Preena Joshi

Question 1

Pathophysiology of rheumatic fever

Answer 1

Autoimmune inflammatory process that develops as a result of streptococcal infection

Cross react with M proteins

Molecular mimicry accounts for the tissue injury that occurs in rheumatic fever- a foreign antigen shares sequence or structural similarities with self-antigens. One proposed mechanism is the expression of T cell receptors on a single T cell. These have dual reactivity leaving the host vulnerable to autoimmune responses

Question 2

How do NSAIDs cause ulcers?

Answer 2

NSAIDs work by inhibiting Cox 1 and 2. Cox1 is present in the majority of cells including endothelial cells, GI cells and platelets. Cox 2 is present in a few cells and is induced by inflammation. NSAIDs inhibit Cox enzymes in the GIT leads to a reduction of PG secretion and its cytoprotective effects in the gastric mucosa and therefore you get mucosal injury and peptic ulcers.

Question 3

Pathophysiology of SLE

Answer 3

global loss of self-tolerance with activation of autoreactive T and B cells (caused by innate immune system). This results in the production of pathogenic autoantibodies, which attack self-tissues and cause the symptoms of gout. Autoimmune antibodies are made against nucleic acids and their binding proteins, which results in the loss of self-tolerance. The autoantigen and autoantibody complexes bind to a Fc receptor, which leads to the activation of the innate immune system, causing the release of inflammatory cytokines.

Question 4

Presentation of SLE

Answer 4

• Arthritis
• Malaise
• Fatigue
• Fevers
• Rash- photosensitive butterfly rash
• Hair loss
• Swollen lymph nodes
• Renal disease
• Weight loss
• Chest pains due to pleuritis or pericarditis
• Abdominal pain
• Headache
• Mood disorder
• Confusion
• Psychosis
• Seizure
• Stroke
• Ulcers in the mouth and nose

Question 5

Management of SLE

Answer 5

• NSAIDs
• Hydroxycholoquini ne (DMARD)
• Corticosteroids
• Immunosuppressive drugs e.g. azathioprine
• Biological agents e.g. rituximab and TNF-a inhibitors
• IV immunoglobulin in special cases

Question 6

Dx of SLE

Answer 6

• Positive anti-nuclear antibody test
• Positive anti-double strand DNA test
• Positive anti-Smith antibody test
• Positive anti-Ro antibody test
• Positive antiphospholipid antibody test
• FBC: Leukopenia, Lymphopenia, Thrombocytopenia, Anaemia
• ESR
• False positive for syphilis

Question 7

complications of SLE

Answer 7

skin scarring, joint deformities, kidney failure, stroke, heart attack, pregnancy complications due to renal disease, hip destruction- avascular necrosis, cataracts, bone fractures.

Question 8

what is the antinuclear antibodies blood test?

Answer 8

Antibodies that attack the nucleus of cells. Found in autoimmune conditions. A homogenous pattern is associated with dsDNA antibodies, while a speckled pattern relates to extractable nuclear antigens

Question 9

what is the anti-dsDNA blood test?

Answer 9

ELISA for the dsDNA in Crithidia lucilae- autoantibody that is associated with SLE.

Question 10

Pathophysiology of nephrotic syndrome

Answer 10

Loss of significant volumes of proteins via the kidneys, resulting in hypoalbuminaemia, damage to glomerular filtration barrier.

Question 11

clinical features of nephrotic syndrome

Answer 11

peripheral oedema, facial oedema, frothy urine, fatigue, poor appetite, recurrent infections, proteinuria (>3.5g/day), hypoalbuminaemia (serum albumin<30g/L), venous/arterial thrombosis due to hypercoagulability caused by the hypoalbulinaemia, xanthelasma, leukonychia, SOB

Question 12

Mx of nephrotic syndrome

Answer 12

dietary sodium restriction, fluid restriction <1.5l/day, diuretics- first line oral loops e.g furosemide, 2nd line thiazides e.g. metolazone. Antiproteinuric therapy- RAAS inhibitor e.g. ACEi ramipril to slow progression and reduce HT, statins to reduce hyperlipidaemia.

Question 13

pathophysiology of nephritic syndrome

Answer 13

Condition involving haematuria, mild to moderate proteinuria (<3.5g/day), hypertension, oliguria and red cell casts in the urine. Glomerular damage

Question 14

clinical features of nephritic syndrome

Answer 14

o More abrupt onset
o Raised JVP
haematuria, oedema, reduced urine output, uraemic symptoms e.g. reduced appetite, fatigue, pruritis, nausea).

Question 15

difference between nephrotic and nephritic syndrome

Answer 15

nephrotic syndrome- protein loss, nephritic- RBCs in urine

Question 16

clinical features of antiphospholipid syndrome

Answer 16

• Blood is sticker than normal
• High BP
• DVT
• Stroke or TIA
• MI
• PE
• Balance and mobility problems
• Vision disturbances such as double vision
• Speech and memory problems
• Pins and needles in arms or legs
• Fatigue
• Headaches and migraines
• Superficial thrombophlebitis- inflammation of the veins just under the skin. Symptoms are similar to a DVT- swelling, redness and tenderness along vein, temperature.

mnemonic to remember:
o	Coagulation defect
o	Livedo reticularis
o	Obstetric- recurrent miscarriage 
o	Thrombocyotpenia

Question 17

Tx of antiphospholipid syndrome

Answer 17

low dose aspirin or warfarin aiming for an INR of 2-3.

Question 18

Pathophysiology of membranous nephropathy

Answer 18

small vessels in the glomerulus become damaged and thickened, which leads to proteinuria. Occurs via the same mechanism as LN.