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Phase 3B > Renal > Flashcards

Renal Flashcards

1
Q

What is an acute kidney injury?

A

-An abrupt loss of kidney function (within 48 hours) resulting in the retention of urea and other waste products = dysregulation of extracellular volume and electrolytes

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2
Q

What are the 3 criteria that defines AKI?

A
  • Increase in serum creatinine of >26.4μmol/L above baseline
  • Increase in serum creatinine of >50%
  • Oliguira <0.5mL/kg/hr for >6hr
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3
Q

Who are high risk patients for AKI?

A
  • CKD
  • Diabetics
  • Diffuse atherosclerotic disease
  • CCF
  • Multiple myeloma
  • Elderly
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4
Q

How can the causes of AKI be classified?

A
  • Pre-renal
  • Renal
  • Post renal
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5
Q

What are the pre renal causes of AKI?

A
  • Volume depletion ie bleeding, D+V, burns
  • Oedematous states ie Cardiac failure, cirrhosis, neprhotic syndrome
  • Hyptension ie sepsis, shock
  • CV
  • Medications ie NSAID, COX-2, ACEi, ARB
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6
Q

What are the renal causes of AKI?

A
  • Glomoerular disease ie glomerulonephritis, thrombosis
  • Tubular injury ie prolonged ischaemia, nephrotoxins
  • Acute interstitial nephritis ie drugs, infection, autoimmune disease
  • Vascular disease ie Polyarteritis nodosa, vasculitis, renal artery stenosis
  • Eclampsia
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7
Q

What are the post renal causes of AKI?

A
  • Prostatic hypertrophy
  • Calculus
  • Blood clot
  • Urethral stricture
  • Tumour
  • Pelvic malignancy
  • Radiation fibrosis
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8
Q

What are the drugs known to cause AKI?

A
  • NSAIDS
  • gentamycin
  • antifungals
  • antivirals
  • radio-iodine contrast
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9
Q

Who is most commonly affected by AKI?

A

-Elderly

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10
Q

What are risk factors for AKI?

A
  • Age >65
  • CKD with eGFR <60
  • Past history of AKI
  • CO-existing illness eg cardiac failure, liver disease, diabetes
  • Neuroimpairment
  • Hypovolaemia
  • Symptoms of urological obstruction
  • Sepsis
  • Use of contrast
  • Nephrotoxic Medications
  • Perioperative period
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11
Q

How does AKI present?

A

-Decreasing urine volume and rise in serum creatinine

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12
Q

What are symptoms of an AKI?

A
  • Decrease in urine output ie oliguria, anuria
  • Nausea and vomiting
  • Dehydration
  • Confusion
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13
Q

What are signs of AKI?

A
  • Hypertension
  • Large painless bladder
  • Fluid overload: ^JVP, pulmonary and peripheral oedema
  • Postural hypotension and dehydration
  • Pallor, rash, bruising
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14
Q

What investigations are required for an AKI?

A
  • Urinalysis and urine microscopy
  • Creatinine blood test along with other normals
  • Blood film
  • Immunology ie bence jones protein, ANCA, complement
  • US (if obstruction suspected)
  • Other radiology for systemic disease
  • BIOPSY
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15
Q

How does CKD differ from AKI?

A

CKD:

  • long duration of symptoms
  • nocturia
  • absence of illness
  • anaemia
  • hyperphosphatemia
  • reduced renal size
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16
Q

How is AKI managed?

A 
-Supportive treatment:
>treat underlying cause
>stop nephrotoxic drugs
>monitor fluid and electrolytes
>treat acute complications ie K+^, acidosis, pulmonary oedema, bleeding
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17
Q

What are the indications for dialysis (renal replacement therapy)

A
  • Hyperkalaemia
  • Pulmonary oedema refractory to medical management
  • Severe metabolic acidaemia due to kidney failure
  • Progressive renal failure (^creatinine)
  • Uraemic complications ie pericarditis, altered mental state)
  • Fluid overload
  • Renal transplant
  • CKD 4 or 5
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18
Q

What is the management bundle for AKI?

A
  • Haemodynamic restoration (fluids and inotropes)
  • Treatment of K+
  • Input/output charting and frequent obs
  • Urinalysis
  • Stop nephrotoxins, drugs with haemodynamic effect, reduce doses of renally excreted drugs
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19
Q

What is CKD?

A

-Abnormal kidney function ie eGFR <60ml/min/1.73m^2 for longer than 3 months
or
-Kidney damage

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20
Q

What is are risk factors for CKD?

