Glomerular disease, Tubulointerstitial nephritis and UTI Flashcards

1
Q

Describe the normal glomerular membrane. (3)

A

Glomerular capillaries lined by fenestrated endothelium that rests on the glomerular basement membrane.
Podocytes are are the visceral epithelial cells of the Bowman’s capsule that make contact with the GBM with finger like projections called foot processes.
This accounts for the tremendous permeability.

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2
Q

What is GFR? (2)

A

Glomerular filtration rate

The permeability of the glomerulus; how much filtrate is formed every minute.

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3
Q

What site difference between glomerulonephritis and glomerulopathies? (1)

A

Glomerulonephritis has inflammation of the glomeruli, glomerulopathies does not.

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4
Q

Which regards to glomerular disease, what is crescent formation referring to? (1)

A

Epithelial cell proliferation with mononuclear cell infiltration in Bowman’s space.

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5
Q

Which regards to glomerular disease, what is membrane alterations referring to? (1)

A

Capillary wall thickening due to deposition of immune deposits or alteration in the basement membrane.

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6
Q

What are the 4 main classifications of glomerulopathies? (4)

A

Nephrotic syndrome
Acute glomerulonephritis (acute nephritic syndrome)
Rapidly progressive glomerulonephritis
Asymptomatic haematuria, proteinuria or both.

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7
Q

What abnormalities are seen in nephrotic syndrome? (4)

What causes these abnormalities? (1)

A

Hypoalbuminaemia
Hypercholesterolaemia
Oedema
Proteinuria (>3.5g in 24 hours)

There is massively increase filtration of macromolecules across the glomerular capillary wall due to structural and functional abnormalities of the podocytes.

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8
Q

What are the most common causes of nephrotic syndrome with “bland” urine sediments? (3)

A

Adults: membranous nephropathy and focal segmental glomerulonephritis.
Children: minimal change nephropathy

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9
Q

What are the causes of membranous nephropathy? (3)

What changes occur histologically? (2)

A

Idiopathic
Drugs: penicillamine, gold, NSAIDs
Autoimmune: SLE, thyroiditis
Neoplasia: lung, colon, stomach, breast, lymphoma
Infections: Hep B and C, Plasmodium malariae
Sarcoidosis
Sickle cell disease

There is IgG and complement C3 deposition in the outer aspect of the GBM.

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10
Q

Which groups of people are more prone to focal segmental nephropathy? (1)

A

Black people

HIV (similar histological type)

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11
Q

Name 2 diseases that may cause a non-immune mediated nephrotic syndrome. (2)

A

Diabetes
Amyloidosis
Polycystic kidneys and reflux nephropathy may cause proteinuria but rarely enough for nephrotic syndrome.

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12
Q

What are the clinical features of nephrotic syndrome? (2)

A

Oedema of the ankles, genitals, abdominal wall are usual findings.
Oedema may also affect the face and arms in severe cases.

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13
Q

What are the 2 main differentials for nephrotic syndrome? (2)

A

CCF (but raised JVP)

chronic liver failure (but other signs of liver disease)

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14
Q

What is the management of nephrotic syndrome? (4)

A

General
Oedema:
dietary salt restriction
diuretic- bendroflumethiazide first then furosemide or amiloride if unresponsive (sometimes IV may be required)
Proteinuria:
ACEi or ARBs
eat normal diet (high protein increases proteinuria)
Thrombotic tendency: long term anti-coguation
Infections: treat aggressively. Annual flu and pneumococcal vaccines.

Specific:
Treat underlying cause e.g. SLE or stop drug e.g. NSAIDs
Only in certain cases: cyclophosphamide and prednisolone.

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15
Q

Who should get specific treatment for glomerulonephropathy/nephritis? (2)
Why? (1)

A

Moderate - severe progressive idiopathic membranous nephropathy should receive specific therapy as there is a high rate of spontaneous improvement.

Treatment is with cyclophosphamide with prednisolone.

Minimal change disease responds to high dose prednisolone for 4-6 weeks or cyclophosphamide or ciclosporin are used in resistant cases.

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16
Q

Name 2 complications of glomerulonephritis. (2)

A

Venous thrombosis: loss of clotting factors in urine predisposes to thrombosis in peripheral and renal veins.

Sepsis: loss of immunoglobulins in the urine

AKI: more a consequence of hypovolaemia or renal vein thrombosis than underlying renal glomerular disease

17
Q

Name 3 causes of acute nephritic syndrome. (3)

A
Post-streptococcal GN
Non-streptococcal post infectious GN
Infective endocarditis
Shunt nephritis
Visceral abscess
SLE
HSP
Cryoglobulinaemia
18
Q

What is the most typical presentation of acute nephritic syndrome? (2)

A

Pose-streptococcal glomerulonephritis occurring gin a child 1-3 weeks after pharyngitis or cellulitis caused by Group A beta-haemolytic streptococcus.

The bacterial antigen gets trapped in the glomerulus leading to an acute diffuse proliferative GN.

19
Q

What are the clinical features of acute nephritic syndrome? (6)

A
Haematuria
Hypertension
Oedema
Oliguria
Uraemia
Proteinuria (<2g in 24 hours)
20
Q

Name 3 management steps in acute nephritic syndrome. (3)

A

Hypertension: Salt restriction, loop diuretics, vasodilators
Fluid balance: monitored with daily weights and recording of fluid input and output.
Oliguric with fluid overload: fluid restriction

21
Q

Name 2 complications of acute nephritic syndrome. (2)

A

Hypertensive encephalopathy
Pulmonary oedema
Severe uraemia

22
Q

Name 3 risk factors for developing UTI’s. (3)

A

Female
Sexual intercourse
Urethral catheterisation
Underlying urinary tract abnormality : urinary obstruction or stasis, previous damage to bladder epithelium, bladder stones, poor bladder emptying.

23
Q

What is pyelonephritis? (2)

What are the clinical features of acute pyelonephritis? (2)

A

Infection ascending through the ureters to the renal parenchyma. There is neutrophil infiltration of the renal parenchyma. Small cortical abscesses and streaks of pus may be present in the medulla.

Fever, nausea, vomiting and loin pain

24
Q

What is the difference between a complicated and uncomplicated urinary tract infection? (4)

A

Uncomplicated: UTI in healthy non pregnant individual with functionally normal urinary tract and will rarely result in kidney damage.

Complicated: UTI in patient with abnormal urinary tracts or systemic disease involving the kidney e.g. diabetes or sickle cell. They are more likely to fail treatment and develop complications.
NB UTI in men are usually considered complicated

25
Q

Name 2 complications of a UTI. (2)

A

Renal papillary necrosis
Renal or perinephric abscess
Gram negative septicaemia

26
Q

What is reflux nephropathy? (2)

A

Vesicoureteric reflux in combination with childhood UTIs causes progressive renal scarring and presents as hypertension or CKD in childhood and adulthood.

27
Q

What is vesicoureteric reflux? (2)

A

Incompetent valve between bladder and ureter allowing reflux of urine from bladder up the ureter during bladder contraction and voiding.
Reflux usually ceases by puberty but the damage is done.

28
Q

What is the difference between a relapsed UTI and a reinfection of UTI? (2)

A

Relapse: failure to eradicate the organism usually associated with anatomical renal tract abnormalities. (recurrence of bacteria within 7 days of treatment completion)

Reinfection: Reinfection with same or different organism more than 14 days after stopping antibiotic treatment.

29
Q

What investigations can help in diagnosis of a UTI? (3)

A
  • Dipstick: nitrites and leucocyte elastase
  • Urine MC&S
  • Contrast enhanced CT: renal tract imaging for anatomical detail of renal parenchyma and peri-nephric area. (only indicated for recurrent UTIs or complicated UTIs, or if symptoms continue 48-72 hours after start of treatment.
30
Q

Name 2 organisms that cause UTIs. (2)

A

E coli

Pseudomonas

31
Q

Give 3 pieces of advice for a woman with frequent UTIs. (3)

A
  • 2L water intake a day
  • voiding at bedtime
  • voiding after sex
  • toilet hygiene
  • avoid spermicidal jellies
32
Q

Why are UTI’s in pregnancy classed as complicated? (2)

A

20% of UTI’s in pregnancy if untreated will develop acute pyelonephritis with significant risk to mother and foetus.
eg septic shock, low birthweight and prematurity.

33
Q

How does TB of the urinary tract present? (2)

How is it diagnosed? (1)

How is it treated? (4)

A

Symptoms of a UI i.e. dysuria, frequency or haematuria.
Classically there is sterile pyuria.
Consider in Asian population of UK.

Diagnosis is with early morning urine sample culturing mycobacteria.

Treat as for pulmonary TB: Rifampicin, Isoniazid, Pyrazinamide, Ethambutol.

34
Q

What is tubulointerstitial nephritis? (2)

A

Primary injury to the renal tubules and interstitial resulting in decreased renal function.

35
Q

Name 2 causes of acute interstitial nephritis. (2)

How do patients present? (2)

A

Allergic drug reaction: NSAIDs, penicillins.
Infections

Fever, eosinophilia, eosinophiluria, normal/mildly elevated proteinuria and AKI.

36
Q

Name 2 causes of chronic interstitial nephritis. (2)

How does it present? (3)

A

Prolonged consumption of analgesics (esp NSAIDs)
Diabetes mellitus
Toxins e.g. lead

Polyuria, nocturia, proteinuria, uraemia.
Necrosis of papillae may cause ureteric obstruction.