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MRCP > Clinical Sciences > Flashcards

Clinical Sciences Flashcards

1
Q

On which chromosomes are the genes which encode for HLA proteins?

A

6

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2
Q

What is the difference between MHC Class I and Class II?

A

Class 1 = Surface of all cells, Allow for Cytotoxic/NK T cells to rcognisde viral/tumour antigens produced within the cell, CD8

Class 2 = Surface of APCs, involved in antigen presenting of extracellular pathogens, CD4

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3
Q

Which diseases are most associated with HLA B27?

A

AS
Post-gonococcal Arthritis
Acute Anterior Uveitis
Reactive Arthritis

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4
Q

Which disease are most associated with HLA DR2?

A

Narcolepsy
Goodpasture’s

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5
Q

Which diseases are most associated with HLA DR3?

A

Autoimmune hepatitis
PBC
T1DM
Dermatitis Herpetiformis
Coeliac
Sjogren’s

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6
Q

Which diseases are most associated with HLA DR 4?

A

RA
T1DM

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7
Q

Which disease is most associated with HLA DR3 and 4 together?

A

T1DM

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8
Q

Which disease is most associated with HLA B47?

A

21-hydroxylase deficiency

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9
Q

Which diseases are most associated with HLA A3?

A

Haemochromatosis

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10
Q

Which HLA is associated with Behcet’s?

A

HLA-B5

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11
Q

What is Felty’s Syndrome?

A

Triad of:
RA
Splenomegaly
Neutropaenia

Highly associated with HLA DR4

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12
Q

What are CD1 molecules?

A

HLA molecules with present lipid molecules

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13
Q

What are CD2 molecules?

A

Found on thymocytes, T cells and some NK cells

Act as a ligand for CD58 and CD59 - signal transduction and cell adhesion

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14
Q

What are CD3 molecules?

A

The signalling component of the T-Cell Receptor

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15
Q

What are CD4 molecules?

A

Co-receptor for MHC Class I

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16
Q

Which receptors are used by HIV units to enter T Cells?

A

CD4

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17
Q

What are CD8 molecules?

A

Co_receptor for HLA Class I
Also found on a subset of myeloid dendritic cells.

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18
Q

What are type I hypersensitivity reactions?

A

IgE mediated anaphylactic reaction provoked by re-exposure to an allergen. Allergies, Hayfever etc = type 1

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19
Q

Which anaphylactoid reactions aren’t IgE mediated?

A

NSAIDs, IV Contrast, Opioids, Exercise-allergy

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20
Q

How do NSAIDs cause anaphylactoid reactions if not IgE mediated?

A

COX-1 inhibition -> Reduced prostanglandins, more leukotrienes = bronchoconstriciton, urticaria and pruritus

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21
Q

What are Type II hypersensitivity reactions?

A

IgG/IgM Mediated
Antibody reacts with cell/matrix associated self-antigen.
Leads to tissue damage/receptor blockade/receptor activation

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22
Q

Which test would be positive in autoimmune haemolytic anaemias and which HS type are they?

A

Direct Coombs
Type II

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23
Q

What are type III hypersensitivity reactions?

A

IgG/IgM immune complex mediated (Ab vs Soluble Ag)

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24
Q

List 4 disease caused by Type III HS reactions

A

Mixed essential Cryoglobulinaemia
Serum Sickness
Polyarteritis Nodosa
SLE

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25
Q

What are Type IV hypersensitivity reactions?

A

T-Cell mediated
Delayed

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26
Q

List 4 diseases caused by Type IV hypersensitivity reactions

A

T1DM
MS
RA
Crohn’s

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27
Q

What is Type V hypersensitivity?

A

IgG mediated tissue damage
Graves’, MG

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28
Q

What are skin prick tests used for?

A

Food Allergies
Pollen
Insect venom (bee stings etc.)

Take 15 mins
Histamine pos. control & H2O neg. control used alongside ?allergen

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29
Q

What is RAST?

A

Radioallergosorbent testins
Grades level of IgE response to allergens
Food, Pollen, Insect venom

Graded 0 (negative) to 6 (strongly positive).

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30
Q

What is skin patch testing used for?

A

Contact dermatitis

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31
Q

What are monocytes

A

APCs produced in BM
Migrate via blood to tissues where they differentiate to macrophages

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32
Q

What roles do IgG antibodies have?

A

Activate Classical complement pathway

Bind to macrophages & neutrophils for enhanced phagocytosis

Bind to NK Cells for antibody-dependent cytotoxicity

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33
Q

Which antibodies can cross the placenta?

A

IgG

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34
Q

What roles do IgA antibodies have?

A

Blocks attachment of bacteria/viruses to mucous membranes preventing internalisation

Exist in bodily secretions

Activates Alternative complement pathway

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35
Q

What roles do IgM antibodies have?

A

First antibody produced in acute immune response

Can activate classical complement pathway

Some exist on surface of B cells as BCRs

36
Q

What roles do IgD antibodies have?

A

Found on surface of B-Cells as B-Cell receptors
Prevent B-cells from generating autoantibodies

37
Q

What roles do IgE antibodies have?

A

Bound to Basophils/Mast cells
Parasitic reactions (Opsonise eosinophils vs parasites/arthropods)
Promote inflammation in external mucous membranes

38
Q

What is deficient in Chronic Granulomatous Disease, Chediak-Higashi Syndrome and Leukocyte adhesion deficiency?

A

Neutrophils

39
Q

What is deficient in IgA Def., bruton’s congenital Agammaglobulinaemia and Common variable immunodeficiency?

A

B-Cells

40
Q

What is deficient in DiGeorge’s and which infections are patients most susceptible to?

A

T-Cells
Viral & Fungal

41
Q

Which immunodeficiency disorders are of mixed T/B cell pathophysiology?

A

Severe Combined
Ataxic telangiectasia
Wiskott-Aldrich Syndrome

42
Q

Describe the inheritance and presentation of Wiskott-Aldrich Syndrome

A

X-Linked recessive
WASP gene mutation
Recurrent bacterial infections, eczema and thrombocytopenia with low plasma IgE

43
Q

What are ANCA?

A

Anti-neutrophil cytoplasmic antibodies.
P=Perinuclear
C=Cytoplasmic

44
Q

Which 2 diseases are most strongly associated with cANCA and what is the most common chemical target?

A

Wegener’s Granulomatosis
Microscopic Polyangiitis
Serine Proteinase 3

cANCA levels = marker of disease activity

45
Q

Which diseases are most commonly associated with pANCA and what is the most common chemical target?

A

Immune Crescentic Glomerulonephritis
Microscopic Polyangiitis
Churg-Strauss
Wegener’s (weakly vs cANCA)

Myeloperoxidase

46
Q

What is complement?

A

A group of 20 tightly regulated, linked proteins produced in the liver and present as inactive molecules in the circulation.

When triggered, enzymatically activate other proteins in a biological cascade resulting in a rapid, highly amplified immune response resulting in the formation of a ‘membrane attack complex’ which punctures holes in bacterial cell membranes.

47
Q

Which protein is, when activated, the catalyst for the major amplification step of the complement cascade?

A

C3

48
Q

What is C1 inhibitor protein deficiency?

A

Complement deficiency resulting in Hereditary Angioedema.

Uncontrolled bradykinin release leads to tissue oedema.

49
Q

Which components are present in the classical complement pathway?

A

C1q
C1rs
C2
C4

50
Q

Which diseases are caused by deficiency of the components of the classical pathway of complement?

A

Immune complex disease ie. SLE, Henoch-Schonlein purpura

(C2 most common - almost all C2 deficient pts have SLE)

51
Q

What happens with C3 deficiency?

A

Recurrent Bacterial infections
Especially encapsulated bacteria (Mening. Haemoph., Streptoc.)

52
Q

Which disease is caused by C5 deficiency?

A

Leiner Disease
A long-term seborrheic dermatitis associated with increased susceptibility to infection (incl. disseminated meningococcal), diarrhoea and wasting.

53
Q

What occurs with C5-C9 Deficiency (Terminal common pathway)?

A

Cannot form MAC
Prone to:
Neisseria meningitides
Haemophilus influenza
Steptococcus pneumoniae

54
Q

How is anion gap calculated?

A

(Na+K)-(Cl+HCO3-)
Pos - Neg
Normal = 10-18

55
Q

What are the main causes of a normal anion gap metabolic acidosis?

A

GI Bicarb Loss
RTA
Drugs (Acetazolamide = common)
Ammonium Chloride injection (used in sev. met. alkalosis)
Addison’s

56
Q

What are the main causes of a raised anion gap metabolic acidosis?

A

Lactic acidosis
Ketoacidosis
Uric (renal failure)
Acid Poisoning (salicylates, methanol)

57
Q

What may cause a metabolic alkalosis?

A

Vomiting/Aspiration
Diuretics
Hypokalaemia
Prim. Hyperaldosteronism
Con. Adrenal hyperplasia
Cushing’s
Bartter’s

58
Q

What is the difference between osmolality and omsolarity

A

Osmolality = Total particles/kg (measured with osmometer in mmol/kg)

Osmolarity = total particles /L (calculated 2(Na+K)+Urea+Glucose)

59
Q

Why is knowing both osmolarity and osmolality useful?

A

Osmolality and Osmolarity should roughly equate, with osmolality being an exact measured figure.

Physiological solutes should just be Na, K, Cl, HCO3, Urea and Glucose.

If there is a difference (raised osmolar gap) then we can assume there are pathological solutes in the blood, such as glucose, ethanol or mannitol.

60
Q

How are true vs pseudo hyponatraemia differentiated?

A

Serum Osmolality
Would be low if true

Lab machines measure Na/Volume and assume it is Na/Water

If Osmolarity = normal/high there is increased volume due to protein/lipid/extra solutes. As such total volume is bigger but Na remains the same, hence is reported by the lab as having been diluted.

61
Q

What is TURP syndrome?

A

Glycine 1.5% is used to irrigate the prostate during resection.

If this is absorbed and metabolised, leads to hyponatraemia

62
Q

What is the first step in assessing a true hyponatraemia?

A

Assess volume status

63
Q

How would you assess and treat a hypervolaemic hyponatraemia?

A

Check urinary Sodium
If >20 = ?Renal = AKI/CKD
If <20 = ?Non-Renal = Cardiac Failure/Cirrhosis/Too much IVI

Fluid Restrict +/- Diuresis
Specialist input

64
Q

How quickly can hyponatraemia be corrected and what is the risk?

A

8-10mMol/24h
Theoretical risk of central pontine myelinolysis (pseudobulbar palsy - evidence is limited)

65
Q

How is euvolaemic hyponatraemia assessed?

A

Check:
TFTs
Short Synacthen
Paired urine/serum osmolality

Can be hypothyroid, addison’s

If not + high uNa + High urine osmolality + low plasma osmolality = ?SIADH

66
Q

What can cause SIADH?

A

Malignancy - Small cell lung most common, pancreatic, prostatic, lymphoma

CNS pathologies

TB, Pneumonia, Chest abscess

Drugs

67
Q

Which drugs can cause SIADH?

A

Opiates
SSRIs
TCAs
Carbamazepine
PPIs

68
Q

How do you treat SIADH?

A

Fluid restrict + Treat the cause

69
Q

How would you assess hypovolaemic hyponatraemia?

A

Urinary Sodium
If low - D/V, Ascites/Burns (£rd spacing) - Kidney is working

if high - Diuretics, Addison’s, Salt-losing nephropathies

70
Q

How does Cirrhosis cause hyponatraemia?

A

Poor breakdown of vasodilators (eg. NO)
= Low BP
= More ADH
= Water retention = Dilution

71
Q

How does Cardiac Failure cause hyponatraemia?

A

Low CO = ADH release
= Water retention = Dilution

BNP also natriuretic which worsens this effect

72
Q

What are the main causes of hypernatraemia?

A

Hypovolaemic =
Low uNa = GI/Skin Losses
High uNA = Loop Diuretics, osmotic Diuresis (HHS), DI, Renal

Euvolaemic = DI, Skin/Breathing losses

Hypervolaemia = Conn’s, IVI

73
Q

How are central/nephrogenic diabetes insipidus treated?

A

Central = Desmopressin
Nephrogenic = Thiazide Diuretics (paradoxical)

74
Q

Which drugs most commonly cause hyperkalaemia?

A

K-Sparing Diuretics (Spironolactone)
ACEi
Cyclosporin

75
Q

What are the main causes of hyperkalaemia?

A

AKI
Drugs
Metabolic Acidosis
Addison’s
Rhabdomyolysis
Massive Transfusion

76
Q

What may cause hypokalaemia with alkalosis?

A

Vomiting
Diuretics
Cushing’s
Conn’s

77
Q

What may cause hypokalaemia with acidosis?

A

Diarrhoea
RTA
Acetazolamide
Partially Treated DKA

78
Q

What is Type 1 RTA?

A

Distal failure of H+ excretion = acidosis & hypokalaemia

Failure of hydrogen-K pump

79
Q

What is type 2 RTA?

A

Proximal bicarb resorption failure -> acidosis -> hypokalaemia

80
Q

What is type 4 RTA?

A

Aldosterone deficiency/resistance = acidosis and hyperkalaemia

81
Q

What are the main causes of hypomagnasaemia?

A

Diuretics
TPN
Diarrhoea
Alcohol
Hypokalaemia
Hypocalcaemia

82
Q

What are the main causes of hypophosphataemia?

A

Alcohol Excess
Liver Failure
DKA
Refeeding
Prim. Hyperparathyroidism
Osteomalacia

83
Q

Where is calcitonin secreted and what does it do?

A

C Cells (parafollicular) in thyroid

On osteoclasts: Causes contraction = limited ability to resorb bone = low Ca (short term effect)

On tubules: Increased diuresis/reduced resorption = low Ca/Po4

84
Q

What does PTH do?

A

Increases:
Renal tubular reabsorption of calcium
Osteoclastic activity
Renal hydroxylation of 25-hydroxy-vit d to 1,25-dihydroxy-vit d
Reduces renal phosphate resorption

85
Q

What does vitamin D do

A

Increased renal tubular resorption or Ca and Po4

Increases gut absorption of Ca
Increases osteoclast activity

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