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Met3b > Dialysis and transplantation > Flashcards

Dialysis and transplantation Flashcards

1
Q

Describe how haemodialysis works.

A
  • during dialysis, blood is exposed to dialyse (mixture which passes through the membrane in dialysis) across a semi-permeable membrane
  • small molecules such as urea and creatinine and electrolytes pass through pores in a partially permeable membrane
  • large molecules such as albumin, IgG and blood cells do not pass through
  • concentration differences across the membrane allow molecules to diffuse down a gradient → allows waste products to be removed and desirable molecules or ions to be replaced
  • water can be driven through the membrane by a hydrostatic force
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2
Q

Describe how peritoneal dialysis works.

A
  • semi-permeable dialysis membrane of the peritoneum comprises the capillary endothelium, supporting matrix and peritoneal mesothelium
  • fluid and solutes move between the fluid-filled peritoneum and blood via the ‘three-pore model’
  • large pores (20-40 nm): allow macromolecules to be filtered between compartments (via venular or lymphatic absorption)
  • small pores (4-6 nm): responsible for the transport of small solutes (Na+, K+, urea, creatinine)
  • ultra small pores (<0.8 nm): transport water alone
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3
Q

What are the different types of haemodialysis?

A
  1. Short daily haemodialysis
  2. In-hospital nocturnal haemodialysis
  3. Nocturnal home haemodialysis
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4
Q

Describe short daily haemodialysis and its benefits.

A
  • 6-7 days/week
  • 1.5-3 hours/session
  • benefits:
    (i) improved BP control
    (ii) reduced LV mass
    (iii) variable reports of quality of life
    (iv) reduced phosphate
    (v) reduced mortality
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5
Q

Describe in-hospital nocturnal haemodialysis and its benefits.

A
  • 3 nights/week
  • 8 hours/session
  • benefits:
    (i) reduced mortality
    (ii) reduced hospitalisation
    (iii) reduced ESA (EPO stimulating agents) requirements
    (iv) reduced intradialytic hypotension
    (v) reduced phosphate
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6
Q

Describe nocturnal home haemodialysis and its benefits.

A
  • 5-6 nights/week
  • 6-8 hours/session
  • benefits:
    (i) improved BP control
    (ii) reduced ESA requirements
    (iii) reduced LV mass
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7
Q

What are the different types of peritoneal dialysis?

A
  1. Continuous ambulatory PD (CAPD)
  2. Automated PD (APD)
  3. Tidal PD
  4. Assisted APD
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8
Q

Describe continuous ambulatory PD and its benefits.

A
  • consists of 3-5 exchanges, with dwell times of 4-10h over 24h
  • usually performed by the patients connecting and disconnecting the PD catheter to dialyse bags
  • at night-time exchange can be performed with a machine
  • benefits:
    (i) simplicity
    (ii) ease of training
    (iii) flexibility → timing of exchanges can be adjusted for convenience (dwells ,3h are discouraged)
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9
Q

Describe automated PD.

A
  • uses a machine at night whilst the patient is asleep
  • machine is usually programmed to perform at least 4 exchanges over 8h
  • machine is programmed to leave the patient ‘dry’ for the daytime
  • machine can also perform a ‘last fill’ leaving PD fluid in the peritoneum → patients may then perform a further exchange during the day
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10
Q

Describe tidal PD.

A
  • machine is programmed to only partially drain out PD fluid at the end of any dwell during the nightly cycles
  • efficiency of dialysis is reduced → useful for patients whose sleep is disturbed through discomfort experienced when ‘dry’
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11
Q

Describe assisted PD.

A
  • poor strength, limited dexterity, decreased vision, or cognitive impairment may mean that some patients are unable to perform PD
  • family member or trained HCA can assist with lifting bags of dialysis fluid and the connection/disconnection of APD
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12
Q

What are the potential complications of haemodialysis?

A
  1. Access-related:
    - local infection
    - endocarditis
    - osteomyelitis
    - creation of stenosis
    - thrombosis or aneurysm
  2. Hypotension (common), cardiac arrhythmias, embolism
  3. N+V, headaches, cramps
  4. Fever: infection central lines
  5. Dialyser reactions: anaphylactic reaction to sterilising agents
  6. Heparin-induced thrombocytopenia, haemolysis
  7. Disequilibration syndrome:
    - restlessness
    - headache
    - tremors
    - fits and coma
  8. Depression
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13
Q

What are the potential complications of peritoneal dialysis?

A
  1. Peritonitis, sclerosing peritonitis
  2. Catheter problems:
    - infection
    - blockage
    - kinking
    - leaks or slow drainage
  3. Constipation, fluid retention, hyperglycaemia, weight gain
  4. Hernias (incisional, inguinal, umbilical)
  5. Back pain
  6. Malnutrition
  7. Depression
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14
Q

What are the absolute and relative contraindications for peritoneal dialysis?

A
  1. Absolute:
    - patients, or carer, unable to train adequately in the technique
    - inguinal, umbilical, or diaphragmatic hernia (esp pleuroperitoneal leak)
    - ileostomy or colostomy
    - abdominal wall infections or intra-abdominal sepsis, e.g. acute diverticular disease
  2. Relative:
    - abdo surgeries (adhesions_ - the more extensive the surgery, the more likely PD will be unsuccessful
    - morbidly obese (inadequate clearance)
    - high polycystic kidneys (insufficient peritoneal space)
    - severe gastroparesis (worsening vomiting)
    - severe lung disease (diaphragmatic splinting)
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15
Q

What is the optimal form of vascular access for dialysis?

A

AV fistula

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16
Q

Describe how AV fistulas are formed.

A
  • require anastomosis of an artery and a vein (under LA or GA)
  • either at the wrist (radiocephalic) or elbow (brachiocephalic, brachiobasilic)
  • vascular mapping with USS may be required
  • maturation for 6-8 weeks minimum prior to needling
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17
Q

Why might a temporary dialysis catheter be required? What are the possible routes?

A
  • Required: for immediate use, for example int he Aki or unresolved sepsis
  • Possible routes: internal jugular, subclavian and femoral
  • ideally leave in situ for ≤2 weeks (femoral <5 days)
18
Q

Where are tunnelled dialysis catheters usually formed?

A

In a central vein → IJV or subclavian

- using femoral vein is less common

19
Q

What are the different types of transplant?

A
  1. Live donor:
    - treatment of choice in ESRD
    - better graft functional and patient survival
  2. Donated after brain death
  3. Donated after cardiac death
20
Q

What are the roles of Class I and II HLAs?

A
  1. Class I:
    - present non-self peptides to cytotoxic CD8+ T cells, leading to their activation
  2. Class II:
    - present peptides to CD4+ T cells, leading to their clonal expansion
    - activated CD4+ cells release cytokines that activate CD8+ cells
21
Q

How are transplanted HLAs recognised by the recipient?

A
  1. Direct:
    - donor APCs present foreign peptides to cytotoxic CD8+ T cells, leading to their activation
    - responsible for early acute cell-mediated rejection
  2. Indirect:
    - donor cells or donor proteins shed from cell surfaces are engulfed by recipient APCs and presented to recipient CD4+ helper T cells
22
Q

The binding of a T cell to an APC leads to the initiation of an immune reactions - describe the 3 signals involved in this process.

A

(i) Signal 1:
- TCR activation
- Binding of APC MHC-peptide complex to the T cell receptor (TCR) activates multiple intracellular pathways
- one of these pathways involves calcineurin (when activated results in the activation of nuclear factors and release of IL-2)
- IL-2 release will only occur in the presence of signal 2

(ii) Signal 2:
- Co-stimulation
- Binding of complementary coo-stimulatory pathway molecules present on APC and T cells
- Activation of tyrosine kinase
- Induction of IL-2 and other T cell activation genes (with signal 1)

(iii) Signal 3:
- Signal 1+2
- Induction of cytokine, cytokine receptors, and cell activation genes (including IL-2 and IL-2R)
- Clonal proliferation

23
Q

Describe the process and consequences of T cell activation.

A
  • involves T cell proliferation and clonal expansion (so all cells express the same TCR)
  • then differentiate into effector cells (which no longer require co-stimulation for activation)
  • CD4+ effector cells include TH1, TH2, regulatory and memory cells:
    1. TH1 → activate macrophages, provide help to B cells, synthesise important cytokines
    2. TH2 → provide help to B cells (e.g. immunoglobulin class switching)
    3. TH17 → inflammatory responses
    4. Regulatory cells → suppress T cell responses
    5. Memory cells → component of immunological memory (ability to respond to promptly and intensely, following antigen re-presentation)
  • CD8+ cells develop into a single cytotoxic effector cell population, involved in the killing of infected and tumour cells
24
Q

What are some of the early and late complications of transplant surgery?

A

Early:

  1. bleeding
  2. wound infection
  3. vascular thrombosis/occlusion
  4. urinary leak
  5. lymphocele
  6. early obstruction

Late:

  1. renal artery stenosis
  2. ureteric stenosis
  3. bladder dysfunction
25
Q

What is hyper acute rejection?

A
  • catastrophic form of rejection that occurs immediately on repercussion of the transplanted kidney
  • due to the presence of pre-formed antibodies
  • antibodies bind to donor endothelial cells where they activate complement and clotting cascades → vascular thrombosis
26
Q

What is acute rejection?

A
  • a sudden deterioration in graft function, associated with specific immunopathological changes
  • either predominantly T-cell or antibody-mediated
27
Q

How does acute rejection classically present?

A
  • fever
  • painful graft
  • oligo-anuria

(this presentation is now very rare → rejection usually presents with an asymptomatic risk in serum creatinine)

28
Q

Describe the mechanisms that increase a person’s risk of malignancy post-transplant.

A
  1. increased risk is more a function of overall immune suppress t burden than of a particular immune suppressive agent
  2. most immunosuppressants impair the cell cycle and cell growth across many different cell types
  3. calcineurin inhibitors up regulate both TGF-beta and VEGF → increased angiogenesis + tumour spread (animal models)
  4. azathioprine interrupts the repair of UV light-associated DNA damage in the skin
    - may be aided by the viral-induced inhibition of p53 tumour suppressor gene
    - (~100x greater risk of non melanoma skin cancer)
29
Q

What causes diabetes after transplant?

A
  • impairment of insulin secretion + increased insulin resistance
30
Q

What are the risk factors for new onset diabetes after transplantation (NODAT)?

A
  • > 60 y/o
  • Use of certain immunosuppressive drugs (steroids, CNIs, and mTOR inhibitors)
  • Non-caucasian
  • BMI >30
  • Family history T2DM
  • History of gestational diabetes
  • HCV +ve patients
31
Q

What are the most common opportunistic infections to occur post-transplant? When do they most often occur?

A

Most common infections:

  • listeria
  • aspergillus
  • pneumocystis pneumonia

When:
- 1-6 months post-transplant

32
Q

List immunosuppressive drugs used in renal transplantation.

A
  1. Antithymocyte globulin
  2. Cyclosporin (CNI)
  3. Tacrolimus (CNI)
  4. Azathioprine
  5. Mycophenolate
  6. Sirolimus + everolimus
  7. Corticosteroids
33
Q

What is the MOA of antithymocyte globulins in immunosuppression?

A

Blocks T-cell membrane proteins

34
Q

What is the MOA of cyclosporin in immunosuppression?

A

Binds to cyclophilin and forms complex that inhibits calcineurin

35
Q

What is the MOA of tacrolimus in immunosuppression?

A

Binds to FKBP12 and forms complex that inhibits calcineurin

36
Q

What is the MOA of azathioprine in immunosuppression?

A

Inhibits protein synthesis

37
Q

What is the MOA of mycophenolate in immunosuppression?

A

Inhibits Inosine monophosphate dehydrogenase

38
Q

What is the MOA of sirolimus/everolimus in immunosuppression?

A

Binds and forms complex with FKBP12 complex that inhibits mTOR

39
Q

What is the MOA of corticosteroids in immunosuppression?

A

Blocks T cell-derived and APC-derived cytokine expression

40
Q

What combination of immunosuppressants is normally used after transplant?

A
  1. Tacrolimus OR Cyclosporin OR Sirolimus
    PLUS
  2. Mycophenolate (either Cellcept or Myfortic)
    PLUS
  3. Prednisolone

Met3b (21 decks)

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