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Block 34 - Metabolic > Chronic kidney disease > Flashcards

Chronic kidney disease Flashcards

1
Q

Define the term chronic kidney disease.

A

Abnormal kidney structure or function which is irreversible and present for >3 months with implications for patient health.

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2
Q

State how chronic kidney disease can be classified.

A

Classification is based upon GFR, presence of albuminuria and the cause of the CKD.

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3
Q

Describe the 6 stages of CKD according to classification based on GFR.

A

1) >90 (normal GFR but presence of structural abnormality. E.G. PCKD).
2) 60-89 (with other evidence of kidney damage; proteinuria/ haematuria/ tubule disorder/ transplant/ pathology on biopsy).
3a) 45-59 (mild to moderate decrease in GFR)
3b) 30-44 (moderate to severe decrease in GFR)
4) 15-29 (severe decrease in GFR and usually the appearance of symptoms)
5) <15 (kidney failure; patient usually on RRT or awaiting transplant).

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4
Q

Name 3 causes of CKD in order from most to least common.

A

1) Diabetic nephropathy
2) HTN
3) AKI

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5
Q

1) In HTN, what happens to the blood vessels walls?
2) What are the effects of narrowing of the blood vessel lumen?
3) Describe the effects of less blood then flowing through the afferent arteriole.

A

1) There is thickening of the blood vessel wall which leads to narrowing of the lumen.
2) Causes less blood flow to the kidneys and nephrons.
3) Decrease in filtration > RAAS activation > further HTN.

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6
Q

Eventually, what damage does continued HTN cause to the kidneys?

A

Eventually, HTN will lead to glomerulosclerosis due to ischaemic injury and this will mean the loss of nephrons, leading to a decreasing GFR.

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7
Q

What proportion of patients with diabetes will develop kidney disease?

A

1/3 patients with diabetes will develop kidney disease within 5-10 years after being diagnosed with DM.

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8
Q

List 4 major Changs seen in the kidneys due to diabetic nephropathy.

A

1) Mesangial expansion and mesangial cell proliferation.
2) Podocytopathy (hypertrophy and then atrophy).
3) GBM thickening
4) GBM sclerosis.

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9
Q

Describe the pathophysiology which leads to the 4 renal changes seen in diabetic nephropathy.

A

Hyperglycaemia = production of ROS > activation of unnecessary growth factors > activation of pro inflammatory cytokine > oxidative stress > changes of nephropathy.

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10
Q

1) In CKD, what can cause uraemia?

2) Initially, what does irreversible loss of nephrons lead to?

A

1) The loss of nephrons.

2) Glomerular hyperfiltration as there is increased blood flow to fewer functioning nephrons.

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11
Q

1) In the early stages of CKD, glomerular hyperfiltration is tolerated, causing what?
2) After a while, what does glomerular hyperfiltration lead to?
3) Further sclerosis causes what?
4) In the late stages of this process, what eventually happens?

A

1) A large increase in GFR.
2) After a while, glomerular hyperfiltration results in sclerosis due to the increased pressure.
3) Glomerulosclerosis leads to the loss of further nephrons.
4) In the late stage, so much kidney function is lost that GF decreases, urine output decreases and waste begins to be retained potentially causing uraemia.

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12
Q

What is the mechanism of Hyperkalaemia in chronic kidney disease?

A

Loss of nephrons > decreased renin production and release > decreased aldosterone > decreased functioning of the Na+/K+ ATPase > K+ retention.

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13
Q

Why should you not use ACEi’s and Potassium sparing diuretics in combination in patients with chronic kidney disease?

A

Because concomitant use can cause aggravation of the hyperkalaemia.

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14
Q

Name 6 possible signs or symptoms that may feature in the presentation of chronic kidney disease.

