immunology/inflammation Flashcards

1
Q

what are the 2 types of immunology

A

innate(non-specific) and adapative (specific)

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2
Q

what are the 6 key points on innate immunity

A

detailed verison :
1. Toll like receptors= identify/respond to bacteria/virus
2.phagoctyes= neutrophils and macrophages get activated to engulf pathogens
3.complement system= protein build up get active if pathogens are present=inflammtion
4. recruit leukocytes(WBC)= neutrophils and monocytes to site of infection
5.lysis= holes in cell membrane of pathogen
6.slow response= takes time to get activated

  • always there present
  • fast acting
  • no memory after encouter
  • first protection against pathogen
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3
Q

what are the 2 types of immunology

A

innate(non-specific) and adapative (specific)

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4
Q

what do complement compounds do?

A

coat/identify antigens making them easy to spot for imune cells to engulf/destroy by phagocytosis

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5
Q

why do complement compounds undergo cytolysis

A

to burst its membrane and trigger inflammation to fight infections (MAC= membrane attack complex)

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6
Q

define opsonisation

A

marks pathogens and acts like tags to see them clearer this helps the process of phagocytosis

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7
Q

what are the 2 proteins that fight infections?

A

lysozome= fights bacteria
interferons = fights virus

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8
Q

define neutrophils and its points

A
  • WBC
  • first to arrive then after macrophages
  • goes to the infected area and fights bacteria/fungal pathogens
  • is an innate immune cell
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9
Q

examples of innate immune cells

A
  • neutrophils
  • natural killers
  • macrophages
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10
Q

define mast cells and what 3 chemicals do they release

A

immune cells that fight allergies/parasites
- found in skin,GI,lungs

  • releases histamine, cytokines (chemical released during allergic reaction and cause symptoms like swelling..) and heparin(stop blood clotting)
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11
Q

monocytes in blood become what in tissues?

A

macrophages

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12
Q

difference between monocytes and basophils?

A

-both are WBC
- basophils have visible granules such as histamine/heparin which help with inflammation and only stay in the bloodstream

  • monocytes don’t have visible granules(mostly cytokines- coordinates/regulates the immune response) and stay in the bloodstream they migrate to tissues and become macrophages
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13
Q

define eosinophilis

A

release cytotoxic chemical on surface of parasites and damage their tissues/membrane

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14
Q

define inflammation

A

response to infection and tissue injury

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15
Q

some points on acute inflammation and name 3 of its key components

A
  • rapid and short-term triggered by injury/infection
  • lots of neutrophils
  1. exudate= fluid/protein leak into tissue during inflammation
  2. diapedesis= WBC squeeze through walls of blood vessels to reach the site of inflammation
  3. chemotaxis= immune cells move towards the site of inflammation
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16
Q

some points on chronic inflammation and what are the 3 cells and what are the 2 responses?

A
  • slow
  • a persistent immune response that leads to tissue damage
  • comes after acute as many lymphocytes and macrophages come

3 cells:
macrophages= remove damages tissue by phagocytosis

plasma cells= emit antibodies

lymphocyte= organise cellular response

2 responses:
granulation tissues= wound healing,ECM (fibroblast+BV)
granulomas = fibrosis= wound healing can be impotant as its not safe for the kidney

17
Q

key points on adaptive (specific) immunity and what are there 2 types of adaptive immunity

A
  • slow but targets responses
  • has a memory of pathogen

2 types of adaptive immunity:

antibody-mediated immunity= B lymph
to neutralise pathogens/toxins flowing in body

cell-mediated immunity= T lymph
target cells that have been affected by pathogens

18
Q

points on T-lymphocytes and what are their 2 types

A
  • Target cell
  • cell mediated
  • directly attacks infected or abnormal cells

Th cells= helper cells
Tc cells= cytotoxic cells= destroy cells

these are good cells

19
Q

points on B-lymphocytes

A
  • antibody-mediated
  • Body fluids
  • recognises/binds to specific antigens
    -develops into plasma cells and make antibodies (Igs) that go in body fluids
20
Q

what does primary and secondary response mean?

A

primary response:
- is the first encounter with antigen
- produces T/B lymphocytes
-slow response

secondary response
-quicker reponses
- memory cells quickly respond to antigen

21
Q

during acute inflammation what 2 responses happen?

A
  1. vasodilation and increased permeability:
    when blood vessels widen more blood flows=more o2 /nutrients to the site
    increased permeability= nutrients flow from blood to tissues causing swelling and redness
  2. cell infiltration= neutrophils go from blood vessel to tissue to fight pathogen
22
Q

points on WBC margination/adhesion molecules

A

margination is used as WBC like neutrophils stick to walls of blood vessels using adhesion molecules before going to respond to inflammation

23
Q

5 stages of leucocytes( WBC like neutrophils) movement out of capillaries

A
  1. Margination = neutrophils move to the inner lining due to slow blood flow
  2. Rolling = make/break adhesion
  3. Pavementing = neutrophils attach tightly to vessel wall using integrin (glue)
    4.Transmigration= move thru vessel gap to enter tissue (diapedesis)
  4. Migration= go to the site of infection (chemotaxis)
24
Q

difference between the complement pathways: classical and alternative pathways

A

classical Pathway: Activated when antibodies “flag” specific antigens like putting a label on them, so the immune system knows what to attack.

Alternative Pathway: Activated when the immune system detects antigens directly, without needing any labels, and it attacks them quickly.

25
Q

examples of chemical mediators in inflammation

A

kinins= blood vessel leak and cause pain

platlets= WBC adhesion

histamine= vasodilation

cytokinises= short distance messenger

26
Q

difference between granulomas and granulation tissue

A

granulomas:
- formed when there persistent responses to infection
- made up of giant cells, macrophages and lymphocytes
- tries to fix by isolating infection from spreading

granulation tissue:
- formed form wound healing
- made up of extracellular matrix,fibroblast and BV

27
Q

process of acute inflammation

A

VEWPRT
Vasolidation= blood vessel dilate and allow blood to site
exudate= fluid protein leaked into tissue =swelling
wbc migrate to site=wbc go to inflammation through blood
phagocytosis=wbc engluf pathogen
release mediators= release hitamine and cytokines that attract more wbc
tissue repair/healing