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Board path > Golj Patho: Cell injury and inflammation > Flashcards

Golj Patho: Cell injury and inflammation Flashcards

1
Q

Myeloperoxidase deficiency
NBT dye test:
Respiratory burst present:
FA 208

A

NBT dye test is positive - blue color because Respiratory burst is present.
Lack MPO which: Cl- + peroxide into bleach.
usually asymptomatic but more prone to candida infections.

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2
Q

Chronic granulomatous disease
what enzyme is defective?
this renders child susceptible to what type of bacteria?
fa 215

A

X-linked R
Lack NADPH oxidase which is responsible for respiratory burst using Oxygen.
Boy is susceptible to catalase + bacteria (staph, aspergillus), but can use the peroxide created in catalase - bacteria (strep) to kill it.

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3
Q

Umbilical cord does not fall off.
defect in what surface protein?
what cell uses this?
FA 227

A

beta integrin defect / CD18 integrin

Neutrophils use it for tight binding to umbilical cord endothelium

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4
Q

Why is angioedema a complication of ACE inhibitor?

FA 386, 555

A

ACE normally degrades bradykinin, a kinin that increases vessel permeability and hence swelling of tissues. (also increases pain, vasodilation)
ACE inhibitors also cause cough.

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5
Q

Actinic keratosis
cause
what type of cell change
FA 443

A

UV-b light damage of skin

causes predisposition of skin cells to squamous cell carcinoma; type of dysplasia

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6
Q

H. Pylori
causes what type of cell change in the stomach?
FA 360

A

glandular metaplasia, precursor for adenocarcinoma of the stomach
stomach should not have glands
Virchow gland is found (left supraclavicular node)

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7
Q

Mechanism of methotrexate use in psoriasis

FA 63

A

methotrexate blocks dihydrofolate reductase, prevents dTMP from being created for DNA synthesis
this blocks S phase

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8
Q

Budd-Chiari syndrome
cause and effect?
FA 370

A

thrombosis or compression of hepatic veins causing necrosis in liver -> congestive liver disease
will see caput medusa (varices), nutmeg liver

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9
Q

nutmeg liver

FA 370

A

may be seen in congestive liver disease; also seen in right heart failure; caused by thrombosis in hepatic vein, which backs the flow of blood.
will see varices as well

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10
Q

cherry-red appearance of skin, decreased SaO2 (oxygen saturation), and headache
FA 257, 605

A

classic presentation of CO poisoning
Co binds to hb therefore not all RBC’s bound to O2; decreased SaO2
cherry-red because Hb is tightly bound to something

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11
Q

what do you ask a patient who was in a fire?

A

do you have headache or confusion?

early signs of CO poisoning, important to ask

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12
Q

membrane blebbing is an example of what cellular damage

A

it is reversible cellular injury caused by hydropic / cell swelling, which was due to hypoxia which impairs oxidative phosphorylation

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13
Q

cardiac troponin in pt is elevated. what has occurred morphologically to their heart myocytes?
FA 224

A

lack of ATP results in sodium build up and hydropic damage (swelling)
plasma membrane damage results in leaking of enzymes and additional calcium will enter cell.
myocytes release CK-MB and troponin
FA 224

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14
Q

three phases of cell death of loss of nucleus

A

nuclear condensation (pyknosis)
fragmentation (karyorrhexis)
dissoluation (karyolysis)

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15
Q

ischemic infarction of brain leads to what necrosis pattern

A

liquefactive necrosis

microglia contain proteolytic enzymes and due to brain’s increased fat content

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16
Q

granulomatous infection in TB resembles what type of necrosis
FA 223

A

caseous necrosis

FA 223

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17
Q

female undergoes trauma to breast in car accident
what type of necrosis ensues and what is the mechanism
FA 223

A

fat necrosis, nonenzymatic in this case.
deposition of calcium allows fatty acid released from trauma to undergo saponification
this would be dystrophic calcification
FA 223

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18
Q

30 y/o pregnant female with preeclampsia
will damage placenta via what necrosis
FA 581 233

A

fibrinoid necrosis of the umbilical cord vessel wall
caused by high blood pressure in mother (preeclampsia)
FA 581, 223

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19
Q

necrotic damage to blood vessel wall; immune reactions in vessels
immune complexes with fibrin
FA 233

A

fibrinoid necrosis
examples are palpable purpura, necrotizing vasculitis
FAA 223

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20
Q

endometrial shedding during menstrual cycle is an example of what cellular process

A

apoptosis

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21
Q

cellular injury, DNA damage, or decreased hormonal stimulation will lead to the inactivation of what factor?
FA path section

A

Bcl-2, which is anti-apoptotic. removal of it will release cytochrome C from mitochondria

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22
Q

CD14 location and what does it bind to

A

Macrophage surface receptor that recognizes lipopolysaccharide (LPS) on the surface of gram negative bacteria

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23
Q

effects of LTC4, LTD4, and LTE4

A 
slow reacting substances of anaphylaxis
1 vasoconstriction
2 bronchoconstriction / spasm
3 increased vascular permeability 
all are smooth muscle contraction
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24
Q

this leukocyte is involved in type I hypersensitivity
releases its granules via IgE crosslinking
can be activated via C3a and C5a

A

mast cells

poma p11

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25
Q

what is the second phase of the mast cell response?
i.e. how is the acute inflammatory response continued (delayed response)
poma 12

A

Leukotrienes
maintain the acute inflammatory response
poma p12

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26
Q

role of C3b

A

opsonization

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27
Q

this inactive proinflammatory protein - once exposed to subendothelial or tissue collage - activates coagulation and kinin system

A

Hageman factor or F XII

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28
Q

what mediates redness and warmth (rubor and calor)

what three important molecules

A

Histamine, prostaglandins, and bradykinin mediate vasodilation which increases blood flow
NOT leukotrienes - these mediate vasoconstriction

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29
Q

where does exudate leak from and what mediates its leakage

poma 12

A

swelling (tumor) is leakage of exudate (protein and liquid) from postcapillary venules
mediated by histamine - which causes endothelial cell contraction - and tissue damage

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30
Q

what mediates pain (dolor) and how

A

bradykinin and PGE2 mediate pain by sensitizing sensory nerve endings

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31
Q

what mediates fever?
two are things released from a certain leukocyte
poma 13

A

TNF and IL-1 are released from MQ in contact with pyrogens (for example, LPS from bacteria) and cause the perivascular cells of hypothalamus COX enzymes to increase activity -> this leads to PGE2 production
PGEEEE - FEEEVER
poma 13

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32
Q

How does aspirin lower fever

poma 13

A

inhibits cyclooxygenase so that PGE2 cannot be formed in the hypothalamus which would otherwise increase the body’s temperature set point

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33
Q

P-selectin is released from what specific intracellular structure upon stimulation by histamine?

A

Weibel=Palode bodies

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34
Q

what induces E selectin formation on endothelial cells

A

TNF and IL-1

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35
Q

where is CD11/18 integrin (beta integrin) located and what upregulates its expression
what are the two integrins called
FA 227

A

located on neutrophils, stimulated by C5a and LTB4 (which also happen to be neutrophil chemotactic factors)
The two integrins are LFA-1 and Mac-1
FA 227

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36
Q

leukocyte adhesion deficiency is due to defect of

FA 215

A

the CD18 subunit on LFA-1 integrin

FA 215

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37
Q

pt lacks pus formation

FA 215

A

leukocyte adhesion deficiency
CD18 subunit
FA 215

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38
Q

pt presents with recurrent pyogenic infections, partial albinism.
what is the mechanism of this disease
FA 215

A

Chédiak-Higashi syndrome is defect in lyososomal trafficking regulator gene (LYST)
can’t fuse phagosome-lyososomes, therefore bacteria that are phagocytosed
pyogenic infections are by staphylococci and streptococci
FA 215

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39
Q

Chediak-Higashi syndrome

FA 215, poma 13

A

LYST lysosomal trafficking regulator gene is defective
sx include light albinism, pyogenic infections by staphyloocci and streptococci, peripheral neuropathy
giant granules are seen in granulocytes, there is pancytopenia, mild coagulation defects.
fa 215, poma 13

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40
Q

Role of superoxide dismutase

FA 208

A

convert superoxide O2- to H2O2

FA 208

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41
Q

myeloperoxidase role

FA 208

A

H2O2 converted into bleach HOCl

FA 208

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42
Q

oxidative / respiratory burst

A

O2 - > O2- superoxide via NADPH oxidase

Neutrophils and monocytes only

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43
Q

Nitroblue tetrazolium test in:
chronic granulomatous disease
MPO deficiency

A

negative (in CGD, do not have NADPH oxidase and therefore no respiratory burst)
positive (have NADPH oxidase)

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44
Q

name bacteria that pts with Chronic granulomatous disease are susceptible to
FA 215

A

susceptible to catalase positive bacteria such as:
staph aureus
Pseudomonas cepacia (very important, because all students already know staph aureus)
Aspergillus
Need PLACESS
FA 215

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45
Q

pt with higher risk of candida infections
what enzyme is lacking
FA 208, poma 14

A 
MPO
myeloperoxidase deficiency 
usually asymptomatic
NBT dye test is positive - have resp burst
FA 208, poma 14
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46
Q

how do macrophages call in more neutrophils to an inflammatory site

A

produce IL-8

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47
Q

how is chronic inflammation initiated

what main cell types mediate this type of inflammation

A

MQ’s ingest the viral microbe, present MHC-II on their surface to activate T helper cells

macrophages and fibroblasts
FA 225, poma 14

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48
Q

chronic inflammation is characterized by what

FA 225, poma 14

A

persistant destruction and repair via fibroblasts and mq’s;
call in lymphocytes and plasma cells into tissue
associated with blood vessel proliferation, fibrosis.
FA 225, poma 14

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49
Q

describe what signals CD4+ T cell activation

FA 203, poma 15

A

B7 on DC binds to CD28
TCR along with CD3 binds to antigen presented on MHCII
FA 203, poma 15

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50
Q

describe what signals B cell activation

FA 203

A

Thelper cell binds to MHCII on B cell
CD40L on Thelper cell binds to CD40 on B cell
Th cell then releases cytokines that determine Ig class switching of that B cell
FA 203

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51
Q

Th1 cell secretion
what stimulates Th1 creation
FA 202

A

IFN-gamma - which activates MQ’s and CD8+ T cells
activated by IFN-gamma and IL-12
FA 202

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52
Q

Th2 cell secretion

what stimulates Th1 creation

A

secretes IL-4 (IgE), IL-5 (eosinphilic cell chemotaxis and activation) and IL-10
IL-4 activates Th2 cells
inhibited by IFN- gamma
FA 202

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53
Q

in what ways to CD8+ cells mediate killing?

FA202

A

perforins and granzyme B
perforins create holes for granzymeB to enter and activate caspases
Expression of FasL, which binds to Fas on target cells activating apoptosis
FA 202, poma 15

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54
Q

what is the key characteristic of a granuloma?

FA 225

A

epitheloid histiocytes / epitheloid macrophages
(macrophage with abundant pink cytoplasm)
FA 225

55
Q

what are noncaseating granulomas

poma 15

A

granulomas that lack central necrosis
remember that caseous necrosis has necrosis in the middle of a granuloma
poma 15

56
Q

what are caseating granulomas

A

granulomas with central necrosis

characteristic of TB, fungal infections

57
Q

histologic hallmark of Crohn’s disease

hallmark of ulcerative colitis
FA 362

A

noncaseating granulomas is Crohn’s (Th1 mediated)

crypt abscesses with ulcers is ulcerative colitis (neutrophils, remember abscesses are neutrophils)
FA 362

58
Q

key differentials for caseating granulomas are

FA 223

A

TB, fungal infections, mycobacterium

FA 223

59
Q

list steps involved in granuloma formation

FA 230, poma 16

A

MQ’s process and present antigen via MHC class II to CD4+ T cells
MQs secrete IL-12 which makes Th1 subtype
Th1 cells secrete IFN-gamma which converts MQ’s to epitheloid histiocytes and giant cells
TNF alpha from mq’s induces and maintains granuloma formation
FA 230, poma 16

60
Q

22q11 microdeletion
third and fourth pharyngeal pouches fail to form
what are symptoms

A

T cell deficiency due to lack of thymus, hypocalcemia (lack of parathyroids), abnormalities of heart, great vessels, face (velocardial syndrome)
DiGeorge Syndrome
FA 214

61
Q

MCC of severe combined immunodeficiency

what’s the other cause

A

defective IL-2R gamma chain (X linked, therefore seen in boys often)
and adenosine daminase deficiency (autosomal recessive)
FA 215, poma 16

62
Q

what enzyme deaminates adenosine and deoxyadenosine for secretion because they would otherwise be toxic to cell?
FA 215, poma 16

A

adenosine deaminase deficiency
in ADA deficiency, these two products accumulate and is toxic to lymphocytes which are making DNA and dividing often
FA 215, poma 16

63
Q

ADA deficiency causes

A

severe combined immunodeficiency syndrome
(SCIDS)
build up of adenosine and deoxyadenosine

64
Q

symptoms of SCIDS

A

failure to thrive, infections by fungal, viral, baceterial, protozoal infections
FA 215, poma 16

65
Q

lack of B cell maturation and defect of BTK (a tyrosine kinase gene) is characteristic of

A

X-linked (Bruton’s) agammaglobulinemia
recurrent bacterial and enteroviral / giardial (no IgA in intestinal mucosa) infections after 6 months when mother’s IgG antibodies are gone
poma 16, FA214

66
Q

findings of Bruton’s agammaglobulinemia

FA 214

A
  • absent B cells in peripheral blood
  • decreased Ig of all classes
    absent lymph nodes and tonsils
    FA 214
67
Q

pt’s serum ab’s are low in IgA, and NL IgG, IgM levels
pt has anaphylaxis to IgA contain products
what dz
FA 214

A

selective IgA deficiency
most common immunodeficency, cause is unknown
FA 214

68
Q

what is the defect in common variable immunodeficiency

A

defect in B cell differentiation, many causes

decreased plasma cells and immunoglobulins

69
Q

pt’s with IgA selective deficiency have increased risk of what types of diseases

anaphylaxis to what?

A

autoimmune; celiac disease; GI infections

anaphylaxis to IgA-containing products

70
Q

X-linked recessive disease that causes increased IgM in serum. Dz?

what is the genetic defect
FA 215, poma 17

A

hyper-IgM syndrome
Defective CD40L on Th cells -> therefore, B cells cannot class switch out of IgM.
FA 215, poma 17

71
Q

serum findings include increased IgM, low IgG, IgA, IgE
how do these patients typically present?
FA 215, poma 17

A

severe pyogenic infections early in life
opportunistic infection with Pneumocystis, Cryptosporidium, CMV
poor opsonization
FA 215, poma 17

72
Q

presentation of Wiskott-Aldrich syndrome

FA 215, poma 17

A 
Thrombocytopenic purpura
Eczema
Recurrent Infections 
W-A-T-E-R
FA 215, poma 17
73
Q

boy child has mutation in WAS gene, rendering T cells unable to reorganize actin cytoskeleton
dz
FA 215

A

Wilskott-Aldrich
X-linked recessive
FA215

74
Q

Neisseria infection susceptibility

A

C5-C9 deficiency

FA 206

75
Q 
pt presents with angioedema (periorbital), and mucosal surfaces 
hereditary angioedema
what dz
what drug is contraindicated
FA 206, poma 17
A

C1 esterase inhibitor deficiency
ACE inhibitors are contraindicated
FA 206, poma 17

76
Q

AIRE mutation results in

poma 17

A

autoimmune polyendocrine syndrome
AIRE is part of negative selection of T cells and allows medullary dendritic cell to present self antigen; if it cannot, T cell can get through and cause autoimmune destruction
poma 17

77
Q

pt presents with triad of
hypoparathyroidism, adrenal insufficiency (addisons), and candida infections due to autoimmunity
what is defective and what is the dz
FA 324, poma 17

A

defective AIRE protein in medulla of thymus
autoimmune polyendocrine syndrome
FA 324, poma 17

78
Q

self reactive T cell binds to self cell and there is no costimulation
what occurs

A

anergy - that T cell is shut off
can also undergo apoptosis by having its FAS (CD95) receptor bound to FasL by the self cell it is trying to bind to
FA 209, poma 17

79
Q

CD25 polymorphism.
what cell type does it effect?
what is it associated with?
FA 202, poma 17

A 
effects Tregs (CD25 is IL-2R)
associated with autoimmune disorders such as MS, Type I DM
FA 202, poma 17
80
Q

Pt presents with an X-linked syndrome that is immune dysregulation.
have diarrhea, damage to thyroid and pancreas
hint.
FA202, poma 17

A

IPEX
mutation of FOXP3 rendering Tregs defected
polyendocrinopathy (thyroid gland and pancreas damage, could lead to DM), enteropathy (hence the diarrhea)
FA202, poma 17

81
Q

women are more commonly affected by autoimmune disorders; why?
poma 17

A

estrogen reduces apoptosis of self-reactive B cells

poma 17

82
Q

what specific trigger events are required for autoimmunity to actually take place

A

genetic predisposition so that self reactive lymphocytes are present
then environmental trigger either by bystander activation or molecular mimicry ( that is, an antigen activates the leukocyte)

83
Q

what ages does bruton’s agammaglobulinemia usually present?
what gene is defective
FA 215

A

bruton’s tyrosine kinase BTK defective in b cells
presents after 6 months after mother’s antibodies have gone away; pt will get recurrent bacterial and enteroviral infections

84
Q

histological findings of amyloidosis

FA 231

A

congo red

apple green birefringence under polarized light

85
Q

define labile tissue.

FA 72, poma

A

tissue contain stem cells that constantly reproliferate and grow back. eg. bone, lung, skin

86
Q

what type of tissue is liver?
Labile, stable, or permanent?
FA 72

A

Stable; hepatocytes will regenerate if damaged

87
Q

what are the labile stem cells of small and large bowel located?
FA 72, poma 21

A

mucosal crypts

88
Q

where are stem cells of skin located?

FA 72, poma 21

A

located in the basal layer

89
Q

The bone marrow stem cells are called …
what is their cell surface marker?
poma 21

A

hematopoeitic stem cells, surface marker is CD 34

90
Q

what are the stem cells of the lung?

FA 600, poma 21

A

Type II pneumocytes

91
Q

How does permanent tissue repair it is damaged if it can regenerate cells?
poma 21, FA 229

A

repairs via fibrous scar;

for example, post MI myocardial tissue will form fibrous scar

92
Q

deep cuts heal with fibrous scar. why?

poma 21

A

because a deep cut through the dermal layer will cut through the basal cells

93
Q

what three main things consist granulation tissue? what is each one’s role?
poma 21, FA 229

A

fibroblasts (deposit type III collagen)
Capillaries (nutrient flow)
myofibroblasts (contract the wound)

94
Q

a scar is what type of collagen? what was replaced and how was it replaced?
poma 21

A

Type I collagen which has higher strength.
Type III collage was initially part of the granulation tissue and is removed via collagenase, which requires Zn as cofactor

95
Q

cofactor required for collagenase?

poma 21, FA 229

A

Zinc

96
Q

role of TGF-beta in wound healing?

poma 21, FA 229

A

decrease inflammation, and it is a fibroblast growth factor

97
Q

Role of PDGF in wound healing? secreted by?

poma 21, FA 229

A

secreted by platelets and macrophages.

helps in vascular remodeling and stimulates endothelium, smooth muscle, and fibroblasts for collagen formation

98
Q

Role of FGF

poma 21, FA 229

A

Angiogenesis

99
Q

role of VEGF?

poma 21, FA 229

A

Angiogenesis

100
Q

Pt has scar that is healed by secondary intention. 6 months later, the wound has gotten a lot smaller. what is the mechanism?
FA 229, poma 21

A

myofibroblasts contraction of wound

101
Q

what can cause delayed wound healing?

A

vitamin C deficiency, infection, diabetes, foreign body

102
Q

what specific step in wound healing / collagen synthesis is delayed by a deficiency of vitamin C?
FA 76, poma 22

A

hydroxylation of pro/lys residues on collagen alpha helix

103
Q

what step does copper deficiency delay wound healing ?

poma 22, FA 76

A

lysyl oxidase which covalently crosslinks lysein-hydroxylysine on collagen fibers

104
Q

pt presents with delayed healing of wound.
they are deficient in Zn. what is the mechanism by which wound healing is delayed
poma 21

A

Type III collagen is not being replaced by type I collagen due to inactivity of collagenase which requires zn as cofactor

105
Q

The rupture of a wound - that is commonly seen post abdominal surgery - is called

A

dehiscence

106
Q

Pt has scar that appears raised but is confined in boundaries. what type of collagen and what is it called?
FA 229, poma 21

A

Hypertrophic scar; too much type I collagen

107
Q

following resection on the face of an african american patient, the wound becomes out of proportion of scar’s boundaries.
what type of collagen?
FA 229, poma 21

A

Keloid scar - Type III collagen is deposited too much by fibroblasts

108
Q

Defect in platelet plug formation due to decreased GpIIb/IIIa?
FA 397

A

Glanzmann thrombasthenia

lack of platelet to platelet plugging

109
Q

anemia of chronic disease is due to release of what from the liver?
what is the mechanism of this anemia?
FA 393

A

chronic inflammation increases hepcidin release from liver.
hepcidin binds ferroportin in macrophages and intestinal mucosal cells.
RBC’s now lack iron.

110
Q

Erythrocyte sedimentation rate of patient with chronic inflammation is elevated.
What is the mechanism?
FA 230

A

products of inflammation (e.g. fibrinogen) coat RBCs and cause aggregation.
Denser RBC’s therefore fall at faster rate in pipette.

111
Q

what enzymes are contained with azurophilic granules of neutrophil? (also called lysosomes)
FA 382

A

proteinases, acid phosphatase, myeloperoxidase (gives blue-green color), beta glucuronidase

112
Q

what enzymes are contained within specific granules of neutrophils?
FA 382

A

ALP (alkaline phosphatase), collagenase, lysozyme, and lactoferrin.

113
Q

role of IL-10; what cells does it inhibit?
what is the mechanism?
FA 207

A 
inhibits activated macrophages and dendritic cells.
decreases expression of MHC class II and Th1 cytokines
114
Q

what HLA subtype predisposes a patient to ankylosing spondylitis ?
FA 201, 637

A

HLA-B27

115
Q

why does a deficiency of early complement proteins increase the risk of systemic lupus erythematous?
FA 433, poma 18

A

because they help in the removal / opsonization of apoptotic bodies.
if they are not present, the antibody-antigen complexes will not be removed from blood and deposit into tissue causing damage.

116
Q

Malar “bufferfly” rash is seen over pt’s cheek bones after sunlight exposure.
dz?
FA 433, poma 18

A

SLE

117
Q

pt presents with orthopnea, and heart failure cells are seen in lungs.
what cells were these originally and what is the mechanism?
FA 297

A

dust cells (MQ’s of the lungs) engulfed RBC’s during pulmonary edema, and they are now hemosiderin-laden macrophages, which gives them an organ-brown appearance.

118
Q

pt findings include hypercoagulability, endothelial damage, and blood stasis.
what is the association?
FA 637, 608

A

Virchow triad, increased risk of thrombosis.

will commonly present with DVT

119
Q

what is the main mechanism of damage in systemic lupus erthematous?
what type of hypersensitivity reaction is this?
fa 433, poma 18

A

antigen-antibody complexes deposit and damage multiple tissues.
this is Type III HSY.

120
Q

what is the cardiac manifestation of lupus?

FA 636, FA 433, poma 18

A

nonbacterial thrombotic endocarditis.

this is when there are nonbacterial, wart-like vegetations on both sides of valve.

121
Q

pt presents with raynaud phenomenon, malar bufferfly rash, and is developing diffuse proliferative glomerulonephritis.
what lab test would confirm the diagnosis?
FA 433, poma 18

A

anti-dsDNA antibodies and anti-smith antibodies.

antinuclear antibodies are sensitive but not specific to SLE; they can be found in other autoimmune diseases.

122
Q

what is the most common cause of death in patients with SLE?
is this true for drug induced SLE?
FA 433, FA 636,

A

lupus nephropathy. nephritic and nephrotic syndromes.

drug induce SLE typically does not result in renal or CNS involvement. poma 19

123
Q

mother is found to have anti-SSA antibodies.
what is the hypersensitivity type of her disease?
what will her child have increased risk of developing?
poma 19, FA 430

A

Sjogren syndrome
Type IV hypersensitivity because antibodies are against own tissues.
child will have increased risk of developing neonatal lupus which includes congenital heart block.

124
Q

pt develops enlarged parotid gland and dry eyes.
what other autoimmune disorder can be expected in this patient?
what type of antibodies will be found?

A

Sjogren syndrome: pt may also have rheumatoid arthritis or SLE.
anti-SSA / anti-SSB (it spells out sjogren syndrome)
FA 430, poma 19

125
Q

pt presents with dry eyes and dry mouth.

what would you see on biopsy and what would you see that would be diagnostic for sjrogen syndrome?

A

lymphocytic sialadenitis on lip biopsy would be diagnostic for sjrogen syndrome.
would see lymphocytic infiltrations in the histo section.
poma 19, poma 20, FA 430

126
Q

what autoantibody is seen in mixed connective tissue disease?

A

anti-U1 RNP (ribonucleoprotein)

poma 20, FA 213

127
Q

anti-U1 RNP is specific for what disease?

A

mixed connective tissue disease

poma 20, FA 213

128
Q

What type of HSR is the Arthus reaction?
What are its characteristics?
Give an example.

A

local, subacute antibody mediated hypersensitivity reaction.
Type III.
Characterized by edema, necrosis, and activation of complement.
Antigen-antibody complexes in the skin.
(FA 211)

Arthus reaction (e.g. swelling and inflammation following tetanus vaccine) (FA 212)

129
Q

What is the mechanism of serum sickness?

what type of HSR?

A

immune complex disease in which antibodies to foreign proteins are produced (5 days)
Complexes deposited in membranes, where they fix complement (leads to tissue damage)
FA 211

Type III

130
Q

48 hours after PPD test, pt notices indurated, raised, erythematous area.
What lymphocyte is responsible?
What type of HSR?

A

Type IV
Delayed T-cell-mediated type - sensitized T cells encounter antigen and then release cytokines (leads to MQ activation; no antibody involved)

FA 211

131
Q

How long does acute transplant rejection take to occur?

What is the pathogenesis (what type of cells)

A

FA 217

weeks to months, CD8+

132
Q

Pt receives second blood transfusion and undergoes anaphylactic shock.
Disease?
What other problems would these patients present with?

A

IgA deficiency, Selective IgA deficiency

GI infections, autoimmune diseases, anaphylaxis to IgA containing products (Blood transfusion)

FA 624, 214

133
Q

24 y/o with increasing malaise; skin facial lesion over cheeks. PE shows mild pitting edema. On auscultation, friction rub is audible over chest.
Lab findings show pancytopenia and serum creatinine of 3 mg/dL.
Urinalysis shows hematuria and proteinuria.
Serologic test for syphilis yields false-positive result.
Renal biopsy shows granular deposits of IgG and complement in the mesangium and along basement membrane.
Mechansim of disease?

will likely develop what life-threatening disease?

A

Defective clearance of apoptotic nuclei (UV light damage)

renal failure / lupus nephropathy

FA 433, SLE

134
Q

24 y/o with increasing malaise; skin facial lesion over cheeks. PE shows mild pitting edema. On auscultation, friction rub is audible over chest.
Lab findings show pancytopenia and serum creatinine of 3 mg/dL.
Urinalysis shows hematuria and proteinuria.
Serologic test for syphilis yields false-positive result.
PT and PTT are elevated.
What is this patient at risk for?
What autiantibodies are likely to be found in serum?

A

Antiphospholipid syndrome
Anticardiolipin antibodies and lupus anticoagulant

risk of thrombosis

FA 433

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