Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

YR5 Immunology > Immuno - case studies > Flashcards

Immuno - case studies Flashcards

1
Q

What is atopy?

A

propensity to develop IgE antibodies against harmless allergens (antigens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is sensitisation?

A

Presence of IgE antibodies + binding to mast cells + basophils (ready to react on next exposure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is allergy?

A

Sensitization (skin prick or blood test) + exposure resulting in allergic reaction (take hx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does an allergic reaction affect different body systems?

A

Skin + mucosa: Urticaria + Angiodema (90%)

Resp: Wheeze, SOB, cough, chest tightness, runny nose, sneezing, stridor (85%)

CVS: hypotension, compensatory tachycardia, reduced consciousness

GI: D+V, cramps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pathophysiology of skin reactions in anaphylaxis?

A

Vasodilation
Increased permeability
Increased peripheral perfusion
Acts on local nerve fibres causing itching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes the respiratory symptoms of anaphylaxis?

A

Smooth muscle contraction causing bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes the cardiovascular symptoms of anaphylaxis?

A

Vasodilatation systemically
Can lose 1/3 of entire blood volume in 10 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes GI symptoms of anaphylaxis?

A

Intestinal oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is anaphylaxis?

A

Severe allergic reaction with sudden onset A B or C problem
+ usually skin changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Immediate management of anaphylaxis - 6 points

A
  1. Remove trigger + lie flat/ sit
  2. IM adrenaline 500mcg (0.5ml)
  3. Airway Mx
  4. High flow O2
  5. Repeat Adrenaline after 5 mins
  6. IV fluid bolus 500-1000ml
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does adrenaline do to help in anaphylaxis?

A

Vasoconstriction: reverses problems in skin, gut + CVS
Bronchodilator: reverse resp problem
Acts on B2 receptor on immune cells: stops release of inflammatory mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why are fluids needed in anaphylaxis?

A

To restore intravascular volume to allow for restoration of cardiac output

If no access to fluids i.e. outside hospital: give adrenaline + raise legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why are antihistamines, bronchodilators and steroids no longer advised in anaphylaxis?

A

Antihistamines: make rash better but distract from life-threatening cardio/ resp manifestations
Bronchodilators: distract from cardio manifestations
Steroids: take hours to have effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why should an anaphylactic patient be kept in for 6h?

A

Anaphylaxis late phase reaction is a repeat of anaphylaxis, but tends to be milder.
Tends to occur in first 6h after initial reaction (though can be up to 72h)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What serum measurement can be used to determine whether a reaction was anaphylactic?

A

Serum tryptase
Baseline + 20% of baseline + 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Disorders associated with recurrent meningococcal meningitis

A

Complement deficiency
Antibody deficiency

Any disruption to BBB: skull fracture, hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which infections if recurrent may indicate a complement deficiency?

A

Encapsulated organisms:
Neisseria meningitis
Gonococcus
H influenzae B
Pneumococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What kinda infections make you suspicious of an immunodeficiency?

A 
SPUR 
Serious
Persistent
Unusual 
Recurrent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Suspected complement deficiency - what Ix are ordered?

A

C3
C4
CH50
AP50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Complement components in classical pathway

A

C1
C2
C4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Complement components of the alternate pathway

A

Factor B H I (from bacterial cells wall)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Complement components of the final common pathway

A

C5-9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is CH50?

A

Functional test of integrity of CLASSICAL complement cascade
All components of the cascade need to be in place for the test to give a +ve (normal) result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is AP50?

A

Functional test of integrity of ALTERNATIVE complement cascade
All components of the cascade need to be in place for the test to give a +ve (normal) result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Normal C3
Normal C4
Absent CH50
Absent AP50

What does this indicate?

A

Deficiency in final common pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How would you manage a patient with deficiency in the final common complement pathway?

A

Meningococcal vaccine
Pneumococcal vaccine
HiB vaccine
Daily prophylactic penicillin
Monitor closely
(v susceptible to encapsulated bacteria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the most specific antibody for SLE?

A

dsDNA antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Tests to investigate lupus nephritis?

A

Urinalysis (proteinuria + haematuria)

urine microscopy - red cells + casts

Renal biopsy: diffuse proliferative nephritis
Immune complex + complement deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What syndrome should SLE patients be screened for? What is the criteria for diagnosis?

A

Anti-phospholipid syndrome
Dx: 1 clinical + 1 lab criteria

30
Q

What are the 2 clinical criteria for anti-phospholipid syndrome?

A

Intravascular thrombosis (arterial + venous)
Recurrent miscarriage (>3)

31
Q

Give 3 signs of anti-phospholipid syndrome on examination/ testing

A

Prominent Lived reticular (mottled skin)
Mild thrombocytopenia
Libmann Sachs endocarditis (sterile)

32
Q

What are the lab criteria for antibphospholipid syndrome?

A

Antibodies to anionic phospholipids: anti-cardiolipid antibodies

Antibodies to beta-2-glycoprotein 1

Lupus anticoagulant test

33
Q

When investigating for anti phospholipid syndrome, what should be remembered?

A

APS is pro-thrombotic in vivo even though it is a/w an anti-coagulant effect in in vitro tests

34
Q

What immunological tests can monitor SLE activity?

A

Immune complexes activate classic complement pathway
Consume complement
The more active the disease, the more complement is consumed
C4 tends to go down first, then C3

35
Q

SLE - what kinda hypersensitivity disorder is it?

A

Type III: immune complex mediated

antinuclear antibodies bind to bare cells. these complexes activate complement + attract WBCs

36
Q

Rituximab - which cells does it deplete?

A

Antibody to CD20
mature B cells (but not plasma cells)

37
Q

Mycophenolate Mofetil - which cells does it affect?

A

T cells > B cells

38
Q

Azathioprine - which cells does it affect

A

T cells

39
Q

Penicillin for CAP –> 3 days later:

Fever, arthralgia, vasculitic skin rash, proteinuria, haematuria, raised transaminases, disorientation

A

Serum sickness

40
Q

WTF is the pathophysiology behind serum sickness

A

Penicillin is recognised as a neo-antigen: SENSITISATION. stimulates a strong IgG response

On next exposure –> IMMUNE COMPLEX FORMATION w circulating penicillin + mass IgG production –> complex deposits in glomeruli + skin + joints

41
Q

Clinical features of serum sickness

A

Arthralgia
Renal dysfunction
Purpuric rash

(immune complex deposition in small vessels)

42
Q

Ix to confirm Dx of serum sickness

A
  • complement levels - LOW due to immune complex activation
  • specific IgG to penicillin
  • Skin and kidney biopsies
43
Q

Serum sickness: Type of hypersensitivity disorder

A

Type III

44
Q

FTT +recurrent infections (tonsillitis, pneumonia, ROM, cellulitis):

Ddx?

A 
CF
DM
Bruton's 
SCID
Hyper IgM
Cytokine deficiency

having ATOPIC DISEASE

45
Q

Evaluation of lymphocyte immunodeficiency - which Ix?

A

T-cells (CD4 + 8)
B-cells
IgM, IgA, IgG

46
Q

Ix for suspected phagocyte deficiency

A

NBT
Neutrophil count
Leukocyte adhesion markers

47
Q

Treatment of Bruton’s

A

Immunoglobulin replacement every 3 weeks

48
Q

Why are multiple myeloma patients susceptible to infections

A

The mass clonal proliferation of one plasma cell –> suppresses production of normal Ig

49
Q

Why are multiple myeloma patients often anemics?

A

Crowding out of normal RBCs in BM by plasma cells

Tumour releases cytokines which inhibits normal BM function

50
Q

Why is ESR elevated in Multiple Myeloma

A

High protein content in plasma –> increases attractant charge

RBCs tend to clump together so they fall more quickly through plasma.

51
Q

X-ray lesions in multiple myeloma

A

lytic lesions “punched out”

52
Q

What is Rheumatoid arthritis? (3)

A

Peripheral, symmetrical, polyarthritis with stiffness
Persists for > 6w
May be a/w RF +/- anti-CCP Ab

53
Q

What is the most specific antibody to test for RA?

A

Anti-citrullinated protein antibodies
(Anti-CCP are a subset of which)

54
Q

How is recent childbirth significant in rheumatoid arthritis

A

Switch of T cell type responses post pregnancy- more likely to develop RA

55
Q

Which class of Ig is rheumatoid factor? what does rheumatoid factor target

A

IgM which targets Fc portion of human IgG

56
Q

what does anti-CCP stand for

A

anti-cyclic citrullinated protein

57
Q

How are CCPs formed?

A

Arginine residues are converted to citrulline residues by PADI enzymes

58
Q

What can affect the degree of CCP generation?

A

Polymorphisms in PADI enzymes
If lose tolerance to CCPs, highly likely to develop RA

59
Q

What 2 situations predispose to RA?

A

Smoking: increases citriilunation of proteins in the lungs (increase in citrilunated protein load)

Gum infections promote citrullination. The causative bacteria is the only bacteria with PADI enzyme.

60
Q

2 HLA associations with Rheumatoid arthritis?

A

DR4 (subtypes Dw4, 14, 15)
DR1

61
Q

PADI stands for?

A

Peptidylarginine deiminase

62
Q

Why are PADI enzymes are important?

A

PADI enzymes act to turn arginine residues into citrulline residues

Polymorphisms (type 2 + 4) of PADI –> more citrulline resiudes –> more likely to develop RA

63
Q

PTPN22 is an enzyme important in rheumatoid arthritis. what is its function?

A

Lymphocyte specific tyrosine phosphatase which suppresses T cell activation

In RA, the 1858T allele increases RA susceptibility (+SLE + T1DM)

64
Q

Genetic predisposition to Rheumatoid arthritis

A
  • HLA DR1 + 4
  • PTPN22 - 1858T allele
  • PADI enzyme (PMs type 2 + 4)
65
Q

1st line tx of rheumatoid arthritis

A

DMARDs inc methotrexate

66
Q

If methotrexate is not tolerated - which DMARds are used for rheumatoid arthritis

A

Sulphasalazine

Hydroxychloroquine

67
Q

name 2 anti-TNFalpha agents

A

infliximab

Adalimumab

68
Q

Tocilizumab - MOA? use?

A

Anti-IL6 receptor

Rheumatoid arthritis

69
Q

Beyond DMARDs - state 4 diff drugs used to treat Rheumatoid arthritis

A

Infliximab (anti-TNFa)
Abatacept (anti-CTLA4)
Tocilizumab (anti-IL6)
Rituximab (depletes B cells, anti-CD20)

70
Q

Natalizumab - MOA? use?

A

MOA: anti-alpha4 intern

Use: relapsing remitting MS

71
Q

Use for basiliximab

A

prevention of transplant rejection

YR5 Immunology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions