IH2 Flashcards

To identify the physical barriers which serve to protect the body from infection • To describe the role of commensal bacteria in host defence • To outline the range of soluble, chemical agents which counteract infection

1
Q

What is the main function of the immune system?

A
  1. Recognition (presence of non-self e.g. pathogen) (significant to organ donation, also immune system doesn’t attack commensal bacteria)
  2. Effector function (contain/eradicate infection)
  3. Regulation (appropriate & measured response)
  4. Memory (immediate & stronger response on second exposure) (the whole basis of vaccination)
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2
Q

Describe the following for the recognition mechanism of the innate immunity:

1) speed of response
2) variance in the way they respond
3) specificity
4) effectiveness of response

A

1) rapid
2) fixed
3) limited number of specificities
4) constant

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3
Q

Describe the following for the recognition mechanism of the adaptive immunity:

1) speed of response
2) variance in the way they respond
3) specificity
4) effectiveness of response

A

1) slow (days to weeks)
2) variable
3) numerous highly selective specificities
4) improve during response

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4
Q

What does the innate and adaptive response have in common?

A

the mechanism for the destruction of pathogens e.g. neutrophils engulf pathogens while B cells selectively engulf pathogens

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5
Q

What are the effector mechanisms of the innate immune response:

  1. +3e.g
  2. +3 e.g.
A
  1. immediate defenses e.g. physical, chemical and microbiological barriers, complement and phagocytosis
  2. Induced defenses e.f. cytokines &chemotaxis, interferon response (signal molecule about virus presence released by infected cells to warn over host cells)
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6
Q

What effector mechanisms are involved in the adaptive immune response?

A
  1. antibodies
  2. cell-mediated immunity
  3. memory
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7
Q

What are the signs and symptoms of :

  1. immediate defenses
  2. induced defenses
  3. adaptive immune response
A
  1. none, natural homeostatic function
  2. temporary disruption of homeostasis acute, localised inflammation
  3. none, longstanding, effective protextion
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8
Q

What is the result of malfunction of the immune response?

A

persistent or inappropriate inflammation, autoimmune disease e.g. Addison’s disease

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9
Q

External body surfaces involved in protection: (3)

A

– Skin (keratin, cell-cell junctions)
– Nails (keratin)
– Ducts (fluid flow)

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10
Q

How does skin protect?

A

– low pH inhibits microbial growth
– lactic acid from sweat glands lowers pH
– fatty acids from sebaceous glands lowers pH

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11
Q

What damadge to the skin can result in penetration by bacteria?

A

Burns-moist surface, vascular damage

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12
Q

why is it that sounds die of measles depsite the fact we have a very effective vaccine for measles?

A

The main reason is in hot climated countries such as Nigeria, the measles vaccine must be stored in a fridge. Furthermore, issues are access people in rural areas.

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13
Q

What is another word for internal body surfaces?

A

mucosal surfaces

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14
Q

Describe the properties of mucosal surfaces (5):

A
  1. Large surface area
  2. No keratin
  3. Mucins (form mucus with water): coat microorganisms preventing attachment
  4. ciliated epithelium (protection and ejection of large particles)
  5. Flow of air and fluid
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15
Q

What addition properties does the GI tract have to protect itself from infection:

A

Acid environment in stomach, bladder, kidney, bile

Digestive enzymes inhibit growth

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16
Q

What addition properties does saliva add to the mouth to protect itself from infection:

A
  • Lysozyme: digests bacterial cell walls

* Lactoferrin: removes iron required by bacteria

17
Q

Give 4 disorders caused by comprimised physical barriers:

A
  • Abnormally thick mucus (e.g. in CF) leads to lung infections e.g. P. aeruginosa infection
  • Corneal and ear infections upon water exposure
  • Smoking damages ciliated epithelia in the airways
  • Higher rate of sepsis after surgery in area of high flora e.g. colon
18
Q

How do commensal bacteria protect surfaces from pathogenic infection?

