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AI Exam 2 > Kidney > Flashcards

Kidney Flashcards

1
Q

What is the functions of the kidney?
REEM

A

Regulatory: fluid volume and composition, bp and pH
Endocrine: Erythropoietin production, renin production, prostaglandin production
Excretory: Excrete waste products and drugs
Need to assess impairment, adjust doses, hold/stop nephrotoxic
Metabolism: Vitamin D metabolism

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2
Q

In renal impairment what happens to Creatinine?

A

Creatinine will increase as there is a build up in the body, due to lack of kidneys excreting this.

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3
Q

eGFR of 90, what stage of renal impairment is this?

A

Stage 1 (G1) - Normal GFR

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4
Q

eGFR of 60-89, what stage of renal impairment is this?

A

Stage 2 (G2) - Mild impairment

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5
Q

eGFR of 45-59, what stage of renal impairment is this?

A

Stage 3 (G3a) -Mild to moderate

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6
Q

eGFR of 30-44, what stage of renal impairment is this?

A

Stage 3B (G3b)- Moderate to severe

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7
Q

eGFR of 15-29, what stage of renal impairment is this?

A

Stage 4 (G4) - Severe impairment

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8
Q

An eGFR of less than 15, what stage of renal impairment is this?

A

Stage 5 (G5) - Established / End stage

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9
Q

Where should Urea be?

A

Should be in the URINE and NOT blood

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10
Q

What can increase urea?

A

Dehydration, muscle injury, infection, haemorrhage, excess protein intake

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11
Q

What does an increased urea indicate?

A

Kidneys are not flushing the urea out, therefore indicates renal impairment

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12
Q

What is proteinuria / ACR a predictor of?

A

Predictor of renal disease development and adverse outcomes

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13
Q

Where should Albumin be found?

A

Albumin is protein bound and should be in the BLOOD and NOT in the Urine!

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14
Q

How do you work out the ACR ratio?

A

Albumin (mg) / Creatinine (g)

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15
Q

What is the ACR range for a diabetic F and M?

A

M - 2.5mg/mmol
F - 3.5mg/mmol

Non-diabetics = 70mg/mmol

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16
Q

As ACR increases and GFR decreases, this increases the risk of adverse outcomes, True or False?

A

True

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17
Q

A patient with diabetes are at an increased risk of issues with the kidneys, what drug should they be put on?

A

ACEi

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18
Q

How does Uraemia in kidney impairment affect drug absorption?

A

-Reduce drug absorption due to diarrhoea and vomiting, and gastrointestinal oedema. -Reduce calcium absorption can lead to less vitamin D activation.

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19
Q

How does a kidney impairment alter protein and tissue binding?

A

Less protein and tissue binding
-Protein - Phenytoin
-Tissue - Digoxin
= Accumulation (Toxicity)

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20
Q

How does kidney impairment affect drug metabolism?

A

-Less vitamin D metabolism = less calcium absorption from the gut and kidneys.
-Less insulin metabolism in Type 1 Diabetes Mellitus.
-Less elimination of pharmacologically active metabolites

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21
Q

As there is less drug excretion in a kidney impairment and doses of drugs need to be adjusted, does this apply to loading doses?

A

NO

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22
Q

When a patient is in end-stage renal failure, can we use nephrotoxic drugs?

A

Yes - Monitor for SIDE EFFECTS

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23
Q

What are the three types of renal failure?

A

Pre-renal, intrinsic and post-renal

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24
Q

What are the causes of pre-renal failure?

A

-Hypovolemia
-Reduced cardiac output
-Infection
-Liver disease
-Heart failure
-Lisinopril
-NSAIDS
-Lactulose overdose

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25
Q

What are the causes of intrinsic renal failure?

A

-Immune-mediated damage,
-Acute tubular necrosis
-Hypertension,
-Infection
-Nephrotoxicity,
-Metabolic conditions,
-Congenital issues,
-Diabetic nephropathy,
-Gentamycin

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26
Q

What are the causes of post-renal failure?

A

-Obstruction to urinary flow, (stones, tumours or strictures)
-Methotrexate
-BPH
-Ovarian tumours

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27
Q

What can cause nephrotoxicity?

A

Hypersensitivity reactions to drugs like phenytoin or penicillin, or direct toxicity from drugs like aminoglycosides, amphotericin, or cyclosporin.

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28
Q

Lactulose overdose, Infection, Liver disease, Lisinopril, NSAIDs, and heart failure can cause what type of renal failure?

A

Pre-renal

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29
Q

Gentamicin, Infection, Acute tubular necrosis, NSAIDs, uncontrolled HTN can cause what type of renal failure?

A

Intrinsic

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30
Q

Methotrexate, BPH, Ovarian tumours can cause what type of renal failure?

A

Post-renal

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31
Q

How do prostaglandins manage the pressure in the kidneys?

A

Dilate afferent arterioles by increasing blood supply to the capillaries

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32
Q

How does Angiotensin II manage the pressure in the kidneys?

A

Constricts efferent arteriole and blood in the capillaries finds it hard to get out.

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33
Q

How does ACEi/ARB affect ANG II?

A

ACEi/ARB inhibit RAS causing dilation of exit efferent arteriole. Dilation occurs meaning the hydrostatic pressure is reduced, and filtration rate is reduced.

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34
Q

How does NSAIDs affect the kidneys?

A

NSAIDS inhibit prostaglandin, therefore constrict the afferent therefore there is less blood in and profusion is reduced.

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35
Q

What is the benefit of ACEi/ARB long term?

A

These are protective as they are preventing any damage from having a high pressure.

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36
Q

What is the ‘triple whammy’ of drugs which must be stopped if a patient is in AKI?

A

NSAID, ACEi, ARB

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37
Q

Is AKI reversible?

A

Yes

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38
Q

Is CKD reversible?

A

NO

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39
Q

Is end stage renal failure reversible?

A

NO

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40
Q

Pt X Serum creatinine rises by 26.5umol/L within 48 hours what could this indicate?

A

AKI

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41
Q

If a patients baseline creatinine is 1.5-1.9 x higher what stage AKI is this?

A

Stage 1

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42
Q

If a patients baseline creatinine is 2 to 2.9 x higher what stage AKI is this?

A

Stage 2

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43
Q

If a patients baseline creatinine is 3 x or more what the baseline what AKI stage is this?

A

Stage 3

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44
Q

What are the risk factors of AKI?

A

-Diabetes
-CKD
-Previous AKI
-Hepatic disease
-CCF or PVD
-65+

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45
Q

What is the cause of AKI?

A

-Hypotension, Sepsis, Infection, Dehydration
-Pre-renal as there is a reduction in perfusion due to low blood volume and reduced circulation

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46
Q

If a patient in renal failure has volume depletion and it is left untreated, what can it cause?

A

Volume overload

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47
Q

What are the symptoms of Volume depletion?

A

-Decreased urine output
-Thirst
-Oliguria
-Dry mouth
-Reduced skin elasticity
-Tachy
-Low bp
Reduced JVP

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48
Q

What are the symptoms of volume overload?

A

-Pitting oedema
-Increase SOB when lying down
-Coughing
-Fluid leaking from the skin
-Pulmonary oedema and crackles
-Ankle Swelling
-SOA

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49
Q

What is the first stage of AKI management?

A

Identify the cause

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50
Q

What is the second stage of managing AKI?

A

Restore and maintain renal function (volume status and BP)

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51
Q

What is the third stage of managing AKI?

A

Electrolyte correction
*Hyperkalaemia

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52
Q

If a patients Potassium is above 6.5mmol/L what can this cause?

A

Muscle weakness, ECG changes, v-fib = cardiac arrest

53
Q

If a patients Potassium is above 6mmol/L and the patient is in AKI what should be done?

A

Should be urgently treated in AKI patients

54
Q

How does ACEi/ARB affect the kidneys?

A
  1. ACE inhibitors (ACEi) and angiotensin receptor blockers (ARBs) prevent angiotensin II (ANGII) from constricting the efferent arteriole.
  2. This leads to vasodilation and reduced hydrostatic pressure.
    3.The reduced pressure in turn lowers the filtration rate.
    4.This mechanism helps prevent a hypertensive cycle caused by sustained vasoconstriction.
    5.If unchecked, the sustained vasoconstriction could lead to efferent arteriole stenosis and nephron function loss.
55
Q

Why do you need to stop ACEi/ARBs in a patient with AKI?

A

We don’t want hydrostatic pressure reduced, filtration rate needs preserving, and hold in acute renal impairment. Long term this needs restarting when the AKI is resolved.

56
Q

In Stage 2 AKI what dose of furosemide can be given?

A

4mg/min MAX rate due to risk of ototoxicity

57
Q

In stage 2 AKI what dose of Dopamine can be given, and in what setting?

A

ITU only
2mcg/kg/min

58
Q

Hope does dopamine work to increase renal perfusion?

A

Renal vasodilation through DA1 receptors increasing perfusion and urine output

59
Q

In Moderate Hyperkalaemia (K=6-6.4) what can be given?

A

Rapid acting insulin! Shift potassium into cells - rapid acting insulin in glucose over 15 mins to stimulate sodium-potassium transporter and dive K+ into cells

60
Q

In severe Hyperkalaemia (K = 6.5+) what can be given?

A

Protect the heart with calcium gluconate 10% IV *to antagonise potassium at cardiomyocyte to protect heart from arrythmias

61
Q

What should be drug should be considered in Moderate-Severe Hyperkalaemia?

A

Salbutamol 10-20mg nebulised. It lowers serum potassium levels by stimulating uptake into cells

62
Q

What is irreversible kidney damage?

A

CKD, It is a progressive and worsening loss of kidney function that can lead to end-stage kidney failure.

63
Q

How is CKD diagnosed?

A

Abnormalities in kidney function or structure are present for more than 3 months,
-Or eGFR of less than 60ml/min/1.732 on at least two occasions 90 days apart, with or without markers of kidney damage

64
Q

What causes irreversible kidney damage?

A

-Acute Kidney Injury (AKI) due to intrinsic damage,
-Hypertension (HTN) leading to vessel thickening and narrowing,
-Diabetes resulting in nephropathy with fibrosis and sclerosis, and diseases like
-Glomerulopathies, Vasculitis, and Polycystic Kidney Disease, all of which can cause sclerosis and loss of nephrons due to increased pressure and hyperfiltration.

65
Q

What are the early stage symptoms of CKD related to water and electrolyte balance?

A

-Polyuria/nocturia,
=Increase in urine production due to medullary damage, the osmotic effect of increased urea, and the loss of ability to concentrate urine, resulting in dilute urine.

66
Q

How does CKD progression affect water and electrolyte balance?

A

Kidneys to excrete Na+ and water, leading to oedema, peripheral and pulmonary oedema, ascites, and volume-dependent hypertension.

67
Q

What is hyperkalaemia and how does it relate to CKD?

A

Kidneys are unable to excrete potassium, increasing the risk of cardiac arrest and ventricular fibrillation.

68
Q

What is acidosis in CKD patients?

A

Inability to remove H+ ions, resulting in reduced bicarbonate levels and changes to blood pH.

69
Q

What is the first line treatment for water and electrolyte imbalance in CKD?

A

Fluid restriction, (1L/day) for those not yet on dialysis and still passing urine,
-possibly 500ml OD for those on haemodialysis without urine output.

70
Q

What is the second line treatment for water and electrolyte imbalance in CKD?

A

Diuretics = furosemide up to 2g daily or bumetanide, especially if there is fluid accumulation in the abdomen.

71
Q

What happens to diuretic use when a CKD patient starts dialysis?

A

STOP when a patient starts dialysis

72
Q

How is the inability to regulate electrolytes treated in CKD?

A

Long-term use of calcium resonium to bind potassium in the GI tract, and sodium zirconium cyclosilicate or patiromer calcium for acute and chronic hyperkalaemia to allow better adherence and longer use of ACEI/ARB.

73
Q

What is the effect of hypertension on circulatory volume in CKD?

A

Circulatory volume expansion due to sodium and water retention

74
Q

How does hypertension affect renal function in CKD?

A

Leads to artery stenosis and then renin release, which increases hypertension and accelerates the rate of renal function decline.

75
Q

What is the relationship between hypertension and proteinuria in CKD?

A

Protein in the urine.
=More than 2g in 24 hours indicates glomerular disease, and more than 5g in 24 hours indicates severe disease (nephrotic syndrome).

76
Q

What is the PTH Target for a patient with CKD ?

A

> 2x and <4x upper limit of normal

77
Q

What is the Phosphate target in someone with CKD?

A

1.1-1.5mmol/l (1.1-1.7mmol in dialysis)

78
Q

What is the calcium therapeutic targets for a patient with CKD?

A

2.2-2.6 mmol/L

79
Q

What is renal bone disease?

A

-Increased bone turnover to release calcium into the bloodstream, weakening the bone architecture.
-Osteopenia and osteoporosis are common, as well as an increased fracture risk and bone hardening (osteosclerosis).

80
Q

How is the metabolism of Ca2+ and phosphate controlled in the context of renal bone disease?

A

Controlled by the parathyroid hormone.
These hormones detect low calcium in the blood and release PTH into the body, which works to stimulate and increase calcium levels in the blood.

81
Q

What is the role of bone in the context of renal bone disease?

A

There is an increase in bone turnover to release calcium from the bone to the bloodstream.
This can damage the bones, leading to osteoporosis, bone hardening, osteopenia, and an increased fracture risk.

