Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

FPP_MSS > Acute & Chronic Inflammation and Hypersensitivity > Flashcards

Acute & Chronic Inflammation and Hypersensitivity Flashcards

1
Q

What are Toll-like receptors?

A

TLRs are surface receptors that respond to patterns on extracellular microbes. Activation leads to release of TNF.

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

What are inflammasomes

A

Inflammasomes are intracellular receptors that detect fragments of dead cells and some microbes. Activation of the inflammasome leads to activation of caspase-1, which in turn activates release of IL-1.

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

Vasodilation is mediated by what?

A

Histamine and nitric oxide (NO)

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

Vascular permeability is mediated by what?

A

histamine and bradykinin

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

Histamine: what is it released by and what does it mediate?

A

Released by: mast cells (stimulated by IL-1 and other inflammatory cytokines) Produces vasodilation and increases vascular permeability

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

Nitric oxide: what is it released by and what does it mediate?

A

Released by: endothelial cells in response to injury Increases vasodilation

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

Bradykinin: what is it released by and what does it mediate?

A

Bradykinin is a plasma protein produced by the liver. It is activated by factors expressed on injured epithelial cells. Bradykinin increases vasodilation, increases vascular permeability, and causes pain

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

Define edema

A

excess fluid in the interstitium

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

Compare/contrast: Trasudate vs. Exudate

A

Transudate: SG < 1.012, protein-poor ultrafiltrate of blood plasma due to increased hydrostatic pressure or lowered plasma osmotic pressure. Non-inflammatory. Exudate: SG > 1.02, protein and inflammatory cell rich fluid released due to increased vascular permeability. Due to inflammatory process.

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

What is pus?

A

Purulent exudate -> exudate rich in neutrophils (PMNs)

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

List the major steps in leukocyte recruitment

A
  1. margination
  2. rolling
  3. adhesion
  4. transmigration
  5. chemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name the receptor associated with each of the following steps of leukocyte recruitment:

  1. rolling
  2. adhesion
  3. transmigration
A
  1. selectins
  2. ICAM-1
  3. PECAM-1 (CD31)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Selectins are expressed on endothelial cells in response to what?

A

Histamine, thrombin, etc

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

ICAM-1 is expressed on endothelial cells in response to what?

A

TNF and IL-1 secreted by macrophages at the site of injury

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

What is diapedesis?

A

Movement of a leukocyte through the epi/endothelial barrier

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

Killing and degradation of microbes/tissues at the site of injury is driven by what two processes?

A
  1. ROS (within phagolysosome)
  2. Enzyme release (example: elastase, extracellular)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name the principal mediators of the following features of inflammation:

  1. Vasodilation
  2. Increased vascular permeability
  3. Chemotaxis and leukocyte recruitment
  4. Fever
  5. Pain
  6. Tissue damage
A
  1. histamine and nitric oxide
  2. histamine and bradykinin
  3. TNF, IL-1, bacterial products
  4. TNF, IL-1
  5. bradykinin
  6. ROS, NO, lysosomal enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name four major morphologies of acute inflammation

A
  1. serous
  2. fibrinous
  3. suppurative
  4. ulcerative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe serous acute inflammation

A
  • mildest form of acute inflammation
  • consists mostly of transudate from injured serious tissues
  • example: pleural/pericardial/peritoneal effusion due to chronic heart failure or fluid overload
  • example: skin blistering from friction, burn, trauma, or viral infection due to leaky epi/endothelia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe fibrinous acute inflammation

A
  • usually secondary to a more severe injury
  • larger vascular leaks, allowing passage of fibrinogen and conversion to fibrin
  • examples: fibrous pericarditis, fibrous peritonitis with ascites, acute rheumatoid fever (ARF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe suppurative acute inflammation

A
  • suppurative = purulent (pus)
  • S. aureus is common
  • formation of an abscess: central necrotic tissue with PMNs enclosed by fibroblasts
  • examples: acute appendicitis, acute bronchopneumonia, acute meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe ulcerative acute inflammation

A
  • local defect on surface of organ or tissue
  • sloughing of surface and necrotic tissue
  • examples: peptic ulcer, skin ulceration (common with diabetes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

A friction rub on cardiac auscultation may be indiciative of what type of inflammation?

A

Fibrinous inflammation

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

Acute appendicities is usually an example of what type of acute inflammation?

A

suppurative inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Tissue macrophages are a hallmark sign of what type of inflammation?
Chronic inflammation
26
What is polymyositis?
Chronic inflammation (autoimmune) characterized by CTL destruction of skeletal myofibers
27
What type of inflammation is defined by the presence of epithelioid macrophages?
Granulomatous inflammation example: sarcoidosis is defined by the presence of granulomatous inflammation
28
What is a multinucleate giant cell?
Fused epithelioid macrophages, induced by IFN-gamma
29
Caseous necrosis with multinucleated giant cells is definitively what disease until proven otherwise?
TB
30
What is SIRS?
a.k.a. Acute Phase reaction Systemic reaction to inflammation that may include the following: 1. Fever: in response to bacterial lipopolysaccharides (endotoxin), elevated endogenous pyrogens (IL-1, TNF), and increased release of prostaglandins (PGE2, increases setpoint of HT) 2. Elevated acute phase protein release from the liver, stimulated by IL-6. Includes: c-reactive protein, fibrinogen, serum amyloid A protein, etc. Produces increased sedimentation (sed) rate. 3. Leukocytosis: stimulated by TNF and IL-1. Produces accelerated release of leukocytes from bone marrow.
31
What is the "sed rate"
Fibrinogen released in response to inflammation binds to erythrocytes (RBCs), forming stacks. In lab tests, these stacks (due to their mass) 'sediment' faster. Inflammation may increase sed rate (part of SIRS)
32
What is a leukemoid reaction?
Extreme leukocytosis (\>20,000)
33
What is a "left-shift"?
Accelerated release of immature neutrophils
34
Give the conditions of the following leukocytoses: 1. Neutropenia 2. Lymphocytosis 3. Eosinophilia 4. Leukopenia
1. bacterial infection -\> may produce a left-shift 2. viral infection 3. allergy, asthma, parasites 4. WBC sequestration in lymph nodes due to certain infections (examples: rickettsia, typhoid, etc)
35
Name the four types of hypersensitivity
* Type I: Immediate, IgE-mediated * Type II: direct antibody-mediated cytolytic * Type III: immune-complex-mediated * Type IV: delayed type cell-mediated
36
What type of hypersensitivity reaction is **Rhus Dermatitis**?
Type IV
37
Describe the sensitization stage of Type I hypersensitivity
1. Specific antigen taken up and presented by APC 2. Presentation to Th2 cell 3. Th2 cell secretes IL-4 and IL-6, inducing B-cell class-switching to IgE 4. B-cell produces IgE against specific antigen 5. Specific antigen IgE is taken up by mast cells
38
What is the difference between an allergen and an irritant?
* Allergen: not dose-dependent, does not affect all individuals, IgE-mediated, affects only those previously sensitized * Irritant: dose-dependent effet, affects all individuals, not Ig-E mediated, tends to be a small molecule
39
What products are secreted by mast cells in the early phase of type I hypersensitivity reactions?
* Histamine * tryptase * PGD2 * thromboxane * LTC4
40
What products are released during the late phase of Type I hypersensitivity reactions?
* LTB4, LTC4 * PGD2, PGE2, PGF2-alpha * kinins * histamine (lower load than early phase) * GM-CSF, IL-5 * Eosinophil products: MBP, ECP, EPO, etc
41
Testing for what mast cell product is a good diagnostic indicator of Type-I hypersensitivity reaction?
Tryptase Lasts for ~4 hours
42
What is the difference between alpha-tryptase and beta-tryptase? What does tryptase do?
* Alpha: released constituitively * Beta: released upon mast cell activation Tryptase triggers remodeling of connective tissue in the ECM
43
What class of drugs are likely to produce a false-negative skin test?
Antihistamines
44
Name the drug(s) that blocks leukotriene synthesis by blocking the action of 5-lipoxygenase
