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Year 3 > Renal > Flashcards

Renal Flashcards

1
Q

For any pt with renal failure need to:

A
  • assess degree of renal impairment
  • make changes
  • change to safer drug
  • avoid nephrotoxics
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2
Q

Routine tests are:

A
  • Plasma

* Urine

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3
Q

Plasma routine tests

A
  • Creatinine
  • Urea
  • eGFR
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4
Q

Urine routine tests

A
  • ACR/Albumin:creatinine ratio
  • Osmolality
  • specific gravity
  • proteinuria/microalbuminuria
  • haematuria
  • mid stream urine
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5
Q

Creatinine

A

GFR = Cr Cl
• freely filtered by kidney
• product of protein metabolism
• 24hr urine collection

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6
Q

Limitations in urine collection/creatinine

A
  • accuracy of urine collection

* time delay

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7
Q

Cockcroft & Gault equation

A

CrCl = [140-age]*IBW / Plasma Cr [umol/l]
* F
(F = 1.23 males, 1.04 females)

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8
Q

Limitations with Cockcroft & Gault equation

A
  • assume average population data
  • unsuitable for children and pregnancy
  • renal fn must be stable
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9
Q

normal CrCl

A

120ml/min

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10
Q

normal CR

A

55 - 125umol/l

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11
Q

Metabolism in kidney impairment

A
  • less vitD activated
  • less insulit met
  • less elimination API metabolites
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12
Q

eGFR 4 variables

A

age, sex, serum Cr, ethnic origin

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13
Q

Stages of eGFR

A 
1 >90 Normal 
2 60-89 Mild impairment 
3a 45-59
3b 30-44 Mod
4 15-29 Severe
5 <15 End stage
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14
Q

eGFR units

A

ml/min/1.73m^2

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15
Q

Stage 1 G1

A

> 90 Normal

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16
Q

Stage 2 G2

A

60-89 Mild impairement

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17
Q

Stage 3A G3a

A

45-59

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18
Q

Stage 3B G3b

A

30-44 Mod

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19
Q

Stage 4 G4

A

15-29 Severe

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20
Q

Severe 5 G5

A

<15 End Stage

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21
Q

Urea - what is it

A

Breakdown product of protein metabolism

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22
Q

Uraemia

A

Urea in blood. >15mmol/l

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23
Q

High urea levels also in:

A
  • dehydration
  • excess protein intake
  • haemorrhage
  • severe infection
  • muscle injury
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24
Q

Proteinuria

A
  • ACR Albumin:Creatinin Ratio
  • predictor of renal disease development
  • predicts risk of AE
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25
Q

ACR

A

Albumin:Creatinine Ratio

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26
Q

uraemia in absorption

A
  • vomiting diarrhoea, GI, oedema
  • reduce Ca2+ absorption
  • phosphate binders
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27
Q

uraemia in distribution

A
  • reduce protein binding in drugs eg phenytoin

* reduce tissue binding in drugs eg digoxin

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28
Q

kidney impairment in metabolism

A
  • VitD - less activation
  • insulin - less met
  • API metabolites - less elimination
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29
Q

dose adjustments - kidney impairment

A
  • reduce dose

* increase dose interval

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30
Q

Loading dose adjustment - kidney impairment

A

none

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31
Q

Ideal drug in renal impairment

A
  • wide therapeutic index
  • liver eliminate
  • not nephrotoxic
  • not affected by changes in fluid balance, tissue or protein binding
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32
Q

kidney fn

A
  • regulatory
  • excretory
  • endocrine
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33
Q

pre renal failure

A

less renal perfusion

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34
Q

intrinsic renal failure

A

damage to renal tissue

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35
Q

post renal failure

A 
obstruction to urinary flow eg 
• Stones 
• structural eg tumour 
• nephrotoxicity 
• outside urinary tract eg ovarian tumour
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36
Q

Eg of urinary flow obstruction

A
  • Stones
  • Structural eg tumour
  • nephrotoxicity
  • outside urinary tract eg ovarian tumour
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37
Q

AKI reversible?

A

Yes

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38
Q

AKi secondary to?

A

decreased circulation (pre-renal failure)

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39
Q

AKI is

A

regulatory & excretory failure

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40
Q

AKI defined in terms of Cr

A

increased Cr ≥ 26 µmol/l

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41
Q

AKI defined in terms of urine output

A

decreased urine output to <0.5ml/kg/hr for >6hrs

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42
Q

Risk factors AKI

A
  • Past AKI
  • pre-existing CRF
  • age >65yrs
  • CCF
  • PVD
  • DM
  • hepatic disease
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43
Q

AKI trigger factors

A
  • sepsis/infection
  • hypovolaemia (dehydration, bleeding)
  • Hypotension
  • drugs eg NSAIDs, ACEIs, ARBs, Diuretics
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44
Q

Drugs that could trigger AKI

A
  • NSAIDS
  • ACEIs
  • ARBs
  • Diuretics
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45
Q

AKI prevention

A
  • avoid nephrotoxic drugs
  • Monitor renal function for drugs known to cause renal impairment
  • Review meds known to exacerbate AKI
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46
Q

Meds that exacerbate AKI

A

ACEI,
CRB,
diuretics

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47
Q

Signs of AKI

A
  • Volume depletion

* Volume overload

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48
Q

Volume depletion signs of AKI

A
  • Thirst
  • Fluid loss ++
  • Oliguria
  • Dry mucosae
  • low skin elasticity
  • tachycardia
  • hypotension
  • low JVP
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49
Q

Volume overload (if left untreated)

A
  • increased orthopnoea/fluid in lungs
  • increased PND/ nocturnal dyspnoea
  • SOA
  • Oedema
  • pulmonary oedema
  • pulmonary crackles
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50
Q

PND

A

paroxysmal noctural dyspnoea

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51
Q

Treatment of AKI - Underlying causes

A
  • Restoration of renal perfusion - IV fluids, blood
  • Dialysis
  • Review drug therapy - stop/withhold nephrotoxic drugs
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52
Q

AKI restoration of renal perfusion

A
  • IV fluids eg NaCl 0.9%

* Blood

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53
Q

AKI Loop diuretics - what,

A

Furosemide IV

• doses 1-2g IV over 24hrs

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54
Q

AKI Loop diuretics - why

A
  • produces diuresis, which decreases tubular cell metabolic demands & renal blood flow.
  • increases renal prostaglandins/PG
  • caution for dehydration
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55
Q

AKI Furosemide max rate IV

A

4mg/min (higher causes ototoxicity)

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56
Q

Ototoxicity

A

damage hear, hearing loss, balance disorders, ringing/tinnitus

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57
Q

Dopamine in AKI why

A
  • renal vasodilation mediated through D1 receptors.

* increases renal perfusion

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58
Q

Dopamine in AKI dose

A
  • low dose (2mcg/min)

* high dose >5mcg/kg/min can cause vasoconstriction

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59
Q

Antibiotics in AKI

A

if cause is infection

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60
Q

CKD

A

Chronic Kidney Disease

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61
Q

CKD what is it

A
  • Regulatory, excretory & endocrine failure
  • secondary to renal tissue damage
  • subtle & slow onset
  • irreversible by the time pt presents with symptoms
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62
Q

CKI reversible?

A

irreversible by the time pt presents with symptoms

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63
Q

ESRF

A

End Stage Renal Failure

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64
Q

ESRF treatment

A
  • renal replacement therapy needed eg.

* dialysis or transplantation

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65
Q

Acute on Chronic Renal Failure

A

• sudden fast decline due to underlying cause eg dehydration. infection, drugs

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66
Q

Clinical manifestations of CKD

A
  • Urinary symptoms
  • Proteinuria
  • Fluid retention
  • Uraemia
  • Anaemia
  • electrolyte disturbance
  • HYP
  • muscle dysfn
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67
Q

Urinary symptoms CKD

A
  • v. early stages only polyuria
  • polyuria
  • medullary damage
  • osmotic effect of urea (>40mmol/l)
  • loss of ability to [urine]
  • nocturia
68
Q

Proteinuria CKD

A
  • degree of proteinuria in all CKD
  • proteinuria >2g in 24hr leads to glomerular disease
  • > 5g in 24hr leads to severe disease = Nephrotic syndrome
69
Q

Nephronic syndrome

A

> 5g in 24hr proteinuria

70
Q

proteinuria

A

protein in urine

71
Q

Glomerular disease

A

> 2g in 24hr

72
Q

Fluid retention CKD

A
  • CKD progress = GFR lowers
  • kidneys can’t excrete Na+ & water leads to peripheral and pulmonary oedema & ascites
  • 80% of CKD pt have volume dependent HT
73
Q

Uraemia CKD

A
  • measurement of toxin level in blood
  • often used to decide when to start dialysis
  • Symptoms eg anorexia, N&V
74
Q

