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BECOM II Exam 4 > Mechanisms of Inflammation/Parasites > Flashcards

Mechanisms of Inflammation/Parasites Flashcards

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1
Q

function of inflammation

A

cause damage while removing harmful agents

bad clinically –> anti-inflammatory drugs; immuotherapeutic agents

good for body –> remove pathogen or toxin & repair damage

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2
Q

calor

A

heat

vasodilation of tissue due to damage - causing inflammation

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3
Q

Rubor

A

redness

RBCs entering due to tissue damage

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4
Q

Tumor

A

swelling

recruit immune cells to the site of tissue damage & due to endothelial cell damage

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5
Q

Dolor

A

Pain

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6
Q

Functio laesa

A

loss of function

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7
Q

inflammation

A

localized rxn - produces symptoms that can be internal or external

adaptive response - triggered by noxious stimuli

protective response to invading pathogen or stimuli; involved in repair

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8
Q

what signals lead to an immune response?

A

PAMPs and DAMPs binding to PRRs on immune cells

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9
Q

necrosis

A

release the contents of the cell; signal that some damage is occurring

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10
Q

acute inflammation

A
  • early response; beneficial
  • remove offending agent & repair tissue
  • positive feedback loop
  • minutes to hours
  • mainly neutrophils
  • mild damage
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11
Q

chronic inflammation

A
  • sum of responses by a tissue against an agent
  • unable to remove offending agent
  • damaging effects –> fibrosis & loss of function; alveolar damage
  • anti-inflammatory drugs beneficial in stopping effects
  • slower - days to occur
  • mainly macrophages/monocytes & lymphocytes
  • severe damage
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12
Q

asbestos

A
  • too big to be killed by alveolar macrophages

- irritate tissue & damage alveoli

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13
Q

steps of an immune reaction

A
  1. recognition of agent/damage
  2. recruitment of leukocytes & proteins
  3. destroy agent
  4. inflammation resolves
  5. tissue repaired
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14
Q

Hemostasis - 0 phase

A

1st step in immune response

vasoconstriction, platelet activation, clot formation

clot - réservoir for chemical mediators; starts recruitment & activation of leukocytes

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15
Q

resident cells

A

mast cells, macrophages, DCs

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16
Q

recruited cells

A

neutrophils, macrophages, B and T cells

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17
Q

NFkB pathway

A

associated with a lot of inflammation

  • big target for drugs
  • IL-1 and TNF-alpha big inflammatory mediators
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18
Q

chemical mediators

A

substance that acts on local tissue to facilitate an inflammatory response
-ex. histamine, prostaglandins, complement, etc.

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19
Q

exogenous sources

A

bacteria & viruses

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20
Q

endogenous sources

A

plasma, leukocytes, endothelial cells, fibroblasts

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21
Q

stages of immune response

A
  1. hemostasis
  2. recognition of pathogen or damage
  3. recruitment of leukocytes and proteins
  4. destroy pathogen through oxidative burst
  5. Inflammation resolves
  6. repair damaged tissue
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22
Q

1st phase of recruitment of leukocytes

A

vasoactive changes

  • vasoconstriction 1st, vasodilation follows
  • increase blood flow
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23
Q

2nd phase of recruitment of leukocytes

A

increase capillary permeability

-endothelial swelling or damage –> exudate & edema

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24
Q

extravasation

A

mobilizes body defenses

  • margination = selectins & ICAMs help leukocytes adhere to wall
  • diapedesis = leukocytes enter tissue
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25
Q

what do selectins, integrins, & ICAMs do?

A

line up on endothelial wall when there is damage

  • attach to WBCs
  • chemokines pull them across
  • selectins (endothelium), integrins (immune cells), ICAMs (both)
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26
Q

role of integrins

A

bring immune cells through endothelial cells to tissue

-ex. CXCL1,7,8 & CCL3,5

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27
Q

big players in acute phase rxn - inflammation

A

IL-1beta, IL-6, TNF-alpha

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28
Q

what does IL-6 do?

A

induces hepatocytes to make acute phase proteins - mannon-binding lectin, fibrinogen, C-reactive protein –> opsonize bacteria & activate complement

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29
Q

oxidative burst

A

usually by neutrophils (also macrophages & DCs)

intracellular killing - release contents of cells

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30
Q

what helps repair tissue damage?

A

activation of fibroblasts - replace damaged epithelial cells

angiogenesis

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31
Q

role of fibroblasts

A

lay down collagen for repair - result in scar if not perfect

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32
Q

role anti-inflammatory molecules

A

shut down the immune response once pathogen is eliminated - apoptosis of immune cells

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33
Q

steps of acute inflammatory rxn

A
  1. recognizing agent/damage
  2. recruitment of leukocytes & proteins
  3. leukocytes & proteins destroy agent
  4. inflammation resolves
  5. damaged tissue repaired
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34
Q

where are acute phase proteins produced?

A

liver

-need cytokines to signal release

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35
Q

what mediators result in fever/inflammation

A

IL-1beta
IL-6
TNF-alpha

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36
Q

what immune cells are recruited for bacterial infection?

