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Medicine block (Y3) > Week 5: Diabetes (2) (pharmacology) > Flashcards

Week 5: Diabetes (2) (pharmacology) Flashcards

1
Q

Type 1 diabetes mellitus
Diagnosis

A
  • Fasting glucose >6.9 mml/L or random plasma glucose >11 mmol/L
  • Plasma or urine ketones
  • HbA1C >48 mmol/mol
  • A single raised plasma glucose without symptoms not sufficient for diagnosis ( would need several blood tests in the absence of symptoms)
  • *Diagnostic factors**
  • Rapid onset symptoms
  • Polyuria (nocturia)
  • Polydipsia (needing to wake at night for water)
  • Weight loss
  • Fatigue/lethargy
  • Generalised weakness
  • Blurred vision
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2
Q

Glucose vs HbA1c

A
  • Glucose = an immediate measure of glucose levels in blood mmol/L
  • Haemoglobin A1c- glycated haemoglobin
    • % of RBC with sugar coating
    • Reflects average blood sugar over last 3 months (mmol or %)
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3
Q

Diabetic ketoacidosis (DKA) Biochemical triad of

A
  1. Hyperglycaemia
  2. Ketonemia
  3. Acidosis
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4
Q

DKA predominantley found in

A
  • T1DM
  • Common in children on diagnosis
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5
Q

When to suspect DKA

A
  • Blood glucose >11 mmol AND
  • Polydipsia
  • Polyuria
  • Abdominal pain
  • Acetonic breath
  • Confusion
  • Lethargy
  • Visual disturbances
  • Symptoms of shock
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6
Q

precipitating factors for DKA

A
  • Infection
  • Trauma
  • Non-adherence to insulin treatment
  • DDIs
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7
Q

diagnosis of DKA

A
  • Blood glucose >11mmol (may not always be present = euglycemia)
  • Test for ketones in blood and urine
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8
Q

DKA treatment

A
  • Initially i.v.i fluid (with potassium) and then i.v.i soluble insulin
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9
Q

Therapeutic insulins

A
  • Historically bovine and porcine (immunogenicity concerns)
  • Now use human insulin
    • Recombinant DNA (bacteria/yeast)
  • Protein therefore must given parenterally to avoid digestion
  • Usually formulation in 100 units/mL
    • Due to obesity and insulin resistance there are higher doses (300 and 500 units/mL(
    • NEVER abbreviate units or international units → dangerous mistake could be made
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10
Q

Emerging therapeutics

A
  • Immunotherapy- monoclonal antibodies for high risk group
    • Delay progression
  • Islet transplantation
  • Islet cell regeneration
  • Inhaled insulin
    • Pharmaceutical challenge
  • SGLT-2 inhibitors
    • TI and TII DM and other CVDs
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11
Q

Pharmacokinetics of insulin therapy

A
  • Routine delivery= subcutaneous injection in upper arm, thighs, buttocks, abdomen
  • Emergency e.g. DKA= i.v.i (IV infusion)

Half life of insulin in plasma is short (5 mins) therefore we need to slow absorption via a few methods

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12
Q

Half life of insulin in plasma is short (5 mins) therefore we need to slow absorption via a few methods:

A
  • For bovine and porcine insulins adding protamine and/or zin complex – used less now
    • Delays dissolving
    • Soluble (neutral) insulin forms hexamers
      • Delaying absorption from site of injection
      • [plasma] insulin will be highest after 2-3 hours (dosing 15-30 min prior to meals)
    • Insulin analogues
      • Recombinant modifications- a few amino acid changes
      • Changes PK and not PD
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13
Q

Effects of different insulin available

A
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14
Q

prescribing insulin

A

Prescribing insulin

  • Many preparations available
  • Combinations often prescribed
    • Short and long-acting mixtures
    • May take them separately
      • Basal bolus dosing- common
  • Methods of injecting
    • Syringes
    • Pens
    • Pumps
    • Inhalers?
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15
Q

drug class of insulin

A

hormonal drug

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16
Q

mOA of insulin

A
  • Insulin binds to insulin receptor
  • Causes cascade of events which causes GLUT4 receptors to translocate from the cytoplasm to the membrane
  • GLUT4 increases uptake of glucose into the cell lowering blood glucose
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17
Q

ADR insulin

A

Adverse drug response

  • Hypoglycaemia
  • Lipodystrophy
    • Lipohypertrophy or
    • lipoatrophy
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18
Q

Basal bolus dosing

A

A common dosing schedule for young active TIDM patients which provides some flexibility if adherence is good

  • Basal- long acting e.g. glargine
    • Given once a day
  • Bolus- rapid acting e.g. aspart
    • Given before meals
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19
Q

management of T@DM

A

Management

  • Lifestyle
  • Education
  • Weight loss
  • Initially non-insulin therapies
    • May form part of treatment plan in poorly managed or later stage disease
  • Treatment with hypoglycaemic agents
    • Can cause weight gain- makes adherence to sustained successful therapy a challenge
  • Treatment of comorbidities
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20
Q

classes of glucose lowering drugs

A

sulphonylureas

biguanides

glitazones

dipeptidyl peptidase-4 DDP (gliptins)

SGLT-2 (gliflozins)

GLP-1 receptor agonists (incretin mimetics)

1

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21
Q

biguanides example

A

metformin

22
Q

sulphonylureas example

A

glicazide

23
Q

glitazone example

A

pioglitazone

24
Q

DDP-4 inhibitor example

A

saxagliptin

sitagliptin

25
Q

SGLT-2 inhibitors

A

canagliflozin

26
Q

GLP-1 receptor agonist

A

exenatide

liraglutide

27
Q

metformin

A

biguanide

  • First line treatment for T2DM
28
Q

metformin MOA

A
  • Reduces hepatic glucose production by inhibiting gluconeogenesis
  • Some gluconegenic activity remains so hypoglycaemia risk reduced
  • Also: suppresses appetite to limit weight gain
29
Q

ADR metformin

A

nausea

vomiting

diarrhoea

30
Q

metformin contraindication

A
  • eGFR <30 mL/min
    • excreted unchanged by kidneys
  • alcohol intoxication
31
Q

metformin DDI

A

Drug-drug interaction

  • ACEi (drugs which impair renal function)
  • Diuretics (drugs which impair renal function)
  • NSAIDs (drugs which impair renal function)
  • Loop and thiazide like diuretics which increase glucose so can reduce metformin action
32
Q

gliclazide

A

sulfonylureas

used

  • Typically in combination with other agents or a first line option if metformin contraindicated
33
Q

gliclazide MOA

A
  • Inhibit ATP-dependent K+ channels causing membrane depolarisation
  • Causes calcium into the cell
  • Stimulate B cell pancreatic insulin secretion by blocking
  • NEED PANCREATIC FUNCTION TO WORKA
  • Can cause weight gain through anabolic effects of insulin
34
Q

ADR glicazide (SU)

A
  • Mild GI upset
    • Nausea
    • Vomiting
    • Diarrhoea
  • Hypoglycaemia (works at low [glucose])
35
Q

contraindication gliclazide (SU)

A
  • Hepatic disease
  • Renal disease
  • Caution of those at risk of hypoglycaemia
36
Q

DDI gliclazide (SU)

A
  • Other hypoglycaemic agents
  • Loop and thiazide like diuretics (increase glucose so can reduce SU action)
37
Q

dapagliflozin

A

SGLT-2 inhibitor

Uses

  • adjunct to insulin in T1DM (high BMI)
  • T2DM as an add on therapy
    • Modest weight loss, hypoglycaemic risk is low
38
Q

MOA of gliflozins

A
  • Competitive reversible inhibition of SGLT-2 in PCT
  • Decrease glucose absorption from tubular filtrate
  • Increase glucose excretion
39
Q

ADR gliflozins

A
  • UTI (sugar urine)
  • Genital infections
  • Thirst
  • Polyuria
40
Q

contraindication gliflozins

A
  • Risk of DKA in T1DM
  • Possible hypotension
41
Q

DDI gliflozins

A
  • Antihypertensives
  • Other Hypoglycaemic agents
42
Q

Physiological effect of GLP-1 (incretin hormone)

A
  • In the pancreas
    • Increases insulin secretion
    • Decrease glucagon secretion
    • Increase insulin biosynthesis
43
Q

Drugs which target GLP-1 actions

A
  • Dipeptidyl peptidase- 5 (DPP-4) inhibitors (Gliptins)
    • Glucagon-like peptide-1 (GLP-1) receptor agonists (incretin mimetics)
44
Q

sitagliptin

A

Dipeptidyl peptidase- 5 (DPP-4) inhibitors (Gliptins)

45
Q

MOA of gliptins e.g. DPP-4 inhibits

A
  • Prevent incretin (GLP-1) degradation – increasing plasma incretin levels
  • Glucose dependent so postprandial action
  • Will not stimulate insulin secretion at normal blood glucose- lower hypoglycaemic risk
  • Supress appetite- due to GLP-1 action in satiety
  • Weight neutral
  • Given subcutaneously like insulin – protein therefore would be digested if given enterally
46
Q

ADR gliptins

A
  1. GI upset
  2. Small pancreatitis risk
47
Q

contraindications gliptins

A
  1. Avoid in pregnancy
  2. History of pancreatitis
48
Q

DDI gliptins

A
  1. Other hypoglycaemic agents
  2. Drugs increase glucose can oppose gliptin action- thiazide like and loop diuretics
49
Q

exenatide

A

GLP receptor agonist- incretin mimetic

50
Q

mode of action of exenatide (GLP-1)

A
  • Increase glucose dependent synthesis of insulin secretion from B cells by activating GLP-1 receptors (resistance to degradation by DPP-4)
  • Subcutaneous injection
  • Promotes satiety- possible weight loss
51
Q

ADR exenatide

A
  • GI upset
  • Decreased appetite with weight loss

Medicine block (Y3) (38 decks)

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