1
Q
Define CKD
A
abnormalities of kidney function or structure present for more than 3 months, with implications for health
2
Q
Why are patients with CKD referred late to nephrology and what is the impact of this?
A
because early CKD is asymptomatic causing late referral, which leads to increased mortality and morbidity
3
Q
How is CKD measured?
A
GFR is measured against ACR
4
Q
What is ACR and how is it measured?
A
- ACR = Urine Albumin Creatinine Ratio
- To measure ACR = Urine sample + dipstick, which is then used to compare Albumin leaked out to creatinine
5
Q
What are the different stages of CKD, their eGFR results and what this means?
A
SEE TABLE ATTACHED
6
Q
What is the main difference between stages 1,2&3 when compared to stages 4&5 of CKD?
A
- Stage 1,2&3 = Kidney functions can still filter waste
- Stages 4&5 = More severe disease, so kidneys may stop working completely
7
Q
What is the general trend between eGFR and kidney function?
A
Lower eGFR = Lower kidney function
8
Q
What are the risk factors associated with CKD?
A
- Diabetes (nephropathy is a complication of diabetes)
- Hypertension (high blood pressure pushes kidneys, causing more damage)
- Kidney disorders (genetic)
- Cardiovascular disease
- AKI (especially if treated late or poorly managed/repeated AKI)
- Infections (especially UTIs/recurrent infections e.g. Pyelonephritis)
- HIV or Hepatitis C
- Medications (e.g. NSAIDs, Lithium)
- Malignancy
- Age
- Family history of CKD
9
Q
How is CKD diagnosed?
A
Diagnosing CKD is done according to the classifications (blood creatinine levels + ACR) as well as certain prompts:
- Persistent microalbuminuria (albumin in urine)
- Persistent proteinuria
- Persistent haematuria (blood in urine), after excluding other causes
- Ultrasound or biopsy
10
Q
What are the 3 main functions of the kidneys and explain each one
A
- Homeostasis - Filtration, absorption, secretion, removal of waste products (e.g. urea), regulating pH of blood, removing potassium and regulating blood pressure
- Hormone function - Release of Renin & Epoetin, activates vitamin D to active form
- Metabolic function - Removal of drugs from the body
11
Q
What are the clinical complications of CKD?
A
- Acidosis (acidic blood - kidneys can’t regulate H+ ions can’t get rid of H+ ions)
- Anaemia (lack of Epoetin, EPO, or iron)
- Dyslipidaemia (abnormal lipid metabolism in CKD)
- Fluid overload (kidneys can’t regulate blood pressure, water or Na+ ions - less secretions = more accumulation, causing oedema in hands and legs)
- Hyperkalaemia (kidneys can’t clear potassium as well as it used to)
- Hypertension (kidneys can’t regulate blood pressure as well as before)
- Mineral and bone disorder (vitamin D, calcium and phosphate)
- Uraemia (kidneys are less able to excrete urea, causing build up)
12
Q
Define acidosis
A
a condition in which the blood becomes too acidic, with an abnormally low pH level
13
Q
What is the cause of acidosis in CKD?
A
- Normally, kidneys maintain the pH of blood by reabsorbing/excreting HCO3- (bicarbonate) and H+
- As CKD progresses, the kidneys are less able to excrete H+/reabsorb HCO3- = acidic blood
14
Q
What is the long-term maintenance treatment for acidosis?
A
PO sodium bicarbonate 1g TDS (long-term treatment)
15
Q
What is the acute treatment for acidosis in a medical emergency?
A
IV sodium bicarbonate (acute treatment)
16
Q
What is the main side effect of sodium bicarbonate and why?
A
fluid retention (swelling of body parts due to trapped fluid) due to secondary increase in sodium because wherever sodium goes, water follows
17
Q
What is renal anaemia?
A
Quality/ quantity of RBCs is below normal
18
Q
Define anaemia
A
when the quality or quantity of red blood cells are below normal
(2) Lack of erythropoietin
19
Q
What are the 2 causes of renal anaemia?
A
- lack of circulating iron (not enough RBCs)
- lack of erythropoietin (EPO)
20
Q
What are the benefits of correcting renal anaemia?
