Chronic Kidney Disease Flashcards

1
Q

What is adult polycystic kidney disease?

A
  • autosomal dominant - genetic

- mutuation in PKD 1 gene

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2
Q

What occurs in APCKD?

A

Cysts grow on the kidney and can grow in the liver as well

-get big kidneys

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3
Q

How is APCKD diagnosed?

A

USS

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4
Q

What is important about the cysts in APCKD?

A

they are fluid filled and can cause secondary complications like pain, bleeding into the cyst, infection and renal stones due to stasis (renal draingae impaired)

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5
Q

What is the most common symptom before full blown APCKD?

A

hypertension - must monitor blood pressure even before cysts develop

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6
Q

How can you manage APCKD?

A
  • treat hypertension (block the RAAS)
  • Diet (fluids, low salt)
  • Tolvaptan - stops reabsorption of water
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7
Q

How can you define CKD?

A

Irreversible and progressive loss of renal function over a period of months to years

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8
Q

What happens to the kidneys in CKD?

A

they are scarred due to tissue damage and tissue is gradually being replaced by ECM or fibrosis from mesangial cells regressing to mesangioblasts which secrete the ECM so the nephrons ability to filter blood is reduced - over time causes CKD

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9
Q

What is CKD associated with?

A

Increased morbidity and morality with cardiovascular diseases

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10
Q

What is the end result of fibrosis and scarring?

A

progressive loss of both excretory and hormone functions of the kidney

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11
Q

NOTE!!!

A

Protein in the urine is a high risk for progression to kidney failure, even is GFR is normal

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12
Q

Why is the incidence of CKD difficult to define?

A

CKD is often asymptomatic

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13
Q

Who is most susceptible to CKD?

A
  • elderly
  • ethnic minorities
  • co-morbidities
  • social deprivation
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14
Q

What would you see in a diseased kidney/H and E stain?

A
  • Scarring, loss of cortex (functioning nephrons)

- fibrotic material, sclerosed glomeruli

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15
Q

What causes CKD?

A
  • diabetes (most common)
  • hypertension
  • glomerularnephritis
  • APCKD
  • infections (HIV)
  • medications (NSAIDS)
  • systemic diseases (Lupus / RA)
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16
Q

What are the risk factors of CKD?

A
  • AKI - includes nephrotoxic injuries and decreased perfusion
  • proteinuria
  • hyperlipidaemia
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17
Q

How would you investigate CKD?

A

-Blood pressure and urine dipstick (assuming they are still able to pass urine and not in ESRD)

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18
Q

What blood tests would you do to diagnose CKD?

A
  • U + E’s
  • LFT (albumin)
  • FBC
  • CRP
  • bone biochemistry
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19
Q

What other investigations would you do?

A
  • kidney scan
  • biopsy
  • renal tumour/stenosis may want to do a scan or angiogram
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20
Q

What does high creatinine levels in blood mean?

A

Poor kidney function - creatinine should be cleared by the kidneys

21
Q

How can CKD be prevented/delyayed progression?

A

Modifiable risk factors e.g. lifestyle, smoking, obesity, lack of exercise, controlled diabetes, correcting hypertension

22
Q

What drug should people with proteinuria be on?

A

ACE inhibitors

23
Q

What is the normal function of the kidney?

A
  • BP regulation
  • Blood volume of regulation
  • pH regulation
  • electrolyte regulation
  • excretion of waste products
  • drug metabolism
  • endocrine function (renin, EPO)
24
Q

Why might a patient with CKD have hyperkalaemia and what should you advise them?

A
  • less potassium is excreted and more builds up in the blood - cardia arrythmias
  • need to stop ACE inhibitor and other drugs that can affect heart failure/kidney etc
  • altering diet to avoid foods with high potassium
25
Q

Why do patients with CKD have anaemia?

A
  • decreased EPO production
  • Blood loss due to clotting problems as CKD gets worse (urea in blood makes platelets less likely to stick to each other)
  • high hepcidin levels stop absorption and utilising oral iron and iron from the liver - can’t access it to make Hb
26
Q

Why is treating anaemia important?

A

Impoving Hb

  • imporves exercise capacity
  • helps regulate LV hypertrophy
  • make patient feel better
27
Q

How do you treat anaemia?

A
  • Check iron stones first
  • If iron low then IV or oral iron
  • Check Hb
  • If Hb low after iron the give EPO
28
Q

What level of Hb are you aiming for?

A

100-110g/L

29
Q

What is the effect on bone of CKD? mineral bone disease

A
  • As kidney function gets worse, stop excreting phosphate, plasma phosphate increases stimulating PT gland glands which excrete more phosphate
  • calcidol helps absorb calcium but less calcidol = hypocalcaemia which also stimulate PT gland to produce phosphate
30
Q

What is the significance of increased PTH release?

A

increase amount of calcidol and how much Ca2+ is reabsorbed

31
Q

Why do bones get thin in CKD?

A

Bone resoprtion due to increased PTH which increases osteoclastic activity

32
Q

How do you treat CKD-BMD?

A

reduce phosphate intake

  • not allowed much fluid or phosphate food
  • may have to give phosphate binders to prevent malnourishment
  • Vit D and 1aCalcidol
33
Q

What are the effects of accumulation of waste products?

A

-contributes to uraemic symptoms e.g. reduced appetite, nausea, itching

34
Q

What is ESRD?

A

When death is likely without renal replacement therapy - eGFR less than 15mls/min

35
Q

What are symptoms of CKD?

A
  • tiredness
  • breathlessness
  • restless legs
  • aches and pains
  • nausea and vomiting - due to urea in the blood
  • itching
  • chest pain
36
Q

What are the symptoms or ESRD?

A
  • Overwhelming fatgiued
  • difficulty sleeping
  • difficulty concentrating
  • sexual dysfunction and
  • reduced fertility
  • increased infections
  • signs and symptoms of volume overload e.g. SoB, oedema
37
Q

When would you give dialysis?

A

GFR less than 10ml.min

38
Q

What is the best treatment for ESRD?

A

transplant - increases quality of life

39
Q

What is + and - of unit-based haemodialysis?

A
  • 4 hrs 3 x a week
  • travel time
  • dialysis times you are tied to
  • big restriction on fluid/food intake
    + less responsibility
    +days off
40
Q

What is + and - of home haemodialysis?

A
\+ allows more dialysis hours
\+ better large molecule clearance
\+patients often feel better
\+fewer medications required
-need someone at home
41
Q

How does peritoneum dialysis works?

A

uses peritoneum as dialysis machine - put fluid there (glucose solution) and it equilibrates to suck in all the waste products including potassium
- either do it only at night or you can do it thourghout the day changing 4/5 times

42
Q

What is + and - of peritoneum dialysis?

A

+ more independence
+ less food and fluid restrictions
+ Fairly easy to travel with
+ Renal function may be better preserved initially
- responsibility
- frequent changes of fluid in peritoneum

43
Q

What is + and - of transplant?

A
\+better quality of life
\+ increased sexual function
\+ better if younger
\+freedom from dialysis
- peri-operative risk
-malignancy risk
-risk of rejection
44
Q

What is the staging of CKD?

A

As GFR decreases, the stage of CKD increases from 1-5

- There is also an ‘a’ rating to indicate the level or proteinuria

45
Q

What happens as proteinuria increases?

A

there is a higher risk of complications and progression of the disease

46
Q

How does hypertension cause CKD?

A
  • the walls of arteries supplying the kidney start to thicken to withstand the pressure causing a narrow lumen
  • less blood and oxygen therefore gets to the kidney
  • results in ischaemic injury to glomerulus
47
Q

How does diabetes cause CKD?

A
  • excess glucose in the blood starts sticking to proteins (non-enzymatic glycation)
  • particularly affects efferent arterioles causing them to stiffen and narrow
  • creates obstruction so blood cant leave glomerulus
  • increases pressure in glomerulus causing hyperfiltration
  • more ECM is laid down in response causing CKD over time
48
Q

What is the effect of failing kidneys on renin release?

A

When kidneys start sensing a lower than normal amount of fluid being filtered, they release renin to increase BP so in CKD, falling GFR leads to more renin release causing increased blood pressure (hypertension)
-remember, hypertension is a cause of kidney disease itself