Session 8 Flashcards

1
Q

Postganglionic neurone neurotransmitter for sympathetic and para branch?

What acts on the m centre?

A

Sympathetic-noradrenaline
Para-ACH

Cortical micturation centre

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2
Q

Two types of kidney failure?

Secondary glomerular injury?

Role of mesangial cells in glomerulus?

A

Blockage of filter or leaking filter (proteinurea/haematurea)

Doesn’t occur at glomerulus but pathology at another site later effects it.

Scaffolding and maintains integrity with nutrient entry.

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3
Q

What is nephrotic syndrome? Symptoms?

Same for nephritic syndrome?

Site of injury in nephrotic?

A

When the kidney looses >3.5grams of albumin in 24 hours to urine. Oedema, hypoalbuminaemia and hypercholestremia.

Acute renal failure,blood in urine, hypertensive,reduced GFR

Subepithelial/podocyte

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4
Q

Primary causes of nephrotic syndrome? Notes on all? Microscopy?

Secondary causes?

A

Minimal change glomerulonephritis-childhood-nephrotic/proteinurea. Foot processes retracted on podocytes.

Focal segmental glomerulosclerosis-scaring of kidney progressive to renal failure.

Membranous glomerulonephritis-immune complex deposits. Can be secondary. Spikes podocytes. PLA2-r antigen on podocytes.

Diabetes mellitus

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5
Q

Causes ofhaematuria? Notes?

Causes of nephritic syndrome? Note that the two above are nephritic.

A

IgA nephropathy-realtionship with mucosal membrane infections, proteinurea, progress to renal failure, deposition of IgA immune complexes causes mesangial cell damage causing leaky to blood. Usually nephrotic.

Thin GBM or Alport (x linked,abnormal collagen IV,abnormal GBM,progress to renal failure).

Vasculitis- systemic disorder associated with ANCA. Subendothelium.

Goodpasture disease-anti GBM disease, causes RPGM, antibodies to a3 chain of type 4 collagen in GBM.

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6
Q

Is glomerulonephritis nephritic or nephrotic?

Causes?

Difference between nephrotic and nephritic?

A

Both

ANCA vasculitis, IgA nephropathy (nephritic), minimal change (nephrotic)

Nephrotic=damage to podocytes leading to proteinurea
Nephritic=inflammation of GBM leading to haematuria

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7
Q

How manage nephrotic syndrome?

Nephritic?

A

Diuretics/ACE inhibitor-to cure oedema.
Steroids-minimal change disease.

BP control with ACE inhibitors.
Immunosuppressants (prednisolone)

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8
Q

What is systemic lupus Erythematosus?

What happens in diabetic nephropathy?

A

Autoimmune causing nephrotic/nephritic.

Kiemelstiel-Wilson nodules (sclerotic areas), thickened GBM, Mesangial expansion, no foot processes, hyperalbuminurea.

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9
Q

Pathology in diabetic nephropathy?

A

Hyper filtration and capillary hypertension/increase GFR.
GBM thickens. (Top two due to hyperglycaemia and glomerularhypertension)
Mesangial expansion.
Podocyte injury.
Glomerular sclerosis and arteriosclerosis.

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10
Q

Relevance of microalbuminurea?

Overt proteinurea?

A

Reversible diabetic nephropathy

Non-reversible

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11
Q

Risk factors for diabetic nephropathy?

Primary prevention?

Managing proteinurea?

A

Race,genetic,hypertension,age,hyperglycaemia

BG control

Inhibiting RAAS-reduces hyperfiltration-because angiotensin II increases glomerular permeability to proteins.

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12
Q

When you get periorbital oedema?

What does low GFR do to creatinine serum?

A

Nephrotic syndrome (minimal change GN)

Higher

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