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REN > Renal replacement therapy > Flashcards

Renal replacement therapy Flashcards

1
Q

What is renal replacement therapy

A

it is life-supporting treatment for renal failure

this can involve dialysis
transplanation

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2
Q

What is the function of the kidneys

A

Filtration & excretion
* Balances electrolytes
* Balances fluid
* Acid-base balance

BP regulation
Regulation of RBC production (EPO is produced here)
Vitamin D activation

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3
Q

When is RRT necessary?

A
  • Stage 5 CKD (requires long term life sustaining therapy)
  • Acute kidney injury (can potentially be revesed)
  • Failure to perfom filtration (can oead to life threatneing consequnces)

RRT is temporary life sustaining therapy for AKI)

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4
Q

What are the causes of needing emergency RRT

A
  • Hyperkalaemia
  • Severe pulmonary oedema
  • Severe acidosis
  • Severe uraemia (pericarditis, seizures)
  • Ingestion of poisons (ethylene glycol)

first three are due to resistant to treatment

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5
Q

What does RRT replace

A

Filtraion and excerition
- it can do regulate electorlytes in a safw way
- regulate fluid balance
- acid base balance

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6
Q

What can’t RRT replace

A
  • can’t replace BP regulations
  • regulates RBC (no EPO)
  • can’t activate vitamin D

transplanation will address all these things

only gets GFR to 15ml/min

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7
Q

RRT: Dialysis

What is dialyis>

A

Removing solutes in a liquid using a semi peremabele membranes

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8
Q

What are the two membranes that are used in dialysis

A
  1. Synthetic (Polysulfone)
  2. Biological (Peritoneum)

with syntehtic you can alter the size of pores, and do rapid clearance or slow

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9
Q

How do partclies move across a membrane

A
  1. Diffusion
  2. ultrafiltraion
  3. convection (solute drag, small solutes move acorss with fluid)
  4. osmosis
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10
Q

Haemodialysis

What is Haemodialysis?

A
  • Intermittent (so about 4 hours, 3x a week)
  • its outside the body (extracorporeal)
  • can be done in hospital or at home (some will do it home)
  • forces used are diffusion and ultrafiltraion)

blood removed, filtred,

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11
Q

Haemodialysis

Haemodialysis structure describe it

A

there’s a dialisier (has many fibrils, that increase surface area)
there is a fluid where a solutes can move into

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12
Q

Haemodialysis

Haemodialysis employs a countercurrent gradint

what does that mean

A

So, blood travels on one side of dialysis
membrane
Fluid travels on other side of
dialysis membrane

you can change membrane pore size, high flux dialysers have larger pores which have enhanced middle molecule clerance

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13
Q

Haemodialysis

What do we need practially do to Haemodialysis?

A

Patient
* Access to blood
* Dialyser
* Dialysis machine
* Ultra-pure water
* Dialysis nurse

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14
Q

Haemodialysis

In an acute setting, how do we get access to blood

A

Temporary dialysis catheter/Vascath

catheter needs to be wide of enough, need a large enough vein

need distance, so blod doesnt mix

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15
Q

In an chronic setting, how do we get access to blood

A

Dialysis
catheter/tunnelled line (tunnels under skin, to stop infection -> which may lead to sepsis)

Arterio-venous fistula/graft

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16
Q

What is the difference between AV fistula v AV graft

A

AV fistula: connection between artery and vein (so the vein enlarges, so you can put needles in, because the vein is now more stable)

AV graft: grafts can clot

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17
Q

What is meant by ultrapure water

A

it’s water that is free from

  • Chlorine
  • Heavy metals
  • XS Mg/Ca
  • Endotoxins
  • Bacteria
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18
Q

Peritoneal dialysis

What is Peritoneal dialysis

A
  • Continuous therapy
  • inside body (corporeal)
  • Semi-permeable membrane (in the Peritoneum)
  • usually done at home
  • uses diffusion, osmosis and convection
19
Q

Why are there limits when it comes to the peritoneal membrane

A

because membrane pores can be variable

20
Q

What happens in peritoneal dialysis

A
  • put fluid in allow it to dwell
  • solution comes out, conaims solutes that contrains excess, fluids, toxins, electorlytes etc
  • the fluid we use in (glucose starches)
  • we put in lacate to create a buffer

use excess glucose solution to get more water out
starches: used to keep water flowing in one direction, as glucose can equlibrate

21
Q

How do we regulate acid base in dialysis

A

as h+ freely moves into tissues, you need to add an ALKALI to patient from the dialysis solution

22
Q

Types of peritoneal dialysis

What are the types of peritoneal dialysis

A

Continuous Ambulatory PD
- involves manual exchnages (around 4x a day)
Automated PD
- this happens overnight, about 6-8 hours)

23
Q

What do we consider when offering PD

A
  • need to think about age, as fraility may mean the person is unable to do the dialysis (they may need someone to help them) -> need to think about vision and dexterity
  • Previous abdominal surgery/Stomas (hard to access peritoenial)
  • Polycystic kidneys

In the home
- need to think about water source being near the bedroom
- need to have regualr hand washing to prevent infections
- need to have somewhere to store the PD fluid

