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Clinical Pharmacy PH2506 > kidneys > Flashcards

kidneys Flashcards

1
Q

Functions of the kidney

A
  • Elimination of waste: carbohydrate; Nitrogenous (urea, creatinine); sulphate and phosphate; water and acid regulation: fluids and electrolytes
  • Endocrine: vitamin D deactivation; secretion of erythropoietin
  • Blood pressure regulation: renin/ angiotensin and volume control
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2
Q

acute kidney injury- facts

A
  • 100,000 deaths a year in hospital are associated with acute kidney injury
  • 30% could be prevented with the right care
  • one in five people admitted to hospital as an emergency has acute kidney injury
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3
Q

Acute kidney injury AKI or ARF

A
  • Serious medical emergency that can develop very quickly (usually within 48 hours)
  • Definition is varied
  • Is not a single state disease with uniform aetiology
  • Prognosis is not good if left untreated in a timely manner
  • Hypovolaemia (shock) main cause-falling renal perfusion pressure. But also nephrotoxicity and acute glomeruli nephritis
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4
Q

Definition of AKI

A
  • A rising serum creatinine of 26 µmol/litre or greater within 48 hours -50% or greater rise in serum creatinine known or presumed to have occurred within the past seven days
  • falling urine output to less than 0.5 mil/kg/hour >6 hrs in adults and >8 hrs in children and young people
  • 25% or greater fall in e GFR in children and young people within the past seven days
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5
Q

RIFLE criteria

A

Risk Injury Failure Loss End stage renal disease

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6
Q

AKIN criteria

A

See BB slides for an illustration of the AKIN criteria

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7
Q

Symptoms Of acute kidney injury

A

• Nausea and vomiting • Dehydration •Confusion • High Blood Pressure • Abdominal Pain • Slide Back out • Oedema

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8
Q

Risk of developing acute kidney injury

A
  • aged over 65
  • patients with existing kidney problems e.g. CKD
  • dehydrated patients who are unable to maintain their fluid intake independently
  • urinary tract blockage
  • sepsis
  • medication : NSAIDs, ACEI, diuretics, antibiotics (gentamicin)
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9
Q

Classification and cause of AKI

A

Pre-renal: reversible decreased perfusion through hypo-perfusion, via hypovoleamia or decreased CO, altered renal vascular regulation; 40-80%

  • Intra renal (including acute tubular necrosis) : renal parachymal injury, tubular necrosis; 10-50%
  • Post-renal: Urinary Tract obstruction, malignancies ; >10%
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10
Q

Pre-renal causes acute kidney injury

A

Occurs before the kidneys blood vessels

Decreased effective extracellular volume

Example: hypovolaemia; decreased cardiac output; systemic dilation Altered renal vascular regulation

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11
Q

intra renal

A

Cause within the kidney Caused by acute tubular necrosis

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12
Q

post renal

A

This occurs after the kidneys: bladder, ureter, urethra Caused by obstruction of the urinary tract e.g.prostate hyperplasia, malignancies

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13
Q

causes of acute tubular necrosis

A
  • Hypoperfusion
  • Radio contrast media (used to diagnose certain conditions)
  • sepsis
  • Rhabdomyolysis (breakdown of muscle from within the cell)
  • Renal transplantation (immunosuppresants cause kindey toxicity)
  • hepatorenal syndrome (End stage liver disease
  • Nephrotoxins: NSAIDS, ahminoglycosides, immunosuppressant, chemotherapy, poisons
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14
Q

Causes of AKI

A
  • reduce fluid intake
  • increased fluid loss
  • urinary tract symptoms (post renal cause)
  • recent drug ingestion
  • sepsis
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15
Q

Phases of recovery of acute tubular necrosis

A
  • Oliguric phase: 10 to 30 days; glomerular and tubular dysfunction
  • Polyuric phase: persisting tubular dysfunction
  • Recovery phase: maybe prolonged-six months or sometimes longer
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16
Q

Investigation of AKI

A

Full history- drug history

Clinical examination, including fluid balance assessment

Urinalysis- if it is conc urine it is pre renal cause; itra-renal or obstructive cause they will have isotonic urine; Obstructive uropathy the patient will have anuria (reduced urine productio) or crystal uria

Blood examination

Ultrasound scan renal tract is mandatory- this is to exclude obstruction and prepare patients for renal biopsy

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17
Q

management of acute kidney injury

A
  • Non-specific remedy
  • Early aggressive intervention at the first sign of oliguria may prevent sustained oliguria-
  • If due to shock-restoration of CVS function may involve transfusion, osmotic erratics or high dose of loop diuretics (furosemide 3mg/kg/6 hours)
  • Otherwise careful management-fluid intake monitoring, may use plasma expanders, use of diuretics depends on a aetiology
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18
Q

Chronic kidney disease

A
  • One in 10 people live in CKD
  • 6 million people in England
  • Progressive loss of renal function over a period of months or years symptoms of worsening kidney function unspecific may include feeling generally unwell,
  • Severity is in five stages: stage I is mildest causing few symptoms so stage V severe illness with poor life expectancy
  • Stage 5 it is called established chronic kidney disease
  • persistent fall in GFR (< 60 mil/Min/1.73 m²) for three months will be considered CKD
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19
Q

Signs and symptoms of chronic kidney disease

A

CNS: confusion; seizures; coma

BLOOD: anaemia; platelet abnormalities

RENAL: polyuria; Na+, H2O retention, noturia

HORMONAL: infertility; loss of libido; impotence

BONE: osteomalacia; pain; osteosclerosis; hyperparathyroidism

CVS (RAAS malfunction): hypertension; HF; vascular disease; peripheral oedema

GI TRACT: nausea; vomiting; weight loss

PERIPHERAL NEUROPATHY

20
Q

Causes of CKD

A
  • Diabetes- 16%
  • Chronic Glomerulonephritis- 19%
  • Pyelonephritis and obstructive uropathy-11%
  • Polycystic Kidneys-10%
  • Hypertension-6%
  • Renovascular disease-3%
  • Other-16%
  • Unknown aetiology-16%
  • Data not sent-3%
21
Q

Urine volumes by definition

A

OLIGURIA (Decreased urine output): in adults <500 ml/day

  • may indicate CKD but may also indicate dehydration or urinary obstruction
  • Anuria is below 50 ml/day

POLYURIA: in adults >2.5 L/day

  • May cause diabetes (osmotic effect), high volume intake, diabetes insipidus
  • May occur in early stage CKD
  • Loss of urine concentrating capacity
22
Q

Renal clearance and GFR

A
  • Direct measurements of clearance is difficult
  • Clearance is used to measure renal function
  • Equals the volume of blood from which a substance completely removed by filtration in one minute
  • Clearance x [plasma] = [urine] x urine vol/min -Clearance = (Uc x Uv) / Pc
  • If a substance were completely cleared and there is no tubular secretion of absorption then clearance = GFR
23
Q

Measurement of GFR

A
  • Inulin: ideal but need to infuse and obtain steady plasma concentration: measure plasma conc and urea conc
  • Creatinine: natural constituent from muscle

+Freely filterd but some tubular secretion

+Somewhat overestimates GFR

+Need 24 hour urine collection- difficult

-Various methods to estimate creatinine clearance and so GFR from single data point e.g. serum creatinine (oppsed to creatinine in urine)

24
Q

Cockroft-Gault equation

A

Derived from average population data 1976

Normal values for GFR fall with age- halve by age 75

-Most medicines that effect renal functions or are predominantly excreated through renal clearance use the cockroft-gault equation to adjust dose dependant on severity of kidney dysfunction (increased half life and so toxicity of drug)

25
Q

MDRD formula

A
  • Developed for use in CKD. No evidence of applicability in acute renal failure
  • Underestimates GFR in healthy (>60 ml/min)

eGFR=186x(serum creatinine (mcmol/L)-1.154x(age)-0.203xK1xK2

  • K1= 0.724 if female
  • K2= 1.212 if afro-American
26
Q

chronic kidney disease epidemiology collaborated

A
  • More accurate than MDRD
  • Clinical labs should: use the CKD epidemiology collaboration (CKD-EPI) creatinine equation to estimate GFR creatinine, using creatinine assays with calibration traceable to standardized reference material
27
Q

Plasma creatinine and GFR

A
  • Plasma Cr inversely related to GFR
  • Initially, relatively large falls in GFR causes small rises in PCr e.g. GFR 50% normal, PCr doubles to 200 mcg/L
  • Serum Cr measurements are not reliable for measuring small changes in GFR
  • Progression of disease best followed by reciprocal plot
  • Serum Cr increases as renal function deteriorates
28
Q

Progression of CKD

A
  • Diminished renal reserve: GFR (120-90 ml/min), urine production UP(normal/mild polyuria)
  • Renal impairment: GFR (90-60 Ml/min), UP (polyuria)
  • early stage renal failure: GFR (60-30), UP (oliguria)
  • Pre-end stage failure: GFR (30-15), UP (oliguria)
  • End-stage renal failure:GFR <15, UP (oliguria)
29
Q

Plasma urea

A
  • Normal <8mmol/L. Some symptoms when 20-25 mmol/L and severe symptoms 50-60 mmol/L
  • Uraemia is common in CKD but urea only one of the nitrogenous products affected
  • Plasma urea still a general index of renal function
  • Affected also by diet, liver function, muscle damage etc
30
Q

Tubular function

A
  • SPECIFIC GRAVITY: (1.01 to 1.02 normal adults)
  • OSMOLARITY (normal adult 50-1400 mOsmol/L; random; 500-800 mOsmol/L 24 hours)
  • Changes reflect concentration and can be used to indicate concentrating capacity e.g. water deprivation (lost in CKD)
  • Also affected by fluid intake and ADH release (diabetes insipidus)
31
Q

Fluid and electrolyte imbalance

A
  • Maybe very slow onset- patients don’t recognize urinary symptoms. Often mild polyuria early (loss of conc, capacity)
  • Later stages inadequate renal function and Na+ and H20 retention. Maybe hypervolemia and oedema- including pulmonary. HF a possibility
  • Late stage hyperkalemia and often acidosis- failure of K+ and H+ secretion
32
Q

Potassium

A
  • Generally Hyperkalaemia
  • Levels over 7mmol/L are life-threatening
  • Acidosis exacerbates hyperkalaemia because of movent of intracellular K+ out of the cell
  • Major ECG changes as a result of hyperkalaemia
  • If allowed to continue to rise will result in cardiac arrest
33
Q

Cardiovascular effect

A
  • Hypertension almost inevitable- number of causes: fluid retention, RA abnormalities
  • Cardiomyopathy associated with Ca2+ and phosphate (PO4) imbalance
  • Cardiac failure- volume overload, oedema, hypertension, anemia
  • Overall CVS events account for over half the deaths in CKD
34
Q

Anaemia

A
  • Bone marrow hypoplasia (wont produce RBC) due to reduced or no erythropoietin
  • Haemoglobin levels fall:<8d/dl Rf 12-18 g/dl
  • Fe and or folate deficiencies exacerbates the above- Poor dietary uptake and losses e.g. bleeding from the GI tract
  • Aggravates effects on heart and major effect on quality of life
35
Q

Calcium and phosphate

A
  • Kidney essential for final stage activation of Vit D
  • Lack of Vit D causes reduction GI Ca2+ absorption and renal reabsorption
  • Hypocalcaemia stimulates PTH release- increased bone resorption. osteomalacia–> renal rickets
  • Poor phosphate excretion leads to solubility product for Ca and PO4 to be exceeded. Ectopic calcification
  • This can be treated by restricting phosphate in the diet however this is hard because it is in alot of food stuff, phosphate binders can be used to absorb them
  • AlOH used to be used as a phosphate binder but patients used to absorb and not eliminate Al so would get neurological side effects including dementia
36
Q

