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Kat's Pathology > Case Studies in Immunology > Flashcards

Case Studies in Immunology Flashcards

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1
Q

40 year old man. Presents to A&E complaining of lip swelling.
Over the next 20mins, he develops: itching of his hands and feet, increasing breathlessness and chest tightness, fall in PEFR to 200l/min, fall in BP to 80/30mmHg, oxygen saturations are 88% on room air.

A

Anaphylaxis

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2
Q

What is the definition of anaphylaxis?

A

A systemic hypersensitivity reaction in which the response is so overwhelming as to be life-threatening

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3
Q

What is the mechanism of anaphylaxis?

A

Type I hypersensitivity response

  • Cross-linking of IgE on surface of mast cells
  • Causes mast cells to degranulate
  • Results in release of specific biological mediators including histamine and leukotrienes (Increase in vascular permeability, smooth muscle contraction, inflammation, increased mucus production)
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4
Q

What are the clinical features of anaphylaxis?

A

Itch of palms, soles of feet and genitalia.
Wheeze, bronchoconstriction.
Flushing, urticaria.
Conjunctival injection, rhinorrhoea, angioedema.
Feeling of impending doom, loss of consciousness, headache, death.
Angioedema of lips and mucous membranes.
Laryngeal obstruction, stridor.
Hypotension, cardiac arrhythmias, myocardial infarct.
Vomiting, diarrhoea, abdominal pain.

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5
Q

What are some causes of collapse? (6)

A 
Myocardial infarction. 
Cardiac arrhythmia. 
Acute asthmatic attack. 
Pulmonary embolus. 
Vasovagal attack. 
Epilepsy.
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6
Q

What is the immediate treatment of anaphylaxis? (6)

A

Oxygen by mask.
Nebulised bronchodilators.
Adrenaline IM - 0.5mg for adults and may repeat.
IV anti-histamines - 10mg chlorpheniramine.
IV corticosteroids - hydrocortisone 200mgs.
IV fluids.

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7
Q

What are some ways of providing respiratory support in a patient presenting with anaphylaxis? (2)

A

Intubation may be required for severe bronchoconstriction.

Trachoestomy if develops upper respiratory tract obstruction (e.g. laryngeal swelling, or severe swelling on tongue)

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8
Q

What is the IM adrenaline dose given to patients presenting with anaphylaxis.

A

0.5mg IM (may repeat)

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9
Q

How does adrenaline help in anaphylaxis? (3)

A

Acts on B2 adrenergic receptors to constrict arterial smooth muscle.

Increases blood pressure.
Limits vascular leakage.
Bronchodilator.

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10
Q

What is the dose and anti-histamine used in anaphylaxis?

A

10mg chlorpheniramine.

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11
Q

Why are anti-histamines indicated in anaphylaxis?

A

They act to oppose the effects of mast-cell derived histamine.

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12
Q

What are nebulised bronchodilators effective in anaphylaxis?

A

Improve oxygen delivery through bronchial dilatation.

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13
Q

What IV corticosteroid is given in anaphylaxis.

A

200mgs hydrocortisone IV.

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14
Q

What is the mechanism of action of hydrocortisone in the treatment of anaphylaxis? (3)

A

Systemic anti-inflammatory agent.
Effect takes about 30mins to start, and does not peak for several hours.
Important in preventing rebound anaphylaxis.

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15
Q

Why are IV fluids given in anaphylaxis?

A

Increase circulating blood volume and therefore increase blood pressure.

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16
Q

What is the immune mechanism of anaphylaxis?

A

IgE mediated mast cell degranulation

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17
Q

What are some common causes of anaphylaxis? (3)

A

Foods (peanuts, tree nuts, fish and shellfish, milk, eggs, soy products).
Insect bites (bee venom, wasp venom).
Chemicals, drugs and other foreign proteins (penicillin and other antibiotics, IV anasethetic agents e.g. suxamethonium, propofol; latex)

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18
Q

What questions would you ask once he has stabilised? (4)

A

What was he doing immediately prior to the onset of symptoms?
As his first symptom was lip swelling, specifically ask what had his lips been in contact with, & what he had eaten.

Does he have any known allergies?

Has anything like this happened before?

How is his general health?

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19
Q

What are the two types of latex allergy?

A

Type 1 hypersensitivity.

Type 4 hypersensitivity.

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20
Q

What is a type 1 hypersensitivity reaction?

A

Acute onset of classical allergic symptoms after exposure e.g. wheeze, urticaria, angioedema, anaphylaxis.
Spectrum of severity
Mucosal route is associated with more severe reactions
Different rubber products vary significantly in their allergenic content.

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21
Q

What is a type 4 hypersensitivity reaction?

A

Contact dermatitis.
Usually affect hands (glove usage) or feet (due to rubber in footwear).
Mainly due to rubber additives eg thiuram rather than latex itself

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22
Q

What are the features of a type 4 hypersensitivity reaction to latex? (4)

A

Symptoms occur 24-48 hours after exposure (Much later than in IgE mediated reactions)
Itch++
Rash well-demarcated, often flaky
Not responsive to anti-histamines.

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23
Q

In what patient groups is type 1 latex allergy a major health problem? (3)

A

Patients undergoing multiple urological procedures.
Preterm infants.
Patients with indwelling latex devices (ventriculoperitoneal shunts)

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24
Q

What percentage of occupational asthma in the UK is associated with latex exposure?

