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Winter 2016 > B&L Unit 4 > Flashcards

B&L Unit 4 Flashcards

1
Q

What are tophi?

A

The deposits of crystalline uric acid and other things in joints, skin, or muscle

Usually part of gout

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2
Q

What are the 4 stages of gouty arthritis?

A

Asymptomatic hyperuricemia
Acute gouty arthritis
Intercritical gout - asymptomatic intervals between acute attacks of gout
Chronic tophaceous gout - deposits of uric acid crystals

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3
Q

What are the 2 ‘big picture’ causes of gout?

A

Underexcretion - 90% of gout patients

Overproduction

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4
Q

What enzyme do humans lack that increases risk of gout?

A

Uricase

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5
Q

Uric acid is a product of _______ metabolism?

A

Purines

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6
Q

Pseudogout is acute episodic arthritis due to _________

A

CPPD (calcium pyrophosphate dihydrate) crystals

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7
Q

In rheumatoid arthritis, what is th emajor cellular component of synovial fluid?

A

Neutrophils

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8
Q

What are 3 pro-inflammatory cytokines we care about?

A

IL-1
IL-6
TNF-a

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9
Q

What are rheumatoid factors?

A

Immunoglobulins that recognize epitopes in the Fc portion of IgG

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10
Q

Which finger joint is often spared in rheumatoid arthritis?

A

DIP

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11
Q

What is the term for when a joint hurts but there is no evidence of inflammation?

A

Arthralgia

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12
Q

What are the 3 types of joints?

A

Synarthrosis - bones come together and interlock (skull)

Amphiarthrosis - bones are joined by fibrocartilage (ribs)

Diarthrosis - bone articulation is cushioned by hyaline cartilage, stabilized by ligaments, moved by muscles and tendons, nourished and lubricate by synovial tissues

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13
Q

What type of collagen are ligaments made out of?

A

Type 1

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14
Q

What are entheses?

A

Where ligaments and tendons insert into bone

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15
Q

What is axial arthropathy?

A

Arthritis involving the spine

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16
Q

What is ankylosis?

A

Joint fixation

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17
Q

What is spondylitis?

A

Inflammation of vertebrae

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18
Q

What is an osteophyte?

A

A bony outgrowth

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19
Q

What is a syndesmophyte?

A

Calcification of a ligament or tendon at the site of bony insertion

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20
Q

What type of collagen is hyaline cartilage made out of?

A

Type II

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21
Q

What are the 2 types of cells in synovium?

A

Type A - macrophage-like

Type B - fibroblast-like

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22
Q

What 3 cells are increased in pannus? What happens to the synovium?

A

Increases in type A, type B, and immune cells

The synovium becomes inflamed and thickened

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23
Q

What is synovium?

A

The thin layer of cells and capsule that covers all intra-articular surfaces other than the cartilage

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24
Q

What are 2 disease categories red joints can indicate?

A

Infection

Crystal disease

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25
Q

What are the synovial WBC levels for inflammatory arthritis?

A

> 2000

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26
Q

What are the 2 nodes on the fingers in osteoarthritis?

A

Heberden’s

Bouchard’s

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27
Q

What joints are not affected by rheumatoid arthritis? (3)

A

DIP

Thoracic and lumbar spine

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28
Q

What’s the deal with pseudogout?

A

Inflammatory synovial fluid with Ca2+ pyrophosphate crystals

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29
Q

What is the NK cell’s special killing mechanism?

A

ADCC - antibody-dependent cell-mediated cytotoxicity

NK cells have receptors for the Fc ends of IgG.
When IgG is bound to a cell, the NK cell can deliver apoptosis signals to the cell

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30
Q

What type of cells are NK cells?

A

Large granular lymphocytes

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31
Q

How does the BiTE drug work?

A

Bi-specific T-cell Engager

2 single-chain antibodies are coupled back-to-back. One against an tumor antigen and another against a T cell receptor.

This somehow gets the immune system to specifically act against the tumor cells

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32
Q

What does Azathioprine do?

What is a related drug?

A

It decreases DNA synthesis and mRNA transcription

It is used in organ transplantation

Mycophenolate mofetil. It has less toxicity

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33
Q

What does cyclosporine do?

A

Decreases IL-2 production.

This downregulates macrophages as APCs and lessens stimulation of T cells

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34
Q

Which 2 drugs for organ transplant rejection bind FKBP-12?

A

Tacrolimus - used in synergy with cyclosporine-A

Sirolimus/rapamycin

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35
Q

What are the 2 mechanisms of anemia in SLE?

A

Anemia of chronic inflammation

Autoimmune hemolytic anemia - IgG and complement to RBCs -> destruction by spleen and liver

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36
Q

What happens with SLE patients produce phospholipid antibodies?

A

Blocks prothrombin activation in the clotting cascade

Leads to increased clotting

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37
Q

What is correlated with SLE morbidity?

A

Kidney damage

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38
Q

What 5 things characterize axial arthropathies?

A 
Axial arthritis
Peripheral arthritis
Enthesitis
Mucocutaneous lesions
Association with HLA-B27
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39
Q

Are males or females affected more in ankylosing spondylitis?

A

Males

7:3

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40
Q

Are males or females affected more in reactive arthritis?

A

Males

5-10:1

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41
Q

What precedes reactive arthritis?

A

Infectious diarrhea or urethritis 2-4 weeks before onset of arthritis

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42
Q

What is the affected joint pattern of reactive arthritis?

A

Asymmetric
Oligoarticular
Usually knees and ankles
Sometimes spine

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43
Q

What sort of tendon inflammation often occurs with reactive arthritis?

A

Dactylitis - diffusely swollen toes (sausage digit)

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44
Q

What genetic finding is most common in ankylosing spondylitis

A

HLA-B27

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45
Q

What is the environmental trigger most suspect for anklyosing spondylitis?

A

Bowel bacteria

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46
Q

4 possible theories of how HLA-B27 can predispose a person to develop ankylosing spondylitis (and reactive arthritis)

A

Arthritogenic peptide hypothesis

Molecular mimicry

Free heavy chain hypothesis - HLA heavy chains can form stable homodimers on a cell surface and trigger NK activation through recognition via killer cell immunoglobulin-like receptors

Unfolded protein hypothesis - HLA can misfold -> unfoldein protein stress response

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47
Q

What are the first 2 drugs types used for spondyloarthropathies?

A

NSAIDs

Indole derivatives

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48
Q

What is the difference between heberden’s and bouchard’s nodes?

A

Heberden’s are distal - DIP

Bouchards are proximal - PIP

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49
Q

What is the fancy word for bunion?

A

Hallux valgus

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50
Q

What is the fancy word for bow-leggedness

A

Genu varus

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51
Q

What is the most common arthropathy?

A

Osteoarthritis

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52
Q

What does IL-1 do to cartilage?

A

Stimulates chondrocytes to make matrix metalloproteases -> matrix degradation

Also stimulates other inflammatory activities like prostaglandin, NO, and IL-6 production

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53
Q

What does TNF-alpha do to acrtilage?

A

Stimulates chondrocytes to make matrix metalloproteases -> matrix degradation

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54
Q

What are the 2 (unusual) elevated things in rheumatoid arthritis?

A

Rheumatoid factor in 85%

Anti-cyclic citrullinated peptide in 70%

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55
Q

What is the WBC for synovial fluid analysis in rheumatoid arthritis

A

> 2000/uL with predominantly neutrophils

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56
Q

Where are rheumatoid nodules located?

A

Extensor surfaces and tendon sheaths

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57
Q

What genotype is most common in rheumatoid arthritis?

A

HLA-DR4 is present in 50% of cases

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58
Q

In the early stage of rheumatoid arthritis, synovial fluid contains predominantly ________ cells

A

Mononuclear

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59
Q

What are the 3 hypothesized causes of rheumatoid arthritis

A
  1. Antibodies to some arthritogenic peptide
  2. T cell selection
  3. The class II peptide is an antigen itself
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60
Q

TNF-A, IL-1, and IL-17 can induce osteocyte lineage cells to express ________, which results in _________

A

RANKL (receptor activator of nuclear factor kB ligand)

Interacts with RANK receptor on osteoclast precursors -> activation -> osteoclastic resorption of bone

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61
Q

What competitively binds RANKL and modulates its activity?

A

Osteoprotegerin

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62
Q

What are the 4 stages of gout?

A

Asympromatic hyperuricemia - elevated serum uric acid levels
Acute gouty arthritis
Intercritical gout - asymptomatic intervals between acute attacks of gout
Chronic tophaceous gout

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63
Q

What do gout crystals look like compared to CPPD crystals?

A

Needle-shaped and negatively birefringent (yellow)

Rhomboid-shaped and positively birefringent (blue)

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64
Q

What channel is important for uric acid reabsorption?

A

URAT1

So, inhibiting URAT1 will increase excetion of uric acid

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65
Q

Humans lack the enzyme ___________, which oxidizes uric acid to ___________

A

Uricase

Allantoin

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66
Q

Overproduction of uric acid can be due to superactivity of ___________or deficiencies of ___________

A

PRPP synthetase

HGPRT

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67
Q

In gout, initial recognition of MSU crystals by ___________ is critical to the inflammatory response

A

Toll-like receptors

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68
Q

3 drugs that can ameliorate an acute gouty attack

A

NSAIDS - anti inflammatory
Colchicine - prevents PMN movement
Corticosteroids - anti inflammatory

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69
Q

Where does pyrophosphate (PPi) come from in CPDD?

A

Metabolism of nucleoside triphosphates, particularly from articular chondrocytes

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70
Q

Can CPDD be cured?

A

No. There is no way to remove CPDD crystald form the joints or to retard further progression

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71
Q

What is used to treat acute pseudogout?

A

Anti-inflammatory drugs

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72
Q

Most of the parts of the coagulation cascade are synthesized by the ___________

A

Liver

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73
Q

Most of the enzymes in the coagulation cascade are ___________

A

Serine proteases

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74
Q

Inactive precursor proteins that are activated through cleavage into active enzymes are ___________

A

Zymogens

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75
Q

7 zymogens in the clotting cascade that become active serine proteases

A

Prekallikrein
Prothrombin (factor II)

Factors 12,11,10,9,7
(XII,XI,IX,X,VII)

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76
Q

Vitamin ___________ is important in clotting

A

K

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77
Q

What does factor XIII do (it is not a serine protease)

A

A transglutaminase that covalently links fibrin molecules together to form a stable clot

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78
Q

What are the 2 things von Willebrand protein does?

A

It is the carrier protein for factor VIII in the plasma

It adheres platelets to exposed collagen (binds to GIb)

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79
Q

Coagulation can be initiated with vascular disruption that leads to exposure of plasma to ___________

A

Tissue factor

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80
Q

Tissue factor binds factor ___________ in the presence of ___________

A

VIIa

Calcium

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81
Q

The 2 clotting pathways meet at factor ___________

A

X (marks the spot)

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82
Q

What are the 3 granules of the platelets?

A

Dense granules - ATP, ADP, serotonin, calcium

Alpha granules - procoagulant proteins, growth factors, factors for platelet activation

Lysosomal granules - acid hydrolases

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83
Q

What attaches to exposed subendothelium and triggers the clotting cascade?

A

von Willebrand factor

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84
Q

What is the most common congenital bleeding disorder?

A

von Willebrand disease

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85
Q

What is Bernard-Soulier syndrome?

A

Expression of GP1b on platelet surface is reduced, leading to defect in platelet adhesion

Autosomal recessive

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86
Q

What si gray platelet syndrome?

A

Deficiency of alpha-granules in platelets

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87
Q

What is Glanzmann thrombasthenia?

A

An autosomal recessive disorder caused by absent/defective GPIIb-IIIa

Platelets can adhere but not aggregate

Signs are petechiae and easy bruising

88
Q

What is the normal platelet range?

A

150,000-400,000/uL

89
Q

What are the 3 treatments for immune thrombocytopenic purpura? (3)

A

Corticosteroids - reduces B cell clone-making autoantibody

IVIg - blocks splenic Fc receptors so they don’t bind to antibody-coated platelets

Splenectomy - so the spleen doesn’t get rid of platelets

90
Q

What is antithrombin? What are the 2 most important things it targets?

A

A serpin that targets lors of things in the clotting cascade (most importantly thrombin and factor Xa)

91
Q

Heparin is a cofactors for _____________

A

Antithrombin

Accelerates rate of protease inactivation

92
Q

What does heparin cofactor II inhibit?

93
Q

What is the cofactor for activated protein C (APC)?

94
Q

What is Factor V Leiden?

A

An abnormal factor V in the clotting cascade

Makes it resistant to APC, so factor Va remains activated longer than normal

Pro-thrombotic

95
Q

Tissue factor pathway inhibitor is expressed by ____________ and inhibits the ___________ part of the coagulation pathway

A

Endothelial cells

Entrinsic

96
Q

The key enzyme in fibrinolysis is ___________

97
Q

What primarily activates plasmin? (2) What enzyme type are they? What makes them?

A

Tissue plasminogen activator
Serine protease
Made by endothelial cells

urokinase plasminogen activator
Serine protease
Made by endothelial cells and kidney cells

98
Q

What does thrombin-activatable fibrinolysis inhibitor do?

A

Is made by binding to the thrombin-thrombomodulin complex

Removes basic amno acids from C-terminal, which decreases plasminogen-binding sites on fibrin

99
Q

What is the primary inhibitor of plasminogen activation?

A

Plasminogen activator inhibitor-1 (PAI-1)
A serpin

It inhibits tissue plasminogen activator

100
Q

What is the primary plasmin inhibitor in blood?

A

alpha2-antiplasmin
A serpin
Inhibits plasmin that is freely circulating

101
Q

What 4 things do endothelial cells express that inhibit thrombosis?

A

Heparan sultfate - cofactor for antithrombin
Ddermatan sulfate - cofactor for heparin cofactor II
Thrombomodulin - cofactor w/ thrombin for activating protein C
TFPI - inhibits extrinsic Xase complex

102
Q

What 3 things do endothelial cells express to prevent platelets from activating?

A

Prostacyclin, nitric oxide - prevent platelet adhesion

Enzyme that metabolizes ADP to AMP and adenosine (a platelet inhibitor)

103
Q

Do RBCs have MHCs? Do platelets?

104
Q

Blood group antigens are ___________

Blood group substances are ___________

A

Glycolipids

Glycoproteins

105
Q

What % of people are blood group substance secretors? What does this mean?

A

80

The glycoproteins are also found in body fluids

106
Q

Whta are isohemagluttinins?

A

Antibodies against A or B antigens in blood

107
Q

What is the most important Rh locus?

A

d/D

The other is c/C and e/E
Rh antigens are on proteins coded for at these loci

108
Q

What is the genotype for Rh phenotypes?

A

Rh+ is DD or Dd

Rh- is dd

109
Q

What on platelets binds von Willebrand Factor?

110
Q

What does ADP do during platelet degranulation?

A

Promotes exposure of GPIIb/IIIa receptor, which is essential for platelet aggregation

111
Q

What on platelets allows aggregation?

A

GPIIb/IIIa

112
Q

Which Ig is implicated in immune thrombocytic purpura?

113
Q

Why does IVIg work for immune thrombocytic purpura?

A

Because splenic macrophages eat it instead of antibody bound to RBCs

114
Q

What happens to RBCs in microangiopathic hemolytic anemia?

A

Schistocytes

Because microthrombi cause shearing

This results in hemolysis

115
Q

What are the 2 underlying causes of microangiopathic heolytic anemia?

A

Thrombotic thrombocytic purpura

Hemolytic uremic syndrome

116
Q

What cuases thrombotic thrombocytic purpura?

A

Decreased ADAMSTS13 enzyme

Can’t degrade von Willebrand multimers

Extra platelet adhesion

117
Q

What causes hemolytic uremic syndrome?

A

Endothelial damage by drugs or infection

Platelets adhere!

118
Q

What is the factor for hemophiliaa A,B, and C?

A

A - factor 8
B - factor 9
C - factor 11

119
Q

aPTT measures the activity of the entire clotting pathway except _______________

A

Factor 7 (VII)

120
Q

Both PT and PTT start with _______________-treated plasma

121
Q

Why do we use the Protime/International Normalized Ratio for clotting time?

A

Thromboplastin varies by manufacturer, so we normalize by adjusting for known potency

122
Q

What does thrombin time detect deficiencies in?

A

Low or abnormal fibrinogen, fibrin split products, heparin

123
Q

What is the cause of death in hemophilia?

A

CNS bleeds

124
Q

What is the abnormal screening test in hemophilia?

A

PTT (vs. PT in factor VII deficiency)

125
Q

What is the abnormal screening test in factor VII deficiency?

A

PT (vs. PTT in hemophilia – VIII and IX deficiencies)

126
Q

How bad is hemophilia C (factor 11 deficiency)

A

Mostly post-operative bleeding, often delayed, especially on sites like prostate, uterus, bladder

Spontaneous bleeding is rare

127
Q

What are the genetics for hemophilia C?

A

Autosomal recessive

Common in Ashkenazi Jews and certain Middle Eastern populaitons

128
Q

What 2 drugs reduce vitamin K/reduce its utiilzation?

A

Warfarin (Coumadin)

Rat poison

129
Q

What is the lupus anticoagulant?

A

IgG against phospholipid

130
Q

What is the bleeding lab finding for lupus anticoagulant presence?

A

Prolonged PTT, since it binds the phospholipid that is added to the test tube to start the reaction

Is a pro-thrombic state though

We can check by seeing if adding normal plasma corrects the problem (it does not in this case)

131
Q

Whan PTT>PT, which disease should we think os?

132
Q

Signs and symptoms of vasculitis

A

Skin lesions
Constitutional symptoms - fever, weight loss, anorexia, weakness, fatigue
Musculoskeletal symptoms - arthralgias, arthritis, myalgias, peripheral neuropathy

133
Q

Laboratory features of vasculitis reflect ____________________

A

Systemic inflammation

Anemia of inflammatory disease
Thrombocytosis
Low albumin
Elevated sedimentation rate and C-reactive protein
Polyclonal gammopathy
Possibly elevated liver enzyme tests
Low complement levels
Cryoglobulins
134
Q

What 2 things characterize polymyositis and dermatomyositis?

A

Chronic muscle weakness

Infiltration of muscle tissue by chronic inflammatory cells

135
Q

Which muscles in dermatomuositis/polymyositis are affected first?

A

Proximal extremeties

can’t comb hair
Also difficulty standing, rising from chairs, climbing stairs

136
Q

What are 3 myositis-specific antibodies in polymyositis/dermatomyositis

A

Anti-synthetase: aminoacyl-tRNA synthetases that help translation

Anti-Mi-2: nuclear helicase. Associated with a good prognosis

Anti-signal recognition particle: translocaiton of newly synthesized proteins into ER

137
Q

What antibody do we use to detect B cells with flow?

138
Q

What do we use single radial immunodiffusion for?

A

Levels of individual immunoglobulin classes

139
Q

What is the best overall test for Th1 activity?

A

A skin test with combos of antigens most people will have positive reactions to

(like the tuberculosis skin test)

140
Q

What can be done to promote visualization of immune complexes in the lab?

A

Chill it for 1-7 days

Immune complexes in serum are often insoluble in cold and precipitate out

141
Q

How is imunohistochemistry different from immunofluorescence?

A

Immunohistochemistry uses a final antibody labelled with an enzyme (vs. fluorophore) like peroxidase that turns the tissue black/brown

Immunohistochemistry lasts longer

142
Q

Direct immunofluorescence is a test for _____________

Indirect immunofluorescence is a test for _____________

A

Antigen

Antibody

143
Q

What is a sandwich/capture ELISA?

A

Use it to find an antigen that is at least divalent
One antibody is on the plate
The other has a fluorophore
The antigen is trapped in the middle

144
Q

What are the 3 parts of the Virchow triad?

A

Decreased blood flow
Altered vessels (inflammation, mechanical injury, hypoxia)
Altered coagulability

145
Q

Arterial thrombi occur under conditions of _____________

A

High shear stress

146
Q

What is the typical composition of arterial thrombi?

A

Aggregated platelets with only small amounts of fibrin and red cells

White thrombi

147
Q

What is the typical composition of venous thrombi?

A

Large amounts of fibrin with lots of RBCs

Red thrombi

148
Q

How are D-dimers formed in thrombosis?

What does testing their levels tell us?

A

When cross-linked fibrin is degraded by plasmin

An indirect measure of amt of clotting. A negative D-dimer result means thrombosis probably isn’t happening

149
Q

How do you detect pulmonary embolisms?

A

Inhale and inject radionucleotides
CT scan
Look for areas of mismatch (areas that ventilate well but are not perfused)

150
Q

What 2 things are given for arterial thrombi in an acute setting?

A

Heparin - prevents further clotting

Fibrinolytic agent like tPA - lyse existing clot

151
Q

What is a nontransforming retrovirus?

A

It is a virus that carries no oncogene

152
Q

What does lentivirus mean?

A

Cause slow, ultimately fatal illnesses

HIV is one

153
Q

What genetic difference do HIV-positive long-term surfvivors have?

Elite controllers?

A

CCR5 mutation, which is an HIV receptor

HLA-B57 - become infected but don’t get AIDS. They make effective CTL to HIV peptides presented on this MHC

154
Q

How does the HIV virus get to the Th cells?

A

It adheres to the dendritic cells in a way that it is not harmed

Then it is taken to the lymph node

155
Q

What is the most common test for HIV?

A

ELISA for antibody to HIV

AND

Western Blot

156
Q

What do the 2 antiretriviral drugs do?

A

Nucleosides - competitive inhibitors and chain-terminators

Non-nucleoside - bind hydrophobic pocket that alters catalytic site

157
Q

What does Maraviroc do as an antiretroviral?

A

CCR5 antagonist - blocks entry of virus intoTh cells

158
Q

What does Raltegravir do as an antiretrovirsl

A

Integrase inhibitor

159
Q

Which antiretroviral is a CCR5 antagonist?

Which one is an integrase inhibitor?

A

Maraviroc

Raltegravir

160
Q

What are 3 pieces of evidence for cance immune surveillance taking place?

A
  1. People with immunodeficiencies have higher rates of tumors
  2. There are lots of activated T cells that recognize tumor-associated antigens
  3. Some tumors spontaneously regress (probs due to an immunologic response)
161
Q

What are tumor antigens?

A

Antigens expressed by tumor cells that are not readily found on the corresponding normal cell

162
Q

How does CTL and NK activity correlate with MHC class I expresion?

A

Binding of MHC class 1 suppresses NK cells but gets CTLs to do there thing. The opposite is also true

163
Q

How do the time courses of ESR and CRP vary?

A

C-reactive protein is upregulated much faster (hours) than erythrocyte sedimentation rate

164
Q

What is the term for calcium deposition in cartilage?

A

Chondrocalcinosis

165
Q

Serine proteases cleave targets at _____________ residues

166
Q

Vitamin K is required for clotting proteins that have a _____________ domain

167
Q

Extrensic tenase complex is made of _____________, _____________, and _____________

A

Tissue factor
Factor 7
Ca2+

Activates factor 10

168
Q

Intrinsic tenase is made of _____________ and _____________

A

Factor 11a
Factor 8a

Activates factor 10

169
Q

Prothrombinase is _____________, and ____________

A 
Factor 10a
Factor 5a (a cofactor)

It catalyzes the conversion of prothrombin to thrombin

170
Q

von Willebrand factor hangs out in ____________s of endothelial cells

A

Weibel-Palade bodies

171
Q

What are the 4 vitamin-K dependent factors?

A

9
7
2 (thrombin)
10

They all go into ten!

172
Q

What 2 proteins (not factors) are vitamin K-dependent

A

Protein C

Protein S

173
Q

Protein C is activated by ____________ and ____________

Protein C inactivates ____________ and ____________

A

Thrombind and thrombomodulintogether

Factor 5a, factor 8a

174
Q

Thrombin activates what 5 things?

What inactivates it?

A

13, 11, 8, 5, 2

Antithrombin III

175
Q

TAFI is activated by ____________ and ____________

A

Thrombin and thrombomodulin (make a complex)

176
Q

TAFI is a ____________, PAI ____________, alpha2-antiplasmin ____________

(enzyme type)

A

Exopeptidase
Serpin
Serpin

177
Q

Platelets adhere to the damaged vessel wall directly via ____________ or indirectly via ____________

A

Collagen

von WIllebrand factor

178
Q

What platelet levels see spontaneous hemorrhage and increased hemorrhage with trauma or surgery?

What platelet levels can see life-threatening spontaneous hemorrhage?

179
Q

What is pseudothrombocytopenia?

A

When people look like they have low platelet counts because they clump and the automated counter doesn’t see them

Make sure you look at the smear to identify if present

180
Q

What are the 3 subtypes of von Willebrand disease?

A
  1. partial quantitative
  2. Qualitative - decreased or increased adhesion to platelets
  3. Almost no vWF

1 is most common, 3 is least

181
Q

What drug is given to treat con Willebrand disease?

A

DDAVP - arginine vasopressin

182
Q

What drug is given for acute DVT/PE?

What is used to prevent additional clots?

A

Heparin

Warfarin

183
Q

What are the 5 known hypercoagulable states (like deficiencies)

A 
Factor 5 Leiden
Prothrombin mutation
Antithrombin III deficiency
Protein S deficiency
Protein C deficiency
184
Q

The prothrombin gene mutation and antithrombin III deficiency are associated with ____________ thrombosis

185
Q

Whatat are the 6 things antithrombin III inhibits?

A

2+7 =9

And 10,11,12

186
Q

What are the 3 types of heparin we give as drugs?

A

Unfractionated - many lengths
Low molecular weight heparin
Fondaprinux - the minimal sequence in heparin for binding antithrombin

187
Q

By which route is heparin administered?

A

IV or subcutaneously

188
Q

What is the main difference in heparin forms in bioavailability and half life?

A

Smaller heparins have longer half lives (and are thus more prediactable) and better bioavailability

189
Q

What is the main difference in heparin forms in their binding?

A

Only heparin containing atleast 18 saccharide units can bind to the antithrombin/thrombin complex. The smaller heparins just bind antithrombin

190
Q

What compound can neutralize heparin?

A

Protamine sulfate

191
Q

What is heparin-induced thrombocytopenia syndrome?

A

The platelet count decreases (by like 50%) 5-10 days after heparin

Caused by the development of antibodies to platelet factor 4/heparin complexes that activates them

192
Q

What does streptokinase do?

A

Complexes and activates plasminogen to make more plasmin

Which makes it a fibrinolytic agent

193
Q

What are the 3 classes of anti-platelet drugs?

A

Aspirin - inhibit formation of platelet products

Prevent activation/aggregation - ADP receptor antagonists

GIIb/IIIa inhibitors - block adhesion proteins

194
Q

What is the difference in lymphocyte behavior between polymyositis and dermatomyositis?

A

Lymphocyte infiltrate directly into the fasicles

Perifascilar lymphocyte infilatration (a bland vasculopathy)

195
Q

What is the difference in lymphocyte type between polymyositis and dermatomyositis?

196
Q

What skin findings are present in dermatomyositis? (6)

A

Gottron’s sign -“an erythematous, scaly eruption occurring in symmetric fashion over the MCP and interphalangeal joints”

Heliotrope rash

Shawl or V sign/Erythroderma/holster sign

Mechanic’s hands

Periungual telangiectasias and erythema

Calcinosis cutis (usually in juvenile dermatomyositis)

197
Q

Polymyositis and dermatomyositis often have anti-________

A

Synthetase

One example is anti-Jo-1

198
Q

What are the EMG findings of dermatomyositis/polymyositis

A

Increased activity when the needle is stuck in
Spontaneous fibrillations
Decreased amplitude of motor unit action potentials

199
Q

________ is overexpressed in myocytes in polymyositis

A

MHC class I

An unfolded protein response made by the ER may be important

200
Q

Categorize the vasculitises

A

Large vessel: Takayasu’s arteritis, termporal arteritis

Medium vessel: Vuerger’s disease, cutaneous vasculitis, Kawasaki disease, polyarteritis nodosa

Small vessel: Chur-Strauss, microscopic polyangiitis, ganulomatous with polyangiitis, cryoglobulinemia

201
Q

What defines ‘large vessels’?

A

Their connective tissues have their own blood supplies

202
Q

What is ANCA?

A

Anti-neutrophil cytoplasmic antibodies

203
Q

What are the 2 types of ANCA?

A

p-ANCA (perinuclear) - myeloperoxidase - microscopic polyanggitis (sorta)

c-ANCA (cytoplasmic) - PR3 - granulomatous polyangiitis

204
Q

What is the main difference between giant cell arteritis and Takayasu’s arteritis?

A

Takayasu’s generally affects young people from Asia and doesn’t affect the temporal artery

Giant cell arteritis mostly affects people of northern european background

205
Q

Is palpable purpura blanchable?

206
Q

Which vasculitis is due to smoking?

A

Thromboangiitis obliterans

Buerger disease

207
Q

Which disease involves heberden’s and bouchard’s nodes?

A

Osteoarthritis

Heberden’s - DIP
Bouchard’s - PIP

208
Q

Which joint does rheumatoid arthritis spare?

209
Q

Which autoantibodies are extremely specific for rheumatoid arthritis?

A

RF AND anti-CCP

Though only like 30% of RA patients have them both

210
Q

Are neutrophils in the synovium in RA?

A

No, just in the synovial fluid

211
Q

What mutation can cause CPPD crystal arthropathy?

A

ANKH gene -> excess intracellular PPi egress from chondrocytes

212
Q

Enthesitis characterizes which arthropathy?

A

Seronegative spondyloarthropathies (like ankylosing spondylitis)

213
Q

What is upregulated in the synovium in seronegative spondyloarthropathies?

214
Q

What joints are affected in reactive arthritis?

A

Lower extremity

215
Q

What genes are lupus associated with?

A

HLA-DR3

C4A null allele

216
Q

Anti-synthetase syndrome is associated with PM/DM and what other disease?

A

Interstitial lung disease

217
Q

What 2 receptors that, when bound, can downregulat CTLs?

A

CTLA-4

PD-1

Winter 2016 (8 decks)

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