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Basic Pathology > Week 1: Innate Immunity > Flashcards

Week 1: Innate Immunity Flashcards

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1
Q

What is a pathogen? Give 5 examples.

A

A microorganism that can cause disease

Virus
Fungus
Bacteria
Protozoa
Helminths
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2
Q

What is an antigen? Give 3 examples.

A

any substance that elicits an immune response (exogenous- coming from external environment or endogenous-coming within our own body)

Proteins
Carbohydrates
Nucleic acids

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3
Q

3 Noninfectious environmental agents (antigens)

A

Pollens
Foods
Bee venom

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4
Q

Clinical products that are antigens

A

Drugs
vaccines
Transplanted tissues

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5
Q

Immune system functions (4)

A

1) Prevent infection and cell injury
2) Distinguish self from non-self
3) Destroy infected and malignant cells
4) Initiates repair

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6
Q

Normal immune response

A

Pruritus: itching
Malaise: general feeling of unwellness
Anorexia: loss of appetite
Limited collateral damage of normal tissue

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7
Q

Abnormal immune responses

A

Immune deficiencies
Hypersensitivities - allergies
Autoimmune disorders

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8
Q

Describe Innate Immunity

A
  • Present at birth
  • Immediate
  • Non-specific
  • Activates inflammation and the adaptive immune response
  • First line of defense
  • What babies use the majority of the time
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9
Q

What is the bridge between specific and non-specific immune response?

A

Inflammation

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10
Q

First line of defense

A

prevent injury/infection

Examples: tears, blinking

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11
Q

Third line of defense

A

adaptive immunity response

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12
Q

Physical borders of innate immunity

A

-Prevent entry
Tight junctions (epithelial tissue throughout GI)
Temperature (cool skin limits bacteria growth)
Epithelium (cornea turnover in 7 days)

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13
Q

Examples of mechanical barriers in Innate Immunity

A 
Blinking
Coughing/sneezing
Mucociliary escalator 
Swallowing
GI tract peristalsis
Vomiting
Defecation
Urination
Ejaculation
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14
Q

7 biochemical barriers and their functions

A 
Tears: antibacterial
Gastric juices: pH
Mucus: antibacterial
Sweat: pH, antibacterial 
Sebum: antibacterial
Earwax: antibacterial
Saliva: digestive enzymes
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15
Q

Normal bacterial flora makes up _____ of the human body mass. What kind of barrier is this?

A

1-3%

Biochemical barrier

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16
Q

What is the second line of defense?

A

Inflammation

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17
Q

What are the goals of inflammation?

A 
Limit infection and further damage
Control bleeding
Interact with adaptive immune system
Prepare the area of injury for healing
Limit and control the inflammatory process
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18
Q

Signs of inflammation

A 
Heat
Redness
Swelling
Pain
Loss of function
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19
Q

True or False: Inflammation is part of the innate immune system.

A

True

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20
Q

Does inflammation respond quickly or slowly? Is it specific or non-specific? Is it repeatable or nonrepeatable?

A

Inflammation responds quickly
It is non-specific
It is repeatable

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21
Q

What 3 things causes inflammation?

A

Activation of immune system components
Mast cell degranulation
Cellular injury

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22
Q

suffix “itis” means

A

inflammation

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23
Q

5 Cardinal signs of inflammation

A

1) Heat - calor
2) Redness - rubor
3) Swelling - tumor
4) Pain - dolor
5) Loss of function - functio laeso