A
  • Stimulate colonic epithelial cells giving a balanced state called physiological inflammation
  • Compete with pathogens for nutrients, attachment sites and living space
  • Fatty acids from propionibacteria are toxic to streptococci
19
Q

dysregulation of the interaction between colonic epithelial cells and commensal bacteria causes disease how?

A
  1. dysregulaiton e.g. antibiotics kill commensal bacteria
  2. pathogenic bacteria get a foot hold and produce toxins that cause mucosal injury
  3. Neutrophils and red blood cells leak into gut between injured epithelial cells
20
Q

Give 3 examples of soluble mediators of the innate immune response:

A
  1. enzymes
  2. complement components
  3. antimicrobial peptides
21
Q

Give examples of enzymes that are soluble mediators of the innate immune response:
2) What is their action?

A

1) lysozyme and phospholipase

2) digest cell walls and membranes respectively (in tears, saliva and phagocytes

22
Q

Give examples of enzymes that are soluble mediators of the innate immune response:
2) What is their action?

A

1) C3a: opsonisation
2) C3a and C5a: chemotaxis
3) C5b: membrane attack complex

23
Q

How many classes of AMP are there?

2) Give examples from 2 classes as well as what cell type in the body makes them:
3) What does AMP stand for?

A

1) 5
2) a)Charged peptides with cysteine e.g. alpha- defensins ,made by neutrophils and paneth cells, beta-defensins made by epithelial cells
b) peptide fragements e.g. lactoferin in saliva by serous epithelial cells
3) Antimicrobial peptides

24
Q

What action do AMPs have?

2) .. by virtue of what property?

A

1) disrupt cell membranes (Kill bacteria, fungi and enveloped viruses by perturbing their membranes )
2) by virtue of their amphipathic properties

25
Q

1) Where are cathelcidins found?
2) What do they do?
3) What is it a type of?

A

1) lysosomes of macrophages and polymorphonuclear leukocytes (PMNs), even epithelial cells
2) ptoent to microbes
3) AMP

26
Q

1) Where are histadins found?
2) What do they do?
3) What is it a type of?

A

1) serous fluid secreted by Ebner’s glands, salivary glands at the back of the tongue
2) play a role in wound-closure and offer proteciton form incoming microbes in the pharynx.
3)

27
Q

1) Where are lectins found?
2) What do they do?
3) What is it a type of?

A

1) leukocytes
2) a) they likely modulate inflammatory and autoreactive processes.
b) help mediate the first-line defense against invading microorganisms.
c) play a role in self-non-self discrimination
3) AMP

28
Q

What are paneth cells?

2) What do they make?
3) WHat do AMPs and enzymes kill?

A

1)Specialised epithelial cells of the small intestine
2) • Make a-defensins (also called cryptidins)
• Make lysozyme and phospholipase

3) enteric (gut) pathogens

29
Q

What are the 3 ways the compliment system can be activated? (IN ORDER OF HOW THEY REACT)

A

1) alternative
2) lectin
3) classical

30
Q

What is the alternative pathway?

A

pathogen surface creates local environment conductive to complement activation

31
Q

What is the lectin pathway?

A

mannose-binding lectin binds to pathogen surface

32
Q

What is the classical pathway?

A

C-reactive protein or antibody binds to specific antigen on pathogen surface

33
Q

What are the 3 main things the complement system does?

A
  1. recruitment of inflammatory cells
  2. opsonization of pathogens, facilitating uptake and killing by phagocytes
  3. perforation of pathogen cell membranes
34
Q

How is perforation of pathogen cell membranes by complement system done?

A

formation of membrane attack complex with consequent disruption of bacterial outer membrane and bacterial cell death

35
Q

Describe what happens in opsonisation:

A

1) encapsulated bacteria cannot be engulfed by neutrophils
2) antibody bound to bacteria activates complement and bonding of C3b to bacteria
3) Engulfment of bacteria by neutrophils is mediated by Fc receptors and complement receptors
4) Granules fuse with pahgosomes rleasing toxic oxygen metabolites killing the bacteria