A
  • Increasing age
  • Diabetes
  • CVD
  • Proteinuria
  • AKI
  • Hypertension
  • Smoking
  • African, afro-carribean or asian ethnicity
  • Chronic use of NSAIDs
  • Untreated outflow obstruction
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21
Q

Classification of CKD?

A
  • Stage 1: normal - eGFR >90 ml/minute/1.73 m2 with other evidence of chronic kidney damage (see below).
  • Stage 2: mild impairment - eGFR 60-89 ml/minute/1.73 m2 with other evidence of chronic kidney damage.
  • Stage 3a: moderate impairment - eGFR 45-59 ml/minute/1.73 m2.
  • Stage 3b: moderate impairment - eGFR 30-44 ml/minute/1.73 m2.
  • Stage 4: severe impairment - eGFR 15-29 ml/minute/1.73 m2.
  • Stage 5: established renal failure (ERF) - eGFR less than 15 ml/minute/1.73 m2 or on dialysis.
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22
Q

What persistent findings may indicate CKD?

A
  • Persistent microalbuminuria
  • Persistent proteinuria
  • Persistent haematuria
  • Structural abnormalities ie PCKD
  • Biopsy proven glomerulonephritis
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23
Q

How does CKD present?

A
  • Usually incidentally on a routine blood or urine test

- Long/progressive disease

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24
Q

What are the symptoms of severe CKD?

A 
Anorexia
Nausea
Vomiting
Fatigue
Pruritus
Peripheral oedema
Dyspnoea
Insomnia
Muscle cramps
Pulmonary oedema
Nocturia
Headache
Sexual dysfunction
Very severe
Hiccups
Pericarditis
Coma
Seizures
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25
Q

What are risk factors that require screening for CKD?

A

-AKI
-CVD
>ischaemic heart disease, chronic HF, PAD, Cerebral vascular disease
-Structural renal tract disease, prostatic hypertrophy
-Multisystem disease ie SLE
-FHX of CKD

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26
Q

Investigations of CKD?

A

-eGFR
-Biochemistry: k+^, bicarb low, phosphate high
-Haematology: anaemia
-Serology: >autoantibodies: ANA, c-ANCA, p-ANCA, anti-GBM
>Hepatitis
>HIV
-Urinalysis
-Imaging: renal US
-Retrograde pyelogram
-Renal radionuclide scan
-CT (Renal artery stenosis)
-Biopsy

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27
Q

Management of CKD?

A
  • Explanation and education
  • Medication review
  • Monitoring of eGFR
  • Immunise against influenza and pneumococcus
  • CVD prevention and blood pressure control
  • Advice for nutrition and physical exercise
  • Manage and monitor bone and mineral disorders and treat with vit d supplementation if required
  • Treat hyperphosphataemia with calcium acetate
  • Renal replacement therapy if required
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28
Q

When should a patient with CKD be referred?

A
  • GFR <30ml/minute/1.73m2 - with or without diabetes
  • ACR >70mg/mmol - unless already known to be caused by DM and being treated
  • ACR >30mg/mmol with haematuria
  • Sustained decrease in GFR of 25%+ within 12 months
  • Hypertension poorly controlled despite >4 drugs
  • Known or suspected rate or genetic causes of CKD
  • Suspected renal artery stenosis
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29
Q

What are some potential complication of CKD?

A
  • Anaemia
  • Coagulopathy
  • Hypertension
  • Calcium phosphate loading: cardiovascular disease, arthropathy, soft tissue calcification
  • Renal osteodystrophy: disorders of calcium, phosphorus and bone
  • Bone changes of secondary hyperparathyroidism
  • Neurological: uraemic encephalopathy, neuropathy
  • Dialysis amyloid: bone pain, arthropathym carpal tunnel syndrome
  • Fluid overload: pulmonary oedema, hypertension
  • Malnutrition: increased mortality and morbidity, poor wound healing, infections
  • Glucose intolerance due to peripheral insulin resistance
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30
Q

What is hyperkalaemia?

A

-Plasma potassium >5.5mmol/L

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31
Q

What are the different severities of potassium and when do the blood tests need to be repeated?

A 
-Mild: .5-5.9
>recheck in a week
-Moderate: 6.0-6.4
>recheck next week
-Severe: >6.5
>requires urgent investigation
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32
Q

Mechanisms of action causing hyperkalaemia:

A
  • Renal causes: decreased excretion of drugs
  • Increased circulation of potassium
  • A shift from intracellular to the extracellular space
  • Pseudohyperkalaemia
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33
Q

When is the greatest risk to experience hyper/hypokalaemia?

A

-At the extreme ends of age

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34
Q

What are the renal causes of hyperkalaemia?

A
  • AKI
  • CKD
  • Hyperkalaemic renal tubular acidosis
  • Mineralocorticoid deficiency
  • Medicines that interfere with RAAS
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35
Q

What drugs can cause hyperkalaemia?

A
  • ACEi
  • ARBs
  • NSAIDs
  • Heparin
  • Ciclosporin
  • Tacrolimus
  • Pentamidine
  • Co-trimaxazole
  • Herbal remedies
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36
Q

What are the exogenous causes of increased potassium?

A
  • Potassium supplementation

- Increased food consumption of soft fruit, veg, chocolate, coffee

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37
Q

What are the endogenous causes of increased potassium?

A
  • tumour lysis syndrome
  • rhabdomyloysis
  • trauma
  • burns
  • crush syndrome
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38
Q

What causes pseudohyperkalaemia?

A
  • Prolonged tourniquet time
  • Difficulty collecting sample
  • Clenched fist
  • Test tube haemolysis
  • Use of wrong haemolysis
  • Excessive cooling of specimen
  • Length of storage of specimen
  • Marked leukocytosis and thrombocytosis
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39
Q

How does hyperkalaemia present?

A
  • Non-specific: weakness and fatigue
  • Muscular paralysis or SOB, chest pain, palpitations
  • Bradycardia
  • Tachypnoea from resp weakness
  • Flaccid paralysis
  • Depressed tendon reflexes
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40
Q

What investigations are required for hyperkalaemia?

A
  • 24hr urine volume and electrolytes
  • FBC
  • Capillary blood glucose
  • ABG
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41
Q

What are the ECG findings of hyperkalaemia?

A
  • Tall tented T waves (in all chest leads)
  • Reduced/loss of P wave
  • Widening of QRS
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42
Q

When are cardiac conduction disturbances most likely when caused by hyperkalaemia?

A

-When there is a rapid rise of potassium

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43
Q

How is hyperkalaemia managed?

A
  • Calcium gluconate 10% - 10mls - over 1-2 minutes

- Insulin immediate release and dextrose 10%

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44
Q

What is hypokalaemia?

A

<3.5 mmol/L

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45
Q

What are the severities of hypokalaemia?

A
  • Mild: 3.1-3.5mmol/L
  • Moderate: 2.5-3.0mmol/L
  • Severe: <2.5mmol/L
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46
Q

What are most cases of hypokalaemia caused by?

A

-Diuretic consumption or loss of GI fluids through vomiting, chronic diarrhoea or laxative abuse.

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47
Q

What are the causes of hypokalaemia?

A
  • Increased loss
  • Transcellular shift
  • Decreased intake of potassium
  • Misc
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48
Q

What causes increased potassium loss via the kidney?

A
  • Thiazide/loop diuretics
  • Renal tubular acidosis
  • Hypomagnesaemia
  • Hyperaldosteronism
  • Tubulointerstitial renal disease
  • Excess liquorice ingestion
  • Activation of RAAS system
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49
Q

What causes increased potassium loss via the GI tract?

A
  • Diarrhoea
  • Vomiting
  • Intestinal fistulae
  • Villous adenoma
  • Pyloric stenosis
  • Laxative abuse
  • Bowel prep
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50
Q

What causes increased potassium loss via the skin?

A
  • Burns
  • Erythroderma
  • Increased sweating
  • Increased loss in sweat ie CF
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51
Q

What are the transcellular shift causes of hypokalaemia?

A
  • Alkalosis
  • Insulin and glucose administration
  • Calcium channel blockers
  • Hypothermia
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52
Q

What are the causes of decreased potassium intake?

A
  • Inadequate potassium replacement on IV fluids whilst NBM
  • Total parenteral nutrition
  • Malnutrition
  • Anorexia nervosa
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53
Q

How does hypokalaemia present?

A
  • Generally asymptomatic
  • General fatigue
  • Generalised weakness
  • Muscle pain
  • Constipation
  • Incidental findings
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54
Q

How does severe hypokalaemia present?

A

-Severe muscle paralysis

>lower extremities moving upwards

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55
Q

What bloods are needed for hypokalaemia?

A 
-Bloods:
>U&amp;E, Bicarb, glucose, chloride, Mg
-ECG:
>Flat t waves, St depression, U waves, Ventricular arrhythmias
-Urine test
>urinary K+, NA+, osmolality
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56
Q

What is the management for hypokalaemia?

A
  • Primary care for 2.5-3.0: compare with previous results, ECG, oral potassium replacement. –>40-120mmol/day
  • TARGET: 4.5mmol/L
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57
Q

What electrolyte needs to managed before others can be corrected?

A

-Magnesium

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58
Q

What is secondary care management for hypokalaemia?

A
  • Oral dose of 20-40mol K+ 2-4 times daily

- IV KCL via peripheral line

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59
Q

What are the complications of hypokalaemia?

A
  • Arrhythmias, sudden cardiac death
  • Muscle weakness
  • Abnormal renal function
  • Iatrogenic hyperkalaemia
  • Digoxin toxicity
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60
Q

How is calcium regulated within the body?

A

-Reduction in serum calcium stimulates PTH
>increases bone resorption
>increases renal calcium reabsorption
>stimulates renal conversion of 25-hydroxyvitamin D3 to 1,25 dihydroxyvitamin D3 (increases intestinal calcium absorption)
>negative feedback

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61
Q

What should serum calcium be?

A

2.25-2.5mol/L

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62
Q

Why should you use corrected (unbound) calcium?

A

-Not bound to albumin so free to take part in cellular activities such as neuromuscular contraction, coagulation

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63
Q

What is hypercalcaemia?

A

Calcium >2.5

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64
Q

What is the most common cause of hypercalcaemia?

A

-Primary hyperparathyroidism

>usually in postmenopausal women

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65
Q

Mneumonic for hypercalcaemic presentation?

A
  • STONES
  • BONES
  • GROANS
  • MOANS
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66
Q

What symptoms may someone experience if they have hypercalcaemia?

A
  • Polyuria/polydypsia
  • Depression
  • Cognitive impairment
  • Muscle weakness
  • Constipation
  • Anorexia
  • Abdominal pain
  • Vomiting
  • Dehydration
  • Coma
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67
Q

What are the PTH mediated causes of hypercalcaemia?

A

-Primary hyperparathyroidism

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68
Q

What are the non-PTH mediated causes of hypercalcaemia?

A
  • Malignancy
  • Granulomatous conditions ie sarcoidosis
  • Endocrine conditions ie thyrotoxicosis
  • Drugs ie thiazide diuretics, vit A and D supplements
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69
Q

What are the 4 mechanisms that malignancy causes hypercalcaemia?

A
  • Ectopic production of PTH related peptide by tumour cells
  • Osteolytic hypercalcaemia
  • Ectopic calcitriol
  • Ectopic PTH produced by tumour cells
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70
Q

What imaging investigations are required for hypercalcaemia?

A
  • X ray: bony abnormalities

- US/CT: urogenital tract imaging >stones or calcification

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71
Q

What bony abnormalities may be detected by xray in someone with hypercalcaemia?

A
  • Demineralisation
  • Bone cyts
  • Bony metastases
  • Pathological fractures
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72
Q

What is the acute management of hypercalcaemia?

A
  • Increase circulating volume with 0.9% saline
  • Bisphosphonates
  • Glucocorticoids
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73
Q

What is the management of asymptomatic hypercalcaemia?

A
  • Conservative treatment with regular bone density monitoring, renal function, serum and urinary calcium levels
  • regular mobilisation
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74
Q

What is the management of symptomatic hypercalcaemia?

A

Removal of parathyroid gland if impaired renal function, hypercalciuria, low bone mineral density, severe hypercalcaemia

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75
Q

What is hypocalcaemia?

A

serum calcium <2.1

76
Q

What level of calcium can result in neuromuscular instability symptoms?

77
Q

What are symptoms of hypocalcaemia?

A
  • Parasthesia (around mouth, toes, fingers)
  • Tetany
  • Carpopedal spasm
  • Muscle cramps
78
Q

What are signs of hypocalcaemia?

A
  • Chvosteks sign
  • seizures
  • prolonged QT interval
  • Laryngospasm
79
Q

What does prolonged hypocalcaemia cause?

A
  • Subcapsular cataract
  • Papilloedema
  • Abnormal teeth
  • Ectopic calcification
  • Dementia and confusion
80
Q

What are the most common causes of hypocalcaemia?

A
  • Hypoparathyroidism
  • Vitamin D deficiency/abnormal metabolism
  • CKD
  • Hypomagnesaemia
81
Q

How should hypocalcaemia be investigated?

A
  • Recheck blood sample
  • Exclude CKD
  • Check mg and p04
  • Serum PTH and vit D
  • ECG
82
Q

How should acute hypocalcaemia be managed?

A
  • Calcium gluconate 10% 10ml IV

- Monitor and further infusion if necessary

83
Q

How should persistent hypocalcaemia be managed?

A

-Supplementary calcium and vitamin D

84
Q

What is hypernatraemia?

A

> 145mmol/L

85
Q

What are risk factors for hypernatraemia?

A 
-Lack of independent access to water 
>children
>elderly patients
>altered mental status
>hypothalamic lesions affecting sense of thirst
>critical illness causing AKI
86
Q

What are the causes of AKI?

A
  • Dehydration
  • Hypotonic fluid loss
  • Hypertonic sodium gain
  • Intracellular shift of water (rare)
87
Q

What are the causes of dehydration which may result in hypernatraemia?

A
  • Inadequate water intake
  • DI
  • Thirst impairment ie dementia
88
Q

What are the causes of hypotonic fluid loss?

A

-Dermal losses ie burns
-GI losses ie diarrhoea and vomiting
-Urinary losses
ie loop diuretics

89
Q

What are the causes of hypertonic sodium gain?

A
  • Iatrogenic ie tube feeding
  • Excess salt ingestion
  • Hyeraldosteronism
90
Q

How does hypernatraemia present?

A
  • CNS dysfunction ie lethargy, weakness, confusion

- Dehydration ie dry mouth, oliguria, tachycardia

91
Q

What investigations are required for hypernatraemia?

A
  • U&E
  • Plasma gluocse
  • Urine and sodium osmolality
  • Neuroimaging if required
92
Q

What is the management of hypernatraemia?

A
  • Treat underlying disorder if possible
  • Correct dehydration and hypovolaemia
  • Monitor progress
93
Q

What are complications of hypernatraemia?

A
  • Cerebral bleeding
  • SAH
  • Permanent brain damage
  • Death
  • Cerebral oedema (if overfast correction)
94
Q

How is hyponatraemia classified?

A
  • Acute vs chronic

- Hypovolaemic vs hypervolaemic vs euvolaemic

95
Q

What are normal sodium levels?

A

136-142.
Mild hyponatraemia <136
Severe hyponatraemia <120

96
Q

How is sodium controlled?

A
  • Kidneys regulate sodicum excretion and level of fluid in the body via the RAAS system.
  • ADH plays a role in regulation
97
Q

Which patient groups are at risk of hyponatraemia?

A

-Children and the elderly

98
Q

What are the causes of hypovolaemic hyponatraemia?

A
  • D+V
  • Addison’s disease
  • Burns
  • Excessive sweating
  • Medications: diuretics
99
Q

What are the causes of hypervolaemic hyponatraemia?

A
  • Cardiac failure
  • Cirrhosis
  • Kidney failure
100
Q

What are the causes of euvolaemic hyponatraemia?

A
  • Neurological ie brain tumour or trauma
  • Lung disorders ie lung cancer, pneumonia
  • Cancers
  • Medications ie SSRIs, PPI, ACEi
  • Pain, postoperative, stress, endurance excercise
101
Q

How does mild hyponatraemia present?

A
  • Anorexia
  • Headache
  • Nausea
  • Vomiting
  • Lethargy
102
Q

How does moderate hyponatraemia present?

A
  • Personality change
  • Muscle cramps
  • Weakness
  • Confusion
  • Ataxia
103
Q

How does severe hyponatraemia present?

A
  • Drowsiness

- Seizures

104
Q

What are signs of hyponatraemia?

A

-Neuro signs: Altered consciousness, cognitive impairment, seziures
-Hypovolaemia signs: dry mucous membranes, tachycardia, reduced skin turgor
-Signs of hypervolaemia: pulmonary rales,
JVP^, peripheral oedema

105
Q

What investigatinos are required for hyponatraemia?

A
  • Fluid status
  • Serum sodium and potassium
  • Urine sodium level
  • Serum TSH and free thyroxine level
  • Random serum cortisol level
  • Imaging
106
Q

What is the acute management for hyponatraemia?

A
  • Hypertonic 3% saline. 150ml over 15 min.
  • repeat after 20 mins if no clincial improvement.
  • Recheck Na at 6,12,24, 48hrs for over correction.
107
Q

How should hypvolaemic hyponatraemia be treated?

A

-0.9% saline

108
Q

How should hypervolaemic hyponatraemia be treated?

A

-Treat underlying cause. ie ccf, renal failure, liver cirrhosis

109
Q

What are the 3 cardinal features of nephrotic syndrome?

A
  • Proteinuria
  • Oedema
  • Hypoalbuminaemia
110
Q

What is the aetiology of nephrotic syndrome?

A

-Often unknown
-Vasculitides
>HSP, SLE,
-Infections
-Allergens ie bee sting

111
Q

What are the clinical features of nephrotic syndrome?

A
  • Periorbital oedema (particularly on waking)
  • Scrotal/Vulval oedema, leg and ankle oedema
  • Ascites
  • Breathlessness (pleural effusion)
112
Q

What investigations are needed to look for nephrotic syndome?

A
  • Urine protein (urine dipstick)
  • Urine microscopy and culture
  • Blood pressure
  • Bloods (FBC, U+E, creatinine, albumin, complement levels - c3+c4 decrease), antistreptolysin O or anti-DNAase B and throat swab
113
Q

What does histology of steroid sensitive nephrotic syndrome look like?

A
  • Light microscopy: normal
  • Electron microscopy: fusion of podocytes
  • Minimal change disease*
114
Q

What features suggest steroid sensitive nephrotic syndrome?

A 
-Age between 1 and 10 years
>Peak between 2+5
-No macroscopic haematuria
-Normal blood pressure
-Normal complement levels
-Normal renal function
115
Q

How is nephrotic syndrome managed?

A
  • Oral corticosteroids (prednisolone) > 60mg/m2/day and reduced slowly from week 4.
  • Blood pressure monitoring
  • Fluid restriction/balance
  • Salt restriction
  • Prophylactic antibiotics
116
Q

What are complications of nephrotic syndrome?

A
  • Hypovolaemia
  • Thrombosis
  • Infection
  • Hypercholesterolemia
117
Q

Why does hypovolaemia occur as a complication from nephrotic syndrome?

A

-Peripheral vasoconstriction and urinary sodium retention

118
Q

Why does thrombosis occur as a complication from nephrotic syndrome?

A
  • Hypercoagulable state due to a loss of antithrombin in the urine
  • Thrombocytosis can exacerbate steroid therapy
  • Increased blood viscosity from raised haematocrit
  • Increased synthesis of clotting factors
119
Q

Why might someone develop an infection if they have nephrotic syndrome?

A
  • Immunoglobulins lost in urine

- Pneumococcus is most common infective bacteria

120
Q

What are the causes of steroid resistant nephrotic syndrome?

A
  • Focal segmental glomerulonephritis
  • Mesangiocapillary glomerulonephritis
  • Membranous nephropathy
121
Q

How is steroid resistant nephrotic syndrome treated?

A
  • Depends on the underlying cause of nephrotic syndrome
  • Azothioprine
  • DIuretics
  • Salt restrictions
  • ACEi
  • NSAIDs
122
Q

What are the 5 functions of the kidneys?

A
  • Elimination of waste material
  • Regulation of volume and composition of body fluid >BP regulation, electrolytes
  • Endocrine functino > production of EPO and renin, activation of vit D
  • Autocrine function > production of endothelin, prostaglandins, renal natriuretic peptide
  • Acid base balance > regulares bicarbonate and H+ excretion
123
Q

What drugs inhibit secretion of creatinine (and therefore eGFR)?

A
  • Trimethoprim
  • Cimetidine (histamine receptor antagonist)
  • Ritonavir (treatment for HIV)
124
Q

What is the role of the proximal convoluted tubule?

A
  • Resorbs 70% of Na+.

- Also absorbs glucose, bicarb and amino acids

125
Q

What hormone acts mainly on PCT?

A

-Angiotensin II

126
Q

What is the role of the distal convoluted tubule?

A

-Regulation of sodium re-absorption (therefore water reabsorption)
-Under the control of aldosterone
>also excretes K+ and H+

127
Q

Why does hypokalaemia and alkalosis occur in Conn’s syndrome?

A

-Conn’s syndrome = hyperaldosteronism
>Na+ reabsorption and K+ excretion in DCT.
>K+ also pulls H+
=hypokalaemic and alkalosis

128
Q

Why does Addison’s disease cause a hyperkalaemic acidosis?

A

-Addison’s disease = adrenal insufficiency
>impaired sodium reabsorption and K+ excretion
>hypotension

129
Q

Which meds can cause hypokalaemia?

A
  • Loop diuretics

- Thiazide diuretics ie bendroflumethiazide, indapamide

130
Q

Which meds can cause hyperkalaemia?

A
  • spinonalactone
  • amiloride
  • ARB
  • Trimethoprim
131
Q

How do thiazide diuretics work?

A

-Block the Na+/Cl- channel in the DCT

>Bendroflumethiazide

132
Q

How do loop diuretics work?

A

-Block Na+K+Cl- in the loop of Henle

>Furosemide

133
Q

How do potassium sparing diuretics work?

A

-Block Na channels in the collecting duct

>amiloride

134
Q

How does spinoralactone work?

A

-Aldosterone antagonist

135
Q

What can kidney stones be made of?

A
  • CALCIUM OXALATE
  • Uric acid
  • Cysteine
  • Calcium phosphate
  • Struvite
136
Q

Where are the 3 most common sites for kidney stones?

A
  • Pelvoureteric junction
  • Pelvic brim
  • Uterovesicular junctino
137
Q

What are risk factors for renal stones?

A
  • Dehydration
  • High calcium
  • Cystinuria
  • High dietary oxalate
  • Renal tubular acidosis
  • Kidney structural acidosis
138
Q

What are risk factors for urate kidney stones?

A
  • Gout
  • Hyperuricaemia
  • Ileostomy pts
  • Myeloproliferative disorders
139
Q

What are the causes of hyperoxaluria?

A

-Dietary causes: increased rhubarb, tea, spinach

140
Q

Which meds increase risk of developing kidney stones?

A 
-Drugs that promote calcium stones;
>loop diuretics
>steroids
>acetozolamide
>theophylline
141
Q

What meds prevent calcium stones from forming?

A

-Thiazide diuretics

142
Q

What are the clinical features of kidney stones?

A
  • Renal colic. Severe intermittent loin pain (loin to groin pain)
  • Writhing pain
  • Haematuria
  • Dysuria
143
Q

Investigations for kidney stones?

A
  • Urine dipstick and CR
  • Serum Cr and electrolytes
  • FBC/CRP
  • Calcium/urate
  • MSSU
  • Plain KUB XR + CT
144
Q

Management for kidney stones?

A

-Strong analgesia
-Most stones pass spontaneously
-Medications:
>alpha adrenergic blockers, calcium channel blockers

145
Q

What are the indications for interventions in kidney stones?

A
  • Persistent pain
  • Infection above site of obstruction
  • Failure of the stone to pass down the ureter
146
Q

How is interventional removal of kidney stones performed?

A
  • Shockwave lithotripsy
  • Ureteroscopy
  • Percutaneous nephrolithotomy
  • Open surgery
147
Q

How are calcium renal stones prevented?

A
  • High fluid intake
  • Low animal protein
  • Low salt diet
  • Thiazide diuretics
148
Q

Why might flash pulmonary oedema occur in AKI?

A

-Reduced renal perfusion activates RAAS which reduces fluid clearance by the kidneys
=fluid overload

149
Q

How should flash pulmonary oedema in AKI be managed?

A
  • O2
  • Diuretics (IV furosemide)
  • Nitrates (GTN infusion)
  • Opiates
  • Haemodialysis if required
150
Q

What is acute tubular necrosis?

A
  • Necrosis of the renal tubular epithelial cells

- In the early stages, it’s reversible

151
Q

What are the causes of acute tubular necrosis?

A
  • Renal ischaemia

- Toxins

152
Q

What are the features of ATN?

A
  • Raised urea
  • Raised Cr
  • Raised K+
  • Muddy brown casts in the urine
153
Q

What is acute interstitial nephritis?

A

-Inflammation of any part of the kidney

154
Q

What are the causes of acute interstitial nephritis?

A
  • Idiopathic
  • Drugs ie penicillin, rifampicin, NSAIDs, allopurinol
  • Infection ie staph
155
Q

What is glomerulonephritis?

A
  • A broad term that refers to a group of parenchymal kidney disease
  • Causes: leaky glomeruli, hypertension, deteriorating kidney function
156
Q

Nephritic vs nephrotic syndrome?

A

-Nephritic: hypertension, inflammation of the glomeruli, oliguria, haematuria (cola coloured) IgA neuropathy
-Nephrotic:
Hypoalbuminaemia, hyperlipidaemia, proteinuria, peripheral oedema

157
Q

What are possible bone disease mainfestations of CKD?

A
  • Osteitis fibrosa cystica (hyperparathyroid bone disease)
  • Adynamic (reduction in cellular activity)
  • Osteomalacia
  • Osteosclerosis
  • Osteoporosis
158
Q

Which drugs need dose alterations if a patient has CKD because they accumulate?

A
  • Most abx ie penicillins, cephalopsorins, gent, vanc
  • Digoxin
  • Atenolol
  • Methotrexate
  • Sulfonylureas
  • Furosemide
  • Opioids
159
Q

What is the distribution of body fluid in an average 70kg person?

A
  • Total volume: 42L
  • Intracellular volume: 28L
  • Extracellular volume: 14L (11L interstitium, 3L plasma)
160
Q

What are physical signs (and symptoms) of hypovolaemia?

A
  • Tachycardia
  • Hypotension
  • Reduced skin turgor
  • Dry mucuous membranes
  • Reduced urine output
  • Weight reduction
  • Thirst
  • Dizziness
161
Q

Which co-morbidities make a patient more at risk of hypervolaemia?

A
  • Chronic kidney disease
  • Heart failure
  • Liver failure
162
Q

What is third spacing?

A 
-FLuid collects in  parts of the body that it shouldn't collect ie
>pleural effusion
>ascites
>bowel obstruction
>obesity
163
Q

When are crystalloid fluids used? What are some examples?

A

-Used when a patient needs hydrating (able to move into the extravascular space and nourish tissue)
>Hartmann’s
>Normal saline
>5% dextrose

164
Q

What are colloid fluids used for? what’s an example?

A

-Used for hypovolaemic patients. (fluid remains in intravascular compartment ->increases blood volume)
-Commonly used in hypovolaemic shock
>Gelofusine

165
Q

What is autosomal dominant polycystic kidney disease?

A

-Most common cause of inherited kidney disease
-2 types: PKD1 (chromosome 16 defect> presents with renal failure early)
PKD2 (chromosome 4 defect)

166
Q

What is PKD associated with?

A
  • Brain, liver and pancreatic cysts
  • Aneurysms
  • Diverticulae
  • Mitral valve prolapse
167
Q

What is vascular disease is PKD associated with

A

-Subarachnoid haemorrhage due to berry aneurysms

168
Q

How do kidney cysts present?

A
  • Polyuria and nocturia
  • Enlarged kidney on US
  • Renal colic (from increased risk of stones)
169
Q

What investigations should be arranged for PKD?

A
  • Family screening
  • US
  • CT scan
170
Q

What is the management for PKD?

A
  • Nephrectomy

- Treat complications

171
Q

What is the most common type of kidney cancer?

A

-Renal cell carcinoma (adenocarcinoma)

172
Q

What are risk factors for renal cell carcinoma?

A
  • Smoking
  • Obesity
  • Hypertension
  • Tuberous sclerosis
  • Renal failure and dialysis
  • PKD
  • Von Hippel Lindau syndrome
  • Heavy metal industry
  • Middle aged men
173
Q

Where does kidney cancer commonly metastasise to?

A
  • Lungs

- Bones

174
Q

What is the pathophysiology of renal cell carcinoma?

A
  • Adenocarcinoma or the renal cortex

- Arises from the proximal convulated tubule epithelium

175
Q

How does renal cell carcinoma present in a classic triad?

A
  • Haematuria
  • Loin pain
  • Abdominal mass
176
Q

What other symptoms may someone present with if they have renal cell carcinoma?

A
  • Fever of unknown origin
  • Left varicocele (occlusion of left testicular vein)
  • Endocrine effects: EPO>polycythaemia, PTH>hypercalcaemia, renin, ACTH
  • Systemic features: malaise, weight loss
177
Q

What are the paraneoplastic syndromes caused by renal cell carcinoma?

A
  • Hypertension
  • Cachexia
  • Weight loss
  • Amyloidosis
  • Elevated ESR
  • Anaemia
  • Abnormal LFT
  • Hypercalcaemia
  • Polycythaemia
178
Q

How is renal cell carcinoma investigated?

A
  • USS
  • CT
  • MRI
  • PET scan (for mets)
  • Bone scan
179
Q

Treatment for localised kidney cancer?

A
  • Radical nephrectomy
  • Partial nephrectomy
  • Cyrotherapy
  • Alpha interferon and interkeukin 2 (reduce tumour size)
180
Q

What is the most common type of bladder cancer?

A

-Transitional cell carcinoma

181
Q

What are risk factors for transitional cell carcinoma of the bladder?

A
  • Smoking
  • Exposure to aniline dyes in printing and textile injury
  • Rubber manufacture
  • Pelvic irradiation
182
Q

What are risk factors for squamous cell carcinoma of the bladder?

A
  • Schistosomiasis
  • BCG treatment
  • Smoking
183
Q

What is the link between schistosomiasis and bladder cancer?

A
  • Schistosomiasis = parasite that cuases chronic inflammation of the urinary tract
  • 20 years later malignancy develops
  • good prognosis
184
Q

How does bladder cancer present?

A
  • Painless haematuria
  • Recurrent UTIs
  • Voiding irritability
  • LUTs
  • Abdo pain
185
Q

Investigations for bladder cancer?

A
  • Urine dipstick
  • Flexible cystoscopy (+/- transurethral resection of the bladder tumour)
  • CT urogram

Phase 3B (14 decks)

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