82
Q

What is hyperphosphatemia and how does it relate to renal bone disease?

A

-Less excretion of phosphate by the kidneys, leading to a build up in the blood. -Phosphate captures calcium, therefore hiding it away from the bones.

83
Q

How is hyperphosphatemia treated in the context of renal bone disease?

A

Dietary phosphate intake control.
First-line treatment with calcium acetate, then sevelamer or lanthanum.
These work by binding with phosphate in the gut.

84
Q

What is the role of vitamin D in the context of renal bone disease?

A

Less activation of vitamin D.
Cholecalciferol is converted to calcitriol by hydroxylation in the liver and kidney. Impaired second step causes defective bone mineralisation and osteomalacia (bone softening).

85
Q

What is hypocalcaemia and how does it relate to renal bone disease?

A

Less vitamin D, leading to less absorption of Ca from the GI tract and kidneys.
More phosphate leads to more sequestering of calcium as calcium phosphate in the bones.

86
Q

What are the targets for treating renal bone disease?

A

-Ensuring adequate vitamin D levels,
-Addressing hypocalcaemia.

87
Q

If Uraemia is >15mmol/L what should be done?

A

Dialysis

88
Q

What are the symptoms of Uraemia?

A

Anorexia, N&V, Constipation, Foul taste, Pruritis, Skin discolouration

89
Q

If Erythropoietin is low, Iron is low, true or false?

A

TRUE

90
Q

What is Erythropoietin?

A

Erythropoietin is a hormone made in the kidneys when there is a low level of oxygen in the tissues, this then makes RBC proliferation in the bone marrow, therefore there are more RBC, more oxygen to the kidneys and this solves hypoxia in the tissues.

91
Q

Why can Erythropoietin reduced?

A

Reduced production in the kidneys = less RBC

92
Q

What is the Hb target for CKD patients?

A

100-120g/L

93
Q

What is the treatment for Renal Anaemia?

A

Recombinant human erythropoietin’s by injection (IV/SC) ‘Epoetin

94
Q

Why must we ensure that Iron levels are efficient before giving the Epoetin injection?

A

Need to ensure that iron stores are sufficient before giving EPO injection because it stimulates RBC production and oxygen delivery: key component in forming Haem group and transporting oxygen via iron. If not a lot of iron in the first place, injection isn’t going to be very effective in giving the transport. IRON replacement to be given first and ensure sufficient levels before giving EPO injection

95
Q

When would iron substitution be given to a patient?

A

Iron levels are less then 200mcg/L

96
Q

What should be avoided in renal anaemia?

A

Blood transfusions in case of future transplants

97
Q

What vaccine should be given to all CKD patients 5 yearly at double the dose?

A

Hepatitis B

98
Q

What vitamins are all removed in dialysis and what can we do to prevent this ?

A

All water soluble vitamins are removed, therefore patients will be put on Renevit

99
Q

What drug does this correspond to ‘Calcimetic which lowers PTH levels’

A

Cinacalcet

100
Q

What drug does this correspond to ‘MHRA warnings of DKA and Fournier’s Gangrene, and sick day rules must be followed’

A

Dapagliflozin

101
Q

What drug group does this correspond to ‘Have a side effect of ankle oedema’

A

CCB’s

102
Q

What drug is a phosphate binder?

A

Sevelamer

103
Q

‘May need to be given Ferrinject to boost iron stores’ before receiving what?

A

Eprex ‘Epoietin alfa’

104
Q

What drug class is contraindicated in renal artery stenosis?

A

ACEi/ARBS

105
Q

What drug group is ineffective when CrCl is less and 25ml/min

A

Thiazide like diuretics (EXCEPT Metolazone)

106
Q

When do we initiate dialysis?

A

-Average GFR is 7ml/min
-MDT and patient discussion
-Life-lengthening but not curative

107
Q

Explain the dialysis principle ‘Mimicking the glomerulus?

A

Ultra-filtration mechanism, to remove fluid - hydrostatic pressure or osmotic gradient. Waste product removal, diffusion from high to low concentration across a semi-permeable membrane.

108
Q

How does haemodialysis get into the patient?

A

Gold standard is a arteriovenous fistula; joined artery and vein together to create two large vessels, takes 6-8 weeks to mature.
- Creates a thick walled artery which is high pressured and then it is joined to thin walled vein at low pressure, this thickens and enlarges, meaning there are two large vessels for access.

108
Q

Explain the dialysis principle ‘Mimicking the proximal/distal convoluted tubule and Loop of Henle’

A

Reabsorption / conversion of wanted molecules. Dialysate fluid composition tailored to the patient’s biochemistry.

