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GERR Pharmacology > Treatment of Diabetes pt2 > Flashcards

Treatment of Diabetes pt2 Flashcards

1
Q

List the 3 causes of hyperglycaemia in T2DM

A
  • impaired insulin secretion
  • receptor and pos receptor defects
  • increased hepatic glucose secretion
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2
Q

Explain LADA , its frequency, signs and features

A
  • latent autoimmune diabetes in adult hood
  • 6-10% of T2DM
  • lack of metabolic syndrome features associated with normal T2DM
  • poor glucose control with oral agents and patient looses weight
  • background autoimmune disease
  • behaves like type 1 diabetes
  • Anti-GAD antibodies attacking B cells
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3
Q

Give an example of steroid induced diabetes cause

A
  • Cushing’s disease : cortisol excess due to tumour secreting TH
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4
Q

Explain MODY , its frequency and features

A
  • maturity onset diabetes of the young
  • rare , genetic form
  • could respond to other treatments that insulin
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5
Q

Diagnostic criteria of T1DM

A
  • DKA
  • rapid weight loss
  • BMI < 25
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6
Q

Diagnostic criteria of T2DM

A
  • HbA1C > 48 ( 2 times 3m apart )
  • Fasting plasma glucose > 7
  • Random plasma glucose > 11.1
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7
Q

Is HbA1c used fro T1DM diagnosis

A

no

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8
Q

When can HbA1c not be used for diagnosis

A
  • increased cell turnover ( pregnancy )
  • anaemia
  • haemoglobinopathies
  • rapid blood glucose level rise ( illness, drugs )
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9
Q

What does an HbA1c less than 48 show

A
  • can still have type 2 diabetes
  • 42-47 is at high risk
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10
Q

What is the target HbA1c based on

A
  • based on the individual
  • usually between 53 to 48
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11
Q

What type of management is used for T2DM (6 factors)

A
  • multifactorial management
    1- education
    2- lifestyle ( smoking, alcohol)
    3- control BP (antihypertensive )
    4- statin for increase lipids
    5- Anti-platelet ( aspirin ) for micro and macro vascular issues
    6- control blood glucose (Metformin )
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12
Q

Non-pharmacological management of T2DM

A
  • education
  • dietician
  • podiatrist ( foot care )
  • retinal photography
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13
Q

What to look out for in DM

A

K- kidneys
E- eyes
V- vascular
I- infection
N- neuropathy
S- skin

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14
Q

What is the list of drug treatments for DM ( 8 ) - good luck

A

1- Biguanides ( metformin )
2- Sulfonylureas ( Gliclazide)
3- Glucagon like peptide (liraglutide, exanitide )
4- Dipeptidylpeptidase IV inhibitors ( sitagliptin)
5- Sodium-glucose cotransport2 inhibitor (dapagliflozin )
6- Thiazolidineodiones (pioglitazone)
7- Meglitinides ( repaglinide)
8- aGlucosidase inhibitors (acarbose)

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15
Q

Choice of therapy for a diabetic patient

A
  • Lifestyle measures for everyone
  • if HbA1c is greater than 48 then start on monotherapy metformin ( first-line)
  • Alternatives if metaformin is not tolerated
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16
Q

What medications should people with high risk of CVD or CKD be using (specify )

A
  • GLP-1 RA or SGLT2 inhibitors
  • patients with CVD risk GLP-1 RA
  • SGLT2 inhibitors for patients with HF , CKD , microalbuminuria
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17
Q

Adverse effects of SGLT2 inhibitors

A
  • feet swell
  • increase risk of amputation
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18
Q

Describe MOA of metformin ( 3)

A

1- activates liver AMP kinase reducing liver glucose output
2- Increases liver, muscle and fat cell sensitivity to insulin
3- Enhances glucose peripheral uptake and utilization ( sensitizes peripheral tissue )

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19
Q

What is a key advantage of metformin

A

enhances natural insulin signal so unlikely to cause hypoglycaemia on its own

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20
Q

Metformin adverse effects

A
  • weight loss
  • GI adverse effects (nausea, wind, diarrhoea )
  • rare : lactic acidosis
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21
Q

How to minimize metformin adverse effects

A
  • start with low dose with meals (once or twice a day)
  • can switch to modified release if still getting adverse effects ( more expensive )
22
Q

What happens if kidney function goes down while patient is on metformin ? At wha level will we have to stop metformin

A
  • stop metformin due to risk of lactic acidosis
  • stop if serum creatinine is above 150 and GFR is less than 30
23
Q

Why is metformin used in patients with adequate renal function

A
  • the cardioprotective gains outweigh lactic acidosis concert if patient has mild to moderate liver dysfunction or cardiac impairment
24
Q

MOA of Sulfonylureas ( SU ). give example drug

A

1 - bind to sulfonylurea receptor , closing ATP K+channels
2- decrease in K efflux increases Ca influx
3- Beta cell depolarizes and insulin releases
- ex : Gliclazide

25
Q

What is the limitation of Sulfonylureas

A
  • only works on t2 diabetes patient with functioning beta cells
  • effect may be antagonized by corticosteroid and thiazide like diuretics
26
Q

Adverse effects of Sulfonylureas

A
  • prolonged hypoglycaemia (forcing pancreas to squeeze out insulin despite blood glucose )
  • weight gain ( insulin is an anabolic hormone so it causes storage )
  • hyponatraemia
  • oedema
  • hepatotoxicity
  • photosensitivity
  • allergy
  • rash
27
Q

