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Year 4 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What type of acid-base disorder is seen in those with mesenteric infarcts

A

Metabolic Acidosis

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2
Q

What conditions are seen in normal anion gaps (metaboic acidosis)

A

GI bicarbonate loss: Diarrhoea, uterosigmoidostomy, fistula
Renal tubular acidosis
Drugs (Acetazolamide)
Ammonium chloride injections
Addison’s

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3
Q

What conditions cause a raised anion gap (metabolic acidosis)

A

Lactate (shock, hypoxia)
Ketones (Diabetic Ketoacidosis, alcohol)
Urate: renal failure
Acid posioning (salicylates, methanol)

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4
Q

What defines a normal anion gap

A

8-14 mmol/L

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5
Q

What medication commonly causes nephrogenic diabetes insipidus

A

Lithium

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6
Q

What psychiatric drug often causes SIADH

A

Fluoxetine (SSRIs)

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7
Q

What medication should all diabetic patients with an albumin:creatinine ratio of 3mg/mmol or more be started on

A

ACEi or ARBs

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8
Q

What does an albumin: creatinine ratio > 2,5 indictae

A

Microalbuminuria

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9
Q

What is the most likely complication for a patient with CKD on haemodialysis

A

Ischaemic Heart Disease

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10
Q

When should someone over the age of 45 be referred for painless haematuria

A

Unexplainied visible haematuria or visible haematuria that persists after UTi treatment

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11
Q

When should someone over the age of 60 be referred for haematuria

A

Unexplained nonvisible haematuria AND dysuria or raiswed WCC

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12
Q

Why is calcium carbonate given to people with hyperkalaemia

A

Protects against arrythmias (but doesn’t correct calcium levels)

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13
Q

What should be given to correct hyperkalaemia

A

Calcium Resonium

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14
Q

ECG changes seen in hyperkalaemia

A

Peaked t waves
Loss of p waves
Broad QRS complex
Sinusoidal wave pattern

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15
Q

How should hyperkalaemia be managed

A

IV Calcium Gluconate

Combined insulin/dextrose infusion

Nebulised Salbutamol

Calcium Resonium or loop diuretics

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16
Q

When should dialysis be considered in hyperkalaemia

A

Persistent + accompanied with AKI

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17
Q

What indicates severe hyperkalaemia

A

6.5mmol/L or higher

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18
Q

Management of severe hyperkalaemia

A

IV Calcium Gluconate
Insulin/dextrose infusion (to shift K+ from ECF to ICD)

Stop ACEi

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19
Q

What creatinine changes indicate AKI

A

> 26 mmol/L in 48 hours

> 50% in 7 days

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20
Q

What urinary output changes indicate AKI

A

<0.5 ml/kg/hour for more than 6 hours

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21
Q

What eGFR increases the risk of AKI

A

<60

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22
Q

When should someone with AKI be referred to nephrologist

A
  1. Renal transplant
  2. Unknown cause
  3. Vasculitis
  4. Myeloma
  5. No repsonse to treatment
  6. Stage 3 AKI
  7. CKD 4 or 5
  8. Meets criteria for dialysis
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23
Q

WHen does acute graft failure occur following a renal transplant

A

6 months

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24
Q

Three signs of an acute graft failure

A

Pyruira
Proteinuria
Rising Creatinine

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25
Q

What is acute tubular necrosis of graft vs acute graft failure

A

Acute graft failure is ASYMPTOMATIC vs symptomatic

Acute tubular necrosis happens in teh first few weeks after a renal transplant

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26
Q

What is the preferred method of access for haemodialysis

A

Arteriovenous fistulas

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27
Q

What drugs should be stopped in an AKI

A

DAMN:

Diuretics
Aminoglycosides and ACEi
Metformin
NSAIDs

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28
Q

If patients have no identifiable cause for an AKI, what should be the next invetsigation of choice

A

Renal USS within 24 hours

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29
Q

What NSAID does not need to be stopped in an ANKI

A

Aspirin if it’s at 75mg (cardiac dose)

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30
Q

When should someone with suspected minimal change disease be given a renal biopsy

A

ONLY if there is no response to prednisolone

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31
Q

What serum level indicates prerenal acute kidney injury over any oter cause

A

Raised serum urea:creatinine ratio

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32
Q

What distinguishes Acute tubular necrosis over other causes of AKIs

A

Hypernatraemia (>30 mmol/L) + low urine outout

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33
Q

Apperaance of urine in prerenal AKI vs acute tubular necrosis

A

Normal vs brown granular with casts

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34
Q

First line management of rhabdomyolysis

A

IV normal saline

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35
Q

How long does it take to develop an arteriovenous fistula for haemodialysis

A

6-8 weeks

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36
Q

What should be given to prevent contrast-induced nephropathy

A

1L IV 0.9% NaCl

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37
Q

How does Lithium cause nephrogenic diabetes inspidus

A

Desensitises the kdiney’s ability to respond to ADH

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38
Q

Signs of Anti-GBM disease

A

Haemoptysis + AKI/proteinuria/haematuria

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39
Q

What is AntiGBM disease

A

Small vessel vasculitis (goodpasture syndrome)

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40
Q

What osmolality level indicates acute tubular necrosis

A

<350

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41
Q

What defines stage 1 AKI

A

1.5-1.9 x baseline

<0.5ml for over 6 hours

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42
Q

What defines stage 2 AKI

A

2-2.9 from baseline

<0.5 ml urine output >12 hours

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43
Q

What defines stage 3 AKI

A

3> baseline

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44
Q

How often does a patient require haemodialysis a week

A

3 times a week

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45
Q

How does a peritoneal dialysis work

A

Has a high dextrose concentration solution to draw waste products from the peritoneum.

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46
Q

How long does a continuous ambulatory peritoneal dialysis last for

A

30-40 minutes

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47
Q

What is an automated peritoneal dialysis

A

Done while the patient is sleeping

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48
Q

At what eGFR should dialysis be considered

A

5-7 ml/min/1.73 m^2

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49
Q

At what age is peritoneal dialysis considered first-line

A

2 or younger

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50
Q

At what Na level is dialysis considered

A

Over 155 or below 120

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51
Q

At what pH level should dialysis be considered in AKI

A

Under 7

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52
Q

At what ureamic level should dialysis be considered

A

> 30 mmol/L

Creatinine over 500

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53
Q

What is the most common side effect of haemodialysis

A

ypotension

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54
Q

Name two contraindications to peritoneal dialysis

A

Intra-abdominal adhesions and abdominal wall stomas

Obesity, resp disease and hernias (relative)

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55
Q

What is the main complication of peritoneal dialysis

A

Peritonitis

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56
Q

What happens to CK levels in tubular cell necrosis

A

Becomes very high (can be caused by rhabdomyolysis)

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57
Q

IgA Nephropathy vs Post-strep glomerulonephritis

A

IgA Nephropathy happens within DAYS of a sore throat

Post-strep glomerulonephritis happens 1-2 weeks after a URTI

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58
Q

What variables are considered when calculating an eGFR

A

CAGE:

Creatinine, Age, Gender, Ethnicity

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59
Q

What are the indications for acute renal dialysis

A

HAVEPEE:

H- Hyperkalaemia
A - Acidosis
V - Volume overload
E- Elevated Urea
P - Pericarditis
E - Encephalopathy
E - Oedema

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60
Q

What is the most common drug that causes acute interstitial nephritis

A

Amoxicillin

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61
Q

What urine results would indicate acute interstitial nephritis

A

Raised urinary WCC and eosinophils

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62
Q

Symptoms of Acute interstitial Nephritis

A

Allergy type reaction: Rash and fever and arthralgia

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63
Q

What defect causes nephrotic syndrome with a hypercoagulable state

A

Antithrombin III deficiency

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64
Q

What is a major complication of membranous glomerulonephritis

A

A hypercoagulable state - look out for DVTs

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65
Q

Acute tubular necrosis vs Acut einterstitial Nephritis on urine dip

A

WCC seen in urine dip vs no raised WCC in urine dip

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66
Q

What defines CKD 1

A

> 90

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67
Q

What defines CKD 2

A

6090

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68
Q

What defines CKD 3a

A

45-59

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69
Q

What defines CKD 3b

A

30-44

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70
Q

What two thing sar eneeded to define CKD stages 1 and 2

A

eGFR and supporting evidence (urinalysis or renal USS abnormal)

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71
Q

What screening test is used for adult PCKD

A

Renal USS

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72
Q

What is the most common infection in those with organ transplants

A

CMV infection

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73
Q

What is the treatment of choice in those with CMV infections

A

Ganciclovir

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74
Q

What is the most common extra-renal manifestation of PCKD

A

Hepatomegaly (hepatic cyst formation)

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75
Q

Where do berry aneurysms commonly occur

A

Anterior communicating artery and anterior cerebral artery

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76
Q

What is the most common cardiac com[lication of ADPKD

A

Mitral valve prolapse

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77
Q

What causes a hyperacute rejection of a renal transplant

A

ABO incompatibility (within minutes of tranpslant)

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78
Q

WHat causes an acute rejection of graft

A

Cell mediated autoimmunity

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79
Q

What malignancy is secondary to immunosupression from transplants

A

Squamous cell carcinoma or Luymphoma

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80
Q

Name causes of prerenal AKI

A

Systolic Heart Failure
Hypoalbuminaemia from decompensated liver disease

Cardiorenal and Hepatorenal syndrome

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81
Q

What symptom is commonly seen across both cardiorenal and hepatorenal syndrome

A

Hypotension

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82
Q

Name some medications that can cause prerenal AKI

A

NSAIDs
ACE-i
ARBs

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83
Q

What is pre-renal AKI

A

Damage to blood vessels supplying the kidney

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84
Q

What is acute tubular necrosis

A

Damage to the tubules following ischaemia (prerenal AKI)

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85
Q

Name some common compounds that can lead to Acute Tubular Necrosis

A

-mycins (e.g., gentamicin)
Methotrexate
Myoglobin (rhabdomyolysis)
Uric Acid

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86
Q

What type of syndrome is seen in membranoproliferative glomerulonephritis

A

Nephrotic syndrome

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87
Q

Proteinuria in nephritic syndrome vs nephrotic syndrome

A

Nephrotic >3,5 g/day

Nephritic 1-3g/day

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88
Q

What can cause renal artery stenosis

A

Atherosclerosis

Fibromuscular dysplasia

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89
Q

Symptoms of renal artery stenosis

A

Persistent Hypertension despite on medication

90
Q

What causes postrenal AKI

A

Obstruction of urine from kidneys

91
Q

What commonly causes postrenal AKI in males

A

BPH and prostatic cancer

92
Q

If one ureter is obsturcted, do we end up with postrenal AKi

A

No

93
Q

Prerenal AKI vs Intrarenal AKI in urine osmolality

A

Urine osmolality >500

urine osmolality <500

94
Q

Why is urine osmolality >500 in prerenal AKI

A

As RAAS system is activated causing more Na+ retention

95
Q

What is the acid-base formula that occurs in the body

A

CO2 + H2O ->/

96
Q

Where is HCO3- ions regulated in the body (ie., excreted)

A

Kidneys

97
Q

How is the level of CO2 regulated by th ebody

A

Lungs

98
Q

What is the normal blood pH in th ebody

A

7.37 -> 7.42

99
Q

Why do pH levels decrease if there is a loss in HCO3- ions

A

CO2 + H20 -> HCO3- + H+

So this equiilibrium shifts to the right, causing more dissociation of H2CO3 into H+ ions

100
Q

If HCO3- ions rise, what happens to the pH

A

Equilibrium shifts to the left, and the pH rises as less H+ ions are formed

101
Q

If CO2 levels rise in the body, what happens to the equilibrium

A

Equilibrium shifts to the right, causing pH to lower

102
Q

What are the four parameters of acidosis/alkalosis

A
  1. pH
  2. pCO2
  3. HCO3-
  4. Compensatory response
103
Q

What causes metabolic acidosis

A

Build up of acid in blood causing equilibrium to shift to the left, causing excess HCO3- loss.

Low bicarbonate levels

104
Q

What symptom is associated with a low pH level (< 7.37)

A

Hyperventilation to lower pCO2

105
Q

Why is lowering pCO2 important

A

Causes less H+ ions to be produced.

106
Q

What is the formula for the anion gap

A

Na+ - (CL- + HCO3-)

107
Q

What does the anion gap show us in metabolic acidosis

A

The anion gap is high

108
Q

What defines a high anion gap

A

> 12

109
Q

What is a normal anion gap

A

8-12

110
Q

What causes the anion gap in metabolic acidosis

A

An excess in H+ ions cause the equilibrium to shift to the left:

CO2 + H20

111
Q

Name three ways we can get a high anion gap (increased organic acid production)

A

Lactic Acidosis: Increased anaerobic respiration causes increased lactic acid

Diabetic Ketoacidosis: Causes increase in ketoacids

CKD: Increase in urea

112
Q

Name two ways we can get a high anion gap (accidental ingestion)

A

Oxalic Acid (Antifreeze)
Formic Acid (Methanol)
Salicylates

113
Q

What three compounds can increase lactic acid production and thus, metabolic acidosis

A

Propylene Glycol
Iron Overdose
Isoniazid overdose

114
Q

What acronym tells us about the causes of metabolic acidosis

A

MUDPILES:

Methanol
Uraemia
Diabetic Ketoacidosis
Propylene Glycol
Iron Tablets/Isoniazid
Lactic Acidosis
Ethylene Glycol
Salicylates

115
Q

What causes a normal anion metabolic acidosis

A

A build up of chloride ions instead:

Na+ - (Cl- + HCO3-)

Cl- increases
HCO3- decreases

116
Q

What is the most common cause of normal anion gap metabolic acidosis

A

Severe Diarrhoea

117
Q

Why does diarrhoea cause metabolic acidosis

A

Inestinal and pancreatic secretions of HCO3- and Cl- cannot be re-absorbed fast enough

118
Q

How does Type 2 renal tubular acidosis cause a normal anion gap metabolic acidosis

A

PCT cannot re-absorb HCO3- ions, causing them to decrease

119
Q

How does Addison’s cause normal anion metabolic acidosis

A

Adrenal glands cannot produce enough aldosterone, so less Na+ is re-absorbed at the DCT, causing less excretion of H+ = metabolic acidosis

120
Q

What drug can cause normal anion gap metabolic acidosis

A

Spironolactone

121
Q

How does Acetazolamide cause a normal anion gap metabolic acidosis

A

Reduces HCO3- reabsorption at the PCT

122
Q

How does IV Saline cause normal anion gap metabolic acidosis

A

Saline has a pH 5.5, so reduces pH in the blood (rare

123
Q

What acronym can help us to remember the causes of normal gap acidosis

A

HARDASS:

H - Hyperalimentation
A - Addison’s
R - Renal Tubular Acidosis
D - Diarrhoea
A - Acetazolamide
S - Spironolactione
S - Saline Infusion

123
Q

What acronym can help us to remember the causes of normal gap acidosis

A

HARDASS:

H - Hyperalimentation
A - Addison’s
R - Renal Tubular Acidosis
D - Diarrhoea
A - Acetazolamide
S - Spironolactione
S - Saline Infusion

124
Q

What range of pCO2 defines if compensation is adequate in metabolic acisosis

A

28.5 -> 32.5

125
Q

If the calculated pCO2 < Measured pCO2, what does this entail

A

Metabolic acidosis WITH associated repiratory acidosis

126
Q

If the calculated pCO2 is greater than the measured pCO2, what does this mean

A

Metabolic acidosis with associated respiratory alkalosis

127
Q

What causes respiratory acidosis

A

Hypoventilation, causing an increase in CO2

Equilibrium shifts to the right causing an increase in H+ ions

128
Q

What compensation occurs in respiratory acidosis

A

The kidneys try to absorb more HCO3- ions to shift the equilibrium to the left (to reduce H+ ions)

129
Q

How long does the compensation by th ekidneys take

A

24 hours

130
Q

Acute vs Chronic respiratory acidosis

A

Acute: pH is VERY low and HCO3- is normal

Chronic: pH is NORMAL and HCO3- is very elevated

131
Q

Two causes of hypoventilation

A

Airway obstruction

Diaphragm or chest wall muscles not working properly (e.g., obesity)

COPD

Opioids etc

132
Q

What causes metabolic alkalosis

A

Loss of H+ ions

133
Q

Describe the compensatory mechanism for metabolic alkalosis

A

Immediate hypoventilation

134
Q

Nma eto GI causes of H+ loss

A

Vomiting

Inability for the pancreas to excrete HCO3- ions

Hyperaldosteronism

135
Q

What drugs can cause metabolic alkalosis

A

Using loop diuretics

Antacids (contain HCO3- ions)

136
Q

What acronym can help us to remember the causes of metabolic alkalosis

A

LAVA

L - Loop Diuretics
A - Antacid Use
V - VOmiting
A - Aldosterone Increase

137
Q

What can cause respiratory alkalosis

A

Hypoxia
Pulmonary Embolisms
High Altitudes

Anything that can cause hyperventilation:

Salicylates overdose (initial)

Anxiety + Panic Attacks
Tumours in the brain

138
Q

What acronym can help us remember the cuases of respiratory alkalosis

A

PAST PH

Panic Attacks
Anxiety Attacks
Salicylates
Tumour

Pulmonary Embolism
Hypoxaemia

139
Q

Why does metabolic acidosis cause hyperkalaemia?

A

In order for H+ ions to enter the cell, K+ ions have to be pushed out (exchanged).

Lots of H+ ions enter the cells, causes lots of K+ ions to be pushed out -> leading to hyperkalaemia

140
Q

How do beta blockers cause hyperkalaemia

A

Block the Na+-K+-ATPase, causing more K+ to be left outside the cell

141
Q

Why does cell lysis (and apoptosis) cause hyperkalaemia?

A

Detsruction of cells causes lots of internal K+ ions (ICF) to be released into the ECF

142
Q

Name three components to tumour lysis sydnrome

A

Hyperkalaemia
Hyperphosphataemia
Hyperurecaemia
Hypocalcaemia

143
Q

What injuries cause hyperkalaemia

A

Crush Injuries

144
Q

Where does aldosterone act

A

Collecting Duct

DCT

145
Q

What cells are responsible for K+ secretion in th ekidneys

A

Principal cells

146
Q

What drugs can cause hyperkalaemia and how?

A

They reduce the effect of aldosterone:

Renin Injbitors
ACE Inhibitors
Angiotensin II receptor antagonist
Selectiev Aldosterone blockers
K+ sparing diuretics

147
Q

How can acute and chronic Kidney Injruy cause hyperkalaemia

A

Impair K+ Excretion

148
Q

What blood test indicates chronic kidney injury

A

Uraemia

149
Q

What are the causes for internal balance shifted hypokalaemia

A

Hyposomolality

150
Q

How does hyponatraemia cause hypokalaemia

A

Water moves back into the cells (as the concentration gradient shifts), bringing back K+ ions with it.

151
Q

How does hyperglycaemic hyperosmolar state cause hypokalaemia

A

Osmolairty is so high, it can cause osmotic diuresis (K+ lost in the urine)

152
Q

How does metabolic alkalosis result in hypokalaemia

A

H+ ions are being secreted from cells to compensate, causing K+ to be exchanged and taken back in - hypokalaemia

153
Q

How does Insulin effect K+ levels

A

An increase causes hypokalaemia, a deficiency causes hyperkalaemia

154
Q

Why does insulin effect K+ levels in the blood

A

Stimulates Na+=K+= ATPase

155
Q

What causes an external balance shift hypokalaemia

A

Reduction in K+ intake: Anorexia, Prolongued fasting and diets

Excretion issues:

Vomiting and Diarrhoea

Sweat (excercise a lot in hot climates)

156
Q

What causes an increased K+ excretion

A

Hyperaldosteronism:

Conn Syndrome
Compensated Heart Failure
Cirrhosis
Loop Diuretics and Thiazides

157
Q

What are the two main readings on an ECG for hyperkalaemia

A

Tall tented t waves
Widened QRS complexes

158
Q

Signs of hypokalaemia on an ECG reading

A

Flattened T Waves
U Waves

159
Q

Signs of hypokalaemia

A

Muscle weakness and cramps

Spasms

160
Q

What cause hypernatraemia

A

H20 loss

161
Q

What causes false hyponatraemia

A

Too much cholesterol

Too much protein (raised) (e.g., multiple myeloma)

Where levels are normal but lab instruments say they’re low

162
Q

What is hypervolaemic hyponatraemia

A

Where total H20 is raised but Na+ stays the same (hyponatraemic)

163
Q

What conditions cause hypervolaemic hyponatraemia

A

Congestive HF
Cirrhosis
Nephrotic Syndrome

ALL PRESENT WITH OEDEMA

164
Q

What cause hypovaelamic hyponatraemia

A

Diarrhoea
Vomiting
Diuretics
Cerebral salt wasting

FLUID loss and Na+ loss

165
Q

What is cerebral salt watsing

A

Intracranail injury (e.g., meningitis) disrupt sympathetic nervous system stimulation of the kidneys (causes loss of Na+)

166
Q

What condition causes euvolaemic hyponatraemia

A

SIADH

167
Q

What causes Parathyroid hormone related protein-mediated hypercalcaemia

A

Squamous cell carcinomas of the lung (mimics the effect of the lung)

168
Q

What medication can cause hypercalcaemia and how

A

Thiazide diuretics

Increase ca2+ absorption at the DCT

169
Q

Symptoms of hypercalcaemia

A

Stones
Bones
Groans
Thrones
Psychiatric overtones

PLUS resistance to ADH = frequent urination + dehydration

Calcium oxalate kidney stones

170
Q

Name a genetic condition which can cause hypocalcaemia

A

DiGeorge Syndrome

171
Q

What vitamin deficiency can cause hypocalcaemia

A

Magnesium Deficiency

172
Q

What condition can result in hypocalcaemia

A

Pancreatitis (acute)

As destroyed fatty acid tissue of the pancrease from high lipase activity binds to calcium ions in the blood.

173
Q

What medical proceedure can cause hypocalcaemia

A

Too many blood transfusions

174
Q

Signs of hypocalcaemia

A

More exciteable

Tetany
Chvostick sign (twitching of facial muscles)
Trousseau sign (BP cuff can cause flexion of the wrist and elbow)

175
Q

Signs of hypocalcaemia on an ECG

A

Prolongued QT interval

176
Q

MOst common cause of hypermagnesemia

A

Kidneys cannot excrete Mg2+

Ingestion of mangnesium drugs or substances

177
Q

Why does lethargy and reduced deep tendon reflexes occur in hypermagnesemia

A

Mg2+ is a cofactor that inhibits passage of neurotransmitters onto receptors

178
Q

How does PTH effect magnesium levels

A

Stimulates the release of Mg2+ into the blood

179
Q

How does hypermagnesemia affect hormone levels

A

Inhibits the release of PTH (hypocalcaemia)

180
Q

Cardiac symptoms of hypermagnesemia

A

Bradycardia
Cardiac Arrest

181
Q

Name four causes of hypomagnesemia

A

Prolongued malnutrition
Mg2+ not absorbed in the GI tract (PPIs, diarrhoea)
Loop and Thiazide diuretics

182
Q

What is hungry bone syndrome

A

Surgical removal of the thyroid causes increased bone formation.

