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NUR3310 > CKD > Flashcards

CKD Flashcards

1
Q

Outline AKI (Acute kidney injury)

A

a sudden, severe impairment of renal function causing a build-up of toxins in the blood

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2
Q

Define pre-renal causes of AKI

A

factors external to the kidneys that reduce renal blood flow and lead to decreased glomerular perfusion and filtration
Eg. hypovalaemia, decreased cardiac output, decreased renovascular blood flow

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3
Q

Define intra-renal causes of AKI

A

conditions that result in direct damage to the renal tissues, causing impairment to nephron function
eg. acute tubular necrosis, renal ischaemia, nephrotoxic injury, contrast, trauma

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4
Q

Define post-renal causes of AKI

A

Mechanical obstruction of urinary outflow. As the flow is obstructed, urine refluxes into the renal pelvis, impairing renal function
eg. renal calculi, renal or bladder tumours, strictures of the urethra, direct trauma

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5
Q

Outline CKD

A

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, decreasing endocrine functionality

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6
Q

What systematic diseases can lead to CKD developing?

A

diabetes, glomerulonephritis, HTN,
cardiovascular disease, UTI,
hereditary defects of the kidneys, complication of renal diseases

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7
Q

How many stages of CKD are there?

A

1, 2, 3(a+b), 4, 5

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8
Q

Outline CKD stage 1

A

Kidney damage with normal or increased GFR, GFR rate of >90, symptoms minimal/none

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9
Q

Outline CKD stage 2

A

Kidney damage with mildly decreased GFR, GFR rate of 60-89

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10
Q

Outline CKD stage 3a

A

Moderately decreased GFR, GFR rate of 45-59

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11
Q

Outline CKD stage 3b

A

Moderate to severe decreased GFR, GFR rate of 30-45, aggressive treatment needed

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12
Q

Outline CKD stage 4

A

Severely decreased GFR, GFR rate of 15-29, preparation for renal replacement therapy required

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13
Q

Outline CKD stage 5

A

Kidney failure (End-stage kidney disease), GFR rate of <15, kidneys can no longer remove metabolic waste, renal replacement therapy required to sustain life

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14
Q

How much GFR can be lost before CKD symptoms present?

A

up to 80% of GFR can be lost with few obvious signs and symptoms, Symptomatic changes do not usually become apparent until renal function declines to less than 25%

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15
Q

Define nephron hypertrophy

A

As nephrons are lost, the remaining nephrons hypertrophy (enlarge) to compensate

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16
Q

Outline how kidney function decline can be represented by urination

A

At stage 1, pt may have polyuria (urination increase) as kidneys lose the ability to concentrate urine
As disease progresses, urine output reduces to oliguria (<30ml urine/hr) and anuria (,100ml urine/24hrs)

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17
Q

How does a reduction in urine output (oliguria/anuria) affect kidney function?

A

azotaemia (retention of nitrogenous waste) becomes evident, identified by increased serum urea levels, increased creatinine levels, and other symptoms

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18
Q

Outline how creatinine is related to CKD

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 (failure of urinary excretion)

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19
Q

Outline how urea is related to CKD

A

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

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20
Q

How does Urea’s relationship to CKD affect other systems?

A

Cardiac - Uraemic toxins cause inflammation, may lead to pericarditis (heart lining inflammation)
Neurological – uraemic toxins produce encephalopathy. can lead to confusion, impaired cognition, and in severe cases seizures/coma
Endocrine – insulin resistance. The ability of the kidney to degrade insulin is reduced. Leads to low BGLs
Digestive - Elevated levels of urea / uraemic toxins are attacked by bacteria in the GIT, releasing ammonia. can lead to uraemic fector (bad breath), nausea, vomiting, diarrhoea, malnutrition
Haematological - Uraemic toxins decrease red blood cell life span. leads to anaemia, lethargy, low haematocrit

21
Q

Outline how sodium & water are related to mod-severe CKD

A

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.
Cardio - increased workload due to reduced circulating volume, leading to hypotension and tachycardia

22
Q

Outline how sodium & water are related to severe-ESC CKD

A

kidneys unable to regulate sodium and water balance. Both sodium and water retained
Cardio - fluid overload, leading to HTN and cardiomyopathy (reduced pump ability)
Resp - fluid overload, congestive heart failure, leading to dyspnoea
skin - oedema

23
Q

Outline how protein is related to CKD

A

Proteins do not usually pass through the fenestrations in the glomerulus.
Damaged nephrons allow protein to pass, resulting in protein in the urine (proteinuria)
Levels of serum protein reduce, with loss of muscle mass. Reduced muscle mass reduces metabolism

24
Q

Outline how potassium is related to CKD

A

Potassium excretion via urine and faeces is maintained until oliguria. With oliguria, potassium levels increase to life-threatening levels
cardio - Cardiac arrhythmias, widened QRS and peaked T wave on ECG

25
Q

Outline how bicarbonate is related to CKD

A

When GFR decreased to 20-25%, decreased bicarbonate reabsorption in tubules, and decreased hydrogen ion elimination.
metabolic acidosis - leading to kussmaul resps (hyperventilation)

26
Q

outline how calcium is related to CKD

A

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), causing CKD-MBD
cardio - Calcium deposits reduce vascular elasticity and cause vascular calcification = vascular disease. Increased risk of heart disease
Endocrine - Hyperparathyroidism decreases insulin sensitivity and impairs glucose tolerance, leading to high BGLs
Calcium phosphate deposits and hyperparathyroidism associated with skin irritation inflammation, pruritus, and excoriation

27
Q

Outline how phosphate is related to CKD

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
Cardio- can cause cardiovascular calcification, increased risk of stroke, disruption of conduction system, and cardiac arrest
mus/ske - CKD-MBD
Phosphate binds with calcium forming calcifications, leading to non-specific symptoms such as pain and stiffness in joints

28
Q

Outline how Vitamin D is related to CKD

A

Vitamin D must be ‘activated’ (hydroxylation) in the kidneys before it can function to help absorb calcium and phosphate
In CKD, Vitamin D is not activated, and therefore calcium & phosphate are not absorbed at usual levels- increased risk of fractures

29
Q

Outline how RBCs are related to CKD

A

Kidneys responsible for production of erythropoietin – as kidneys fail, erythropoietin production decreases, decreasing red blood cell production
Cardio - Declining RBC production causes anaemia, thereby increasing cardiac workload. Defective platelet aggregation increase risk of bleeding, leading to cardiomyopathy due to anaemia (and fluid overload), GI bleeding, haemorrhage
Haem - ureamic toxins decrease RBC lifespan, leading to anaemia, lethargy, low haematocrit
Skin - anaemia causes pale skin

30
Q

Outline how magnesium is related to CKD

A

As the kidney is the major regulator of serum magnesium; accumulation may occur with progressive renal impairment leading to hypermagnesaemia, leading to vomiting, lethargy, muscle weakness, hypotension, arrhythmias

31
Q

Define CKD-MBD (Mineral Bone Disorder)

A

Alterations in the metabolism of calcium, phosphate and vitamin D are part of an inter‐related cascade that causes bone loss and joint destruction. Of significant clinical consideration is the impact of CKD‐MBD on vascular calcification which substantially contributes to mortality

32
Q

define bone remodelling

A

Bone mass is recycled by adding or removing bone cells from the skeleton on a daily basis. Each week 5 to 7% of bone mass is recycled.
Bone is deposited by osteoblasts and reabsorbed by osteoclasts

33
Q

Outline the three types of renal bone disease

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
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

34
Q

What are the 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

35
Q

What are some airway related signs and symptoms of CKD?

A

SOB, Kussmaul respirations, pulmonary oedema, pleural effusion

36
Q

What are some circulatory related signs and symptoms of CKD?

A

polyuria, oliguria/anuria, HTN, cardiac arrythmias, cardiomyopathy & heart failure, anaemia

37
Q

What are some disability related signs and symptoms of CKD?

A

confusion/altered cognition, muscle/tissue wasting, neuromuscular twitching/cramps, weight loss, infection, increased risk of fractures, itchy skin

38
Q

What are some diagnostics that can be performed to assess for CKD?

A

> Urine screen for protein- proteinuria is a common indicator. Persistent proteinurina should be investigated by pathology to determine serum urea, creatine and creatinine levels
GFR levels indicate kidney function and determine the stage of kidney disease
kidney ultrasound to identify size of kidneys and for obstructions
Biopsy for renal bone disease

39
Q

What are some principles for CKD management?

A

treatment of HTN, anaemia, hyperglycaemia, and detection of proteinuria
?Control HTN, aim for <130/80
>encourage weight loss, administration of > >erythropoietin to treat anaemia, improve diet
>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)

40
Q

What are the traditional functions of the kidney?

A

Fluid and electrolyte balance
Removal of waste (creatinine & urea)
Acid base balance
Erythropoietin (EPO)
Renin production
Activation of Vitamin D

41
Q

outline fluid balance management of CKD

A

dehydration is common in early CKD (inability to concentrate urine), and fluid overload common in later CKD (oedema)
In later stages, restrict fluid intake and record output

42
Q

Define Dialysis as a renal replacement therapy

A

a method of removing waste products and excess fluid from a patient’s body after the kidneys have failed. Dialysis is an artificial process that performs the two main functions of the kidneys:
>filtering waste from the blood; and
>balancing the body’s fluid levels

43
Q

When would dialysis be considered?

A

Typically commenced when the patient’s uraemia can no longer be controlled with conservative medical management, though it can be commenced sooner, to conserve the kidney
Severe complications of CKD may also require urgent dialysis

44
Q

Define what happens in 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. Wastes are then removed from the body by removing the dialysis solution
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

45
Q

What are the two types of dialysis?

A

peritoneal dialysis and haemodialysis

46
Q

Define Peritoneal dialysis

A

Uses the peritoneum, a natural membrane lining the cavity of the abdomen . A catheter is inserted into the abdomen in a minor procedure. Some of the catheter remains outside the body. Bags of dialysis fluid (dialysate) are attached to the patient’s body with a small, soft plastic tube, called a PD catheter
During the dwell phase (the time dialysate remains in the abdomen) excess water and waste products from the blood are drawn into the dialysate. Removal of waste (toxins) occurs via a process called diffusion. The removal of excess water occurs via osmosis. Changeover of the dialysate is called an exchange

47
Q

Define Haemodialysis

A

a machine-assisted blood filtration method which removes waste and excess fluid from the blood in a dialyser (or artificial kidney) outside the body
There are two types of permanent access – a fistula (surgical linking of an artery to a vein) and a graft (tube surgically placed under the skin linking an artery to a vein)
During treatment two needles are inserted into the access point. Plastic tubes attached to these needles connect them to a dialyser
The blood is drawn from the body via one needle and pumped through the dialyser. An artificial membrane separates the blood from the dialysis fluid but allows waste and excess water to diffuse through from the blood.
The clean blood is then returned to the body via the second needle or tube and the needles are removed at the end of each session

48
Q

Outline a kidney transplant

A

The only definitive treatment for patients with ESKD
Can reverse many of the pathophysiological changes associated with kidney disease

NUR3310 (9 decks)

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