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NUR3310 > Wk 2: Renal > Flashcards

Wk 2: Renal Flashcards

1
Q

Define CKD

A

= umbrella term that describes kidney damage, or a decrease in the glomerular filtration rate (GFR) for 3 months or more.
- It reflects the progressive and irreversible destruction of kidney structures.
- Chronic kidney disease decreases the endocrine and excretion functions of the kidney.

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2
Q

What are some causes of CKD?

A
  • diabetes,
  • glomerulonephritis,
  • hypertension,
  • cardiovascular disease,
  • urinary tract obstruction/infection,
  • hereditary defects of the kidneys, or
  • as a complication of renal diseases (e.g. failure to resolve AKI).
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3
Q

Why is the prevalence of CKD increasing?

A
  • aging population
  • increasing rate of obesity
  • increased incidence of diabetes
  • increased incidence of hypertension
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4
Q

What are some risk factors for CKD?

A
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5
Q

What are the stages of CKD? their GFR range and the management for them?

A

Stage 1
= Kidney damage with normal or increased GFR.
- GFR: >90 ml/min/1.72m2
- Action: Diagnosis & treatment, Rx of co-existing conditions, CVD risk reduction.

Stage 2
= Kidney damage with mildly decreased GFR
- GFR: 60-89 ml/min/1.72m2
- Action: estimation of progression

Stage 3a
= Moderately decreased GFR
- GFR: 45-59 ml/min/1.72m2
- Action: Evaluation & Rx of complications

Stage 3b
= Moderate to severe decreased
- GFR: 30-45 ml/min/1.72m2
- Action: Frequent evaluation and aggressive treatment of complications

Stage 4
= Severely decreased
- GFR: 15-29 ml/min/1.72m2
- Action: Preparation for renal replacement therapy

Stage 5
= Kidney failure (End-stage kidney disease) - GFR: <15 ml/min/1.72m2
- Action: Kidneys cannot remove metabolic waste. Renal replacement required to sustain life.

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6
Q

Explain the pathophysiology of CKD

A

= unhealable nephron loss that reduces the fucntion of the kidney.
- In stage one, the patient may have polyuria (increased urine output) as the kidneys lose their ability to concentrate urine.
- Symptomatic changes do not usually become apparent until renal function declines to less than 25% of normal.
- As the disease progresses, urine output reduces to oliguria (<30mL urine / hr) and anuria <100 mL / urine / 24-hours).

With a reduction in urine output, azotaemia (retention of nitrogenous waste) becomes evident, identified by;
- increased serum urea levels
- increased creatinine levels
- other more general signs and symptoms.

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7
Q

What are some clinical manifestations of CKD?

A
  • polyuria-> oliguria-> anuria
  • often progressive and goes unnoticed as kidneys have good functional reserves
  • up to 80% of GFR can be lost with few obvious signs and symptoms.
  • As nephrons are lost, the remaining nephrons hypertrophy (enlarge) to compensate.
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8
Q

What are the pathophysiological effects of deranged creatin secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

= Creatinine is a by-product of creatine breakdown. Creatine is released by muscles, and is exclusively excreted by the kidneys.

Elevated serum creatinine is a marker of CKD.

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9
Q

What are the pathophysiological effects of deranged urea secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

= Urea is the by-product of protein breakdown – both dietary and via metabolism.
- Urea is excreted by kidneys.
- Reduced kidney function causes an elevation in urea levels (uraemia) and other toxic (nitrogenous) waste.

System affected
- Cardiac: Uraemic toxins cause inflammation
- Neurological: uraemic toxins produce encephalopathy
- Endocrine: insulin resistance. The ability of the kidney to degrade insulin is reduced, and insulin half-life is prolonged
- Digestive: Digestive - Elevated levels of urea / uraemic toxins are attacked by bacteria in the GIT, releasing ammonia.
- Haematological: Uraemic toxins decrease red blood cell life span

Signs and symptoms:
- Cardiac: Inflammation may lead to pericarditis, compromising cardiac output.
- Neurological: Confusion, drowsiness, impaired concentration, memory loss, impaired judgment. In ESKD may progress to seizures, coma
- Endocrine: Low BSLs
- Digestive: Uraemic fetor (bad breath), nausea, vomiting, anorexia, bleeding, diarrhoea, constipation. Weight loss. Malnutrition is common in CKD.
- Haematological: Anaemia, lethargy, dizziness, low haematocrit

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10
Q

What are the pathophysiological effects of deranged sodium and water secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

Patho:
- When GFR decreases to 25%, obligatory osmotic loss of 20-40mmol sodium per day as kidneys unable to concentrate urine.
- Elevated renin stimulates secretion of aldosterone, increasing sodium reabsorption.

Later patho:
- In later CKD, kidneys unable to regulate sodium and water balance. Both sodium and water retained.

System affected
Inital
CVS: increased cardiac workload due to reduced circulating volume.

Late
CVD: fluid overload
Resp: fluid overload, congestive heart failure.
Integumentary

Signs and symptoms
Initial
CVD: Hypotension due to excess fluid loss, Tachycardia (compensatory)

Late
CVD: Excess sodium and water cause hypertension. Cardiomyopathy due to fluid overload (and anaemia)
Res: Dyspnoea
Ingu: odema

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11
Q

What are the pathophysiological effects of deranged protein secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

Patho: Proteins do not usually pass through the fenestrations in the glomerulus.
- Damaged nephrons allow protein to pass, resulting in protein in the urine (proteinuria).

System affected:
- MSK

Sign and symptoms:
- Loss of muscle mass
- Muscle weakness

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12
Q

What are the pathophysiological effects of deranged Potassium secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

Pathophysiology
- Potassium excretion via urine and faeces is maintained until oliguria (end-stage kidney disease). With oliguria, potassium levels increase to life-threatening levels.

System affected
- CVS

Signs and symptoms
- arrhythmias
- widened QRS and peaked T wave on ECG

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13
Q

What are the pathophysiological effects of deranged bicarbonate secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

Pathophysiology
- When GFR decreased to 20-25%, decreased bicarbonate reabsorption in tubules, and decreased hydrogen ion elimination.

System affected
- metabolic acidosis

Signs and symptoms
- Kussmaul respirations (fast a deep in response to metabolic acidosis)

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14
Q

What are the pathophysiological effects of deranged calcium secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

Pathophysiology
- When GFR decreased to 25%, calcitrol production in kidneys is impaired, and calcium absorption in intestine is reduced. Hypocalcaemia stimulates parathyroid hormone secretion with mobilisation of calcium from bone (hyperparathyroidism)

System affected
CVS: Calcium deposits reduce vascular elasticity and cause vascular calcification = vascular disease. Increased risk of heart disease, stroke, peripheral vascular disease.
Endocrine: Hyperparathyroidism decreases insulin sensitivity and impairs glucose tolerance.
MSK: CKD metabolic bone disorder (CKD-MBD) = Increased risk of fractures.
Integumentary: Calcium phosphate deposits and hyperparathyroidism associated with skin irritation inflammation, pruritus, and excoriation.

Signs and symptoms
- Endo: high BGLs

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15
Q

What are the pathophysiological effects of deranged Phosphate secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

= Renal phosphate excretion decreased (hyperphosphataemia). Increased serum phosphate binds to calcium, further compounding hypocalcaemia.
= Increased phosphate level also increases production of parathyroid hormone (PTH). Increased production of PTH results in more calcium being released from bones into blood. This leads to weak and brittle bones= increased fractures

Systems affected
- Cardiovascular - Can cause cardiovascular calcification, increased risk of stroke, disruption of conduction system, and cardiac arrest.
- Musculoskeletal - CKD metabolic bone disorder (CKD-MBD) = Increased risk of fractures.
- Phosphate binds with calcium forming calcifications, leading to non-specific symptoms such as pain and stiffness in joints

S+S
- increased fractures

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16
Q

What are the pathophysiological effects of deranged Vit D secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

Pathophysiology
= Vitamin D must be ‘activated’ (hydroxylation) in the kidneys before it can function to help absorb calcium and phosphate.

System affected
- In CKD, Vitamin D is not activated, and therefore calcium & phosphate are not absorbed at usual levels.

Signs and symptoms
- Increased risk of fracture

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17
Q

What are the pathophysiological effects of deranged Red blood cells secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

Pathophysiology
- Kidneys responsible for production of erythropoietin – as kidneys fail, erythropoietin production decreases, decreasing red blood cell production.

System affected
- Cardiovascular - Declining erythropoietin production causes anaemia, thereby increasing cardiac workload. Defective platelet aggregation increase risk of bleeding.
- Haematological - Uraemic toxins decrease red blood cell life span
- Integumentary – anaemia causes skin pallor, and may cause bruising from increased bleeding

Signs and symptoms
- Cardiovascular: Cardiomyopathy due to anaemia (and fluid overload). GI bleeding, epistaxis, cerebrovascular haemorrhage.
- Haematological: Anaemia, lethargy, dizziness, low haematocrit
- Integumentary: Pale / yellowed skin, bruising

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18
Q

What are the pathophysiological effects of deranged magnesiums secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

Pathophysiology
- As the kidney is the major regulator of serum magnesium; accumulation may occur with progressive renal impairment leading to hypermagnesaemia.

System affected
Hypermagnesaemia may cause vomiting, lethargy, muscle weakness, skin burning, hypotension and cardiac arrhythmias.

Signs and symptoms

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19
Q

What are the three categories of renal bone disease (CKD-MBD)? and explain them

A

Low bone turnover with inadequate mineralization secondary to diminished vitamin D (osteomalacia) or from over‐suppression of parathyroid gland (adynamic bone disorder). Low turnover increases fracture rate. This is managed by prescribing Calcitrol and phosphate binders (e.g. calcium carbonate binds to phosphate in food).

High bone turnover related to hyperparathyroidism (osteitis fibrosa cystica). Increased bone reabsorption and accelerated rates of disordered bone being formed.

Mixed osteodystrophy (elements of high and low bone turnover). Results in poorly constructed soft bone that is not being regenerated at a normal rate.

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20
Q

What are some signs and symptoms of CKD-MBD?

A
  • Muscle weakness and bone pain
  • Fractures and stiff joints
  • Pruritus (severe itching)
  • Calciphylaxis
  • Soft tissue calcification
  • Periarthritis
  • Skeletal deformities
  • Calcification of lung, skeletal muscle
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21
Q

What are some clinical manifestations of CKD? (by system)

A

Psychological
- anxiety + depression

Neuro
- fatigue
- headache
- sleep disturbances
- encephalopathy

Ocular
- hypertensive retinopathy

Metabolic
- carbohydrate intolerance
- hyperlipidaemia

Airways + breathing
- Short of breath
- Kussmaul respirations
- Pulmonary oedema
- Pleural effusion
- uraemic pleuritis
- pneumonia

Circulation/CVS
- Polyuria
- Oliguria / Anuria
- Hypertension
- Cardiac arrhythmias
- Cardiomyopathy & heart failure
- Anaemia
- Bleeding tendencies
- Discolouration of skin
- heart failure
- coronary heart disease
- pericarditis
- peripheral artery disease

MSK
- vascular and soft tissue calcifications
- osteomalacia
- osteitis fibrosa

Haematological
- anaemia
- bleeding
- infection

Gastro-intestinal
- anorexia
- nausea
- vomiting
- GI bleeding
- gastritis

Endo/reproductive
- hyperpara-thyroidism
- thyroid abnormalities
- amenorrhoea
- erectile dysfunction

Peripheral neuropathy
- paraesthesias
- restless leg syndrome

Disability
- Confusion / Altered conscious state
- Muscle / tissue wasting
- Neuromuscular twitching, cramps
- Weight loss
- Infection
- Increased risk of fractures

Integumentary
- pruritis
- ecchymosis
- dry, scaly, skin

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22
Q

What patient assessments would you complete for suspected/diagnosed CKD?

A
  • DRSABCD
  • Obtain a history
    - Identify existing kidney disease, family history, risk factors
    - Ask about current medications (many medications are nephrotoxic)
    - Ask about diet – what have they been eating / drinking?
    - How they are feeling?
  • medication history (some over-the-counter drugs are nephrotoxic, e.g. aspirin, ibuprofen)
  • assess dietary habits
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23
Q

What diagnostic studies may be ordered for a pt with suspected CKD?

A
  • Urine screen for protein, heamaturia and cellular casts= proteinuria is often the first indication of kidney damage.
  • Persistent proteinuria should be investigated with pathology: serum urea, creatine and creatinine clearance levels (creatinine exclusively excreted by kidneys).
  • Glomerular filtration rate (GFR) to assess degree of disease
  • Kidney ultrasound to identify size of kidneys, and any obstructions.
  • Biopsy for renal bone disease (early identification enables intervention to slow progression)
  • risk assessment for risk of CVD
    • as reduced GFR and albuminuria are risk factors
24
Q

What are the general principles of CKD management?

A

Key points
- Detect and treat reversible causes
- preserve current function
- slow progress
- reduce risk of CVD
- manage hypertension
- nutritional therapy
- anemia
- hyperglycemia
- Dyslipidaemia
- Hyperkalaemia
- Patient education
- Referrals
- Kidney replacement therapy
- Control serum urea and creatinine
- Control hyperkalaemia by restricting high-potassium foods and drugs.
- Limit dietary phosphate to minimise risk of CKD-MBD.
- Sodium restriction (varies from 2-4g/day)
- Protein - some controversy re protein in diet. Recent evidence suggests ‘avoid high protein meals, but otherwise normal protein intake’ for patients who are not receiving dialysis.

  • Treatment of hypertension, anaemia, hyperglycaemia and detection of proteinuria all help slow disease progression and improve patient outcomes.
  • Control hypertension - aim to keep BP <130/80, encourage weight loss (if needed), exercise,
  • Early referral to commence renal replacement therapy
  • Administer exogenous erythropoitin (EPO) to treat anaemia

Diet:
- Nutritional management is critical in supporting the patient with CKD.
- CKD is associated with the accelerated breakdown of body proteins (catabolism) which creates a negative nitrogen balance. - Poor nutritional status is associated with increased mortality and morbidity; people with malnutrition are at higher risk of sepsis and haemorrhage.

25
Q

How would we correct or manage fluid balance in CKD?

A

In end stage:
- restrict fluids in late stage to 500-600mls (insensible loss= sweat, saliva) plus an amount equivalent to previous day’s urine output
- monitor for fluid over load in late stage
- daily weight

*Patients may be dehydrated due to diuresis in early stages of CKD (inability of the kidneys to concentrate urine) or have fluid overload in later stages of CKD.

26
Q

How would we correct or manage hypertension in CKD? and what would this do?

A

Management of hypertension will:
- Reduce the progression of CKD
- Reduce cardiovascular risk

Target BP <130/80

Meds
- Ace inhibitor (e.g. Captopril, Ramipril) to slow prodcution of angitension 2 and thus vasoconstriction
- Angiotension II receptor blocker (e.g.
Irbesartan, Candesartan)

27
Q

How would we manage nutrition in CKD?
Consider; protein, salt, phosphate, potassium, fluid, carbonated beverages

A
  • encourage balanced diet
  • maintain nutritional status while minimising accumulation of toxic waste production
  • GFR<30= individualised diet prescribed
  • Malnutrition may be due to anorexia, nausea, vomiting, due to CKD

The nutritional targets for those with CKD and eGFR>30ml/min/1.73
- Protein= 0.75‐1.0 g/kg/day (no restriction necessary)
- Salt= No greater than 100 mmol/day (or 2.3 g sodium or 6 g salt per day) Avoid addingsalt during cooking or at the table Avoid salt substitutes that contain high amounts of potassium salts
- Phosphate= No restriction necessary in Stages 1‐3. In ESKD, phosphate restriction to 1g/day.
- Potassium= If persistent hyperkalaemia present, consult dietitian regarding restricting intake and avoiding food high in potassium
- Fluid= Drink water to satisfy thirst. In Stages 1‐3, fluid restriction is not required.
- Carbonated beverages= Avoidance is preferable. Minimise intake to less than 250 mL per day

28
Q

What are the pathophysiological effects of deranged glucose secondary to CKD?
- Pathophysiology
- System affected
- signs and symptoms

A

= when excess glucose is in the blood it needs to be excreted and because it is a larger molecule it injurs the glomeruli.

29
Q

What is renal bone disease (CKD-MBD)?

A

= kidneys cant balance calcium and phosphate levels so when phosphate levels rise, calcium is drawn out of the bones making them weak.
- Causes vascular calcification which contributes to mortality in patients with CKD.
- caused by sever hyperparathyroidism (HPT)
- thus must manage phosphate

30
Q

How are phosphate level in CKD-MBD managed?

A
  • limit dietary phosphorus
  • administer phosphate binders/calcium supplements to prevent/manage hyperphosphataemia
    - calcium binds with phosphate in food in bowel and is excreted with faeces
    - administered with meals
  • supplement vit D to help absorb calcium and phosphate
31
Q

How does CKD cause anemia?

A
  • failing kidneys are unable to complete the function of erythropoietin production thus resulting in anemia.
  • uraemic toxins also decrease RBC life span
32
Q

What is the management of anaemia in CKD?

A
  • Administer Erythropoietin therapy / EPO stimulating agents (IV or SC 2-3 times / week).
  • ensure we also manage their anemia so they can actually produce RBCs

Note. EPO is associated with cardiovascular disease risk, hypertension is a contraindication

33
Q

Explain how CKD can cause hyperglycemia

A
  • CKD is associated with insulin resistance resulting in hyperglycemia.
  • can lead to a loss of kidney function
    = can lead to increased loss of kidney function and CVD due to the glucose molecules being larger in size and thus damaging the membranes they permeate when needing to be excreted in urine.
34
Q

What is the management of hyperglycemia for patients with CKD?

A
  • metformin should not be prescribed to patients with GFR < 30, due to possibility of fatal lactic acidosis.
  • Other diabetic agents can be used
35
Q

How id dyslipidemia caused and managed in CKD?

A
  • Dyslipidaemia is thought to be caused by a range of contributing factors in CKD, including reduced lipoprotein lipase (LPL) activity, increased concentration of apo C-III (a specific inhibitor of LPL) in plasma, secondary hyperparathyroidism, insulin resistance.

*Dyslipidaemia increases the risk of cardiovascular disease.

Dyslipidaemia management
- Treat with statins, e.g. atorvastatin

36
Q

What occurs in CKD related hyperkalaemia? and what is the management?

A
  • potassium excretion via urine and faeces is maintained until oliguria (Stages 4-end stage).
  • without oliguria, potassium levels increase to life-threatening levels causing cardiac arrhythmias.
  • diagnosis vis blood test

Management:
- Cardiac monitor: Look for prolonged PR, wide QRS, tall peaked T waves, VT, VF
- Reduce potassium in diet
- Medications: Resonium (O or PR) which binds to K+ in the bowel and this it is excreted, Calcium (cell membrane stabliser), Insulin & glucose, Sodium bicarbonate (no ones sure how it works so is a last resort).
- in emergencies use insulin out of the bloodstream and into the cells. (we also need to give glucose so we don’t cause a hypo)
- this is temporary and the K+ will move back out but at this time risonium will be clearing it out.
- Dialysis

37
Q

What are some important points of pt education regarding CKD?

A
  • Diet,
  • Medications (to take, and to avoid),
  • Follow-up care
  • Daily BP measurement
  • Activity intolerance due to anaemia
  • Energy conservation
  • Discuss future treatment options (dialysis, kidney transplant)
  • Educate patient re medication excretion, and to monitor for signs of toxicity
38
Q

What are some early refferals you may complete for a pt with CKD?

A
  • Dietitian
  • Nephrologist / kidney nurse practitioner (?transplant)
  • Psychologist
  • Nurse Practitioners and Clinical Nurse Consultants: access, anaemia,
39
Q

What are the two forms of kidney replacement therapy?

A
  • dialysis
  • kidney transplant
40
Q

What is dialysis and what are the two types?

A

= Dialysis is the diffusion of solute molecules across a semipermeable membrane from an area of higher concentration to one of lower concentration.
= Dialysis is used to remove excess fluid and metabolic waste products in the patient with renal failure.
- commenced when the patient’s uraemia can no longer be controlled with conservative medical management, although there is a move to starting dialysis sooner, to conserve the kidney.

Two functions
1. filtering waste from the blood;
2. balancing the body’s fluid levels.

Types
- Heamo dialysis (outside body)
- peritoneal dialysis (inside body)

41
Q

Explain haemodialysis

A
  • A procedure in which blood passes by an artificial semipermeable membrane outside the body
  • May be intermittent dialysis or continuous renal replacement
  • Needs a permanent vascular access site
  • 3-4 times weekly in hospital or at home overnight.
  • need a finsula
42
Q

Explain peritoneal dialysis

A
  • Uses the peritoneum surrounding the abdominal cavity as the dialysing membrane
  • 2-3L dialysate fluid infused
  • Fluid must be changed 4-5 times per day
    Types
    1: Continuous Ambulatory Peritoneal Dialysis (CAPD)
    2: Automated Peritoneal Dialysis (APD)
43
Q

Explain a kidney transplant as a form of CKD management

A
  • only definitive treatment for end stage.
  • During a transplant the donated kidney is placed inside recipient’s pelvis and attached to their blood vessels and urinary tract. Their own kidneys are usually left in place.
  • After a successful
    transplant, the recipient no longer needs dialysis or special diets.
  • Immunosuppression required to avoid rejection, e.g. prednisolone, mycophenolate,
    cyclosporine
44
Q

What is the conservative treatment of CKD?

A
  • preserve function as long as possible
  • comfort and quality of life are prioritised

*they know this will not stop the degradation of the CKD

45
Q

What are some complications of CKD that may require urgent dialysis?

A
  • encephalopathy
  • neuropathies
  • uncontrolled hyperkalaemia
  • pericarditis
  • accelerated hypertension
46
Q

Explain the process of dialysis

A

= waste and excess water pass from the blood across a semi-permeable membrane, into the dialysis solution (dialysate) for removal from the body.
- A thin layer of natural tissue (in peritoneal dialysis) or of artificial (synthetic) membrane (in haemodialysis), known as the dialysis membrane, keeps the blood separate from the dialysis fluid. - Smaller molecules that pass freely through the semi-permeable membrane (e.g. urea, creatinine, potassium) are able to be removed from the blood via diffusion.
- Blood cells are too large to pass through the dialysis membrane, so remain in the blood.
- Wastes are then removed from the body by extracting the dialysis fluid.

47
Q

What are the three processes of dialysis and explain them

A
  1. diffusion
  2. osmosis
  3. ultrafiltration

Diffusion is the movement of solutes from an area of high concentration to an area of low solute concentration. Urea, creatinine, uric acid and electrolytes move by diffusion.

Osmosis is the movement of fluid from an area of low concentration to an area of high concentration of solutes.
- Glucose is usually added to the dialysate and creates an osmotic gradient across the membrane, pulling excess fluid from the blood.

