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Clinical Therapeutics Sem 2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Actions of Insulin

A

Major anabolic hormone (effect to increase energy storage in the body )
RAPID - active transport of glucose and amino acids from blood into the tissues
INTERMEDIATE - promotes actions of enzymes that cause glucose to glycogen conversion in liver
LONG TERM- Promotion of growth

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2
Q

Normal diurnal variation

A

Insulin levels tend to Lag shortly behind BG levels
Biphasic secretory response - onceBG levels increase the insulin that has a,ready been formed is released quickly from the panscrwas.
If BS levels remain hugh despite initial insulin release, more insulin is formed and released ~ 45 mins
Always some insulin (basal/serum insulin ) being released at low levels throughout the day - responsible for growth.

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3
Q

What is diabetes

A

This is a condition where the amount of glucose in the blood is too high

This can be due to -
The pancreas not producing any insulin
The pancreas not producing enough insulin
The body not responding appropriately to insulin that is produced ( insulin resistance)

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4
Q

T1DM classification

A

Body cannot produce any insulin
Acute onset
Normally presents <40 years
Accounts for ~ 8-10% DM cases

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5
Q

T2DM classification

A

CNnot produce enough insulin or insulin produced does not work properly (insulin resistance )
Often present for years before diagnosis
Generally presmets >40 years
Accounts for ~ 85-90% of all people with diabetes

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6
Q

T1DM pathology

A

Absolute insulin deficiency (no insulin produced at time of diagnosis )
Most frequent I’m children , young people and young adults
Autoimmune destruction of pancreatic beta cells
Viral infection ? Envurornmtnal toxins ?
Not inherited
Can be a predisposition- more likely to get with certain genes

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7
Q

T1DM symptoms

A

Onset is relatively wxuick , over a few weeks (body gets from hav7ng enough b cells to cope to b cells stop working

CONSEUQNCE OF HUGH BG LEVELS
excessive urination (polyuria)
Thirst (polydypsia)
Visual disturbances - water drawn out of eye into blood by osmosis
Fungal infections - usually uti. So much glucose in urine , rich media for bacteria to grow

CONSEQUENCE OF IMPAIRED GLUCOSE UTILISTSIOM
fatigue - no glucose as source of energy
Hunger
Weight loss- no glucose for use in cells. Fat and protein broken down in cells instead
Ketone production (breath and urine ) can lead to diabetic ketoacidosis (DKA)

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8
Q

T1DM diagnosis

A

Symptoms plus one of the following
Fasting venous glucose of >= 7mmol/L
Venous plasma glucose >= 11.1 mmol/L 2 hours after OGTT (oral glucose tolerance test )
Random venous plasma glucose of >= 11.1 mmol/L

HBA1c not suitable for diagnosis of T1DM as onset it too rapid

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9
Q

T2DM causes

A

Absolute insulin deficiency (end point)
Relative insulin deficiency (not enough produced or notenough to meet increased metab9ic needs eg obesity)
Insensitivity to insulin (tissue not responding to insulin produced )

Increased in prevalence with age

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10
Q

T2DM risk factors

A

> 40 years
Asian and African Caribbean backgrounds (>25yrs)
History of gestestional diabetes
HBD, HD and stroke
Family history of T2DM
overweight (BMI >30)
Increased Waist circumference
Little or no exercise

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11
Q

T2DM Presentation

A

A lot of time brought up by screening if they have risk factors

INITIALLY (over a couple of yrs)
Thrush
Blurred vision
Slow healing of cuts /wounds
Chest pains
Erectile dysfunction

EVENTUALLY (increased BG)
Polydypsia
Polyuria
Extreme tiredness
Weighloss (loss of muscle bulk)

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12
Q

T2DM diagnosis

A

Random plasma glucose >11.1 mmol/L
SYMTOMS PLUS ONE OF THE FOLLOWING
Fasting plasma glucose > 7.0 mmol/L
Oral glucose tolerance test >11.1 mmol
Testing on 2nd day essential if symptoms absent

HBA1C > 48 mmol/mol 6.5%)

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13
Q

Complications or diabetes overview

A

As a result of poorly controlled diabetes (usually type 2)
ACUTE
diabetic ketoacidosis
Hypoglycaemia

LOMG TERM
microvascular (small vessel disease)
Macrovascular (large vessel disease )

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14
Q

Diabetic ketoacidosis cause

A

Can occur in T1DM when BG levels are increased for prolonged Periods of time due to lack of insulin.
Glucose requires the prescence of insulin for utilisation as an ernery source by fat and muscle.
When glucose isn’t available as a pin energy source, stored fats are ,metabolised as an attempt to generate energy to keep the body functiosning.

As a result the increased BG levels and increased free fatty acids in the blood oxidise in the body to form ketone pbodies .
Ketones are acidic and cause a decarese in the bodies ph leading to ketoacidosis. Ketone in the blood cause vomiting (causing further dehydration in the body ) netutarlsiing factors in the body eg bicarbonates are therefore decreased further causing further intracellukar dehydration and can eventually lead to a coma and death .

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15
Q

When is DKA most likely to occur

A

In new,diagnosed patients (25%) where they haven’t had insulin in a while

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16
Q

What is DKA a result of

A

Omission of insulin
Or
Insuffeinct insulin due too
Emotional disturbances
Drugs (interfering with insulin)
Infection
Acute illness
Trauma

Presenting symtom of type 1

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17
Q

DKA Symptoms

A

Ketosis (increased ketones in blood)
Thirst
Increased dehydration
Vomiting
Hyperventilation (body mistakes ketoacidosis for the retention of c02 and increases resp drive)
Tachycardia
Hypotension
Confusion
Coma
Weakness
Drowsiness

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18
Q

What would you use to treat a patient with diabetic ketoacidosis ?

A

Needs treated asap

(Monitor BG and electrolytes to ensure treatment is effective);
INSULIN
inhibits glucose production and fat breakdown
Facilitates uptake of glucose from cells
Ensured the body in utilising glucose for energy and not stored fats
Usually only stopped when pt is stable and can eat

IV FLUIDS
Eg nacl to replace lost fluids

IV K+
Eg kcl
Prevents low k which may occur as a result of the insulin.

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19
Q

DKA- sick day rules

A

Continue to take insulin and tablets when unwell
Testing BG levels atleast 4x per day
Test urine for ketones
Drink plenty of fluids
If not we’ll enough to eat meals eplace with carb containing drinks
Contact GP if unsure what to do when sick

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20
Q

Hypoglycaemia defentiotiom

A

Blood glucose levels below 4mmol/L with or without symptoms

Patients can experience hypoglycaemia at higher blood glucose levels (experience triggered by relative change in blood glucose )

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21
Q

Hypoglycaemia causes

A

Too much insulin /tablets
Missed or late meals
Too little food
Exercise - uses up glucose
Alcohol - inhibits glucose production
Weather - warm weather increases rate of abs of insulin at inj site
Weight loss without dose adjustment - may require less insulin

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22
Q

Hypoglycaemia symtoms

A

All symptoms are not the same
Majority will learn to recognise and deal with their symptoms before they get serious
EARLY WARNING
hunger pangs
Shaking
Sweating
Feeling sick to stomach
Pale skin
Fast heart beat

COGNTIITVE DYSFUNCTION
mood changes
Irrational behaviour
Vagueness
Uncoordinated movement

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23
Q

Hypoglycaemia treatemnt (conscious )

A

Quick acting sugar (15-20g) liquid preferred (absorbs faster)
✅ small glass of sugary non diet drink
✅4-6 dextrose tablets
✅small carton of pure fruit juice
✅glucogel 25g pod
✅ soft sweet eg 5 jelly beans

Repeat after 5-10 mins if necesssary

Follow up with slow acting carbohydrate eg bisuuit, bread to prevent blood sugars dipping again

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24
Q

Hypoglycaemia treatemnt (unconscious)

A

GLUCAGEN HYPOKIT
➡️1mg glucagon
➡️if unconscious
➡️IM/SC/IV ROUTE
➡️after 10-15 mins causes the liver to replete its stores of glycogen as glucose

Emergency services if unresponsive after tgus
Exp date outside fridge - 18 months
Once conscious, pt should be given long acting carbohydrate

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25
Q

Hypoglycaemia complications

A

Frequent episodes are harmful
Area of the brain that monitors glucose levels readjusts and considers low levels as normal
Leads to loss of awareness - normal response not triggered until levels are dangerously low

