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Ch 2 pathoma > .2 > Flashcards

.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
Q

wiskott aldrich syndrom is caused by a mutation in the

A

wiskot aldrich syndrome X LINKED!!!

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26
Q

compliment deficiency

A

C5-‘C9 deficiency can cause a risk for Neisseria infection

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27
Q

if there is a deficiency of C1 inhibitor can cause

A

over activation of c1 causing over activation of complement

causes include vasodilation increased vascular permeability. Periorbital edema

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28
Q

Hereditary angio edema is and example of

A

compliment deficiency with a periorbital edema caused by over activation of complement because of a c1 inhibitor deficiency

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29
Q

autoimmune desease, we constantly creating lymphocytes buy they are

A

usually apoptotic, or become anergic (go to sleep) generally effect woman more than men at child bearing age.

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30
Q

Etiology of autoimmune disorders

A

Environmental trigger in a genetically susceptible individuals, increased incidence in twins and associated with certain HLA subtypes

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31
Q

first autoimmune disease

A

SLE

32
Q

SLE Systeic autoimmune disease involves

A

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
Q

Long list of lupus

A 
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
Q

Lupus common cause of death is from

A

Renal damage - diffuse proliferative glomeruloephritis

INFECTION

35
Q

lupus is Characterized by a ANA

A

Anti nutruphil body and a anti DS DNA

36
Q

Lupus can also be drug induced by what drugs

A

ANTI HISTONE ANTIBODY Hydralazine procainamide and isoniazid

removal of drug will get rid of disease

37
Q

Antiphosphlipid syndrome also accounted with lupus

A

antibody against phosophlipds specifically
anticardiolipin, (false postive syphilis test)
lupus anticoagulant, interfering a ppt (false elevation)

38
Q

Antiphospholipid syndrome in lupus actually causes

A

arterial and venous thrombosis

Deep venous thrombosis and hepatic vein thrombosis, placental thrombosis and stroke

39
Q

what is required life long when diagnosed with antiphsopholipid syndrome.

A

Anticoagulation medication

40
Q

Bud keori syndrome is caused by and most commonly found with

A

Deep venous thrombosis

polly cithemia verra

41
Q

Sjorgren syndrome

A

lacrimal and salivary glands are filled with fibrosis due type 4 hypersensitivity

42
Q

common symptoms,

A

dirt in eye and multiple carries

43
Q

Sjorgren syndrome is characterized by

A

Antiribonucleoprotein antibodies

antibody has the SS-A SS-B

44
Q

What is the target of SS-A and SS-B

A

Ribonucleoproteins

45
Q

Most auto immune diseases is associated wit h

A

rhematoid arthritis

46
Q

A increased risk of what with sjorgens and swollen partied gland, and unilateral growth the partied gland

A

B cell lymphoma is what they are looking for.

47
Q

Scleroderma

A

autoimmune both diffuse and localized

Tough skin from excess amounts of collagen in the skin

48
Q

Scleroderma diffuse type is what

A

exhibits skin and early visceral involvement

Esophogus is commonly affected causing disorder motility (dysphagia for solids and liquids)

49
Q

Scleroderma diffuse is Characterized by

A

Anti DNA topoisomerase 1 (Scl-70 antibody)

50
Q

Localized scleroderma is CREST syndrome which is

A 
Calcinosis and Anti Centromere antibodies
Raynaud phenomenon
Esophageal dysmptility
Sclerodactyly (hands)
Telangiectasia's of skin
51
Q

Mixed connective tissue disease

A

Tissue damage with features of SLE, 100% have antibodies against U1 ribonucleoprotein

52
Q

common damage with mixed features

A

of SLE, systemic sclerosis and polymyotsitis

53
Q

Wound healing

A

regeneration and repair, replace tissue with collagen and fibrosis

54
Q

3 types of tissues based of regenerative capacity

A

labile tissues
Small and large bowel,(stem cells in mucosal crypts)
skin (stem cells basal cells)
bone marrow (hematopoietic stem cells)

55
Q

where are the stem cells of the bowel

A

crypts

56
Q

where are the stem cells for bone marrow

A

hematopoietic stem cells CD34+

57
Q

what is the stem cell of the lung

A

type 2 phnemocytes

58
Q

Stable tissues is the 2nd tissue

A

quiscent (sit out side of cell cycle and can reenter) Liver example will produce additional cells and then reenters quiescence also kidney

59
Q

the third is permeant tissues

A

lacks regenerative abilities
cardiac and skeletal muscle and neurons.
REPAIR not REGENERATION

60
Q

if the stem cell layer are damaged what will happen instead of regeneration fro a cut

A

Repair will accrue not regeneration

61
Q

repair cycle

A

Granulation tissue will become a scar
fibroblasts
capillaries
myofibroblasts

62
Q

granuloma,

A

epithelhoid histiocyte

formed by by IL 12 from macrophage hits the the CD4 t cell turns it into the t herper cell

63
Q

name collagen 1 through 4 and what they are used for

A
  1. used in bone
  2. used in collagen
  3. used in blood vesssels
  4. basement membrane
64
Q

What is the cofactor for collegase in wound repair (scar)

A

Zinc!!!!!!!

65
Q

What is the mechanism of regeneration and repair

A

paracrine signalling via growth factors by macrophages

66
Q

TGF-alpaha

A

epithelial and fibroblast growth factors

67
Q

TGF-Beta

A

important fibroblast growth factor inhibits inflammation also works with IL 10

68
Q

PDGF-

A

endothelium smooth muscle fibroblast growth factor

69
Q

FGF, very important

A

angiogenesis( helps to grow blood vessels) , skeletal development

70
Q

VEGF

A

angiogenesis

71
Q

Cutaneous healing can occur by two mechanisms

A

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
Q

delayed wound healing

A

infection is the most common cause with continued inflammation which delay healing.
WE need VIT C!!!

73
Q

What are important assisting substances in healing

A

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
Q

Other causes of delayed wound healing

A

ischemia, foreign body, dehiscence, diabetes colitis, hypertrophic scar, malnutrition.j

75
Q

hypertrophic scar

A

excess deposition of type 1 collagen

76
Q

Keloid is what

A

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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