Diabetes Flashcards

1
Q

What is the MOA of Insulin

A

Aim to maintain a stable BGL that avoids hyper/hypoglycaemia

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2
Q

What are the adverse effects of Insulin

A

Hypoglycaemia - low sugars, do not drive if experiencing
Weight gain - educate on a healthy eating plan
Lipohypertrophy - from not rotating injection sites

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3
Q

Patient education for insulin

A

Educate on checking BGL levels, how to treat a hypo/hyperglycaemic event, weight management, lifestyle,

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4
Q

What is the MOA of Metformin

A

Increase glucose uptake and utilisation in skeletal muscles
Reduce glucose production in liver
Increase insulin sensitivity
Reduces low and very low density lipoproteins

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5
Q

What are the adverse effects of Metformin

A

GI upset- nausea, abdominal discomfort, diarrhoea, metallic taste
Lactic acidosis

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6
Q

What is some patient education about Metformin

A

Take with food
Start with low dose
Avoid alcohol
Encourage healthy diet and excersie

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7
Q

Metformin contradictions

A

Poor liver or renal function - increase risk of lactic acidosis
GI disturbances- diarrhoea= dehydration - potential lactic acidosis
Any condition causing decrease tissue oxygenation that may result in lactic acidosis

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8
Q

Types on insulin

A

Rapid acting, short acting, long acting, intermediate acting

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9
Q

What are the contraindications of insulin

A

hypoglycaemia, hypersensitivity to insulin, diabetic ketoacidiosis

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10
Q

What is the MOA of Empagflozin

A

Acts on sodium glucose co-transporters in the renal tubules to inhibit reabsorption of glucose

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11
Q

What are some adverse effects of Empagflozin

A

Urinary tract infection
Hypoglycaemia
Increased urination and increased thirst
Constipation
Puritis

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12
Q

What is some patient education for Empagflozin

A

Take with food at same time everyday
Seek medical attention if symptoms of diabetic ketoacidosis
Keep genitals clean to avoid thrush
Stop if unwell
Avoid Keto diet while on this medication
Healthy diet and exercise

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13
Q

What are some contraindications of Empagflozin

A

Keep genitals clean - pass more during (glucose); increase risk thrush/groin infections
Any changes to diet should be mentioned, increase risk ketoacidosis
Pregnancy
sick day; stop empaflozin until otherwise
Seek medical attention if s/s of diabetic ketoacidosis

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14
Q

Glycogenesis

A

The formation of glycogen from sugar.

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15
Q

Gluconeogenesis

A

The process of making glucose (sugar) from its own breakdown products or from the breakdown products of lipids (fats) or proteins

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16
Q

Lipogenesis

A

The formation of fats from surplus glucose

17
Q

Glycogenolysis

A

Break up of glycogen into glucose

18
Q

Lipolysis

A

Break up lipids for gluconeogenesis

19
Q

What are some short term signs and symptoms of hyperglycaemia

A

Polyuria, this, polydipsia, fatigue, blurred vision, recurrent infection, unexplained weight loss

20
Q

Long term complications of hyperglycaemia

A

Degeneration of unmyelinated sensory neutrons

21
Q

Treatment for T1DM and monitoring

A

Insulin
Short acting admin 15-30min before meals
Oral hypoglycaemic agents cannot be used with T1

22
Q

T1DM risk factors

A

Prone to hypoglycemia and ketoacidosis
Insulin dependent
Often effects young people
Immune infiltration of pancreatic islets

23
Q

Risk factors of T2DM

A

Pre-diabetic
Metabolic syndrome
Physical inactivity
Unhealthy diet
Smoking
Genetics

24
Q

Name non-pharmacological interventions for T2 diabetes

A

Diet management
Increase physical activity - small achievable goals
Smoking cessation

25
Q

The blood test HbA1c is used in diagnosing and monitoring diabetes. Explain what the blood test is and what factors would need to be considered for a pt

A

Is known as glycated haemoglobin - the higher the glucose levels, more will bind to haemoglobin
Measures glycated haemoglobin over 2-3 months
Normal is under 40mmol/ml in person without diabetes
Older age increase hyperglycaemia, irregular eating patterns, alone, poor motility

26
Q

Why is Metformin the first line med for T2 Diabetes

A

Effective for individuals that are overweight and increase lipid profile due to increase effectiveness of available insulin and reducing LDL and VLDL
Has the benefit for not causing weight
Does not affect Beta cells = does not increase insulin production and therefore does not have risk of hypoglycaemia

27
Q

What important drugs may cause hyperglycaemia and hypoglycaemia

A

Hyper - Corticosteroids, atypical antipsychotics, Beta 2 agonists, oral contraceptive, thyroid hormones
Hypo - insulin, oral hypos, NSAIDs, alcohol, ACE inhibitors, beta blockers

28
Q

Education on how to manage hypoglycaemia

A

if in doubt treat
Eat/drink one serving of quick acting carb e.g jelly beans
After 10 mins test BGL if below 4mmol/l eat another

29
Q

Discuss the implications of taking prednisone with Empagflozin

A

prednisone may cause increase BGL as it inhibits glucose uptake in cells and inhibits glucose utilisation - decreasing effect of Empagflozin

30
Q

How should someone manage their diabetes while on prednisone

A

Check BGL more regularly due to risk of hyperglycaemia - could be 4x a day
Monitor for ketones

31
Q

What is a basal bolus regime and rationale

A

Basal bolus regime - basal insulin injected once per day to ensure insulin in body at all times
Mimics body natural rhythms of insulin release
Short acting before eating to manage the post prandial rise and the intermediate/long acting insulin before bed to manage BGL

32
Q

Education on storage and handling insulin

A

Never freeze insulin
Keep stock in fridge 2-5 days
Admin at room temp
Discard after one month of opening
Don’t shake

33
Q

Can pts take diabetic ‘pills’ instead of insulin injections

A

T1 diabetes means the body doesn’t produce insulin so tabs not effective - they influence insulin already in body
Tabs get broken down in gut and ceases to be insulin

34
Q

Two main adverse effects of insulin therapy and how to avoid those

A

Weight gain and hypos
Diet/exercise management - caution increases of sugar, carbs and alcohol
Hypoglycaemia - monitor BGL, educate s/s, don’t skip means, care with alcohol