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HHD 2 > Drugs to treat Diabetes > Flashcards

Drugs to treat Diabetes Flashcards

1
Q

What is the normal range of blood glucose before a meal?

A

4-6mmol/L

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2
Q

What is the normal range of blood glucose after a meal?

A

7-8mmol/L

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3
Q

What is hypoglycaemia ?

A

this is when the blood glucose is below normal <4mmol/L

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4
Q

What are the consequences of hypoglycaemia ?

A

confusion and loss of consciousness; as the brain cells are starved of glucose
hypoglycaemia coma and possible death if not treated promptly

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5
Q

What is the treatment for hypoglycaemia ?

A

to administer glucose

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6
Q

What is hyperglycaemia?

A

this is when blood glucose levels are above normal
fasting levels >7mmol/L
random levels >11mmol/L

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7
Q

What are the consequences of hyperglycaemia

A

damage to endothelial cells lining the lumen of the blood vessels
microvascular complications- damage to capillaries in retina (retinopathy), kidneys (nephropathy)
macrovascular complications: poor peripheral circulation leading to tissue damamge (heart attack, stroke)
peripheral nerve damage (peripheral neuropathy)
damage to insulin producing cells in the pancreas
diabetic ketoacidosis
hyperglycaemic coma

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8
Q

What is ketoacidosis?

A

this is a metabolic state that is associated with pathologically high levels of serum and urine concentrations of ketones.
Occurs in hyperglycaemia and insulin deficiency which causes unopposed lipolysis and the oxidation of free fatty acids thus resulting in ketone production

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9
Q

What us diabetes mellitus?

A

this is a condition where the body cannot regulate the use of glucose properly so blood glucose levels become too high

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10
Q

Diabetes mellitus is the 9th leading cause of death with 1.5 million deaths caused by DM. True or false

A

True

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11
Q

The NHS spends what percentage of its budget on treating DM and its complications?

A

10%

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12
Q

What are the causes of diabetes mellitus ?

A

genetics
gender
relocation
lifestyle- diet, exercise

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13
Q

When was the earliest known record of diabetes made? What was reported?

A

1552 BC by a physician Hesy- Ra who reported/mentioned frequent urination

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14
Q

When was diabetes first named? What are the origins?

A

Greek Physician Aretaeus of cappadocia named the condition diabetes in 100 AD
Diabetes is greek for siphon; came about since people with diabetes urinated so often

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15
Q

How was diabetes originally diagnosed in the 1100s AD?

A

urine of those with diabetes thought to be sweet tasting
Water tasters drank urine of those thought to have diabetes

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16
Q

When was mellitus added to diabetes? What are the origins of mellitus ?

A

1700s AD by an edinburgh trained surgeon John Rollo
comes from Latin and Greek words meaning honey

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17
Q

When were important discoveries made regarding better understanding and treatment of diabetes mellitus?

A

1800’s and onwards

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18
Q

What are the two types of cells in the pancreas?

A

exocrine cells (secrete pancreatic fluids containing digestive enzymes)
endocrine cells

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19
Q

What are the islet of langerhans?

A

regions of the pancreas that contains endocrine cells discovered by a German medical student Paul Langerhans
Help produce the hormone insulin

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20
Q

The islet of langerhans make up __% of the pancreas

A

4.5%

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21
Q

What cells in the pancreas are responsible for the production of digestive enzymes?

A

acinar cells

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22
Q

What is a hormone?

A

a chemical messenger produced by a particular gland or cells of the endocrine system

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23
Q

What is endocrine signalling?

A

this is when signalling molecules from the signalling cel travel through the bloodstream to the target cell

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24
Q

What is paracrine signalling?

A

this is when the signalling and target cell are close together

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25
Q

What is autocrine signalling?

A

this is when the signalling and target cell are the same cell

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26
Q

Glucagon is produced by …

A

alpha cells of the pancreas

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27
Q

What is the effect of glucagon on blood glucose?

A

raises blood glucose levels
causes the liver to convert stored glycogen into glucose which is released into the blood stream

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28
Q

Insulin is produced by which cells?

A

beta cells

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29
Q

What is the effect of insulin on blood glucose?

A

lowers blood glucose levels
cells in the liver, muscle and fat tissue take up glucose from the blood, storing it as glycogen in the liver and the muscle

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30
Q

The islet of langerhans contain four type of cells. List them and what they produce

A

Alpha cells- glucagon
Beta cells- insulin
Delta cells - somatostatin
P(F) cells- pancreatic polypeptide

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31
Q

What hormone is released by the pancreas in hypoglycaemia ?

A

glucagon
(raise blood glucose levels)

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32
Q

What hormone is released by the pancreas in hyperglycaemia?

A

Insulin
to lower blood glucose levels

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33
Q

What is the effect of glucagon on hepatocytes?

A

glucagon binds to receptors on hepatocytes and causes glucose channels to open

this then switches on enzymes that breakdown glycogen into glucose

this allows glucose to flow through the cell membrane out of the cell (via the glucose channels)

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34
Q

What is glycogenolysis?

A

breakdown of glycogen into glucose

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35
Q

Describe on a molecular level what occurs in order to resolve hyperglycaemia in liver cells

A

(liver/muscle/fat cells)
Insulin is released by beta cell in the islet of langerhans in response to high blood glucose
insulin binds to receptors on hepatocytes
this causes glucose transporters (GLUT2) to open
this allows glucose to flow though the cell membrane into the cell
insulin binding also switches on enzymes that convert glucose to glycogen

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36
Q

What is gluconeogenesis?

A

It is a pathway by which non-hexose precursors such as glycerol, lactate, pyruvate and glucogenic amino acids are converted into glucose for storage

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37
Q

What is the main glucose transporters expressed in hepatocytes?

A

GLUT2

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38
Q

What is the main glucose transporter expressed in striated muscle?

A

GLUT4

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39
Q

Describe on a molecular level what occurs in order to resolve hyperglycaemia in striated muscle cells

A

insulin binds to receptors on the striated muscle cells
this opens glucose transporters (GLUT4)
this allows glucose to flow through the cell membrane into the cell
insulin binding also switches on enzymes that converts glucose to glycogen

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40
Q

Describe on a molecular level what occurs in order to resolve hyperglycaemia in adipocytes

A

insulin binds to receptors on the adipocytes
this opens GLUT4 transporters
this allows glucose to flow through the cell membrane into the cell
glucose undergoes a number of actions to form glycerol
one glycerol molecule binds to 3 fatty acid molecules to form a triglyceride

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41
Q

As opposed to glycogen, what transformation to glucose is performed in adipocytes?

A

glucose forms glycerol

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42
Q

What is insulin resistance?

A

this is a pathological condition in which cells fail to respond normally to the hormone insulin

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43
Q

What does a disruption in the insulin signalling pathway in hepatocytes, skeletal muscle cells and adipocytes lead to ?

A

prevent the uptake of glucose into these cells
resulting in elevated blood glucose levels
Leads to type 2 diabetes

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44
Q

Briefly describe how glucose sensing leads to insulin release in beta cells

A

glucose enters beta cells via GLUT2 glucose transporters
glucose is metabolised by GCK (glucokinase)
metabolism of glucose causes an increase in ATP:ADP ratio
increase in ATP:ADP ratio is detected by Katp channels (potassium channels)
The K+ channels close (preventing loss of K+ ions) which leads to depolarisation of the cell- as it becomes more positive
depolarisation to opening of voltage gated calcium ion channels which allow calcium ions diffuse into the cell
Ca2+ induced exocytosis of insulin occurs

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45
Q

Aside from glucose, what other molecules can cause the pancreatic beta cell to release insulin?

A

amino acids
hormones
neurotransmitters

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46
Q

Briefly describe a mechanism outside of glucose sensing by which beta cells release insulin

A

Incretins such as GLP1 (glucagon like peptide) are hormones released from intestinal endocrine cells

they travel in the blood (as per endocrine signalling) and bind to receptors on beta cells which result in intracellular signalling

Intracellular signalling causes released of calcium ions from intracellular stores

Calcium induced exocytosis of insulin occurs

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47
Q

How are drugs designed to treat type 2 diabetes?

A

the drugs can target the disrupted pathways to try and correct insulin release

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48
Q

What are the other names of type I diabetes?

A

insulin dependent diabetes mellitus
juvenile diabetes

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49
Q

When does T1DM develop?

A

usually before the age of 20
with a peak at 12 years old

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50
Q

What is the cause of T1DM?

A

autoimmune destruction of pancreatic beta cells
insufficient or non existent production of insulin

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51
Q

Symptoms of T1DM often develop quickly. What are they?

A

tiredness
excessive urine production (polyuria)
weight loss
increased thirst (polydipsia)
blurred vision
in extreme cases, coma
blood glucose levels >11mmol/L (random)
muscle cramps
GI symptoms such as nausea and vomiting, abdominal pain and changes in bowel movement
diabetic ketoacidosis (serum and urine ketones due to unopposed lipolysis)
UTIs

52
Q

What is the treatment of T1DM?

A

insulin injections and lifestyle changes which include diet control and regular exercise

53
Q

What is are the other names for T2DM?

A

non insulin dependent diabetes mellitus
adult onset diabetes

54
Q

What is the onset of T2DM

A

usually after the age of 40
increase in obesity leading to younger sufferers (in 90% of cases obesity is the cause in <40 sufferers)

55
Q

What is the cause of T2DM?

A

reduced amount of insulin or cells stop responding to insulin produced (insulin resistance)

56
Q

What are the symptoms of T2DM

A

tiredness
excessive urine production
weight loss
increased thirst and blurred vision

57
Q

What is the difference in symptom presentation between T1DM and T2DM?

A

T2DM symptoms are less severe and may go undetected for many years

58
Q

What are the treatments on offer for T2DM?

A

Lifestyle change - diet control, exercise
oral medication
sometimes insulin injections

59
Q

What test can indicate the presence of glucose in the urine?

A

a simple strip test

60
Q

When is T2DM often most diagnosed?

A

during health screening tests

61
Q

How is T2DM diagnosed ?

A

simple blood and urine tests may be sufficient for some people
others may take OGTT (oral glucose tolerance test)

62
Q

Describe a simple diagnostic test for T2DM (OGTT)

A

Patients are not allowed to eat for 12 hours before the test
blood sample is taken to measure the patients fasting glucose level
then the patient is given a drink containing 75g of glucose
this absorbed quickly and blood glucose is measured over the next 2 hours
individuals with diabetes become hyperglycaemic and blood glucose is above normal
(fasting >7mmol/L, 2 hours post glucose >11mmol/L)

healthy individual will release insulin which regulates their glucose back to normal

63
Q

List treatment options available for T1DM
(in T1DM, insulin resistance is not developed, receptors still respond to insulin)

A

injecting insulin to control blood sugar levels
insulin pens
pumps that deliver controlled amount throughout the day
nanopumps which deliver insulin from pumps the size of skin patches

64
Q

Natural insulin was purified from porcine or bovine pancreas, why was this stopped?

A

development of allergic reactions

65
Q

Natural insulin is now provided in what form?

A

human insulin using recombinant DNA technology

66
Q

How is insulin administered?

A

usually subcutaneously but can be given IV or IM in emergencies

67
Q

Natural insulin once absorbed has a short half-life of 10 minutes; how is the half-life prolonged?

A

protamine
zinc

68
Q

Insulin preparations can be divided into what 3 types?

A

short duration
intermediate duration
long duration

69
Q

What are short duration insulin preparations?

A

soluble insulin, rapid acting insulin analogues

70
Q

Give examples of short duration insulin preparations

A

insulin aspart
insulin glulisine
insulin lispro

71
Q

What are intermediate duration insulin preparations?

A

Intermediate-acting analogues

72
Q

Give examples of intermediate action preparations

A

isophane insulin

73
Q

Give examples of long acting insulin analogues

A

Protamine zinc insulin
insulin detemir
insulin glargine

74
Q

What are the side effects of insulin treatment?

A

hypoglycaemia
neuroglycopenia (shortage of glucose in brain)
rebound hyperglycaemia

75
Q

What is the cause of rebound hyperglycaemia following insulin induced hypoglycaemia?

A

due to release of counter hormone, adrenaline, glucagon, glucocorticoids to an attempt to raise blood glucose levels

76
Q

What are the insulin treatment regimens for T1DM?

