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Blood and Lymph > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Osteoarthritis

A

degeneration of articular cartilage with hypertrophy of bone, joint space loss, subchondral cysts, sclerosis and osteophytes

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2
Q

what joints are involved in OA?

A

DIPs, PIPs, 1st CMC, weight bearing - hips and knees, Spine - cerivical and lumbar, 1st MTP

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3
Q

Heberden’s

A

DIPs

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4
Q

Bouchard’s

A

PIPs

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5
Q

Predisposing factors to OA

A

Age, obesity, occupational risks, trauma, or secondary OA due to inflammatory disorders like RA, spondylo, or metabolic disorders

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6
Q

sports and OA

A

no increased risk, exercise may be protective

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7
Q

Cartilage components

A

avascular and no nerves 1) collage II 2) proteoglycans 3) matrix proteins 4) chondrocyes 5) 70% water

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8
Q

Proteoglycans

A

in cartilage - chondroitin and keratin sulfate linked to hyaluronic acid - hydrophilic

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9
Q

Matrix proteins in cartilage

A

Metalloproteinases - like collagenases, gelatinases, stromeylsins and Tissue inhibitors of metalloproteinases TIMPS

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10
Q

Chondrocytes

A

main cell of cartilage that produces the proteins in cartilage

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11
Q

aggrecans

A

chondroitin and keratin sulfates bound to collagen. Forms a weave that acts like a sponge to hold onto water

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12
Q

changes to cartilage in OA

A

increase chondrocytes, increase MMPs, decrease TIMP, proteglycans, Increase water. This is due to a mechanical injury, inflammation, metabolic hit of cartilage. Looses the weave and forms a dish rag instead of a sponge.

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13
Q

Does OA have systemic feaures?

A

NO - lacks them

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14
Q

Synovial fluid in OA

A

non-inflammaotry, type I fluid with 200-2000 WMC

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15
Q

Pathophysiology of OA

A

chondrocytes and synovium produce inflammatory mediators for cartilage destruction - IL1, NO, protsaglandins; they also activate complement and adipokines.

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16
Q

IL-1 release in OA

A

stimulates MMPs, PGE2, NO, IL6 produciton

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17
Q

NO release in OA

A

increases MMPs, inhibits protoglycan, induces chondrocyte apoptosis.

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18
Q

Prostaglands in OA

A

increase production and activation of MMPs

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19
Q

what other cytokines are produces in OA?

A

TNF, IL6, IL17, IL18

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20
Q

Adipokines

A

are our own fact cells that make IL6 that go into the liver to make acute phase reactants like CRP. - metabolic aspect of OA.

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21
Q

Radiological findings in OA

A

Joint space loss, sclerosis, subchondral cysts, osteophytes

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22
Q

Patient will tell about OA

A

localized pain, worse with use. Stiffness for less than 30 minutes.

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23
Q

Rheumatoid Arthritis - basic

A

systemic, inflammatory, autoimmune disorder that results in peripheral, symmetric, *synovitis with cartilage and bone destrcution.

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24
Q

Joint involvement in RA

A

Bilateral and symmetric small joints of hands and feet (sparing DIPs), medium and large too.

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25
Q

X-rays of RA

A

marginal joint erosions and deformities

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26
Q

Etiology of RA

A

arthritogenic peptide in host genetically suseptible due to a HLA-DR4 and HLA-DR1 mutation.

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27
Q

HLA-DR4

A

mutation in 3rd hypervariable region of the MHC II binding cleft that increases the susceptibility and severity of the RA.

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28
Q

RF

A

antibody that detects Fc profession of IgG. usually composed of IgM, but can be IgG and IgA. Not a very sensitive marker of RA (85%). Produced in synovial tissue by plasma cells. RF-IgG immune complexes are pathogenic and form rheumatoid nodules over extensor system and lungs

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29
Q

Anti CCP

A

anti cyclic citrullinated peptide antiboides that react with synthetic peptides contains citrulline.

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30
Q

Cirulline

A

modified arginine residue that is commonly seen in RA patients

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31
Q

Sensitivty vs. Specificity of anti-CCP

A

90% senstivie and 90% specific

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32
Q

RF sensitivity and specificy

A

80% sensitive, 80% specific

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33
Q

RF and anti-CCP sensitivity and specificity

A

rare only 40% sensitive and 100% specific

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34
Q

how often do anti_CCP occur

A

most frequently in those with HLA-DR4 epitope, due to enhanced binding of peptides to cirullination.

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35
Q

Pannus

A

characteristic of RA, containing major T lymphocytes, macrophages, and some fibroblasts, plasma cells, DCs. Located adjacent to bone and cartilage that chews away the erosions at margins of the joint.

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36
Q

Basic one liner of RA

A

disease of synovium

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37
Q

basic one liner for OA

A

disease of cartilage

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38
Q

cell types in synovial fluid of RA

A

PMNs

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39
Q

where are PMNs in RA?

A

in synovial fluid, but NOT synovium tissue.

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40
Q

Synovium tissue in RA contains…

A

contains CD4 lymphocytes and Th17; more often than B-cells and plasma cells; IL2 and IFNgamma are sparse. no PMNs

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41
Q

Role of cells in RA synovium

A

CD4 memory cells modify and amplify local immune response through nation recognition.

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42
Q

Extra-articular manifestations of RA

A

RF-IgG compelx caues induced vasculitis; rhematoid nocules, eye lung, pericardium, peripheral nerves.

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43
Q

Pathophy of RA

A

unknown antigen is consumed by immune system at diagnosis, but altered proteoglycans, collagen, cirulinated peptides propogate the disease (not the antigen)

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44
Q

what patient experiences in RA

A

morning stiffness, fatigue, pain that improves with activity, rest makes worse

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45
Q

Lab values in RA

A

elevated RF, ESR, CRP, anti-CCP antibodies

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46
Q

Imaging of RA

A

loss of joint space, erosion of marginal distribution, soft tissue swelling, osteopenia

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47
Q

Risk factors of RA

A

female, any age, smoking

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48
Q

Gout - definition

A

Tissue deposition of Monosodium urate crystals due to hyeruricemia (MSU supersaturation of extracellular fluid)

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49
Q

Joints in Gout

A

1st MTP (podagra), Cool peripheral joins of lower and upper extremities.

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50
Q

Hyperuricemia

A

over production or under excretion of uric acid. (90% are under excretors)

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51
Q

Uric Acid

A

produce of purine metabolism, but humans lack the Uricase enzyme to oxidize uric acid into allegation form.

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52
Q

X-linked conditions for overproduction or uric acid

A

PRPP synthtase overactivity, and HGPRT deficiency.

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53
Q

Diagnosis of Gout

A

arthrocentesis - needle biopsy with needle shaped crystals, negatively birefringement.

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54
Q

Increased PRPP synthetase

A

incrases production of PRPP-glutamine to cause the pathway to form uric acid

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55
Q

decreased HGPRT

A

inhibits the reaction from going backward to promote more uric acid instead of guanlyic acid or inosinic acid.

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56
Q

Xanthione oxidase

A

inhibited by allopurinol and febuxosat that covers Xanthine into uric acid.

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57
Q

Inflammation induced Gout

A

Endogenous MUS crystals trigger TLR2/4 of inflammatory response. These are on monocytes, macrophages, synovial cells and activate NFkB to pour out inflammaotry cytokiesn and attract PMNs. 2) MSU crystals are internalized to activate NLRP3 inflammation via activation of Caspase 1 to results in IL-1 cleavage and release.

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58
Q

Self limiting nature of Gout

A

Cellular response due to protein coatings: gig coating promotes phagocytosis by PMNs. As time goes on you switch to ApoB coating that inhibits phagocytosis and the immune response.
2) phagocytosis decreases crystal concentrations
3) heat of inflammation, increases solubility
4) ACTH secretion supresses inflammation
5) IL1 and TNF anti antibodies are produced to modulate the inflammation

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59
Q

Calcium Pyrophosphate Dihydrate deposition

A

Abnormal pyrophosphate metabolism (PPi) - metabolism of NTPs from chondrocytes., PPi contacts calcium to form crystals.

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60
Q

PPi generation on chondrocytes

A

NTP pyrophosphohydrolase NTPPPH hydrolyzes phosphodiester1 bond to make NMP and PPI.
2) mutations in ank gene (ANKH) case transmembrane PPi transporter to all egression of excess PPi.

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61
Q

Visualization of Ca Pyrophospahte dehydrate deposition

A

PPi precipitates with Ca to form crystals in midzonal cartilage layers - shedding, strip mining. Rhomboid shape with positive birefringement

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62
Q

Predisposition to Gout

A

Men over 30, shelfish, alcohol

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63
Q

Underexcretion of uric acid

A

activation of URAT1 to decrease excretion

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64
Q

Lesch-Nyhan

A

complete deficiency in HGPRT

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65
Q

Seronegative spondylarthropaties

A

Axial arthritis of spine, sacroilitis, periphery (small and large), characterized by *enthesitis, mucocutaneous lesions, Uveitis

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66
Q

Enthesitis

A

characterisitc of seronegative spondylarthropaties. - inflammation where ligament, tendon, and fibrossseous junction meet bone.

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67
Q

Systemic effects of Ankylosing Spondylitis

A

osteoporosis, uveitis, microscopic colitis

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68
Q

lab values of Ankylosing spondylitis

A

High ESR, negative RF, negative ANA

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69
Q

Genetic predisposition to Spondylarthropaties

A

HLA-B27 - associated with negative RF and ANA (sero negative).

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70
Q

what is in the synovium of Spondylarthropaties

A

increased expression of TNFalpha

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71
Q

HLA-B27

A

Increased prevalence in Caucasians (6-9%), but relative low incidence of sponylarthropaties (0.1-0.2%. Thus there is low chance of having Spondyloarthropaties, and a 20% if you have the mutation and first degree relative. Only accounts for 40% of genetic risk -

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72
Q

Concordance of spondyloarthropties

A

60%

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73
Q

Reative Arthritis

A

due to infectious diarrhea or urethritis. Asymmetric, oligoarticular of the lower extremities, dactylitis, hips spared

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74
Q

Triggers of Reactive arhritis

A

transporttion of bacteria inside by monocytes (chlamydia) via molecular mimicry, arthritogenic peptide, Heavy chain theory, Unfolded protein hypothesis, TH2 response.

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75
Q

systemic effects of Reactive arthritis

A

inflammatory eye, musculocutaneous lesions, aortas, cardiac conduction defects

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76
Q

Arthritogenic peptide hypothesis

A

unique presentation of process peptide by HLA-B27

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77
Q

HLA-B27 heavy chain theory

A

causes NK cell activation

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78
Q

Reiter’s syndrome

A

conjunctivitis, urthritis, arthritis

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79
Q

HLA-B27 ER stress response

A

misfolded HLA-B27 initiates stress response to cuase IL23, IL17 to response to IL-6.

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80
Q

ERAp1

A

helps trim proteins as they feed into the ER

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81
Q

Systmic Lupus Erythromatses

A

chronic, autoimmune disease that affects multiple organs - skin, joints, serial, luns, kidneys, CNS

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82
Q

What causes SLE?

A

disdirectied recognition of self as foreign; requires both the T and B cell lectures; misdirected recognition of self as foreign.Antibody response requires antigen driven CD4 cells.
loss of t and b cells can happen

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83
Q

Pathophysiology of SLE

A

1) auto reactive B and T cells; Nucleic acids stimualte TLR receptors on DC cells to pump out IFN-alpha to represent to auto reactive Tcells. This leads to B cell stimulation and autoantibody creation. 2) NETOSIS - when apoptosis occurs of PMNs, they spew their nucleus out and trap bacterial pathogens. They trap, but the trap is made of DNA —> more autoAb.

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84
Q

Genetics of SLE

A

Increased risk among relatives, 35% concordance rate, associated with HLA_DR3 and C4A null allel (greatest risk)

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85
Q

Popualtions of SLE

A

AA, asians, hispanic americans

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86
Q

Environmental factors of SLE

A

female is 9x more likely, increased risk in childbearing age, sun exposure exacerabates systemic disease

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87
Q

Antinulcear Antiboides

A

hallmark of abnormala b in SLE, >95% of SLE have ANA. Ab directed to multiple nuclear antignes

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88
Q

ANA -dsDNA

A

renal disease

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89
Q

ANA anti-histone

A

SLE and drug induced lupus

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90
Q

Ab to Non-DNA, non Histone

A

SSA, SSB, Smith, RNP

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91
Q

SLE diagnostic criterai

A

4/11: Malar rash, discoid rash, photo sensitivity, oral ulcer, Arthritis, serositis, renal invomvement, CNS - seizures, psychosis, hematologic disease, immunologic disorders, ANA

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92
Q

SLE pathophysiolgy

A

1) Type III specific antibodies mediated to cause HM, neurophenia, thrombopenia, anti phospholipid ab to block prothrombin activation of clotting. Immune complex form with anti-dsDNA and DNA immune complex that can cause the lump and bumpy IF.

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93
Q

Vasculitis - basic definition

A

inflammation of vessel

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94
Q

Pathology of vasculitis

A

varying degress of lymphs, monocytes, histiocytes, eosinophils, PMNs. Granulmonas or giant cells form in some types
large vessels: disruption of elastic lamina + intimal thickening
small vessels: fibroid necrosis (leukocutclastic vasulitis)

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95
Q

large artery vasculitis

A

Takayasus (claudication of upper extremities + CNS), Giant Cell (temporal artery + headache)

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96
Q

Medium Artey vasculitis

A

Classic polyartheritis nodes (skin + joint + peripheral nerves); Kawasaki (acute fever in infants, rash, coronary vasculitis)

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97
Q

small artery vasculitis

A

Wegener’s granulomatosis (ANCA+, respiratory), microscopic pohylangitis (pulmonary hemorrahge + glomerulonephritis), churg-strauss syndrome (asthma+eos)

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98
Q

Arteriole/capillary venule vasculitis

A

Cryoglobinemia (RF ab and Hep C ab), Cutaneous leukoclastic vasculitis (palpablr purpuric lesions + althralgia), Henoch-schonlein purpura (palpable purpra + abdominal pian + IgA)

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99
Q

Major pathophysiology of Vasculitis - one word

A

immune complexes

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100
Q

detailed pathophys of vasculitis

A

inflammation —> platelet activating factors —> increased vascular permeability —> IC deposition; papable purpura.
ANCAS. anti-endothelial ab; T cell mediated endothelial injury,

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101
Q

T cell dependent mediated endothelial cell injury

A

HLA-DR4 in giant cell arthritis, suggests antigen driven vascular inflammation

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102
Q

Source of immune complexes in vasculitis

A

Drugs, bugs, CT disease, malignancy

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103
Q

ANCA

A

antinuetrophil cytoplasmic antibodies in vasculitis; amplifies inflammatory response - not the cause.

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104
Q

c-ANCA

A

cytoplasmic ANCA, acts on proteinase-3 in primary granules of PMNs; associated with GPA

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105
Q

p-ANCA

A

perinuclear, acts on MPO in primary granules of PMNs associated with MPA

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106
Q

treatment of vasculitis

A

remove inciting agent, steroids, plasmapheresis, rituximab

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107
Q

Polymyositis and Dermatomyositis

A

Inflammatory myopathies with muscle weakness, low endurance, idiopathic, but may overlap with CTDs or neoplastic disease. DM has skin rashes - Guttron’s papules, heliotrope rash, V sign, shawl-sign, mechanics hands, periungual changes/erythema

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108
Q

Systemic effects of PM and DM

A

GI dysphagia, pulmonary fibrosis, mycocarditis, Ranaud’s phenomenon, Anti-synthetase

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109
Q

Anti-synthetase syndrome

A

PM or DM presenting with **instertitial lung disease, Fever, arthritis, mechanics hands, raynaud’s phenomenon.

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110
Q

Anti-synthetase antibodies

A

anti-aminoacyl-tRNA synthetase in cyto,, Anti-Jo-1 = anti histadyl-tRNA synthetase; not pathologic of myotoxic

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111
Q

PM - lab finding

A

distribution of inflammatory CD8 cells surrounding and invading muscle fibers

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112
Q

DM

A

Perivascular and perifascicular inflammation of CD4 cells; complement mediated, vasulopathy

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113
Q

pathophysiology of DM/PM

A

CTL directly attacks muscles
Immune complex damage skin
MHC class I overexertion on myocytes —> ER stress response and NFkB production
Viral infections

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114
Q

Etiology of PM and DM

A

Virus! Flu and HIV —> viral particles are detected, but not live virus.; DM microarray of mRNA shows interferon responsive pathways

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115
Q

Juvenile DM

A

increase ab to coxackie B

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116
Q

Seasonal DM

A

Anti-Jo1 ab in the spring

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117
Q

Treatment of DM and PM

A

Corticosteroids, immunosuppressives, PT

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118
Q

Musculocutaneous bleeds are a sign of…

A

primary hemostasis - disorder of platelet of vWF

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119
Q

Soft tissue or joint bleeds are a sign of…

A

secondary hemostasis - coagulation disorder

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120
Q

aPTT

A

tests the procoagulant activity of intrinsic pathway most often F XI, VIII, IX; NOT VII.

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121
Q

PT

A

tests the procoagulant activity of the extrinsic pathway and common pathway - sensitive to II, VII, V, X, Vit K, liver disease

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122
Q

TT

A

tests procoagulant activity of fibrinogen and affect of heparin and fibrin split. Detects heparin contamination and fibrinogen def/dysfunction.

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123
Q

PFA-100

A

standardized bleeding time test; Collage/Epi and Collagen/ADP;
Abnormal Epi and normal ADP = aspirin effect
Both abnormal: platelet function effect.

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124
Q

Ristocetin

A

chemical added to blood to test the activity of vWF binding to GP1b

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125
Q

vWF Disease - mechanism

A

qualitative platelet disorder due mut/under production of vWF —> decreased adhesion and unstable VIII

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126
Q

vWF

A

binds to subendothelial collagen and GP1b receptor on platelets for adhesion! stabilizes Factor VIII

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127
Q

GP1b

A

receptor on platelets that binds to vWF for adhesion

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128
Q

GPIIb/IIIa

A

exposed on surface of platelets with ADP release from dense granules, used as linkage for platelet aggregation

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129
Q

Epidemiology of vWF disease

A

AD, but can be acquired by autoab

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130
Q

Clinical signs of vWF disease

A

mild mucosal and skin bleeding - GI bleed, menorrhagia, NO joint or mucosal bleeds.

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131
Q

Types of vWF

A

Type 1 = partial quantitative deficiency, type 2: qualitative def type 3: near complete absence

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132
Q

Diagnostic lab tests of vWF disease

A

Normal PT, Long PTT, decrased vWF antigen, decreased F VIII, abnormal ristecetin

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133
Q

Treatment of vWF

A

DDAVP desmopressin - arginine vasopressin to enhance release of vWF from endothelial stores, or humane P (vWF and Factor VIII)

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134
Q

Bernard-Soulier Syndrome

A

Qualitative platelet disorder due to GP1b mutation to decrease adhesion; AR; unaffected PT or PTT

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135
Q

Gray Platelet syndrome

A

qualitative platelet disorder due to reduced/absent alpha granules, AR

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136
Q

Afibrogenemia

A

qualitative platelet disorder due to lack of fibrinogen —> no platelet aggregation due to lack of GPIIb/IIIa-fibrinogen binding and no GPIIb/IIIa cross linking; AR; has both mucosal and deep muscle bleeds; prolonged PT and PTT

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137
Q

Ganzman Thrombasthenia

A

qualitataive platelet disorder, defective/low GPIIb/IIIa leads to decreased aggregation; AR, PTT and pT are unaffected.

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138
Q

Abciximab

A

GPIIb-IIIa antagonists

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139
Q

Thrombocyopenia

A

low platelet count due to decreased production, increased destruction, sequestration

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140
Q

Decreased platelet production

A

BM disorders, aplastic anemia, MDS, leukemia, TB, B12/Folate def, viral infection

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141
Q

Increased platelet destruction

A

ITP, autoimmune, DIC, TTP, HUS

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142
Q

Thrombocytopenia - clinical characteristics

A

Mucosal bleeds and skin bleeds - petechiae

143
Q

ITP

A

immune thrombocytopenia purpura - AutoAb to GPIIb/IIIa to cause removal by macrophages in spleen. Can be acute or chronic

144
Q

Acute ITP

A

occurs in children and is proceeded by a virus. Sudden severe onset, but no treatment require. Presents with petichiase and nosebleeds, risk of Intracranial hemorrhage

145
Q

Chronic ITP

A

occurs in adults with concurrent autoimmune, lymphoma, HIV. requires treatment

146
Q

Labs for ITP

A

decreased platelet count, normal PT and PTT, increased megakaryocytes in marrow

147
Q

Treatment of ITP

A

Rituximab, steroids, IVIG, splenectomy, Thrombopoetin receptor agonist

148
Q

Rituximab - ITP treatment

A

depletes b cells form making autoAb

149
Q

Steroids in ITP treatment

A

dampens B-cell clones

150
Q

IVIG in ITP treatment

A

blocks Fc receptors to prevent splenic destruction

151
Q

Thrombopoetin receptor agonists

A

stimulates platelet production in BM

152
Q

what should ITP patients avoid?

A

aspirin and Ibuprofen, contact sports

153
Q

TTP

A

Thrombotic Thrombocytopenic Purpura - increased platelet consumption due to autoab to ADAMTS13

154
Q

ADAMTS13

A

proteast that cleaves vWF into active monomers

155
Q

Mutation in ADAMTS13

A

leaves vWF as inactive multimers that lead to abnormal adhesion and micro thrombi

156
Q

HUS

A

hemolytic uremic syndrome - increase platelet consumption due to bacterial toxin or drug that damages endothelium and leads to increased adhesion and activation —> microthrombi; often seen in childen with E. coli

157
Q

Clinical Signs of TTP and HUS

A

fever, renal insuff (HUS), microanggiopathic hemolytic anemia, Purpura, mental changes

158
Q

Lab values for TTP and HUS

A

low platelets, normal PT and PTT, anemia with schistiocytes, increase megakaryocites in BM, creatinine.

159
Q

Microangiopathic hemolytic anemis

A

microthrombi causes shearing of RBC and destruction leading to hemolytic anemia

160
Q

Treatment of TTP

A

plasmaphoresis and replacement of ADAMTS13

161
Q

Hemophilia A

A

Factor VIII deficiency (intrinsic), X linked or from new mutations.

162
Q

Hemophilia B

A

Factor IX deficiency, X linked or from new mutations

163
Q

Hemophilia clinical signs

A

spontaneous hemorrhage in joints, soft tissue, retroperitoneal space, bleeding after surg/trauma

164
Q

Lab values in hemophilia

A

Long PTT, Mix = abnormal after 2 hours, Normal PT, platelet count, BT

165
Q

HemophiliaC

A

Factor XI def, AR; post op delayed bleeding, but rare spontaneous bleeds

166
Q

Acquired hemophilia

A

Factor VII deficiency (extrinsic), AR, same symptoms as A and B; prolonged PT normal PTT

167
Q

Liver Disease - bleeding

A

Decreased Vit K dependent carboxylation of II, VII, IX, X, decreased fibrinogen, increased fibrinolysis, increased platelet consumption.

168
Q

Liver disease - lab testing

A

Prolonged PT and pTT and TT, decreased fibrinogen, presence of FSP and D dimers, decreased platelet count, defects in protein S and C

169
Q

Vitamin K deficiency

A

cannot make II, VII, IX and X - common in newborns because the lack GI bacteria to synthesize Vit K, or with long term antibiotic use, malabsorption.

170
Q

Vitamin K deficiency lab values

A

Increased PT and PTT (normal to slight increase)

171
Q

DIC

A

simultaneous bleeding and clothing due to systemic activation of coagulation to cause thrombosis but also platelet depletion to cause bleeding.

172
Q

DIC is due to

A

sepsis, trauma, malignancy, obstetric complications, vascular disorders, toxins, immunologic disorders

173
Q

DIC lab values

A

Prolonged PT and PTT and TT, delevated FSP and D dimer, low platelets, low fibrinogen, low factors

174
Q

Treatment of DIC

A

treat underlying disorder, replace platelets and fibrinogen

175
Q

lupus anticoagulant (APLA)

A

IgG ab binds to PL in platelet membranes - causes venous and arterial thrombosis, hepatic vein thrombosis, recurrent miscarriage, headaches

176
Q

Lupus Anticoagulant lab values

A

Prolonged PTT (thrombic disorders), Pt mixing - no correcting at time 0

177
Q

Arterial Thrombosis

A

due to high shear stress and vWF, cause aggregated platelets with small amounts of fibrin and RBCs - white in color

178
Q

Associated conditions of arterial thrombosis

A

Hypertension, atherosclerosis, endothelial injury

179
Q

Venous Thromobsis

A

slow blood flow with low shear stress, clots with large amounts of thrombin - red in color.

180
Q

Associated conditions of venous thrombosis

A

Stasis - right heart failure, tumor with extrinsic vascular compression, obesity, chronic venous insufficiency, surgery, altered coagulability, defect in fibrinolysis, contraceptives, pregnancy.

181
Q

DVT symptoms

A

Swollen, painful, blue leg, (phelegmasia cerulean dozens)

182
Q

Phelegmasia curelean dolens

A

signs of DVT - swollen, painful blue leg

183
Q

Consequences of DVT

A

Postthrombotic syndrome, intermitten obstruction, PE

184
Q

Postthrombotic syndrome

A

chronically swollen, painful extremities that lead to cutaneous ulcers

185
Q

Intermittent obstruction

A

recurrent bouts of pain due to DVT

186
Q

Signs of PE

A

sudden chest pain, dyspnea, anxiety, cough, syncope, cyanosis, hemoptosis

187
Q

Diagnosis of PE

A

Ultrasound, D-dimer assay, spiral CT, Ventilation/Perfusion scan

188
Q

Treatment of DVT

A

heparin to prevent further clots, fibrinolytic to lyse existing clots.

189
Q

Arterial thrombosis tx

A

main goal is anti platelet therapy

190
Q

Venous thrombosis tx

A

main goal is inhibition of coagulation.

191
Q

Inherited thrombotic disorders

A

Prothrombin G20201A, Protein C def, protein S, anithrombin def,

192
Q

Prothrombin G20210A

A

Highest prevalence of inherited thrombotic disorders; AD, cause elevated plasma prothrombin and thrombin levels. long term treatment is not necessary for heterozygotes, asymptomatic is not treated

193
Q

Protein C defiency

A

2ND most common inherited thrombotic disorder, AD, inability to inactivate Factor V and VIII to inhibit coagulation.

194
Q

Complication of protein C deficiency

A

Homozygotes lead to neonatal purport fulminans - fatal
Warfarin induced skin necrosis - increased thrombosis of skin in adults

195
Q

Protein S deficiency

A

similar to above, but due to inability to activate Protein C.

196
Q

Treatment of Protein C and S deficiency

A

NO treatment of asymptomatic, but with 1st Thrombotic event 6-12 months therapy; >1 is long term terapy

197
Q

Anithrombin deficiency

A

AD, antithrombin in unable to activate thrombin (as well as factor X, IX, XI, XII)

198
Q

Tx of Antithrombin Def

A

1st event 3-6 months; Massive = therapy; prophylaxis for pregnant and surgery

199
Q

Hyperhomocytenemia

A

inherited or acquired; enhanced platelet activation and adhesion due to endothelial injury

200
Q

impaired fibrinolysis is due to..

A

plasminogen and tPA deficiency

201
Q

high risk factors for thromosis

A

increased Factor VIII, oral contraceptives

202
Q

Heparin mechanism

A

activates antithrombin II to increase rate of thromin inactivation and accelerated rate of decay for factors IX, X,XII; prevents conversion of fibrinogen to fibrin

203
Q

Subtypes of Heparin

A

Unfractionated, low MW, fondaparinux

204
Q

Unfractionated heparin

A

long version that can bind to antithrombinthrombin complex to inhibit thrombin directly

205
Q

LMWH

A

produced by depolarization of heparin to 1/2 the size

206
Q

Fondaparinus

A

synthetic version of lmwh

207
Q

LMWH vs. Fonaparinus vs. unfractionated

A

LWMH and fona do not bind directly to thrombin, but only antithrombin to inactive factor X

208
Q

Pharmacokinetics of unfractionated heparin

A

IV or SC, short half life of 1-5 hours, acts in the blood rapidly. Must be administered in hospital; does not cross placenta

209
Q

Pharmacokinetics of LMWH and fonaparinus

A

Give SC, better bioavailability than unfractionated and longer half life —> less monitoring. Action in blood and rapid

210
Q

Clinical use of heparin

A

Venous thromosis, PE, angina, Acute MI, cardiopulmonary bypass

211
Q

Adverse effects of heparin use

A

Bleeding, heparin induced thrombocytpenia, osteoporosis, Drug/drug interactions

212
Q

heparin induced thrombocytopenia

A

development of ab to heparin bound platelet factor IV to cause thrombosis and cytosine about 5-10 days after use. Tx with direct thrombin inhibitors like argatroban or lepirudin

213
Q

Warfarin - mechanism

A

a vitamin K analoge that inhibits gamma carboxylation of of II, VII, IX, X and C and S. It also acts on VKORC1 (activator of vitamin K) a vitamin K epoxide reductase that develops polymorphisms.

214
Q

Pharmacokinetics of warfarin

A

oral anticoag with 90 min absoprtion, T1/2 is 36-48 hours; acts in the liver with a very slow onset of action. Duration of action days/chronic. IT CROSSES the placenta

215
Q

Warfarin vs. Heprin

A

Heparin is only for acute cases and administered IV or SC; acts in the blood and with rapid onset of action; short half life. Does not cross placenta
Warfarin is for chronic use and is administered orally, acts in liver with very slow onset and long half life; crosses the placenta.

216
Q

warfarin uses

A

venous thrombosis, systemic embolism, stroke, recurrent infarction

217
Q

Adverse rxns with warfarin use

A

Hemorrhage, skin necrosis, food and drug interactions

218
Q

Hemorrhage due to warfarin

A

tx with vitamin K or plasma transfusion

219
Q

Treatment of hemorrhage with heparin

A

protamine sulfate

220
Q

Drugs that increase action of warfarin

A

Aspirin, antibiotics (decrease vit K synthesis), drugs that displace warfarin from plasma proteins, reduce metabolism

221
Q

Drugs that decrease action of warfarin

A

barbituates and rifampin (increase metabolism), decreased GI absorption

222
Q

advantages of direct thrombin or factor Xa inhibitors

A

rapid onset, absence of food interactions, do not require monitoring

223
Q

disadvantages of direct thrombin or factor Xa inhibitors

A

contraindicated with kidney disease, GI bleeding, short 1/2 life

224
Q

Dabigatran, Etexilate

A

Inhibitor of thrombin that is used for atrial fibrillation and has lower rates of stroke, systemic embolism and intracranial hemorrhage than warfarin.

225
Q

Rivaroxaban

A

inhibitor of Factor Xa that is used for atrial fibrillation, VTE, is better then warfarin at preventing stroke and emboli

226
Q

Fibrinolytic agents - mechanisms

A

converts plasminogen to plasmin to degrade fibrin clots

227
Q

Subtypes of fibrinolytic agents

A

Tissue plasminogen activator (TPA (Alteplase)) and Urokinase (u-PA) (Abbokinase); Streptokinase

228
Q

T-PA

A

serine protease that binds to fibrin to increase cleavage from plasminogen to plasmin; given via bolus injection

229
Q

U-Pa

A

enzyme from renal cells that convert plasminogen to plasmin, but does not bind to fibrin.

230
Q

Streptokinase

A

non enzymatic protein from beta-hemolytic streptococci that forms a complex with plasminogen to convert to plasmin.

231
Q

Use of fibrinolytic agnets

A

Acute MI, stroke, DVT, PE

232
Q

Adverse effects of fibrinolytic agents

A

hemorrhage, systemic lytic state, allergic reaction

233
Q

ADP receptor antagonists

A

binds to ADP receptor P2Y12 to block activation of ADP to inhibit secretion of alpha granules and block GPIIb/IIIa adhesion proteins

234
Q

Theinopyridine vs. Ticagrelor

A

ADP receptor antagonists Theinopyridine binds irreversibly, ticagrelor binds reversibly and has more rapid action

235
Q

Pharmacokinetics of Thienopyridine

A

rapidly absorbed but slow onset of action (5-7 days), prodrugs that require liver metabolism; Ticagrelor requires no metabolism

236
Q

use of ADP receptor antagonists

A

prevent cardiac events and deaths in patients with atherosclerosis and angina without major bleeding.

237
Q

Glycoprotein IIb/IIIa inhibitors

A

block receptor and prevents platelet aggregation.

238
Q

Glycoprotein IIb/IIIa inhibitor subyptes

A

Abciximab, eptifibatide, triofiban

239
Q

Amciximab

A

GP IIb/IIIa inhibitor; monoclonal ab

240
Q

Eptifibatide

A

GP IIb/IIIa inhibitor; cyclic peptide inhibitor of binding site

241
Q

Tirofiban

A

GP IIb/IIIa inhibitor; small molecule inhibitor

242
Q

Pharmacokinetics of GP IIb/IIIa inhibitors

A

IV

243
Q

Use of GP IIb/IIIa inhibitors

A

unstable angina, following coronary angioplasty, MI

244
Q

Risks of GP IIb/IIIa inhibitors

A

bleeding thrombocytopenia

245
Q

Immunomodoulation

A

use of drugs to change the function of the immune system

246
Q

Biological Response Modifiers

A

target cytokines or their receptors, or cellular signaling molecules, antagonists or agonists and most are antibodies.

247
Q

Monoclonal Antibodies

A

Biological response modifier - derived from single B cell that has been fused with multiple myeloma tumor cells to result in hybrid that can grow forever in tumor. — very costly!

248
Q

Chimeric antibiodes

A

enginerred to have different strain of variable domains (ie mouse) and human constant domains -making them less likely to be recognized by own immune system.

249
Q

Humanized antibodies

A

only CDRs of the V domain are mouse

250
Q

NK cells

A

natural killer cells that are large granular lymphocytes in the blood (5-10% of lymphocytic cells); have killer mechanism like CTL but no V(D)J genes or thymic derived. Recognize DAMPS - innate immune system

251
Q

Antibodie dependent cell mediated cytotoxicity

A

ADCC - NK cells have receptor for Fc end of IgG; IgG binds to target cell and NK cell binds to Fc end of antibody. Cell dies of apoptosis.

252
Q

Passive Antibody Therapy

A

evoke ADCC; antibodies are tagged with poison or radioisotope (modifed antibodies called immunotoxins) that provide highly-targeted delivery of toxic moiety.

253
Q

BiTE

A

Bispecific T-cell Engager - two single chained antibodies are coupled together one against CD19 and on against CD3 (on T-cell) for tumor cell death.

254
Q

Azathioprine

A

decreases DNA syntehsis and mRNA transcription - repalced by mycophenolate mefetil - less toxic - organ trasnplant drug

255
Q

Cyclosporin A

A

decreases IL2 production works with steroids to down regulate macrophage function and lessen T-cell stimulation

256
Q

Tacrolimus

A

synergizes with cyclosporin A to decrease IL-2 secretion

257
Q

Sirolimus (rapamycin)

A

binds to FKBP-12 to hinbit target of rapamycin (mTOR) needed for T-cell activation.

258
Q

Anti-thymocyte globulin

A

prepare BMT recipeints

259
Q

why can we transplant blood easier than organs

A

RBCs do not have MHC and antigens they carry are less polymorphic

260
Q

Blood group antigens

A

glycolipids on surface of all body cells - including RBCs; lipid backbone spans plasma membrane and terminal sugars confer antigenic specificity.

261
Q

Secretor phenotype

A

blood type can be determined by sweat and cigarette buts.

262
Q

H Antigen

A

core sugar chain on all RBCs

263
Q

O allele

A

amorphic - does not code for working transferase - basic core H only

264
Q

A allele

A

have glycosyl transferase on the 3rd sugar

265
Q

B allele

A

different sugar on the 3rd sugar.\

266
Q

Bombay Phenotype

A

lack the transferase gene the puts the final sugar on the core - all blood is foreign!

267
Q

isohemagglutinins

A

antibodies arising form natural exposure of IgM class.

268
Q

Rh.

A

proteins coded for at two loci d/D and c/E or e/E (most important is D). Not naturally occurring isohemagglutinins

269
Q

when you donate blood…

A

ABO, Rh, syphilus, hep B and C, HIV, west nile; reverse typing

270
Q

Antiglobulin Coombs test

A

antibody against human Ig detects human Ig on surface of RBC or plasma

271
Q

DAT asks?

A

is there antibody on the cells i am interested in?

272
Q

IAT

A

is there antibody to the red cell antigens in the plasma of the potential recipeint. (red cells, add plasma, rinse, add antiblogulin.

273
Q

hemolytic disease of newborns

A

erythroblastosis fetalis - RhD+ babies of RhD- mothers. Baby’s RBC enter mothers circulation, mother makes anti RhD antibodes. In subsequent pregnancy, if fetus if RhD+, ab attach fetus’s RBC and fetus is jaundiced and cause damage basal ganglia —> cerebral palsy, fetal death

274
Q

Prevention of Hemolytic disease of newborns

A

given IgG to Rh(D) after first baby, these ab combine with fetal red cells, opsonizing them and destroying them before they can a chance to immunize her.

275
Q

Heterophile antibodies

A

cross reactive antibodies

276
Q

full blown AIDS

A

CD4 below 200/ul

277
Q

how many people live with HIV in US?

A

1.1 million

278
Q

how many people don’t know they have it

A

16% of people with HIV

279
Q

HIV-1

A

nontransforming retrovirus, reverse trasncriptase -

280
Q

Lentiviruses

A

slow, ultimately fatal illnesses - HIV

281
Q

Why is HIV antigenically variable?

A

Rerverse transcripatse is highly error prone - many variants

282
Q

Long Term survivors of HIV

A

homozygous for 32 BP deletion in gene for chemokine receptor CCR5, an HIV correcpetor. They never become ill

283
Q

Elite controllers

A

group in LTS that become infected but do not progress to AIDS due to an HLA-B57 allele. They make effective CTL to HIV

284
Q

Pathogenesis of HIV

A

single exposure —> high blood virus at 6 weeks —> loss of CD4 in gut mucosa and increased gut permeability. HIV spreads systemically. HIV peaks at 9 weeks and virus level falls for about 9.5 year.

285
Q

DC sign

A

vHIV adherence to lectin on dendritic cells and uses these cells to get to lymph nodes where HIV binds to p120 on Th cells.

286
Q

gp120

A

binding site of HIV in lymph nodes, binding triggers conformational change to allow binding to corrector CCR5; this binding changes conformation of GP41 glycoprotein to expose hydrophobic region and melt away T-cell membrane - cell and viral fusion where dsDNA issued and inserted via integrase into random breaks in DNA.

287
Q

HIV genome

A

9 genes - gag, pol, env (all retroviruses have), and 6 regulate latency and virulence.

288
Q

how may polypeptides can HIV make?

A

3 large precurose and by splicing 16 polypeptides

289
Q

Clearance in early HIV

A

entire viral population is replaced daily and CD4 cells every 3 days.

290
Q

what is unique about HIV spread

A

not extracellular - gp120/gp41 is made early and virus is inserted into plasma mebrane. This allow fusion of infected cell to nearby uninfected CD4. Thus antibody is useless

291
Q

Steps in HIV clinical symptoms

A

serpositive without symptoms —> opportunistic infection (candida, fevers, night sweatws, weight loss, fatigue —> major opportunistic infections like TB, malignancy, CD4 below 200 (AIDS dementia)

292
Q

Common malignancy of AIDS

A

kaposi sarcoma, burkitt lymphoma

293
Q

Diagnosis of HIV

A

antibody measured by ELISA, western blot to conrifm, PCRR

294
Q

RT inhibitors (nucleosides)

A

competative inhibitors and chain terminators - HIV drug

295
Q

Non-nucleside RT inhibitors

A

bind to hydrophobic bocket and change conformation and activity of RT.

296
Q

Protease inhbitors in HIV

A

to inhibit the cleavage of gag, pol, and env proteins

297
Q

Enfuvirtide

A

binds to gp41 so membrane cannot fuse

298
Q

Maraviroc

A

CCR5 antagonst to block viral entry into CD4 *HIV)

299
Q

Raltegravir

A

integrase inhbiitor in HIV, so HIV cant insert DNA from virus

300
Q

Art

A

combines two NRTIs awith an NNRTIs

301
Q

Vaccine problems with HIV

A

difficult betcuase we need a vaccine to preferentially stimulate Th1 and CTL - not antibody response. Key epitope of HIV is concealed in p120 and p41 and is invisible to B cells. but 20% HIV positiv apple make a broadly neutralizing antibody that blocks infection by almost all HIV strains and mutant forms. (but rare)

302
Q

Immune survelliance

A

T-cells are constantly monitoring surface of cells in body to detect abnormal cells before they become mutant.

303
Q

Evidnece of immune survelliance

A

1) immunodefienct peole have higher tumor incidences 2) activated T cells that recognize Tumor antigens are easily identified 3) some tumors spontaneously regress 4) paraneoplastic syndrome

304
Q

Paraneoplastic syndrome

A

symptoms at a distant organ that do not contain tumor cells due to rxn of antibodies or T cells to another organ that expresses that anigen.

305
Q

Nude Mice

A

have no thymus and get tumors readily, but spontaenous tumors are rare. These mice don’t have Tcells, but they have NK cells that kil the cancer.

306
Q

Immunoediting proces

A

1) elimination 2) equilibrium 3) escape

307
Q

Elimination in immune editing

A

malignant clone is recognized by DAMPs to activate innate immunity and cytokine secretion activates T cells and CTLs

308
Q

Equilibrium in immune editing

A

When tumor and lymphocytes exist in equilibrium

309
Q

Escape

A

tumor cells fight back and overpower T cells. CTL inhibitor surface receptors are engaged and down regulate CTL cytotoxic activity.

310
Q

Tumor escape mechanisms

A

immunosupression by TGFb, decoy CTLs, reuce expression of MCH Class I

311
Q

Tumor associated antigens

A

most often over expressed on tumor

312
Q

Tumor rejection antigens

A

subclass of TAA, recognized by t cells that leads to destruction of tumor

313
Q

Driver vs passengers

A

Driver: activate oncogenes and inactive tumor suppressor genes; passenger genes have numerous other mutations that dont’ affect growth rate, but make mutated proteins.

314
Q

Immunotherapy focuses on…

A

passener mutations —> more mutations = better response.

315
Q

Microbial Gene products

A

tumors caused by viruses

316
Q

Oncofetal antignes

A

normal fetal tissue not found in adults but reexpressed in tumor

317
Q

Differntiation anitgens

A

lineage specific antigens that are overexposed and represent TAA

318
Q

Clonal Antigens

A

expressed uniquely in malignant clone

319
Q

CTL

A

kill tumor cells by inducing apoptosis via perforin of Fas mediated (transmembrane signaling pathways)

320
Q

Specific immunization for immunotherapy

A

a tumor vaccine that is therapeutic but not preventative.

321
Q

Innocent bystander killing

A

BCG (TB vaccine) injected into tumor, leads to delayed type hypersensitivity and tumor cells are killed by M1 macrophages.

322
Q

Tumor-Infiltrating lymphocytes

A

autologous cell therapy where Tcells are expanded in culture using IL2; patients immune system is partially depleted by irradiation and T-cells are reintroduced to kill tumor cells.

323
Q

Chimeric Antigen Receptors

A

rearmed CTLs with antibody/TCR chimeric receptors. Stitched together High affinity antibody linked to transmembrane region and t-cell intracellular tumor agent with high affinity and chosen specificy. (CD3) This allows CTL to bind to tumor with high affinity and chosen specificity with no MHC restriction.

324
Q

Split car

A

chimeric antigen receptor that requires small molecule for association and function. To stop working discontinue small molecule

325
Q

CD28

A

upregualted when T cell engages APC. Binds to CD80 and CD86 for T cell activation

326
Q

CTLA-4

A

after a few days of CD28 upregualtion, it is down regulated and CTLA-4 appears on T-cell surface and binds to CD80/86 to be inhibitory of T-cell activation

327
Q

PD-1

A

later after CTLA-4, PD1 is engaged by PD-L1 ligand to exhaust T-cell and inhibit CTLs.

328
Q

Nivolumab and Pembrolizumab

A

blocking monoclonal Abs against PD1

329
Q

ipilimumab

A

blocking monoclonal ab against CTLA-4; toxic!

330
Q

ID blood testing

A

Syphilis, Hep A, B, C, HIV, HTLV, WNV, CMV, (CJD

331
Q

A allele extra

A

N-acetylgalactosamine

332
Q

B allele extra

A

D-galactose

333
Q

pretransfusion testing

A

ABO, Rh, antibody screen for ab other than ABO

334
Q

Crossmatch

A

Major: serum + donor cells —> agglutination; Coomb’s to lok for IgG and complement

335
Q

Emergent blood transfusion

A

O, RhD negative; or O RhD positive for males and non-childbreaing female

336
Q

Abbreviated (30 min) transfusion

A

ABO, Rh type, Ab screen negative

337
Q

if blood is positive for specific alloantibodies

A

must use blood with negative antigens

338
Q

if blood has auto antibodies but no alloantibodies

A

re-evaulate transfusion

339
Q

cyroprecipiates

A

F VIII, vWF ag, fibrinogen, Factor XIII, fibronectin

340
Q

random donor platlets vs ampheresis platelets

A

RD is more concentration in smaller volume;

341
Q

what cannot be stored in blood transfusions

A

granulocyte concetnration

342
Q

Whole blood is given for

A

decreased oxygen carrying capacity and volume, must be crossmatched

343
Q

PRBCs are given for

A

low oxygen carrying, chronic anemia, acute blood loss, cross matching is a must

344
Q

FFPs are given for

A

coagulopathy related to DIC, liver failure, Vit K def, can use specific clotting factors, must be ABO specific but no crossmatch. Given under 4 hours

345
Q

Cyroprecipitate is given for…

A

low fibrinogen levels, of vWF disease, must be ABO; infusion over 30-45 min

346
Q

Platelets are given for..

A

bleeding due to low or dysfunctional platelets, thrombocytopenia, ABO type , infusion 30-1 hr

347
Q

Granulocyte concentate is given for..

A

severe infection with patients with ANC

348
Q

Acute hemolytic transfusion rxn.

A

preformed alloantibodes (ABO) cause intravascualr hemolysis and activation of DIC, inflammatory mediators and renal failure. fever, nasuea, chills, hypotension, dyspnea, dark urine.

349
Q

Tx of Acute hemolytic transfusion rxn

A

stop trasnfusions, maintain IV fluids, heparin

350
Q

Delayed hemolytic transfusion rxn

A

formation of alloantibodes post transfusion to cause extravasualr heomlysis, fewer signs could include jaundice, anemia.

351
Q

Febrile reactions

A

due to leukoagglutinins in recpeient cytokines.

352
Q

Allergic rxns due to transfusion

A

result of antibodies to IgA, typcial allergic signs

353
Q

Transfusion acute lung injury

A

4 hours post, due to infection, surgery, cytokine therapy, lipids, antibodies, cytokines.

Blood and Lymph (6 decks)

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