IM 2 Flashcards

1
Q

what category is immune responses?

A

internal defenses

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

what are the 2 types of immune responses?

A

innate and adaptive

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

what’s the encoutner stage?

A

where pathogen and cell meet

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

what are locations for encoutner stage?

A

resident immune cell populations and in circulatin

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

what is resident immune cell populations?

A

immune cell in fixed location, pathogen brought by circulation (lymph or blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is circulation for encounter stage?

A

both pathogen and immune cell in circulation and come together in non-fixed location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are innate immune responses

A

general, 2nd line of defense, rapid but limited response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the recognition stage?

A

pathogen and immune cell binding

-general recognition
-toll receptors on immune cell membrane act as pattern-recognition receptors (can recognize large number of patterns)
-resulting binding triggers innate immune responses

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

what’s innate and adaptive difference?

A

innate responses contain and limit spread of pathogen while adaptive mounts more specific response

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

explain the interferon

A
  • cell infected with virus produce proteins called interferons to interfere with viral replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the process of a type 1 interferon

A

-virus infected cell releases type 1 interferon from cell surface into IF
-most cells have type 1 interferon receptor for binding
-if binding occurs on a non-infected cell, the non-infected cell will start producing antiviral proteins
-if at some point later, the cell becomes virus infected, the antiviral proteins will prevent viral replication

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

what’s a phagocyte and what are types?

A

any cell that can do phagocytosis, neutrophils and macrophages

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

what are neutrophils

A

quickest response

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

what are macrophages

A

have largest capacity

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

what’s the 4 step process for phagocytosis

A
  1. recognition
  2. ingestion
  3. digestion
  4. kill
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the components of the alternative complement pathway?

A

complement proteins, opsonization, membrane attack complex

17
Q

what are complement proteins?

A

plasma proteins from liver that circulate inactive in blood
-inactive C3 binds pathogen to activate
-activated proteins complement or enhance immune reactions

18
Q

what is opsonization

A

portion of active C3 (C3b) left attached to pathogen because the phagocyte has a receptor for C3b and then C3b acts as an opsonin (marker) so that makes recognition easier which enhances phagocytosis

19
Q

what the membrane attach complex?

A
  • cascade of activations after C3 activates C5-C9
  • pore formed by inserting activated C5-C9 into pathogen cell membrane
  • inflow of fluid/material into pathogen intracellular environment → apoptosis triggered (programmed cell death)
20
Q

What are sources of inflammation?

A

pathogens, abrasions, chemical irritants, cell distortion or disturbance, extreme temperature

21
Q

what are characteristic symptoms of inflammation?

A

redness, pain, heat, swelling (also loss of tissue function in damage site sometimes)

22
Q

what are the goals of inflammation?

A

-isolate, destroy or inactivate pathogen
-remove debris
-prepare for wound healing and tissue repair

23
Q

what’s stage 1 of inflammation?

A

release of inflammatory mediators

types: cytokines, prostaglandins, histamine

24
Q

what are the local effects for stage 1 inflammation?

A

-vasodilation microcirculation
-increased permeability of blood vessels

25
Q

what are the non-local effects for stage 1 inflammation?

A

-stored immune cells released into circulation, especially from spleen and lymph nodes
-red bone marrow proliferation of new immune cells

26
Q

what is stage 2 of inflammation?

A

-phagocyte movement into damage site from blood (start within 1 hour)
-neutrophils early, monocytes mature into wandering macrophages arriving later

27
Q

what are the steps of stage 2 inflammation?

A

-margination
-diapedesis
-chemotaxis

28
Q

what is margination?

A

phagocytes and local endothelium each form adhesion molecules for attachment to local area

29
Q

what is diapedesis?

A

phagocyte migration through blood vessel walls into IF

30
Q

chemotaxis

A

phagocyte migration to damage site guided by cytokines using chemoattraction

31
Q

what is stage 3 of inflammation?

A

worn out or damaged or dead cells replaced

includes
-angiogenesis
-tissue repair leaving scar
-remodelling after repair

32
Q

what is the purpose of angiogenesis in inflammation?

A

a new network of small blood vessels to help remove debris and deliver needed nutrients and oxygen