Brainscape's Knowledge GenomeTM

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


See full index

CC2 > Immunology > Flashcards

Immunology Flashcards

1
Q

Signs to ?immunodeficiency

A

Severe, recurrent or invasive infections
Severe, recurrent or disproportionate inflammation
Unusual site/organism of infection
Unexplained lymphoproliferation

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

What is SCID

A

Severe combined immunodeficiency
Group of inherited genetic disorders characterised by a deficiency in lymphocytes
T cells are absent in most forms, B and NK vary
X linked is most common = boys = t neg, B +

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

Lymphocyte count of <2 in an infant <6 months is what until proven otherwise

A

SCID

? up to 1 yr really

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

SCID symptoms

A 
Severe, recurrent infection
Failure to thrive
Chronic diarrhoea
?absent lymph
?erythematous rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which vaccines are CI in SCID kids

A

Live:

1) BCG
2) rotavirus
3) polio
4) VZV (chickenpox)
5) MMR
6) yellow fever
7) LAIV

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

How is SCID diagnosed

A
  1. Lymphocyte phenotyping, flow cytometry
  2. Lymphopenia
  3. May see eosinophelia
  4. Absent thymic shadow on CXR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is SCID managed

A
  1. Gene therapy, BMT before infection
  2. prophylactic antifungal, abx, antiviral, igg
  3. No live vaccine
  4. No breast feeding (CMV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Characteristic presentation of an antibody deficiency and give eg

A 
Recurrent
1) otitis media/sinusitis
2) conjunctivitis
3) pneumonias 
tend to present when maternal igG wanes (6-9m)
XLA (brutons)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is hyper igM syndrome

A 
Raised or normal igM, deficient igG,A,E because inability for B cells to class switch 
eg secondary to T C40L abnormality (X linked)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tx of antibody deficiency

A

Prophylactic abx

replace igG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is primary antibody deficiency diagnosed

A
  1. Serum igG,A,M + repeat
  2. FBC to look for wider lymphopenia (SCID), anaemia, thrombocytopenia and neutropenia
  3. Flow cytometry and genetic testing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How would an absolute neutrophil deficit present?

A

Mouth ulcers
Stomatitis
Recurrent fever
Neutropenic sepsis

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

Causes and tx of absolute neutrophil deficiency

A

SCN
Cyclical
Secondary eg to chemo
Treat: GCSF ?AML

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

Cause, presentation + tx of neutrophil chemotaxis defect

A 
Leukocyte adhesion deficiency (Cd18)
No pus at site of infection 
Skin infection, perianal fistula
Delayed umbilical cord detachment
Enlarged lymph node
tx: stem cell transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do chronic granulomatous diseases present

A

Early onset deep seated catalase + infections (staph, Aspergillus, Norcardia, Serratia)
IBD like disease, perianal abscess

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

Tx of CGDs

A

AlloBMT, gene therapy

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

Describe normal complement pathway

A

Add pic + MAC

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

Deficiency in which part of complement increases risk of nicerria meningitidis

A

C5b-9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is CVID

A

Common variable immune deficiency is a hypogammoglobulinaemia of unknown genetic causes especially in adulthood
Can have recurrent infections, autoimmunity and other manifestations
Tx: IgG replace, rarely alloBMT

20
Q

What infections do PPIs give rise to

A

C diff, enterobacter, norovirus

21
Q

Which infections do anticholinergics give rise to

A

Dental, UTi

22
Q

Which infections does chemo give rise to

A

Neutropenia -> fungal and extracell bac eg E coli, staph aureus

23
Q

What is rituximab, indications

A

Anti Cd20 antibody acting on peripheral B cells for lymphoma, leukaemia and some AI
SE: immunodeficiency because hypogammaglobulinaemia

24
Q

What is infliximab, indications

A

Anti TNFr igG a cytokine used in RA

TNF a = bone erosion, cartilidge destruction, inflammation, malaise etc

25
Q

What is Entanercept

A

Binds to TNFa itself unlike infliximab

26
Q

Link between infliximab, entarecept and TB

A

tnf a is produced by cells that maintain granulomas so anti tnfa therapy = worsen latent tb

27
Q

What is tocilizumab, indication, se

A

Anti il6 cytokine for RA
stop inflammation but
- skin and soft tissue infection without redness
- diverticulitis

28
Q

What is eculizumab and SE

A

C5 complement blocker for rare diseases where MAC haemolyses RBCs eg atypical haemolytic, uraemic syndrome, paroxysmal nocturnal haemoglobinuria
but less c5
- risk of meningococcal and gonococcal infection

29
Q

Describe the natural process of preventing autoimmunity

A

Positive and negative t cell selection occurs in thymus
If a t cell receptor binds tightly to mhc on thymus cells = negative selection
If a t cell receptor binds lightly = induce t reg cell (can also occur in periphery)
rest go to periphery as naive cd4 and cd8 cells

30
Q

Function of t reg cells

A

Immunosuppression Il10 and tgfB
Limit APC activity (AI) via ctla4
Disrupt other T cell expansion
Kills immune cells

31
Q

Define autoimmunity

A

Inappropriate, self directed inflammation caused by autoreactive T and B cell responses when central/peripheral tolerance/reg mechanisms fail

32
Q

Drugs causing SLE (AI)

A
  1. Procainamide (antiarrhythmia)
  2. Quinidine (antiarrhythmia)
  3. Hydralazine (antihypertensive)
33
Q

Principles of AI management

A
  1. Steroids = modulate gene expn of inflamm cells
  2. Antimetabolites = target dna synthesis of rapidly dividing lymphocytes in inflammation
  3. Calcineurin inhibitors stop IL2 mediated cell proliferation but chronic renal toxicity eg cyclosporine, tacrolimus, and pimecrolimus
  4. Biologic
34
Q

Describe how a type 1 hypersensitivity reaction works

A
  1. Exposure to allergen
  2. Sensitisation = APC takes antigen to naive t cell. T cell responds -> Th2 cell specific to the antigen is primed
    Th2 releases il4 so that B cell switches from igM to igE
    the igE is attached to mast cell/eosinophil/basophil
  3. Re exposure to allergen = mast cell degranulation to release:
    Histamines, prostaglandins, leukotrienes, PAF, tryptase
  4. Long term exposure can -> chronic inflammation, tolerance
35
Q

Describe how T2 hypersensitivity works

A

igG response to antigen on a cell eg transfusion reaction

36
Q

Describe how T3 hypersensitivity reaction works

A

igG response to circulating antigens -> complexes that damage eg RA, vasculitis

37
Q

Describe how T4 hypersensitivity reactions work

A

Antigen sensitised to allergen -> >th1 primed
T cells release cytokines, recruit macrophages etc on re-activation

NOT b cell mediated
EG contact dermatitis

Takes >4 hours usually 1-2 days post exposure, longer to resolve, not life threatening

38
Q

How is allergy confirmed

A
  1. History
  2. ssIgE if history +
  3. total igE
  4. skin prick test = igE mediated local histamine reaction in 20 mins
39
Q

Allergic rhinitis

A

Type 1 to aeorallergens
nasal and eye symptoms
Tx includes steroids, antihistamines, ipratroprium bromide, LTRA

40
Q

Allergic asthma

A

type 1 igE mediated initially but the hypersensitive bronchus then responds to non allergic stimuli
TX: avoid, b2a, steroids, LTRA, sodium chromoglycate in kids to stabilise mast cells

41
Q

What is atopic triad

A
  1. Allergic rhinitis
  2. Allergic asthma
  3. Atopic dermatitis

1 is an independent risk factor for 2

42
Q

Atopic dermatitis

A

Complex response to multiple allergens likely due to genetic barrier defect (filaggrin keratinocyte layer)
so have allergic skin disease + immunodeficiency + chronic inflammation
IgE v high, strong link with food allergy as kid
TX: avoid, prevent scratching, moisturise, abx creams, steroids, tacrolimus (calcineurin inhibitor of t cell proliferation)

43
Q

common drugs which have been linked to steven johnsons syndrome

A 
allopurinol
carbamezapine
phenytoin
lamotrigine
sertraline
sulfasalzine
44
Q

Define anaphylaxis

A

Severe , life threatening, systemic type 1 hypersensitivity reaction usually occuring within 60 minutes of exposure to pre-sensitised allergen
the response may be biphasic (2nd attack in 8 hours)

45
Q

Differentials for anaphylaxis

A
  1. CSU (hives but longer onset, recurrent, longer to resolve)
  2. Asthma attack
  3. Anxiety induced hyperventilation
  4. Vocal cord dysfunction (esp in asthmatics)
  5. Hereditary angiodema (c1 esterase inhibitor deficiency, no rash)
  6. Mastocytosis
  7. Scombroid poisoning from not cooling fish quickly
  8. Carcinoid syndrome (paraneo) - flush, diorrhoea
  9. Opiods
  10. Excercise induced
  11. Hypotension, syncope
46
Q

Acute anaphylaxis management

A
  1. AtoE
  2. IM 1 in 1000 0.5ml (auto pen wait 5 mins)
  3. high flow ox
  4. Fluid challenge 500ml 4 times
  5. Bronchodilators
  6. 200mg IV hydrocortisone or 40mg oral
  7. 10mg IV chlorphenamine (antihistamine)

CC2 (8 decks)

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