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Clinical Pharmacology Year V NIŠ > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is Diabetes?

A
  • group of metabolic disorders
  • characterised by hyperglycaemia
  • results from defect in insulin secretion, insulin action or both
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2
Q

What are the symptoms of Diabetes?

A
  • polyuria
  • polydypsia
  • weightloss
  • fatigue
  • blurred vision

*chronic = susceptible to certain infections

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3
Q

What are some acute life threatening consequences of uncontrolled diabetes?

A
  • Ketoacidosis
  • non ketoacidosis hyperosmolar syndrome
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4
Q

What are the types of diabetes? Explain.

A

Type 1:
- auto immune mediated
- juvenile
- absolute deficiency of insulin

Type 2:
- life style dependent
- combination of resistance to insulin action and inadequate compensatory insulin secretory response

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5
Q

Do individuals with normal glycemic control need insulin?

A
  • No
  • Individuals with adequate insulin glycemic control with weight reduction, exercise, oral glucose lowering agents do not require insulin
  • Individuals with some residual exogenous insulin for adequate glycemic control can survive without it
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6
Q

Do individuals with extensive b-cell destruction with no residual insulin secretion need insulin?

A

Yes

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7
Q

What are the glucose levels according to the ADA on an empty stomach and 2 hours after a meal?

A
  • Empty stomach: > 7 mmol/L (126mg/dl)
  • 2 hours after a meal: > 11.1 mmol/L (200mg/dl)
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8
Q

What are some long term complications from diabetes?

A
  • retinopathy: potential vision loss
  • nephropathy: leading to renal failure
  • peripheral neuropathy: risk of foot ulcers & amputations
  • autonomic neuropathy: GI, GU, CV symptoms and sexual dysfunction
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9
Q

What is type 1 diabetes?

A
  • auto immune destruction of B cells in pancreas
  • usually leads to absolute insulin deficiency
  • level of B cell destruction varies
  • 5-10% of people who are diabetic
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10
Q

What is idiopathic diabetes?

A
  • T1DM some forms have unknown causes
  • Some with permanent insulinopenia and prone to ketoacidosis
  • often no evidence of autoimmunity
  • varying degrees of insulin deficiency
  • strongly inherited
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11
Q

What is type 2 diabetes?

A
  • non-insulin dependent diabetes
  • insulin resistance and with relative insulin deficiency
  • most common type of diabetes
  • initially, do not require insulin to survive
  • Most of these diabetic patients are obese and this can cause some degree of insulin resistance
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12
Q

What are the risks of developing type 2 diabetes?

A
  • increasing age
  • obesity
  • lack of exercise
  • hypertension
  • women who had GDM before
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13
Q

What are the treatment goals for diabetes?

A
  • control glycemia
  • control of CV risk factors
  • patient active participation
  • improve QOL
  • prevent complications
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14
Q

Why is self monitoring blood glucose SMBG beneficial?

A
  • Beneficial for patients on intensive insulin regimen
  • multiple doses or a continuous insulin infusion
  • Should blood glucose before meals, postprandial, before sleeping, before exercise, before major efforts or when suspecting low blood glucose
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15
Q

What is Hb1Ac?

A
  • Glycosylated Hb (Hb1Ac) is the average value of plasma glycemia over the previous 2-3 months in a single measurement
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16
Q

Hoe are patients with T1DM treated?

A
  • most patients require multiple doses of insulin injections or continuous subcutaneous insulin injections
  • they should use insulin analogues to reduce their risk of hypoglycemia
  • Choice of glycemic target and drugs used varies and should be individualised to the patients
17
Q

What are biguanides? MOA? Contraindications? Side effects?

A
  • e.g. metformin
  • first line medication for T2DM

MOA:
- Reduction in insulin resistance via modification of glucose metabolic pathways
- Inhibits mitochondrial glycerophosphate dehydrogenase (mGPD) → ↓ hepatic gluconeogenesis and intestinal glucose absorption
- Increases peripheral insulin sensitivity → ↑ peripheral glucose uptake and glycolysis
- Lowers postprandial and fasting blood glucose levels
- Reduces LDL, increases HDL

  • most preferred way of reducing glucose in T2DM patients
  • Well tolerated drug
  • Contraindicated in lactation and pregnancy
18
Q

When can dual therapy be used in treating diabetes?

A
  • Hb1Ac is 9% or higher to achieve glycemic control more quickly

e.g. biguanides can be combined with sulfonylureas derivatives or SGLT-2 Inhibitors

19
Q

What are sulfonylureas derivative drugs? MOA? Side effects? Contraindications?

A
  • e.g. Glibenclamide
  • oral medication which lower glucose by stimulating insulin secretion

MOA:
-Block ATP-sensitive potassium channels of the pancreatic β cells → depolarization of the cell membrane → calcium influx → insulin secretion
- Extrapancreatic effect: ↓ hepatic gluconeogenesis, ↑ peripheral insulin sensitivity

Contraindications: B blockers, obesity, severe CV comorbidities

Side effects: weight gain, risk of hypoglycemia
- others SU derivates e.g. Glipizide or Glicazide have a lower risk of hypoglycemia

20
Q

What are Meglitinide drugs? MOA? Side effects? Contraindications?

A
  • e.g. Repaglinide or Nateglinide (less effective)
  • stimulate insulin secretion
  • shorter half life than SU derivatives

Side effect: risk of weight gain,

21
Q

What are alpha-glucosidase inhibitor drugs? MOA? Side effects? Contraindications?

A
  • e.g. Miglitol and acarbose
  • Inhibit alpha-glucosidase (a brush border enzyme expressed by intestinal epithelial cells) → delayed and ↓ intestinal glucose absorption and ↓ carbohydrate breakdown, resulting in ↓ hyperglycemia after food ingestion
  • primarily lower post-prandial glucose levels without causing hypoglycemia

Contraindications: severe renal failure, IBD

Side effects: increase transaminases, flatulence, abdominal pain

22
Q

What are thiazolidinedione drugs? MOA? Side effects? Contraindications?

A
  • e.g. Pioglitazone and rosiglitazone

MOA:
- activation of the transcription factor PPARγ (peroxisome proliferator-activated receptor of gamma type in the nucleus) → ↑ transcription of genes involved in glucose and lipid metabolism → ↑ levels of adipokines such as adiponectin and insulin sensitivity → ↑ storage of fatty acids in adipocytes, ↓ products of lipid metabolism (e.g., free fatty acids) → ↓ free fatty acids in circulation → ↑ glucose utilization and ↓ hepatic glucose production

  • increase insulin sensitivity and offer high glucose lowering efficacy
  • TZDs increase HDL and assist in lowering CVD risks and hepatic steatohepatitis
  • Side effects: fluid retention, weight gain and possible worsening of CHF and bone fracture, therefore contraindicated in CHF and severe liver failure
23
Q

What are SGLT2 drugs? MOA? Side effects? Contraindications?

A

E.g. Dapaglifzolin, Empaglifzolin and Canaglifzolin

*renal function determines the drugs efficacy on glucose lowering

MOA:
- reversible inhibition of SGLT-2 in the proximal tubule of the kidney → ↓ glucose reabsorption in the proximal convoluted tubule of the kidney → glycosuria and polyuria
- reduce plasma glucose by enhancing urinary excretion of glucose
- decreases BP

Side effects: UTI’s, dehydrations, weight loss, orthostatic hypotension, severe diabetic ketoacidosis

Contraindications: chronic kidney disease, recurrent UTI’s

  • CAUTION when combined with ACEi or ARBs
24
Q

What are GLP-1 agonist drugs? MOA? Side effects? Contraindications?

A
  • e.g. Exenatide, liraglutide
  • Incretins: Endogenous hormone secreted by cells in the GI tract - potentiate insulin secretion postprandially depending on glucose
  • exert effects by various G-protein coupled receptors on B cells

Incretin mimetic drugs bind to the GLP-1 receptors and are resistant to degradation by DPP-4 enzyme → ↑ insulin secretion, ↓ glucagon secretion, slow gastric emptying (↑ feeling of satiety, ↓ weight)

Side effects: GI symptoms, satiety, pancreatitis, weight loss (liraglutide shown to reduce CV events)

Contraindicated: existing GI motility dysfunction, chronic pancreatitis or family history of pancreatic tumors

25
Q

What are DPP-4 inhibitor drugs? MOA? Side effects? Contraindications?

A

e.g. Saxagliptin, alogliptin and sitagliptin
- Increase insulin secretion and reduce glucagon secretion

MOA:
- indirectly increase the endogenous incretin effect by inhibiting the DPP-4 that breaks down GLP-1 → ↑ insulin secretion, ↓ glucagon secretion, delayed gastric emptying

  • when in combo with SU derivatives, risk of hypoglycemia increases by 50%

Side effects: diarrhea/constipation, arthralgia, satiety, increased risk of pancreatitis, worsening renal function

Contraindications: liver failure or renal failure

26
Q

What is the role of insulin for diabetes therapy?

A
  • Insulin lowers glucose in a dose dependent manner over a wide range

Side effects: weight gain, glucose monitoring, constant titration for optimal dose

Different formulations: intermediate and long term
- different onset of action, duration of action and risks of hypoglycemia

27
Q

What is basal insulin? Uses?

A

E.g. Degludec and glargine (U300 & U100)

  • Degludec reduce risk of hypoglycemia
  • Glargine reduces risk of nocturnal hypoglycemia (U300 compared to U100)
  • Long acting insulin that covers the body’s basal metabolic insulin requirement in contrast to a bolus or prandial insulin
  • preferred initial insulin formulations in patients with T2DM

Clinical Pharmacology Year V NIŠ (9 decks)

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