zileuton
45
Name the drug(s) that block leukotriene receptors
montelukast / zafirlukast
46
Does psychological stress lower or raise the mast cell sensitivity threshold?
lower
47
Name 3 drugs or classes of drug that raise the sensitivity threshold of mast cells?
1. Corticosteroids 2. Antihistamines 3. Cromolyn sodium
48
Describe the cytokines released by mast cells during the late phase reaction
* IL-4 and IL-13: stimulate Th2 cells and IgE class switching * IL-3, IL-5, GM-CSF: activate and promote survival of eosinophils * TNF: endothelium activation and adhesion expression
49
Describe the major chemokines released by mast cells during the late phase
* CCL3: macrophage and leukocyte chemotaxis * RANTES (CCL5) and eotaxin (CCL11): T-cell and eosinophil chemotaxis
50
Describe the major lipid mediators released by mast cells during the late phase reaction
* LTC4, LTD4, LTE4: eosinophil migration, smooth muscle contraction, increased vascular permeability, mucus hypersecretion * PAF: attracts leukocytes, activates eosinophils/neutrophils/platelets
51
Name 5 major caused of increased eosinophil count (eosinophilia)
NAACP: 1. neoplasia 2. asthma 3. allergy 4. connective tissue disease 5. parasite
52
Describe the mechanism by which corticosteroids suppress eosinophils
1. Directly block IL-5, reducing eosinophil release from bone marrow and promoting eosinophil apoptosis 2. Bind GR-alpha, inhibiting AP-1 and NFkB
53
Give 4 clinical examples of Type I hypersensitivity
1. Allergic rhinitis 2. asthma 3. anaphylaxis 4. urticaria
54
Why is early life viral infection significant in the context of hypersensitivity reactions?
Early childhood viral infections increases the risk of development of allergies
55
What cells type(s) infiltrates are commonly seen in asthma? Sudden-death asthma?
Asthma: eosinophils and lymphocytes Sudden-death asthma: neutrophils
56
What is denudation?
Destruction of airway epithelium
57
Give the 5 major morphological features of asthma
1. Denudation 2. Mucus gland hyperplasia and hypersecretion 3. smooth muscle hyperplasia 4. submucosal edema and vascular dilation 5. fibrin deposition and airway remodeling
58
Why must administration of a skin test wait 4-6 weeks after an allergic event?
Mast cells need time to 'reload'
59
What type of hypersensitivity reaction is **Myasthenia Gravis**?
Type II
60
What is the name for the Type II hypersensitivity reaction caused by Rh-factor mismatch between mother and child?
erythroblastosis fetalis
61
What type of hypersensitivity reaction generally features a soluble antigen? A matrix-bound antigen?
* Type III * Type II
62
Name 4 major sites of immune complex deposition in Type III hypersensitivity reactions
1. Kidney 2. Skin 3. joints 4. blood vessels
63
What is the **Arthus Reaction**?
Skin reaction when sensitized individuals are exposed to a specific antigen. The reaction is caused by leukocyte activation via FC(gamma)III receptors with no complement involvement - therefore Type III
64
What is serum sickness?
Systemic reaction following injection of a large quantity of foreign antigen. Reaction occurs 7-10 days post-exposure (sweet spot of Ab:Ag complex formation). Symptoms: flu-like condition (fever, vasculitis, arthritis, nephritis)
65
**Farmer's Lung** features what type of hypersensitivity reaction?
Type III - reaction to hay dust and mold spores
66
**Systemic Lupus Erthematosus** is what type of hypersensitivity reaction?
Type III
67
Describe Type IV hypersensitivity
* Delayed-type, cell-mediated, does not generally involve antibodies * Process: antigen enters skin and binds self-protein, antigen-protein complex is presented to T-cells, resulting in T-cell proliferation * Cellular response is mediated by CD4+ Th1 cells and/or CD8+ CTLs
68
Name the plant-based chemical involved in Rhus Dermatitis?
pentadecacatechol

FPP_MSS (30 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions