New diabetic drugs, When to start dialysis, Diabetic nephropathy,Type 2 Diabetes and its complications, Elderly on Dialysis, Chronic disease pathway Flashcards
How do you treat diabetes
1.st line: Metformin
2nd line: DPP-4 inhibitor, SGLT2 inhibitor, Glp1 receptor agonist (these reduce death)
What are clinical feature of diabetic nephropaty
Hypertension
proteinuria
derranged kidney function
What is the best way to check for diabetic nephropathy?
look at proteinuria first thing
creatinine goe up higher later
What are you particularly at risk of if you have diabetes with diabetic nephropathy?
much higher risk of cardiovascular events
What are the histological features of diabetic nephropathy?
- glomerular:
- Mesangial expansion
- basement membrane thickening
- Glomerulosclerosis
- vascular
- tubulo interestial
How long does it take for someone with diabetes to develop reanal failure
30-40 years
WHat are risk factors that impact whether someone get diabetic nephropathy
age at which you get diabetes
racial factors
age of presentation
loss due to cardiovascular morbidity
What are ways to prevent the onset of diabetic nephropathy in someone with diabetes
- diabebetic control
- blood pressure control
- suppression of RAAS
- stop smoking
What are the antihypertensives that you give to diabetics
ACE inhibitor
If someone get’s a cough with an ACE inhibitor and is diabetic, what is the next drug you would give
ARB
Which of the following are feature of diabetic nephropathy:
A. affects all patient with diabetes over time
B associated with decreased BP
C. progressively increasing proteinuria
D. Unrelated to glycaemic control
E, Associated with a low risk of cardiovascular events
C. progressively increasing proteinuria
Regarding ACE inhibition in patients with diabetes
A. ACE inhibitors cause improvement in the creatinine within days of starting
B. Ace inhibitors cause an increase of the creatinine within days of starting
C. ACE inhibitors increase microalbuminuria
B
What happens if you give somone with renal artery stenosis an ACE inhibitor?
fall in GFR
Regarding ACE inhibitors in patients with diabetes
A. ACE inhibitors are useful in patients with diabetes and resultant renal artery stenosis
- ACE inhibtors increase microalbuminuria
- ACE inhibitors prevent end stage renal failure
- ACE inhibitors cause hypokalaemia
- ACE inhibitors prevent end stage renal failure
if you give some an ACE for their diabetic nephropathy what happens to their kidney function
inititally drops off massively but then it plateau and the fall is much less than without and therefore over many years it is more favourable
What should you do if someone has been given an ACE inhibitor and they have renal artery stenosis
you have to take them off it
AND THEN
call a nephrologist might need to be dialised for a while
BUT they will fully recover
What are the problems/ implications of renal failure
- Electrolyte imbalance: hyponatraemia, hyperkalaemia
- ACIDOSIS
- fluid retention
- retention of waste products: urea, creatinine, urate, phosphate, middle molecules
- LESS secretion of EPO and Vitamin D
WHat are symptoms of renal failure
tiredness - anaemia (lack of EPO)
SOB and oedema
Pruritus - renal bone disease (lack of vit. D)
nocturia, feeling cold, twitching (later on)
poor apetite, nausea, loss of taste, weight loss
What are the complications that occur if renal replacement is not started in time
Hyperkalaemia- arrthmias, cardiac arrest
Pulmonary oedema- fluid retention
Nause and vomitting- acidosis
Malnutrition cachexia - loss of apetite and taste
Fits & increasing coma - hypnatraemia
DEATH
What are renal replacement therapies?
Where are they done?
Dialysis
-
haemodialysis:
- HOSPITAL based but can be done at home
-
peritoneal dialisis
- HOME treatment
Transplantation
What are the aims of renal replacement therapy
correct electrolytes
remove waste product
restore fluid balance
improve symptoms
maintain quality of life
When do you refer for renal replacement therapy?
Do you start it then?
eGFR of below 20
No just discuss and organise
and then you may start at 10ml/min (benifits outweigh the risks)
Need to start at 6 or less
What do you need to tell the patient about
Risks of renal failure
types of renal replacement failure and then establish the access
What are the different accesses for renal replacement therapy
fistula
PD catheter
transplant assesment
At what eGFR does someone have to be on dialysis?
At what eGFR woudl it be beneficial?
At what eGFR does someone have to be on dialysis? 10
At what eGFR woudl it be beneficial - 6
What are the risks adn benifits of dyalisis?
Benifit
improve uraemic syndrome (reduce pruritus, nausea and tiredness)
correct fluid balance (less SOB and oedema)
Avoid life threatning complication like acidosis, hyperkalaemia and pulmunary oedema resistant to diuretics
RISKS
infection
hypotension
reduces quality of life (travel, family life)
What does dialysis not treat
anaemia
vitamin D (renal bone diasease)
AND comorbidities
SLE, diabetes and vascular disease
What are the 2 different type of dialysis
haemodialysis: 3 times a week - 4 hours (needs a fistula and catheter)
peritoneal dialysis: Home base: daily and continuous, less haemodynamic stress but need a peritoneal access
GOOD becauses avoid the swings, done at home and less dietary and lfuid restrictions
WHat are the benifits and risks of transpantation
benefits:
- better renal replacement - because also good for anaemia and renal bone disease
- Costs less in long term
- prolongues life
- good for quality of life
RISKS:
- older and sicker patients not eligible
- immunosuppression (increased infection and malignancy)
- surgical complications
- worse off if the transplant fails
how do you predict survival of patients on dialysis?
What do it take into account
body mass index
heart failure
peripheral vascular disease
dysrhythmia
active malignancy
severe behavioural disorder
total dependency
unplanned dialysis
Is dialysis always beneficial?
no study where people over 75 year of age with 2 comorbidities were put on dialysis
SURVIVAL Was the same
What is the normal range for proteinuria?
<30mg/24hr.
What is conservative care in ESRF?
Non-dialysis pathway chosen by patient after shared decision making with predialysis team.
Active management of anaemia with ESA and IV iron.
BP control- slow rate of decline and lower stroke risk.
Optimise fluid balance- avoid over and under hydration.
Symptom control, including pain.
Joint management with palliative care team at end of life phase.
NOT in the lecture but on her flashcards (thought might be useful)
True or false? Half of the patients with type 2 diabetes in the UK do not know they have it.
True
NOT in the lecture but on her flashcards (thought might be useful)
What can you see on fundoscopy of patient with background diabetic retinopathy?
Hard exudates (cholesterol). Microaneurysms (dots). Blot haemorrhages.
What treatment should we use for background diabetic retinopathy?
a) glasses or contact lenses
b) laser treatment
c) nothing
d) improve blood pressure control
e) improve blood glucose control
Improve blood glucose control.
What is likely to be seen on fundoscopy of pre-proliferative diabetic retinopathy?
Cotton wool spots: previously called soft exudates, indicate ischaemia.
Cotton wool spots suggest which of the following?
a) retinal cholesterol deposits
b) retinal ischaemia
c) retinal hypertension
Retinal ischaemia.
What is the management plan for patients with background diabetic retinopathy?
Improve control of blood glucose.
Warn patient that warning signs are present.
What is the management plan for patients with pre-proliferative diabetic retinopathy?
Cotton wool spots, suggest general ischaemia. Without treatment, new vessels will grow.
Pan-retinal photocoagulation.
What is the management plan for patients with proliferative diabetic retinopathy?
Proliferative = visible new vessels.
Pan-retinal photocoagulation.
How long does it take to see benefit from good glucose control in diabetes?
15 years.
How is hyperglycaemia managed?
Diet and exercise.
Biguanide (metformin).
Sulphonylureas (e.g. gliclazide).
Insulin sensitiisers: thiozolidinediones such as pioglitazone.
Insulin analogues.
Incretins (GLP-1 analogues).
Gliptins (DPP-4 inhibitors).
What is the problem with insulin use in T2DM?
When soluble natural insulin is given subcutaneously, it forms a hexameter under the skin, which delays release.
Inject 30mins before meals.
Why are short acting insulin analogues better than insulin in the treatment of T2DM?
Very rapid acting and mean that patients can inject and eat- no waiting, no risk of hypos if forget to eat.
Gives patients a licence to inject immediately before meals.
Many were doing this anyway with the old insulins.
Profile more closely mimics insulin profile of insulin following a meal.
X Twice the cost of soluble insulin X
What are the effects of GLP-1?
GLP-1 is secreted from the gut and signals to the pancreas to make even more insulin.
Direct effect on appetite and reduces gastric emptying.
Increases hypothalamic satiety.
List GLP-1 analogues.
Exanatide
Liraglutide (Victoza or Saxenda)
Semaglutide
How do SGLT2 inhibitors work?
Blocks sodium-glucose cotransporters in renal tubules.
Impairs glucose reabsorption.
Decreasing blood glucose levels.
How do GLP-1 agonists work?
Increase insulin secretion.
Decrease glucagon.
Decreasing blood glucose levels.
How do DPP-4 inhibitors work?
Increase incretin levels (GLP-1 and GIP).
Increase insulin and decrease glucagon.
Decreasing blood glucose levels.
Why do patients gain weight on insulin treatment?
If glycosuria stops, many calories saved.
Increased appetite.
Improved wellbeing.
Set point of body weight (hypothalamic).
Poor glucose control enables weight loss.