Uraemia symptoms

A 
anorexia 
N&V
constipation 
foul taste 
skin discoloration 
• pruritis
75
Q

Anaemia CKD

A
  • failure of kidney to produce erythropoetin hormone
  • regulates RBC proliferation in bone marrow
  • symptoms eg fatigue
76
Q

Anaemia symptoms

A
  • fatigue and lethargy
  • breathlessness
  • angina
77
Q

Electrolyte disturbance CKD

A
  • hyperkalaemia

* Acidosis

78
Q

Hyperkalaemia

A
  • kidneys unable to remove K+

* >7mmol/l = medical emergency & risk of cardiac arrest

79
Q

Acidosis

A
  • kidneys cant remove H+

* reduce plasma bicarbonate

80
Q

Hypertension

A
  • majority CKD pt have it
  • mainly due to circulatory volume expansion due to Na+ retention
  • increases rate of decline of renal fn
81
Q

Muscle dysfunction

A
  • cramps & restless legs
  • especially at night
  • general nutritional deficiencies & electrolyte disturbances
82
Q

Renal bone disease/ osteodystrophy from what?

A
  • Cholecalciferol (inactive precursor of vitD) absorbed from GIT & produced in dkin from sunlight
  • To produce active vitD calcitriol, cholecalciferol needs hydroxylation in 25 position in liver and 1𝒶 position in kidney.
  • leads to VitD deficiency
  • defective bone mineralisation
  • osteomalacia/ bone softening
83
Q

osteomalacia

A

bone softening

84
Q

How VitD deficiency?

A
  • cholecalciferol needs hydroxylation in 25 position in liver. 1𝒶 position in kidney.
  • ESFR cannot do this.
  • active vitD decrease
  • vitD deficiency
  • defective bone mineralisation
  • osteomalacia/ bone softening
85
Q

vitD leads to?

Why low Ca2+?

A
  • vitD cannot absorb Ca2+ from gut
  • less vitD = less Ca2+
  • low bone mineralisation/ osteomalacia
86
Q

hypocalcaemia leads to?

A
  • release of PTH/parathyroid hormone
  • 2º/leads to hyperparathyroidism/hyperplasia of parathyroid gland
  • disrupt bone structure
  • bone hardening/osteosclerosis
87
Q

hypocalcaemia can be exacerbated by

A
  • hyperphosphataemia as kidney cannot excrete phosphate

* Phosphate ions can sequester Ca2+ into calcium phosphate in bones.

88
Q

Why hyperphosphataemia?

A
  • kidney cant excrete phosphate

* leads to hypocalcaemia as Phosphate ions sequester Ca2+ as calcium phosphate in bones.

89
Q

Hyperphosphataemia can lead to?

A
  • lead to pruritis
  • leads to hypocalcaemia
  • disturb bone architecture
  • osteosclerosis/ bone hardening
  • bone pain
90
Q

PTH

A

parathyroid hormone

91
Q

PTH in osteodystrophy

A
  • Ca2+ and Phosphate met controlled by PTH
  • kidney cant respond to PTH to increase renal Ca2+ reabsorption
  • persistent hyperparathyroidism.
  • persistent hyperplasia of thyroid glands - may have to remove.
  • hyperparathyroidism
92
Q

Treat CKD two areas?

A
  • conservative eg diet and drugs, treat symptoms

* renal replacement therapy

93
Q

Renal replacement therapy CKD

A
  • dialysis

* transplantation

94
Q

Drug treatment with HYP & CKD

A
  • diuretics
  • BB
  • alpha blockers
95
Q

Diuretic CKD & HYP

A
  • only LOOP eg Furosemide
  • occasionally used for HYP mainly for oedema.
  • thiazides ineffective at CrCl<25ml/min
  • K sparing increases risk of hyperkalaemia
96
Q

Diuretic thiazide

A

except metolozone, ineffective at CrCl<25ml/min

97
Q

BB CKD & HYP

A
  • cardioselective eg metoprolol, atenolol, bisoprolol
  • Metoprolol cleared through liver
  • start low dose, titrate up
98
Q

Why metaprolol for HYP & CKD

A
  • cardioselective

* cleared via liver

99
Q

CCB HYP & CKD

A

• can produce oedema
especially Nifedipine
• confusion with symptoms of fluid overload

100
Q

ACEis/ARB

A
  • can decline renal fn
  • fine is ESFR but increases risk of SE
  • C/I: renal artery stenosis
101
Q

Renal artery stenosis

A

blood flow to kidney relied upon Angiotensin 2 vasoconstriction

102
Q

alpha-blokers

A

eg. doxazosin

• cleared through liver

103
Q

vasodilators CKD & HYP

A
  • eg hydralazine, minoxidil
  • reserved when HYP not controlled by others
  • SE: fluid retention so use w diuretic, reflex tachycardia
104
Q

BP targets

A

<140/90

& DM: <130/80

105
Q

Oedema CKD

A
  • pulmonary
  • diuretic
  • LOOP in pre-dialysis stage
  • Furosemide up to 2g OD (500mg tablet)
  • Fluid and Na2+ restriction
  • stop when dialysis starts
106
Q

Hyperkalaemia CKD

A
  • > 7mmol/l imperative due to risk of cardiac arrest.

* emergency treatments calcium gluconate, insulin + glucose, calcium resonium

107
Q

Emergency treatment for hyperkalaemia & doses

A
  • Calcium gluconate [10ml 10% IV over 5-10min]
  • Insulin (20IU soluble) + Glucose (50ml 50% IV)
  • Calcium resonium [15-30g powder oral/enema] with Lactulose 10ml/ 15g dose
108
Q

Why Insulin & Glucose in hyperkalaemia treatment - pharmacology

A
  • Insulin stimulates intracellular K+ uptake

* Glucose prevent hypoglycaemia

109
Q

Why calcium resonium in hyperkalaemia treatment - pharmacology

A
  • Ion exchange resin binds to K+ in GIT & releases Ca2+ in exchange
  • always give with lactulose 10ml for each 15g dose as very constipating
110
Q

Acidosis why & treatment

A
  • kidney cant excrete H+ ions
  • sodium bicarbonate 500-600mg TDS tab or powder
  • only problem in pre-dialysis
111
Q

Hyperphosphataemia why & treatment

A
  • kidney cant excrete phosphate

* Phosphate binders eg Aluminium hydroxide, calcium carbonate, calcium acetate, sevelamer

112
Q

Phosphate binder eg

A
  • Aluminium hydroxide
  • Calcium carbonate
  • Calcium acetate
  • Sevelamer
113
Q

Phosphate binder pharamcology

A
  • bind with phosphate in food in gut
  • take with or just before meal
  • dose by meal size
114
Q

Hypocalcaemia why & treatment

A
  • kidney cant produce active vitD
  • Calcitrol 250ng OD- fully active
  • Alfacalcidol 500ng-1mcg OD- partial active
115
Q

Anaemia why & treatment

A
  • kidney cant produce EPO, erythropoetin
  • Recombinant human erythropoetins injections IV/SC
  • Iron therapy
  • avoid blood transfusions
116
Q

Iron therapy in anaemia CKD. eg

A
  • Iron sucrose [Venofer]

* Ferric cerboxymaltose [Ferinject]

117
Q

Iron sucrose brand

118
Q

Ferric carboxymaltose brand

119
Q

Venofer

A

Iron sucrose

120
Q

Ferinject

A

Ferric carboxymaltose

121
Q

Recombinant human erythropoetin inject SE

A

HYP

pure red cell aplasia

122
Q

Cramps & restless legs CKS

A
  • cramps at night/on dialysis

* restless leg syndrome

123
Q

Cramps treatment CKD

A

• Quinine sulphate 300mg

124
Q

Restless leg syndrome treatment

A

• Clonazepam 0.5-1mg nocte

125
Q

Vitamin supplements CKD

A
  • eg Renavit
  • dietary advice
  • water soluble vit removed by dialysis
126
Q

Hepatitis B vaccine

A
  • CKD pt
  • get booster every 5yr
  • HD pt monitored annually for antibodies and re-immunised if needed
  • 3 doses of 40mcg [double normal dose]
127
Q

which vaccine do CKD pt need

A

Hepatitis B
• every 5 years, booster
• monitor HD pt yearly

128
Q

Dialysis types

A
  • Haemo

* peritoneal

129
Q

principal of dialysis

A
  • artificial kidney, mimics normal kidney.

* mimic ultrafiltration & reabsorption

130
Q

Membranes in dialysis HD and peritoneal

A
  • HD = artificial membrane

* peritoneal = pt own peritoneal membrane

131
Q

Ultrafiltration in dialysis

A
  • remove waste

* remove water

132
Q

How waste removed in dialysis

A
  • diffuse down conc grad across membrane

* waste solutes from blood (high conc) to dialysate fluid (low conc)

133
Q

how water removed in HD

A

hydrostatically with negative pressure grad from pump in HD machine

134
Q

how water removed in peritoneal dialysis

A

osmotically using dialysate fluids containing various glucose concentrations

135
Q

How reabsorption in dialysis

A

dialysate fluid = desired substances at normal conc to prevent diffusion/ no conc gradient.

136
Q

Haemodialysis what is done?

A
  • atrial blood taken from body
  • anticoagulated (heparin)
  • passed through artificial kidney
  • countercurrent dialysate fluid bathes fibres & maximises conc grad.
  • return to vein & dialysate discarded
137
Q

Artificial kidney in HD made from?

A

hollow fibres.

• semi permeable membrane

138
Q

HD where?

A

• hospital or home

139
Q

HD when?

A

2-3 times a week, 3-4 hours.

140
Q

HD fluid restriction

A

should not put on >1.5Kg above dry weight

141
Q

Gain vascular access in HD

A
  • subclavian

* ateriovenous fistula

142
Q

Ateriovenous fistula in HD

A
  • artery joined to vein
  • matures over 6 wks
  • 2 enlarged blood vessels to allow needling
  • dont cover tightly or injure
143
Q

Sub-clavian

A
  • tunnelled under skin to subclavian vein

* temporary risk of infection

144
Q

Ateriovenous shunt in HD

A

• two silastic tubes w Teflon connector inserted into vein and artery

145
Q

Why Peritoneal membrane?

A

peritoneal membrane lines all internal organs & has rich blood supply

146
Q

Peritoneal dialysis how?

A
  • 1.5/2L sterile dialysis fluid run into peritoneal cavity under gravity
  • fluid in abdomen for set time period
  • diffusion occurs
  • fluid drained out under gravity & discarded
  • new fluid drained in
  • repeated QDS
147
Q

Access PD

A
  • indwelling silastic catheter
  • tunnelled through abdominal wall & distal end sits in peritoneal cavity
  • aseptic techniques required when changing bags
  • Peritonitis risk
  • other risks eg loss of protein.
148
Q

Types of PD

A
  • CAPD - continuous ambulatory PD
  • APD - automated peritoneal dialysis
  • IPD - intermittent peritoneal dialysis
149
Q

CAPD

A

continuous ambulatory PD

150
Q

APD

A

automated PD

151
Q

IPD

A

intermittent PD

152
Q

Diet in PD

A
  • healthy [low fat, low salt, high fibre]
  • low K
  • low phosphate
  • high protein in CAPD
153
Q

Fluid restriction

A

HD: urine output + 500ml/day

PD: urine output + 750ml/day

154
Q

HD drugs removal

PD drugs removal

A
  • low % plasma protein bound
  • low Vd
  • low m. wt/ molecular weight
  • increase water solubility
  • increase renal clearance in normal RF
155
Q

increase HD via dialysis

A
  • duration
  • blood flow
  • type of membrane
  • flow rate & composition of fluid
156
Q

Increase PD via dialysis

A
  • composition of dialysate
  • pathology of peritoneum
  • volume & exchange rate of dialysate in peritoneal cavity • osmotic concentration gradient
157
Q

Pre renal nephrotoxicity

A
  • diuretics
  • g.i.losses [D&V, laxative abuse]
  • NSAIDs
  • ACEIs
158
Q

Classification of nephrotoxicity

A
  • Pre-renal
  • Intra-renal
  • Post-renal
159
Q

Intra-renal what? eg?

A

hypersensitivity reactions & unpredictable
• Glomerular lesions
• Interstitial damage

160
Q

Glomerular lesions

A
  • passive trapping of immune complexes in glomerulus causing inflammatory response
  • eg gold, penicillamine, phenytoin, penicillins
161
Q

Interstitial damage

A
  • inflammation of cells lying between nephrons

* eg penicillins, allopurinol, azathioprine

162
Q

Directly toxic and more predictable in dialysis

A
  • can occur with single dose

* eg aminoglycosides, cyclosporin, amphotericin

163
Q

Post renal what? eg?

A
  • urinary tract obstruction eg methotrexate
  • causing crystalluria
  • crystals block outflow of urine, leads to back pressure, leads to damage to kidneys
164
Q

Nephrotoxic drugs in renal patients?

A

sometimes essential
• monitor renal fn and signs of toxicity constantly
• ESFR, fine to use.

165
Q

pruritis

A

itchy skin due to hyperphosphataemia

Year 3 (4 decks)

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