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2a Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Where do stones form in renal colic?

A

Collecting ducts.

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2
Q

What are upper urinary tract stones?

A

Renal and ureteric.

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3
Q

What are lower tract stones?

A

Bladder, prostate and urethral.

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4
Q

What is the most common reason for the formation of bladder stones?

A

Urinary stasis due to failure of optimal emptying.

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5
Q

Who is more at risk of renal stones?

A

Males.

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6
Q

What is the lifetime risk of renal stones?

A

10-15%.

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7
Q

What are the 4 main causes of renal stones?

A
  1. Anatomic (can be congenital or acquired e.g. obstruction)
  2. Hypercalciuria (most commonly from hyperparathyroidism)
  3. Infection induces struvite (UTI with organisms that produce urease. Urease hydrolyses urea to ammonia which makes alkaline urine which favours stone formation)
  4. Hyperoxaluria: caused by dietary hyperoxaluria (spinach, rhubarb, tea, malabsorption of calcium so less binding to oxalate and rare autosomal recessive enzyme deficiency resulting in high oxalate levels).
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8
Q

What causes cystine stone formation?

A

An autosomal recessive condition affecting cystine and dibasic amino acid transport. Excessive urinary excretion of cystine (least soluble amino acid) leads to formation of crystals and calculi.

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9
Q

What causes uric acid stones?

A

Hyperuricaemia. With or without gout.

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10
Q

What is the pathophysiology of renal stones?

A

Urine is made up of water (solvent) and particles (solute). When solutes become too concentrated it becomes supersaturated and solute precipitates and forms crystals.

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11
Q

What is the most common composition of a stone?

A 
Calcium oxalate (forms in acidic urine).
Calcium phosphate (forms in alkali urine).
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12
Q

What is the most common site for stones to get stuck?

A

Pelviureteric junction (PUJ).

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13
Q

What causes renal colic?

A

Stones in the kidney, renal pelvis or ureter causing dilatation, stretching and spasm of the ureter.

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14
Q

What makes the pain worse in renal colic?

A

Moving. Often writhing in agony.

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15
Q

What are the signs of a bladder stone?

A

Urinary frequency and haematuria.

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16
Q

What are the signs of a ureteric stone?

A

Causes bladder outflow obstruction so anuria and painful bladder distension.

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17
Q

What is the first line investigation in renal colic?

A

X-ray of kidney, ureter and bladder.

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18
Q

What is the gold standard investigation for renal colic?

A

Non-contrast CT of kidney, ureter and bladder.

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19
Q

What would an ultrasound show in renal colic?

A

Hydronephrosis (can cause permanent renal damage).

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20
Q

What are differential diagnosis for renal colic?

A

Diverticulitis is left-sided pain and appendicitis is right-sided pain.

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21
Q

What is a preventative measure for stone formation?

A

Over hydration.

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22
Q

What is the treatment for a small stone <5mm?

A

It will pass spontaneously in a few weeks.

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23
Q

What is the treatment for a large stone >5mm?

A

ESWL (extracorporeal shock wave lithotripsy) for stones <1cm.
Ureteroscopy for stones >2cm..

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24
Q

What describes an AKI?

A

Rapid decline in GFR.

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25
Q

What conditions are associated with AKI?

A

Diarrhoea, haematuria, haemoptysis, hypotension, urine retention.

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26
Q

What are the 3 main causes of an AKI?

A
  1. Pre renal: reduced blood flow to the kidney e.g. hypovolaemia (due to diarrhoea, vomiting, haemorrhage), hypotension and thrombosis/stenosis.
  2. Renal: kidney can’t filter blood properly so cells damaged e.g. acute tubular necrosis, nephrotoxins (NAIDs inhibit COX which causes excess vasoconstriction of afferent arteriole), glomerulonephritis, vasculitis.
  3. Post-renal: anything that can cause blockage of the kidney reducing outflow e.g. BPHm stones, cancer and urethral stricture.
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27
Q

At what age is AKI most likely?

A

> 75.

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28
Q

What are the symptoms of an AKI?

A

Oliguria (decreased urine output), nausea and vomiting, confusion, fever SOB due to pulmonary oedema due to volume overload.

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29
Q

What is the criteria for diagnosis of an AKI?

A
  1. Rise in creatinine >26micromol/L in 48 hours above baselines.
  2. Rise in creatinine >50% from best figure in last 6 months.
  3. Urine output <0.5ml/kg for >6 consecutive hours.
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30
Q

What suggests glomerulonephritis as a cause of AKI on a dipstick?

A

Haematuria and proteinuria. Also red cell casts on urine microscopy.

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31
Q

What should be stopped in an AKI?

A

Nephrotoxic drugs: NSAIDs, ACE-inhibitors, gentamicin, amphotericin.

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32
Q

What is the medical emergency in AKI?

A

Hyperkalaemia as kidneys can’t excrete potassium.

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33
Q

What are the features of hyperkalaemia on an ECG?

A

Tall peaked T waves, small or absent P waves and a wide QRS complex.

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34
Q

What is the management of hyperkalaemia?

A 
Calcium gluconate (membrane stabiliser of the heart which protects).
Also insulin and dextrose (insulin drives potassium from blood into cells).
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35
Q

What GFR classifies as chronic kidney disease?

A

<60ml/min/1.73m for 3 months or longer.

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36
Q

Who is more at risk of chronic kidney disease?

A

Females and increasing age.

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37
Q

What are the 3 main causes of chronic kidney disease?

A
  1. Hypertension: walls thicken to withstand pressure and so narrow which causes ischaemic injury.
  2. Diabetes mellitus (type 2> type 1): excess glucose in the blood sticks to proteins which creates obstruction particularly in the efferent arteriole.
  3. Glomerular disease (IgA nephropathy, Wegener’s granulomatosis, amyloidosis): proteinuria (nephrotic syndrome) damages capillary cell wall.
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38
Q

What are other causes of chronic kidney disease?

A

Polycystic kidney disease, AKI, chronic NSAID use, SLE, tubular sclerosis, obstructive uropathy, myeloma.

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39
Q

What is the pathophysiology of CKD?

A

In CKD, where many nephrons have failed and scarred, the burden of filtration falls to fewer functioning nephrons. Functioning (remnant) nephrons experience hyperfiltration (increased flow per nephron as blood flow remains the same), and adapt with glomerular hypertrophy, and reduced arteriolar resistance. Increased flow, increased pressure and increased shear stress causes a vicious cycle of raised intraglomerular capillary pressure and strain, which accelerates remnant nephron failure. This increased flow and strain may be detected as new/increasing proteinuria.

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40
Q

How does CKD cause bone disease?

A

Renal phosphate retention and impaired production of 1,25-dihydroxyvitamin D which leads to compensatory release of PTH and sustained skeletal decalcification.

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41
Q

How does CKD cause anaemia?

A

Reduced erythropoietin production and increased blood loss.

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42
Q

What are the symptoms of CKD?

A

Early is asymptomatic. Then:

  1. Normocytic anaemia
  2. Bone disease (renal osteodystrophy embraces osteomalacia, osteoporosis, osteosclerosis, hyperparathyroidism as compensatory mechanism)
  3. Hypertension
  4. Fluid overload and oedema
  5. Malaise (oliguria, haematuria, weight loss)
  6. CVD disease due to hypertension and cardiac arrhythmias due to hyperkalaemia.
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43
Q

What is a normal or high GFR?

A

> 90.

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44
Q

What GFR is kidney failure?

A

<15.

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45
Q

What is the treatment for CKD?

A

Fluids, stop nephrotoxic drugs, manage high blood pressure to less than 120/80. Statins for GFR<60.
Vitamin D and bisphosphonates for bone for GFR <30.
Treat hyperkalaemia with calcium gluconate, insulin and dextrose.

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46
Q

What is haemodialysis?

A

The surgical construction of AV fistula in forearm (join an artery and vein to make large vessel).

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47
Q

What is peritoneal dialysis?

A

Involves infusing a sugary solution into the abdomen which draws off toxins.

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48
Q

What is nephrotic syndrome?

A

Protein leaks due to inflammation of podocytes.

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49
Q

What are the 4 signs of nephrotic syndrome?

A
  1. Proteinuria (>3.5g/day): damaged glomerulus more permeable so more protein come across from blood into nephron and causes proteinuria
  2. Hypoalbuminaemia: albumin leaves blood
  3. Oedema (periorbital and arms): oncotic pressure falls due to less protein in blood and so lower osmotic pressure and water driven out of vessels into tissues
  4. Hyperlipidaemia and lipiduria: loss of protein means less lipid synthesis and more lipids in blood and so more in urine.
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50
Q

What is nephritic syndrome?

A

Acute glomerulonephritis where blood vessels are inflamed so blood leaks out.

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51
Q

What are the signs of nephritic syndrome?

A
  1. Haematuria: visible or non-visible (red clast cells on microscopy)
  2. Reduced GFR: hypercellular glomeruli so decreased blood flow and leaky bone marrow so reduced filtration rate
  3. Oliguria
  4. Proteinuria (<2g in 24 hours)
  5. Oedema (periorbital, leg and sacral)
  6. Hypertension.
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52
Q

What are the 4 primary causes of nephrotic syndrome?

A
  1. Membranous glomerulonephritis: thickening of glomerular capillary wall due to IgG deposition in sub-epithelial surface so damaged glomerulus allowing protein to leak out.
  2. Minimal change disease: accounts for 80%, most common in children (2-3). Cytokines attack foot processes of podocytes which causes shrinkage/blunting of podocytes and so protein leakage.
  3. Focal segmental glomerulosclerosis: sclerosis forms in parts of the glomeruli in some kidneys. Podocytes are damaged which allows proteins and lipids to pass into urine. Overtime, these get trapped in glomerulus causing hyalinosis (glassy appearance on histology).
  4. Membranoproliferative glomerulonephritis: can present as both nephritic and nephrotic.
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53
Q

How do you diagnose membranous glomerulonephritis?

A

Renal biopsy and electron microscopy show thickened capillaries and glomerular basement membrane spike and dome pattern and effacement of foot processes, and PLA2R antigen.

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54
Q

What is the treatment for membranous glomerulonephritis?

A
  1. Supportive (control of oedema, hypertension, hyperlipidaemia and proteinuria)
  2. Immunosuppression with steroids and cyclophosphamide
  3. RAAS blockade
  4. Anti-coagulation.
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55
Q

How do you diagnose minimal change disease?

A

Based on renal biopsy and electron microscopy.

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56
Q

What is the management for minimal change disease?

A

Corticosteroids ± cyclophosphamide or cyclosporine (for frequent relapsing cases).

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57
Q

How do you diagnose focal segmental glomeruloslcerosis?

A

Renal biopsy and histology show segmental sclerosis and hyalinosis, effacement of foot processes and immunofluorescence (non-specific deposits of IgM and complement).

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58
Q

What is the treatment for focal segmental glomerulosclerosis?

A

Steroids.

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59
Q

What is the treatment for membranoproliferazive glomerulonephritis?

A

Steroids.

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60
Q

What are the seondary causes of nephrotic syndrome?

A

Diabetic nephropathy, SLE, amyloidosis (amyloid deposition), Hepatitis B/C, myeloma, drugs (NSAIDs, lithium).

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61
Q

What are the 3 primary causes of nephritic syndrome?

A
  1. IgA nephropathy: most common cause of nephropathy worldwide. Type III hypersensitivity so inflammation occurs at deposition site not site of formation. Presentation is usually in childhood and during GI or respiratory infection.
  2. Mesangiocapillary GN.
  3. Diffuse proliferative GN.
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62
Q

How do you diagnose IgA nephropathy?

A

Biopsy (diffuse mesangial IgA deposits, sub-endothelial and sub-epithelial deposits), light microscopy (mesangial proliferation) and urine dipstick.

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63
Q

What is the management for IgA nephropathy?

A 
Management is supportive care so blood pressure control, diet, lower cholesterol. 
Also immunosuppression (induction is steroids + cyclophosphamide and remission is steroids + azathioprine).
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64
Q

What are the secondary causes of nephritic syndrome?

A
  1. Post-Streptococcal GN with Lancefield Grouping A beta haemolytic strep
  2. Vasculitis: multisystem necrotising small vessel vasculitis Treatment is immunosuppression, steroids, cyclophosphamide, rituximab, plasma exchange.
  3. SLE: rash, arthralgia, kidney failure, pericarditis, pneumonitis. Anti-nuclear antibody (ANA) positive and double stranded DNA positive. Low complement C3 and C4. Treatment with immunosuppression (steroids, cyclophosphamide, rituximab).
  4. Goodpasture’s: autoimmune condition that attacks the type IV collagen in the basement membrane of the lungs and kidneys.
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65
Q

What are the causes of rapidly progressing GN?

A
  1. Background of acute nephritic syndrome
  2. Glomerulus becomes crescent shaped: vasculitis is ANCA positive, Goodpasture’s is anti-GBM disease with lung involvement and low GFR.
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66
Q

How is rapidly progressing GN diagnosed?

A

Light microscopy showing crescent shaped glomeruli.

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67
Q

What is the treatment for rapidly progressing GN?

A

Anticoagulants, plasmapheresis, immunosuppressants, dialysis and transplant.

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68
Q

What are the symptoms of nephrotic syndrome?

A

Oedema, swelling, breathlessness, protein in urine dipstick.

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69
Q

What are the symptoms of nephritic syndrome?

A

Haematuria, oliguria, blood and protein on urine dipstick, hypertension, AKI symptoms.

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70
Q

What would urine microscopy show in nephritic syndrome?

A

Red cell clasts.

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71
Q

What is the management for nephrotic syndrome?

A

Steroids in children, diuretics for oedema and ACE-I/ARBs for proteinuria.

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72
Q

What is the management for nephritic syndrome?

A

Corticosteroids and hypertension treated with ACE-I, salt restriction, loop diuretics e.g. oral furosemide and calcium channel blockers e.g. amlodipine.

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73
Q

What are the complications of nephrotic syndrome?

A

Infections, thromboembolism, hypercholesterolaemia.

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74
Q

What are the stages of CKD?

A

Stage 1: > 90 ml/min with evidence of renal damage Stage 2: 60-89 ml/min with evidence of renal damage Stage 3a: 45-59 ml/min with or without renal damage Stage 3b: 30-44 ml/min with or without renal damage Stage 4: 15-29 ml/min with or without renal damage Stage 5: <15 ml/min, established renal failure

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75
Q

What are the 6 types of polycystic kidney disease?

A
  1. Simple: most common, benign
  2. Polycystic: multiple cysts
  3. Hydronephrosis: when ureter blocked, and kidney dilates and gets bigger
  4. Dysplasia: not formed correctly
  5. Medullary sponge: dilation of collecting ducts
  6. Acquired cystic disease: medullary uraemic, dialysis cystic.
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76
Q

What percentage of people over 50 have a renal cyst?

A

50%.

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77
Q

What are the causes of renal cysts?

A

Simple: develop over time.
Acquired: CKD.
Drugs: lithium (used for treating depression).
Autosomal dominant/recessive: genetic cause.
Syndromic disease: tuberous sclerosis.

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78
Q

What are the symptoms of renal cysts?

A

Cysts often asymptomatic and found incidentally on ultrasound examination. Occasionally cause pain and/or haematuria if large, or bleeding may occur into cyst.

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79
Q

What is autosomal dominant polycystic kidney disease?

A

Multiple cysts develop gradually and progressively throughout the kidney resulting in renal enlargement, kidney tissue destruction and gradual renal failure .

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80
Q

When does PKD usually present?

A

20-30.

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81
Q

Who is more at risk of PKD?

A

Male.

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82
Q

What genes cause PKD?

A

Mutation in PKD1 gene (85%) on chromosome 16: more severe, earlier onset.
Mutations in PKD2 (15%) on chromosome 4: less severe, later onset.

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83
Q

What does PDK1 code for?

A

PKD1 encodes polycystin 1. It regulates tubular and vascular development in kidneys.

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84
Q

What does PKD2 code for?

A

PKD2 encodes polycystin 2 which functions as a calcium ion channel.

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85
Q

What is the pathophysiology of PKD?

A

The polycystin complex occurs in cilia that are responsible for sensing flow in the tubule.
Disruption of the polycystin pathway results in reduced cytoplasmic Ca2+, which, in principal cells of the collecting duct, causes defective ciliary signalling and disorientated cell division resulting in cyst formation.
Progressive loss of renal function is usually attributed to mechanical compression, apoptosis of the health tissue and reactive fibrosis.

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86
Q

What are the symptoms of renal cysts?

A

Acute loin pain due to cyst haemorrhage or infection, or urinary tract stone formation.
Abdominal discomfort caused by renal enlargement.
Nocturia.
Haematuria.
Renal colic due to clots.

87
Q

What are the extra-renal manifestations of renal cysts?

A

Sub-arachnoid haemorrhage: intracranial and berry aneurysms more common in ADPKD patients.
Liver cysts.
Mitral valve prolapse.

88
Q

What appears on an ultrasound to be diagnostic of PKD?

A

With family history: <30 at least 2 cysts.
15-39 years: > 3 cysts (uni/bilateral).
40-59 years: > 2 cysts (each kidney).
> 60 years: > 4 cysts (each kidney).

89
Q

What is the treatment of PKD?

A

No treatment shown to slow disease progression.

Laparascopic removal of cysts, nephrectomy or renal replacement in end stage renal failure.

90
Q

What are 5 functions of the kidney?

A
  1. Blood volume/fluid
  2. Waste/toxin/drug excretion
  3. Red cell production (generates erythropoietin)
  4. Vitamin D metabolism (vitamin D to 1-Hydroxyvitamin D)
  5. Acid-base regulation (excretes H+ ions and reabsorbed HCO3 ions).
91
Q

How is kidney function measured?

A
  1. Creatinine: waste product of muscle metabolism, low in people with low muscle and vice versa. Purely excreted by kidneys. Longstanding measure of kidney function
  2. eGFR.
  3. Proteinuria and albuminuria: protein with urine dipstick (depends on hydration)
  4. Albumin Creatinine Ratio: albumin in urine can be diluted or concentrated depending on urine volume. Creatinine is excreted in the urine at a constant rate. Therefore, the ratio of albumin to creatinine should be constant irrespective of urine volume.
92
Q

What is glomerular filtration?

A

When the filtrate passes through the glomerulus into the Bowman’s capsule.

93
Q

What is tubular secretion and tubular reabsorption?

A

Tubular secretion is when the peritubular capillaries secrete substances into the kidney tubules.
Tubular reabsorption is when the peritubular capillaries reabsorb substances from the kidney tubules.

94
Q

What is the pathway of renal blood flow?

A

Renal artery -> interlobar artery -> arcuate artery -> interlobular artery -> afferent arteriole -> glomerular capillary -> efferent arteriole -> peritubular capillary around tubules.

95
Q

Is secretion and absorption to and from the peritubular artery and filtrate active or passive?

A

Often active so requires energy and oxygen.

96
Q

How do you calculate GFR clinically?

A

(Urine concentration (creatinine) x urine flow)/plasma concentration creatinine.

97
Q

What is the average GFR?

A

125ml/min.

98
Q

Why is creatinine used as a marker for GFR?

A

It is freely filtered, not metabolised, not secreted and not reabsorbed.

99
Q

How much blood supply do the kidneys receive?

A

1L/minute which is 20% of the cardiac output so 10% to each kidney.

100
Q

What is the average urine flow?

A

1ml/minute.

101
Q

What is the favouring filtration at the glomerulus?

A

Hydrostatic pressure from glomerular capillary. This is the greatest pressure because there is forward action.

102
Q

What is the opposing filtration at the glomerulus?

A

Hydrostatic pressure from Bowman’s capsule and oncotic pressure from glomerular capillaries.

103
Q

How do you calculate GFR using pressures?

A

GFR= Hydrostatic pressure of capillaries - (oncotic pressure of capillaries + hydrostatic pressure from Bowman’s capsule).
=60 -(29+15) = 16mmHg.

104
Q

What is auto regulation?

A

Increase blood flow in afferent arteriole which causes stretch of wall so smooth muscle contract and there is arteriolar constriction.
Systemic circulation BP doesn’t affect renal circulation.

105
Q

What are the cells involved in tubuloglomerular feedback?

A

Macula densa cells.

106
Q

Where are the macula densa cells found?

A

In the distal convoluted tubule.

107
Q

What do the macula densa cells detect?

A

NaCl.

108
Q

What does low levels of NaCl at the macula densa cells cause?

A

Release of prostaglandins and so granular cells release renin which activates RAAS system.

109
Q

What does high levels of NaCl at the macula densa cells cause?

A

Sends signal to afferent arteriole causing vasoconstriction which will decrease GFR and lower BP.

110
Q

What are the 4 factors affecting GFR?

A
  1. Pressure
  2. Rate of glomerular filtration
  3. Renal clearance
  4. Tubules.
111
Q

Where is hydrostatic pressure greatest along the capillary?

A

Hydrostatic pressure is constant along the length of the capillary.
Pressure is greater than in the capillary than Bowman’s Capsule so pushes filtrate from the capillary into here.

112
Q

Where is oncotic pressure highest along the capillary?

A

Oncotic pressure increases along length so is higher in the efferent arteriole.

113
Q

Are there proteins in the capillary?

A

Yes.

114
Q

Are there proteins in Bowman’s Capsule?

A

No. This means fluid would move from here into the capillary by osmosis but the hydrostatic pressure in the capillary is higher so this does not happen.

115
Q

Why does oncotic pressure increase along the capillary?

A

Fluid is pushed out of the capillary along the length by the hydrostatic pressure.

116
Q

How do you calculate net glomerular filtration pressure?

A

Kf x ((PGC –PBS) – (πGC – πBS)).

117
Q

What parts of the glomerular filtration rate can be changed?

A

Hydrostatic pressure and surface area.

The permeability of the membrane and oncotic pressure can not be altered,.

118
Q

How is GFR decreased?

A
  1. Constrict afferent to reduce blood flow in
  2. Dilate efferent to increase blood flow out
  3. Contract mesangial cells to decrease surface area.
119
Q

How is GFR increased?

A
  1. Constrict efferent to keep blood in
  2. Dilate afferent to get more blood into capillary
  3. Mesangial cells dilate to increase surface area.
120
Q

How is filtration fraction calculated?

A

Filtration fraction = GFR/renal plasma flow.

Renal blood is 1000ml/min but as 60% of blood is plasma then the renal plasma flow is 600ml/min. So FF = 125/600 =20%.

121
Q

What is renal clearance?

A

The volume of plasma from which a substance is completely removed by the kidney per minute.

122
Q

How is renal clearance calculated?

A

(Urine concentration x urine volume)/plasma concentration.
So if a substance is all filtered, not reabsorbed and not secreted, it will be 125ml/min.
If the substance is all filtered and partially reabsorbed, this will be lower (i.e. urea = 65ml/min),
If the substance is all filtered and completely secreted, this will be higher (i.e. PAH = 625ml/min).
If the substance is all filtered and completely reabsorbed, this will be lower (i.e. glucose = 0ml/min).

123
Q

Where does the majority of reabsorption take place?

A

Proximal tubules.

124
Q

How much H2O is reabsorbed?

A

70%.

125
Q

How much Na+ is reabsorbed?

A

70%.

126
Q

How much K+ is reabsorbed?

A

90%.

127
Q

How much glucose is reabsorbed?

A

100%.

128
Q

How is Na+ absorbed into cells?

A

Passively via a glucose symporter (SGLT2) and a phosphate symporter (NKCC2).

129
Q

Is the ascending limb permeable or impermeable to water?

A

Impermeable.

130
Q

What 3 things does the filtration barrier consist of?

A
  1. Fenestrated capillary endothelial cells
  2. Basement membrane
  3. Podocyte foot processes.
131
Q

Is the filtration barrier negatively or positively charge?

A

Negatively so repels positively charged molecules.

132
Q

What area is responsible for filtration?

A

The slit diaphragm between the foot processes of the podocytes.
Globulin repels albumin.
Nephrin causes presence of cysteine crosslinks in slit diaphragm.
Podon brings nephrin to cell membrane.
CDPA2 links podocyte to actin skeleton.

133
Q

What effect does diabetes have on the filtration barrier?

A

Thickens it so it becomes leakier to proteins.

134
Q

What is the protective urinary protein?

A

Tamm Horsfall protein, has anti-microbial properties so is an important defence against infection.

135
Q

What makes up the renal corpuscle?

A

Glomerulus and Bowman’s capsule.

136
Q

What are the two types of nephron:

A
  1. Corticol nephron: glomeruli in outer cortex, short loop of Henle, doesn’t go deep into medulla.
  2. Juxtamedullary nephron: glomeruli near corticomedullary border, long loop of Henle, goes deep into the medulla with vasa recta which are vital in the concentration of urine.
137
Q

What parts are in the cortex?

A

PCT.
DCT.
Renal corpuscle.

138
Q

What parts are in the medulla?

A

Loop of Henle and collecting ducts.

139
Q

What occurs in the loop of Henle?

A

Urinary dilution.

140
Q

What are the cells in the glomerulus?

A

Smooth muscle mesagnial cells and capillary endothelial cells.

141
Q

What is the glomerulus stained with?

A

Periodic acid-Schiff.

142
Q

What are the cells in the PCT?

A

Cuboidal epithelium.

143
Q

What are adaptations of the PCT?

A

Cells have microvilli that increase surface area.

Contains lysosomes degradation of small molecules that are reabsorbed in urinary space.

144
Q

What is reabsorbed from the PCT?

A

Na, Cl, proteins, amino acids.

145
Q

What does the PCT excrete?

A

H+.

146
Q

Where does angiotensin II act?

A

On the PCT to increase Na+ reabsorption.

147
Q

Where is water reabsorbed?

A

The descending loop of Henle.

148
Q

How is water reabsorbed from the descending loop of Henle?

A

Through aquaporins.

149
Q

What part of the loop of Henle is insoluble to sodium?

A

The descending limb.

150
Q

Which part of the loop of Henle has the highest osmolarity?

A

The bottom of the loop of Henle. The top has the lowest osmolarity.

151
Q

What channels are found in the ascending loop of Henle?

A

NKCC2 channels to absorb NA, Cl and K+.

ROMK channels to remove the K+ that was reabsorbed.

152
Q

What channels are found in the distal convoluted tubule?

A

NCC channels.

153
Q

Where does aldosterone work?

A

On the DCT to reabsorb Na+.

On the collecting ducts where the more aldosterone, the more ENaC channels.

154
Q

What is secreted from the DCT?

A

K+ and H+.

155
Q

Where does ADH act?

A

On the DCT and collecting ducts.

Increases water reabsorption in the collecting ducts.

156
Q

Where do urinary buffers act?

A

On the DCT.

157
Q

Which cells contain ENaC channels?

A

Principle cells in the collecting duct.

158
Q

Is the medullary interstitial surround the collecting ducts hypertonic or hypotonic?

A

Hypertonic.

159
Q

What is the function of ADH?

A

V2 receptors and inserts aquaporins in the apical membrane to increase water permeability.

160
Q

Which cells in the collecting ducts act to regulate acid base?

A

Intercalated cells.

161
Q

How do intercalated A cells work?

A

They work in acidosis.
CO2 + H2O -> H+ + HCO3-, HCO3- /Cl_ transporter pumps HCO3- into cell. K+ released in DCT is pumped into cell in exchange for H+. NH3 from body is pumped out of the cell and joins with H+ forming NH4- which decreases the pH.

162
Q

How do intercalated B cells work?

A

They work in alkalosis. CO2 + H2O -> H+ + HCO3-, HCO3- /Cl_ transporter pumps HCO3- out of the cell. H+ reabsorbed by H+/K+ transporter which increases pH.

163
Q

How much is reabsorbed in the PCT?

A

60%.

164
Q

How much is reabsorbed in the thick ascending loop of Henle?

A

25%.

165
Q

How much is reabsorbed in the DCT?

A

10%.

166
Q

How much is reabsorbed in the collecting ducts?

A

4%.

167
Q

Where do carbonic anhydrase inhibitor diuretics work?

A

PCT.

168
Q

Where do loop diuretics work?

A

Ascending limb of the loop of Henle.

169
Q

Where do thiazide diuretics work?

A

DCT.

170
Q

Where do K+ sparing diuretics work?

A

DCT.

171
Q

What is the juxtaglomerular apparatus?

A

Between the DCT and the glomerulus.

172
Q

What do macula densa cells detect?

A

Decreased blood pressure by detecting decreased Na+ and then causing renin release.

173
Q

What do juxtaglomerular “granule cells” release?

A

Renin.

174
Q

What is the function of mesangial cells?

A

Contractile cells surrounding the efferent and afferent capillaries to alter GFR.

175
Q

What do loop diuretics inhibit?

A

The Na+/K+/2Cl- cotransporter that transports the ions into the cell and water follows.

176
Q

What are examples of loop diuretics?

A

Furosemide, bumetanide.

177
Q

What are the adverse effects of loop diuretics?

A

Dehydration, hypotension and hypokalaemia.

Metabolic alkalosis.

178
Q

What is the action of K+ sparing diuretics?

A

Inhibits the reabsorption of sodium and therefore water from the DCT and so there is sodium and water excretion. There is potassium retention.

179
Q

What are examples of K+ sparing diuretics?

A

Amiloride and spironolactone.

180
Q

What are the adverse effects of K+ sparing diuretics?

A

GI upset, hyperkalaemia and metabolic acidosis.

181
Q

What is the action of thiazide diuretics?

A

Acts on the sodium/chloride transporter so sodium is not retain.
Longer acting than loop diuretics but not as effective.

182
Q

What are the adverse effects of thiazide diuretics?

A

Hypokalaemia, metabolic alkalosis, hypovolaemia, hyponatraemia and hyperglycaemia in diabetics.

183
Q

What removes water in the nephron?

A

Vasa recta.

184
Q

How does sodium leave the ascending limb?

A

Actively pumped out.

185
Q

Which part of the medulla is the most hypertonic?

A

The furthest bit in.

186
Q

What is the action of angiotensin II?

A

Acts on the PCT:
1. Causes thirst
2. Causes increased SNS activity
3. Causes ADH release by stimulating posterior pituitary (where ADH is stored)
4. Causes aldosterone release by stimulating adrenal glands
5. Causes an increase in PCT reabsorption so increases Na+ reabsorption
6. Causes vasoconstriction to increase BP.
All of these act to increase BP.

187
Q

What is the action of aldosterone?

A

Acts on the DCT and collecting ducts:

  1. Increases Na+ reabsorption by NCC channels
  2. Promotes K+ secretion
  3. Binds to cytoplasmic receptors which is transported to the nucleus
  4. Increases ENaC and Na/K ATPase
  5. Increases circulating volume.
188
Q

What is the action of ADH?

A

Acts on the DCT and collecting ducts.
ADH release from posterior pituitary is triggered by increased plasma osmolality (decreased water).
Detected by hypothalamic osmoreceptors because H2O diffuses out posterior pituitary in response to the increased Na+ pulling it out.
ADH acts on V1 receptors on blood vessels to cause vasoconstriction.
ADH acts on V2 receptors in basolateral side of collecting ducts.
Increases insertion of aquaporin 2 on apical membrane so increased water reabsorption.
Works by aquaporin insertion in collecting ducts.
Also helps maintain hypertonicity of medulla by increasing urea permeability of collecting duct.

189
Q

Where is ADH produced?

A

Hypothalamus. It is stored in the posterior pituitary.

190
Q

What converts angiotensinogen to angiotensin 1?

A

Renin.

191
Q

What converts angiotensin I to angiotensin II?

A

ACE.

192
Q

Where is renin produced?

A

The kidney.

193
Q

What is ANP?

A

Atrial natriuretic peptide. Released from the atria in response to increased BP/increased blood volume.

194
Q

Why is ANP released from the atria?

A

The atria are stretched due to high BP.

195
Q

What is the action of ANP?

A
  1. Increases vasa recta blood flow which washes out NaCl and urea out of the medullary so decreases osmolarity and there is less reabsorption.
  2. Dilates afferent glomerular arterioles and constricts effort arteriole and relaxes mesangial cells to increase GFR so excretion can be increased.
  3. Blocks NCC transporter in DCT and ENaC in CT, preventing sodium reabsorption in the DCT and so promoting Na+ and water excretion.
  4. Inhibits renin secretion so no aldosterone release.
  5. Systemic vasodilator.
196
Q

What are the effects of PTH?

A

Directly increases distal Ca2+ reabsorption and blocks proximal phosphate reabsorption, increasing HPO43- excretion.
Also stimulates formation of the active form of Vitamin D..

197
Q

Why is PTH released?

A

Released by parathyroid glands in response to decreases in Ca2+ levels.

198
Q

Where is vitamin D obtained from?

A

Produced by the skin from UVB and ingested in diet.

Converts 7-dehydrocholesterol to Vitamin D3 (cholecalciferol).

199
Q

Where is Vitamin D first hydrolysed?

A

In the liver by 25-hydroxylase to from 25-hydroxylase-vitamin D (calcidiol).

200
Q

Where is Vitamin D further hydrolysed?

A

In the kidneys by 1-hydroxylase to form 1,25 dihydroxy-vitamin D (calcitriol) which is active Vitamin D.

201
Q

What is the action of vitamin D?

A

Increases calcium absorption into intestines and bones.

Decreases phosphate levels.

202
Q

Who does ARPKD affect?

A

It is a disease of infancy, the child is born with multiple cysts on both kidneys.

203
Q

What causes ARPKD?

A

PKHD1 mutation on chromosome 6.

204
Q

What are the symptoms of ARPKD?

A

Congenital hepatic fibrosis.
Can cause renal failure before birth: fetus has less urine so oligohydramnios (low amniotic fluid) so potter sequence (developmental abnormalities) such as clubbed feet and flattened nose.
Enlarged polycystic kidneys.
30% develop kidney failure.

205
Q

What are the investigations for ARPKD?

A

Ultrasound
CT and MRI to monitor liver disease
Genetic testing.

206
Q

What is the management for ARPKD?

A

Currently no treatment.
Blood pressure control with ACE-inhibitor.
Laparoscopic removal of cysts.
Nephrectomy.
Renal replacement therapy for end stage renal failure.

207
Q

What is the pathophysiology of nephrotic syndrome?

A

Gaps in the podocytes allow proteins to leak into urine. Albumin is lost and so there is decreased intravascular oncotic pressure. Fluid moves into surrounding tissue causing oedema. The hypalbuminaemia causes liver compensation and a side effect of this is lipid production so there is hyperlipidaemia.

208
Q

What is the pathophysiology of nephritic syndrome?

A

Inflammation causes podocytes to develop large pores, which allows blood to flow into the urine. Red cell clasts are characteristic. Low renal function leads to low urine output.

209
Q

What is the investigation for nephrotic and nephritic syndrome?

A

Urine dipstick for haematuria/proteinuria.

210
Q

What are the 3 hallmarks of minimal change disease?

A
  1. Diffuse loss of podocyte foot processes
  2. Vacuolation
  3. Appearance of microvilli.
211
Q

What is seen under a light microscope in minimal change disease?

A

Nothing. Abnormal podocytes seen under electron microscope.

212
Q

Where in the adrenal gland is aldosterone produced?

A

Zona glomerulosa.

213
Q

What type of hypersensitivity is Goodpasture’s?

A

Type II hypersensitivity with anti-GBM antibodies.

214
Q

What is the presentation of Goodpasture’s?

A

Haemoptysis, haematuria and proteinuria. Diagnosis with renal biopsy.
Treatment with corticosteroids/cyclophosphamide, immunosuppression and remove antibody via plasma exchange.

2a Medicine (11 decks)

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