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Nephrology - Passmedicine Flashcards

1
Q

How do you calculate an anion gap?

A

(Na + K) - (bicarb + Cl)

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2
Q

What is considered a normal anion gap?

A

8-14mmol/L

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3
Q

What are the two types of metabolic acidosis?

A

Normal anion gap (aka. hyperchloraemia) metabolic acidosis

Raised anion gap metabolic acidosis

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4
Q

List causes of a normal anion gap (aka. hyperchloraemia) metabolic acidosis

A 
GI bicarbonate loss - diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs, e.g. acetazolamide
Ammonium chloride injection 
Addison's disease
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5
Q

List causes of a raised anion gap metabolic acidosis

A 
Lactate: shock, hypoxia
Ketones: DKA, alcohol
Urate: renal failure
Acid poisoning: salicyclates, methanol
5-oxoproline: chronic paracetamol use
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6
Q

What is the anion gap?

A

Measure of the difference between cations and anions

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7
Q

If the serum is neutral in charge why does an anion gap exist?

A

We are only measuring 4 ions to calculate it (there are a lot of significant anions not included, e.g. phosphate, negatively charged plasma proteins e.g. albumin)

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8
Q

What does a high anion gap mean?

A

The negatively charged ions and proteins (not accounted for) are taking up a larger proportion of the serums negative charge than usual

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9
Q

What causes a high anion gap?

A

Increased organic acid in the blood, e.g. lactate anions

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10
Q

Explain why there is an increased anion gap in lactic acidosis

A

Lactic acid breaks down into lactate and H+, H+ is buffered by bicarb so there is less bicarb and more of the negative proportion of the serum being made up by lactate so the anion gap is increased

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11
Q

What essentially causes a normal anion gap?

A

Bicarbonate loss

Kidneys compensate by reabsorbing more Cl keeping serum electroneutral

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12
Q

What is the most common cause of bicarbonate loss causing normal anion gap?

A

Diarrhoea

Then renal tubular acidosis

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13
Q

Does vomiting cause a metabolic acidosis?

A

Usually no

You are losing H+ ions in gastric acid

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14
Q

Define acute interstitial nephritis

A

Pattern of kidney inflammation localised to the kidney tubulo-interstitial space

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15
Q

What tends to trigger acute interstitial nephritis?

A

Medications, esp. antibiotics

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16
Q

What antibiotics commonly cause acute interstitial nephritis?

A 
Penicillin
Rifampicin
NSAIDs
Allopurinol
Furosemide
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17
Q

What are causes of acute interstitial nephritis other than medications?

A

Systemic conditions - SLE, sarcoidosis, Sjogrens

Infections: Hanta virus, staphylococcus

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18
Q

What do you see on histology in acute interstitial nephritis?

A

Marked interstitial oedema and interstitial infiltrates in the connective tissue between renal tubules

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19
Q

What are the clinical features of acute interstitial nephritis?

A

Fever, rash, arthalgia
Eosinophilia
Mild renal impairment
HTN

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20
Q

What can you see on investigation in acute interstitial nephritis?

A

Sterile pyuria
White cell casts
Raised urea and Cr

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21
Q

Who does tubulointerstitial nephritis with uveitis tend to affect?

A

Young females

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22
Q

What are features of tubulointerstitial nephritis with uveitis?

A

Fever
Wt loss
Painful, red eye

Urinalysis shows leukocytes + protein

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23
Q

How do you manage acute interstitial nephritis?

A

Usually managed by stopping the offending medication

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24
Q

What is the most common cause of a nephrotic syndrome in children/young people?

A

Minimal change disease

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25
Q

What causes the majority of cases of minimal change disease? What are other causes?

A

Idiopathic mostly

Drugs: NSAIDs, rifampicin
Hogdkin’s lymphoma, thymoma
Infectious mononucleosis

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26
Q

What is the pathophysiology of minimal change disease?

A

T-cell + cytokine mediated damage to the glomerular basement membrane –> polyanion loss
Resultant reaction of electrostatic charge –> increased glomerular permeability to albumin

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27
Q

What are the features of minimal change disease?

A

Nephrotic syndrome
Normotension usually
Highly selective proteinuria (only medium sized proteins (e.g. albumin and transferrin) leak

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28
Q

What investigation will confirm a diagnosis of minimal change disease?

A

Renal biopsy

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29
Q

What will you see on electron microscopy of the renal biopsy in minimal change disease?

A

Fusion of podocytes + effacement of foot processes

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30
Q

How is minimal change disease managed?

