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ESA 3 - Urinary System > CKD > Flashcards

CKD Flashcards

1
Q

What is adult polycystic kidney disease?

A
  • An autosomal dominant condition that occurs in roughly 1 in 1000 births.
  • The mutation occurs in either the PKD 1 gene (85%) or PKD 2 gene.
  • Cysts grow with age and generally present in aduithood.
  • Prognosis depends in rate of increase in kidney size and age.
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2
Q

How do you diagnose APCKD?

A
  • Ultrasound - can’t exclude if under 30.
  • Genetic testing isn’t wide spread - only donw in specfic senarios e.g. if donating a kidney.
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3
Q

What secondary complications can occur because of APCKD?

A
  • Pain
  • Bleeding into cyst
  • Infection
  • Renal stone
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4
Q

What other diseases occur alongside APCKD?

A
  • Hypertension (very common)
  • Aneurysms
  • Heart valve abnormalities
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5
Q

How do you manage APCKD?

A
  • Treat hypertension - block RAAS
  • Diet
    • Lots of fluids
    • Low salt
    • Normal but not excessive protein
  • Tolvaptan - block ADH
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6
Q

What is normal GFR?

A

90-120ml/min

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7
Q

Define CKD

A

The irreversible and sometimes progressive loss of renal function over a period of months to years.

Renal injury causes renal tissue to be replaced by extracellular matrix in response to tissue damage.

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8
Q

Why does CKD matter?

A

In some patients CDX inexorably worsens with progressive loss of renal function.

It is also accociated with substntial crdiovascular morbidity and mortality even with mild CKD.

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9
Q

How do you stage CKD?

A

Look at GFR and at the amount of protein in urine.

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10
Q

In who is CKD more common?

A
  • Elderly
  • Ethnic minorities
  • Multi-morbid
  • Social deprivation
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11
Q

What are the causes of end stage renal disease?

A
  • Diabetes (common)
  • Hypertension (common)
  • Immunilogical - Glomerulonephritis
  • Infection - Pyelonephritis
  • Genetic - APCKD / Alports
  • Obstruction and reflux nephropathy (OU)
  • ATN
  • Vascular
  • Systemic disease - myeloma
  • Unknown
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12
Q

How do you investigate CKD?

A
  • Define degree of renal impairment
  • Define cause of renal impariment
  • Provide patient with diagnosis and porgnosis
  • Identify complications of CKD
  • Plan long term treatment (delay long term progression and plan for dialysis and transplantation)
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13
Q

What do we need to measure in CKD?

A
  • BP
  • Urine Dipstick
  • Creatinine
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14
Q

In who is eGFR accurate and when is a corretion needed?

A
  • Only accurate in adults
  • Correction of blacks (not asians)
  • Not useful in AKI
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15
Q

What general blood tested need to be done when assessing CKD?

A
  • U&E
  • Bone biochemistry
  • LFTs (Albumin)
  • FBC
  • CRP
  • Iron (ferritin, iron, reticulocyte, haemoglobin)
  • PTH
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16
Q

What specific blood tests can be done to determine the cause of CKD?

A

If there is clinical suspision of the following:

  • Auto-antibody screen (autoimune diseases)
  • Complement levels (autoimmune diseases)
  • Anti-neutrophil cytoplasmic antibody - ANCA (vasculitis)
  • Serumimmunoglobulin screen (myeloma)
  • Protein electrophoresis and serum free light chain measurement (myeloma)
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17
Q

What other investigations can be done when investigating CKD?

A
  • USS
    • Kidney size,
    • Obstruction (hydronephrosis).
  • Kidney biopsy
    • Unknown,
    • Haematuria,
    • Proteinuria.
  • Other:
    • CT,
    • MRI,
    • MR angiogram.
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18
Q

How do you prevent / slow progression of CKD?

A
  • Modifiable risk factors:
    • Lifestyle
    • Smoking
    • Obesity
    • Lack of exercise
  • Uncontrolled diabetes
  • Hypertension
  • Proteinuria (ACE-inhibitors, ARBs)
  • Lipids (Statin)
19
Q

What does the kidney do?

A
  • Regulation of:
    • BP
    • Blood volume
    • pH
    • Electrolytes
    • Osmolality
  • Excretion of waste products
  • Metabolism of drugs
  • Endocrine - 1-alpha cacidol, renin, erythropoitin
20
Q

Ho do you control water and salt?

A
  • Anti-hypertensive
  • Diuretics
  • Fluid restrict

80-85% od CKD patients are hypertensive

21
Q

What is the effect of CKD on water / salt handling by kidney?

A

Reduced GFR

Loose ability to maximally dilute and concentrate urine - much lower range.

Small glomerular filtrate but same solute load causes osmotic diuresis (reduces maximum concentraing ability and response to ADH) .. nocturia.

Low volume of filtrate reduced maximum ability to excrete urine therefore maximum urine volume is much smaller.

22
Q

When during CKD could hyperkalaemia occur?

A

Can occur once eGFR < 20 mls/min

Less likely when good urine output is maintained.

23
Q

How do you treat hyperkalaemia?

A
  • Stop ACE-inhibitor / ARB
  • Avoidance of other drugs that can increase K+ (amiloride, spironolactone, trimethoprim)
  • Altering diet to avoid foods with high potassium (e.g. McDonalds or bananas)
24
Q

What are the symptoms of acidosis?

A
  • Central
    • Headache
    • Sleepiness
    • Confusion
    • Loss of consciousness
    • Coma
  • Muscular
    • Seizures
    • Weakeness
  • Intestinal
    • Diarrhoea
  • Resporatory
    • Shortness of breath
    • Coughing
  • Heart
    • Arrhythmia
    • Increased heart arte
  • Gastric
    • Nausea
    • Vomitting

Treat with oral NaHCO3 tablets.

25
Q

What are the causes of anaemia in CKD?

A
  • Decreased EPO
  • Absolute Fe deficiency
  • Blood loss
  • Short RBC life span
  • Co-morbidities
  • Bone marriw suppression
  • CKD mineral and bone disorder
  • Meds
  • B12 and folate deficiency
26
Q

Why is treating anaemia important?

A
  • Improves exercise capacity
  • Improves cognitive function
  • Help regulate LVH
  • Slows progression of renal disease
  • Reduces mortality
  • Makes patients feel better
27
Q

How do you treat anaemia in CKD?

A

Check iron stores first

If Fe low, replace Fe first

When iron supplies okay, re-check Hb

If Hb still low, start EPO stimulating agent.

28
Q

What is mineral bone disease?

A

The kidney normally convert vitamin D into its active form (calcitriol) but, when its not working, the kidney cant do this.

This means there is less calcitriol so, vitamin D cannot be absorbed as well from the gut (it needs calcitriol to do this).

It also means that phosphorus is not properly removed from the blood so, there are high levels of phosphorus.

These high levels of phosphorus combine with calcium and create bone calcifications in joins and arteries and the skin.

Also, in response to disregulated Ca and phosphate, PTH is released in higher quantities from the parathryoid glands. This takes Ca from the bones (by increasing osteoclast activity) to increase the levels in the blood so the bones are even worse off.

29
Q

How do you manage CKD-BMD?

A
  • Reduce phosphate intake
  • Phosphate binders -many contain Ca (can’t give too much)
  • 1-a-calcidol
  • Vitamin D
30
Q

How does drug metabolism change?

A

Alter dose due to reduced metabolism and / or elimination

Drug sensitivity can increase even if elimination unimparied meaningside effects are more liekly e.g. statins

31
Q

What effect does the accumulation of waste product have?

A
  • Contribute to uraemic symptoms
  • Reduced appetite
  • Nausea and vomiting
  • Pruritis
32
Q

Define ESRD

A

When death is likely without renal replacement therapy.

eGFR < 15ml/min

33
Q

When is renal replacement therapy required?

A
  • Required when native renal function declines to a level no longer adequate to support health.
  • Usually when eGFR 8-10ml/min (normally about 100)
34
Q

What are the symptoms of ESRD?

A
  • Tiredness - overwhelming fatigue, physically and mentally incapacitated, feeling of guilt and ineptitude at needing rest.
  • Difficulty sleeping
  • Difficulty concentrating
  • Volume overload (SoB, oedema)
  • Nausea and vomitting / reduced appetite
  • Restless leg /cramps
  • Pruritus
  • Sexual dysfunction / reduced fertility
  • Increased infections (reduced cellular and humeral immunity)
35
Q

What are the options when kidneys fail?

A
  • Haemodialysis
  • Peritoneal dialysis
  • Conservative care
  • Transplant
36
Q

What is haemodialysis? What are the pros and cons?

A

4 hours, 3 times per week

Night time

Designated slot

Good:

  • Less responsability
  • Days off

Bad:

  • Travel time / waiting
  • ‘tied’ to dialysis times
  • Big restriction on fluid / food intake.
37
Q

What are the contraindication of HD?

A
  • Failed vascular access
  • Heart failure
  • Coagulopathy
38
Q

What are the complications of HD?

A
  • Lines: infection, thrombosis, venous stenosis
  • AVF: thrombosis, bleeding, access failure, steal syndrome
  • CVS instability
  • Feel chronically unwell
  • Accululate morbidity (CVS, bone ect.)
39
Q

How is home or nocturnal HD different?

A
  • More hours dialysis
  • Better large molecules clearance
  • Patients often feel better
  • Patients often need fewer medications (BP meds, phosphate, binders ect)
  • Home HD requires someone at home with you
40
Q

What is peritoneal dialysis?

A

2 options:

  • CAPD: 4-5 bags throught the day, 30min exchange)
  • APD: overnight dialysis

You are responsible for your care.

41
Q

What are the advantages and disadvantages of PD?

A

Good:

  • Self-sufficient
  • Generally less fluid / food restrictions
  • Family easy to travel with CAPD
  • Renal function many be better preserved initially

Disadvantage:

  • Frequennt daily exchanges or overngiht
  • Responsability
42
Q

What are the contra-indications of CAPD?

A

Contra-indications:

  • Failure of peritoneal membrane
  • Adhesions, previous abdo surgery, hernia, stoma
  • Patient (or carwe) unable to connect / disconnect
  • Obese or large muscle mass (relative CI)
43
Q

What are the complications of CAPD?

A
  • Peritonitis, exit or tunnel site infections
  • Ultrafiltration failure
  • Leaks (scrotal, diaphragmatic)
  • Development of herniae
44
Q

What are the pros and cons of transplant?

A
  • Reduced mortality and morbidity compared to dialysis
  • Between quality of life
  • Peri-operative risk
  • Malignancy risk
  • Infection risk
  • Risk of diabetes, hypertention for meds

ESA 3 - Urinary System (20 decks)

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