Diabetes Notes PDF

Ngwarraye Ross, R. (2015). Bush flowers and bush medicine plants [acrylic on linen]. Medical History Museum.  Have opinions count Check your inbox for the SES – open 30 July to 1 September. Help shape the future of higher education in Australia. Have a say about your course and a chance to win $...

Ngwarraye Ross, R. (2015). Bush flowers and bush medicine plants [acrylic on linen]. Medical History Museum.  Have opinions count Check your inbox for the SES – open 30 July to 1 September. Help shape the future of higher education in Australia. Have a say about your course and a chance to win $1,000 – complete now for more chances to win! qilt.edu.au/ses Terms and conditions apply This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  Diabetes This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Learning outcomes Explain the action of incretin and insulin in the body Recall the drugs used in the management of diabetes Explain the pharmacodynamics and pharmacotherapeutics of drugs used to manage diabetes This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Why learn about Diabetes? 1 in 20 Australians were living with diabetes in 2021 Prevalence largely stable over the past 10 years Some of the drugs to manage diabetes are in the top 50 most dispensed in Australia Metformin (#7) Gliclazide (#47) People with type 2 diabetes often have other comorbidities including hypertension, hypercholesterolaemia and renal disease This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Diabetes Diabetes is: A condition where someone has elevated blood glucose levels (BGLs) A disorder of insulin deficiency or cellular resistance to insulin’s actions (or both) Three “types” of diabetes: 1. Type I diabetes: Insulin not produced by the pancreas Treatment: diet PLUS physical activity PLUS parenteral insulin PLUS manage CV risk factors 2. Type II diabetes: Insulin resistance - impaired glucose uptake, increased production of glucose by liver, decreased production of insulin Treatment: diet PLUS physical activity PLUS oral/injectable drugs for diabetes; sometimes parenteral insulin, PLUS manage CV risk factors 3. Gestational diabetes: diabetes that appears during pregnancy (and resolves after pregnancy) Treatment: diet PLUS physical activity; add medication if indicated This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Physiology of incretin and insulin Glucose levels in the body are primarily regulated by insulin Insulin is a hormone produced by the beta cells of the pancreas which regulates energy conservation and storage in the body Stimulates cellular uptake of glucose and amino acids in the periphery Promotes synthesis of complex molecules (e.g., glucose à glycogen in the liver, amino acids à proteins in muscle, fatty acids à triglycerides in the adipose) Also acts to oppose the above by: inhibiting glucose production and release in the liver, inhibiting proteolysis and lipolysis Primary stimulus for insulin release is an increase in BGL Other stimuli for release: incretin hormones and sympathetic nervous system stimulation (beta-2 receptor activation) This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Physiology of incretin and insulin Incretin hormones (including GLP-1) are released from the gut in response to food intake à slow gut emptying à stimulate glucose-dependant insulin release à suppress appetite à inhibit post-prandial release of glucagon Inactivated by DPP-4 This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes Insulin Metformin Others: Acarbose Pioglitazone Sulfonylureas GLP-1 analogues Sodium-glucose co-transporter-2 (SGLT2) inhibitors DPP-4 inhibitors Figure 30.4 from: Bryant, B., Knights, K., Darroch S., Rowland, A. (2019). Pharmacology for Health Professionals. Elsevier. This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes Insulin “Natural” insulin PLUS many modified insulins Modified insulins are classified by their pharmacokinetic profile (onset and duration of effect) Ultra short acting Short acting Intermediate acting Long acting Also available as “pre-mixed” Figure 57.2 from: Burchum, J.R. & Rosenthal, L.D. (2019). Lehne’s Pharmacology for Nursing Care E-Book : Lehne’s Pharmacology for Nursing Care E-Book: Vol. 10th edition. Saunders. This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes Insulin Side effects: hypoglycaemia, hypokalaemia, weight