A

60%

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25
What groups of people have a greater tendency to have latex allergies? (2)
``` Healthcare workers (10% versus <1% of the general population) Latex or manufacturing industry workers. ```
26
What is latex fruit syndrome?
People with type 1 hypersensitivity to latex have cross reactivity with some foods.
27
What foods are particularly associated with latex fruit syndrome? (9)
``` Avocado. Apricot. Banana. Chestnut. Kiwi. Passion fruit. Papaya. Pear. Pineapple. ```
28
How would you confirm that someone has a latex allergy?
In vivo allergy testing. In vitro IgE test for latex allergy. If there is a history of anaphylaxis, blood tests are preferable to skin tests because of the small but significant risk of inducing anaphylaxis. It is not very sensitive (70-80%) or specific (60-80%) NB: Blanket testing to other allergens which have not been implicated will not aid diagnosis.
29
What type of allergy does skin prick testing look for?
Type 1 hypersensitivity reaction.
30
What type of allergy does patch testing look for?
Type 4 hypersensitivity reaction.
31
What would a skin biopsy show if there was a type 4 hypersensitivity allergy? (2)
Infiltrating T lymphocytes. | Granuloma.
32
What is part of the long term management of patients with anaphylaxis. (2)
Referral to an allergist/immunologist. | A plan of allergy avoidance should be made in conjunction with the occupational physician.
33
What common household and health care products contain latex? (14)
``` Balloons. Condoms. Dish-washing gloves. Sports equipment. Rubber bands. Shoe soles. Erasers. Health care gloves. Blood pressure cuffs. Catheters. Face masks. Rubber stoppers. Bandages. Stethoscope tubing. ```
34
What forms part of a latex avoidance plan? (3)
Alert health professionals prior to any procedure, especially dentists. (latex free equipment, patient should be first on the list to reduce the risk of latex exposure, peri-operative antihistamines and corticosteroids may be considered). Avoidance of cross reactive foods. Major occupational health issue.
35
What is advised to people who have latex allergies to carry with them? (2)
Medical alert bracelet. | Epi-pen (self-injectable adrenalin)
36
Who are epi-pens provided to.
Only those who have had anaphylaxis previously.
37
What allergies can desensitisation work for? (2)
Insect venom. | Some aero-allergens (e.g grass pollen)
38
What disorders are associated with recurrent meningococcal menigitis? (2)
Immunological (complement or antibody deficiency). | Neurological (any disruption of the BBB).
39
What immunological disorders are associated with recurrent meningococcal menigitis? (2)
Complement deficiency (recurrent infection with encapsulated organisms e.g. neiseria meningitis, gonococcus, H.influenza, B pneumococcus). Antibody deficiency (recurrent bacterial infections, especially of the upper and lower respiratory tract)
40
What neurological disorders are associated with recurrent meningococcal meningitis? (2)
Occult skull fracture. | Hydrocephalus.
41
What important questions regarding the history of other infections have to be included in a patient presenting with recurring infection?
Serious Persistant Unusual Recurrent
42
What is important to ask about PMH in patients presenting with recurrent meningococcal meningitis? (2)
Neurological disease. | Head injury.
43
What is important to ask about general well being and health in a patient presenting with recurrent meningococcal meningitis? (4)
Energy. Weight loss. Sleep. Work status.
44
What is important to ask in the family history of a patient presenting with meningococcal meningitis? (2)
Consanguinuity. | History of meningitis.
45
What components of the complement would you look for in the blood tests for a patient presenting with meningococcal meningitis? (3
C3 and C4. CH50. AP50.
46
What immunoglobulins would you look for in a patient presenting with meningococcal meningitis? (2)
Serum IgA, IgG, IgM | Protein electrophoresis
47
What is a CH50?
Functional test of integrity of the classic complement cascade. All components of the cascade need to be in place for the test to give a positive (normal) result.
48
What are the components of the classical pathway? (3)
C1 C4 C2
49
What is an AP50?
Functional test of integrity of the alternative complement cascade. All components of the cascade need to be in place for the test to give a positive (normal) result.
50
What are the aspects of the common pathway in the clotting cascade? (5)
C5-9.
51
How would you manage a patient with a deficiency in the clotting pathway (common one)? (3)
Meningovax, pneumovax, HIB. Daily prophylactic penicillin. High level of suspicion.
52
What deficiency is associated with recurrent meningococcal infection?
Any deficiency of the complement pathway. In particular, the alternative pathway and the final common pathway.
53
In a patient who is ANA +ve, what other investigations do you want to do? (3)
dsDNA ENA Cytoplasmic (t-RNA synthetase, SPR, mitochondria).
54
What condition is characterised by ANA +ve and dsDNA +ve
SLE
55
What immunological tests indicate SLE? (2)
ANA +ve | dsDNA +ve
56
What condition is characterised by ANA +ve and ENA +ve? (4)
SLE. Sjogrens. Diffuse cutaneous scleroderma. Myositis.
57
What condition is characterised by ANA +ve and SRP +ve
Myositis
58
What do anti-centromere antibodies suggest?
Limited cutaneous scleroderma.
59
In the context of SLE, what do low levels of C4 and 3 indicate
Active disease.
60
What can be used to determine disease activity in SLE (3)
C4/3 levels (low levels = increased disease activity). | ESR and dsDNA.
61
What tests would you request in a patient with SLE? (3)
``` Urinalysis (proteinurua, microscopic haematuria). Urine microscopy (red cells, red cell casts). Renal biopsy (diffuse proliferative nephritis, immune complex and complement deposition) ```
62
What is the predominant mechanism of disease in terms of the Gel and Coombs classification in SLE?
Type 3 hypersensitivity response (involves complement activation and neutrophil and macrophage infiltration)
63
What drugs can be used to treat SLE? (7)
Prednisolone - widely used immunosuppressant. Azathioprine - widely used anti-proliferative immunosuppressant - check TPMT status before use. Hydrozychloroquine - alters pH and affects antigen presentation/processing. Inhibits production of some cytokines. Upregulates apoptosis/clearance. Rituximab - antibody to CD20 that depletes B cells. IVIG - effective immunosuppressive agent. Precise mechanisms is unclear. Mycophenolate Mofetil - anti-prolieferative immunosuppressant with preferential effect on lymphocytes. Cyclophosphamide - cytotoxic immunosuppressant.
64
Why can adalimumab not be used in the treatment of SLE?
May precipitate cutaneous lupus.
65
What is serum sickness?
Can occur after treatment with penicillin.
66
What is the mechanism of action of serum sickness?
Penicillin can bind to cell surface proteins. Acts as 'neo-antigen' - stimulates very strong IgG antibody response. Individual is 'sensitised' to penicillin. Subsequent exposure to penicillin stimulates formation of immune complexes with circulating penicillin and the production of more IgG antibodies. These immune complexes are then deposited in small vessels (causes small vessel vasculitis)
67
What organs are most affected in small vessel vasculitis? (3)
Renal dysfunction Arthralgia in joints In skin - purpuric vasculitis.
68
How would you confirm a diagnosis of serum sickness? (3)
Low serum C3/C4 Specific IgG to penicillin. Characteristic biopsy features (skin, kidneys)
69
What does low serum C3 and C4 indicate in serum sickness
Indicative of classical complement pathway activation.
70
What is seen on biopsy in a patient with suspected serum sickness (2)
Infiltration of macrophages and neutrophils | Deposition of IgG, IgM and complement.
71
Who is renal function affected in serum sickness?
Deposition of immune complexes causes local complement activation and neutrophil and macrophage infiltration. Results in inflamamtion of the glomeruli. Results in increase in serum creatinine, proteinuria and haematuria.
72
Who can patients become disorientated with serum sickness?
Small vessel vasculitis affects cerebral vessels and may compromise oxygen supply to the brain.
73
Who do patients with serum sickness develop purpura?
Inflamed blood vessels are likely to leak resulting in local haemorrhage. Vessels also become plugged with clots, further compromising oxygen delivery.
74
How would you manage a patient with serum sickness. (3)
Discontinue penicillin immediately. Decrease systemic inflammation with corticosteroids. Ensure appropriate fluid balance.
75
What does recurrent upper and lower respiratory tract infections with failure to thrive indicate?
An immunodeficiency.
76
What are the features that are suggestive of an immunodeficiency? (7)
Severe infections. Recurrent minor infections/failure to respond to conventional antibiotics. Evidence of early end-organ damage. Unusual organisms. Opportunistic organisms. Unusual sites of infection. Concomitant problems (e.g. failure to thrive, family history, etc...)
77
What factors can cause a child to have too many infections? (4)
Allergic rhinitis, sinusitis, asthma. Non-immunological disorders (cystic fibrosis, local factors e.g. foreign body, ciliary disorders). Over estimation of infections. Immune deficiency.
78
What investigations would you do in a child presenting with a history of recurrent infections? (7)
``` FBC U&Es, creatinine LFTs CRP Sweat test (CF) CXR Immunoglobulins ```
79
How can you quantify lymphocyte populations?
Flow cytometry using lymphocyte surface markers.
80
What is a-gamma-globulinaemia
X-linked cause of immunodeficiency. | Failure of pre-B-cells to mature in bone marrow, so failure to produce any immunoglobulin.
81
What is the management of agammaglobulinaemia
Immunoglobulin replacement therapy
82
What does immunoglobulin replacement therapy involve? (3)
Pooled serum immunoglobulins. Administered every 3 weeks. Indefinite treatment.
83
64year old lady seen in A&E after slipping and injuring her left hip when getting out of the bath. Swollen, tender hip with marked limitation of movement. Clinically anaemic. Persistent back pain and generalised lethargy for 12 months. Three episodes of pneumococcal pneumonia in last 2 years. Post-menopausal – on HRT. What is the differential diagnosis?
Multiple myeloma. Osteoporosis and Sjogren's syndrome. Osteoporosis and SLE
84
What bone lesion is characteristic of multiple myeloma
Punched out/lytic lesions.
85
What is multiple myeloma
Neoplastic proliferation of plasma cells, resulting in massive expansion of single plasma cell clone.
86
What are the biochemical markers of multiple myeloma? (3)
Production of excess amounts of a single immunoglobulin molecule with single specificity (usually both heavy chain and light chain) Increased numbers of abnormal plasma cells in the bone marrow. Lytic lesions of bone.
87
What are patients with multiple myeloma susceptible to recurrent infections?
Suppression of production of normal immunoglobulin by the malignant close results in functional antibody deficiency - known as immune paresis.
88
Why do patients with multiple myeloma tend to be anaemic? (2)
Space limitation - expansion of malignant clone crowds out normal red cell and white cell precursors in the bone marrow. Inhibitors - tumours may produce local cytokines which inhibit normal bone marrow function.
89
What does ESR measure?
Measures the rate of fall or erythrocytes through plasma. Normally, erythrocytes do not clump - repellent negative surface charge > attractant charge of the plasma constituents. However, if protein constituents of plasma increase or change - increases attract charge, causes erythrocytes to clump together, and clumped erythrocytes fall more quickly through the plasma....further increasing the ESR.
90
What blood film abnormality can you see in multiple myeloma?
Rouleaux formation of RBCs.
91
When do you have a high index of suspicion for multiple myeloma?
Unusual or vertebral fractures.
92
What are some initial clues that point towards a diagnosis of multiple myeloma? (3)
Anaemia. High ESR. High calcium.
93
What investigations need to be done in a patient you suspect of having multiple myeloma? (3)
Igs and electrophoretic strip. Urinary BJP. Skeletal survey.
94
32 year old lady. 3 month history Pain and stiffness of joints - Particularly hands. Previously entirely well Recently given birth. Family history of gout and rheumatoid arthritis. Smokes 20/day. Anti-CCP >300. Raised ESR. What is the diagnosis?
Rheumatoid arthritis.
95
What is rheumatoid arthritis?
Peripheral, symmetrical, polyarthritis with stiffness.
96
How long do you need to have symptoms of rheumatoid arthritis for a diagnosis to be made?
6 weeks.
97
What tissue markers may rheumatoid arthritis be associated with? (2)
Rheumatoid factor. | Anti-CCP antibodies.
98
When can rheumatoid arthritis present suddenly?
Post-partum.
99
What is rheumatoid factor?
Antibody directed at the Fc region of human IgG. Assays usually look for IgM RF although patients may sometimes also have IgG and IgA RF. Approximately 60-70% sensitive. Approximately 60-70% specific (found in other diseases)
100
What is anti-CCP antibody (cyclic citrullinated protein)
Arginine residues may be deiminated to form citrulline residues by peptidyl arginine deiminase (PADI) enzymes. Polymorphisms within PADI enzymes may increase generation of citrullinated residues in patients who develop RA. Loss of tolerance to the citrullinated residues results in production of antibodies specific for citrullinated proteins in ~60-70% individuals (sensitivity similar to RF). Development of anti-citrullinated peptide antibodies is associated with RA in ~95% individuals (highly specific)
101
What are the genetic factors that predispose to rheumatoid arthritis? (4)
``` Twin concordance (30% identical, 5% non-identical). HLA-DR4 (present in 60-70% of patients). PADI type 2 and 4. PTPN 22 (lymphocyte specific tyrosine phosphatase) ```
102
What HLADR4 subtypes predispose to rheumatoid arthritis? (4)
DR1, DW4, DW14, DW15
103
What conditions does PTPN22 predispose to? (3)
Rheumatoid arthritis. SLE. T1DM.
104
What is first-line treatment for rheumatoid arthritis?
Disease modifying drugs to include methotrexate. Sulphasalazine, hydroxychloroquine, leflunomide also frequently used in addition or if methotraxate is not tolerated.
105
What further treatment is available for patients with rheumatoid arthritis if DMARDs do not work/are not tolerated? (4)
TNF alpha antagonsit - inhibits downstream events in inflammation. Rituximab - antibody specific CD20 - depletes B cells. Abatacept - CTLA-4 Ig fusion protein which binds to ligands of CD28 and thereby inhibits T cell activation. Tocilizumab - antibody specific for IL-6 receptor - widespread effects.
106
What must be done before starting a patient with rheumatoid arthritis on immunosuppressive medication? (2)
Consider risk of infection, especially prior to use of biologic agents. Consider risk of malignancy.

Kat's Pathology (105 decks)

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