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.2 Flashcards

1
Q

digeorge syndrome

A

will not have items from 3rd and 4th pouch

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2
Q

What deficiency’s would be found in digeorge syndrome

A

T cell deficiency (thyroid)
hypocalcemia (parathyroid)
abnormalities of heart, great vessels and face

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3
Q

SCID are effected by

A

defected humoral and cell mediated immunology

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4
Q

Etologies of SCID

A 
defects cytokine receptor
adenosine deaminase deficenty
MHC class 2 deficency
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5
Q

Adenosine deaminase deficiency

A

build up of adenosine and oxydenosine can cause a build up in neutrophils causing immunodeficiency

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6
Q

CD4+ Tcells

A

help b cells mature and help CD8 fight infections

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7
Q

Cytokine receptors deficiency can cause

A

immunodeficeny

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8
Q

MHC class 2 are able to activate

A

CD+4 causeing a deficency in t and b cells

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9
Q

Patients with SCID

A

don’t have t cells and will get fungal and viral infections
They also don’t have b cells and will get protezoal and bacterial infection
also have problems with live vaccines and are worse than aids patients

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10
Q

SCID treatment include

A

sterile isolation and stem cell transplant

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11
Q

Why are they given stem cell transplants

A

the stem cell transplant can differentiate into b and t cells.

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12
Q

X linked agammaglobulinemia

A

Complete lack of immunoglobulin

disordered b cell mutation problem hence not allowing them to mature into plasma cells

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13
Q

Tyrosine kinase

A

To help b cells mature into plasma cells

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14
Q

the lack of tyrosine kinase will cause

A

bacterial, enterovirus and giardia infections.

after 6 months of life. because of the lack of IgG IgA, IgA in that order. No live vaccines given

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15
Q

the x linked aggamagobulinemeia is due to a mutation in what

A

Bruton tyrosine kinase

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16
Q

Common variable Immune disease

A

Low immunoglobulin due to B-cell or helper T-cell defects

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17
Q

What are the common infections with CVID

A

autoimmune disease and lymphoma in late adulthood.

when younger there will be bacterial infections, enterovirus, and giardia.

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18
Q

IgA deficiency

A

Increase mucosal viral infections

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19
Q

celiac disease

A

cause by IgA deficeincy

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20
Q

Hyper IgM syndrome is cause by a mutation in the

A

CD40 2nd way of being activated not working so 2nd pathway for IGA and IgG and IgE, prevents class switching.

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21
Q

2 ways b cells are activated

A
  1. antigen binds IgM making a IgM secreting plasma cell
  2. B cell can internalize the antigen and present MAclass 2 and a CD 40 stimulus is expressed on the b cell for T cell and will activate CD4 and produce IL4 and IL 5 and will go back to the b cell and allow it to mature and class switch to produce IGA IgG IgE
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22
Q

IgA and IgG and IgE are created from the b cell class switching cause by IL4 and IL5 what will not be activated with someone with Hyper IgM syndrome

A

The CD40 will not be expressed for the t cell so IL4 and IL 5 will not be produced preventing the b cell from class switching. meaning there will be high IgM but low IgA IgG IgE

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23
Q

what are common problems with Hyper IgM syndrome

A

mucosal infections

puss forming recurrent infection

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24
Q

Wiskott Aldrich Syndrome

A

a triad of
Thrombocytopenia
Excema
recurrent infection

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25
wiskott aldrich syndrom is caused by a mutation in the
wiskot aldrich syndrome X LINKED!!!
26
compliment deficiency
C5-'C9 deficiency can cause a risk for Neisseria infection
27
if there is a deficiency of C1 inhibitor can cause
over activation of c1 causing over activation of complement | causes include vasodilation increased vascular permeability. Periorbital edema
28
Hereditary angio edema is and example of
compliment deficiency with a periorbital edema caused by over activation of complement because of a c1 inhibitor deficiency
29
autoimmune desease, we constantly creating lymphocytes buy they are
usually apoptotic, or become anergic (go to sleep) generally effect woman more than men at child bearing age.
30
Etiology of autoimmune disorders
Environmental trigger in a genetically susceptible individuals, increased incidence in twins and associated with certain HLA subtypes
31
first autoimmune disease
SLE
32
SLE Systeic autoimmune disease involves
multiple organs have antibodies by binding and causing damage type 2 cytotoxic or Type 3 antigen antibody complex Hyper sensitivity reaction deposited in the tissue.
33
Long list of lupus
``` fever wight loss, Mallar butterfly rash Arthritis Pleuritis pericarditis CNS cycosis ANY HEART LAYER LEADMANSACKS endocarditis vegetation of both sides of the valve. ANEMIA THROMBOCYTOPENIA LEUKOPENIA ```
34
Lupus common cause of death is from
Renal damage - diffuse proliferative glomeruloephritis | INFECTION
35
lupus is Characterized by a ANA
Anti nutruphil body and a anti DS DNA
36
Lupus can also be drug induced by what drugs
ANTI HISTONE ANTIBODY Hydralazine procainamide and isoniazid | removal of drug will get rid of disease
37
Antiphosphlipid syndrome also accounted with lupus
antibody against phosophlipds specifically anticardiolipin, (false postive syphilis test) lupus anticoagulant, interfering a ppt (false elevation)
38
Antiphospholipid syndrome in lupus actually causes
arterial and venous thrombosis | Deep venous thrombosis and hepatic vein thrombosis, placental thrombosis and stroke
39
what is required life long when diagnosed with antiphsopholipid syndrome.
Anticoagulation medication
40
Bud keori syndrome is caused by and most commonly found with
Deep venous thrombosis | polly cithemia verra
41
Sjorgren syndrome
lacrimal and salivary glands are filled with fibrosis due type 4 hypersensitivity
42
common symptoms,
dirt in eye and multiple carries
43
Sjorgren syndrome is characterized by
Antiribonucleoprotein antibodies | antibody has the SS-A SS-B
44
What is the target of SS-A and SS-B
Ribonucleoproteins
45
Most auto immune diseases is associated wit h
rhematoid arthritis
46
A increased risk of what with sjorgens and swollen partied gland, and unilateral growth the partied gland
B cell lymphoma is what they are looking for.
47
Scleroderma
autoimmune both diffuse and localized | Tough skin from excess amounts of collagen in the skin
48
Scleroderma diffuse type is what
exhibits skin and early visceral involvement | Esophogus is commonly affected causing disorder motility (dysphagia for solids and liquids)
49
Scleroderma diffuse is Characterized by
Anti DNA topoisomerase 1 (Scl-70 antibody)
50
Localized scleroderma is CREST syndrome which is
``` Calcinosis and Anti Centromere antibodies Raynaud phenomenon Esophageal dysmptility Sclerodactyly (hands) Telangiectasia's of skin ```
51
Mixed connective tissue disease
Tissue damage with features of SLE, 100% have antibodies against U1 ribonucleoprotein
52
common damage with mixed features
of SLE, systemic sclerosis and polymyotsitis
53
Wound healing
regeneration and repair, replace tissue with collagen and fibrosis
54
3 types of tissues based of regenerative capacity
labile tissues Small and large bowel,(stem cells in mucosal crypts) skin (stem cells basal cells) bone marrow (hematopoietic stem cells)
55
where are the stem cells of the bowel
crypts
56
where are the stem cells for bone marrow
hematopoietic stem cells CD34+
57
what is the stem cell of the lung
type 2 phnemocytes
58
Stable tissues is the 2nd tissue
quiscent (sit out side of cell cycle and can reenter) Liver example will produce additional cells and then reenters quiescence also kidney
59
the third is permeant tissues
lacks regenerative abilities cardiac and skeletal muscle and neurons. REPAIR not REGENERATION
60
if the stem cell layer are damaged what will happen instead of regeneration fro a cut
Repair will accrue not regeneration
61
repair cycle
Granulation tissue will become a scar fibroblasts capillaries myofibroblasts
62
granuloma,
epithelhoid histiocyte | formed by by IL 12 from macrophage hits the the CD4 t cell turns it into the t herper cell
63
name collagen 1 through 4 and what they are used for
1. used in bone 2. used in collagen 3. used in blood vesssels 4. basement membrane
64
What is the cofactor for collegase in wound repair (scar)
Zinc!!!!!!!
65
What is the mechanism of regeneration and repair
paracrine signalling via growth factors by macrophages
66
TGF-alpaha
epithelial and fibroblast growth factors
67
TGF-Beta
important fibroblast growth factor inhibits inflammation also works with IL 10
68
PDGF-
endothelium smooth muscle fibroblast growth factor
69
FGF, very important
angiogenesis( helps to grow blood vessels) , skeletal development
70
VEGF
angiogenesis
71
Cutaneous healing can occur by two mechanisms
Primary wound edges brought together for minimal scar formation secondary- wound edges remain open and granulation tissue fills in the defects. causes contraction of the the area. (myofibroblasts)
72
delayed wound healing
infection is the most common cause with continued inflammation which delay healing. WE need VIT C!!!
73
What are important assisting substances in healing
VIT C-( used to hydroxolate or add a OH to proline or Lysine on collagen) for strengthening collagen Copper- (lysyl oxidase) used to crosslink collagen making it stronger Zinc- used to convert type 3 to type 1 collagen for collagenase.
74
Other causes of delayed wound healing
ischemia, foreign body, dehiscence, diabetes colitis, hypertrophic scar, malnutrition.j
75
hypertrophic scar
excess deposition of type 1 collagen
76
Keloid is what
Excess production of scar, excess type 3, genetic predisposition on african americans, classically seen on the ear lobe

Ch 2 pathoma (3 decks)

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