A

80% corticosteroid responsive

If steroid resistant –> cyclophosphamide

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31
Q

What is the prognosis of minimal change disease?

A

1/3rd –> 1 episode
1/3rd –> infrequent relapses
1/3rd –> frequent relapses which stop before adulthood

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32
Q

What is a nephrotic syndrome?

A

Damage to glomeruli allows leakage of proteins into urine –> proteinuria

Albumin leaving blood –> hypoalbuminaemia –> low oncotic pressure –> oedema

Unknown process –> hyperlipidaemia (which can also leak into urine)

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33
Q

What are the 4 hallmarks of nephrotic syndrome?

A

Proteinuria
Hypoalbuminaemia
Oedema
Hyperlipidaemia/lipiduria

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34
Q

What are the 3 layers of the glomerulus?

A

Endothelial cells (which line capillaries), basement membrane, podocytes

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35
Q

What are podocytes named podocytes?

A

They have foot like processes

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36
Q

How are the podocytes charged?

A

Negatively - helps them repel plasma proteins (e.g. albumin) and therefore podocytes act as a charge barrier

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37
Q

What happens in minimal change disease that means that proteins can leak into bowen’s capsule?

A

T-cells release cytokines which specifically damage the foot processes of podocytes making them flatten out (effacement) –> reduced charge barrier and albumin can slip into nephron

NB larger proteins, e.g. Ig aren’t allowed through

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38
Q

What technique do you need to see foot effacement in minimal change disease?

A

Electron microscopy

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39
Q

What is acute tubular necrosis?

A

Ischaemic/nephrotoxic injury to the kidney which leads to cell death

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40
Q

What area is most prone to AKI and why?

A

Renal medulla (it is relatively hypoxic making it prone to renal tubular hypoxia)

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41
Q

What is the best indicator of renal function?

A

eGFR

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42
Q

What parameters are required to estimate eGFR?

A

Serum creatinine, age, race, gender, body size

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43
Q

What sort of things may cause an AKI?

A

Nephrotoxic stimuli, e.g. aminoglycosides, contrasts –> apoptosis

Myoglobulinuria (e.g. after compartment syndrome) + haemolysis –> necrosis

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44
Q

What patients are more likely to be affected by post-op renal failure?

A

Early pts, with PVD, high BMI, COPD, on vasopressors or nephrotoxic medications

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45
Q

Avoiding hypertension/hypotension will reduce the risk of renal tubular damage

A

Hypotension

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46
Q

What is a typical history of acute tubular necrosis?

A

Worsening renal function

Muddy brown casts

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47
Q

What are the three types of AKI?

A

Prerenal - cause before kidneys
Intrarenal - cause within kidneys
Post-renal - cause after kidneys

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48
Q

When is rhabdomyolysis typically seen?

A

After a fall or prolonged epileptic seizure

May be in those who have AKI on admission

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49
Q

What are features of rhabdomyolysis?

A 
AKI with disproportionately raised creatinine
Elevated CK
Myoglobulinuria
Hypocalcaemia
Elevated phosphate
Hyperkalaemia
Metabolic acidosis
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50
Q

Why do you get hypocalcaemia in rhabdomyolysis?

A

Myoglobin binds calcium

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51
Q

Why do you get elevated phosphate in rhabdomyolysis?

A

As it is released from myocytes

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52
Q

Why do you get hyperkalaemia in rhabdomyolysis?

A

Secondary to renal failure

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53
Q

What can cause rhabdomyolysis?

A 
Seizure
Collapse/coma
Ectasy
Crush injury
McArdle's syndrome
Drugs - statins, esp. if co-prescribed with clarithromycin
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54
Q

How is rhabdomyolysis managed?

A 
IV fluids (normal saline) to maintain good urine output
Urinary alkalinization is sometimes used
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55
Q

What is used as a diagnostic criteria in rhabdomyolysis?

A

CK >5x normal

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56
Q

How is Alport’s syndrome inherited?

A

X linked dominant

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57
Q

What genetic defect causes Alport’s syndrome?

A

Defect in gene which codes for IV collagen –> abnormal glomerular basement membrane

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58
Q

When does Alport’s syndrome tend to present?

A

Childhood

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59
Q

What are features of Alport’s syndrome?

A 
Microscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus
Retinitis pigmentosa
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60
Q

What is lenticonus?

A

Protrusion of the lens into the anterior chamber

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61
Q

What do you see on renal biopsy in Alport’s syndrome?

A

Splitting of the lamina dense on electron microscopy (basket weave appearance)

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62
Q

How is Alport’s syndrome diagnosed?

A

Molecular genetic testing

Renal biopsy

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63
Q

At what K level should you give calcium gluconate etc. to treat hyperkalaemia?

A

> 6.5 OR ECG changes

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64
Q

What biochemical pattern is more characteristic of dehydration as opposed to AKI?

A

Raised urea and cr but urea is proportionately more raised

Hypernatraemia

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65
Q

Is eGFR more inaccurate in high or low muscle mass?

A

Both - it is most inaccurate at extremes of muscle mass

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66
Q

What are causes of transient non-visible haematuria?

A

UTI
Menstruation
Vigorous exercise
Sexual intercourse

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67
Q

What are causes of persistent non-visible haematuria?

A 
Cancer (renal, bladder, prostate) 
Stones
BPH
Prostatitis
Urethritis
Renal causes - e.g. IgA nephropathy
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68
Q

What things may mimic haematuria but no blood is actually in the urine?

A

Foods - beetroot, rhubard

Drugs - rifampicin, doxorubicin

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69
Q

What is the test of choice for haematuria?

A

Urine dipstick

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70
Q

Define persistent non-visible haematuria

A

Blood in 2/3 samples tested 2-3 weeks apart

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71
Q

Which patients with haematuria should be urgently referred (within 2 weeks)?

A

Age >=45 AND unexplained visible haematuria in absence of UTI or visible haematuria that persists/recurs after treatment of UTI

Age >= 60 AND unexplained non-visible haematuria and either dysuria or raised WCC on blood test

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72
Q

Which patients with haematuria merit a non-urgent referal?

A

Age >=60 with recurrent or persistent unexplained UTI

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73
Q

Do patients under 40 with haematuria, with normal renal function, who are normotensive and have no proteinuria need to be referred?

A

No - they can be managed in primary care

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74
Q

Which test is most useful in distinguishing between acute tubular necrosis and prerenal uraemia?

A

Urinary sodium

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75
Q

What age group is HUS typically seen in?

A

Young chlidren

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76
Q

What are the triad of features of HUS?

A

AKI
Microangiopathic haemolytic anaemia
Thrombocytopenia

77
Q

What classically causes HUS?

A

Shiga toxin producing E. coli 0157 (90% cases)

78
Q

What other things can cause HUS?

A

Pneumococcal infection
HIV
Rare: SLE, drugs, cancer

79
Q

What investigations should be done in suspected HUS?

A

FBC
UE
Stool culture

Severe cases - plasma exchange may be req.
Eculizumab

80
Q

How is HUS managed?

A

Supportively, e.g. fluids, transfusion, dialysis

NO ANTIBIOTICS

81
Q

What are the commonest causes of polyuria?

A

Diuretics, caffeine, alcohol
DM
Lithium
Heart failure

82
Q

What are some infrequent causes of polyuria?

A

Hypercalcaemia

Hyperthyroidism

83
Q

What are some rare causes of polyuria?

A

Chronic renal failure
Primary polydipsia
Hypokalaemia

84
Q

What is a very rare cause of polydipsia?

A

Diabetes inspidius

85
Q

What is Henoch-Schonlein prupura?

A

An IgA mediated small vessel vasculitis

86
Q

What condition does HSP overlap with?

A

Berger’s disease

87
Q

When is HSP most commonly seen?

A

Following an infection in children

88
Q

What are the features of HSP?

A

Palpable purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs
Ab pain
Polyarthritis
Features of IgA nephropathy may occur, e.g. haematuria, renal failure

89
Q

How is HSP treated?

A

Analgesia

Nephropathy usually treated supportively

90
Q

What is the prognosis of HSP?

A

Usually self limiting

1/3rd relapse

91
Q

What are the two disease loci for ADPKD?

A

PKD1 and PKD2 which code for polycystin 1 and 2

92
Q

How many types of ADPKD are there?

93
Q

What is the best screening for relatives of ADPKD?

A

Abdominal US

94
Q

What is the ultrasound diagnostic criteria for ADPKD in those with +ve FH?

A

2 cysts (uni/bilateral) if <30
2 cysts in both kidneys if 30-59
4 cysts in both kidneys if >60

95
Q

What drug may be used in ADPKD and what patients can use it?

A

Tolvaptan (vasopressin receptor 2 antagonist)
Only used in adults to slow the rate of cyst development if they have CKD 2/3 at the start of treatment, there is evidence of rapidly progressive disease

96
Q

How much glucose should nil by mouth patients be given per day to avoid starvation ketosis?

A

50-100g/day of glucose

97
Q

What is diabetes inspidus?

A

Deficiency of ADH (cranial DI) or insensitivity to antiduretic hormone (nephrogenic DI)

98
Q

What are causes of cranial DI?

A 
Idiopathic
Post head injury
Pituitary surgery 
Craniopharyngiomas
Histocystosis X
Wolfram's syndrome
Haemochromatosis
99
Q

What are the features of Wolfram’s syndrome?

A

DIDMOAD - cranial DI, DM, optic atrophy, deafness

100
Q

What are causes of nephrogenic DI?

A

Genetic - most common affects vasopressin receptor, less common results from mutation in AQP2 channel
Electrolytes: hypercalcaemia, hypokalaemia
Lithium, demeclocycline
Tubulo-interstitial disease (obstruction, sickle cell, pyelonephritis)

101
Q

What are the clinical features of DI?

A

Polyuria, polydipsia

102
Q

What investigation results would you expect in DI?

A

High plasma osmolality, low urine osmolality

Urine osmolality >700mOsm/kg excludes DI

103
Q

What test can you do for DI?

A

Water deprivation test

104
Q

How is nephrogenic DI treated?

A

Thiazides, low salt/protein diet

105
Q

How is central DI treated?

A

Desmopressin

106
Q

What is erythropoietin?

A

A haemopoietic growth factor that stimulates production of erythrocytes

107
Q

What stimulates the kidneys to make EPO?

A

Cellular hypoxia

108
Q

List side effects of EPO

A

Accelerated HTN potentially leading to encephalopathy + seizures
Bone aches
Flu like symptoms
Skin rashes, urticaria
Pure red cell aplasia (due to Abs against EPO)
Raised PCV increases risk of thrombosis
Iron deficiency

109
Q

Why might patients fail to respond to EPO?

A 
Fe deficiency 
Inadequate dose
Concurrent inflammation/infection 
Hyperparathyroid bone disease
Aluminium toxicity
110
Q

What is there an increased risk of in patients with nephrotic syndrome?

A

VTE (LMWH prophylaxis indicated)

111
Q

When might a patient with CKD require dialysis?

A

Uraemia (e.g. encephalopathy/pericarditis)

112
Q

What are features of ADPKD?

A 
HTN
Recurrent UTIs
Abdominal pain
Renal stones
Haematuria 
CKD
113
Q

What are the extra-renal manifestations of ADPKD?

A

Liver cysts (hepatomegaly)
Berry aneurysm (SAH)
CV - mitral valve prolpase, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
Cysts in other organs, e.g. spleen and pancreas

114
Q

How does spironolactone work?

A

Aldosterone antagonist that acts in the cortical collecting duct

115
Q

What are indications for spironolactone?

A 
Ascites
HTN
HF
Nephrotic syndrome
Conn's syndrome
116
Q

What adverse effects are associated with spironolactone?

A

Hyperkalaemia

Gynaecomastia

117
Q

If a patient gets troublesome gynaecomastia with spironolactone what can it be substituted with?

A

Eplerenone

118
Q

How is hyperkalaemia classified?

A

Mild: 5.5-5.9mmol/L
Moderate: 6-6.4mmol/L
Severe: >= 6.5mmol/L

119
Q

At what K level should a patient undergo an urgent ECG?

120
Q

How do the timing of onset of PSGN and IgA nephropathy differ after URTI?

A

PSGN develops 1-2 weeks post URTI

IgA nephropathy develops 1-2 days after URTI

121
Q

What is the normal range for the anion gap?

A

10-18mmol/L

122
Q

How do you calculate an anion gap?

A

(Na + K) - (Cl + HCO3)

123
Q

What are causes of a normal anion gap metabolic acidosis?

A 
GI bicarb loss - diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs, e.g. acetazolamide
Ammonium chloride injection 
Addison's disease
124
Q

What are causes of a raised anion gap metabolic acidosis?

A

Lactate: shock, sepsis, hypoxia
Ketones: DKA, alcohol
Urate: renal failure
Acid poisoning: salicyclates, methanol

125
Q

What are the two types of lactic acidosis?

A

A: sepsis, shock, hypoxia, burns
B: metformin

126
Q

In intrinsic AKI what is the urinary sodium and urine osmolality like and why?

A

It is high because the kidneys are not able to concentrate urine or retain sodium —> urine osmolality low, urine sodium high

127
Q

What is the urinary sodium and urine osmolality like in pre-renal AKI?

A

Urine osmolality high, urine sodium low

Kidneys act to concentrate urine and retain sodium

128
Q

On what chromosome is HLA coded for?

129
Q

What are post-op renal transplant problems?

A

ATN of graft
Vascular thrombosis
Urine leakage
UTI

130
Q

What kinds of graft rejection can you get post-kidney transplant?

A 
Hyperacute rejection (minutes to hours) 
Acute rejection (<6 months)
Chronic rejection (>6 months)
131
Q

What is the pathophysiology of hyperacute rejection?

A

It is due to pre-existing antibodies against donor HLA type 1 antigens (this is v. rare due to HLA matching)

132
Q

What is the pathophysiology of acute rejection?

A

Usually due to mismatched HLA

Other causes incl. CMV infection

133
Q

Can acute rejection be treated?

A

May be reversible with steroids + immunosupressants

134
Q

What happens in chronic graft failure?

A

Both antibody and cell mediated mechanisms cause fibrosis to the transplanted kidney
May get recurrence of original disease

135
Q

How does acute rejection often present?

A

With signs and symptoms of infection

136
Q

How do you confirm the acute graft rejection?

137
Q

What is commonly see in the urine of someone with acute tubular necrosis?

A

Brown granular casts

138
Q

What is reflux nephropathy?

A

Chronic pyelonephritis secondary to vesico-uretic reflux

139
Q

How long does scarring take to occur in reflux nephropathy?

A

Usually occurs in first 5 years

140
Q

How can reflux nephropathy lead to HTN?

A

Renal scarring may produce increased amounts of renin

141
Q

How is reflux nephropathy best diagnosed?

A

On micturating cystography

142
Q

How should all diabetic patients be screened for diabetic nephropathy?

A

Annual urinary albumin:creatinine ratio (ACR) from an early morning specimen

143
Q

Define microalbuminuria

144
Q

How is diabetic nephropathy managed?

A 
Dietary protein restriction 
Tight glycaemic control
BP aim <130/80mmHg
ACEi and ARBs can be used 
Control dyslipidaemia, e.g. statins
145
Q

What are signs of a negative fluid balance?

A 
Tachycardia
Hypotension
Oliguria
Sunken eyes
Reduced skin turgor
146
Q

What are signs of an over-filled fluid balance?

A

Ascites
Crackles
Tachypnoea
Elevated JVP

147
Q

Why does rhabdomyolysis cause AKI?

A

Myoglobin released from muscle tissue is toxic to the kidneys

148
Q

What are complications of nephrotic syndrome?

A

Inc. infection risk due to urinary Ig loss
Inc. TE risk due to loss of antithrombin III and plasminogen in urine (most common site - renal vein thrombosis)
Hyperlipidaemia
Hypocalcaemia (vitamin D and binding protein lost in urine)
Acute renal failure

149
Q

Is renal biopsy always indicated in minimal change disease?

A

No - only indicated if response to steroids is poor

150
Q

What is cyclosporin?

A

A calcineurin inhibitor

151
Q

What are SEs of mycophenolate mofetil?

A

GI SEs

Bone marrow suppression

152
Q

What monitoring do those on long-term immunosupression for organ transplants require?

A

CV - tacrolimus + ciclosporin can cause HTN and hyperglycaemia, tacrolimus can –> hyperlipidaemia
Renal failure - nephrotoxic effects of tacrolimus + ciclosporin
Malignancy - esp. SCC and BCC

153
Q

What is the first indicator of diabetic nephropathy?

A

Microalbuminuria

154
Q

What is the recommended fluid challenge (in those with no heart failure)?

A

500ml normal saline STAT

Reassess and decide if patient req. another 500ml

155
Q

What is the recommended fluid challenge in those with heart failure?

A

250ml normal saline

156
Q

What diuretic is used in high doses to prevent the reformation of ascites in patients with chronic liver disease?

A

Spironolactone

157
Q

When does Wilm’s nephroblastoma tend to present?

A

Typically in children under the age of 5

158
Q

What are features of Wilm’s nephroblastoma?

A

Abdominal mass
Flank pain
Painless haematuria
Anorexia, fever

159
Q

What is the best way to differentiate between acute and chronic renal failure on US?

A

CRF tend to have small bilateral kidneys

(EXPECTIONS -

  • AKPKD
  • Diabetic nephropathy
  • Amyloidosis
  • HIV associated nephropathy
160
Q

What electrolyte abnormality is more suggestive of chronic renal failure as opposed to acute renal failure?

A

Hypocalcaemia (due to lack of vit D)

161
Q

What is the most common extra-renal manifestation of ADPKD?

A

Liver cysts

162
Q

How can you remember the eGFR variables?

A 
CAGE
C - serum Creatinine
A - Age
G - Gender
E - Ethnicity
163
Q

Who should you consider a diagnosis of fibromuscular dysplasia in?

A

Young female patients who develop AKI after starting an ACE inhibitor

164
Q

What does fibromuscular dysplasia cause?

A

Proliferation of cells in the walls of arteries causing the vessel to bulge/narrow

165
Q

What is the classical appearance of fibromuscular dysplasia on US?

A

String of bead appearance of the renal arteries

166
Q

What are the features of fibromuscular dysplasia?

A

HTN
CKD or acute renal failure (e.g. secondary to ACEi initiation)
Flash pulmonary oedema

167
Q

What is the classic triad of symptoms seen in renal cell carcinoma?

A

Haematuria
Loin pain
Abdominal mass

Other features - left varicele (due to occlusion of L testicular vein)

168
Q

What is dialysis disequilibrium syndrome?

A

A rare complication of dialysis that usually affects those who have just started RRT

Caused by cerebral oedema, exact mechanism is unclear

169
Q

How do you calculate maintenance fluids for children for a 24h period?

A

100ml for first 10kg
50ml for next 10kg
20ml for subsequent kgs

170
Q

How do you calculate maintenance fluids for children per hour?

A

4ml for first 10kg
2ml for next 10kg
1ml for subsequent kgs

171
Q

What is someone with CKD on haemodialysis most likely to die from?

172
Q

What are features of renal artery stenosis (secondary to atherosclerosis)?

A

HTN
CKD
Flash pulmonary oedema

173
Q

What renin level will you see in someone with renal artery stenosis?

A

High renin (reduced perfusion –> decreased stimulation of baroreceptors in wall of afferent arteriole so RAAS is activated -> increased aldosterone (K low, Na high)

174
Q

What are the WHO classes of lupus nephritis?

A 
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis
175
Q

How is lupus nephropathy managed?

A

Treat HTN
Corticosteroids
Immunosupressants, e.g. azathioprine/cyclophosphamide

176
Q

What things can cause metabolic alkalosis?

A

Loss of hydrogen ions or gain of bicarbonate

Mainly due to GI problems or kidney problems

177
Q

List causes of metabolic alkalosis

A 
Vomiting/aspiration
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia
178
Q

What may cause a respiratory acidosis?

A

COPD
Decompensation in other respiratory conditions,e .g. life-threatening asthma/pulmonary oedema
Sedatives: benzos, opiate OD

179
Q

What can cause respiratory alkalosis?

A 
Anxiety --> hyperventilation
PE
Salicyclate poisoning
CNS disorders - stroke, SAH, encephalitis
Altitude
Pregnancy
180
Q

When do nice recommend referring to a nephrologist from primary care in CKD?

A

If eGFR falls below 30 or by >15 in a year

181
Q

What is the maximum recommended rate of potassium infusion via a peripheral line?

A

10mmol/hour

182
Q

What are clinical features of hypokalaemia?

A

Muscle weakness, hypotonia
Palpations
Ascending paralysis

183
Q

Hypokalaemia prediposes to toxicity from which drug?

184
Q

What are the ECG features of hypokalaemia?

A

U waves
Small/absent T waves
Prolonged PR interval
ST depression

185
Q

What are causes of hypokalaemia?

A

Inc. K loss (e.g. thiazides, laxatives, glucocorticoids, antibiotics)
GI loss: diarrhoea, vomiting, ileostomy
Dialysis
Endocrine disorders: hyperaldosteronism, Cushing’s

Transcellular shift (e.g. insulin/glucose therapy, salbutamol, theophylline, metabolic alkalosis)

Decreased K intake

Mg depletion (assoc with increased K loss)

186
Q

Define mild-moderate hypokalaemia

187
Q

Define severe hypokalaemia

188
Q

How is mild-moderate hypokalaemia treated?

A

Oral K (if asymptomatic + no ECG changes)

189
Q

How is severe hypokalaemia managed?

A

IV replacement (dilute K to low concentrations as higher concs can be pheblitic)

E.g. - 3 bags 0.9% saline with 40mmol KCl

Renal/Urology (29 decks)

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