Nephrology Flashcards

(22 cards)

1
Q

Glomerulonephritis

A

Renal biopsies show any changes of glomerulonephritis along with renal scarring from longstanding hypertension or urinary tract infections

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2
Q

Nephrogenic Diabetes Insipidus

A

V2 ADH mutation is usually X linked recessive.
Nephrogenic DI related to vasopressin-2 receptor mutation is X linked. This fits best with only male members of the family being affected by the condition. Nephrogenic DI may also occur as a sporadic condition or be autosomal recessive, although drugs are the commonest precipitants.

Autosomal recessive nephrogenic DI is related to mutations in the aquaporin-2 gene,

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3
Q

Nephrotic Syndrome

A

The triad of proteinuria, hypoalbuminaemia and oedema typifies the nephrotic syndrome.

The minimum threshold for proteinuria which is defined as ‘nephrotic’ is 300 mg/mmol.

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4
Q

Symptomatic Nephrotic syndrome caused by membranous nephropathy

A

Immunosuppression in the form of alternating steroids and cyclophosphamide is indicated in those patients with symptomatic nephrotic syndrome caused by membranous nephropathy

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5
Q

ADPKD

A

Abdominal ultrasound has a sensitivity approaching 100% for autosomal dominant polycystic kidney disease (ADPKD) patients above 20 years of age.

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6
Q

Rhabdomyolysis

A

The biochemical features of rhabdomyolysis are raised creatine kinase, hypocalcaemia (especially early after injury), hyperkalaemia and acute kidney injury.

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7
Q

Phosphate excretion in dialysis

A

Dialysis is able to remove about 2700 mg of phosphate per week in a patient who is anuric. This is half of the normal kidney’s ability.

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8
Q

Staghorn calculus ( Struvite)

A

Ammonium magnesium phosphate
- Associated with proteus infections.
- Urease inhibitors + Abx

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9
Q

Renal stones

A
  • Cystine stones- cystinuria
  • Oxalate stones- Short Bowel syndrome
  • Calcium phosphate stones- Renal tubular acidosis
  • Urate stones- Gout
  • Struvite stones- Proteus
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10
Q

Minimal change disease

A

Features
- nephrotic syndrome
- normotension - hypertension is rare
- highly selective proteinuria

-Renal biopsy
normal glomeruli on light microscopy.
electron microscopy shows fusion of podocytes and effacement of foot processes

Management
- oral corticosteroids: majority of cases (80%) are steroid-responsive
- cyclophosphamide is the next step for steroid-resistant cases

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11
Q

Peritoneal Dialysis Complications

A

1 - Peritonitis
coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause. Staphylococcus aureus is another common cause
Antibiotics should cover both Gram positive and Gram-negative organisms
- the BNF recommends vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid
OR vancomycin added to dialysis fluid + ciprofloxacin by mouth
- Aminoglycosides are sometimes used to cover the Gram negative organisms instead of ceftazidime.
2- Sclerosing peritonitis

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12
Q

Renal cell cancer

A

Renal cell cancer is also known as hypernephroma and accounts for 85% of primary renal neoplasms. It arises from proximal renal tubular epithelium. The most common histological subtype is clear cell (75 to 85 percent of tumours).

Associations
more common in middle-aged men
smoking
hypertension
obesity
von Hippel-Lindau syndrome
tuberous sclerosis
incidence of renal cell cancer is only slightly increased in patients with autosomal dominant polycystic kidney disease

Features
classical triad:
- haematuria
- loin pain
- abdominal mass

pyrexia of unknown origin
endocrine effects
may secrete erythropoietin (polycythaemia)
parathyroid hormone-related protein (hypercalcaemia), renin
ACTH
25% have metastases at presentation
paraneoplastic hepatic dysfunction syndrome
varicocele
majority are left-sided
caused by the tumour compressing veins

Stauffer syndrome
a paraneoplastic disorder associated with renal cell cancer
typically presents as cholestasis/hepatosplenomegaly
it is thought to be secondary to increased levels of IL-6

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13
Q

Minimal Change Disease

A

Minimal change disease nearly always presents as nephrotic syndrome, accounting for 75% of cases in children and 25% in adults.

The majority of cases are idiopathic, but in around 10-20% a cause is found:
Drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

Pathophysiology
T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
the resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin

Features
- nephrotic syndrome
- Normotension - hypertension is rare
highly selective proteinuria
only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus.

Renal biopsy
Normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes

Management
- oral corticosteroids: majority of cases (80%) are steroid-responsive
- Cyclophosphamide is the next step for steroid-resistant cases

Prognosis is overall good, although relapse is common. Roughly:
1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood.

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14
Q

Anemia in CKD

A

Elevated hepcidin levels in patients with CKD are a contributory factor to the development of iron-deficiency anaemia

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15
Q

Causes of anemia in renal Failure

A

Causes of anaemia in renal failure
reduced erythropoietin levels
the most significant factor in CKD causing anaemia
CKD is associated with a decrease in the production of erythropoietin, a hormone produced by the kidneys that stimulates erythropoiesis in the bone marrow
reduced erythropoietin levels → diminished red blood cell production
reduced absorption of iron
hepcidin is an acute-phase reactant
in CKD, hepcidin levels are often increased due to inflammation and reduced renal clearance
elevated hepcidin levels lead to decreased iron absorption from the gut and impaired release of stored iron from macrophages and hepatocytes, reducing the iron available for erythropoiesis
additionally, metabolic acidosis, a common condition in CKD, can inhibit the conversion of ferric iron (Fe³º) to its absorbable form, ferrous iron (Fe²º), in the duodenum → reduced iron absorption.
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due to capillary fragility and poor platelet function
stress ulceration leading to chronic blood loss

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16
Q

Renal tubule is impermeable to water.

A

The thin ascending limb of the loop of Henle is impermeable to water

17
Q

Pre-eclampsia

A
  • New-onset blood pressure ≥ 140/90 mmHg after 20 weeks of pregnancy, AND 1 or more of the following:
    proteinuria
    other organ involvement (see list below for examples): e.g. renal insufficiency (creatinine ≥ 90 umol/L), liver, neurological, haematological, uteroplacental dysfunction

Potential consequences of pre-eclampsia
- Eclampsia
- Other neurological complications include altered mental status, blindness, stroke, clonus, severe headaches or persistent visual
- scotomata
- fetal complications
- intrauterine growth retardation
- prematurity
- Liver involvement (elevated transaminases)
- haemorrhage: placental abruption, intra-abdominal, intra-cerebral
cardiac failure

Features of severe pre-eclampsia
- hypertension: typically > 160/110 mmHg and proteinuria as above
- proteinuria: dipstick ++/+++
- headache
- visual disturbance
- papilloedema
- RUQ/epigastric pain
- hyperreflexia
- platelet count < 100 * 106/l, - abnormal liver enzymes or HELLP syndrome.

Management
Women with blood pressure ≥ 160/110 mmHg are likely to be admitted and observed

Further management
Oral labetalol is now first-line following the 2010 NICE guidelines. Nifedipine (e.g. if asthmatic) and hydralazine may also be used
Delivery of the baby is the most important and definitive management step.

18
Q

Complications of Peritoneal Dialysis

A

1- coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause. Staphylococcus aureus is another common cause
antibiotics should cover both Gram positive and Gram negative organisms
the BNF recommends vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth
aminoglycosides are sometimes used to cover the Gram negative organisms instead of ceftazidime
2- sclerosing peritonitis

19
Q

Reflux Nephropathy ( VUR Vesicoureteral reflux)

A

Micturating cystography ( MCUG) is the investigation of choice for reflux nephropathy.

20
Q

Gitelman’s Syndrome

A

Gitelman’s syndrome is due to a reabsorptive defect of the NaCl symporter in the DCT.
-normotension
hypokalaemia
hypocalciuria
hypomagnesaemia
metabolic alkalosis

21
Q

Metabolic Alkalosis

A

Causes
1- vomiting / aspiration
(e.g. peptic ulcer leading to pyloric stenos, nasogastric suction)
Vomiting may also lead to
2- hypokalaemia
3- Diuretics
4- iquorice, carbenoxolone
hypokalaemia
5- primary hyperaldosteronism
6- Cushing’s syndrome
7- Bartter’s syndrome

22
Q

Rapidly progressive Glomerulonephritis

A

Causes
Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritis