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Inflammation and Immunity > I2 Diseases > Flashcards

I2 Diseases Flashcards

1
Q

• Mutation in Bruton Tyrosine Kinase (BTK)
○ Required for B cell to become plasma cell
○ Autoimmunity:
• BTK required in signaling in central tolerance.. When you don’t get negative signals you produce self-recognition

A

X-Linked Agammaglobulinemia

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2
Q

Inhibits antigen presentation Inhibits proteasomal activity

Removal of MHC I molecules from ER. Degrades NKG2D on NK cells.

A

CMV (cytomegalovirus)

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3
Q

CATCH-22. Developmental failure of the 3rd & 4th pharyngeal pouches. T-/B+/NK+

A

DiGeorge Syndrome

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4
Q

IgG autohemolysin binds RBCs @ low temps

Causes intravascular hemolysis after warming

A

Autoimmune hemolytic anemia

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5
Q

Defective VDJ recombination results in low lymphocyte numbers (b/c can’t get out of primary lymphoid organs) Mutations in a DNA repair enzyme. Gait abnormalities. IgA deficiency and cerebellar problems leading to ataxia and, in this case, multiple falls

A

Ataxia-Telangiectasia (ATM)

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6
Q

Defective resistance or abnormal responses to intestinal microbes. Defective NOD signaling pathway.

A

Chron’s disease

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7
Q

Chronic mast cell activation with increased mucous secretion and bronchoconstriction. Eosinophil recruitment which can initiate damage to mucosal epithelium

A

Allergic Asthma

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8
Q

Found in Central and Southeastern US. Dimorphic fungi that is a granulomatous disease.

A

Blastomyces dermatitidus

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9
Q

Howell-Jolly bodies and loss of IgM and T-independent response. Susceptibility to encapsulated bacteria

A

Asplenia

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10
Q

CD18 deficiency leading to poor neutrophil adhesion and poor opsonophagocytosis.

A

LAD-1

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11
Q 
Disease results from: 
	1. CD4+ T cells & ANAs 
	2. Vascular damage 
Fibrosis 
	A. 2 ANAs: 
		1. DNA topoisomerase 1 Ab = AKA Scl-70
Anticentromere Ab
A

Scleroderma

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12
Q

Pathogenesis MOA:
- Main players: Th1 & macrophages
- Infection proceeds from initial infection of macrophages to a Th1 response that both contains the bacteria & causes tissue damage
- Process:
1. Bacteria uptake by macrophages
2. Blockage of phagolysosomal fusion
3. TB PAMPs recognized by innate receptors, initiating a Th1 response
4. Th1 cells produce IFN-y
IFN-y = the critical mediator that enables macrophages to contain the TB infection

A

Tuberculosis

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13
Q

• Disease causes release of cytotoxic enzymes leading to widespread keratinocyte cell deal w/ blistering & sloughing of the skin
• Majorly involved molecules:
1. CD8+ T cells
2. Fas
3. Perforin
4. Granzyme B
• Proposed mechanism:
1. Meds binds MHC I & TCR
2. Leads to CTL clonal expansion
3. CTLs kill keratinocytes via cell-mediated cytotoxic rxn via death domains
a. Dysregulation of Fas-FasL death ligand receptor on keratinocytes
4. NK cell recruited & they secrete soluble death mediators
Massive apoptosis

A

Stevens-Johnson Syndrome

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14
Q

Ab’s against streptococci cross-react w/ myocardial antigen

A

Rheumatic fever

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15
Q

Low Ig due to B cell or CD4+ T cell defects
Pathogenesis results from reduced serum IgG, IgA, IgM levels
Poor Ab response to infections
Recurrent infections, autoimmunity & lymphomas
They have normal B cell #’s but Ab’s either aren’t produced or don’t work

A

CVID

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16
Q

Defective phagolysosomal formation results in:
Impaired granule release from NK & CTLs
Frequent & severe bacterial infections

A

Chediak-Higashi Syndrome

Give away: partial albinism due to defective MT trafficking of melanin from melanocytes to keratinocytes

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17
Q

Systemic granulomatous disease of unknown cause that may involve many d/f tissues & organs

A

Sarcoidosis

18
Q

CD4 is less than 400 and patient has an opportunistic infection

A

AIDS

19
Q
  • W prophylactic GvHD medications (tacrolimus, cyclosporine) we have shut down CTLs that would normally kill EBV
    Virus runs rampid
A

PTLD EBV-related

Post-transplanted Lymphoproliferative Disorder

20
Q

Impaired NADPH oxidase activity. Granulomas form in lungs, liver & spleen when microbes that can’t be killed are walled off

A

Chronic Granulomatous Disease

21
Q

Type IV Autoimmune

Immune atack of myelin sheath that covers nerve fibers

A

Multiple Sclerosis

22
Q

Mutation in TAP1/TAP2/Tapasin expression. Low CD8+ T cells counts No MHC I expression. Viral infections.

