5 mutants are immune to infection with HIV)
- co-receptor is super important in the process of getting HIV

CXCR4 and CCR5, gp41, gp120 spikes, V3 loop, APC, MHCII, CD4, peptide, T-cell receptor

34
Q

molecular transmission of HIV

A

HIV is present as both free virus particles and viruses within infected immune cells

  • HIV primarily infects CD4+ T cells and macrophages through interaction with CD4 RECEPTORS on cell surface and GP120 SPIKES on virus
35
Q

CD4 vs macrophages in HIV

A

CD4: 90% of viral load
- most of HIV is in CD4
- SHORT LIVED once infected

macrophages:
- some is in here but not much
- LONG-LIVED and infections make them live longer
- may be part of the reason why it’s hard to treat HIV

36
Q

CD4 T cell abnormalities (all the things that can happen to an infected CD4)

A
  • depletion/ cell death, reduced proliferation/ regeneration
  • direct destruction by infection
  • direct/ indirect destruction by viral proteins
  • immune activation
  • anti-cellular effects of CD8

less than 1% of cells are infected at any point during infection, so indirect effects play a role in the development of immune pathology and progression to AIDS

37
Q

HIV receptors and routes of entry

A
  • HIV also uses other “non-classical” receptors and routes of entry (lots of other receptors HIV will bind to, but these other sites won’t do much)
  • CD4 cells are the MOST PREDOMINANTLY INFECTED and REPLICATE THE HIGHEST amount of virus
  • CD4 CELLS ARE THE MAIN TARGET OF HIV
  • progressive CD4 T cell infection and eventual depletion of CD4 T cells is a marker of disease progression (lots infected, start depleting = disease progression)
38
Q

cytopathic effects of HIV

A

1-2% OF CD4 T CELLS ARE INFECTED AT A GIVEN TIME

infected:
- cell-cell fusion
- accumulation of unintegrated viral DNA
- alteration of cell permeability/ lipids

infected and uninfected:
- apoptosis
- release of toxic cytokines by infected cells
- direct cellular toxicity of HIV and viral proteins
- destruction by immune responses
- inhibition of growth factors
- degradation of cellular mRNA, reduction in protein synthesis
(not only the infected cells get damaged from HIV, there are other things that happen as a result)
(CD4, CD8, B cells, macrophages, DCs, NK cells, thymus, neutrophil dysfunction, general disorders - all cause bad things)

39
Q

HIV replication and genetic variability

A

(replicates fast and mutates fast, lots of variability) - b/c it’s a retrovirus (we only have tx for DNA -RNA)

  1. fast replication cycle (generation of trillions of virus particles every day)
  2. high mutation (1/cycle) rate combined with recombination events (2-20/cycle)
  3. no fidelity for RT in eukaryotes
  4. many variants of HIV in a single infected patient in the course of one day
  5. over time, a single patient will accumulate several variants of HIV virus
  6. rapid mutational changes in HIV and large numbers of viruses being produced provides an adaptive advantage to HIV
  7. 8-10% changes in host virus over the course of the infection
40
Q

stages of HIV infection throughout the body

A
  1. HIV infection of mucosal tissues
  2. massive depletion/ death of mucosal and memory CD4 cells (DAYS)
  3. infection established in LN (spreads to activated T cells)
  4. infection spreads throughout the body (high viral load) (WEEKS)
  5. immune response partially controls viral replication (viral load decreased)
  6. clinical latency, steady and gradual (MONTHS)
    - not active phase, but things are still replicating
    - increase in viral load
    - decrease in immune functions
    - decrease in CD4 cell counts
    - patient probably doesn’t know that there’s anything wrong
  7. quicker progression (YEARS)
    - AIDS
    - loss of immune function
    - susceptibility to opportunistic infections/ cancer
    - death
    - destruction of lymphoid tissue, depletion of CD4
41
Q

when does HIV become AIDS?

A

when CD4 COUNT DROPS BELOW 200 (CD4 count drops as infection spreads/ progresses)

  • healthy individual has 800-1500 CD4 T cell in 1uL of blood
  • immune deficits start to emerge below 500
  • once this number drops below 200, the individual is described as having AIDS
    -they are then susceptible to dying from any infection of cancers, many of which we are constantly exposed to, and easily dealt with by a healthy immune system
42
Q

index of disease

A

if you want to monitor someone’s disease, you can count their CD4 or test how much VIRAL HIV RNA they have

viral RNA replication: measure the amount of viral RNA in blood
- virus replicates in LN, but amount of viral RNA in blood reflects extent of viral replication in LYMPHOID TISSUE

damage to immune system:
- measure number of CD4 lymphocytes in blood
- NORMAL: 800-1200
- BELOW 400-500: risk of opportunistic infections
- BELOW 200: risk of major HIV complications

43
Q

CD8 T cells - the EFFECTORS of cell mediated immunity

A
  • CD8 ARE THE MAIN CONTROLLERS OF HIV
  • important in combatting intracellular pathogens (like HIV), controlling infection and destroying infected cells using:
    1. cell to cell contact:
  • MHC1 presented HIV antigens (HIV is presented by APC on MHC1 for CD8 to kill?)
  1. secreted factors to:
    - destroy infected cells (PERFORIN/ GRANZYME A,B)
    - inhibit virus production/ promote immune activation (IFN-y, TNF-a, IL-2, MIP1a/B, RANTES)
    (or cytokines)

CD8 aren’t. infected by HIV YET, so they can help control

44
Q

cytotoxic T cells (CD8) and HIV

A
  • eventually, CD8 does get infected
  • CD8 dysfunction can be caused by:
    1. cytokine/ receptor dysregulation
    2. direct effect of HIV soluble factors
    3. cell death/ apoptosis
    4. other immune dysfunction
    5. anergy
    (not all from direct effect infection of HIV)
45
Q

progressive loss of CD8 T cell mediated immunity in HIV

A
  • there is a progressive loss of CD8 T cell mediated immunity
  • LOSS OF CD8 ANTIVIRAL ACTIVITY PRECEDES CD4 T CELL DEPLETION
  • viral-specific CD8 T cells remain present in the circulation at relatively normal frequencies even in patients with advanced disease
  • unresponsive, fail to proliferate, express Perforin or demonstrate cytolytic activity in response to antigens

(when CD4 is depleted, CD8 sticks around for a while until they also deplete later on)

  • in vitro model: effect of CD8 T cells on viral control in co-cultures also supports the role of CD8 T cells in control of HIV infection
46
Q

strong, moderate and weak anti-HIV CTL(CD8) activity

A

STRONG activity is associated with LTNP/ Elite controllers, degree of control of HIV infection, and in turn, SLOWER DISEASE PROGRESSION
(weak –> rapid progression)
- strong response depends on type 1 cytokine production and genetic background

47
Q

early manifestations of HIV infection

A

asymptomatic
mild febrile (fever) illness

48
Q

late manifestations of HIV infection

A

generalized LN enlargement
nonspecific symptoms
fever, weakness, chronic fatigue, weight loss, thrombocytopenia (low platelet count)
AIDS

49
Q

Antibody response to HIV

A
  • Ab formed within 1-6 months
  • detection of Ab provides evidence of HIV infection
  • Ab do not get rid of virus (THEY ARE NOT PROTECTIVE, they are a marker of infection)
  • virus is detectable by lab tests (VIRAL RNA) - the fast replicating thing
    (Ab are not detectable after infected for up to 6 months)
    (person should take post-exposure prophylaxis right away if there’s a risk they picked it up)

symptoms (take many forms)
- persistent generalized LYMPHADENOPATHY caused by impaired function of CD4 cells (immunodeficiency)
- nonspecific symptoms: weight loss, fatigue, night sweats, fevers related to altered function of immune system
- NEUROLOGIC symptoms resulting from HIV encephalopathy and infection of neuroglial cells

50
Q

complications of AIDS

A

OPPORTUNISTIC INFECTIONS for organisms not normally pathogenic or limited pathogenicity
- pneumocytosis carinii pneumonia
- candidiasis
- mycobacterium avium complex
- parasitic infections: toxoplasmosis, cryptosporidosis
- rapidly progressive TB or histoplasmosis
(or any viral infections/ anything that was latent or not expressed before will now be expressed)

MALIGNANT TUMORS IN AIDS PATIENTS
- kaposi sarcoma: human herpesvirus 8
- malignant tumors of B lymphocytes
- cancers of oral cavity, rectum, uterine cervix

REEMERGENCE OF DORMANT INFECTIONS LIKE…
- TB
- CMV (cytomegalovirus)
- EBV (ebstein-barr virus)
- HSV (herpes)
(they come out and manifest themselves again (because you never get rid of these, and now you don’t have an immune system to keep them under control)

51
Q

HIV pathogenesis sequence

A
  1. HIV enters T-cells and macrophages through primary interaction with CD4 and secondary interactions with coreceptors (CXCR4 and CCR5) which are required for virus: membrane fusion
  2. although different cell types can be infected or carry HIV, OVER 90% of virus in the body is produced by actively infected CD4 cells
  3. HIV integrates into the host genome where it can actively produce more virions or remain dormant for years as provirus, until reactivated by various stimuli
  4. in the early stage of infection, HIV destroys large numbers of T cells at mucosal sites, which are never fully restored
  5. CD4 depletion is an indicator of disease progression but is not in itself responsible for all aspects of HIV dependent immune deficiency (other things are also responsible for immune system falling apart)
  6. An initial strong immune response to the virus wanes over time (5-10 years) until the immune system fails, leading to disease progression and development of AIDS (CD4 count below 200)
  7. this TRANSITION PERIOD TO AIDS is marked by increased virus production, lack of CD8 T cell anti-viral responses, and rapid CD4 T cell depletion and susceptibility to opportunistic infections and cancers
  8. destruction of CD4 T cells and functional deficits in CD8 T cells are mediated by direct and indirect effects from both viral (whole virus and secreted viral proteins) and host factors (all other things body is doing)

(infected for life)
- when virus proliferates in infected cells and sheds virus particles, the virus is then present in blood and body fluids

52
Q

treatment of HIV infections

A

NO CURE
- treatments don’t get rid of HIV, they just try to STOP REPLICATION at any stage
- ANTI-RETROVIRAL THERAPIES

primary therapy: use of various COMBINATIONS and different types of antiretroviral agents to maximally INHIBIT HIV VIRAL REPLICATION with fewest adverse reactions
- various stages of life cycle of HIV are targeted during therapy to suppress viral replication (so you have less HIV)
- treatment schedules are revised as new drugs are developed and as advantages and side effects of various drug combinations are recognized

(live a long and healthy life as long as they stay on medications)

53
Q

Main groups of HIV treatments/ AIDS

A

antiviral drugs given in combination to target different phases of the virus life cycle
if you can block INTEGRATION AND REVERSE TRANSCRIPTION, the viral infection is pretty easy to control!!

  1. nonnucleoside reverse transcriptase inhibitors
  2. nucleoside reverse transcriptase inhibitors (nucleoside analogs)
  3. integrase inhibitors (main choice of drug now, effective and few side effects)
    - BLOCK INTEGRATION OF VIRAL RNA INTO THE CELLS OWN DNA
    if this is stopped, it can’t produce its own HIV viral cells
  4. protease inhibitors

additional treatment:
- supportive therapy
- nutritional support
- psychological support
- social (housing)

54
Q
  1. protease inhibitors
A

block action of viral protease in viral replication (needed for protein processing)
- block protease so less cleavage of protein and can’t produce virus

55
Q
  1. reverse transcriptase inhibitors
A
  • interfere with copying of viral RNA into DNA by the enzyme reverse transcriptase (block transcription)

NRTI DRUGS: substitute a nucleoside analog that resembles normal nucleosides used by virus to construct DNA, virus cannot distinguish between analog and normal nucleoside, interrupting viral DNA synthesis!!

NNRTI: binds to functional sites on reverse transcriptase inhibiting function!!

56
Q
  1. integrase inhibitors (main choice of drug now, effective and few side effects)
A

BLOCK INTEGRATION OF VIRAL RNA INTO THE CELLS OWN DNA

57
Q

PrEP and PEP

A

PrEP: treatment as prevention (pre-exposure prophylaxis)
- before exposure to HIV

PEP: prophylaxis within 72h (28 days of treatment)
- after exposure to HIV

barriers: coverage varies in provinces (Ontario covers 75%, full in BC, SK, Que)
cost (generic 250/month), perception of risk

58
Q

costs of treatment for HIV

A
  • financial-number of federal and provincial assistance programs (varies province to province)

Ontario Drug Benefit (ODB), Trillium Drug program
- constant treatment required - 10% struggle with care and not an effective treatment in Canada
- social: stigma
- mental and physical health

*as soon as you get off drugs, it will come back quickly, matter of weeks, virus may work its way around certain drugs so you may need to get different drugs available

pathophysiology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions