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Basic Pathology > Week 1: Innate Immunity > Flashcards

Week 1: Innate Immunity Flashcards

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
Q

Why does temperature increase when immune system activated?

A

Pyrogens act on the hypothalamus to increase the temp.

26
Q

Vascular response when immune system activated

A

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
Q

What happens to vasculature when immune system is activated?

A 
Brief vasoconstriction
Mast cells release histamine 
Vasodilation
Increased capillary permeability
Exudation- leakage/buildup of fluid and cells (emigration)
28
Q

a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation.

A

exudate

29
Q

watery exudate that indicates early inflammation

A

serous exudate

30
Q

thick, clotted exudate that indicates more advanced inflammation. Can lead to dysfunctional wound healing

A

Fibrinous exudate

31
Q

Exudate that contains pus and indicates bacterial infection

A

Purulent Exudate

32
Q

Exudate that contains blood; indicates vascular disease

A

Hemorrhagic exudate

33
Q

What type of exudate is central serous chorioretinopathy?

A

Serous exudate

34
Q

What type of exudate is pseudomembrane?

A

Fibrinous exudate

35
Q

What type of exudate is bacterial conjunctivitis?

A

Purulent conjunctivitis

36
Q

What type of exudate is diabetic retinopathy?

A

Hemorrhagic exudate

37
Q

Examples of inflammation in the eye

A 
Hordeolum
Dry eye syndrome
Conjunctivitis 
Trauma
Ocular Rosacea 
Thermal and Chemical burns
Scleritis
Vitritis/ retinitis/ chorioretinitis
38
Q

7 Cellular mediators of inflammation

A 
Mast cells
Natural Killer Cells
Platelets
Granulocytes
Monocytes
Dendritic cells
Lymphocytes
39
Q

What are the cellular mediators activated by?

A

Plasma protein system products
Inflammatory cell secretions
Microbial molecules
Debris from cellular destruction

40
Q

What are pattern recognition receptors (PRR’s)? Where are they found?

A

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
Q

4 step process of Pattern recognition receptor when interacting with pathogen/microbe.

A

Attachment of pattern recognition receptor to pathogen
Pseudopodia forming a phagosome
Granule fusion and killing of pathogen
release of microbial products

42
Q

Describe phagocytic mobilization when inflammation is occurring.

A

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
Q

Describe process of phagocytosis

A 
Opsonization, recognition, and adherence 
Engulfment 
Phagosome formation
Fusion with lysosomal granule 
Destruction of the target
44
Q

Describe mast cells. Where are they located?

A

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
Q

What can stimulate mast cells? (4)

A

Pathogens
Allergens
Physical injury
chemical agents

46
Q

What are 2 products of mast cell degranulation? Describe them.

A

1) Histamine:
- Increased glandular production
- Vasoactive amine
- has CNS effects

2) Chemotactic factors
- Neutrophil chemotactic factor
- Eosinophil chemotactic factor of anaphylaxis (ECF-A)

47
Q

What are 2 mast cell synthesis products? Describe them.

A

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
Q

In atopic individuals (frequent inflammation), describe the mast cells in these individuals.

A

More numerous mast cells
higher number of antigen receptors
Mast cells more easily activated

49
Q

What do natural killer cells do?

A

Cell mediator that recognizes and eliminates virus infected cells and cancer cells.
Release perforin and granzyme

50
Q

Describe platelets

A 
Contribute to clot formation
Have multiple triggers
Degranulate upon activation 
Contribute to wound healing
Pro and anti-inflammatory
51
Q

Describe neutrophils. What is another name? What happens when dysfunction occurs?

A

AKA polymorphonuclear neutrophils (PMNs)
Early rescindants in inflammation (within hours)
Ingest bacteria, dead cells, and cellular debris
Dysfunction increases risk of bacteria influx

52
Q

Describe Eosinophils

A

Mildly phagocytic
Defend against parasites
Implicated in allergies and asthma
Regulate vascular mediators

53
Q

Describe Monocytes/ Macrophages.

A

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
Q

What happens at the end of inflammation?

A

Removal of an offending agent usually ends response

55
Q

What checks are present to control course of inflammation

A

Neutrophil life span is short
Inflammatory mediators degrade rapidly
Anti-inflammatory cytokines

56
Q

Outcomes of acute inflammation

A

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
Q

Describe chronic inflammation

A

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
Q

thickening and scarring of connective tissue (fibrin)

A

fibrosis

59
Q

Production of new blood vessels

A

Angiogenesis

60
Q

walling off of offending agents

A

Granuloma formation

61
Q

Possible outcomes of chronic inflammation

A

Dense infiltration of lymphocyte and macrophages
Fibrosis
Angiogenesis
Granuloma formation

62
Q

What biochemical immune response does the eye use?

A

Lysosome enzyme

Basic Pathology (16 decks)

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