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Phase 2 Metabolic > Other Renal Conditions > Flashcards

Other Renal Conditions Flashcards

1
Q
  1. What is nephrolithiasis?

2. How does it typically clinically manifest as?

A
  1. formation of urinary calculi in the kidney, which may deposit anywhere along the entire urogenital tract
  2. sudden onset colicky flank pain that radiates to the groin; usually associated with haematuria
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2
Q
  1. What are renal stones usually the result of?

2. What are most kidney stones composed of?

A
  1. elevated levels of urinary solutes (calcium, uric acid, oxalate, sodium) plus decreased levels of stone inhibitors (citrate, magnesium). Leads to urine supersaturation
  2. calcium oxalate and phosphate
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3
Q

Name causes/aetiological factors for nephrolithiasis (9)

A
  1. chronic dehydration
  2. high protein intake (associated with hyperuricosuria, hypocitraturia, and hypercalciuria)
  3. high salt intake (associated with higher urinary sodium and calcium levels, and decreased urinary citrate)
  4. hypercalcaemia - primary hyperparathyroidism, high dietary intake, excessive bone resorption
  5. Obesity
  6. chronic infection - results in large stones, forming a staghorn calculus
  7. primary renal disease
  8. Medications
    • thiazides
    • loop diuretics
    • theophylline
    • glucocorticoids
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4
Q

How may a patient with bladder stones present?

A

frequency, dysuria and haematuria
if the calculus is locared at the bladder neck or obstructing the urethra, patient may present with bladder outflow obstruction (anuria; painful bladder distension)

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5
Q

Name investigative tests for renal stones (5)

A
  1. urine dip (may be normal or positive for red cells, protein, white cells, bacteria)
  2. chemical analysis of passed stones (can give indication of cause)
  3. bloods - U&E, creatinine, eGFR, calcium
  4. ultrasound (can miss ureteric stones0
  5. CT KUB - high sensitivity for stones but significant radiation exposure
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6
Q

How is a patient with symptomatic nephrolithiasis managed?

A
  1. analgesia - NSAIDs
  2. good hydration
  3. alpha blockers (tamsulosin) - helps expulsion of distal ureteral stones
  4. urological/radiological intervention for stones >1cm
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7
Q

How can recurrent kidney stones be prevented?

A
  1. high fluid intake
  2. calcium restruction
  3. limit salt intake
  4. reduction of animal proteins
  5. thiazide diuretic (for calcium stones)
  6. prophylactic antibiotics
  7. allopurinol
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8
Q

Name the 3 characteristics of HAEMOLYTIC URAEMIC SYNDROME

A
  1. anaemia
  2. AKI
  3. thrombocytopenia
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9
Q
  1. What are the initial symptoms of haemolytic uraemic syndrome?
  2. What are the later manifestations of haemolytic uraemic syndrome?
A
  1. GI symptoms - bloody diarrhoea, vomiting, stomach cramps, fever
  2. oliguria, hypertension, bleeding/bruising (due to thrombocytopenia), jaundice, seizures
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10
Q
  1. What is the most common cause of haemolytic uraemic syndrome?
  2. What does the underlying mechanism of the disease involve?
A
  1. E. coli (O157:H7) infection; S. pneumonia, shigella, salmonella
  2. SHIGA TOXIN
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11
Q

How does the shiga toxin cause renal damage in haemolytic uraemic syndrome?

A

binds to renal glomerular endothelial cells, causing damage which exposes the basement membrane, leading to toe formation of microthrombi in glomerular capillaries.

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12
Q

how is haemolytic uraemic syndrome managed?

A

SUPPORTIVE TREATMENT

  • dialysis
  • steroids
  • blood transfusion
  • plasmapheresis
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13
Q
  1. What is the inheritance pattern of polycystic kidney disease?
  2. What are the 3 major characteristics of the disease?
A
  1. autosomal dominant
  2. multiple renal cysts
    extra-renal cysts
    intracranial aneurisms
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14
Q
  1. Where within the kidney do cysts develop in PKD?

2. Why is there a loss of renal function

A
  1. tubular portion of the nephron and the collecting ducts
  2. mechanical compression of renal architecture and infrarenal vasculature
    apoptosis of healthy tissue
    reactive fibrosis
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15
Q

describe clinical features of polycystic kidney disease (6)

A
  1. loin pain and/or haematuria
  2. loin or abdominal discomfort (due to increasing size of the kidney)
  3. subarachnoid haemorrhage (associated with berry aneurism rupture)
  4. complications of hypertension
  5. complications of associated liver cysts
  6. symptoms of uraemia and/or anaemia associated with CKD
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16
Q

Name 5 complications associated with PKD

A
  1. renal calculi (often composed of uric acid)
  2. hypertension (early feature; ACEi useful in management)
  3. hepatic cysts
  4. mitral valve prolapse
  5. intracranial aneurism
17
Q
  1. What is common finding on physical examination of a patient with PKD?
  2. How is a definitive diagnosis of PKD made?
A
  1. palpable, bilateral, non tender upper abdominal masses

2. ultrasound

18
Q
  1. What are tubulointerstitial renal disorders?
  2. How do patients with tubulointerstitial disorders commonly present?
  3. What is a common consequence of tubulointerstitial disorders?
A
  1. diseases characterised by inflammation of the renal tubules, that can spread to the interstitium (which may progress to fibrosis)
  2. non specific signs and symptoms such as painless haematuria and white cells in urine
  3. AKI which can lead to CKD
19
Q
  1. What is the most common cause of acute tubulointerstitial nephritis?
  2. How do patients present?
  3. How is this cause of the condition managed?
  4. Name 3 other aetiologies of acute tubulointerstitial nephritis
A
  1. hypersensitivity to drugs (particularly antibiotics and NSAIDs)
  2. painless haematuria, flank pain, sterile pyuria, peripheral eosinophilia, rash
  3. discontinue drugs and administer IV fluids
  4. infection
    systemic disease - SLE, sarcoidosis, Sjörgren’s syndrome
    Autosomal dominant tubulointerstitial kidney disease
20
Q
  1. What are the most common causes of chronic tubulointerstitial nephritis (2)
  2. Name 3 other aetiologies of chronic tubulointerstitial nephritis
A
  1. analgesic nephropathy (NSAIDs)
    myeloma (due to filtration of light chains)
  2. drugs - mesalazine, lithium
    systemic diseases - SLE, sjörgren’s syndrome
    metabolic disturbance - hyperuricaemia, hypercalcaemia
21
Q
  1. Why are the renal papillae vulnerable to ischaemia?
  2. What does renal papillary necrosis result in?
  3. Name causes of Renal Papillary Necrosis
A
  1. they are supplied by small caliber arteries that are liable to obstruction
  2. Sloughing (collapse) of tubular epithelial cells into the lumen, resulting in haematuria
  3. POSTCARDS mnemonic:
    - Pyelonephritis
    - Obstruction of the urogenital tract
    - Sickle cell disease
    - TB
    - cirrhosis of the liver
    - analgesia/alcohol abuse
    - renal vein thrombosis
    - diabetes mllitus
    - systemic vasculitis
22
Q

What investigations are useful for patients presenting with ?tubulointerstitial disease?

A
  1. urinalysis - proteinuria, haematuria, sterile pyuria, WBC casrs
  2. serum urea and creatinine - elevated
  3. FBC - may demonstrate eosinophilia if cause is hypersensitivity
  4. ANCA if systemic disease is suspected as cause
  5. Anti-nuclear antibody if SLE is suspected
  6. ultrasound - kidneys oedematous if acute; shrunken if chronic
  7. intravenous urography (test of choice for renal papillary necrosis)
23
Q

What are renal tubular disorders characterised by?

A

dysfunction of transporters and channels in the renal tubular system; leads to fluid loss and abnormalities in electrolytes and acid-base homeostasis

24
Q
  1. What is acute tubular necrosis?
  2. Name 2 common causes of acute tubular necrosis
  3. How do patients present?
  4. What is revealed on urinalysis?
A
  1. necrosis of tubular epithelial cells
  2. hypotension (kidneys not adequately perfused)
    nephrotoxic drugs (aminoglycosides, statins, cisplatin based chemotherapies)
  3. AKI
  4. muddy brown casts of epithelial cells
25
Q
  1. What is the anion gap?
  2. What is it used to determine?
  3. What does a raised anion gap indicate?
  4. What does a normal anion gap indicate?
A
  1. estimation of unmeasured plasma anions (phosphate, ketones and lactate)
  2. the cause of metabolic acidosis
  3. increased production or decreased excretion of organic acids (lactate, urate, ketones)
  4. due to bicarbonate loss of acid ingestion
26
Q
  1. What is the anion gap in renal tubular acidosis?
  2. How does it arise?
  3. What is the presentation?
A
  1. normal
  2. defects in tubular transport of bicarbonate and/or acid
  3. mostly asymptomatic
27
Q
  1. What is the cause of Type 1 renal tubular acidosis?
  2. What does it result in?
  3. What is the cause of Type 2 renal tubular aciosis?
  4. What does it result in?
  5. What is the cause of type 4 renal tubular acidosis
  6. What does it result in?
  7. Which is the most common type?
A
  1. intercalated cells unable to secrete acid
  2. positive anion gap and hypokalaemia
  3. proximal tubule unable to reabsorb bicarbonate
  4. negative anion gap; hypokalaemia
  5. aldosterone deficiency and/or resistance
  6. hyperkalaemia and positive anion gap
  7. type 4
28
Q

What is fanconi syndrome?

A

rare disorder with generalised dysfunction of proximal tubule

  • aminoaciduria
  • glucosuria
  • phosphaturia
  • type 2 renal tubular acidosis
  • rickets/osteomalacia
29
Q
  1. What are 2 common causes of renal artery occlusion?
  2. What does it result in?
  3. How does a patient present?
A
  1. atherosclerosis; embolisation
  2. renal infarction (part or whole kidney)
  3. dull flank pain, macroscopic haematuria and varying degrees of CKD

Phase 2 Metabolic (12 decks)

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