A

Bare lymphocyte Syndrome Type I

23
Q

Characterized by a triad:

1. Thrombocytopenia 
2. Eczema 
    3. Recurrent pyogenic infections
A

Wiskott-Aldrich Syndrome

24
Q

ii. Silver stain- BAL GMS DIAGNOSTIC
· Thick-walled, rounded w/ inctracystic bodies
Encysted organisms have cup or “goblet shape”

A

Pneumocystis jirovecii

25
Q 
○ Any type III hypersensitivity reaction against some kind of therapy 
Local reaction = arthus reaction
○ Clinical findings: 
	• Vasculitis 
	• Hemorrhage arthralgia 
	• Skin rashed 
Nephritis
A

Serum sickness

26
Q

Due to mutations in Sialyl Lewis X receptor for selectins • Defective leukocyte adhesion
Defects in selectin or selectin ligand binding

A

LAD-2

27
Q

“soap bubble appearance” on histolgical staining. India ink staining. Presents with meningitis.

A

Cryptococcus

28
Q

Congestion of RBCs in capillary, strings of fibrin in the air space, and neutrophil infiltrate. Need to put patients on antibiotics to prevent scarring of lung tissue.

A

Acute Pneumonia

29
Q

Mutations in 1 of 4 genes encoding TFs regulating MHC II expression. No MHC II expression. Responsible for internalizing extracellular antigens. Lack CD4+ T cells.

A

Bare Lymphocyte Syndrome Type II

30
Q

Infective arthroconidia

Blocks phagolysosomal fusion. Found in desert southwest. Sphericles with endospores. Cauliflower White Staining.

A

Coccidiodes immitus

31
Q

Problems with formation of the MAC complex leads to infections by what?

A

Nesseria

32
Q
  1. Necrotizing inflammation of blood vessel walls
    1. Causes vessels to have increased permeability & fibrin moves in
    2. Thrombosis in vessel walls
      • Clinical presentation is widespread from this:
        Pain in the vessel being obstructed
        Type III
A

Polyarteritis Nodosa

33
Q
  1. Reaction to foreign material
    1. Sarcoidosis
    2. Beryllium exposure
    3. Chrohns disease
      Cat scratch disease
      These all have what in common
A

Noncaseating granulomas

34
Q

• Results from a deficiency in enzyme that creates an anchor that tethers DAF & MCP to the membrane
• Makes a stable membrane-bound C3 convertase
Pathogenesis: Sporadic hemolysis due to spontaneous C4 activation on RBC membranes

A

Paroxysmal Nocturnal Hemaglobinura (PNH)

35
Q

. Process of pathogenesis:
1. Infected macrophage drains to LN
2. Here, activates CD4+ * CD8+ T cells
3. Macrophages & T cell activation leads to granuloma formation
Granulomas develop central necrosis (Caseous necrosis)

A

Mycobacterium TB

36
Q

Defective elimination of self reactive lymphocytes. FAS:FASL disorder.

A

Human ALPS

37
Q 
Intracellular pathogen residing in phagocytes 
• Induces cell-mdeiated imunity 
	• CD4+ 
	• IFNy 
Heat-shock proteins 
	○ Elicits granulomas 
Some caseate (mimics TB)
A

Histoplasmosis

38
Q

Ab inhibits acetylcholine binding–> down modulates the receptor

A

Myasthenia gravis

39
Q

• Ab-mediated stimulation of TSH receptors

Agonistic thyroid-stimulating Ab’s

A

Graves Disease

40
Q

• IgG Ab against NC1 domains of the alpha-3/alpha-5 chain of type IV collagen (basement membrane) of the kidney
Predominantly IgG1 & IgG3

A

Goodpasture Syndrome

41
Q 
Type 3 Hypersensitivity
Anti-dsDNA Ab
• Ab's against nuclear antigens 
	1. dsDNA 
	2. snRNP 
• Criteria for SLE classification: 
	1. Malar rash 
	2. Discoid rash 
	3. Photosensitivity 
	4. Oral ulcers 
	5. Arthiritis 
	6. Serositis 
		- Pleuritis 
		- Pericarditis 
	7. Renal disorder 
	8. Neurologic disorder 
	9. Hematologic disorder: 
		- Hemolytic anemia (w/ reticulocytosis) 
		- Leukopenia 
		- Lymphopenia 
		- Thrombocytopenia
	10. Immunologic disorder 
ANA
A

SLE

42
Q

C1 inhibitor absence lead to ongoing cleavage of C4 and C2. Presents with random swelling.

A

Hereditary angiodema

Inflammation and Immunity (51 decks)

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