Can cause oroblems with those who keep tight control of their BG

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26
Q

Diabetes long term complications

A

More common in type 2 (50% or more will suffer from one or more complications at time of diagnosis )
😔macrovascualr (disease of small vessels)
Prolonged exposure to hugh blood glucose levels damages tissues throughout the body by damaging small blood vessels, initially changes are reversible but if the BG levels are persistently hugh this can lead ro irreversible damage
👁️retinopathy -damage to eye
😩nephropathy- damage to kidney (can result in kidney failure)
🧠neuropathy (damage to peripheral nerves)

🙁macrovascular (damage to large vessels )
Occur as a result of damage rk the walls bvs, which can then become blocked and result in a range of issues such as
🫀progressive heart failure
🫀stroke
🫀angina

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27
Q

Retinopathy 👁️

A

Damage to the eyes
Can lead to visual disturbances and blindness
Main cause of blindness in uk
More common in type one
Increase risk of cataract and glaucoma
Diabetics should have annual eye checks

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28
Q

Retinopathy 👁️ risk factors

A

Poor glycemic control ( consistently hugh BG levels)
HTN
Duration of diabetes
Microalbuminuria and proteinuria
Dyslipidaemia (abnormal lipid profile )
Pregnancy
Smoking

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29
Q

Nephropathy

A

Damage to the kidneys
Indicative to type 1 and 2 diabetes

DIABETIC NEPHROPATHY
Diagnosed clinically
Urinary albumin exretion >300mg/24hr I’m a person either diabetics and nk other renal disease present

MICROALBUMINURIA
Early marker that kidney function may not be as good as it should be
Early sign of diabetic nephropathy
Marker for alotcof other diseases down the linen

Without intervention , there would be a Greatly increased amount of diabetics with Microalbuminuria and increased risk if renal diseases.

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30
Q

Nephrotoxicity risk factors

A

Age
Duration of diabetes
Uncontrolled BG levels
Dyslipidaemia
HTN
Presence of retinopathy
Smoking

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31
Q

Neuropathy

A

Result of hyperglycaemic damage to motor, sensory and autonomic nerves
Can manifest as
Foot problems
(Common);numbness and neuropathic pain
Erectile dysfunction
Efffects on bowel and bladder

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32
Q

Neuropathy risk factors

A

Patients age
Duration of diabetes
Hyperglaecemapeia
Smoking ans diastolic bp

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33
Q

Micro vascular complications frisk factors

A

Increasing age
Hyperglaecemia
HTN
smoking
Dyslipidaemia
Duration of diabetes

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34
Q

Prevelance of macrovascualr conditions with diabetes

A

2-3 x more likely to have MI or stoke
3-5 x more likely to suffer heart failure
IRRESPECTIVE OF OTHER RISK FACTORS

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35
Q

CV risk factors with diabetes

A

Smoking
Microalbuminuria
Hyperglycaemia
HTN
Dyslipidaemia (increases ldl and decrease Hdl)

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36
Q

Monitoring of diabetes

A

BIOCHEMICAL CONTROL
glucose
Ketones
HbA1C

CLINICAL MONITORING (annual review)
Feet
Eye
Renal
Neurological
Cardiovascular

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37
Q

Another name for HBA1C

A

Glycated haemoglobin

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38
Q

HbA1C

A

Useful for assessing long term control of diabetes
Is the fraction of Hb irreversibly bound to glucose. (Indication of amount of glucose in blood).
Hb stays in the blood for around 3 months - reflects BG levels of pervious 3 months.
Gold standard for long term monitoring

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39
Q

How often should HBA1C be measured .

A

Every 3-6 months type 1
Every 6-12 months in well controlled type 2

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40
Q

Units for HbA1C

A

OLD (%). NEW (MMOL/mol)
6. 42
6.5 48
7. 53
7.5. 59
8. 64
9. 75
10. 86

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41
Q

Ideal control HBA1c

A

48-59 mmol/mol (6.5-7.5%)

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42
Q

HBA1c and patient outcome

A

<6 (42)- tight control , risk of hypoglycaemia

6- 7.5 (42-59) ideal control ,risk of complication and hypoglycaemia reduced

7.5-8 (59-64) minimal symptoms but increased risk of complications

> 8 (>64) high risk of diabetic complications

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43
Q

Types of insulin

A

Short acting 🐶
Rapid acting insulin analogues
Soluble insulin

Intermediate acting 🐶

Long acting 🐶
Prolonged acting analogues

Biphasic insulin🐶
Mixture of 2 different insulins to reduce no of injections eg short acting and intermediate acting

