Diabetes Mellitus T2 Flashcards

1
Q

def of T2DM

A

increased peripheral resistance to insulin, impaired insulin secretion & increased hepatic glucose output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

aetiology of T2DM

A

combination of genetics & environment

1 genetic (risk for a 1st-degree relative of a patient with T2DM is 5-10 times higher)
2 obesity
-high plasma free FA levels & adipokines (leptin, TNF-a) secreted from adipocytes contribute to peripheral insulin resistance
-chronic hyperglycaemia can damage beta cells
-high free FA levels can damage beta-cell function
3 secondary diabetes
-pancreatic diseases (chronic pancreatitis, pancreatic cancer, resection)
-endocrinopathies (Cushing’s, acromegaly)
-drugs (corticosteroids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

epi of T2DM

A

5-10% prevalence in UK
people of asian, african & hispanic descent are at greater risk
incidence has increased as obesity has increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

history of T2DM

A

polyuria & polydipsia
patients may present with hyperosmolar hyperglycaemic state (hyperosmolar non-ketotic state)
infections (foot ulcers, candidiasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

examination findings in T2DM

A

determine BMI, waist circumference, blood pressure

observe for diabetic foot (ischaemic such as dry skin, reduced foot pulses, ulcers & neuropathic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

investigations for suspected T2DM

A

diagnosed if one or more of the following are present:
-symptoms of diabetes & random plasma glucose >11.1mmol/l
-fasting glucose >7mmool/l
-two hour plasma glucose >11.1mmol/l after a 75g oral glucose tolerance test
additionally monitor hba1c, UEs, lipid profile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

overview of management of T2DM

A

1 glycaemic control
2 screening for & management of complications
3 screening & treatment of CVS risk factors
4 advice & patient education
5 hyperosmolar hyperglycaemic state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

(glycaemic control) management of T2DM

A

monitor control of symptoms
monitor capillary blood glucose
monitor hba1c every 3 months

Step 1 (diagnosis)
-lifestyle & metformin
-if hba1c >7% after 3 months progress to step 2
Step 2
-lifestyle & metformin & sulphonylurea
-if hba1c >7% after 3 months progress to step 3
Step 3
-lifestyle & metformin & basal insulin
-if hba1c >7% after 3 months & fasting blood glucose <7mmol/l progress to step 4
Step 4
-add premeal rapid-acting insulin

metformin inhibits hepatic gluconeogenesis
sulphonylureas (gliclazide) block ATP-sensitive K channels in beta cells stimulating insulin release
thiazolidinedione (pioglitazone) activates PPAR-gamma and reduces insulin resistance

if weight loss is desired use SC exenatide (GLP-1 agonist - glucose-like-peptide-1 agonist)
GLP-1 is produced by the L-cells in the gut & increase glucose-stimulated insulin secretion, decrease glucagon release, gastric emptying & appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

(screening for & management of complications) management of T2DM

A

retinopathy (regular digital retinal photography)
nephropathy (monitor UEs, K, & estimated GFR, BP control, ACE inhibitors/ARBs)
neuropathy (examination for foot ulcers)
vascular disease (examination of foot pulses)
diabetic foot (examine feet regularly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

(screening & treatment of CVS risk factors) management of T2DM

A

lose weight
stop smoking
BP control
all diabetic patients should be started on a statin (CARDS trial)
aspirin given in patients with diabetes & an additional CVS risk factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

(advice & patient education) management of T2DM

A

INFORM PT

Information (diabetic nurses, websites, etc. explaining diabetic control, complications)
Nutrition (complex carbs as opposed to simple sugars, reduce fat intake)
Foot care (regular inspection)
Organisations (support groups)
Recognition & treatment of hypoglycaemia
Monitoring of capillary glucose

Pregnancy (strict glycaemic control & planning conception)
Treatment (action, duration, administration technique for insulin, change injection site to avoid lipohypertrophy, explain need of exercise)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

(hyperosmolar hyperglycaemic state) management of T2DM

A

similar to treatment of DKA
but use 0.45% saline if serum Na >170mmol/l & a lower rate of insulin infusion
DVT prophylaxis with SC heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

complications of T2DM

A

1 hyperosmolar hyperglycaemic state
-due to insulin deficiency like DKA
-patient is usually older than DKA patients
-longer history
-dehydration, high Na, high glucose (>35mmol/l), high osmolality (>340mmol/kg)
-no acidosis
2 neuropathy
-distal symmetrical sensory neuropathy
-mononeuritis (IIIrd nerve palsy)
-autonomic neuropathy (postural hypotension)
-impotence
-urinary retenion
3 nephropathy
-microalbuminuria, proteinuria & eventually renal failure
4 retinopathy
-background (dot and blot haemorrhages, hard exudates)
-pre-proliferative (cotton wool spots & venous bleeding)
-proliferative (new vessels on disc)
-maculopathy (macular oedema, exudates &/ haemorrhage within 1 disc of fovea associated with decreased visual acuity)
-also prone to glaucoma & cataracts
5 macrovascular complications
-IHD
-stroke
-peripheral vascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

prognosis of T2DM

A

intensive glycaemic control decreases the risk & progression of microvascular complications
early intensive glycaemic control decreases risk of MI and overall mortality

pre-diabetes

  • diagnosed based on fasting blood glucose or an oral glucose tolerance test
  • impaired fasting glucose (IFG) defined as fasting plasma glucose of 5.6-6.9mmol/l
  • impaired glucose tolerance (IGT) defined as plasma glucose of 7.8-11mmol/l measured 2h after 75g oral glucose

patients with IFG & IGT are at considerable risk of developing T2DM over next 5yrs (40%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are GLP-1 receptor agonists

A

glucagon-like receptor agonists
for treatment of T2DM
lower risk of causing hypoglycaemia
also inhibits appetite & aids with weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

liraglutide

A

long acting GLP-1 receptor agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are dipeptidyl peptidase 4 inhibitors

A
also known as gliptins
oral hypoglycaemic
blocks DDP-4
treats T2DM
e.g. sitagliptin

as glucagon increases blood glucose levels, DPP-4 inhibitors reduce glucose & therefore blood glucose levels
DDP-4 inhibitors increase incretin levels (GLP-1 & GIP) by preventing breakdown, which inhibits glucagon release, which in turn increase insulin secretion and result in decreased blood glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the normal non-diabetic hba1c

A

<36mmol/mol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the hba1c level for diabetics

A

> 48mmol/mol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

metformin

A

first line treatment for T2DM
often true for overweight patients
also used as treatment for PCOS

part of the biguanide class
MOA
-decreases hepatic glucose production
-increases insulin sensitivity across the body

used because it is cheap, functional, & weight neutral (patients will not gain weight while using this)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

gliclazide

A

for T2DM
a sulfonylurea
increases insulin levels

however can cause weight gain & hypos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

thiazolidinedione

A

also know as glitazones
for treatment of T2DM

activates PPAR-gamma receptor (are PPAR-gamma agonists)
causes an increase in FA storage in adipocytes
therefore decreases FAs in circulation
as a result increase in cellular glucose oxidation, causing decreased blood glucose levels
decreased insulin resistance

pioglitazone

side effects include water retention leading to HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the contraindications of metformin use

A

renal failure

EGFR<30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

SGLT2 inhibitors

A

sodium-glucose like transporters
giflozins

inhibits renal glucose reabsorption in the kidneys
causes an increase in glycosuria
causes weight loss due to loss of glucose
lowers BP
decreases risk of cardiac events

however increases risk of UTI in due to increase glucose in urine
used for T2DM as glucagon:insulin ratio is affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how does regular exercise help diabetes

A

during & after exercise muscles increase expression of GLUT4 receptors
glucose is taken up by GLUT4 receptors into the muscles
blood glucose levels decrease

26
Q

hyperosmolar hyperglycaemia

A

in T2DM
common in elderly, those with recent infection
causes an increase in glucose

27
Q

what happens if sodium levels are corrected too quickly

A

osmotic demyelination occurs

central pontine myelinolysis

28
Q

what is diabetes mellitus

A

a chronic condition characterised by abnormally raised blood glucose levels

29
Q

what is T1DM

A

autoimmune disorder where insulin producing beta cells of islets of langerhans in the pancrease are destroyed by immune system
this results in an absolute deficiency of insulin which causes raised glucose levels

30
Q

what are the signs + symptoms of T1DM

A

weight loss
polydipsia
polyuria

31
Q

what are the signs + symptoms of diabetic ketoacidosis in T1DM

A

abdominal pain
vomiting
reduced consciousness

32
Q

what are the signs + symptoms of T2DM

A

polydipsia

polyuria

33
Q

why does polydipsia and polyuria occur

A

water is removed from the body due to the osmotic effects of glucose being excreted in the urine

34
Q

what are the 4 main investigations for blood glucose

A

1 finger-prick bedside glucose
2 one off blood glucose (fasting or non-fasting)
3 HbA1c
4 glucose tolerance test

35
Q

what are the diagnostic criteria for diabetes mellitus set out by the WHO

A
patient symptomatic:
-fasting glucose >7.0mmol/l
-random glucose >11.1mmol/l
patient asymptomatic:
-above criteria must occur on two separate occasions
36
Q

what is the level by which the HbA1c is diagnostic of DM

A

HBA1c >6.5% (48mmol/mol)

37
Q

what are the diagnostic criteria for prediabetes

A

HbA1c 42-47mmol/mol or 6-6.4%

fasting glucose 6.1-6.9mmol/l

38
Q

what must all T1DM patients be treated with

A

insulin

as they have an absolute insulin deficiency

39
Q

what is the ROA for insulin

A

subcutaneous

40
Q

what are the SEs of insulin

A

hypoglycaemia
weight gain
lipodystrophy

41
Q

what is the MOA of metformin

A

increases insulin sensitivty

decreases hepatic gluconeogenesis

42
Q

what is the ROA for metformin

A

oral

43
Q

what are the SEs of metformin

A

GI upset

lactic acidosis

44
Q

when can metformin not be given

A

an eGRF <30ml/min

45
Q

what is the MOA for sulfonylureas

A

stimulates pancreatic beta cells to secrete insulin

46
Q

what is the ROA of sulfonylureas

A

oral

47
Q

what are the SEs of sulfonylureas

A

hypoglycaemia
weight gain
hyponatraemia

48
Q

give 2 examples of sulfonylureas

A

gliclazide

glimepiride

49
Q

what is the MOA of thazolidinediones

A

activates PPAR-gamma receptor in adipocytes to promote adipogenesis and FA uptake

50
Q

what is the ROA of thazolidinediones

A

oral

51
Q

what are the SEs of thazolidinediones

A

weight gain

fluid retention

52
Q

what is the MOA for DPP4 inhibitors (gliptins)

A

increases incretin levels which inhibit glucagon secretion

53
Q

what is the ROA for DPP4 inhibitors (gliptins)

A

oral

54
Q

what is the risk of DPP4 inhibitors (gliptins)

A

increased risk of pancreatitis

55
Q

what is the MOA for SGLT-2 inhibitors (gliflozins)

A

inhibits reabsorption of glucose in the kidney

56
Q

what is the ROA of SGLT-2 inhibitors (gliflozins)

A

oral

57
Q

what is the risk of SGLT-2 inhibitors (gliflozins)

A

UTI

58
Q

what type of drug is gliclzide

A

sulfonylureas

59
Q

what is the MOA of GLP-1 agonists (-tides)

A

incretin mimetic which inhibits glucagon secretion

60
Q

what is the ROA of GLP-1 agonists (-tides)

A

subcutaneous

61
Q

what are the SEs of GLP-1 agonists (-tides)

A

N+V

pancreatitis

62
Q

what do SGLT-2 inhibitors (gliflozins) + GLP-1 agonists (-tides) result in

A

weight loss