A

neutrophils

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37
Q

what immune cells are recruited for viral infection?

A

lymphocytes

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38
Q

what leads to fever during inflammation?

A

new hypothalamic set point by cytokines

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39
Q

Transudate

A

smaller holes in endothelial

  • low protein and cell content (low specific gravity)
  • no coagulation (clear sample)
  • no inflammatory cells
  • acute response
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40
Q

Exudate

A

larger holes in endothelial (larger things pass)

  • high protein and cell content (high specific gravity)
  • RBCs and immune cells can enter
  • has coagulation (opaque)
  • has inflammatory cells
  • chronic response
41
Q

Suppurative (purulent) inflammation

A

severe acute inflammation w/ pus

-pyogenic bacteria: staph aureus, strep pyogenes, E. coli

42
Q

what is pus?

A

fluid that contains dead neutrophils, bacteria, plasma proteins, and necrotic tissue

43
Q

Non-suppurative inflammation

A
  1. serous - runny nose, watery fluid, blisters, less proteins and cells
  2. serofibrinous - snotty nose, fibrin rich, more proteins and cells
  3. catarrhal - rhinitis, mild inflammation w/ mucus membrane and watery secretion
  4. Pseudomembranous
  5. hemorrhagic
  6. necrotizing
  7. allergic
44
Q

cells in acute inflammation

A

neutrophils (Mickey Mouse), not many T cells, less macrophages

45
Q

cells in chronic inflammation

A

lymphocytes (large round nucleus), more macrophages

46
Q

pathological outcomes of inflammation

A
  • resolution (resolve inflammation; wound healing)
  • abscess (aren’t healing)
  • ulcers
  • fistula
  • chronic inflammation (cannot resolve problem)
  • scars (fibrosis)
  • allergies
47
Q

role of fibroblasts

A

make collagen to initiate wound healing - improper wound healing leads to scars

48
Q

transition from acute to chronic inflammation

A
  • no resolution
  • shift from neutrophils to macrophages and lymphocytes
  • cycle b/w inflammation, damage, and repair
  • fibrosis (collagen deposition)
49
Q

what immune cells are recruited in acute inflammation?

A

neutrophils - innate immunity

50
Q

how can you get rid of bacteria that induce cell damage?

A

can activate compliment if they are opsonized with antibodies

51
Q

role of mast cells in acute inflammation

A
  • lead to hypersensitivities
  • degranulation by IgE
  • release histamines, prostaglandins, leukotrienes
52
Q

how do immune cells enter through endothelial cells?

A

inflammatory mediators use receptors to stop and bind the immune cells to enter the endothelial layer –> margination/diapedesis

53
Q

what is a marker of chronic inflammation?

A

formation of granulomas

  • mainly from activated macrophages
  • occurs during fibrosis
54
Q

what immune cells are recruited during chronic inflammation?

A

lymphocytes (B, T, plasma) and macrophages

-macrophages most prominent

55
Q

chronic inflammation characteristics

A
  • longer duration (weeks, months, years)
  • delayed type hypersensitivity rxn
  • fibrosis
  • formation of new blood vessels (angiogenesis)
  • not resolved immediately
56
Q

causes of chronic inflammation

A
  • persistent infections (bacteria, viruses, fungi, etc.)
  • hypersensitivity disease (RA, MS, asthma, inflammatory bowel disease etc.)
  • prolonged exposure to toxic agents (silicosis, atherosclerosis, alzeihmers, diabetes)
57
Q

silicosis

A

body tries to encapsulate particulate silica in a chronic inflammatory process, but silica never goes away (not harmful)

58
Q

atherosclerosis

A

cholesterol deposition in the arterial walls

-NOT arteriosclerosis (hardening of arteries)

59
Q

features of chronic inflammation

A
  1. infiltration of site with macrophages, lymphocytes, and plasma cells
  2. tissue destruction by organism, agent, or inflammatory mediators
  3. healing by angiogenesis or fibrosis
    - granulomas caused by fibrosis
60
Q

role of macrophages

A
  • release cytokines and growth factors for lymphocyte activation
  • destruction and clean up during chronic inflamm.
  • release ROS and enzymes to degrade agent
  • produce inflammatory response (IL-1, IL-12,IL-23)
  • initiate tissue repair
  • display antigens to T cells
61
Q

M1

A

classical pathway for macrophage activation

-activated by Th1 cells and IFN-gamma

62
Q

M2

A

alternative pathway for macrophage activation

-activated by Th2 cells and IL-4,5,13

63
Q

what do Th17 cells recruit

A

recruit neutrophils and monocytes through the release of IL-17

64
Q

B cells and plasma cells in chronic inflammation

A

-may have antibody response to multiple antigens which can cause autoimmunity

65
Q

what is a tertiary lymphoid organ?

A

clusters of macrophages and antibodies

-area of [] immune cells

66
Q

other immune cells in chronic inflammation

A
  • eosinophils = major basic protein (MBP) –> toxic to parasites
  • mast cells = prominent in chronic
  • neutrophils = mostly in acute, can also be in chronic if they hand around inflammation sites
67
Q

granulomas

A

nodular collection of epithelioid macrophages surrounded by lymphocytes (often Th1)

  • reorganization of tissue w/ persistent inflammation
  • sometimes associated with necrosis
  • transform macrophages to epithelioid Macs by IFN-gamma
68
Q

what are giant cells?

A

fused cluster of macrophages - mulitnucleated

69
Q

2 types of granulomas

A
  1. foreign body = form around material such as talc, sutures, or food
  2. immune granulomas = cell mediated, agent hard to eradicate –> Macs activate T cells to release cytokines forming granuloma to wall off infection
70
Q

Caseating vs. noncaseating granulomas

A 
Caseating = always associated with TB; epithelioid macrophages, cheese like material, necrotic
Noncaseating = sarcoidosis; activated macrophages; always has cells in it, non-necrotic
71
Q

protozoa

A

single celled eukaryotes

72
Q

helminths

A

worms

73
Q

ectoparasites

A

bugs

74
Q

what is a diagnostic test for trichomonas vaginalis?

A

cervical wet prep

75
Q

blood/tissue protozoa is transmitted how?

A

via mosquitos, tick, or sandfly

76
Q

protozoa cysts stage

A

often mode of infection

-initially dormant and enter this stage when exposed to harsh environment

77
Q

protozoa trophozoite stage

A

metabolically active, reproductive, and feeding

78
Q

what 2 protozoa are acid fast?

A
  • cryptosporidia (4 microns; small) - always stains but are unevenly stained
  • cyclospora (size of RBC) - sometimes stains, but not always
79
Q

Acanthamoeba

A

can enter the brain

-get under contacts causing corneal lesions

80
Q

Naeglaria

A

can enter brain through cribriform plate

81
Q

GI protozoa

A
  • giardia lamblia
  • cryptosporidium
  • cyclospora
  • entamoeba histolytica (outside US)
82
Q

Giardia lamblia

A

“farting sulfur”

  • sulfurous belching/flatulence
  • uncontrollable diarrhea, fat rich floating stool
  • # 1 protozoa cause of diarrhea
  • high risk when camping (outdoors)
  • alien face
83
Q

cryptosporidium parvum

A
  • watery diarrhea in immunocompetent
  • severe diarrhea and dehydration in AIDS patients
  • cause of epidemic community diarrhea outbreaks
84
Q

entamoeba histolytica

A

traveler’s dysentery = bloody diarrhea, fever, cramps

  • can escape gut and cause abscess in liver, lung, brain
  • trophozoite contains RBCs in it
  • positive fecal leukocyte test
85
Q

amoebic vs. bacterial dysentery

A

both have tenesmus (bowel movements) and bloody diarrhea and + fecal leukocyte

  • amoebic = variable fever
  • bacterial = high fever
86
Q

CNS protozoa

A
  • toxoplasma gondii
  • acanthamoeba
  • Naegleria fowleri
  • Trypanosoma brucei
87
Q

Toxoplasmosis gondii

A

“cat poop parasite”

  • risk to pregnant women who have cats
  • cat poop, undercooked meat, unwashed vegetables
  • ring enhancing lesions found scattered across brain on CT –> neurological deficits (ex. hydrocephaly)
88
Q

Acanthamoeba

A

get under contacts causing corneal lesions

-can travel to brain

89
Q

Naegleria

A

brain eating disease (rare)

-enters through cribriform plate

90
Q

trypanosoma brucei

A

African sleeping sickness (not in US)

  • insomnia or sleepiness
  • transmitted by tsetse fly
  • trypomastigote on blood smear
91
Q

Hematologic protozoa

A
  • plasmodium falciparum - Malaria - transmitted by mosquito (not in US)
  • babesia - similar to malaria but transmitted by tick (in US)
92
Q

plasmodium falciparum

A
  • transmitted by mosquitos
  • black water fever –> pee lysed blood
  • cerebral hemorrhage
  • cyclic fever
  • infects ALL RBCs
  • banana shaped gametocyte
93
Q

babesia

A
  • transmitted by tick
  • fever and hemolytic anemia
  • easily confused with malaria
  • often coinfected with Lyme disease
  • diagnostic test –> Maltese cross
94
Q

Leishmania donovani

A
  • transmitted by sandfly
  • cutaneous (slow healing skin ulcers)
  • visceral (fevers that can be fatal)
  • macrophages with amastigotes
95
Q

trypanosoma Cruzi

A

“kissing bug”

  • chagas disease - large heart, esophagus, and colon
  • romana sign - periorbital swelling
  • trypomastigote in blood smear
96
Q

trichomonas vaginalis

A
  • vaginitis - green discharge
  • sexual - cannot survive outside body
  • strawberry cervix
  • cervical wet prep (motile, swimming pear-shaped trophozoites)
97
Q

pediculosis pubis

A

pubic “crab” lice

  • will not burrow or jump
  • found in course hairs
  • passed through close body contact
  • pubic itching, burning, irritation
  • worse at night
98
Q

scabies

A

sarcoptes scabiei - a burrowing mite

  • don’t jump - passed b/w close contact
  • 7 year itch
  • someone who is immunocompromised
  • worse at night

BECOM II Exam 4 (10 decks)

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