Ultrafiltration uses the changes in pressure gradient to remove excess fluid.

48
Q

Explain peritoneal dialysis (PD)

A

= uses the peritoneum, a natural membrane lining the cavity of the abdomen
- The peritoneal membrane, a thin layer of natural tissue, separates the blood from the dialysate (this solution is usually glucose).
- membrane has tiny holes that waste products and fluid filter through from blood.
- need a minor procedure to insert peritoneal dialysis catheter. Sits with aprox 18cms of the catheter remain outside the body allowing for easy dialiate change.
- Bags of dialysis fluid (dialysate) are attached to the patient’s body with a small, soft plastic tube, called a PD catheter.

Phases:
Dwell phase (the time dialysate remains in the abdomen)
- excess water and waste products from the blood are drawn across the patient’s peritoneal membrane into the dialysate.
- Removal of waste (toxins) occurs via diffusion.
- The removal of excess water occurs via osmosis, is aided by another substance within the dialysis fluid (glucose).

While blood cells are too large to pass through the semi-permeable membrane, excess water is drawn into the dialysate by the glucose. The excess water and waste (filtrate) now in the dialysate needs to be changed in a process called an exchange.

  • renal physician will prescribe number of exchanges per day and the amount and type of dialysate to be used.
  • there are two types of PD.
49
Q

What are the two types of peritoneal dialysis?

A
  1. Continuous Ambulatory Peritoneal Dialysis (CAPD)
    - involves three-to-five exchanges per day.
  2. Automated peritoneal dialysis (APD)
    - Is performed by a machine, called a cycler, while the patient sleeps.

At renal units, patients are educated to perform CAPD or APD treatments safely, so they may continue their treatment at home, returning regularly to the renal unit for check-ups.
- Both types of PD allow the patient to be relatively independent and manage their own care at home.

50
Q

What are some risks of peritoneal dialysis?

A
  • Infection at catheter site
  • Heat loss (if not warmed)
  • Raised intra-abdominal pressures
  • Bowel perforation
  • Peritonitis
  • Loss of amino acids
51
Q

When may dialysis be indicated?

A
  • AKI
  • to remove drugs or toxins from the body
52
Q

Explain haemodialysis

A
  • completed with a dialisier machine outside the body via a fistula.
  • requires the creation of a permanent access point to pts blood stream. This can be via a fistula or a graft.
  • two needles are inserted into the access point. Plastic tubes attached to these needles connect them to a dialyser.
  • can be completed at home or in hospital
  • Shorter duration dialysis means fluids exchanged at higher speeds. Patient must be haemodynamically stable for rapid exchange.

Fistula: surgically link between artery and vein
Graft: surgically placed tube under the skin linking artery to vein.

53
Q

What are some nursing considerations when caring for a pt with a fistula?

A
  • never take a BP or venepuncture from the fistula arm.
54
Q

When may a kidney transplant be indicated?

A
  • end-stage kidney disease
55
Q

What are the positives and negatives of a kidney transplant?

A

Pros
- only definitive treatment fro pts with ESKD.
- improve quality of life.
- removes need for ongoing dietary restrictions and dialysis
- reverses many pathological changes associated with kidney disease.
- after the first year, kidney transplant is cheaper then dialysis

Challenges of a kidney transplant
- a lack of donated organs
- some patients are physically or mentally unsuitable for transplantation
- some patients do not want a transplant.
- require immuno suppression to avoid rejection.

56
Q

Explain paired organ donation

A

= a donor/recipient pair who are incompatible or a poor match with each other, find another donor/recipient pair with whom they can exchange kidneys. Thus a spouse (Person A) who wants to donate their kidney to their wife (Person B), for example, but is incompatible, is paired with another donor/recipient pair involving a son with ESKD (Person C) and his mother (Person D). In this example, person A would donate his kidney to Person C, and Person D would donate her kidney to Person B.

NUR3310 (9 decks)

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