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Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What are the causes and risk factors of chronic kidney disease?

A
  • Diabetes, hypertension, older age, glomerulonephritis, PCKD
  • Medications-> NSAIDs, PPIs, lithium
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2
Q

How does chronic kidney disease usually present?

A

Asymptomatic, itching, loss of appetite, nausea, oedema, muscle cramp, peripheral neuropathy, pallor, hypertension

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3
Q

What are the investigations for chronic kidney disease?

A
  • eGFR via U+Es-> 2 tests 3 months apart
  • Proteinuria-> urine albumin:creatinine (>3mg/mmol is significant)
  • Haematuria-> dipstick, 1+ is significant (warrants malignancy investigation)
  • Renal US-> obstruction etc
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4
Q

What are the stages of CKD and what are they based on?

A

Look at eGFR + albumin:creatinine ratio

  • eGFR-> >90 (1), 60-89 (2), 45-59 (3a), 30-44 (3b), 15-29 (4), <15 (5)
  • Albumin-> <3mg/mmol (1), 3-20 (2), >30 (3)
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5
Q

When is CKD diagnosed?

A

When eGFR <60 or proteinuria

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6
Q

What are the complications of CKD?

A

Anaemia, renal bone disease, CVD, peripheral neuropathy, dialysis problems

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7
Q

How is CKD managed?

A
  • Reduce CVD + complication risks-> atorvastatin 20mg + weight
  • Refer to specialise when meet criteria
  • Treat glomerulonephritis
  • Optimise diabetes + HTN treatment
  • Sodium bicarb-> for metabolic acidosis
  • Iron + erythropoietin-> for anaemia
  • Vitamin D
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8
Q

What are the criteria for referral to a specialist in CKD?

A
  • eGFR <30
  • ACR >70
  • eGFR decreases by 15 or 25% or 15ml/min in 1 year
  • Uncontrolled HTN after 4+ medications
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9
Q

How is hypertension managed in CKD?

A
  • ACE-i’s 1st line
  • Aim for BP <140/90 or <130/80 if ACR >70mg/mmol
  • Monitor serum K+-> hyperkalaemia risk
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10
Q

Why does anaemia occur in CKD?

A

Erythropoetin deficiency in CKD-> RBC production lower

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11
Q

How is anaemia in CKD managed?

A
  • Exogenous EPO
  • Transfusions-> can get allosensitisation
  • IV/oral iron
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12
Q

What is renal bone disease and why does it occur?

A
  • Osteomalacia, osteoporosis and osteosclerosis
  • High serum phosphate due to reduced excretion
  • Low vitamin D as not metabolised to active form-> calcium absorption + bone turnover not regulated
  • Low calcium + high phosphate causes pituitary to excrete more PTH-> more osteoclast activity-> absorb calcium from bone-> secondary hyperparathyroidism
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13
Q

What are the X-ray changes seen in renal bone disease?

A

Vertebral sclerosis, osteomalacia in centre of vertebrae (rugger jersey sign)

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14
Q

What causes osteomalacia in renal bone disease?

A

Increased turnover without adequate calcium

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15
Q

What causes osteosclerosis in renal bone disease?

A

Osteoblasts increase activity to match osteoclasts but low calcium means tissues not mineralised properly

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16
Q

What causes osteoporosis in renal bone disease?

A

-Can be a co-morbidity eg due to age or steroids

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17
Q

How is renal bone disease managed?

A

Give active vitamin D + bisphosphonates

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18
Q

What is the function of the kidney?

A
  • Filter + excrete waste products from the blood-> urine

- Water and electrolyte balance

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19
Q

What is the anatomical position of the kidneys?

A
  • Retroperitoneal
  • Extend from T12 to L3
  • Adrenal glands superior to the kidney within renal fascia
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20
Q

What is the internal anatomy of the kidney (ie the different layers)?

A
  • Outer cortex + inner medulla
  • Renal pyramids-> cortex extending into medulla + dividing it into triangles
  • Renal papilla-> apex of renal pyramid
  • Minor calyx-> collects urine from oyramids
  • Major calyx-> minor calices converge to form one + where urine passes through
  • Renal pelvis-> where urine drains to ureter
  • Renal hilum-> where renal vessels + ureter enter/exit
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21
Q

What is the arterial blood supply of the kidneys?

A
  • Renal arteries-> directly from abdominal aorta

- Renal artery-> anterior + posterior division-> 5 segmental ateries from these

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22
Q

What is the venous drainage of the kidneys?

A
  • Left + right renal veins

- Left renal vein-> longer as IVC sits more to right

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23
Q

What are the different parts of the nephron?

A
  • Glomerulus ie Bowman’s capsule
  • Proximal convoluted tubule
  • Loop of Henle
  • Distal convoluted tubule
  • Collecting duct
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24
Q

How does the glomerulus of the kidney work?

A
  • Not permeable to plasma proteins

- Permeable to sodium, potassium, amino acids, creatinine etc

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25
Q

What are the definitions/criteria of acute kidney injury?

A
  • Acute drop in function measured by serum creatinine
  • Rise in creatining of >25micromol/L in 48 hours
  • Rise in creatinine of >50% in 7 days
  • UO of <0.5ml/kg/hour for >6 hours
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26
Q

What are the risk factors for acute kidney injury?

A

Acute illness, infection, operations, older, cognitive impairment, CKD, HF, DM, liver disease, NSAIDs, ACE-i’s, contrast medium for CTs

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27
Q

What are the three types/causes of AKI?

A

Pre-renal, renal and post-renal

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28
Q

What are the causes of pre-renal AKI?

A

Inadequate blood supply-> dehydration, hypotension, heart failure

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29
Q

What are the causes of renal AKI?

A

Intrinsic kidney disease, glomerulonephritis, interstitial nephritis, acute tubular necrosis

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30
Q

What are the causes of post-renal AKI?

A

Obstruction + back pressure-> stones, cancer, strictures, BPH, prostate cancer

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31
Q

What is the most common type/cause of AKI?

A

Pre-renal

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32
Q

What are the investigations for AKI?

A
  • U+Es-> creatinine rise, electrolyte imbalance etc
  • Urinalysis-> leucocytes + nitrites (infection) or protein + blood (acute nephritis, infection) or glucose (diabetes)
  • Ultrasound-> obstruction
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33
Q

What is the management of AKI?

A
  • Prevention-> IV fluids + avoid nephrotoxic meds
  • Treatment-> fluids, stop meds, relieve obstruction
  • If severe-> renal input + dialysis
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34
Q

What are the potential complications of AKI?

A

Hyperkalaemia, fluid overload, HF, pulmonary oedema, metabolic acidosis, uraemia leading to encephalopathy or pericarditis

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35
Q

What is dialysis?

A

Artificial filtration of the kidneys in end stage disease-> remove fluid, solutes and waste

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36
Q

What are the indications for acute dialysis?

A

AEIOU

  • Acidosis
  • Electrolytes (eg hyperkalaemia)
  • Intoxication
  • Oedema
  • Uraemia (symptoms- seizure, reduced consciousness)
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37
Q

Indications for long-term dialysis?

A

CKD stage 5, acute indications long term (AEIOU)

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38
Q

What is peritoneal dialysis?

A
  • Add dialysis solution + dextrose to peritoneal cavity-> ultrafiltration from blood across peritoneal membrane to solution-> replace + take away waste
  • Can be continuous ambulatory-> solution in at all times ie 2 fluid 4x daily
  • Can be automated-> overnight for 8-10 hours
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39
Q

What are the potential complications of peritoneal dialysis?

A

Spontaneous bacterial peritonitis, peritoneal sclerosis (scarring), ultrafiltration failure, weight gain, psychosocial implications

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40
Q

What is haemodialysis?

A
  • Blood filtered
  • 4 hours ish 3 times a week
  • Some-> catheter in subclavian/jugular vein + sits in SVC or RA long term
  • Some-> AV fistula
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41
Q

What is an AV fistula in the context of haemodialysis

A
  • Surgical operation-> connection by bypass capillaries + flow under high pressure from artery to vein
  • Usually radio-cephalic, brachio-cephalic or brachio-basilic
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42
Q

What clinical signs might someone with an AV fistula have?

A

Machinery murmur + thrills

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43
Q

What are the complications of an AV fistula?

A
  • Aneurysm, infection, thrombosis, stenosis
  • STEAL syndrome-> inadequate blood flow distally (‘steals’ from limb) so flows into venous system + cause distal ischaemia
  • Heart failure as flow quick from arterial to venous-> rapid return to heart-> increase preload + hypertrophy
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44
Q

What are the benefits of renal transplant?

A

In end stage renal failure adds 10 years compared to with just dialysis

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45
Q

How are donors matched in renal transplant?

A
  • Based on human leucocyte antigen (HLA) types A, B and C

- Don’t have to fully match-> can get desensitisation treatment

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46
Q

What scar might be present in someone who’s had a renal transplant?

A
  • Hockey stick incisional scar

- Can palpate kidney in iliac fossa

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47
Q

What do patients require after a renal transplant?

A

Lifelong immunosuppression regime to reduce rejection risk-> tacrolimus + mycophenolate + prednisolone

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48
Q

What are the potential complications of renal transplant?

A
  • Rejection-> hyperacute, acute, chronic
  • Failure
  • Electrolyte imbalances
  • Related to immunosuppressants-> T2DM, HIS, infections, non-Hodgkin lymphoma, skin cancers
49
Q

What is glomerulonephritis?

A

Non-specific inflammation of the kidneys-> umbrella term

50
Q

What is nephritic syndrome and what are its features?

A
  • A group of symptoms not a diagnosis
  • Haematuria-> micro or macroscopic
  • Oliguria-> reduced UO
  • Proteinuria-> <3g in 24 hours
  • Fluid retention
51
Q

What is nephrotic syndrome and what are its features?

A
  • Group of symptoms without a specific cause
  • Peripheral oedema
  • Proteinuria-> >3g in 24 hours
  • Serum albumin <25g/L
  • Hypercholesterolaemia
52
Q

What is the typical presentation of nephrotic syndrome?

A

Oedema and frothy urine (due to proteinuria)

53
Q

What are the complications of nephrotic syndrome?

A

Pre-disposition to thrombosis, hypertension and hypercholesterolaemia

54
Q

What type of nephrotic syndrome is most common in kids?

A

Minimal change disease

55
Q

How is minimal change disease managed?

A

Steroids-> usually idiopathic

56
Q

How is the most common type of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis?

57
Q

What are the different types of glomerulonephritis?

A
  • Nephrotic and nephritic syndromes fit into this
  • Minimal change disease, focal segmental glomerulosclerosis, membranous glomerulosclerosis, IgA nephropathy, post-strep glomerulonephritis, Goodpasture syndrome
58
Q

What is the most common primary glomerulonephritis?

A

IgA nephropathy

59
Q

What are the features of IgA nephropathy?

A
  • Peaks in 20’s

- IgA deposits + glomerular mesangial proliferation on histology

60
Q

What are the features of membranous glomerulonephropathy?

A
  • Presents in 20’s and 6’s
  • 70% idiopathic
  • Some due to NSAIDs and cancers
  • IgG and complement deposits in basement membrane
61
Q

What are the features of post-streptococcal glomerulonephritis?

A
  • Presents in under 30’s
  • 1-3 weeks after strep infection-> tonsillitis or impetigo
  • Nephritic syndrome
  • Usually make full recovery
62
Q

What are the features of Goodpasture syndrome?

A
  • Anti-GBM antibodies attack glomerulus + pulmonary basement membranes
  • Glomeruponephritis + pulmonary haemorrhage
  • AKI + haemoptysis
  • Can cause rapidly progressive glomerulonephritis
63
Q

What are the features of rapidly progressive glomerulonephritis?

A
  • Acute illness
  • Often secondary to Goospasture’s
  • Histology-> crescentic
  • Responds well to treatment
64
Q

What is interstitial nephritis?

A
  • Inflammation of interstitium of kidney-> between cells + tubules
  • Different to glomerulonephritis
  • Acute or chronic
65
Q

What is glomerulosclerosis?

A

Damage and scarring of glomerulus tissue due to other pathology

66
Q

What can cause glomerulosclerosis?

A
  • Glomerulonephritis
  • Obstructive uropathy
  • Focal segmental glomerulosclerosis
67
Q

How are most types of glomerulosclerosis treated?

A
  • Steroids-> for immunosuppression

- ACE-is or ARBs-> BP control + block RAAS

68
Q

What is the pathology behind diabetic nephropathy?

A

Glomerulosclerosis-> chronic passing of high levels of glucose through glomerulus causes scarring

69
Q

What is the main feature of diabetic nephropathy?

A

Proteinuria-> damage causes leakage into urine

70
Q

How is diabetic nephropathy screened for?

A
  • Albumin:creatinine ratio

- U+Es

71
Q

How is diabetic nephropathy managed?

A
  • Optimising BMs and blood pressure

- ACE-i’s-> start when nephropathy regardless of BP level

72
Q

What is acute interstitial nephritis?

A
  • Inflammation of space between kidney cells + tubules (interstitium)
  • AKI and HTN due to acute inflammation
73
Q

What is the presentation of acute interstitial nephritis?

A
  • Rash
  • Fever
  • Eosinophilia
  • AKI
  • HTN
  • Can be reaction to NSAIDS or antibiotics or due to infection
74
Q

How is acute interstitial nephritis managed?

A
  • Treat the underlying cause

- Steroids

75
Q

What is chronic tubulointerstitial nephritis?

A
  • Inflammation of space between cells + tubules (interstitium)
  • CKD due to inflammation
76
Q

What causes chronic tubulointerstitial nephritis?

A

AI, infection, iatrogenic

77
Q

How is chronic tubulointerstitial nephritis managed?

A
  • treat the underlying cause

- steroids

78
Q

What is acute tubular necrosis?

A
  • Damage + necrosis of epithelial cells in tubules
  • Reversible as epithelium regenerates
  • Common cause of AKI
79
Q

What can cause acute tubular necrosis?

A
  • Hypoperfusion-> shock, sepsis, dehydration

- Toxins-> radiology contrast dye, gentamycin, NSAIDs

80
Q

How is acute tubular necrosis investigated?

A

Urinalysis-> muddy brown casts (pathognomonic) + maybe renal tubular epithelial cells

81
Q

How is acute tubular necrosis managed?

A

Supportive-> IV fluids, stop meds, complication management

82
Q

What is renal tubular acidosis?

A
  • Metabolic acid due to pathology in tubules

- Tubules usually balance H+ and bicarb ions between blood + urine to maintain pH-> pathology causes issues

83
Q

What is type 1 renal tubular acidosis?

A

Distal tubule pathology-> unable to excrete H+

84
Q

What causes type 1 renal tubular acidosis?

A

Genetic, SLE, Sjogren’s, PBC, hyperthyroidism, sickle cell, Marfan’s

85
Q

How does type 1 renal tubular acidosis present?

A

FTT, hyperventilation (to compensate for acidosis), CKD, osteomalacia

86
Q

What blood and urine results may be apparent in type 1 renal tubular acidosis?

A
  • Hypokalaemia + acidosis

- Acidic urine (pH 6 or more)

87
Q

What is the treatment for type 1 renal tubular acidosis?

A

Oral bicarbonate-> correct electrolyte imbalances

88
Q

What is type 2 renal tubular acidosis?

A

Proximal tubule pathology-> unable to resorb bicarbonate so excess in urine

89
Q

What is the main cause of type 2 renal tubular acidosis?

A

Fanconi syndrome

90
Q

What is the management of type 2 renal tubular acidosis?

A
  • Bloods-> hypokalaemia + acidosis
  • Urine-> acidic urine (pH 6 or more)
  • Give oral bicarbonate-> correct electrolyte imbalances
91
Q

What is type 3 renal tubular acidosis?

A

A mixture of type 1 and 2 renal tubular acidosis-> very rare

92
Q

What is type 4 renal tubular acidosis and what can cause it?

A

Renal tubular acidosis due to reduced aldosterone-> adrenal insufficiency, ACE-is, spironolactone, SLE, diabetes, HIV

93
Q

Which is the most common type of renal tubular acidosis?

A

Type 4

94
Q

What investigations are done in renal tubular acidosis?

A
  • Bloods-> hyperkalaemia, high chloride, metabolic acidosis

- Urine-> low pH

95
Q

How is type 4 renal tubular acidosis managed?

A
  • Fludrocortisone
  • Sodium bicarb
  • Hyperkalaemia treatment if present
96
Q

What is haemolytic uraemic syndrome?

A

Medical emergency in which many thrombi occur throughout the body-> often triggered by shiga toxin (E.coli + Shigella)

97
Q

What is the pathophysiology of haemolytic uraemic syndrome?

A
  • Triggered by shiga toxin-> from E.coli 0157 or shigella
  • Blood clots consume platelets-> thrombocytopaenia
  • Clots chop up RBCs as pass by-> haemolysis + anaemia
  • Blood flow through kidneys affected by clots + damaged RBCs-> AKI
98
Q

What infections often trigger haemolytic uraemic syndrome?

A
  • Shiga toxin-> from E.coli 0157 or Shigella

- Higher risk if antibiotics or anti-motility medications used

99
Q

How does haemolytic uraemic syndrome present?

A
  • E.coli infection-> gastroenteritis + bloody diarrhoea
  • 5 days after-> reduced urine output, haematuria or dark urine, abdominal pain, lethargy, confusion, hypertension, bruising
  • ‘Triad’-> haemolytic anaemia + AKI + thrombocytopaenia
100
Q

What is the ‘triad’ of pathologies that occur in haemolytic uraemic syndrome?

A

Haemolytic anaemia + AKI + thrombocytopaenia

101
Q

How is haemolytic uraemic syndrome managed?

A
  • Self limiting illness

- Supportive-> anti-HTNs, transfusions, dialysis

102
Q

What is rhabomyolysis?

A

Break down of skeletal muscle + release of products into blood due to extreme underuse, overuse or trauma

103
Q

What is the pathophysiology of rhabdomyolysis?

A
  • Extreme under or overuse or trauma-> skeletal muscle breaks down + releases products
  • Myocytes apoptose-> release myoglobin, potassium, phosphate and CK into blood
  • Cause hyperkalaemia-> arrhythmias
  • Cause myoglobulinaemia-> toxic to kidneys in high concentrations-> AKI + accumulation
104
Q

What causes rhabdomyolysis?

A
  • Anything that can damage cells
  • Prolonged immobility-> frailty + falls
  • Rigorous exercise
  • Crush injuries
  • Seizures
  • Statins
105
Q

What are signs and symptoms of rhabdomyolysis?

A

Muscle aches, oedema, fatigue, confusion, red-brown urine

106
Q

What are the investigations for rhabdomyolysis?

A
  • U+Es-> AKI + hyperkalaemia
  • ECG-> for hyperkalaemia
  • Urine dip-> red-brown with +ve for blood (myloglobinurea)
  • Blood CK-> very high, rise till 12 hours, stay up for 1-3 days, then gradually fall
107
Q

How is rhabdomyolysis managed?

A
  • IV fluids-> rehydrate + encourage breakdown product filtration
  • IV sodium bicarb-> make urine more alkaline + reduce myoglobin toxicity
  • IV mannitol-> after correcting hypovolaemia to increase eGFR + reduce oedema
  • Treat complications
108
Q

What are the causes of hyperkalaemia?

A
  • AKI, CKD, rhabdomyolysis, adrenal insufficiency, tumour lysis syndrome
  • Meds-> NSAIDs, ACEis, ARBs, aldosterone antagonists (spironolactone etc)
109
Q

What investigations should be done in hyperkalaemia?

A
  • U+Es-> K+, creatinine, urea, eGFR

- ECG-> need when K+ >6mmol/L + may see tall peaked T-waves, flattened/absent P waves, broad QRS

110
Q

What ECG findings may be present in hyperkalaemia?

A

Tall peaked T-waves, flattened/absent P waves, broad QRS

111
Q

How is hyperkalaemia managed?

A
  • Local policy, close ECG monitoring + renal input
  • Need urgent treatment if >6mmol/L K+
  • Calcium gluconate-> stabilise cardiac muscle cells + reduce arrhythmia risk
  • Insulin + dextrose-> drive carbs into cells + take K+ in to reduce blood levels
  • Nebulised salbutamol
  • IV fluids-> increase UO + encourage K+ loss
  • May use oral calcium resonium, sodium bicarbonate, dialysis
112
Q

What is polycystic kidney disease?

A

Genetic condition in which kidneys develop cysts leading to significant impairment and sometimes extra-renal problems

113
Q

What are the different types of polycystic kidney disease?

A
  • PKD-1-> autosomal dominant (chromosome 16)
  • PKD-2-> autosomal dominant (chromosome 4)
  • Autosomal recessive polycystic kidney disease (ARPKD)-> chromosome 16
114
Q

What extra-renal manifestations can occur in autosomal dominant polycystic kidney disease?

A
  • Cerebral aneurysms
  • Cysts-> hepatic, splenic, pancreatic, ovarian, prostatic
  • Mitral regurgitation
  • Colonic diverticula
  • Aortic root dilatation
115
Q

What are the complications of autosomal dominant polycystic kidney disease?

A

Chronic loin pain, HTN, CVD, gross haematuria (eg cyst rupture), renal stones, end stage renal failure

116
Q

What is the presentation of autosomal recessive polycystic kidney disease?

A
  • Oligohydramnios-> as foetus doesn’t produce enough urine
  • Underdeveloped lungs + respiratory failure after birth
  • Dysmorphic features-> low set ears, flat nasal bridge
  • End stage renal failure before adulthood
117
Q

How is autosomal recessive polycystic kidney disease managed?

A

-May need dialysis in first few days of life

118
Q

How is polycystic kidney disease diagnosed?

A
  • Ultrasound

- Genetics

119
Q

How is polycystic kidney disease managed (in general)?

A
  • Tolvaptan-> vasopressor receptor antagonist, can slow cyst developement
  • Complications support-> anti-HTNs, analgesia (colic), antibodies/drainage of infected cysts, dialysis, transplant
  • Avoid contact sport-> cyst rupture
  • Avoid anti-inflammatories + anti-coagulants
  • Regular US + bloods + BP monitoring
  • Regular MR angiograms-> cranial aneurysms
  • Genetic counselling

Medicine (13 decks)

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