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Pharmacy Yr3 Renal and hepatic diseases > week 2- Clinical manifestations & treatment of CKD+ Dialysis & Nephrotoxicity > Flashcards

week 2- Clinical manifestations & treatment of CKD+ Dialysis & Nephrotoxicity Flashcards

1
Q

what are the clinical manifestations for CKD?

A

-urinary symptoms
-Proteinuria
-fluid retention
-uraemia
-anaemia
-electrolyte disturbance
-Hypertension
-Muscle dysfunction
-Renal bone disease (renal
osteodystrophy)

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2
Q

what are the urinary symptoms in CKD?

A 
– Very early stages only
– Polyuria
– Medullary damage
– Osmotic effect of urea (>40
mmol/l)
– Loss of ability to
concentrate urine
– Nocturia
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3
Q

what are the Proteinuria symptoms in CKD?

A 
-IF PROEIN IS FOUND IN URINE 24HR SAMPLE IS COLLETED.
– Degree of proteinuria
occurs in all CKD
– Proteinuria >2g in 24 hr 
glomerular disease
– >5g in 24hrs  severe
disease = Nephrotic
Syndrome
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4
Q

what are the fluid retention symptoms in CKD?

A 
– As CKD progresses, GFR
decrease very low levels
– Kidneys unable to excrete
Na+ & water
– leading to peripheral & pulmonary
oedema & ascites
– 80% of CKD patients will
have volume dependent
HT
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5
Q

what are the uraemia symptoms in CKD?

A 
-greater than 50mmol/l
– Measurement of level of
“toxins” in blood
– Often used to decide when
to start dialysis
– Symptoms:
• anorexia
• N&V
• constipation
• foul taste
• skin discoloration (gets deposited in the skin)
• pruritis
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6
Q

what are the anaemia symptoms in CKD?

A 
– Due to failure of kidney
to produce the hormone
erythropoetin
– Regulates red blood cell
proliferation in the bone
marrow
– Symptoms:
• fatigue & lethargy
• breathlessness
• angina
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7
Q

what are the Electrolyte

disturbances symptoms in CKD?

A 
– Hyperkalaemia
• due to kidneys inability
to remove K+
• >7mmol/l leading to medical
emergency & risk of
cardiac arrest
– Acidosis
• due to kidneys inability
to remove H+
• leads to decrease plasma
bicarbonate
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8
Q

what are the hypertension symptoms in CKD?

A 
-80 of ppl with CKD have hypertension
– Vast majority of CKD
patients will have HT
– Mainly due to circulatory
volume expansion due to
Na+ retention
– HT can also increase the
rate of decline of renal
function
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9
Q

what are the Muscle dysfunction symptoms in CKD?

A 
– Cramps & restless legs
– Especially at night
– General nutritional
deficiencies & electrolyte
disturbances
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10
Q

what are the different processes for Renal bone disease (renal
osteodystrophy)?

A

– Cholecalciferol (inactive precursor of Vitamin D)
absorbed from GI tract & produced in skin due to
sunlight
– Production of active vitamin D - 1,25-
dihydroxycholecalciferol (calcitriol) requires
hydroxylation in 25 position by liver and 1
position in kidney (does not occur in renal
failure)
– lead to Vitamin D deficiency
– lead to Defective bone mineralisation
– lead to Osteomalacia (bone softening)

– low Vitamin D
– leads to low calcium absorption from gut
– leading to Hypocalcaemia

–Hypocalcaemia due to lack of vitamin D is made worse by Hyperphosphataemia due to failure to excrete phosphate via kidneys
– leading to Hypocalcaemia because phosphate
ions sequester calcium as calcium phosphate in bones which would decrease calcium levels even more
– Hyperphosphataemia leading to pruritis (deposition of the phosphates)

– Metabolism of calcium & phosphate
controlled by parathyroid hormone (PTH)
produced by the parathyroid glands
– Kidney unable to respond to PTH by increased renal
calcium reabsorption
– leading persistent hyperparathyroidism &
hyperplasia of thyroid glands (may require
removal)
– Hyperparathyroidism leading disturbance in
normal bone architecture
– leading Osteosclerosis (bone hardening)
– leading to Bone pain

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11
Q

what is the treating of chronic kidney disease?

A

there are two broad areas
-conservative= diet and drugs (hat would treat the manifestations)
aim is to treat symptoms and decrease the decline in renal failure
-renal replacement therapy= dialysis and transplantation

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12
Q

what is often the treatment for end stage renal failure?

A

the 3 D’s

diet, drugs and dialysis

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13
Q

What is the propose of drugs, dialysis and transplant?

A
  • drugs used to treat the manifestations and symptoms

- dialysis and transplant is to cure the underlying cause

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14
Q

what kind of drugs are used to treat hypertension in CKD?

A
  • Diuretics
  • ß- blockers
  • Calcium channel blockers
  • ACEIs
  • Angiotensin II inhibitors
  • alpha - blockers
  • Vasodilators
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15
Q

what are some main facts about diuretcis?

A 
– Only LOOPs (e.g.
furosemide)
– Only occasionally used for
HT - mainly for oedema
– Thiazides (except
metolozone) ineffective at
CrCl<25ml/min
– Potassium sparing  risk of
hyperkalaemia
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16
Q

what are some main facts about beta-blocker?

A 
– Cardioselective
– E.g. Metoprolol, atenolol
– Metoprolol cleared through
liver
– Start with low dose and
titrate up
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17
Q

what are some main facts about CCB?

A

– Can produce oedema
(especially Nifedipine)
– LEADS TO confusion with
symptoms of fluid overload

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18
Q

what are some main facts about ACEI’s/Angiotensin II

inhibitors?

A 
– Can cause decline in renal
function but not an issue in
ESRF (although increased risk of
other side-effects)
– C/I: Renal artery stenosis
(where blood flow to kidney
relies upon Angiotensin II
vasoconstriction)
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19
Q

what are some main facts about alpha-blocker?

A

– E.g. Doxazosin

– Cleared through liver

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20
Q

what are some main facts about vasodilators??

A 
– E.g. Hydralazine, Minoxidil
– reserved when HT
inadequately controlled by
others
– S/E:
• Reflex tachycardia (use
with ß- blocker)
• Fluid retention (use with
diuretic)
• Minoxidil leading to excess hair
growth!!
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21
Q

what is Bp target for most patients?

A

<140/90

if type 1 diabetic <130/80

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22
Q

what is oedema as a consequence of CKD?

A 
Mainly pulmonary
• Best controlled with dialysis
• Loop diuretics in pre-dialysis stage
• Furosemide - up to 2g daily (500mg tablet)
• Fluid & sodium restriction
• Stop when dialysis starts
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23
Q

what is hyperkalaemia as a consequence of CKD?

A

• >7mmol/l dialysis imperative due to risk of cardiac arrest
• Emergency treatment:
– Calcium gluconate [10ml 10% iv over 5-10mins]
– Improves myocardial stability
– Insulin (20 IU soluble) + Glucose (50ml 50% iv)
– Insulin stimulates intracellular K+ uptake
– Glucose to prevent hypoglycaemia
– Calcium Resonium [15-30g powder orally or
enema]
– ion exchange resin binds to K+ in GI tract &
releases Ca2+ in exchange
– Always give with lactulose 10ml for each 15g dose
as very constipating

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24
Q

what is the pre-haemodialysis target for pottassium?

