Mar26 M2-Infection and immunity Flashcards

1
Q

things that influence the symptoms of a disease with inflammation

A
  • immune system impaired
  • infant (not same symptoms as adults)
  • being on a statin
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2
Q

biologic drugs used in many diseases: what they do

A

immune system modifiers

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3
Q

statins effect on the immune system

A
  • compromise the immune system

- compromise macrophages (supposed to cause plaque rupture). ats not stopped but plaque rupture stopped

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4
Q

fever, malaise, was in quinolone resistant malaria strain area when travelled in Africa = number 1 on ddx

A

acute viral illness infection (malaria is only number 2)

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5
Q

concept of route of infection in the body

A
  • diff routes of entry of pathogens (airways, GIT, reproductive tract, external surface, wounds, insect bites)
  • each route has its pathogens
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6
Q

important pathogens in airway, GIT and reproductive tract routes

A

airways = influenza
GIT = salmonella, rotavirus
reproductive tract = HIV, treponema pallidum

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7
Q

4 classes of pathogens

A
  1. EC bacteria, parasites, fungi
  2. IC bacteria, parasites
  3. viruses (IC)
  4. parasitic worms (EC)
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8
Q

1st symptom of malaria

A

periodic fever

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9
Q

malaria type of infection

A

intracellular parasitic infection (enters and lives in RBCs)

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10
Q

immunologicla charact of RBCs

A

no MHC 1, malaria invisible to immune system in RBC. when RBC full, bursts, malaria goes in other RBCs

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11
Q

how microbes get through epithelial barriers of the body

A
  1. mechanical effects (cuts, breaks, bites)
  2. chemical (they can secrete stuff to compromise our barrier)
  3. compromised gut flora (serves as protection normally)
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12
Q

factors that influence the incubation period of a virus (3)

A
  • amount of inoculum you got (how much virus)
  • virulence of the infection (how many substances released and that serve as stimulus)
  • immune system reaction
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13
Q

3 steps of immune response after infection (3 time categories)

A
  • innate immunology (0-4 hours) = non specific receptors
  • early induced response (4-96 hours) = PAMPs
  • adaptive immune response (clonal expansion of B and T cells)
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14
Q

when does adaptive immune system act in infection and how long before you see an Ab

A
  • doesn’t act until at least 4 days

- see first Ab after 2 weeks

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15
Q

there’s a certain level of Ag needed for the adaptive immune response to be involved: name of that concept

A

antigenic window (is a threshold) (at threshold, end of incubation period)

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16
Q

def of incubation period

A

time to onset of symptoms = time to threshold (of adaptive immunity)

17
Q

(imp) 5 acute phase cytokines + def of that

A
  • cytokines released first and that cause the first blush of symptoms
  • IL-1, IL-6, IL-8 (CXCL8), IL-12, TNF-alpha
18
Q

why route of infection is key in immunity

A
  • will try to localize infection to its original site
  • systemic dissemination and infection that spreads = LOT of inflam + HARD to target (bc cytokines released everywhere by macrophages = confusing for neutrophils)
19
Q

what helps localize an infection to its original site

A

antibodies

20
Q

liver role in inflammation

A

produces acute phase reactants

  • platelets
  • CRP (acts as an opsonin on bacteria + activates the complement). important for abcesses bc they can hide
21
Q

abscess management and prognosis if watch and wait

A

management = drain, give Abx, until microbes gone

watch and wait = abscess will win and spread

22
Q

3 things that can happen if you stop Abx (for an abscess for ex) too soon (the 3 Rs)

A
  1. reappearance of the abscess
  2. resistance (if new microbe grows again)
  3. regrowth
23
Q

how to follow an abscess and know when it’s gone

A

watch CRP and follow until back to normal

24
Q

CRP still elevated after normal Abx time 2 things to do

A
  1. rethink dx

2. continue Abx

25
Q

most common pathway to deal with viruses

A
  1. virus infected host cell releases IFN-a and IFN-b
  2. resistance to viral replication in all cells
  3. more MHC class 1 expression
  4. NK cells activation
26
Q

3 immune branches involved in virus elimination (in order) and ones that are more involved

A
  1. IFN-a, IFN-b, TNF-a, IL-12 production + NK-cell mediated killing of infected cells (Most of the job)
  2. T cell mediated killing of infected cells
27
Q

2 advantages of infected cell killing (virus) with T cells (CD8)

A
  1. cell implodes (apoptosis)

2. protects surrounding

28
Q

consequence of a disease of macrophage activation

A
  • primary immunodeficiency

- can get adenitis (lymph node infection) bc macrophage engulfs bacteria but doesn’t kill it

29
Q

time before primary immune response really acts vs secondary immune response

A

12 days

secondary = immediately

30
Q

why secondary response is faster and stronger

A

faster bc of memory cells
stronger bc of somatic hypermutation
*only high affinity cells and high affinity memory cells remain at end of primary response

31
Q

substance that marks, flags microbes in the body

A

antibodies

32
Q

4 things Abs do

A
  1. neutralization + eventually leads to ingestion by macrophage
  2. opsonization (coat + macrophages eat)
  3. complement
  4. independent Ab mediated cell toxicity (target pathogen bound with Ab for other cells)
33
Q

4 ways microbes can make you sick (4 sites)

A
  • interstitial spaces, lymph, blood
  • epithelial surfaces
  • cytoplasmic
  • vesicular (IC)
34
Q

whooping cough like pertussis, diphteria and others, why makes you sick

A

Are toxemias. it’s the toxin that causes the cough.

35
Q

2 most common causes of death in influenza

A
  • secondary bacterial infection

- heart attack

36
Q

how long influenza effect can last

A

4 months

-can show up with pneumonia 4 months after infection

37
Q

HIV infects what cells in the body

A

CD4+ T cells (helper)

38
Q

CASE: fever, malaise, was in quinolone resistant malaria strain area when travelled in Africa: investigation

A

smear for malaria (viral infection still #1 on ddx)

39
Q

name of healthy infection

A

commensals