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CEP > Treatment Of Diabetes > Flashcards

Treatment Of Diabetes Flashcards

1
Q

What does insulin stimulate through enzymatic activity

A

Catalyses oxidation of glucose for ATP prod
Polymerises glucose to glycogen
Converts glucose to fat

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2
Q

How does the body respond to insulin deficiency

A

Decreased uptake of glucose uptake and utilisation
Glycogenolysis
Protein catabolism
Gluconeogenesis
Lipolysis
Ketogenesis

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3
Q

Conditions due to diabetes mellitus

A

Hperglycemia
Glycosuria - glucose in urine
Osmotic diuresis - increased urine
Lipidemia + ketoacidosis
Ketonuria
Loss of Na and K
Electrolyte and acid base imbalances

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4
Q

Signs and symptoms of diabetes mellitus due to hyperglycaemia

A

Polyuria - dehydration and soft eyeballs
Poydipsia - thirst
Polyphagia - hunger
Fatigue
Weight loss

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5
Q

Signs and symptoms due to ketoacidosis

A

Acetone breath
Hypernea
Nausea/ abdominal pain
Cardiac irregularities
CNS depression

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6
Q

How is secretion of insulin regulated

A

Mostly by glucose levels
GI hormones

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7
Q

Mechanism of how insulin is secreted

A

Glucose enters beta cells via GLUT 1/3 transporter
Produce ATP (via glycolysis pathway)
Reduces activity of ATP sensitive K channel
Reduces K efflux causing depolarisation (when glucose low beta cell in hyperpolarised state)
Opens Ca channels which cause exocytosis of insulin

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8
Q

Diabetes caused due to glucose transporters becoming:

A

Unresponsive
Less sensitive

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9
Q

What is biphasic insulin release

A

Allows glucose to reach cells to be metabolised
2 peaks of insulin secretion
1st peak: stimuli of food causes pancreases to rapidly secrete insulin. Allows feelings of satiety.
2nd peak: when food passed through to stomach to small intestine. Allows glucose absorption.

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10
Q

Which peaks do type 1 and type 2 miss in the biphasic release of insulin

A

Type 1: both peaks not present
Type 2: 1st peak missing
So diabetes patients can eat more because dont have feelings of satiety (1st peak)

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11
Q

Biological structure of insulin receptor

A

2 alpha subunits - extracellular binding site
2 beta subunits - transmembrane tyrosine kinase

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12
Q

What happens when substrate binds to insulin receptor

A
  1. Phosphorylation of insulin receptor substrate proteins
  2. Enzyme activation and gene transcription
  3. Increase in glucose uptake via expression of GLUT 4 transporter
  4. Increased glycogen synthesis
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13
Q

What are the main groups of drug given by injection

A

Insulin in various forms/ formulations
Incretin mimetics e.g. exenatide, liraglutide - mimic hormones tat regular activity of insulin (GI hormones)

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14
Q

Main groups of oral drugs

A

Biguanides - metformin
Sulfonylureas & related drugs
Thiazolidinediones
Gliptins
Glucose transporter inhibitors

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15
Q

Causes of diabetes mellitus type 1

A

Genetics
Autoimmune response leading to beta cell loss

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16
Q

Management of type 1

A

Carbohydrate counting
Dietary advice
Managing insulin doses to minimise glucose fluctuations when changing diet (patient specific)

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17
Q

How exercise effects type 1 diabetes patients

A

Reduced cardiovascular risk
Effects to insulin dosage and carb intake
Regular HbA1c measurement (lower the measurement the better)

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18
Q

Self monitoring of plasma glucose

A

Finger prick
Continuous monitoring devices

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19
Q

Why does insulin need to be injected

A

Peptide hormone
Broken down by digestive tract enzymes

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20
Q

Types of human (recombinant DNA) insulin

A

Short acting: onset 30 mins, peak 2-4 hrs, soluble insulin, insulin lispro

Long acting: onset 1-2 hrs, peak 4-12 hrs, insulin complexes , insulin glargine

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21
Q

Different Dose regimes for insulin

A
  1. Short acting 3 times before meals + intermediate/ long acting once or twice
  2. Pre mixed short and intermediate acting insulin
  3. Continuous infusion - for patients that poorly manage treatment
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22
Q

Complications of insulin treatment

A

Fluctuations of blood glucose: hypo/hyper
Allergy
Lipodystrophy - inject to same set can cause change in fat consumption

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23
Q

Contraindications of insulin

A

Insulin compliance - psychosocial impacts (complex and demanding patients)
Eating disorders
Restrictions - driving/ jobs

24
Q

Complex cause of diabetes mellitus type 2

A

Genetics
Socioeconomic factors - poor diet due to poverty
Demographic factors - diff populations have diff likelihood

25
Q

Causes of type 2 diabetes

A

No major loss of beta cells
Increased basal insulin levels in blood
Loss of 1st phase of insulin secretion

26
Q

How is insulin resistance caused in type 2 diabetes

A

Dysfunction of IR signalling cascade proteins
Associated with inflammation in adipose tissue

27
Q

Management of Pre diabetic

A

Vaccine? None successful yet

28
Q

Primary management of type 2 diabetes

A

Diet
Exercise
Lifestyle modification
Intermittent fasting
VLCD - very low calorie diet

29
Q

Type 2 management, if primary defence doesnt work and HbA1c still high:

A

Drugs (ACE inhibitors, statins)
One third of patients will eventually need insulin

30
Q

Effects of biguanides (metformin) that lower blood glucose

A

Decreases gluconeogenesis
Via activation of AMP activated protein kinase (AMPK) - gene expression is decreased

Decreases carbohydrate absorption in intestine

Increases glucose uptake by skeletal muscle

31
Q

Side effects of using biguanides

A

No high appetite
Lactic acidosis esp. with alcohol use
Gastrointestinal disturbances

32
Q

Treatment for obese diabetics

A

Biguanides with acarbose (reduce carb absorption in gut)

33
Q

What is acarbose?

A

Alpha glucosidase inhibitor - decreases CHO absorption
Used for obese
May be gastrointestinal disturbances

34
Q

Examples of sulfonylureas

A

Tolbutamide
Glibenclamide
Glipizide

35
Q

Mechanism of sulfonylureas

A

Beta cells - bind to SUR (part of K(ATP) channel)
Binding causes channel to close
Depolarisation of beta cell
Ca entry and increases insulin secretion

Secondary effect: Increases tissue sensitivity to insulin

36
Q

Duration of action of Sulfonylureas

A

Long acting - glibenclamide (active metabolite 10hr
Short acting - tolbutamide 4hr

37
Q

Side effects of sulfonylureas

A

Hypoglycaemia
Diuretic actions

38
Q

Examples of other SUR modulators

A

Repaglinide
Nateglinide

39
Q

What is repaglinide

A

No sulfonylurea moiety!
Binds to SUR (sulfonylurea receptors) - decreases K(atp) activity
Shorter duration of action: less potent
More selective for K(atp) channels in B cells (as there are K(atp) channels on cardiac cells)
Administered prior to meal

40
Q

Side effects of SUR drugs

A

Hypoglycaemia (less with repaglinide)
Stimulate appetite (don’t use for obese patients)
Contraindicated in pregnancy/ breastfeeding

41
Q

What are SUR and how they can increase insulin secretion

A

Sulfonylurea receptors in contact with K(atp) channels
Sulfonylurea and glinides (SUR modulators) can bind to SUR
Activation of SUR blocks K(atp) channel
Causing depolarisation
And Ca influx
Increasing insulin secretion

42
Q

Actions of thiazolidinediones (e.g. pioglitazone)

A

Binds to TF: affects gene expression
Primary action: adipose tissue. Increase fatty acid uptake and lipogensis
Secondary affect: decreases plasma fatty acids. Increases glucose update. Decreases gluconeogenesis.

43
Q

Primary action of thiazolidinediones on adipose tissue

A

Increased fatty acid uptake
Increased lipogenesis

44
Q

How does insulin affect fatty acid oxidation

A

Insulin decreases fatty acid oxidation
Decreases triglyceride breakdown
So more fatty acid substrate

45
Q

Secondary effect of thiazolidinediones on lowering plasma fatty acids

A

Increased glucose uptake
Decreased gluconeogenesis

46
Q

Side effects of thiazolidinediones

A

Weight gain
Liver toxicity
Heart failure due to fluid retention
Used less frequent now due to bad side effects

47
Q

What are drugs based on incretin actions

A

Incretins: GI hormones. Created in gut and released after meal regulate insulin.
Regulate insulin secretion

48
Q

How do incretin acting drugs act like GLP-1 agonists:

A

Act on pancreas and increase insulin
Slows gastric emptying
Lowers BGL after meal
Induce satiety

49
Q

What are incretin hormones and examples

A

GLP-1
GIP
Released from GIT in response to nutritional absorption

50
Q

What are sodium glucose transporter 2 (SGLT2) inhibitors

A

Canagliflozin
Rapidly absorbed
Peak plasma conc in less than 2 hours

51
Q

Examples of sodium-glucose transporter 2 (SGLT2) inhibitors

A

Empagliflozin
Canagliflozin (usually used in combination)

52
Q

Mechanism of sodium-glucose transporter 2 (SGLT2) inhibitors

A

Kidney - proximal convoluted tubule
Increased glucose and Na loss
Promotes osmotic diuresis
So less glucose reabsorbed from tubule
Excess glucose passed out into urine

53
Q

Cautions and side effects of sodium glucose transporter 2 (SGLT2) inhibitors

A
  • Peripheral vascular disease
    Hypotension
    Dehydration
  • Ketoacidosis
    Urinary tract infections
54
Q

What are thiazolidiediones used in combination with

A

SU (sulfonylureas) or metformin

55
Q

How do gliptins work

A

E.g. linagliptin
Block breakdown of incretins
Inhibitors of dipeptidyl peptidase-4 (membrane)

56
Q

What is exenatide

A

GLP-1 agonists
Expensive
Used in combination
Slows gastric emptying (for obese)

CEP (12 decks)

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