Brainscape's Knowledge GenomeTM

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


See full index

MOD > Immuno Pathology > Flashcards

Immuno Pathology Flashcards

1
Q

Which chromosome are the HLA receptors on?

A

Chromosome 6

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

Fact of each Ig

A

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

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

Natural Killer cell receptor

A

NKG2D- cell damage

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

Job of

IL-4
IL-5
IL-13

A

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

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

3 mechanisms of type 2 hypersensitivity

A

Opsonization and Phagocytosis

Complement mediated inflammation (Neutrophil ROS)

Antibody attack (activated or inhibiting)

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

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

Type 2- ipsonization/phagocytosis examples(2)

A

Autoimmune hemolytic anemia

Autoimmune thrombocytopenia purpura

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

Type 2 Hypersensitivity - complement(2)

A 
Goodpasture (protein in kidney/lung basement membrane)
Rheumatic  fever( post strep heart valve attack)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Type 3 hypersensitivity examples (4)

A

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

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

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

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

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

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

3 things to have “autoimmune Reactions”

A

Immune response to self antigens

Immune response is responsible for pathology

No other pathophysiology responsible

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

Ankylosis spondylitis

What? What gene increase susceptibility?

A

Class 1 HLA-B27

Fusion of vertebrae from disc inflammation

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

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

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

Lupus Nephritis usually seen as….

A

Diffuse Lupus Nephritis

Scattered/grainy/granular immunoflouresence

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

Liebman Sachs endocarditis

A

Fibrin deposits in heart valves from SLE

Not from infection, can embolize

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

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

Systemic Sclerosis

Where?

Signs

A

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
Q

CREST syndrome

What related to? How different?

Acronym?

A

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
Q

Mixed Connective Tissue Disraeli

Molecular signature?

Symptom?

A

High titer Anti-ribonucleoprotein

Usually seen with Raynaud phenomenon

28
Q

IgG4 related disease

Disease associated (6)

A 
Autoimmune pancreatitis
Riedel thyroiditis
Mikulicz’s syndrome(salivary)
Idiopathic retroperitoneal fibrosis
Inflammatory pseudo tumors(lung, eye, other)
Inflammatory aortitis
29
Q

Rejection types (5)

A

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
Q

Rejection treatment

Down sides?

A

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
Q

Immunodeficiency syndromes

5 primary

2 secondary

A

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
Q

Consequences of deficiencies:

B cell
T cell
Complement

A

B cell- pyogenic bacteria, enteric bacteria

T cell- viral/intercellular, cancers

Innate- pyogenic bacteria, nisseria( variable)

33
Q

Cherish higashi

A

Autosomal recessive
Failure of phagokysosome fusion
Fatal

Giant granules
Albinism/grey hair
Clotting deficient
Vision/central nervous system

34
Q

Chronic granulomatous disease

A

Poor superoxide production

35
Q

MAC deficiency

A

C5,6,7,8,9

Increase neisseria infections

36
Q

Hereditary angioedema

A

Autosomal dominant

Decrease C1 inhibitor= excess complement activation

37
Q

SCID- 2 types

A

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
Q

DiGeorge

A

Catch 22

Cardiac
Abnormal facies
Thymus
Cleft lip/palate
Hypocalcemia(hypoparathyroid)- tetany
39
Q

X linked agammaglobulinemia

A

Bruton tyrosine kinase mutation

Can’t make “pre-B cells”

40
Q

Hyper IgM

A

Many encapsulated bacteria infections

Defect in CD40/CD40L(can’t class switch)

41
Q

Common variable immunodeficiency

A

Most common significant immunodeficiency

Pyogenic bacteria(sinus/lung)
Granulomas
Diarrhea(giardia)
Autoimmune(anemia,thrombocytopenia)

42
Q

IgA deficiency

First notice when??

A

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
Q

Wiskott Aldrich syndrome

A

Thrombocytopenia
Eczema
Infections(reduced T cell, hypogammaglobunemia)
WASP mutation

44
Q

Ataxia Telangiectasia

A

Ataxia- neurological
Telangiectasia- swollen vessels

Respiratory, autoimmune, cancer

Mutated ATM gene- no DNA repair

45
Q

4 areas of HIV genome and their proteins

A

LTR- transcription/translation factors

Gag- interior proteins(p24 capsid protein)

Env- surface glycoproteins(gp 120, 41)

Pol- viral enzyme(reverse transcriptase, protease, integrate)

46
Q

HIV infection steps

A

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
Q

How is transcription stimulated?

A

Antigens are suppose to cause the T cell response(NF-kappa B)

But with LTR it hijacks signal to make viral proteins

48
Q

Resiviors for HIV other then T cells

A

Macrophage, dendritic, microglia

49
Q

HIV testing timelines

What marker when?

A

HIV RNA (NAT)- 7-14 days

P24(gag)- 14-25 days

HIV antibodies- 21+days

50
Q

Acute retro viral syndrome symptoms

A

Fever, sore throat, muscle ache

Starting to infect cells, immune system is working to try and limit it.

51
Q

Amyloidosis- What? Where?

Local vs systemic

A

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
Q

AL vs AA amylodosis?

A

AL- amyloid light chains
- abnormal production from plasma cells

AA- inflammation causing abnormal protein production

53
Q

What stain used for amyloidosis?

A

Congo Red

Polarized Congo red (Apple green)

MOD (6 decks)

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