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24
Q

Signs throughout the whole body (Systemic) when immune system is activated

A 
Fever
Increased Pulse
Increased blood pressure 
Leukocytosis- white blood cells increase  
Increase Plasma protein synthesis
Cytokine Effects (TNF-a, IL-1)
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25
Why does temperature increase when immune system activated?
Pyrogens act on the hypothalamus to increase the temp.
26
Vascular response when immune system activated
Send WBC and other immune components to area. Dilute the bacteria at injury site. Provide nutrients and oxygen for immune cells and wound repair
27
What happens to vasculature when immune system is activated?
``` Brief vasoconstriction Mast cells release histamine Vasodilation Increased capillary permeability Exudation- leakage/buildup of fluid and cells (emigration) ```
28
a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation.
exudate
29
watery exudate that indicates early inflammation
serous exudate
30
thick, clotted exudate that indicates more advanced inflammation. Can lead to dysfunctional wound healing
Fibrinous exudate
31
Exudate that contains pus and indicates bacterial infection
Purulent Exudate
32
Exudate that contains blood; indicates vascular disease
Hemorrhagic exudate
33
What type of exudate is central serous chorioretinopathy?
Serous exudate
34
What type of exudate is pseudomembrane?
Fibrinous exudate
35
What type of exudate is bacterial conjunctivitis?
Purulent conjunctivitis
36
What type of exudate is diabetic retinopathy?
Hemorrhagic exudate
37
Examples of inflammation in the eye
``` Hordeolum Dry eye syndrome Conjunctivitis Trauma Ocular Rosacea Thermal and Chemical burns Scleritis Vitritis/ retinitis/ chorioretinitis ```
38
7 Cellular mediators of inflammation
``` Mast cells Natural Killer Cells Platelets Granulocytes Monocytes Dendritic cells Lymphocytes ```
39
What are the cellular mediators activated by?
Plasma protein system products Inflammatory cell secretions Microbial molecules Debris from cellular destruction
40
What are pattern recognition receptors (PRR's)? Where are they found?
Recognition pathogen-associated molecular patterns (PAMPs). Is not specific but can identify whether molecule is pathogen or not. Found on surface of resident and circulating immune cells Also recognize cellular debris.
41
4 step process of Pattern recognition receptor when interacting with pathogen/microbe.
Attachment of pattern recognition receptor to pathogen Pseudopodia forming a phagosome Granule fusion and killing of pathogen release of microbial products
42
Describe phagocytic mobilization when inflammation is occurring.
Neutrophils, eosinophils, and macrophages emigrate toward the source. They flow to the walls of the blood vessel (Margination) They attach to the walls of the vessel (Adherence) They move through the walls of the capillaries (Diapedesis) They migrate to the injured area in response to concentration gradients of extracellular signals. (Chemotaxis)
43
Describe process of phagocytosis
``` Opsonization, recognition, and adherence Engulfment Phagosome formation Fusion with lysosomal granule Destruction of the target ```
44
Describe mast cells. Where are they located?
Key initiator of inflammation and immune respone Located in loose connective tissue in high risk areas of the body (GI tract, lungs, skin, mucosal tissue) Sensitive and stimulated by multiple stimuli Immediate degranulation Delayed synthesis
45
What can stimulate mast cells? (4)
Pathogens Allergens Physical injury chemical agents
46
What are 2 products of mast cell degranulation? Describe them.
1) Histamine: - Increased glandular production - Vasoactive amine - has CNS effects 2) Chemotactic factors - Neutrophil chemotactic factor - Eosinophil chemotactic factor of anaphylaxis (ECF-A)
47
What are 2 mast cell synthesis products? Describe them.
1) Leukotrienes - Product of the arachidonic acid cascade - Similar effects to histamine in later stages 2) Prostaglandins - Induce pain - Pro and anti-inflammatory properties
48
In atopic individuals (frequent inflammation), describe the mast cells in these individuals.
More numerous mast cells higher number of antigen receptors Mast cells more easily activated
49
What do natural killer cells do?
Cell mediator that recognizes and eliminates virus infected cells and cancer cells. Release perforin and granzyme
50
Describe platelets
``` Contribute to clot formation Have multiple triggers Degranulate upon activation Contribute to wound healing Pro and anti-inflammatory ```
51
Describe neutrophils. What is another name? What happens when dysfunction occurs?
AKA polymorphonuclear neutrophils (PMNs) Early rescindants in inflammation (within hours) Ingest bacteria, dead cells, and cellular debris Dysfunction increases risk of bacteria influx
52
Describe Eosinophils
Mildly phagocytic Defend against parasites Implicated in allergies and asthma Regulate vascular mediators
53
Describe Monocytes/ Macrophages.
Produced in bone marrow Mature and replicate at inflammatory site (3 to 7 days) Ingest bacteria and cellular debris Contribute to activation of adaptive immune system Initiate wound healing
54
What happens at the end of inflammation?
Removal of an offending agent usually ends response
55
What checks are present to control course of inflammation
Neutrophil life span is short Inflammatory mediators degrade rapidly Anti-inflammatory cytokines
56
Outcomes of acute inflammation
1) Complete resolution - structure and function recoverable 2) Scarring- substantial damage to connective tissue 3) Abscess formation- pus confined in a closed space. Active proteases produce fluid increasing osmotic pressure. Usually have to drain. 4) Progression to chronic inflammation- Body can't remove offending agent. Persistent bacteria/toxins or autoimmune disease
57
Describe chronic inflammation
Lasts longer than 2 weeks Related to unsuccessful acute inflammation response Caused by high lipid and wax content of microorganism, ability to survive inside the macrophage, toxins, chemicals, particulate matter, physical irritants
58
thickening and scarring of connective tissue (fibrin)
fibrosis
59
Production of new blood vessels
Angiogenesis
60
walling off of offending agents
Granuloma formation
61
Possible outcomes of chronic inflammation
Dense infiltration of lymphocyte and macrophages Fibrosis Angiogenesis Granuloma formation
62
What biochemical immune response does the eye use?
Lysosome enzyme

Basic Pathology (16 decks)

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