What is Incretin and MOA

A
  • 30 amino acid polypeptide hormone
  • stimulated by lipid and carb in meal , release GLP-1
  • binds to G protein receptors in beta cells to increase insulin secretion
28
Q

How is Incretin degraded

A
  • degraded by dipeptidyl peptidase IV ( DPP-IV)
  • inhibits glucagon secretion , glucose output , gastric emptying
  • promotes satiety
29
Q

How to promote Incretin effect and give examples of each method

A

1- make artificial GLP-1 : resistant to DPP-IV , promotes insulin signal for longer
ex: exenatide
2- promote going on of natural GLP-1 signal by switching off DPP-IV signal
ex: sitagliptin

30
Q

How is GLP-1 RA administered and adverse effects

A
  • subcutaneous infection
  • effects : GI disturbance , weight loss , hypoglycaemia if used with other med , increase pancreatitis risk
31
Q

NICE guidelines for GLP-1 RA

A
  • stop after first 6 months is HbA1c and weight hasn’t dropped
  • don’t use in patients with gastroparesis ( stomach not emptying already )
32
Q

Which is more effective GLP1-RA or DPPIV inhibitors

A

GLP1-RA

33
Q

How is DPPIV inhibitors administered and adverse effects

A
  • tablet
  • effects : increase hypoglycaemia risk , small weight gain or neutral , Resp infection , nausea , headache
34
Q

NICE guidelines for DPPIV inhibitors

A

stop after 6 months if HbA1c hasn’t decreased 5-6mmol

35
Q

What are the SGLT isoforms and what does each of them do

A
  • two isoforms : 1 & 2
  • large proteins that help absorb sugars
  • SGLT1 : made in small intestine and responsible for glucose and galactose absorption
  • SGLT2 : manages reabsorption in PCT of glucose ( reabsorbs about 99% of filtered glucose )
36
Q

What is the MOA of SGLT2 inhibitors. Give drug example

A
  • drug dapagliflozin blocks SGLT2 action in PCT
  • reduce renal threshold for glucose = excess glucose is excreted in urine as reabsorption is decreased
  • lowers blood glucose levels
37
Q

What contradicts SGLT2 inhibitors

A
  • if kidney function is not good and eGFR is below 45
38
Q

Adverse effects of SGLT2 inhibitors

A
  • weight loss
  • small decrease in SBP
  • polyuria
  • increase urinary tract infections
  • increase acute kidney injury
  • ketoacidosis
  • increase osteoporosis risk
  • increase amputation risk (stop if there’s limb complications )
39
Q

How is SGLT2 inhibitors used

A
  • add on therapy to metformin or insulin
40
Q

What is the advantage with Empaglifozin

A
  • may reduce risk of adverse CV outcomes such as CV death and heart failure
41
Q

SGLT2 inhibitors drug interactions

A
  • diuretics
  • ACE
  • NSAID
42
Q

Use of Insulin in type 2 diabetes (along with what , what is stopped , intensity ?)

A
  • added onto oral therapies (usually metformin ) because it reduces weight gain and offers CV protection
  • stop Sulfonlyureas and TZD for hypoglycaemia and heart failure risk
  • patient starts with single dose of intermediate acting insulin
  • intensifying insulin regimen could be required depending on patient
43
Q

Indication for insulin use in T2DM ( 7 )

A
  • significant hyperglycaemia at present
  • hyperglycaemia despite maximal oral doses
  • surgery
  • pregnancy
  • renal disease
  • allergy to oral drugs
  • decompensation : uncontrolled weight loss , ketonuria , injury
44
Q

What does the insulin regimen of a patient depend on

A
  • predictable caloric consumption = stable insulin regimen
  • unpredictable patients : intensified insulin regimen ( short )
45
Q

What are Thiazolidinediones

A
  • drugs impacting fatty acid metabolism by binding to PPAR receptors
  • located in adipose tissue , skeletal muscle and large intestine
  • only work in presence of insulin
46
Q

MOA of Thiazolidinediones

A
  • cause PPAR complex to bind with DNA to promote transcription of genes involved in insulin signalling
  • increase sensitivity of tissues to insulin by recruiting GLUT
  • overall : reduce insulin resistance , uptake of glucose and fatty acids
47
Q

When is Thiazolidinedione used

A
  • T2DM patients with inadequate control of hyperglycaemia & significant insulin resistance
  • not T1DM since they have no endogenous insulin
48
Q

Thiazolidinediones adverse effects

A

1- Hepatotoxic : LFT monitored
2- weight gain
3- potential for heart failure esp with insulin combination

49
Q

What are Meglitinides and how often are they used

A
  • non-sulfonylurea oral hypoglycaemic agents
  • stimulate insulin secretion from B cells but faster than sulfonylurea
  • rarely used
50
Q

What is Acarbose, its purpose, adverse effects any how often is it used

A
  • intestinal Disaccharidase inhibitors
  • inhibit carbohydrate absorption in gut
  • High GI side effects
  • not used due to low tolerability
51
Q

What is usually used along with Diabetic treatments

A

1- ACE I and ARB if not contraindicated to control BP
2- Atorvastatin for lipid management

52
Q
A

GERR Pharmacology (9 decks)

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