A

1) SOB/ oedema (symptoms of fluid retention)
2) Anorexia
3) Restless legs
4) Bone pain
5) Pruritis
6) Amenorrhoea
7) Weakness
8) Impotence
9) N+V

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15
Q

Give a basic description of why the following signs or symptoms might occur in patients with CKD:

a) Fatigue
b) Oedema
c) N+V
d) Pruritis
e) Anorexia

A

a) Due to anaemia
b) Periorbital and peripheral oedema due to salt and water retention.
c) Due to accumulation of toxic waste products in circulation.
d) Due to accumulation of toxic waste products in circulation.
e) Due to accumulation of toxic waste products in circulation.

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16
Q

Name 5 other potential presenting factors of chronic kidney disease.

A

1) Arthralgia
2) Enlarged prostate
3) Frothy urine
4) Coca-cola urine
5) Rashes
6) Dyspnoea
7) Orthopnoea
8) Seizures
9) Retinopathy

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17
Q

Describe a list of investigations which you might carry out in a patient with suspected CKD.

A

1) Bloods: U&Es, FBC, Creatinine, glucose, Calcium, Phosphate, PTH and eGFR.
2) USS
3) Urinalysis and micro-albumin
4) AXR
5) Biopsy
6) CT abdomen

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18
Q

Describe the pathogenesis of anaemia and osteodystrophy in patients with CKD.

A

In late stage CKD, there is decreased renin production > causes decreased BP, decreased EPO and decreased calcitriol > anaemia and osteodystrophy.

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19
Q

Name 4 treatments that might be used to slow renal disease progression in CKD.

A

ACEi/ARB
Anti-hypertensives
Glycaemic control
Lifestyle advice

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20
Q

Name 5 complications of CKD which may require management.

A 
Anaemia
Oedema
Acidosis
Bone mineral disorders
Restless legs/ cramps
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21
Q

When might it be reasonable to start long term dialysis treatment?

A

When dialysis (RRT) is necessary in order to manage one or more symptoms of renal failure.

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22
Q

Name 5 symptoms of renal failure which are criteria for renal replacement therapy (i.e. dialysis) if they are not managed via other means?

A 
Inability to control volume status (including pulmonary oedema)
Inability to control BP
Serositis
Acid-base or electrolyte abnormalities
Pruritis
N+V
Deterioration in nutritional status
Cognitive impairment
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23
Q

1) At the commencement of dialysis, generally what is a patient’s GFR?
2) What are the two options for dialysis when transplantation is awaited or not possible?
3) When should planning for RRT in patients with progressive CKD begin?

A

1) 5-10 (stage 5 CKD)
2) Haemodialysis or peritoneal dialysis.
3) When risk of renal failure is 10-20% within a year.

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24
Q

Describe basically how haemodialysis works.

A

Blood passed over semi-permeable membrane
Dialysis fluid flows in the opposite direction
Diffusion of solutes occurs down concentration gradient
Hydrostatic gradient used to clear excess fluid as required

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25
Q

1) How is access created for haemodialysis and why is this preferred?
2) When should this type of access be created?
3) How often is haemodialysis required and where is it completed?
4) Why should haemodialysis be started gradually?

A

1) Arteriovenous fistula as this provides increased blood flow and longevity.
2) Prior to a need for RRT to avoid infection risk associated with central venous dialysis catheters.
3) 3 times weekly or more at a dialysis unit (home haemodialysis should be offered to all suitable patients).
4) Because of the risk of dialysis disequilibrium.

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26
Q

Name 4 problems which can occur with haemodialysis.

A

Arteriovenous fistula: thrombosis, stenosis, tunnelled venous line, infection, blockage, recirculation of blood.

Dialysis disequilibrium: between cerebral and blood solutes leading to cerebral oedema.

Hypotension

Time-consuming process

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27
Q

What 3 areas does renal replacement therapy focus on?

A

1) Residual renal function
2) Symptom control
3) Advanced planning

** conservative management is offered for those who opt out of RRT.

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28
Q

Describe basically how peritoneal dialysis works.

A

Peritoneum is used as a semi permeable membrane.
Catheter inserted into peritoneal cavity.
Fluid is infused.
Solutes diffuse slowly across peritoneum.