A

single daily injection
twice daily injections
multiple injections
continuous subcutaneous infusion
intravenous insulin or intramuscula
intraperitoneal infusion (injection into peritoneal cavity)

77
Q

Single daily injections of insulin is the treatment regimen often adopted by…

A

elderly people with T2DM

78
Q

Twice daily injections of insulin is the treatment option suitable for …

A

stable activity and eating habits

79
Q

Multiple insulin injections are suitable for …

A

younger active people, flexibility

80
Q

Continuous subcutaneous infusions of insulin are suitable for what type of patients?

A

patients with recurrent hypos
the continuous therapy leads to improved glucose level control and reduced hypoglycaemia

the insulin induced hypoglycaemia is better controlled with continuous therapy

81
Q

Intramuscular or intravenous insulin is usually reserved for …

A

medical emergencies

82
Q

Intraperitoneal infusion is reserved for …

A

those who fail to reach adequate glycaemic control despite intensive subcutaneous intervention

83
Q

Give the classes of hypoglycaemic agents used to treat T2DM

A

Biguanide
Sulfonylureas
Thiazolidinediones (glitazones)
a-glucosidase inhibitors
inhibitors of renal glucose transport

84
Q

Give an example of a bisguanide used to treat T2DM

A

metformin

85
Q

What is the only biguanide used to treat T2DM

A

metformin

86
Q

Although the MOA of metformin is unclear, what does it cause?

A

reduction of hepatic glucose production (suppressing gluconeogenesis)
faciliation of glucose up-take and utilisation by skeletal muscle (reduces insulin resistance)
reduction of glucose absorption at the intestines
reduction of low density lipoproteins
reduction in appetite (less weight gain) useful in overweight patients

87
Q

What are the adverse effects of metformin?

A

does not cause hypoglycaemia ????
mainly dose related GI disturbances (anorexia, diarrhoea, nausea)
lactic acidosis (leading to a reduction in the body pH)
metallic taste

88
Q

Give examples of first generation sulfonylureas

A

tolbutamide

89
Q

Give examples of second generation sulfonylureas

A

glibenclamide
glipizide
glicazide
glimepiride

90
Q

Glibenclamide is a _____________ agent and therefore is not used in elderly. Give an example of a suitable sulfonylurea for elderly and state why.

A

long acting
Tolbutamide is suitable because there is a lower risk of causing hypoglycaemia

91
Q

What are the characteristics of sulfonylureas?

A

rapid absorption
highly protein bound
metabolised by the liver
excreted by the kidneys

92
Q

What is the mechanism of action of sulfonylureas?

A

they bind to Katp channels of beta cells(in pancreas)
they block the Katp channels (under normal circumstances this would have been blocked by ATP:ADP ratio)
this causes depolarisation of the beta cell, VGCC are opened as a result
this causes calcium mediated /induced insulin release

93
Q

What are the side effects of sulfonylureas?

A

hypoglycaemia
stimulated appetite causing weight gain (a concern in obese T2DM patients)

94
Q

What is the effect of the following drug interactions:
sulfinpyrazone (uricosuric drug to treat gout)
antibacterial drugs (trimethoprim, chloramphenicol)
imidazole antifungals
on sulfonylureas??

A

They compete with metabolising enzymes and plasma proteins thus inhibit metabolism of sulfonylureas and thus increase systemic exposure (toxicity)

This can as such lead to hypoglycaemia

95
Q

Briefly describe the interaction between alcohol and sulfonylureas

A

Alcohol decreases hepatic glucose production
in combination with sulfonylureas which stimulate the release of insulin
Patients are at an increased risk of hypoglycaemias

96
Q

The mechanism that causes an increased risk of hypoglycaemia when MAOI and sulfonylureas are taken concurrently is unclear. True or false

A

True

97
Q

What sulfoynlurea increases the risk of hepatotoxicity when Bosentan (for pulmonary arterial hypertension) is concurrently administered?

A

Glibenclamide

98
Q

Pioglitazone is a _______________.

A

Thiazolidinedione (glitazone)

99
Q

___________ is the only thiazolidinedione (glitazone) still clinically in use.

A

Pioglitazone

100
Q

Pioglitazone is marketed as a combination tablet with __________.