Management of CKD

A
  • BP control: ARBs, ACEI this is used bevause they reduce protein uria and progression of CKD
  • Anaemia management
  • Oral bicarbonate supplement for management of metabolic acidosis
  • Encourage those with CKD to exercise, achieve a healthy weight and stop smoking
  • Offer dietary advice about K+, PO4, calorie and salt intake, but patient needs dietary assessment to prevent malnutrition
  • Low protein diets are no longer offered
37
Q

Drug use in renal impairment

A
  • Avoid drugs that are likely to cause further damage
  • Many drugs are excreted by the kidneys
  • Some drugs may need to be excreted in order to work
  • ADRs are more likely with many drugs
38
Q

Drug use in renal impairment

A

PATIENT FACTORS: degree of renal impairment; stable, improving or deteriorating; concomitant medication/disease

DRUG FACTORS: is the drug essential; How quickly is needed; what proportion is renally cleared; is the drug nephrotoxic; does the drug have a narrow therapeutic index; measure safety/efficacy parameter; our ADRs more likely in renal impairment; mechanism of action; half life

39
Q

Renal replacement therapy

A
  • Towards end-stage CKD-how shall require an organ transplant
  • there is a waiting list
  • the best option for most CKD patients
  • 2929 Kidney Transplants Took Pl; aprox one third were live donors
  • major limiting factor is donors-UK one of the worst in Europe for diners
40
Q

Dialysis

A

Peritoneal: up to 25 L of sterile fluid into the peritoneal cavity under gravity. The exchange between peritoneal capillaries and fluid. drain out under gravity

Haemodialysis-artificial kidney with large area exchange membrane. Arterial blood pumped by peristaltic pump countercurrent flow of dialysis fluid

continuous venovenous haemofiltration- short-term treatment using ICU patients with acute or chronic renal failure. Blood is passed through hemofilter

-Dialysis fluid is adjusted to the individual- low in ions to be removed and high in those to be added to patient plasma

41
Q
A
42
Q

Erythropoietins

A
  • Recombinant human erythropoietins
  • Epoetin alpha, beta, theta and zeta and darbepoetin (hydroxylated derivative with longer half life)
  • Can be used in CKD
  • MRHA warning on use in cancer- increase in mortality- 2008
  • Revised NICE guidelines- erythropoiesis stimulating agents are recommednend, within their MA as options for treating anaemia in people with cancer who are having chemotherapy
43
Q

Dialysis

A
  • This is taking toxins out of the blood
  • The blood passes through a semi permeable membrane that lets low MW compounds through
  • This is via difusion which is dependant on conc gradients as well as movement of dialysis pores of membrane so small moleucles are cleared better
  • This can be done with pressure changes
  • The movement of substances can be done by convection- small molecules move with ultrafilrate
44
Q

Peritoneal dialysis

A
  • Rarely used but is used when Haemodialysis
  • A catheter is then placed into the peritoneal cavity
  • 1-2L of dialysis fluidis then placed into the abdomen and left for around 30 minutes then drained into bag
  • This can be carried out up to 20 times a day
  • This is keep and simple and doesn’t need specialist kidney untis or staff
  • However this can take a long time and be tiring for the patient; Cause infection of peritoneum as well as protein loss
45
Q

Haemodialysis

A
  • A dialysis line is used, this is placed in a vein and an artery
  • This can be intermittent of continuous
  • This is expensive bevcause it has to be in a renal unit as well as specialist staff (this can be inconvient, travel)
46
Q

Continuous venvenous haemofiltration

A
  • Blood is passed through a haemofilter
  • For each case the dialysis fluid is adjusted dependant on electrolyte and needs for the specific patient

Clinical Pharmacy PH2506 (20 decks)

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