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44
Q

Rapid acting insulin analogues

A

Have modifications made to their insulin chain that allows them to be absorbed from subcutaneous injection site into the blood stream v quickly.
Provide a insulin profile similar to physiological insulin.
Quick onset (15min) and short duration (2-5hrs )
Peak effect after one hour
Inject immediately before meals
Less changed of hypoglycaemia than solubke insulin

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45
Q

Types of rapid acting insulin analogues

A

Inulin aspart (novorapid)
Insulin lispro (humalog)
Insulin glulisine (apidra)

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46
Q

Soluble insulins

A

Not as commonly used as insulin analogues
Human (bovine /porcine) insulin
Slower onset of action (30-60min) compared to analogues
Peak action -1-4hrs after injection
Duration - up to 9 hrs
Should be injection 15-30 mins prior to meal
Significant post prandial / nocturnal hyperglycaemia (this insulin has a longer duration of action than rapid acting analogues )

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47
Q

Examples of soluble insulins

A

Actarapid

Humulin S
Insulin soluble human

48
Q

Intermediate acting insulins

A

Rarely prescribed besides when part of a biphasic routine
Absorbed slowly after injection
Onset- 1-12 hours
DOA- 11-24 hrs
Peak action - 3-12 hrs (Broad values, depends on patient )

49
Q

Examples of intermediate acting insulins

A

Insulin isophane human
Insulatard

50
Q

Prolonged acting insulins

A

Insulin released at steady state from injection site
Peakless plateau ~ 90 mins after injection
Relatively instant insulin release over 24hours
Decreases chance of hypoglycaemia
Decreases amount of weight loss

51
Q

Examples of prolonged acting insulins

A

Insulin glargine (lantus)
Insulin detemir (levemir(0)
Insulin deglude (tresbia)

52
Q

Biphasic insulin

A

2 phases,
Immediate part to cover meal which follows inj eg breakfast eg shirt actinf insulin
Longer acting part to cover lunch or overnight

Decreases the number of injections required

Less flexibility due to fixed ratio, therefore may require a regeminted diet

53
Q

Example of biphasic insulin

A

Human Mixtard

54
Q

Diabetic syringes

A

Calibrated in UNITS (100 units per ml of insulin)
Not commonly used
Not as discrete as other devices
Requires skill to use
Disposal issues

55
Q

Reusable insulin pens

A

Usually used in conjunction with 3ml insulin cartridges

56
Q

Disposable pre filled insulin pens

A

One off use
Available for a range of insulins

57
Q

Innolet

A

Ideal for patients with poor dexterity and /or sight problems
Large dial
Pre filled with 3ml insulin
Large injection button
Audible clocks during dial up of dose (known from no of clicks the units of insulin given )
available for
Insulin determir (levemir )- prolonged action insulin
Insulatard - intermediate

58
Q

Insulin pump

A

Small, practical, reliable, safe
Decreased variability of absorption and closer to physiological insulin release
Dosage instructions entered into pumps small computer and appropriate volume of insulin is injected into the body in a calculated , controlled manner

59
Q

Injection sites

A

Abdomen (fastest absorption 0)
Buttocks
Upper arm
Thighs (slowest )

Skin rotation essential - risk of lipohypertrophy (lump under skin caused by accumulation of fat at injection site ) and subsequent erratic absorption of injection site is over used

60
Q

Storage of insulin

A

Fridge at 2-8 degreees c for long term stability
Do not freeeze - store at front of fridge
In use insulin stable for 4-6 weeks at room temp - allows pt to use day to day without need for refrigeration
Avoid direct sunlight - cap after use and stole vials in cardboard packaging

61
Q

What are the types of continuous glucose monitoring ?

A

Intermittently scanned (flash) CGM ,isGCM
real time CGM, rtCGM

62
Q

What is isCGM?

A

Intermittently scanned (flash ) continuous glucose monitoring eg free style libre
Intermittent - not continuous - need to hold to sensor to get results
Constantly measures BG levels

Made up of-
A sensor you stick to your arm (usually lasts about 14 days then needs replaced)
A reader- a small device you use to scan the sensor to see BGL

can also use smart phone app to scan the sensor
Still need to do finger prick tests for things like driving , BSL gone low etc

63
Q

What is real time continuum glucose monitoring?

A

BGL show up on device or smart phone automatically via Bluetooth
Range of systems available

64
Q

What are the advantages of continuous glucose monitoring?

A

Time in range data - % time that BSL are in the target range that has been decided by the diabetic team
Can share the data online with HCP

65
Q

Patients unwilling to use CGM

A

Can use capillary blood glucose monitoring
At least four times per day including before each meal and before bed

66
Q

Target blood glucose levels type one

A

HBa1C of 48mmol/mol or 6.5% or lower

GLUCOSE LEVELS
fasting blood glucose levels on waking - 5-7 mmol/L
Blood glucose levels before meals at any other point of the day - 4-7 mmol/L
Blood glucose level of 5-9 mmol/L at least 90 mins post meal
Should be ATLEAST 5Mmol/l when driving

67
Q

Treatment plan - T1DM

A

Insulin therapy
Healthy diet
Regular exercise
Diabetes education
Regular checkups at diabetes clinic

68
Q

Diet -T1DM

A

Does not differ from guidelines for the rest of the population
Should have alcohol in moderation

69
Q

Exercise in T1DM

A

Decreases blood glucose levels
Increases uptake of glucose into exercising muscles
Increases sensitivity of muscles to insulin

70
Q

Names of clinical trails that were important clinical evidence in treating diabetes

A

Diabetic control and complications trail DCCT
Epidemiology of diabetes interventions and complications (EDIC)- follow up trail

71
Q

Diabetes control and complications trail

A

1993
Showed that intensive treatment with insulin designed to decrease blood glucose levels decreased the microvascular complications of type one diabetes

Big trail - 1400 subejctcs

Compared the effects of conventional vs intensive therapy off the development of complications

INTENSIVE
3or more daily insulin injections
4 or more blood glucose tests per day
Frequent dietary instruction
Monthly clinical visits
Insulin doses were adjusted according to BG, diet, exercise etc

CONVENTIONAL
1 or 2 daily injections (normal at the time )
Daily self monitoring
Standard diet and exercise regimen

RESULTS
Intensive therapy dramatically decreased the risk of microvascular complications in particular such as neuropathy , retinopathy, nephropathy.
However, hypoglycaemia increased 3 fold in this group.

72
Q

Epidemiology of diabetes intervention and complications

A

Followed up patients in DCCT after it finished.
Showed risk decreased risk of microvascular complications seen in DCCT were maintained well beyond their period of implementation shown during DCCT.
THEREfore shows d the benefits of intensive insulin therapy

There was a later study in 2015 that showed decreased mortality in intensive group compared to the conventional group

73
Q

DCCT and EDIC - overall conclusions

A

STRICT control of blood glucose can decrease the risk of MICROVASCULAR complications in T1DM (retinopathy , neuropathy , nephropathy)

74
Q

3 key insulin regimes

A

Basal bolus
2x daily using biphasic insulin mixes
Continuous SC insulin infusion via pump

75
Q

Basal bolus regemine

A

Bolus of RAPID ACTING or short acting insulin before Breakfast lunch or evening meal (adjustment of dose made on BGL before eating or size of the meal);
Injection of PROLONGED or intermediate acting insulin once or TWICE daily
Close to physiological insulin production
Great flexibility- patient choses when to eat and how much
Tighter control but multiple injections

76
Q

Basal in basal bolus regemin

A

Usually long acting (prolonged acting analogue )
Eg twice daily insulin detemir

77
Q

Bolus in basal bolus regime

A

Usually a rapid acting insulin analogue
Eg insulin apsart, glulisine, lispro

78
Q

Twice daily with biphasic Insulin regmine

A

More often used in older patient s

Patients injects themselves with biphasic insulin twice a day
Usually contains a short acting or rapid acting insulin and an intermediate acting insulin
2/3 of the dose administered before breakfast and 1/3 before evening meal
Does NOT match physiological insulin
Risk of hypoglycaemia due to inappropriate amount of insulin in circulation between meals (snacks required)- therefore regeminted diet required - need to eat at certain times

79
Q

Typical prescriptions for twice daily biphasic insulin

A

Novomix 30
Humalog mix 25

80
Q

Continuous SC infusion via insulin pump

A

Uses short acting or very fast acting insulin
Mimics physiological insulin delivery
Intensive patient education required
24 hour access to diabetes team needed

81
Q

Nice guidelines on continuous SC infusion via insulin pump use

A

Only to be offered to patients who suffer DISABLING HYPOGLYCAEMIA while attempting to achieve their target HBA1c levels
OR
have hugh HBA1C (69 mmol/mol or above 8.5%) with multiple daily injections

82
Q

Closed ‘loop’ systems

A

Insulin released automatically by pump in response to blood glucose levels detected by rtCGM sensor
Better glucose control , reduces risk of hyperglycaemia and removed the need for finger pricking

83
Q

Who is eligible for a closed loop system

A

Those who are unable to control their condition using an insulin pump or CGM and if their long term average HBa1C is 8% or more

84
Q

What might a patient adjust dose depending on

A

The amount of carbohydrate to be consumed
Pre meal blood glucose reading
Planned activity

85
Q

Aims of therapy of T2DM

A

Alleviate hyperglycaemia symptoms
Improve lipids, glucose amd bp
Acid excessive weight gain (increase insulin need)
Improvement or neutral impact on quality of life
Decrease risk of hypoglycaemia

ALL PREVENT LONG TERM COMPLICATIONS

86
Q

Clinical evidence for treatment of T2DM

A

UNITED KINGDOM PROSPECTIVE DIABETES STUDY - UKPDS

> 5000 newly diagnosed patients
Meadian age - 54 years
Lasted >20 years , median follow up - 10 years

AIM.
determine if intensive blood glucose control could decrease the risk of micro and macro vascular complications

ADDITIONAL SUB TRIAL
effect of tight v less tight control of Bp on risk of macro and microvascukar complications

87
Q

United Kingdom prospective diabetes study - control group

A

(Conventional therapy )
Dietary advice from dietician every 3 months
Minimal drug treatment if fasting plasma glucose > 15 mmol/L

88
Q

United Kingdom prospective diabetes study - intervention group

A

(Intensive therapy )
Advice from dietician every 3 months
Initiation of sulfonylurea or insulin treatment

89
Q

United Kingdom prospective diabetes study - goals of treatemnt

A

CONTROL GROUP
Keep FPG < 15 mmol/L without symptoms of hypoglycaemia

INTERVENTION GROUP
keep FPG <6 mmol/L

90
Q

United Kingdom prospective diabetes study - resukts

A

HBA1c
Conventional - initial drop then slowly in carried again with time
Intensive - sharper initial drop and levels constantly remained lower with a more gradual increase

FBG
conventional- no real drop and gradually increased with time
Intensive - sharp drop in fbg and more gradual incline than conventional. FPG levels always remained lower

MICROVASCULAR COMPLCIATUIMS
25% drop in microvascular complications with intensive therapy

MICROVASCULAR COMPLICATIONS
no significant change observed from either group

91
Q

Target levels for type 2 diabetes

A

Daubers managed by lifestyle and diet and single drug not associated with hypoglycaemia- HBA1c- 48mmol/mol (6.5%)
Drug associated with hypoglycaemia- Hba1C- 53 (7%)
Targets agreed eith patients being realistic

92
Q

Classes of oral anti diabetics

A

SENSITISE THE BODY TO INSULIN AND OR DECREASE GLUCOSE PRODUCTION
biguanides, thiazolidinediones (glitazones)

BLOCK GLUCOSE REABSORPTION FROM KIDNEYS (used less often now)
Sodium glucose cotransporter 2 inhibitors (sglt 2) inhibitors

STIMULATE INSULIN PRODUCTION
sulfonylureas

TARGET INCRETIN SYSTM
DPP-4 inhibitors (gliptons)
GLP-1 agonists (incretin mimics )

SLOW ABS OF STARTCH ( rarely usd - GI side effects)

93
Q

Metformin MOA

A

biguanide
INTESTINE
⬇️glucose reabsorption
⬆️anaerobic metabolism of glucose

LIVER
⬇️glucose production
⬇️glycogenolysis
⬇️fatty acid oxidation

SKELETAL MUSCLE
⬆️insulin mediated glucose uptake
⬆️glycogengenis
⬇️fatty acid oxidation

THESE ALL ⬇️BGL WHICH IN TURN ⬇️HYPERGLYCAEMIA

94
Q

Metformin advantages and disadvantages

A

ADVANTAGES
enhances weight loss (drug of choice for overweight )
Improves lipid profile (⬇️ CVD risk)

DISADVANTAGES
gastric intolerance (naseau, diahorrea, abdominal pain)
C/I in impaired renal failure
Lactic acidosis (⬆️ in blood lactic acid levels)

95
Q

Metformin dosage

A

Titrated to decrease side effects
500mg OD after main meal increase to 500mg TID (over 2-3 weeks)
Normal dose - 500mg TID OR 850 BD
Max dose - 2g daily
MR prep available for those with gi side effects but more expensive

96
Q

SGLT2 inhibitors

A

More prominant in last 6 months and year
Blocks reabsorption of glucose in kidneys
Promotes excretion of excess glucose in urine
Urine will test positive for glucose
Effectiveness depends on kidney function
Increased incidence of genetial and urinary infections

97
Q

SGLT2 inhibitors examples

A

Dapagliflozin
Canagliflozin

98
Q

Advantages of SGLT2 inhibitors

A

May promote weight loss
Improve CV outcomes in some patients
Decreased risk of CKD progression , mortality and CV events in adults with T2DM and CKD

99
Q

Cautions with SGLT2 inhibitors

A

Rik of DKA needs ro bc e assessed before commenced, increased risk if had previous episode
Caution if on v low ir ketogenoic diet (take off sglt2 inhibitor )

100
Q

Sulfonylureas

A

Stimulate beta cell insulin secretion
Require residual beta cell activity

Reduce hba1c by about 1%
Max effect at 6 months

101
Q

Sulfonylureas urea’s examples

A

1st gen - tolbutamide (short doa, useful for elderly )
2nd gen - gliclazide
3rd gen- glimepiride (longer doa , increased hyp risk )

102
Q

Sulfonylureas side effects

A

Increased hypo risk if don’t eat frequently, especially with longer acting eg glimepiride
Weight gain , caution in over weight
GI disturbances

103
Q

Thiazolidinediones

A

Glitazones eg pioglitazone

Referred to as insulin sensitising drugs , enhances the effects of 8nsulin in adipose tissue and d skeletal muscle

Inhibits gluconeogenisis in liver

104
Q

Thiazolidinediones advantages

A

Effective in insulin resistant patients (type 2)
Decreased risk of hypoglycaemia
Positive effect on lipids

105
Q

Thiazolidinediones disadvantages

A

Increased risk of heart failure ( result of oedema - more of an issue If taken along side insulin - not recommended for use in those with chronic heart failure)

Increased risk of bladder cancer

C/I In renal impairment

Weight gain (fluid retention)

106
Q

Pioglitazone and Liver

A

Some reports it use causes disturbances in liver function
Therefore need monitoring of liver function

Baseline LFTs - every 2 months for a year , periodically after thus

Symtoms suggesting liver diases, seek medical attention
Jaudice, discontinue use

107
Q

What are incretins

A

Gi hormones released in response ro meals to increase insulin secretion

108
Q

Normal INCRETIN response

A

2 gut peptides -
GLP-1 (glucagon like peptide )
GIP(glucose independent insulinotrophic peptide)
Rapidly degraded in circulation by DPP-4 enzyme

109
Q

Incretin effect type 2 diabetes

A

INCRETIN effect in type 2 diabetes
GLP-1 levels decrease
GIP levels defective or abscent

Decreases INCRETIN response in type 2 is due to both

110
Q

DPP4 inhibitors moa

A

Block dpp4 enzyme
Incretin and GLP-1 levels increase
Stimulates insulin realease ans inhibits glucagon release
Bg lowered

111
Q

DPP4 inhibitors examples

A

OD- alogliptin
Bd- vildaglitpin

112
Q

DPP4 inhibitors advantages

A

Weight neutral
Well tolerated

113
Q

DPP4 inhibitors disadvantage

A

Liver / renal dose adjustments needed

114
Q

GLP-1 receptor agonists

A

Mimics gulp-1 , increasing insulin secretion wnd suppressing glucagon secretion

115
Q

GLP-1 agaonists dosing

A

Sc inj
Once/ gp twice daily - liraglutide
Once weekly - semaglutide
Start with low dose and increase to maintenance

116
Q

Glp-1 receptor agonists advantages and disadvantages

A

Slight weight loss

Side effects - such as naseua and hypoglycaemia esp with sulfonylureas

Clinical Therapeutics Sem 2 (1 decks)

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