A

4.0-6.0 mmol/l

25
what is Acidosis as a consequence of CKD?
• Due to kidneys inability to excrete H+ ions • Sodium bicarbonate 500-600mg tds -is given if patient has low levels (tablets or powder) • Usually only a problem pre-dialysis
26
what is the target for bicarbonate levels?
18-24 mmol/l
27
what is Hyperphosphataemia as a consequence of CKD?
• Due to kidneys inability to excrete phosphate ions • Phosphate binders: – E.g. Aluminium hydroxide, calcium carbonate, calcium acetate, sevelamer – bind with phosphate in food in gut – take with or just before meals – dose according to size of meal (advice given by renal dieticians)
28
what is Hypocalcaemia as a consequence of CKD?
• Due to kidneys inability to produce active Vitamin D • Vitamin D: – Calcitriol [1,25-dihydroxycholecalciferol] – Alfacalcidol [1 alpha-hydroxycholecalciferol]
29
what are the targets for calcium, phosphate and level?
``` • PTH (Parathyroid hormone ): – >2x and <4x upper limit of normal • Phosphate: – 1.1-1.7mmol/l (pre-dialysis in HD pts) • Calcium (corrected): – 2.2-2.6mmol/l ```
30
what is anaemia as a consequence of CKD?
• Due to failure of kidney to produce the hormone Erythropoetin [EPO] • Recombinant human erythropoetins by injection (iv/sc): • Eg: Epoetin alfa [Eprex] Epoetin beta [Neo-Recormon] Darbepoetin [Aranesp] ▪ S/E: hypertension, pure red cell aplasia (Eprex sc only) ▪ Methoxyl Polyethylene Glycol-Epoetin Beta[Mircera] - continuous erythropoietin receptor activator •give Iron therapy for people with low ferrtin levels as it doesnt matter about how much erythropoetins: – Eg Iron sucrose [Venofer], Ferric carboxymaltose [Ferinject] (Oral iron – limited effectiveness) • Avoid blood transfusions theres a risk of antibodies and can cause problems with possible future transplant matching
31
what are the target Hb and ferritin levels for someone who has CKD?
``` • Hb: – 100-120 g/l • Ferritin: – >100 µg/l [aim for 200-500 µg/l & stop if >800 µg/l ] ```
32
what is Cramps & restless legs as a consequence of CKD?
``` • Cramps: – Often at night or on dialysis – Quinine sulphate 300mg • Restless leg syndrome: – Clonazepam 0.5-1mg nocte ```
33
what vitamin supplements are given to patients with CKD and the problem of water soluble ones?
• Eg Renavit – dietary advice – water soluble vitamins removed by dialysis process
34
why are people given hepatitis B vaccine for CKD?
``` • All patients with CKD + booster every 5 years • HD patients monitored annually for antibodies and re-immunised if necessary • 3 doses of 40mcg [double normal dose] ```
35
what are the 2 different types of dialysis?
* Haemodialysis | * Peritoneal dialysis
36
how does a normal kidney work? 2 process?
ultrafiltration- occurs through glomerulus removal of water reabsorption- occur distal and proximal convoluted tubule and loop of Henle partial recooping of useful molecules
37
what is the princle of dialysis?
-aims to micmic the 2 main process occurring in a normal functioning kidney ultrafiltration and reabsorption -artifical kiney used in dialysis the kidney glomerular basement membrane – Haemodialysis = artificial – Peritoneal dialysis = patient's own peritoneal membrane
38
what is the aim of ultrafiltration?
removal of waste products and removal of water
39
how does removal of waste products occur during ultrafiltration?
– Diffusion down concentration gradient across membrane – Waste solutes from blood (high conc.)to dialysate fluid (low conc.)
40
how is the removal of water occurring in ultrafiltration?
– HD - removed hydrostatically with negative pressure gradient produced by pump in HD machine – PD - removed osmotically using dialysate fluids containing varying concentrations of glucose (1.5%, 2.3%, 4,25%)
41
what is the aim for reabsorption in dialysis?
conversation of useful substances
42
how does conservation of useful substances occur in reabsorption?
– Dialysate fluid loaded with desired substances at normal concentrations and therefore prevents diffusion ( as no concentration gradient)
43
how does haemodialysis work?
``` • Arterial blood taken from body, anticoagulated (heparin so it does clot) & passed through artificial kidney (made of hollow fibres - semi-permeable membrane) • Countercurrent dialysate fluid bathes fibres & maximises conc. gradient • Return to vein & dialysate discarded • 3-4 hours, 2-3 times a week (depending on fluid regulation between treatments - must not put on >1.5Kg above ‘dry weight=after dialysis’) -between dialysis have to be very strict with fluid intake so they dont have too much fluid can cause pulmonary oedema and cardiac problems • Hospital [mainly] or home ```
44
how is the fluid removed from the patient to flow through the artificial kidney?
``` • Sub-clavian – tunnelled under skin to subclavian vein – temporary - risk of infection • Ateriovenous fistula leading to – Artery joined to vein – ‘Matures’ over 6 weeks – Two enlarged blood vessels to allow needling – Do not cover tightly or injure • Ateriovenous shunt – Two silastic tubes with Teflon connector inserted into vein and artery ```
45
how does peritoneal dialysis?
``` • Peritoneal membrane lines all internal organs & has rich blood supply • 1.5/2l sterile dialysis fluid run into peritoneal cavity under gravity • Fluid remains in abdomen for set period of time [dwell time] - diffusion occurs • Fluid drained out under gravity & discarded • New fluid drained in • Repeat 4 times/ day (“exchanges”) ```
46
how is access occur into the body?
``` • Indwelling silastic catheter • Tenckoff catheter • Tunnelled through abdominal wall & distal end sits in peritoneal cavity- Dacron cuffs sit on either sideof abdominal wall & hold in place • Aseptic technique required when changing bags • Complication of PERITONITIS [Intra Peritoneal antibiotics eg Vancomycin/gentamicin] • Other problems: – hyperglycaemia – loss of protein – catheter blockage – local infection – sclerosing peritonitis ```
47
what are the types of peritoneal dialysis?
• CAPD: – Continuous ambulatory peritoneal dialysis= 4 types a day bag exchange • APD: – Automated peritoneal dialysis=in hospital till they can go home on a machine, or if patient has problem with fluid overload for 24hrs • IPD: – Intermittent peritoneal dialysis= machine at home hooked up over night less efficient than COPD
48
what is the management of diet for being on dialysis?
* Healthy [low fat, low salt, high fibre] * low potassium, due to inability to remove, chocolate and potatoes * low phosphate, found in protein * high protein in CAPD
49
what is the management of diet for being on dialysis?
• Haemodialysis: – urine output + 500ml/day including sauces, ice cream • Peritoneal dialysis: – urine output + 750ml/day
50
what are some of the complication for dialysis with drugs?
-haemodialysis increases removal
51
what are the causes that can increase drug removal during haemodialysis due to the drug?
``` – low molecular.wt [<500] • vancomycin 1448 • gentamicin 543 • metronidazole 171 – low % plasma protein bound – low Vd – high water solubility – high renal clearance in normal RF ```
52
what are the causes that can increase removal during haemodialysis?
``` – duration – blood flow – type of membrane – flow rate & composition of fluid ```
53
what are the causes that can increase drug removal during peritoneal dialysis due to the drug?
``` – low molecular.wt [<500] • vancomycin 1448 • gentamicin 543 • metronidazole 171 – low % plasma protein bound – low Vd – high water solubility – high renal clearance in normal RF ```
54
what are the causes that can increase removal during peritoneal dialysis?
``` • Dialysis – composition of dialysate – pathology of peritoneum – volume & exchange rate of dialysate in peritoneal cavity – osmotic concentration gradient ```
55
what are the different classifications for nephrotoxicity?
-depends where damage occurs • Pre-renal • Intra-renal • Post-renal
56
what is pre renal nephrotoxicity?
Under perfusion of kidney: – Diuretics – g.i.losses [Diarrhoea and vomiting, laxative abuse] – NSAIDs (Cycloxygenase inhibition leads to inhibition if vasodilatory PGs) therefore redcues renal blood flow – ACEIs
57
what is intra-renal nephrotoxicity?
-within kidney Hypersensitivity reactions & unpredictable: – Glomerular lesions [glomerulonephritis]: • eg. gold, penicillamine, phenytoin, penicillins • Passive trapping of immune complexes in glomerulus causing inflammatory response – Interstitial damage [interstitial nephritis] • eg penicillins, cephalosporins, allopurinol, azathioprine • inflammation of cells lying between nephrons Directly toxic and more predictable: – Eg aminoglycosides (damage proximal tubules), amphotericin, cyclosporin – Can occur with a single dose
58
what is intra-renal nephrotoxicity?
Due to urinary tract obstruction: – Eg. high dose suplhonamides, methotrexate – Causing crystalluria – Crystals block outflow of urine leading to back pressure leading to damage/scarring to kidneys
59
why is there conflict for the use of nephotoxic drugs and what can be done?
``` • Often essential to use nephrotoxic drugs in renal patients; • leads to Constant monitoring of renal function and signs of toxicity • leads to Once in ESRF, cannot cause any further renal damage or decline in renal function BUT patients will be at risk of other side-effects associated with toxic accumulation ```

Pharmacy Yr3 Renal and hepatic diseases (5 decks)

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