Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 6 Week 1 > Hunter: Innate Immunity > Flashcards

Hunter: Innate Immunity Flashcards

1
Q

This is the FIRST line of defense. Contains these components:
Epithelial Barriers
Anti-Microbial Enzymes and Peptides
The Complement System
Macrophages, Dendritic Cells, and Neutrophils (myeloid cells)
Pattern Recognition Receptors (germline encoded)
Inflammation (rubor, calor, tumor, and dolor)
Cytokines, Chemokines, Adhesion Molecules, and Acute Phase Proteins
Interferons and NK Cells

A

innate immunity

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

About how long does it take for innate immunity to take action?

A

0-4 hours

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

What are some ways in which pathogens enter mucosal surfaces?

A

airway
GI tract
reproductive tract

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

What are some ways in which pathogens enter external epithelia?

A

physical contact
wounds and abrasions
insect bites

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

List three sources of pathogens

A

the environment
humans
animals

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

These reside ON or IN your body but cause disease only when the host is immunosuppressed.

A

opportunistic pathogens

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

What are some MECHANICAL barriers to adhesion, colonization, and infection by pathogens?

A

epithelial cells with tight junctions
longitudinal flow of air or fluid
movement of mucus by cilia
tears, nasal cilia

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

What are some CHEMICAL barriers to adhesion, colonization, and infection by pathogens?

A 
fatty acids
low pH
enzymes like pepsin
pulmonary surfactant
enzymes in tears
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is one MICROBIOLOGICAL barrier to adhesion, colonization, and infection by pathogens?

A

microbiota

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

What are some DIRECT mechanisms of tissue damage by pathogens?

A

exotoxin production *toxins penetrate tissues to get nutrients they need to survive
endotoxin production
direct cytopathic effect *take over the cell to accomplish their mission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some INDIRECT mechanisms of tissue damage by pathogens?

A

formation of immune complexes
anti-host antibodies
cell-mediated immunity

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

Microbes produce enzymes that can destroy our tissues. As defense, we produce enzymes that can fight back. List a few.

A

lysozyme
pepsin
secretory phospholipase A2

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

What are these examples of?
Defensins
Cathelicidins
Histatins

A

anti-microbial peptides

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

When anti-microbial peptides are activated via proteolysis, what do they release?

A

amphipathic peptides

**made in almost all tissues of the body

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

In what time period does the early induced innate response occur?

A

early: 4-96 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Discuss what happens to a pathogen when it gets past an epithelial barrier and encounters a macrophage.

A

Macrophages will recognize pathogens via TLRs.
Release cytokines which cause vasodilation and increased vascular permeability, as well as upregulation of adhesion molecules.
Kinin and coagulation systems upregulated.
Chemokines attract neutrophils and monocytes as a second line of defense.
Phagocytic cells and complement rid of the pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is one PAMP found on gram-positive bacteria, such as streptococcus pyogenes?

A

peptidoglycan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is one PAMP found on gram-negative bacteria, such as escherichia coli?

A

lipoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Macrophages have different receptors which recognize different PAMPs. What does TLR-4 recognize?

A

LPS endotoxin (gram-negative bacteria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

These are PAMP receptors. There are 10 genes that code for them. Some are on cell surface, while others are intracellular.

A

TLRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When TLRs are activated, what transcription factor is produced to induce the production of inflammatory mediators?

A

NF-kB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

These are similar in structure to TLRs, they detect cytoplasmic bacteria, and signal inflammation.

A

NOD-like proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

These are similiar to TLRs, but detect viral RNA in the cytoplasm and induce inflammation

A

RIG-like proteins *retinoic acid inducible gene-I-like proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Explain what happens when TLRs bind a pathogen to ultimately lead to increased gene expression.

A

PAMP binds to TLR, TLRs dimerize, induce intracellular signaling, increased gene expression for trx factors like NF-kB, inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Rare autosomal recessive defect which involves poor response of monocytes to TLR agonists, thus causing a defect in the NF-kB pathway and the response to pyogenic bacterial infections.

A

IRAK4 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the two most important phagocytic cells?

A

neutrophils

macrophages

27
Q

Where are most microbes killed and digested?

A

in the phagolysome

28
Q

This forms in the phagolysosomal membrane during phagocytosis of microbes. It generates ROS to cause a hostile environment, with a low pH, which causes death of the microbes.

A

NADPH oxidase

29
Q

What makes the phagolysosome so toxic to microbes?

A 
low pH
reactive oxygen species
NO
antimicrobial peptides
enzymes like lysoszyme
30
Q

This disease results from a failure of the assembly of NADPH oxidase in phagolysosomes.

A

Chronic granulomatous disease

31
Q

How does chronic granulomatous disease present?

A

granulomatous lesions in the skin and various internal organs due to pyogenic bacteria and fungi

32
Q

What test is used to determine if a patient has chronic granulomatous disease?

A

dihydrohodamine test using flow cytometry - this reveals a defective respiratory burst

33
Q

How can you treat chronic granulomatous disease?

A

antibacterial and antifungal agents, or IFN-gamma, or bone barrow transplant

34
Q

NADPH oxidase generates antimicrobial superoxide, hydrogen peroxide, and other reactive oxygen species. This is referred to as (blank).

A

respiratory burst

35
Q

This is an autosomal recessive disease with a defect in microtubule polymerization which decreases phagolysosome formation and impairs killing of bacteria.

A

Chediak-Higashi Syndrome

36
Q

How does Chediak-Higashi Syndrome usually present?

A

as recurrent pyogenic infections (i.e. staph and strep) in early childhood, particularly gingival infections

37
Q

What clinical cues can help you make a diagnosis of Chediak-Higashi syndrome?

A

partial albinism

large lysosomal vesicles in neutrophils and eosinophils

38
Q

How to treat Chediak-Higashi Syndrome?

A

prophylactic antibiotics

bone marrow transplants

39
Q

What is the most common defect in granulocyte-mediated host defenses?

A

neutropenia

40
Q

What is neutropenia?

A

decreased absolute neutrophil count *like less than 1500 cells/mm3

41
Q

What are two forms of acquired (common) neutropenia?

A

drug-induced *cancer drugs

autoimmune *anti-neutrophil antibodies

42
Q

What are these examples of?
Familial (benign, ethnic) neutropenia
Infantile genetic agranulocytosis (severe congenital neutropenia)*
Cyclic neutropenia

A

hereditary neutropenia *rare

43
Q

What is one common way to induce neutropenia?

A

cytotoxic anti-cancer drugs

44
Q

A variety of pyogenic bacteria and fungi can cause this to occur.

A

neutrogenic sepsis

45
Q

How to treat neutropenia?

A

broad-spectrum antibiotics

hrG-CSF prior to chemotherapy

46
Q

A genetically and phenotypically heterogeneous group of hereditary neutropenias seen in infants

A

severe congenital neutropenia

47
Q

How do infants with severe congenital neutropenia usually present?

A

recurrent infections of skin, soft tissues, lungs, deep organs
ANC below 200/ul

48
Q

At what stage are neutrophils typically “stuck” in patients with SCN?

A

stuck at premyelocyte of myelocyte stage

*can treat w bone marrow transplant

49
Q

How are neutrophils called to sites of inflammation?

A

by macrophages

50
Q

Rare autosomal recessive disorder presenting with recurrent bacterial infections due to defects in neutrophil adhesion

A

Leukocyte adhesion deficiency

51
Q

What occurs as a result of adhesion molecule defects?

A

Neutrophils cannot undergo chemotaxis, so there will be large numbers of neutrophils in the plasma. Infants will suffer from infections like omphalitis, pneumonia, gingivitis, peritonitis, because they cannot get neutrophils to site of infection.

52
Q

In leukocyte adhesion deficiency, what molecule is not working properly? How is this condition diagnosed?

A

CD18, which is a subunit of the leukocyte CAM;
diagnosed by finding low CD18 and via flow cytometry
*treat w bone marrow transplant

53
Q

The acute phase response is mediated by acute phase proteins. List one opsonin which is used to identify patients with active inflammatory processes.

A

C-reactive protein

54
Q

This binds to and sequesters iron to inhibit microbial growth.

A

ferritin

55
Q

This is a coagulation factor, which is telling of the rate of RBC sedimentation

A

fibrinogen

56
Q

What happens to albumin production during an acute phase response?

A

it is downregulated

57
Q

Viral RNA induces the gene expression of what inflammatory agent?

A

Interferon alpha/beta

58
Q

When viral RNA enters a host, it activates (blank), which degrades the viral mRNA and causes apoptosis. Then, interferon alpha/beta increases the expression of (blank) on nucleated cells.

A

RNAse L; MHC class 1 molecules

59
Q

What lineage are NK cells derived from?

A

lymphoid progenitor cells

60
Q

NK cells produce large amount of (blank)

A

interferon gamma

61
Q

What do NK cells do?

A

kill virus-infected cells, cells containing pathogens, and tumors by using cytotoxic granules full of nasty stuff. They don’t kill normal cells that have MHC class 1 molecules on their surface, but if there is abnormal MHC class 1 expression or a cell expressing stress molecules, they will attack

62
Q

If there is a deficiency in NK cells, what are you more susceptible to?

A

infection with HERPES viruses

63
Q

If a pathogen is coated in antibody, these cells can bind to that pathogen and induce death.

A

NK cells

*antibody dependent cell-mediated cytotoxicity (ADCC)

Block 6 Week 1 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions