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MICRO 360 > Diseases > Flashcards

Diseases Flashcards

1
Q

Hereditary angioedema

A

This is a complement disease when you are deficient in C1 INH which inhibits C1 cleaving C2 and C4 (start of the classical complement pathway)

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2
Q

Chronic granulomatous disease

A

you have a mutation in phagocyte oxidase which creates ROI needed for macrophage peptide degradation

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3
Q

Allergic Rhinitis

A

also known as hay fever

type one hypersensitivity reaction caused by EARLY PHASE MEDIATORS (histamine). Upper respiratory tract (nose) inflammation, mucosal edema,

treated with antihistamines

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4
Q

Bronchial asthma

A

hypersensitivity type one reaction

lower respiratory tract inflammation and bronchoconstriction due to LATE PHASE MEDIATORS
primary cells = eosinophils and Th2

key inflammatory molecule = LCT4

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5
Q

What is MIP1-alpha?

A

a late phase mediator that attracts neutrophils

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6
Q

what do cromolyn and corticosteroids do?

A

used to treat bronchial asthma

cromolyn - satbilises mast cell membrane

corticosteroids - block production of inflammatory cytokines

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7
Q

what are Urticaria and atopic eczema?`

A

Urticaria –> acute hives
atopic eczema –> chronic hives

typically caused by food allergies

type one HS

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8
Q

The transfusion reaction

A

hypersensitivity two deals with membrane-bound antibodies (typically IgG).

Type O = universal donor –> expresses no membrane anitgen
Type AB = universal acceptor –> expresses both A and B antigens (i.e. does not contain any antibodies)

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9
Q

Hemolytic disease of the newborn

A
  1. Rh - mom has a kid who is Rh+
  2. blood mixes and mom makes anti-D antibodies (D refers to antigen expressed by Rh+ people)
  3. if the next kid is Rh+ -> IgG antibodies that are anti-D can cross the placenta and attack the child’s blood
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10
Q

Farmers lung

A

type 3 hypersensitivity rxn

antigens in hay dust enter alveoli and cause inflammation (not the same as broncho asthma)

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11
Q

Arthus reaction

Serum Sickenss

A

both are type 3 HS rxns

arthus rxn –> vaccinate someone who already has Ab’s to vaccine = local inflammation / redness

serum sickness –> systemic inflammation / redness

cutanous vasulitis = vasodilation leading to skin redness

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12
Q

Tuberculin reactions

A

TD tests –> type 4 HS rxn

cell mediated HS

often involves metals and haptens

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13
Q

EPSTEIN-BARR Virus (EBV)

molecular mimicry

release of sequestered anitgen

A

these are different ways tolerance can be broken

EPSTEIN-BARR Virus (EBV) –> gives rise to polyclonal antibodies some of which may recognise self antigen

molecular mimicry –> by chance a antigen has the same peptide seuqence as a self peptide

release of sequestered anitgen –> injury can release hidden Ag which T cells have never seen and therefore think is foriegn (eyes, brain, testes)

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14
Q

Type 2 Auto immune disease

Streptococcos infection

A

Streptococcos infection is a type 2 AI disease –> therefore antigen is cell surface bound

in this case, the antigen from Streptococcos infection iis very similar to a heart protein leading to cardititis (molecular mimicry)

rhematic fever can also occur –> inflammatory disease that develops after a streptococcos infection

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15
Q

Type 2 AI

Graves disease

A

Graves disease is a type two AI –> antigen is cell surface bound.

antibodies recognise TSH receptor on the theyroid and bind with efficacy causing constant production of thyroid hormone

fatigue, weight loss, etc.

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16
Q

Type 2 AI

Myasthenia Gravis

A

Myasthenia Gravis is a type two AI –> antigen is cell surface bound.

self antigen is acetlycholine receptors at neuromuscualr junctions –> antibodies bind this and cause Ach receptor internalization

muscles become weak, droopy eyelids (ptosis)

17
Q

Type 3 AI

Rhemaoid arthritis

A

Rhemaoid arthritis is a type 3 AI –> soluble antigen is detected and an immune complex forms.

TNF-alpha cytokine is detected as a foreign antigen. Antibodies bind this and form a complex that is too large for macrophages to engulf –> gets deposited into joints (a lot in hands) and causes destrcution.

18
Q

what is Rheumatoid factor?

A

this is a gene that 80% of people with RA express.

RF is an IgG or IgM antibody that binds other antibodies

However, not everyone expresses this with RA so its not a given that you can’t develop it if you lack the RF.

19
Q

Type 3 AI

Systemic Lupus Erythenatosus

A

Systemic Lupus Erythenatosus is a type 3 AI –> soluble antigen is detected and an immune complex forms.

antbody detects your own DNA!

when a cell lyses due to apoptosis sometimes DNA is let out –> antibody (usually IgG in all these cases) binds it and forms an immune complex that can be deposited in many different tissues

vasculititis --> vessel inflammation 
cardititis --> heart inflammation 
synvotitis --> joint inflammation 
dermatitis --> butterfy face 
glomerulophritis --> kidney inflammation

butterfly rash in face and kidney inf –> characteristic of lupus

20
Q

Type 4 AI diseases

a. insulin dependent daibetes
b. rheumatoid arthritis (again)
c. multiple sclerosis

A

these three are type 4 AI –> cell mediated AI

a. insulin dependent daibetes
- pancreatic beta cell Ag –> destroys pancreas

b. rheumatoid arthritis (again)
- sinonovial joint Ag –> joint destruction

c. multiple sclerosis
- myelin is the anitgen
- demyelination of neurons leads to retardation

21
Q

Primary immunodeficiency

chronic granulomatous disease

A

Innate immunity defect

when you are deficient in phagocyte oxidase which means you cannot form ROI which are essential in macrophage degradation of peptides (along with nitric oxide and elastase)

22
Q

Primary ID

Complement ID

A

Innate immunity defect

macrophages lack C3b receptor (which is the opsonin often used for opsonization)

23
Q

Primary ID

Bruton’s Disease

A

specific immunity defect

mutation in Bruton tyrosine kinase which is important in B cell development

person with Bruton’s disease will have very few B cells and antibodies

X linked disease

24
Q

Why do children with Bruton’s disease only get infections after 3 months of living?

A

first three months the IgG placental antibodies given by the mother via passive immunity are still functional. Also, IgA antibodies in breast milk are given to the kid.

25
Q

Primary ID

DiGoerge Syndrome

A

specific immunity defect

lack of proper thymus development leads to an inability to mature T cells –> lack CD4 CD8 NKT cells and lack B cells too since Th cells are needed for B cell activation.

live vaccine can be life-threatening

26
Q

Primary ID

Hyper IgM syndrome

A

specific immunity defect

Mutation of the CD40L on CD4 Th cells

no CD40L-CD40 interaction with B cells inhibits T cell-dependent activation of B cells. Recall that Th2 produces Il-4 (and IL-5 and Il-13) which interacts with STAT 6 to produce an IgE class switch.

in Hyper IgM syndrome, there is no class switching

prone to infection in area’s IgM cannot go

27
Q

What is Pneumocystis carinii?

A

Pneumocystis carinii is a fungal infection often developed by people with hyper IgM syndrome

28
Q

Primary ID

Common Variable Id (CVID)

A

specific immunity defect

randomly cannot mature B cells perfectly causing a reduction in IgA or IgG or both depending on severity.

hypogammaglobulinaemia –> refers to a reduction in gamma globulins

treatment: IVIG aka IVGG

29
Q

Primary ID

Adenosine deaminase deficiency (ADA)

A

specific immunity defect

Adenosine deaminase deficiency (ADA)

this is also called combined B and T cell immunodeficiency.

lack of the AD enzyme causes accumulation of deoxyadenosine which is toxic to lymphocytes leading to their death

must be homozygous recessive to get this disease

30
Q

Primary ID

Sever combined ID (SCID)

A

specific immunity defect

lack of RAG 1 and 2 enzymes due to mutation meaning you cannot perform gene rearrangements at RSS sequences for either B or T cells. = no lymphocytes

treatment = bone marrow transplant

31
Q

Primary ID

MHC 2 deficiency

A

specific immunity defect

bare lymphocyte syndrome is aka MHC 2 deficiency

mutation leading to no MHC2 –> no CD4 positive selection and no T cell-dependent B cell activation and no CD8 cell activation via Th1

treatment = bone marrow transplant

32
Q

rather than primary ID (which are congenital/inherited) what is the main acquired ID?

A

HIV / AIDS

33
Q

Explain HIV

A

a virus that infects macrophages and CD4 Th cells.

They target CD4 as their receptor to enter our cells

typically infects macrophages first then Th cells in the second wave.

34
Q

HIV

explain

CD4
CCR5
GP120
GP41

A

CD4 –> main HIV receptor for infection
CCR5 –> co-receptor, also binds MIP (recall MIP is a late phase mediator in type 1 HS)
GP120 –> glycoprotein binds CD4 and other molecules
GP41 –> required for endocytosis of HIV

35
Q

allograft rejections

hyperacute
acute
chronic

A

hyperacute –> preformed antibodies to graft –> rejection takes 24 hours
acute –> CMI (t cells) –> takes 10 days - 2 weeks

chronic –> constant battle to keep graft in (2-10 years)

minor H antigen such as H-Y antigen
or battle with therapy

36
Q

cancer arises from

abnormal activity of a proto-oncogene –>

failure of a tumor supressor –>

defects in apoptosis –>

A

abnormal activity of a proto-oncogene –> RAS gene

failure of a tumor supressor –> P53 gene

defects in apoptosis –> BAD gene

37
Q

what are tumor infiltrating lymphocytes

A

adaptive immunity lymphocytes that fight cancer

also b cells produce anti-tumor Ab’s to try cause NK ADCC

38
Q

what are myeloid-derived suppressor cells (MDSC’s)?

A

myeloid-derived suppressor cells (MDSC’s) are recruited by T reg cells and they produce more Anti-inflammatory cytokines

MICRO 360 (12 decks)

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