pathoma > Chapter 2 - Inflammation > Flashcards

Chapter 2 - Inflammation Flashcards

Inflammation (68 cards)

Study These Flashcards
1
Q

Hallmark cells of acute inflammation

A

Neutrophils

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

Hallmark cells of chronic inflammation

A

Leukocytes

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

Transcription factor that induces further inflammation

A

NF-Kb

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

2 pathways of arachidonic acid

A

Cyclooxygenase –> Prostaglandins
5- lipooxygenase - Luekotrienes

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

Prostaglandin E2 mediates what?

A

Fever and pain

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

Which leukotriene attracts neutrophils? What other cytokines attract neutrophils?

A

LTB4
Also C5a and IL-8

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

Leukotrienes mediate what system changes?

A

Vasoconstriction, bronchospasm, and increased vascular permeability

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

Prostaglandins mediate what system changes?

A

Vasodilation and membrane permeability

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

Which complement substances mediate mast cell degranulation?

A

C3a, C5a

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

Describe Hageman factor

A

Activates coagulation and fibrinolytic systems, complement, and the kinin system

It cleaves HMWK to bradykinin –> vasodilation, vascular permeability, and pain

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

Redness and warmth is due to what vascular changes?

A

Vasodilation
Mediated by histamine, prostaglandins, and bradykinin

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

Fever is mediated by what substances

A

IL-1, TNF-a, Cox activity/Prostaglandins (E2)

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

Selectins (located on endothelial cells) are mediated by what substances

A

P-selectin - Weibel Pallade bodies
E selectins - TNF-a and IL-1

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

Leukocyte Adhesion Deficiency (LAD) symptoms

A

Late separation of umbilical cord
Absence of pus
Dysfunction neutrophils

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

Leukocyte Adhesion Deficiency pathophysiology

*Think about margination, rolling, ect. of neutrophils
Silly soldiers like ice pops

A

Autosomal recessive mutation of integrins on neutrophils (LFA-1) leading to decrease in adhesion

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

Chediak-Higashi Syndrome pathophysiology

A

Impaired trafficking of phagolysosome (neutrophil + lysosome) which leads to inability of neutrophils to degrade substances

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

Chediak-Higashi Syndrome symptoms
PLAIN

A

Progressive neurodegeneration
Leukohistiocytosis
Albinism
Increased pyogenic (pus) infections
Neuropathy

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

Which enzymes are involved in the respiratory burst/formation of free readicals

A

NSM
NADPH oxidase
Superoxide dismutase
Myeloperoxidase

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

What is the order of free radicals formed in neutrophils

A

O2–> Superoxide –> Hydrogen peroxide –> Hydroxyl

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

Chronic granulomatous disease pathophysiology

A

Deficiency/Mutation of NADPH oxidase –> unable to perform respiratory burst

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

Chronic granulomatous disease patients are at increased risk of what kind of infections?

Normal = able to use hydrogen peroxide from bacteria to make hydroxyl
CGD = catalase positive bacteria is able to neutralize the peroxide = no hydroxyl

A

Infection with Catalase positive organisms

(Catalase Positive: Notoriously Big Bubbling HASSLE)
Candida
Pseudomonase
Nocardia
Burkholderia
Bordetella
H. pylori
Aspergillus
Staphylococci
Serratia
Listeria
E. coli

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

What are the 2 signals needed to activate T Helper cells

A

CD4/MHCII
CD28/ B7

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

TH1 cells secrete which cytokines

A

IL-2 = T cell growth
IFN-y = macrophage growth

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

CD40L and FASL are located on T cells or target cells

A

T cells
CD40L binds to B cells
FASL binds to target cells for apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the 2 signals needed to activate B cells
MHCII/CD4 CD40/CD40L
26
Non-caseating granulomas are indicative of what kinds of infections?
Sarcoidosis, beryllium, crohn disease, cat scratch
27
Caseating granulomas are indicative of what kinds of infections?
TB or fungus (think walling off an infection)
28
Macrophages and T cells work together to form granulomas via what signals?
Macrophages secrete IL-12 which makes Th cells Th1 cells make IFN-y to mature the macrophages
29
List 3 T cells disorders
Thymic aplasia (DiGeorge) IL-12 receptor deficiency Hyper IgE syndrome
30
DiGeorge Syndrome is due to a failure of what pharyngeal pouches to form?
3rd and 4th pharyngeal pouch --> lack of thymus and parathyroids CATCH-22 Cardiac Abnormal facies Thymic aplasia Cleft palate Hypocalcemia
31
Describe IL-12 receptor deficiency
T cells (specifically TH1 cells) rely on IL-12 signal from macrophages to form. Without IL-12, T cells remain naive --> decreased IFN-Y, maturation of macrophages, CD8 cells, and
32
Hyper IgE syndrome (Job) pathophysiology
STAT3 mutation leads to a decrease in Th17 --> low IL-17 which is a neutrophil chemotaxin Low neutrophil response and low IL-17 response --> High Th2 response ABCDE Abscess (cold, no neutrophil) Baby teeth Coarse face Dermatologic issue E - excess IgE (due to Th2) Fractures from minor trauma
33
Name 3 B cell disorders
Bruton agammaglobinemia CVID IgA deficiency
34
X-linked Bruton agammaglobulinemia pathophysiology
X linked mutation of BTK protein which is a tyrosine kinase involved in the maturation (exiting of B cells from the bone marrow). Leads to an absence of B cells in the periphery and recurrent bacterial and GI infections **after 6 months**
35
Common Variable Immunodeficiency pathophysiology
Either an issue with B cells or T cells which lead to low levels of antibodies/ B cell differentiation Leads to recurrent bacterial and GI infections **later in childhood**
36
IgA deficiency pathophysiology
Cause is unknown, associated with Celiac Disease Can cause false-negative celiac disease test and false-positive pregnancy test
37
List 4 B and T cell combined immunodeficiencies
Wiskott-Aldrich SCID Ataxia-Telangiectasia Hyper IgM syndrome
38
Wiskott Aldrich pathophysiology
X linked mutation in WASP gene which leads to inability of leukocytes and platelets to present antigen WATER Wiskott Aldrich Thrombocytopenia Eczema Recurrent pyogenic infections
39
SCID pathophysiology
1. Adenosine deaminase deficiency (girl) 2. X-linked IL-2 receptor deficiency (most common, boy) IL-2 receptor deficiency --> T cell deficiency --> B cell deficiency Failure to thrive, recurrent, viral, bacterial, fungal, and protozoal infections
40
Ataxia-telangiectasia pathophysiology
Autosomal recessive defect in ATM gene leading to a defect in ability to detect DNA damage --> mutations/risk of cancer Ataxia Spider Angiomas IgA deficiency Increase AFP
41
Hyper IgM pathophysiology
Either CD40 or CD40L defect causing a decrease in activation of B cells. Only antigen is able to bind to IgM causing IgM producing B-cells.
42
Positive selection of T cells happen in the cortex or medulla
Cortex
43
When a T cell binds to MHCII without B7 (second signal) it is said to be self reactive. The T cell will express what to induce apoptosis?
FasL will be expressed which will bind to FAS (CD95) on itself.
44
Lupus pathophysiology
Type III HS which causes self antigen (nuclear) to bind to antibody and those complexes deposit around the body leading to inflammation
45
Positive antibodies found in Lupus
Positive ANA (non specific) Anti-dsDNA and Anti-Sm Antiphospholipid antibody
46
Which antibody in Lupus can cause a false positive syphillis test?
Antiphospholipid antibody (Anticardiolipin)
47
Deficiency in early or late complement can increase the risk for Lupus?
Early Complement (especially C2). These are used to clear the antigen/antibody complexes. If deficiency, it won't get cleared.
48
Diagnostic criteria for Lupus
1. Malar/Discoid rash 2. Arthritis 3. Serositis 4. Renal damage 5. Anemia/ thrombocytopenia/ leukopenia (Type 2 HS)
49
What antibodies are found in Drug induced lupus?
Positive ANA (not specific) Anti-histone
50
What drugs commonly cause drug induced Lupus?
Procainamide, Isoniazid, Hydralazine
51
Sjogren Syndrome pathophysiology
T-cell mediated autoimmune destruction of lacrimal and salivary glands (Type IV HS)
52
Common symptoms for Sjogren Syndrome
"Can't eat a cracker, got dirt in eye" Dental carries, joint, skin, CNS issues
53
Sjogren Syndrome puts patients at increased risk for what kind of cancer?
B-cell lymphoma (enlarged parotid gland)
54
Diagnostic criteria for Sjogren Syndrome
Positive ANA Positive Antiribonucleoprotein (SSA/SSB) Lymphocytic sialadenitis
55
If Anti SSA crosses the placenta, what is the outcome for the fetus?
Lupus and congenital heart block
56
Sjogren Syndrome is also associated with what MSK disease?
Rheumatoid arthritis. RF is typically increased.
57
Scleroderma pathophysiology
Hardening of the skin and visceral tissues due to deposition of collagen after endothelial damage
58
Diagnostic criteria for Scleroderma (CREST)
Calcinosis/Anti-centromere Raynaud Esophageal dysmotility Sclerodactyly Telangiectasis of skin
59
Antibody found in Scleroderma (limited skin type)
Anti-centromere (CREST)
60
Antibody found in Scleroderma with diffuse involvement (organs)
Anti-DNA topoisomerase I
61
Describe labile, stabile, and permanent tissues
Labile - constantly dividing (skin) Stabile - able to reenter growth phase (liver) Permanent - limited stem cells, do not regenerate (cardiac, nerve, muscle)
62
What cofactor is needed to replace Type III collagen to Type I collagen in wound healing?
Zinc
63
TGF-a is a signal used to stimulate what in wound healing?
Fibroblast and epithelial cells
64
TGF-b is a signal used to stimulate what in wound healing?
Stops inflammation and stimulates fibroblasts
65
Platelet derived growth factor (PDGF) is a signal used to stimulate what in wound healing?
Endothelium, smooth muscle, fibroblasts
66
Fibroblast growth factor is signal used to stimulate what in wound healing?
Angiogenesis, skeletal development
67
Which 2 growth factors stimulate angiogenesis?
Fibroblast growth factor VEGF
68
pathoma
flashcards
Decks in class (8)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions