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Exam 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

Rheumatoid Arthritis -

Blood tests? specific to RA

A

Anticyclic citrolinated protein - shows severity of RA

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2
Q

Rheumatoid Arthritis Blood checks?

A
  • Rheumatoid factor - autoantibody of RA
  • Antinuclear antibody - against nucleus for RA
  • Hb for anaemia
  • Anticyclic citrolinated protein/anti-CCP if Rh factor -ve
  • Xray/Radiology - shows inflammation & damage
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3
Q

Rheumatoid Arthritis Acute phase tests?

A
  • Erythrocyte sedimentation Rate (ESR) - measure inflammation within 24hrs.
  • Works after hour but could be activated by surgery, injury & infections.
  • C-reactive protein (CRP) -
  • measures inflammation via protein made in innate system, • increases 4-6hr after inflammation.
  • Could be activated by surgery, injury & infections.
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4
Q

C-reactive protein (CRP) in Rheumatoid Arthritis Blood test

A
  • measures inflammation via protein made in innate system, • increases 4-6hr after inflammation.
  • Could be activated by surgery, injury & infections.
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5
Q

Erythrocyte sedimentation Rate (ESR) in Rheumatoid Arthritis Blood test

A
  • measure inflammation within 24hrs.

* Works after hour but could be activated by surgery, injury & infections.

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6
Q

Rheumatoid Arthritis additional checks (.not blood)

A
  • Xray
  • functional ability of pt eg health assessment questionnaire
  • baseline tests for comparison in the future
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7
Q

NICE Rheumatoid Arthritis first line

A
  • conventional/ cDMARD
  • monotherapy
  • eg MTX, leflunomide, sulfasalazine
  • ASAP
  • hydroxychloroquine if mild symptoms - weak DMARD.
  • treat to target, aim for remission
  • escalate dose as tolerated.
  • consider short term bridging with corticosteroid/ steroid cover whilst DMARD starts to work
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8
Q

cDMARD stands for?

A

conventional disease modifying anti-rheumatic drug

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9
Q

Why add corticosteroid short term bridging with cDMARD in Rheumatoid Arthritis?

A
  • as DMARD has lag time until effects seen.

* review corticosteroid & remove once DMARD effects.

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10
Q

weak DMARD eg

A
  • hydroxychloroquine.

* used if mild symptoms. not usually given.

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11
Q

Rheumatoid Arthritis considerations before treatment?

A
  • Pt preference
  • Pt characteristics eg co-morbidities
  • drug characteristics
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12
Q

CI/Cautions with MTX

A
  • Active infection
  • immunodeficiency syndromes
  • Ascities/pleural effusion
  • severe renal impairment
  • Alcoholism
  • NSAIDs
  • Blood dyscrasias - myelosuppression = SE
  • Pregnancy
  • Elderly - reduced hepatic and renal fn, reduced folate reserves.
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13
Q

MTX CI with Active infection why?

A
  • reduce immune system efficacy

* immunodeficiency syndromes

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14
Q

MTX CI with Ascities/pleural effusion why?

A

• MTX into fluid, accumulates, re-excreted, prolong serum 1/2 life, toxicity increase.

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15
Q

MTX CI with Alcoholism/NSAIDS

A
  • severe renal impairment - MTX renal cleared
  • Alcoholism - increased risk of hepatotoxicity
  • NSAIDs - risk to renal fn and MTX excretion
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16
Q

MTX CI with pregnancy why?

A
  • Pregnancy - MTX teratogenic.

* Contraception for both during treatment and 3-6months after.

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17
Q

MTX strength of tablets in RA

A

• 2.5mg, 10mg NEVER for safety incase of accidental overdose.

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18
Q

RA - MTX weekly adjustments?

A

• increase by 2.5-5mg every 2-6 weeks to 20mg max dose or highest tolerated dose below max.

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19
Q

RA - MTX supply of tablets

A

only supply up to next appx to reduce risk of incorrect administration.

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20
Q

MTX - folic acid?

A
  • 1/7 , take on different days.

* given to reduce antifolate SE of MTX

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21
Q

MTX - corticosteroid?

A
  • DMARD delay up to 3 months.
  • oral prednisolone course or one off IM or IV methylprednisolone.
  • stopped appropriately
22
Q

MTX pt discussion

A
  • MTX - immunosuppressant
  • MTX monday, Folic acid Friday
  • miss dose = take next day, unless 3+ days late. continue on normal day following week.
  • long? 6wk to 3months to work. Corticosteroid til then = pain relief.
  • cytotoxic - away from children
  • teratogenic - contraception
  • MTX booklet - carry, fill in, keep up to date.
  • blood tests for A.SE/ adverse SEs
23
Q

MTX SE

A
  • GI
  • CNS - inform prescriber
  • hair thinning - fine once stopping med

Report:
• SOB, dry cough, fever - pulmonary toxicity
• Yellowing of eyes, N&V - hepatic impairmetn

24
Q

Avoid with MTX

A
  • contact with chicken pox
  • live vaccinations
  • OTC NSAIDs, ibuprofen
  • non-pasteurised foods
25
Q

Contraception w MTX length?

A

3 - 6 months before and after

26
Q

MTX tests and investigations?

A
  • LFTs - MTX = hepatotoxic
  • RF - ensure MTX cleared and doesn’t accumulate.
  • FBC - neutropenia, thrombocytopenia, lymphopenia, bone marrow suppression
  • Chest X ray - pulmonary toxicity
27
Q

MTX Tests for newly started pt

A

LFTs/RT, FBC
• before starting
• 1-2 wks until stabilised
• 2-3 months

28
Q

DAS28 what is it?

A

28 joints in body tested for swelling, tenderness and ESR/CRP

29
Q

DAS28 >5.1

A

active disease

30
Q

DAS28 <3.2

A

low disease

31
Q

DAS28 <2.6

A

remission

32
Q

RA Step up therapy after MTX

A 
• additional cDMARD 
eg sulfasalazine, leflunomide
• bridging corticosteroid 
• symptomati relief 
• optimise new therapy 
• increased monitoring until stabilised
33
Q

after 2nd line RA MTX & cDMARD

A

by EULAR could consider bDMARD or tDMARD

34
Q

failure of cDMARD in RA, NICE recommend..

A

DAS28 >5.1

give bDMARD

35
Q

Infliximab is a?

A

TNFa inhibitor

tumour necrosis factor alpha

36
Q

Infliximab binds to?

A
  • with high affinity to monomers & trimers of soluble TNF & transmembrane TNF
  • form complexes of each.
  • prevents pro-inflammatory TNF binding to its receptors.
37
Q

Infliximab made of?

A
  • chimeric protein - human and murine origin
  • IgG light and heavy chains
  • fragment of antigen bindings - TNF binding areas
  • Fc region
38
Q

Infliximab prevents inflammation by inducing.. ?

A 
Induce: 
• reducing cytokine & chemokine production 
• reduce activation & proliferation 
• inflammatory cell apoptosis
• reduced angiogenesis
• reduced effect on bone
39
Q

Pro inflammatory cytokine egs

A 
IL-1
TNF-a
IL-12
IL-6
IFNa/ß
CXCL8 
CCL2
40
Q

IL-1

A
  • causes inflammation & fever

* induces acute phase proteins/ APP

41
Q

TNF-a

A
  • inflammation
  • induce APP/ acute phase proteins
  • induce cell death
  • neutrophil activation
  • cachexia (muscle wasting)
42
Q

IL12

A
  • Nk cells

* promotes Th1 to produce T-lymphocytes

43
Q

IL6

A
  • in liver
  • induce APPs
  • induce adaptive system (proliferation & antibody secretion via B-cells)
44
Q

IFNa/ß

A
  • induces antiviral state

* activates Nk cells

45
Q

CXCL8

A

attracts neutrophils

46
Q

CCL2

A

attracts monocytes

47
Q

NFkB bound to?

A

Ikb

48
Q

When NFkB released?

A

When cytokines released/ bacterial components etc, Ikb kinase activated and breaks down Ikb. (NFkB bound to Ikb)

49
Q

After NFkB released?

A
  • migrates to the nucleus to bind on the promoter sequences to transcribe pro-inflammatory cytokines.
  • DNA to RNA
50
Q

Describe signalling pathway that leads to production of prostaglandins & leukotrienes

A
  • Stimulus activates phospholipase A2 which activates phospholipids.
  • then arachidonic acid
  • then COX1, COX2 lipoxygenases.
  • lipoxygenases -> leukotrienes
  • COX -> different prostaglandins eg PGG2
51
Q

Process that leads to a fever?

A
  • Macrophage ingests toxin
  • broken down in a vacuole
  • releases endotoxins
  • macrophage proces IL1.
  • IL1 goes into blood stream then hypothalamus
  • IL1 induces production of prostaglandins which increase temp of body’s thermostat.
  • fever

Exam 1 (11 decks)

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