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29
Q

1) How is peritoneal dialysis performed?

2) How is ultrafiltration achieved in peritoneal dialysis?

A

1) A continuous process with intermittent drainage and re-filling of the peritoneal cavity, performed at home.
2) Ultrafiltration is achieved by adding osmotic agents to the fluid.

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30
Q

List 4 potential problems that may occur with peritoneal dialysis.

A

Catheter site infection
Peritonitis
Hernia
Loss of membrane function over time.

31
Q

Describe basically how haemofiltration works.

A

Water is cleared by positive pressure which drags solutes into waste by convection.
Ultrafiltrate is replaced with volumes of water before or after the membrane.

32
Q

1) When is haemo-filtration used?

2) When might harm-filtration be used in the long term?

A

1) Used when there is decreased haemodynamic stability when haemodialysis is not possible, for example in critical care.
2) When in combination with haemodiafiltration during haemodynamic instability allowing middle molecule clearance.

33
Q

What does uraemia cause which increases mortality rates?

A

Uraemia causes granulocyte and T cell dysfunction which causes increased sepsis related- mortality.

34
Q

In patients requiring long term dialysis, what causes carpal tunnel syndrome, arthralgia and visceral effects?

A

Beta-2 microglobulin accumulates in patients needing dialysis long term.

35
Q

When should renal transplantation be considered for patients?

A

Should be considered for every patient with or progressing towards stage 5 CKD.

36
Q

Give examples of the following types of contraindications to renal transplant:

a) absolute
b) temporary
c) relative

A

a) cancer with metastases
b) active infection, HIV with viral replication, unstable CVD.
c) CHD or CVD.

37
Q

What are the 2 classifications for sources of kidney transplants?

A

1) heart beating and non-heart beating (cadaveric donor)

2) related and non-related (live donor)

38
Q

Describe what is meant by the following:

1) Cadaveric heart beating donor
2) Cadaveric non-heart beating donor

A

1) the patient has severe brain injury and has brainstem death but is still breathing due to artificial ventilation.
2) patient has already died and the hea rt has stopped beating prior to organise retrieval.

39
Q

Describe what is meant by the following:

1) Related live donor
2) Unrelated live donor

A

1) Kidney donor is living and has a blood or emotional relationship with recipient.
2) Donors and recipients are paired and pooled, and organs are swapped between incompatible donor-recipient pairs.

40
Q

What is an altruistic kidney donor?

A

This is when the kidney donor and recipient do not know each other.

41
Q

Where is a transplanted kidney placed?

A

Into an exztraperitoneal position in the left or right iliac fossa.

** the native kidney is left in situ.

42
Q

1) How does ABO blood grouping classify people?
2) Describe what is meant by the following with regards to antigens and antibodies:

a) Blood group A
b) Blood group B
c) Blood group AB
d) Blood group O

A

1) Based on the A/B antigens on RBCs.

2a) A antigens and anti-B antibodies
2b) B antigens and anti-A antibodies
2c) A and B antigens, no antibodies
2d) No antigens, anti-A and anti-B antibodies

43
Q

List the acceptable blood donors for the following blood groups:

1) A
2) B
3) AB
4) C

A

1) A/O
2) B/O
3) Any (A/ B/ O)
4) O

44
Q

1) What are major histocompatibility complexes?
2) Name the class 1 HLAs and state where they are found.
3) Name the class 2 HLAs and state where they are found.

A

1) Genes which code for human leukocyte antigens
2) HLA-A/ B/ Cw found on all nucleated cells.
3) HLA-DR/ DQ/ DP found on APCs, B lymphocytes and activated T cells.

45
Q

1) For transplants, which HLAs are of most interest?
2) How is closeness of HLA matches expressed?
3) What is graft vs. host disease?

A

1) HLA-A/ B/ DR
2) As mismatches of A, B and DR.
3) Where immune cells in the donated tissue begin to attack a recipient’s body cells.

46
Q

1) Why are there large differences in HLAs?

2) With regards to graft vs. host disease, what are MHC genes involved in?

A

1) Because the genes coding for MHC I and II are very variable, causing large differences in the antigens.
2) They are involved in recognising if cells are self/ non-self.

47
Q

In graft vs. host disease, what does the transplanted organ do in the beginning?

A

A transplanted organ will release immune cells which will recognise MHC molecules of the recipient as foreign.

48
Q

What are the 3 elements which must be present in order for graft Vs. host disease to take place?

A

1) Graft tissue must contain immune cells.
2) Host’s immune system must be suppressed.
3) The host must be immunologically different to the donor.

49
Q

Describe the basic role of a dendritic cell in graft Vs. host disease.

A

Dendritic cells pick up foreign antigens and travel to the nearest lymph node where they present the foreign antigen on an MHC molecule to a T helper cell.

50
Q

Describe the role of T helper cells in graft Vs. host disease.

A

If donor T helper cell recognises antigen presented by dendritic cell as foreign, then they differentiate into type 1 T helper cells.

51
Q

What do type 1 T helper cells do?

A

Release the cytokines IL-2 and IFN-gamma which cause themselves and other T cells to proliferate.

52
Q

What do the cytokines IL-2 and IFN-gamma do?

A

Induce expression of more MHC class II proteins on host cells (makes it easier for donor helper T cells and host APCs to interact).

53
Q

1) What does IFN-gamma do specifically in this context?
2) Name 3 pro-inflammatory cytokines involved in graft Vs. host disease.
3) What action do activated macrophages also do in graft Vs. host disease?

A

1) Activates phagocytes such as macrophages which release pro-inflammatory cytokines which recruit new immune cells to the area.
2) TNF-alpha, IL-1, IL-6.
3) They secrete lysosomal enzymes which directly damage tissue.

54
Q

1) As well as helper T cells, what other type of T cells are present in graft Vs. host disease?
2) What is the function of these T cells?

A

1) Grafted cytotoxic T cells are also present.

2) These recognise antigens presented on MHC class 1 molecules.

55
Q

1) What do cytotoxic T cells do if they recognise antigens presented to them as foreign?
2) What do perforin and granzymes do?

A

1) They begin to secrete perforin and granzymes.
2) Perforin: perforates target cells by forming pores. Granzymes: enter cells through pores created by perforin and induce apoptosis in the cell.

56
Q

In graft Vs. host disease, which types of tissues tend to be affected more frequently and severely?

A

Skin
Liver
GIT

57
Q

1) What is meant by acute graft Vs. host disease?
2) What is meant by chronic graft Vs. host disease?
3) How is graft Vs. host disease diagnosed?

A

1) Occurs within 3 months of transplant.
2) Occurs more than 3 months post transplant.
3) Based on signs and symptoms, lab tests such as LFTs ad U&Es (these are useful to address damage caused), and tissue biopsies of affected organs which can confirm a diagnosis.

58
Q

Describe the signs and symptoms which may occur in graft Vs. host disease in the skin in acute disease.

A

Skin can be painful and itchy.
There may be a rash on the soles of the feet and palms of the hands.
The rash can blister and peel and may progress to cover the whole body.

59
Q

Describe the signs and symptoms which may occur in graft Vs. host disease in the liver in acute disease.

A

Acute disease is normally asymptomatic in the liver.

There may be increased bilirubin, ALP, ALT and AST.

60
Q

Describe the signs and symptoms which may occur in graft Vs. host disease in the GIT in acute disease.

A

Can cause diarrhoea, intestinal bleeding and abdominal pain.

Particularly will affect the distal small intestine and colon.

61
Q

Describe how chronic graft Vs. host disease could affect the following organs:

a) skin
b) eyes
c) GIT
d) others

A

a) Skin thickening is the most commonly seen.
b) eyes and lacrimal glands affected by burning sensations and photophobia.
c) main effects on proximal digestive tract (mouth and salivary glands) with a dry mouth, sensitivity to acidic/ spicy foods and odynophagia.
d) SOB, cramps and weakness occur less frequently.

62
Q

What is the mainstay of treatment for graft Vs. host disease?

A

IV glucocorticoids to suppress the T cell mediated response.

63
Q

Aside from graft Vs. host disease, describe 4 other types of complication which may result as a result of renal transplantation.

A

1) Surgical complications: bleeding, thrombosis, infection, urinary leaks, lymphocyte hernia.
2) Delayed graft function: more common from deceased donors, affecting 40% grafts.
3) 3-5x increased risk of CVD
4) Increased risk of all infections

64
Q

Name 4 classes of drug which can be used for immunosuppression.

A

1) Calcineurin inhibitors
2) Antimetabolites
3) Mammalian target of rapamycin inhibitors (mTOR inhibitors)
4) Monoclonal antibodies

65
Q

Give examples of and describe a basic mechanism of action for the following classes of immunosuppressing drugs:

a) calcineurin inhibitors
b) mTOR inhibitors
c) antimetabolites
d) monoclonal antibodies

A

a) inhibit cell nuclear activation (tacrolimus/ ciclosporin)
b) inhibit cell cycle activation (sirolimus/ everolimus)
c) inhibit nucleic acid synthesis (azathioprine/ mycophenalate)
d) anti-CD3 (inhibits T cells binding APCs), anti-CD52 (depletes B and T lymphocytes), anti-IL-2 receptor 2 (inhibits IL-2 binding to receptors which blocks clonal proliferation of activated T cells).

66
Q

When could a hyper acute rejection to organ transplant occur?

A

Occurs when a recipient has pre-formed antibodies to a donor kidney (e.g. with blood group incompatible transplant).

67
Q

Briefly describe the hyperacute rejection pathophysiology.

A

Antibody binds antigens on capillary endothelium in kidney.
Endothelial damage caused by complement activation and inflammatory cell infiltration.
Renal infarction then caused by platelet adhesion and vascular thrombosis.

**In these cases, infarction will occur within minutes of implanting the graft.

68
Q

What reaction is similar to a hyperacute rejection reaction and give 3 examples of when this might happen.

A

The same process occurs in sensitisation reactions. These occur when patients have previously been exposed to HLA from other patients or individuals.

For example, in pregnancy, blood transfusions or previous transplants.

69
Q

Which types of patients may be able to have a simulations kidney and pancreas transplant?

A

Those with end stage renal failure secondary to type 1 diabetes mellitus.

70
Q

Describe 3 pieces of lifestyle and diet advice for patients with CKD.

A

1) Exercise to achieve a healthy weight
2) Smoking cessation
3) Dietary advice about potassium, phosphate, calorie and salt intake, appropriate for the severity of CKD.

**Do not advise people with CKD to have low protein diets.

71
Q

1) What should BP target be for patients with CKD?

2) What should BP target be for patients with CKD and DM?

A

1) <140/90

2) <130/80

72
Q

1) What is the primary management for preventing and treating CVD in patients with CKD?
2) In CKD patients, what is used for secondary prevention of CVD?

A

1) Statins.

2) Oral antiplatelets and anticoagulants.

73
Q

In basic terms, state how you would treat the following complications of CKD:

a) Osteoporosis
b) Anaemia
c) Hyperkalaemia
d) Metabolic acidosis

A

a) bisphosphonates and vitamin D supplements (vitamin D supplements for deficiency, not management).
b) education, iron therapy, EPO stimulating agent therapy.
c) Patriomer can be used in adults but only if there is acute, life-threatening Hyperkalaemia. Calcium gluconate can also be used.
d) Oral sodium bicarbonate supplementation for people with both GFR <30 and serum bicarbonate <20mmol/litre.

74
Q

What 3 criteria can determine if a patient is suffering from persistent hyperkalaemia if they are between at stages 3b to 5 of CKD or if they have CHF?

A

1) K+ >6mmol/litre.
2) The patient is not taking a RAAS inhibitor for increased K+
3) The patient is not on dialysis

Block 34 - Metabolic (18 decks)

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