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Clinical Sciences Flashcards

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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
What are Type IV hypersensitivity reactions?
T-Cell mediated Delayed
26
List 4 diseases caused by Type IV hypersensitivity reactions
T1DM MS RA Crohn's
27
What is Type V hypersensitivity?
IgG mediated tissue damage Graves', MG
28
What are skin prick tests used for?
Food Allergies Pollen Insect venom (bee stings etc.) Take 15 mins Histamine pos. control & H2O neg. control used alongside ?allergen
29
What is RAST?
Radioallergosorbent testins Grades level of IgE response to allergens Food, Pollen, Insect venom Graded 0 (negative) to 6 (strongly positive).
30
What is skin patch testing used for?
Contact dermatitis
31
What are monocytes
APCs produced in BM Migrate via blood to tissues where they differentiate to macrophages
32
What roles do IgG antibodies have?
Activate Classical complement pathway Bind to macrophages & neutrophils for enhanced phagocytosis Bind to NK Cells for antibody-dependent cytotoxicity
33
Which antibodies can cross the placenta?
IgG
34
What roles do IgA antibodies have?
Blocks attachment of bacteria/viruses to mucous membranes preventing internalisation Exist in bodily secretions Activates Alternative complement pathway
35
What roles do IgM antibodies have?
First antibody produced in acute immune response Can activate classical complement pathway Some exist on surface of B cells as BCRs
36
What roles do IgD antibodies have?
Found on surface of B-Cells as B-Cell receptors Prevent B-cells from generating autoantibodies
37
What roles do IgE antibodies have?
Bound to Basophils/Mast cells Parasitic reactions (Opsonise eosinophils vs parasites/arthropods) Promote inflammation in external mucous membranes
38
What is deficient in Chronic Granulomatous Disease, Chediak-Higashi Syndrome and Leukocyte adhesion deficiency?
Neutrophils
39
What is deficient in IgA Def., bruton's congenital Agammaglobulinaemia and Common variable immunodeficiency?
B-Cells
40
What is deficient in DiGeorge's and which infections are patients most susceptible to?
T-Cells Viral & Fungal
41
Which immunodeficiency disorders are of mixed T/B cell pathophysiology?
Severe Combined Ataxic telangiectasia Wiskott-Aldrich Syndrome
42
Describe the inheritance and presentation of Wiskott-Aldrich Syndrome
X-Linked recessive WASP gene mutation Recurrent bacterial infections, eczema and thrombocytopenia with low plasma IgE
43
What are ANCA?
Anti-neutrophil cytoplasmic antibodies. P=Perinuclear C=Cytoplasmic
44
Which 2 diseases are most strongly associated with cANCA and what is the most common chemical target?
Wegener's Granulomatosis Microscopic Polyangiitis Serine Proteinase 3 cANCA levels = marker of disease activity
45
Which diseases are most commonly associated with pANCA and what is the most common chemical target?
Immune Crescentic Glomerulonephritis Microscopic Polyangiitis Churg-Strauss Wegener's (weakly vs cANCA) Myeloperoxidase
46
What is complement?
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
Which protein is, when activated, the catalyst for the major amplification step of the complement cascade?
C3
48
What is C1 inhibitor protein deficiency?
Complement deficiency resulting in Hereditary Angioedema. Uncontrolled bradykinin release leads to tissue oedema.
49
Which components are present in the classical complement pathway?
C1q C1rs C2 C4
50
Which diseases are caused by deficiency of the components of the classical pathway of complement?
Immune complex disease ie. SLE, Henoch-Schonlein purpura (C2 most common - almost all C2 deficient pts have SLE)
51
What happens with C3 deficiency?
Recurrent Bacterial infections Especially encapsulated bacteria (Mening. Haemoph., Streptoc.)
52
Which disease is caused by C5 deficiency?
Leiner Disease A long-term seborrheic dermatitis associated with increased susceptibility to infection (incl. disseminated meningococcal), diarrhoea and wasting.
53
What occurs with C5-C9 Deficiency (Terminal common pathway)?
Cannot form MAC Prone to: Neisseria meningitides Haemophilus influenza Steptococcus pneumoniae
54
How is anion gap calculated?
(Na+K)-(Cl+HCO3-) Pos - Neg Normal = 10-18
55
What are the main causes of a normal anion gap metabolic acidosis?
GI Bicarb Loss RTA Drugs (Acetazolamide = common) Ammonium Chloride injection (used in sev. met. alkalosis) Addison's
56
What are the main causes of a raised anion gap metabolic acidosis?
Lactic acidosis Ketoacidosis Uric (renal failure) Acid Poisoning (salicylates, methanol)
57
What may cause a metabolic alkalosis?
Vomiting/Aspiration Diuretics Hypokalaemia Prim. Hyperaldosteronism Con. Adrenal hyperplasia Cushing's Bartter's
58
What is the difference between osmolality and omsolarity
Osmolality = Total particles/kg (measured with osmometer in mmol/kg) Osmolarity = total particles /L (calculated 2(Na+K)+Urea+Glucose)
59
Why is knowing both osmolarity and osmolality useful?
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
How are true vs pseudo hyponatraemia differentiated?
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
What is TURP syndrome?
Glycine 1.5% is used to irrigate the prostate during resection. If this is absorbed and metabolised, leads to hyponatraemia
62
What is the first step in assessing a true hyponatraemia?
Assess volume status
63
How would you assess and treat a hypervolaemic hyponatraemia?
Check urinary Sodium If >20 = ?Renal = AKI/CKD If <20 = ?Non-Renal = Cardiac Failure/Cirrhosis/Too much IVI Fluid Restrict +/- Diuresis Specialist input
64
How quickly can hyponatraemia be corrected and what is the risk?
8-10mMol/24h Theoretical risk of central pontine myelinolysis (pseudobulbar palsy - evidence is limited)
65
How is euvolaemic hyponatraemia assessed?
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
What can cause SIADH?
Malignancy - Small cell lung most common, pancreatic, prostatic, lymphoma CNS pathologies TB, Pneumonia, Chest abscess Drugs
67
Which drugs can cause SIADH?
Opiates SSRIs TCAs Carbamazepine PPIs
68
How do you treat SIADH?
Fluid restrict + Treat the cause
69
How would you assess hypovolaemic hyponatraemia?
Urinary Sodium If low - D/V, Ascites/Burns (£rd spacing) - Kidney is working if high - Diuretics, Addison's, Salt-losing nephropathies
70
How does Cirrhosis cause hyponatraemia?
Poor breakdown of vasodilators (eg. NO) = Low BP = More ADH = Water retention = Dilution
71
How does Cardiac Failure cause hyponatraemia?
Low CO = ADH release = Water retention = Dilution BNP also natriuretic which worsens this effect
72
What are the main causes of hypernatraemia?
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
How are central/nephrogenic diabetes insipidus treated?
Central = Desmopressin Nephrogenic = Thiazide Diuretics (paradoxical)
74
Which drugs most commonly cause hyperkalaemia?
K-Sparing Diuretics (Spironolactone) ACEi Cyclosporin
75
What are the main causes of hyperkalaemia?
AKI Drugs Metabolic Acidosis Addison's Rhabdomyolysis Massive Transfusion
76
What may cause hypokalaemia with alkalosis?
Vomiting Diuretics Cushing's Conn's
77
What may cause hypokalaemia with acidosis?
Diarrhoea RTA Acetazolamide Partially Treated DKA
78
What is Type 1 RTA?
Distal failure of H+ excretion = acidosis & hypokalaemia Failure of hydrogen-K pump
79
What is type 2 RTA?
Proximal bicarb resorption failure -> acidosis -> hypokalaemia
80
What is type 4 RTA?
Aldosterone deficiency/resistance = acidosis and hyperkalaemia
81
What are the main causes of hypomagnasaemia?
Diuretics TPN Diarrhoea Alcohol Hypokalaemia Hypocalcaemia
82
What are the main causes of hypophosphataemia?
Alcohol Excess Liver Failure DKA Refeeding Prim. Hyperparathyroidism Osteomalacia
83
Where is calcitonin secreted and what does it do?
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
What does PTH do?
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
What does vitamin D do
Increased renal tubular resorption or Ca and Po4 Increases gut absorption of Ca Increases osteoclast activity

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