109
Q

What dialysis method is this ‘
Artificial kidney. Hollow fibres create a semi-permeable membrane. For diffusion, pump generates hydrostatic pressure facilitating osmotic pressure’

A

Haemodialysis

109
Q

How does haemodialysis work?

A

Arterial blood from the body,
1) Patient is anti-coagulated with heparin to prevent blocking of the tubes.
3) Blood is passed through a dialyser counter current of dialysis fluid to bath blood and maximise concentration gradient.
3) Cleaned blood is returned to the body via vein and the dialysate fluid is discarded.

110
Q

What type of dialysis is this? ‘The peritoneal membrane lines the internal organs creating an abdominal space which is rich in blood supply it normally holds a small amount of fluid. The Dialysate fluid runs into the cavity by gravity. There is a dwell time, where the concentration gradient takes time to effect, there is a high glucose solution so fluid moves out via osmosis. The fluid is then drained out under gravity. ‘

A

Peritoneal

111
Q

Where does a patient do Peritoneal dialysis?

A

4 exchanges a day every day, but this happens at the patients own home.

112
Q

What is CAPD dialysis?

A

An indwelling Tenckhoff catheter, which is inserted under local/general anaesthetic through the abdominal wall and sits in the cavity. It is stitched on either side of the abdominal wall to hold in place, scar tissue will form and become watertight over time. Patient requires post operative antibiotics for prophylaxis.

113
Q

What is automated peritoneal dialysis?

A

Exchanges carried out via a machine overnight over 8-10 hours. 1-3L drained into peritoneum. It wells for 1-3 hours then is replaced. The incidence of peritonitis is decreased. Although the patient needs to do this more frequent and has shorted dwell times so improved dialysis adequacy, this is better for a patient as blood is refreshed more often.

114
Q

What are the advantages of Peritoneal dialysis?

A

1) Reduced anaemia as less loss of blood at needling sites
2) Less aggressive so does not leave patients as fatigued as HD
3) Better for cardiac stability - gentle rate of fluid removal
4) Can be done at home, more independence
5) Dietary and fluid restrictions not as strict

115
Q

What are the disadvantages of Peritoneal dialysis?

A

1) Risk of PD peritonitis (Cloudy bag, IV Vanc an oral ciprofloxacin is needed)
2) Membrane can become fibrosed and inefficient
3) Risks of hypoglycaemia due to high glucose content solutions
4) Requires a lot of equipment and good technique
5) Less clearance of smaller molecules, (urea and creatinine)

116
Q

What is the max amount a patient can gain?

A

1.5kg but each patient had a tailored ‘dry weight’

117
Q

Diet and Fluid whilst on dialysis?

A

-Healthy diet - low fat and salt, high fibre
-Low potassium - chocolate, potatoes, caffeine
-Low phosphate - in proteins - BUT need high protein = balance
-High protein in CAPD - can lose protein through CAPD fluid
* Urine output
HD +500ml/day
Peritoneal +750ml/day

118
Q

What drug factors increase the likelihood of removal during dialysis?

A

-Low molecular weight
-Low plasma protein binding
-Low volume of distribution
-High water solubility
-High renal clearance in usual kidney function

119
Q

What dialysis factors affect drug removal?

A

-Membrane type (HD)
-Dialysis duration
-Fluid composition, concentrations and volume (osmotic concentration gradient (PD)
-Peritoneum pathology (PD)
-Blood flow rate (HD) - Increase rate, increase pressure = loss increased.

120
Q

What should be considered regarding fluid management when a patient is on dialysis?

A

STOP diuretics unless residual function to pass urine

121
Q

What should be stopped regarding Acid/Base balance when a patient is on dialysis?

A

STOP Sodium Bicarbonate

122
Q

How should hypertension be managed in a patient on dialysis?

A

Monitor pre and post dialysis BP, likley to be lower afterwards, but still needs management.

123
Q

How should renal bone disease be managed in a patient having dialysis?

A

Remain on treatment

124
Q

Should a patient on dialysis remain on erythropoietin?

A

Risk of blood loss is increased on dialysis, so still required and usually given with IV iron on dialysis (HD)

125
Q

What can we use if a patient is exhibiting Hyperphosphatemia?

A

Phosphate binders to reduce absorption of some drugs

126
Q

If a patient is only passing 0.5ml/kg/hour for 6 hours what diagnosis could this be?

A

AKI

127
Q

If a patient’s serum creatinine rises by 1.5x from baseline what can this indicate?

A

AKI

AI Exam 2 (16 decks)

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