Bone are ‘hungry’ for ions so consume all the Mg2+ in the blood

183
Q

What electrolyte imbalance causes Torsades de pointes

A

Hypomagnesemia

184
Q

Why are hypomagnesemia and hypokalaemia related

A

Diarrhoea and diuretics cause BOTH

185
Q

What inherited disease can result in fanconi Syndrome

A

Wilson’s

186
Q

What cancer can result in fanconi Syndrome

A

Multiple Myeloma

187
Q

How does multiple myeloma cause fanconi syndrome (Kidney Damage)

A

Plasma cells produce abnormally shaped immunoglobulins which damage the PCT

188
Q

Signs of Fanconi Syndrome

A

Damage to the PCT causes loss of HCO3- ions: Renal tubular acidosis type 2 (Metabolic Acidosis)

Damage to PCT causes loss of phosphate ions (hypophosphataemia)

189
Q

What GI complication can PCKD result in

A

Divrticulitis

190
Q

Name three peices of advice to give someone with CKD

A

Avoid Salt containing food
Avoid phosphate containing foods (e.g., meat and dairy foods)

191
Q

What happens to phopsphate levels in later stages of CKD

A

They become very raised (as the kidneys are unable to excrete them)

192
Q

What is the problem with raised phosphate levels in the blood

A

Can cause hypocalcaemia

193
Q

How long should cefalexin/co-amoxiclav be used to treat Pylonephritis

A

7-14 days

194
Q

What drugs should be stopped in hyperkalaemia

A

Digoxin
Beta blockers

195
Q

If ECG does not normalise with calcium gluconate, what should ve done

A

Give 10ml every 10 minutes (up to 50ml)

196
Q

Should calcium gluconate be given in the absence of ECG changes?

A

No

197
Q

Name two ways potassium can be shifted into cells

A

10 units of insulin + 25g glucose

10% glucose infusion over 5 hours + 7.0 mmol/L glucose

198
Q

Why is glucose given alongside insulin

A

Prevent hypoglycaemia

199
Q

What medication is used to remove potassium from the body

A

Calcium Resonium + Lactulose

200
Q

If glucos and IV insulin continue to have no impact on hyperkalaemia, what should be done

A

Dialysis or Sodium Bicarbonate

201
Q

What is the main presentation of hypercalcaemia (2.8 mmol or less)

A

Polyuria and Polydipsia

Dyspepsia

202
Q

At what calcium levels do people get ECG changes

A

> 3,5 mmol/L

203
Q

What is the most common cause of raised calclium levels

A

Primary Hyperparathyroidism

204
Q

In conjuction with what other serum level does hypercalcaemia indicate dehydration as the cause

A

Raised albumin

205
Q

If there is hypercalcaemia in the presence of NORMAL ALP, what is the cause

A

Myeloma

206
Q

If there is hypercalcaemia in the presence of raised calcitonin levels, what is the likely cause

A

B-cell Lymphoma

207
Q

Managmenet of acute hypercalcaemia

A

0.9% 2-3L of Calcium to increase urinary output

THEN bisphosphonates

208
Q

What hormone does phosphate stimulate and why

A

PTH, hyperphosphataemia in CKD can cause PTH to be released (secondary hyperparathyroidism)

209
Q

Why do we not get hypercalcaemia in CKD caused secondary hyperparathyroidism

A

Because PTH mechanisms tend to fail, so phosphates usually stay elecated and calcium levels remain normal

210
Q

What is the role of ANP

A

Stops RAAS activation + lowers BP

211
Q

What diagnostic is used for vesicoureteric reflux

A

Micturating Cystourethrogram

212
Q

What investigations is used to check renal perfusion

A

DTPA

213
Q

Role of podocytes

A

Has foot processes which allow filtration in the kidneys

214
Q

Management of focal segmental glomerulonephiritis

A

Prednisolone

215
Q

What is distinctive of rapidly progressive glomerulonephritis under microscopy

A

Crescent shapes: Aggregated of macrophages and epithelial cells in the Bowman’s capsules

216
Q

What immunosuppressive agent is used in kidney transplants

A

Tacrolimus

217
Q

What does a urine sample show for pre-renal AKI

A

No proteins and no blood

218
Q

Management of mild hyponatraemia (130-135 mol/L)

A

Stop medication causing the issue or check for underlying issues at primary care

219
Q

Define accelerated progression of CKD

A

A sustained decrease of 15 in eGFR over 12 months

220
Q

What albumin:creatinine ratio describes proteinuria that should require referral to nephrology

A

70 or more

221
Q

At what urianry albumin: creatinine ratio, should antihypertensives be considered in

A

<30 mg/mmol

Year 4 (16 decks)

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