A
Increased:
- Quality of life
- Exercise capacity
- Endocrine function
- Immune function
- Muscle metabolism
- Sleep patterns
- Cognitive function
- Nutrition
Decreased:
- Bleeding tendency
- Transfusions
- Depression
- Hospitalisation
21
Q
What are the causes of a lack of circulating iron?
A
- Increased blood loss → Haemodialysis (HD)/blood samples
- Dietary inadequacy → many patients are on a renal diet to restrict phosphate intake
- Poor iron absorption due to uraemia (uric acid) or use of phosphate binders
- Reduced or impaired erythropoiesis due to lack of erythropoietin or iron
22
Q
What is the treatment for a lack of circulating iron in pre-dialysis patients?
A
- Oral iron OD usually for 3 months maximum
- E.g. Ferrous sulphate or ferrous fumarate
- If no improvement in oral iron, give IV iron
23
Q
What are the side effects of PO iron?
A
- GI irritation
- Black stools
- Constipation
- Diarrhoea
(2) Black stools
24
Q
What is the treatment for a lack of circulating iron in dialysis patients?
A
- V iron given after a dialysis session
- Many different type of iron IV but usually given Ferinject
25
What is Erythropoietin (EPO) and its function?
- Erythropoietin (EPO) is a naturally occurring hormone produced by the kidneys
- It stimulates the bone marrow to produce red blood cells
26
What are the levels of Erythropoietin (EPO) in CKD patients like?
patients have low or no circulating EPO
27
What is ESA?
Erythropoietin stimulating agents
28
What are the treatment options for a lack of Erythropoietin (EPO) in CKD?
Multiple treatment options known as Erythropoietin stimulating agents (ESA):
- Eprex - recombinant human EPO
- can be given s/c once weekly (usually self administered by patient)
- can also be given IV 3x weekly to dialysis patients usually at the end of the dialysis session
- Aranesp - novel erythropoiesis stimulating protein (longer half-life than Eprex)
- given IV to dialysis patients usually at the end of the dialysis session
- can be given once weekly due to longer half-life
- Mircera (longest half-life that provides continuous activity)
29
What ESA has the longest half-life?
Mircera > Aranesp > Eprex
30
Why can Aranesp be given only once a week?
Longer half-life than other ESAs
31
What is dyslipidaemia?
the imbalance of lipids such as cholesterol, low-density lipoprotein cholesterol, (LDL-C), triglycerides, and high-density lipoprotein (HDL)
| - Mainly hypertriglyceridaemia
32
What is the treatment for dyslipidaemia in CKD?
Atorvastatin 20mg OD (can be on a higher dose if already taking statins for other cardiovascular conditions)
33
What is the cause of fluid overload (oedema) in CKD?
occurs due to the kidneys decreased ability to maintain sodium/fluid balance in CKD
34
What is the treatment for oedema in CKD?
- restrict dietary sodium
- restrict fluid intake (need to balance as patient can become dehydrated, developing AKI on top of CKD)
- offload fluid with diuretic therapy - Thiazides
- if CrCl <20ml/min = Loop diuretic in higher doses (e.g. Furosemide)
- if medication ineffective → dialysis
35
Define hyperkalaemia
High levels of potassium in blood
36
What is the cause of hyperkalaemia in CKD?
CKD patients are less able to excrete potassium and develop hyperkalaemia (medical emergency, as high levels of potassium are damaging to the heart - arrhythmias)
37
What is the treatment for hyperkalaemia?
- Phosphate restriction
- Calcium resonium PO TDS or Lokelma
- IV calcium gluconate (stabilise heart)
- Actrapid insulin (push K+ into cells)
- If above is ineffective → dialysis = last resort
38
What is the target blood pressure for those with hypertension in CKD?
140/90mmHg
39
What is the treatment for hypertension in CKD?
- ACEi or ARB - titrate to maximum tolerated dose → Renoprotective in CKD (Nephrotoxic in AKI)
- If ACEi or ARB unsuitable then Doxazosin (alpha blocker) is a common option
40
In CKD hypertension, what is a common treatment option if ARBs and ACEis are unsuitable?
Doxazosin
41
Why are ACEi and ARBs used in CKD but not in AKI?
because they are renoprotective in CKD but nephrotoxic in AKI
42
Why are the kidneys important in mineral and bone density (rebuilding bones)?
because they balance the levels of phosphorus and calcium in the blood
43
What are the 4 constituents involved in mineral bone disorder (MBD)?
- Calcitriol (active vitamin D)
- Calcium
- Phosphorus (Phosphate)
- Parathyroid hormone
44
What are the 2 roles of healthy kidneys in MBD?
- Activate a form of vitamin D into Calcitriol (the active form of the vitamin), which maintains blood calcium levels by promoting calcium absorption from the gut
- Remove excess phosphorus/phosphate
45
What is the cause and pathophysiology of MBD?
- CKD causes the production of calcitriol to stop
- This causes a reduction of calcium in the blood
- Phosphorus/phosphate levels in the blood rise
- = vitamin D deficiency + hyperphosphataemia + hypocalcaemia
- Hyperphosphataemia stimulates calcium to be released from the bones
- Hypocalcaemia activates the release of parathyroid hormone (PTH) to stimulate calcium to be released from the bones
- This results in breakdown of the bone, where effects of bone changes do not appear for many years
- vitamin D deficiency + hyperphosphataemia + hypocalcaemia = hyperparathyroidism
46
How does hyperphosphataemia cause hypocalcaemia?
Hyperphosphataemia stimulates calcium to be released from the bones
47
What does vitamin D deficiency, hyperphosphataemia, and hypocalcaemia lead to?
Hyperparathyroidism
48
What is the treatment for calcitriol deficiency in MBD?
Alfacalcidol (activated vitamin D)
49
Why is activated vitamin D (Alfacalcidol) given to treat calcitriol deficiency in CKD rather than inactivated vitamin D such as Adcal D3?
because Adcal D3 contains calcium with colecalciferol, but colecalciferol is the inactivated form and giving Adcal D3 to CKD patients won’t be beneficial as their kidneys can’t function to convert it into vitamin D)
50
What is the treatment for hyperphosphataemia?
- Phosphate binders e.g. Sevelamer or Lanthanum carbonate
- Restricted phosphate diet
51
What is the role of phosphate binders and why do they need to be taken with meals?
remove excess phosphate from diet by reducing absorption in the GI tract, so need to be taken with meals
52
Why does hyperparathyroidism persist when calcitriol deficiency and hyperphosphatemia have been treated in CKD?
- continued stimulation of the parathyroid gland results in it becoming enlarges and continues to release PTH despite correcting vitamin D/phosphate levels
- continued PTH levels will still result in hypercalcaemia
53
What is the treatment for hyperparathyroidism in CKD?
Cinacalcet or parathyroidectomy
54
What is uraemia?
Reduced ability to excrete waste products such as urea and nitrogenous compounds
55
How do calcium levels differ in early and late stages of CKD?
- Early stage CKD = may have low levels of calcium due to vitamin D deficiency
- Late stage CKD = may have high levels of calcium due to overstimulation of parathyroid hormone
56
Define uraemia
a build up of waste products in your blood (e.g. urea)
57
What is the cause of uraemia in CKD?
the kidneys are less able to excrete waste products such as urea and other nitrogenous products
58
What are the complications of uraemia in CKD?
Various medical emergencies:
- Encephalopathy
- Pericarditis
- Confusion
- Coma
59
What is the treatment for uraemia in CKD?
dialysis (to remove waste products from their blood)
60
What medication and dose is used to treat acidosis?
Sodium bicarbonate 1g TDS
61
What medication and dose is used to treat renal anaemia?
- Ferrous fumarate 210mg OD
- S/C or IV ESA
| (2) SC/ IV ESA
62
What medication and dose is used to treat dyslipidaemia?
Atorvastatin 20mg ON
63
What medication and dose is used to treat oedema (fluid overload)?
Diuretics, usually high doses of Furosemide BD
64
What medication and dose is used to treat hyperkalaemia?
Calcium resonium TDS/Lokelma
65
What medication and dose is used to treat hypertension?
Antihypertensive
E.g. Ramipril OM or Doxazosin OM
66
What medication and dose is used to treat vitamin D deficiency?
Alfacalcidol up to OD
67
What medication and dose is used to treat hyperphosphataemia?
Sevelamer or Lanthanum TDS with meals
68
What medication and dose is used to treat hyperparathyroidism?
Cinacalcet OD
69
Are ACEis/ ARBs used in AKI, CKD, or neither?
CKD - because renoprotective
Not AKI - because nephrotoxic
70
Which bloods are used to classify CKD stage?
Compare Albumin-Creatinine Ratio and GFR
71
What is a side-effect of phosphate binders?
Decrease absorption of iron
72
When are thiazide diuretics less effective?
When CrCl is <20mL/min
73
In CKD hypertension, what is the first line treatment?
ACEi or ARB
Titrated to maximum dose
74
What should be considered in patients with hypertension and CKD?
- ACEi/ARBs are renoprotection in CKD but nephrotoxic in AKI
- Calcium channel blockers are safe in renal failure but they cause/exacerbate fluid overload
75
Why are ARBs/ ACEis used in treatment of CKD?
HTN
Renoprotective
76
What effect does high phosphate levels in the blood have on the bones?
Causes calcium to move out of the bones
77
What is alfacalcidol and what is it used for?
Activated vitamin D
Given to treat low levels of calcitriol
78
What is an example of phosphate binders used in treatment of CKD?
Sevelamer
| (2) Lanthanum carbonate
79
What should be considered in patients with diabetes and CKD?
- Metformin is first line but contra-indicated if CrCl <30ml/min
- Sulphonylureas should be used with caution in renal failure as there is an increased risk of hypoglycaemia, especially for older patients and risk of falling (low doses given, titrate up)
- Pioglitazone (and others) fine in renal failure but contra-indicated in heart failure
- Complications of insulin - can the elderly administer insulin themselves?
80
When is pioglitazone contraindicated?
Heart failure
81
When is metformin contraindicated?
CrCl <30mL/min
82
When are SGLT2 inhibitors (flozins) contraindicated?
CrCl <60mL/min
83
What is a side-effect of calcium channel blockers for CKD patients?
Cause/ exacerbate fluid overload (oedema)
84
What should be considered in patients with pain management and CKD?
- Paracetamol is fine to give
- Codeine, tramadol and morphine accumulate in renal failure (low doses given, titrate up)
- Oxycodone is safer than codeine, morphine and tramadol as it bypasses the kidneys
- Patches such as fentanyl and buprenorphine are not appropriate for acute pain
- Ease of administration - elderly (risk of falls)
85
Which type of painkillers accumulate in renal failure?
- Codeine
- Tramadol
- Morphine
86
What types of painkiller are available for patients with renal failure requiring pain management stronger than paracetamol?
- Fentanyl patch
- Oxycodone
- Buprenorphine patch
- Tapentadol
87
Why do pharmacists have an impact in the management of CKD patients?
- Medication management in patients with CKD is complex, further complicated by multi-morbidities
- CKD medications need fine management
- Need a really good understanding of the principles of pharmacokinetics and pharmacodynamics plus and understanding of your drug and patient to manage them safely
88
Why does Atorvastatin need to be taken at night?
because the body makes the most amount of cholesterol at night
89
Why should Lanthanum be taken with meals?
it is a phosphate binder which removes excess phosphate from diet by reducing absorption in the GI tract, so need to be taken with meals
PM4B - Antonio
flashcards
Decks in class (28)
# Cards
-
(SYNOPTIC) Cancer - Cancer Recap30
-
(SYNOPTIC) Complications of Chemotherapy56
-
(SYNOPTIC) Cancer Metastases47
-
(SYNOPTIC) New + Emerging Cancer Treatments10
-
(SYNOPTIC) Renal - AKI33
-
(SYNOPTIC) Renal - CKD89
-
(SYNOPTIC) Dialysis + Drugs64
-
(SYNOPTIC) Poisoning & Antidotes27
-
(SYNOPTIC) Surgery97
-
(SYNOPTIC) Liver Disease & Management112
-
(SYNOPTIC) Neonates + Paediatrics28
-
(SYNOPTIC) Palliative Care21
-
(SYNOPTIC) Women's Health14
-
New Pharmacy Service22
-
Role of the Pharmacist4
-
Advanced Drug Delivery181
-
Motivational Interviewing4
-
Personalised Medicine15
-
Medication Safety25
-
OSCEs253
-
OSCE – Counselling3
-
OSCE – RTS4
-
OSCE – Prescriber Interaction3
-
OSCE – Drug Chart22
-
OSCE – RTS Referral Criteria40
-
Pharmacy Law165
-
Pharmacy Ethics4
-
Metallotherapeutics31