A

Metformin

101
Q

Why are the other thiazolidinediones not clinically use?

A

caused serious cardio and hepatotoxicity

102
Q

What is the MOA of pioglitazone?

A

increases endogenous insulin sensitivity and lowers blood glucose (reducing hepatic glucose output)

may reduce the need for exogenous insulin

binds to peroxisome proliferator activated receptor y (gamma)
PPAR-y

103
Q

What are the adverse effects of pioglitazone?

A

weightgain
oedema
increases osteoporotic fractures

104
Q

What are the results of the interaction between clopidogrel (anti-platelet) and pioglitazones?

A

increase the exposure to pioglitazones by inhibiting CYP2C8 mediated biotransformation

Prevents pioglitazones from being metabolised

105
Q

What are the results of the interaction between Gemfibrozil (lowers lipid levels) and pioglitazones?

A

increase the exposure to pioglitazones by inhibiting CYP2C8 mediated biotransformation

Prevents pioglitazones from being metabolised

106
Q

What is the MOA of a-glucosidase inhibitors like Acarbose?

A

they delay glucose absorption
this reduces postprandial increase in blood glucose

107
Q

What are the side effects of a-glucosidase inhibitors?

A

diarrhoea
bloatedness
flatulence

108
Q

What is the MOA of dapaglifozin?

A

inhibits sodium- glucose transporter (SGLT2) which is responsible for 90% of glucose reabsorption in the kidney

Reduces glucose reabsorption in the renal tube

lower blood glucose levels; more in urine

109
Q

Dapaglifozin is well absorbed from the gut. True or false

A

True

110
Q

Where is dapagliflozin metabolised?

A

Liver

111
Q

What are the adverse effects of dapagliflozin?

A

more glucose in urine leads to UTIs
Increased risk of bladder cancer

112
Q

Give examples of incretin mimetics

A

exenatide
Liraglutide

113
Q

What are incretin mimetics?

A

They are agonists of the GLP(glucagon like peptide)-1 receptor on beta cells which potentiate glucose dependent insulin synthesis and secretion (increase release of calcium ions from intracellular stores)

114
Q

What are the effects of incretin mimetics?

A

suppress glucagon secretion
slow gastric emptying
reduce food intake (modest weight loss)

115
Q

Incretin mimetics are not absorbed in the gut therefore they are delivered…

A

subcutaneously

116
Q

What drug combination is appropriate with incretin mimetics?

A

metformin with or without sulfonylurea pioglitazone, insulin

117
Q

What are the adverse effects of incretin mimetics?

A

hypoglycaemia
GI effects (nausea and vomiting)
dizziness
headache
fatigue

118
Q

What is the mechanism of action of dipeptidylpeptidase-4 (DPP4) inhibitors?

A

Incretins like GLP1 are broken down by DPP4 enzumes which reduces their effects with potentiating insulin release

DPP4 inhibitors inhibit the DPP4 enzymes preventing them from breaking down incretins. This allows the incretin signalling on beta cells and thus subsequent insulin release

119
Q

Give examples of DPP-4 inhibitors

A

gliptins
sitagliptin
vildagliptin
saxagliptin
linagliptin

120
Q

How are DPP-4 inhibitors administered?

A

orally

121
Q

DPP-4 inhibitors are absorbed by the gut and metabolised by _________ and excreted by __________

A

liver
kidneys

122
Q

DPP-4 inhibotors have a short half life. True or false

A

False
long half life, extended binding to DPP-4 enzyme

123
Q

What are the adverse effects of DPP-4 inhibitors?

A

weight neutral
GI effects- nausea, vomiting, dyspepsia
dizziness
risk of pancreatitis

124
Q

What are the oral complications of diabetes mellitus?

A

dental caries (increased glucose, bacteria)
periodontal disease (delayed healing)
xerostomia
candidiasis
oral mucosal disease
burning mouth syndrome

125
Q

How is a hypoglycaemic incident managed in the dental practice?

A

omit hypoglycaemic agents (agents that induce hypoglycaemia)
reduce or stop insulin (we want to increase blood glucose)
give glucose, orally (if conscious) or IV (unconscious)
glucagon (increase blood glucose)
follow hypoglycaemia protocol and kit in practice

HHD 2 (37 decks)

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