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ZCP311 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What are the secretory cells of the pancreas?

A

The alpha cells secrete glucagon. The beta cells secrete insulin and amylin.

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2
Q

How is insulin released?

A

GLUT 2 transporters facilitates glucose uptake in Beta cells, intracellular ATP increases. Then K channels are closed (depolarisation). Then voltage-gated Calcium channels open and this stimulates release of insulin from Beta cells.

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3
Q

What inhibits insulin release?

A

Stimulation of alpha adrenoreceptors, amylin, chronic hyperglycaemia, phenytoin, verapamil, colchicine

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4
Q

What are the types of diabetes?

A

Type 1 DM - typically involves non-obese patients. Treatment is insulin.
Type 2 DM - involves obese patients. Insulin resistance improves with weight reduction, physical activity and pharmacological treatment.

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5
Q

List 5 risk factors of type 2 DM

A

Visceral fat, family history, hypertension, dyslipidaemia, Smoking, use of drugs (antidepressants, atypical antipsychotics, thiazide diuretics, NRTIs)

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6
Q

What are some symptoms of DM?

A

Polydipsia, polyuria, glycosuria, blurred vision, nausea and vomiting, infections, tingling of hands and feet.

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7
Q

What are some factors affecting HbA1c?

A

Sickle cell disease, pregnancy (2nd and 3rd trimesters), HIV, Hemodialysis.

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8
Q

What are the main aims of therapy of DM?

A

Improve glycaemic control, avoid hypoglycaemia, decrease the risk of developing microvascular and macrovascular complications.

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9
Q

What is diabetic ketoacidosis?

A

Mainly associated with type 1 DM. Occurs when beta cells are severely compromised and insulin secretion is impaired. Brain can only use glucose or ketone bodies as energy source. Body goes into starvation which leads to fast breakdown of fats (ketones are metabolised fatty acids). High blood levels of ketones lead to decreased blood pH.

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10
Q

What are some triggers of diabetic ketoacidosis?

A

Trauma, heart attack, stroke, pancreatitis and pregnancy

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11
Q

What are signs and symptoms of diabetic ketoacidosis?

A

Deep rapid breathing, severe dehydration, GIT symptoms, blood pH of less than 7.3

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12
Q

What is hypoglycaemia?

A

Any glucose level below 3.9 mmol/L

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13
Q

What are some symptoms of hypoglycaemia?

A

Sweating, hunger, tremor, anxiety, palpitations.

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14
Q

What is hypoglycaemic unawareness?

A

Less autonomic warning signals of hypoglycemia, patients cant take action immediately, may feel weak, have seizures and cant take action by themselves.

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15
Q

What is the management of severe hypoglycaemia?

A

Rapid IV dextrose water 50% 20-50ml and assess response. Continue infusion with 1L dextrose 10% over 6 hours

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16
Q

What is the somogyi effect?

A

Rebound hyperglycaemia. Due to hypoglycaemia at 2am the body releases cortisol, adrenaline and glucagon. This is caused by missed meals, wrong timing of insulin admission. Patients must reduce evening insulin dose.

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17
Q

What are some clinical uses of glucacon?

A

Hypoglycaemia in unconscious patients, beta-blocker poisoning (raises cAMP levels), relaxation of bowel smooth muscles.

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18
Q

What are the examples of insulin we can get?

A

Short-acting (lispro,aspart,glulisine), regular insulin
Long-acting (degludec, determir, glargine)

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19
Q

What is the dose for insulin in adults?

A

0.3-0.6 units/kg/day in adults.
In the elderly, its 0.25-0.35 units/kg/day. In biphasic insulins, 2/3 of the dose is given in the morning and 1/3 of the dose is given at night.

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20
Q

What is added to intermediate acting insulin?

A

It is combined with protamine and zinc. Cloudy insulins are only used subcutaneously

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21
Q

When can insulin requirements be increased?

A

Medical illness, stress, puberty, 2nd and 3rd trimester pregancy

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22
Q

When can insulin requirements be decreased?

A

Renal or hepatic impairment, some endocrine disorders, coeliac disease.

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23
Q

What are some factors affecting insulin absorption?

A

Exercise, lipohypertrophy, site of injection, smoking, depth of injection and type of insulin.

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24
Q

What are some side effects associared with insulin use?

A

Hypoglycaemia, weight gain, lipodystrophy, allergic reactions.

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25
Q

What is the physiological action of metformin?

A

Lowers fasting and post prandial hyperglycaemia, does not cause hypoglycaemia and reduces insulin resistance. Off-label, improve insulin sensitivity in patients with PCOS.

26
Q

What is metformin’s MOA?

A

Inhibits mitochondrial respiration, lowers intracellular ATP and increases AMP. Activates AMP kinase. This decreases hepatic and renal gluconeogenesis and stimulates glucose uptake and use.

27
Q

What is special about the pharmacokinetics of metformin?

A

It can be used without major concerns in patients with an eGFR of 45-60ml/min

28
Q

What are some adverse effects associated with metformin usage?

A

GIT (N&V, Metallic taste, Diarrhoea)
Decreased Vit B12 absorption

29
Q

When is metformin contraindicated?

A

Renal and hepatic disease, alcohol intoxication, DKA, Pregnancy. 1000mg daily for patients with an eGFR of 30-45ml/min

30
Q

What is the physiological activity of pioglitizone?

A

They activate PPARy receptors, it decreases insulin resistance in muscle, liver and fat tissue. It also increased GLUT 1 and GLUT 4 expression.

31
Q

What are its pharmacokinetics?

A

Its metabolized by CYP2C8 and CYP3A4 metabolites, attention to drug interactions

32
Q

What are adverse effects of pioglitazone?

A

Oedema, weight gain, hypoglycaemia, Anaemia.

33
Q

What are some contraindications of pioglitazone?

A

Pregnancy and breast feeding. Cardiac failure, significant liver disease. Avoid in patients with renal impairment

34
Q

What is the mechanism of action of sulphonylureas?

A

They bind to SUR1 found on Beta cells, K efflux is inhibited, there is then B cell depolarisation, voltage-gated calcium channels open, Ca moves in and insulin is released from beta cells

35
Q

What are sulphonylureas’s Pka?

A

Food and hyperglycaemia reduce absorption. Strong binding to plasma albumin. Metabolized by the liver, mainly renally excreted. They cross the placenta and breast milk.

36
Q

What factors do we think of when selecting sulfonylureas?

A

Short-acting agents (allows for discontinuous use, lower risk of hypoglycaemia, safer for elderly and in renal impairment)
Long-acting (better control of overnight glycaemia, better avoided in elderly and renally impaired patients.

37
Q

What are some drug interactions of sulfonylureas?

A

Drugs that amplify the hypoglycaemic effect (aspirin, alcohol, MOAIs, TCAs, Warfarin). Inducers like rifampicin and pheytoin.

38
Q

What are adverse effects associated with sulfonylurea use?

A

Hypoglycaemia, weight gain and cardiovascular.

39
Q

What are some contraindications to sulfonylureas?

A

T1DM patients, late stage type 2 DM (insulin resistance), pregnant and breastfeeding women

40
Q

What is the PKA of meglitinides?

A

Rapaglinide has a half-life of 1hr. DOA of 4-7hr and is metabolised by CYP3A4.

41
Q

What is repaglinides MoA?

A

Will only stimulate B-cells in presence of glucose. Binds to ATP sensitive K+ channel.

42
Q

What are contraindications of repaglinides?

A

Gemfibrozil decreases metabolism of rapaglinide, causing severe hypoglycaemia. T1DM, Diabetic Ketoacidosis, severe renal/hepatic impairment.

43
Q

Where are incretins secreted?

A

GIP (Gastric Inhibitory Peptide) is secreted by the K cells. GLP-1 (Glucagon like peptide 1) is secreted by the L cells.

44
Q

What is the incretin effect?

A

Glucose is ingested, incretins are released, increases insulin secretion. Increased C-peptide levels of oral glucose.

45
Q

What are some advantages of DPP-IV inhibitors?

A

They are safe in patients with CVS comorbidities. They are weight neutral, except for saxagliptin, can be used in heart failure and can be used in renal impairment.

46
Q

What are adverse effects of DPP-IV inhibitors?

A

Risk of pancreatitis and joint pain.

47
Q

Why are GLP-1 Receptor agonists used?

A

Not metabolized by DPP-IV. It also elicits a glucose-dependent response. Patients also have low appetite.

48
Q

What are some advantages of GLP-1 RAs?

A

They are associated with high efficacy, weight loss, added benefit in pts with MACE. Safe in pts with HF. Can be used in pts with DKD.

49
Q

What are adverse effects of GLP-1 RAs?

A

GIT effects (temporary), pancreatitis.

50
Q

What is the MoA of SGLT2 Inhibitors?

A

They stop the reabsorption of glucose in the kidney. Leads to glycosuria and lower BG levels. They have a higher efficacy when HbA1c levels are elevated.

51
Q

What are effects of SGLT2 inhibitors?

A

Reduces HbA1c (by 0.7% -1% in monotherapy), sustained weight loss, improved fasting and PP glucose. Also decreases blood pressure by 2-4mmHg. Also reduces MACE.

52
Q

What are adverse effects of SGLT2 inhibitors?

A

Slight decrease in GFR - caution renal impairment
Increased UTIs in women, polyuria, empagliflozin - slight increase of LDL levels

53
Q

What are FDA warnings for SGLT2 Inhibitors?

A

Increased risk of fractures, DKA, serious urinary tract infections.

54
Q

What are some drugs that may accelerate the onset of diabetes?

A

Glucorticoids, thiazide diuretics, beta blockers, loop diuretics, protease inhibitors.

55
Q

What are some factors to consider when adding the second agent?

A

Efficacy of the add on therapy, hypoglycaemic risk, effect on weight, presence of CVD, presence of renal disease and adverse effects.

56
Q

What is the relationship between CVD and Diabetes?

A

Adding SGLT2 inhibitors or GLP-1 RA that have demonstrated CVD benefit is recommended in pts with ACVD, HF and CKD.

57
Q

What are targets for CV risk?

A

Weight:
BMI: <25
Lose 5-10% of body weight and maintain

BP:
Systolic 130mmHg
Diastolic 80mmHg

Cholesterol:
Total <4.5mmol/L
LDL >1mmol/L (men), >1.2 mmol/L (women)
TG < 1.7 mmol/L

Waist circumference
Male <94cm
Female <80cm

58
Q

Why and when do we recommend aspirin?

A

It is strongly recommended for secondary prevention of CV disease in Type 2 Diabetes (who have had a cardiavascular event)

59
Q

Why not use aspirin?

A

Increase in intracranial bleeds and GIT bleeds. All patients who have established ASCVD to use low dose aspirin

60
Q

When to initiate statin therapy?

A

Existing CVD, CKD, >40 years or DM > 10 Years.

Initiate if LDL > 1.8 mmol/L in pts with lower risk no CVD/CKD, <40 years or DM < 10 years

ZCP311 (11 decks)

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