24
Q

HD

What are the problems with haemodialysis

A

Need to think about access
* Risk of clotting
* Central venous stenosis

Infection –more likley in lines over AVF
* Bacteraemia
* Endocarditis
* Osteomyelitis/discitis

  • Haemodynamic instability
  • Can cause fatigue
25
Q

What are the benefits of HD over PD

A

Short/ intermittent treatment time
It’s in a hospital
Defined fluid removal

26
Q

What are the benefits of PD

A

Continuous/daily treatment
Less chance of haemodynamic instability
it’s at home
can have a more “liberal diet” potentily
Offers flexiblity for holidays

27
Q

What are the disadvantges to HD

A

Access complications
Lifestyle disruption
Holidays
Stricter diet
Muscle cramps/Fatigue
Haemodynamic instability

28
Q

What are the disadvanatges of PD

A

Access Peritonitis risk
Peritoneal sclerosis
Membrane failure risk
storage of kit at home

29
Q

What are the problems with PD

A

PD tube dysfunction
* Constipation tube can be blocked
* Migration
* Occlusion e.g. fibrin

Infection
* Peritonitis abdominal pains
* Gram +ve > -ve bacteria

*Membrane failure
* Encapsulating Peritoneal Sclerosis (EPS)

  • Encapsulating Peritoneal Sclerosis (EPS): can end up with adhesions, can cause obsurtcion and nurtional difficulties
30
Q

problem with dialysis…

When you have haemodialysis what happens with CV risk

A

it increases due to
* Cardiac disease
* LVH due to hypertension, anaemia, fluid overload
* Calcification of arteries, lipid abnormalities

31
Q

problem with dialysis

What are the other risks/problems with dialysis in general

A

-infections can happen
-does not correct anaemia
-does not correct bone disease
-can lead to malnutrion

32
Q

Transplanation

Why is transplanation the treatment of chocie

A

mproved quality of life
* Improved survival
* Recovery of renal function(there’s now EPO and Vitamin D production)

33
Q

Where do kidney transplant go

A

typically in right or left illiac fossa
ureter will be in the bladder, blood supply put in aorta

34
Q

How are the donors for transplanation

A

Live Donor
* Deceased Donor (Cadaveric – brain/cardiac death) – “Waiting List

35
Q

Assessing the transplant opp

what does transplanation depend on

A

Age-related comorbidity: Frailty Scoring
* Cardiovascular risk
Immunosuppression risk (need to think about maligancies)
Surgical factors:
* BMI >30
* Vascular anatomy & intra-abdominal space (PKD)
* Immunological factors
- if they have certain antibodies hard to find a sutible match

36
Q

Complications of transplants

What are the early/medium term complications

A
  • CV morbidity/mortality (period of risk)
  • Infection (immunosupression load is higher)
  • Rejection (first years)
37
Q

Complications of transplantation

What are the long term complications of transplanation

A

Increased CVD risk
* Transplant-associated diabetes because of steriods
* Opportunistic infections / Viral reactivation
* Malignancy esp. non-melanoma skin cancer & virus associated e.g. PTLD
(EBV) -> can happen years later sometimes

38
Q

How are donor and recipeent matched

A

Need to look at

must ve matched acorss Species

  • Blood group antigens (ABO) – not always (possible to desensitize)
  • need to matched acorss blood type antigens

HLA antigens
* Class I A/B
* Class II DR
cannot have pregormed HLA antibodies that are directed by the donor HLA type, quickly can attack the donor kidney

basically more tightly matched,

39
Q

How do we match HLA antigens

A

do tissue typing (analysing HLA types)

40
Q

How do people get pre-existing anti HLA antibodies

A
  1. Pregnancy
  2. transfusion
  3. previous transplant
41
Q

*

Why do we immunosupress

A
  • to reduce the ablity of t cells to fight the kidney (reduce ablity to fight infectiosn and cancer though)
  • because 30-40% may still be rejected, but this can be treated

use a triple therapy
CNI (calcineurin inhibitors) e.g. Tacrolimus ( prescribed by BRAND NAME, OD/BD)
* Antiproliferative agents e.g. Mycophenolate (MMF), Azathioprine
* Corticosteroids – prednisolone

can also use Basiliximab – anti-CD25

42
Q

Explain transplant immunology

A
  1. APC presents non self anigen to t cell
  2. t cell recpetor trigger
  3. co stimulation from t cell
  4. this releases calcineurin
  5. which transcibes nculeus of IL-2
  6. IL-2 gets secreted, acts on cells
  7. sends signals for proliferation
  8. proliferate cells that recognise that non self antigen
  9. which will lead to rejection
43
Q

How do we stop the transplant immunology pathway

A
  1. Block calinurin being released by using Tac CyA
  2. steriods block transcription
  3. sirolimus blocks TOR pathway
  4. use antiproliferatiev agents
44
Q

What risks do we need to consider when doing immunosupression

A

Leaves you at risk of Infection like
* CMV
* Fungi/oral thrush
* Pneumocystis

High dose steroids
* GI protection  PPI
* Bone protection (becasue you get some bone thinning) -> so we need calcium supplementation

REN (6 decks)

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