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Immuno Pathology Flashcards

1
Q

Which chromosome are the HLA receptors on?

A

Chromosome 6

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2
Q

Fact of each Ig

A

IgG- fetal protection
IgM- vase Ig. x5
IgA- mucosal defense. Breast milk
IgE- allergy. Eosinophils.

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3
Q

Natural Killer cell receptor

A

NKG2D- cell damage

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4
Q

Job of

IL-4
IL-5
IL-13

A

4 - class switching
5- eosinophils activation
13- increase IgE production

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5
Q

3 mechanisms of type 2 hypersensitivity

A

Opsonization and Phagocytosis

Complement mediated inflammation (Neutrophil ROS)

Antibody attack (activated or inhibiting)

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6
Q

examples of type 2 hypersensitivity antibody attacks(4)

A

Graves’ disease (activating TSH)
Myasthenia Gravis (inhibit ACH)
Pernicious anemia (intrinsic factor-B12 absorption-iron)
Insulin resistant diabetes( inhibit insulin binding)

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7
Q

Type 2- ipsonization/phagocytosis examples(2)

A

Autoimmune hemolytic anemia

Autoimmune thrombocytopenia purpura

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8
Q

Type 2 Hypersensitivity - complement(2)

A 
Goodpasture (protein in kidney/lung basement membrane)
Rheumatic  fever( post strep heart valve attack)
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9
Q

Type 3 hypersensitivity examples (4)

A

Vasculitis/pleuritis/pericarditis
Arthritis
Arthur’s reaction
Glomerular nephritis(post strep complexes….)

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10
Q

Type 4 hypersensitivity

Hallmarks?
Examples (7) what target?

A

T-cells (helper or cute toxic)
Granulomas

Rheumatoid arthritis-collagen?
MS- myelin
Type 1 DM- pancreatic Beta cells by cytotoxic
Inflammatory Bowl- enteric bacteria or self
Psoriasis- unknown
Contact sensitivity- chemicals (poison oak, metals)
Tb skin test

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11
Q

What cell is on?
What binds it bind to?
Action?

B7(CD80/86)
CTLA-4
CD28
PD-1
PDL-1
A

B7= APC, binds to T cells, costimulatory for attack

CTLA-4= T cells, bind B7, inhibitory signal for T cells

CD28= T cells, bind B7, co stimulators for attack

PD-1= T cells, bind PDL-1, reduces/kills T cells

PDL-1= self cells(cancer), binds PD-1, inhibits immune reaction against self cells (or cancer/infection)

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12
Q

Main signal on T-Regs?

Actions caused by…..

A

FoxP3
CD25- IL-2 receptor

Immune suppression by increase

IL-10
TGF-Beta
CTLA-4 = remove B7 off APC

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13
Q

IPEX stand for?

What mutation? Mechanism?

A

Immune dysregulation
Polyendocrinopathy
Enteropathy
X-linked

FoxP3- needed for Treg development. If mutated than less Tregs around= increase autoimmunity

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14
Q

3 things to have “autoimmune Reactions”

A

Immune response to self antigens

Immune response is responsible for pathology

No other pathophysiology responsible

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15
Q

Ankylosis spondylitis

What? What gene increase susceptibility?

A

Class 1 HLA-B27

Fusion of vertebrae from disc inflammation

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16
Q

Crohn disease

Gene increasing susceptibility?

A

Poor ability to kill enteric bacteria

NOD-2 mutation= innate immunity can’t kill bacteria

Increase lymphocyte activity to kill= exaggerates immune response

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17
Q

What test are specific for…..

Lupus
Sjogren
Systemic sclerosis
CREST syndrome

Immunofloresence pattern

A

Lupus: anti-dsDNA, Anti- Smith
Homogeneous

Sjogren: anti Ro(Ss-A), anti La(SS-B)
Speckled

Systemic sclerosis: anti topoisomerase(Scl-70)
Speckled

Crest Syndrome: anticentromere, centromere

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18
Q

SLE

Genetic predisposition?
Criteria?

A

Common HLA- DQ, females

Criteria-: Malar Rash- butterfly
Discoid Rash-underpigmented
Photosensitivity
Oral ulcer
Arthritis-aches
Serositis
Renal disorders-edema,proteinuria, 
Neurologic disorder
Hematologic disorder- fatigue/anemia
Immunologic disorder-fever, endocarditis
Antinuclear antibodies- Anti DNA, Anti Smith
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19
Q

Lupus Nephritis usually seen as….

A

Diffuse Lupus Nephritis

Scattered/grainy/granular immunoflouresence

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20
Q

Liebman Sachs endocarditis

A

Fibrin deposits in heart valves from SLE

Not from infection, can embolize

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21
Q

L-E cell?

A

Phagocyte that injests nucleus of damaged cell but can’t break it down.

Looks like damaged nucleus is “sealing the phagocyte nucleus

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22
Q

Discoid Lupus

Characteristics

A

Mainly just face/scalp lesions
no renal or blood effects.

Positive ANA, but not anti-DNA

23
Q

Drug induced Lupus

Characteristics

Drugs and Genetic disposition

A

Arthralgia, fever, discoid rash
Also blood symptoms

Positive ANA, Positive anti-HISTONE

Goes away with drug cessation

Hydralazine: HLA-DR4
Procainamide: HLA- DR6

24
Q

Sjogren Syndrome

Signs
Diagnosis/tests
Complications

A

Dry eyes, mouth, root caries

Anti Ro/anti La
Biopsy minor salivary glands (lips)

May lead pulmonary fibrosis and lymphomas

25
Systemic Sclerosis Where? Signs
Fibrosis in skin, GI, Kidney, heart, lungs, Vasculature. Bent, hook like fingers. Lead to Raynaud disease. Vascular hyalinazation (thick walls) reflux, ulceration Renal/lung disease
26
CREST syndrome What related to? How different? Acronym?
Form of limited sclerosis. Better prognosis than systemic. No lung, renal or heart components. ``` Calcinosis- in skin Raynauds- vascular constrict Esophageal- reflux Sclerodactyly- hook fingers Telangiectasias- red marks blood dilation ```
27
Mixed Connective Tissue Disraeli Molecular signature? Symptom?
High titer Anti-ribonucleoprotein Usually seen with Raynaud phenomenon
28
IgG4 related disease Disease associated (6)
``` Autoimmune pancreatitis Riedel thyroiditis Mikulicz’s syndrome(salivary) Idiopathic retroperitoneal fibrosis Inflammatory pseudo tumors(lung, eye, other) Inflammatory aortitis ```
29
Rejection types (5)
Hyper acute- preformed antibodies (blood type) Acute- tubulitis/endothelium (no complement) Acute antibody mediated= 5-9 day C4d positive stain Chronic Chronic antibody mediated - fibrosis of vessels(Trichrome Stain)
30
Rejection treatment Down sides?
Corticosteroids T cell rejection- Tacrolimus Antibody rejection- rituximab(CD20 antibody) Immunosuppressive- rare virus/fungal infections(polyomavirus,cytomegalovirus) -increase viral cause tumor(lymphoma, kaposi sarcoma)
31
Immunodeficiency syndromes 5 primary 2 secondary
1) leukocyte function-chediak hegashi Complement function- hereditary angioedema Lymphocyte maturation-SCID, Di George Lymphocyte function-hyper IgM, igA deficiency Systemic disease- wiskott Aldrich, ataxia-telangiectasia 2)Immunosuppression AIDS
32
Consequences of deficiencies: B cell T cell Complement
B cell- pyogenic bacteria, enteric bacteria T cell- viral/intercellular, cancers Innate- pyogenic bacteria, nisseria( variable)
33
Cherish higashi
Autosomal recessive Failure of phagokysosome fusion Fatal Giant granules Albinism/grey hair Clotting deficient Vision/central nervous system
34
Chronic granulomatous disease
Poor superoxide production
35
MAC deficiency
C5,6,7,8,9 Increase neisseria infections
36
Hereditary angioedema
Autosomal dominant Decrease C1 inhibitor= excess complement activation
37
SCID- 2 types
No T cell production, impaired B cell with no T-helpers X linked-mutated IL receptors Autosomal recessive- adenosine deaminase deficient - toxic purine accumulation
38
DiGeorge
Catch 22 ``` Cardiac Abnormal facies Thymus Cleft lip/palate Hypocalcemia(hypoparathyroid)- tetany ```
39
X linked agammaglobulinemia
Bruton tyrosine kinase mutation Can’t make “pre-B cells”
40
Hyper IgM
Many encapsulated bacteria infections Defect in CD40/CD40L(can’t class switch)
41
Common variable immunodeficiency
Most common significant immunodeficiency Pyogenic bacteria(sinus/lung) Granulomas Diarrhea(giardia) Autoimmune(anemia,thrombocytopenia)
42
IgA deficiency First notice when??
Can’t defend unhedged/inhaled pathogens Sinus, urinary, GI infections Transfusion reaction- host antibodies against IgA as never seen before (Must “wash” RBC before transfusion)
43
Wiskott Aldrich syndrome
Thrombocytopenia Eczema Infections(reduced T cell, hypogammaglobunemia) WASP mutation
44
Ataxia Telangiectasia
Ataxia- neurological Telangiectasia- swollen vessels Respiratory, autoimmune, cancer Mutated ATM gene- no DNA repair
45
4 areas of HIV genome and their proteins
LTR- transcription/translation factors Gag- interior proteins(p24 capsid protein) Env- surface glycoproteins(gp 120, 41) Pol- viral enzyme(reverse transcriptase, protease, integrate)
46
HIV infection steps
1) Entry-Gp 120 bind to CD4 - Gp 41 drills in 2) reverse transcriptase 3) protease/integrase into host DNA 4) LTR controls transcription
47
How is transcription stimulated?
Antigens are suppose to cause the T cell response(NF-kappa B) But with LTR it hijacks signal to make viral proteins
48
Resiviors for HIV other then T cells
Macrophage, dendritic, microglia
49
HIV testing timelines What marker when?
HIV RNA (NAT)- 7-14 days P24(gag)- 14-25 days HIV antibodies- 21+days
50
Acute retro viral syndrome symptoms
Fever, sore throat, muscle ache Starting to infect cells, immune system is working to try and limit it.
51
Amyloidosis- What? Where? Local vs systemic
Improper folding of proteins into beta-pleated sheets that can’t be broken down Generally heart, liver, kidney, brain, Local- caused by tumor or diseae(mutation) Systemic- caused by plasma cell disorder or inflammation?
52
AL vs AA amylodosis?
AL- amyloid light chains - abnormal production from plasma cells AA- inflammation causing abnormal protein production
53
What stain used for amyloidosis?
Congo Red | Polarized Congo red (Apple green)

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