gain, lipodystrophy/atrophy at injection site Drug of choice for T1DM and GDM Monitoring: BGLs and HbA1C monitored Drug interactions: many drugs can affect blood glucose levels, including: Beta-blockers Corticosteroids Thyroid replacement hormone Thiazide diuretics Oral contraceptives CAUTION: Beta blockers can also mask the signs of hypoglycaemia This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes Metformin (a biguanide) Mechanism of action: a biguanide drug that: Reduces glucose absorption from the GIT Decreases hepatic glucose production Increases peripheral use of glucose Increases glucose uptake into cells Improves glucose sensitivity of tissues Side effects: GI upset, malabsorption of vitamin B12, lactic acidosis (rare) and acute hepatitis (rare) First-line drug therapy for T2DM Renally cleared Dose adjustments required if renal function is reduced Extra care if patient has condition that may affect renal function or cause tissue hypoxia or acidosis This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes Sulphonylureas (glibenclamide, gliclazide, glimepiride, glipizide) Mechanism of action: Stimulate insulin release from the pancreas May also inhibit gluconeogenesis à increase the number of insulin receptors Side effects: hypoglycaemia and weight gain (common), SJS (rare) May be added to metformin as second-line therapy Cheap Good outcomes in established chronic kidney disease This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes DPP-4 inhibitors (alogliptin, linagliptin, saxagliptin, sitagliptin, vildagliptin) Aka: dipeptidyl peptidase-4 inhibitors, “gliptins” Mechanism of action: DPP-4 is the enzyme responsible for breakdown of incretin hormones, inhibition à more GLP-1 and other incretins àIncrease glucose-dependent insulin secretion àReduce glucagon production (à less glucose being released by liver) Side effects: hypoglycaemia, musculoskeletal pain, pancreatitis (rare) Different clearance mechanism depending on drug: Linagliptin excreted in bile Vildagliptin is hepatically cleared, but dose adjustment required in renal dysfunction Others are renally cleared This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes SGLT2 inhibitors (dapagliflozin, empagliflozin, ertugliflozin) Aka: sodium-glucose co-transporter 2 inhibitors Mechanism of action: Reduce glucose reabsorption in the kidney through inhibition of SGLT2 Side effects: genital infections, polyuria, UTI, thirst, renal impairment, euglycaemic ketoacidosis Image from: Tulane University. (2017). PharmWiki: Medical Pharmacology|SGLT-2 Inhibitors. https://tmedweb.tulane.edu/pharmwiki/doku.php/sglt-2_inhibitors This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes GLP-1 analogues (exenatide, liraglutide, dulaglutide, semaglutide) Aka: Glucagon-like-peptide-1 analogues Mechanism of action: Analogues of the incretin hormone GLP-1 Delay gastric emptying à slow glucose absorption Decrease appetite Increase glucose-dependent insulin secretion Suppress inappropriate glucagon secretion Side effects: n/v in 50% of patients at start of therapy (worse in short-acting agents), GORD, fatigue, weight loss Can cause cholecystits, pancreatitis, and rarely, precipitate or worsen renal failure (all rare) Sub-cutaneous administration Different agents and formulations administered at different intervals This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Drugs for diabetes Others (acarbose, pioglitazone) Acarbose Pioglitazone Mechanism of action: Delays Mechanism of action: regulates intestinal absorption of genes associated with lipid and carbohydrates by inhibiting glucose metabolism Increase sensitivity of peripheral alpha-glucosidase enzymes in tissues to insulin the small intestine à reduces Decrease hepatic glucose release postprandial hyperglycaemia Rarely used due to poor safety Side effects: flatulence, profile: oedema, weight gain, diarrhoea, abdominal distension myalgia, increased fracture risk, & pain macular This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  Drug for diabetes General considerations Metformin is generally first-line Other drugs are added to obtain HBA1c reductions of at least 0.5% after 3 months of therapy Drug choice guided by: patient’s comorbidities (CVD, CKD, heart failure), side effect profile, and cost Image (RIGHT) from: The Royal Australian College of General Practitioners. (2020). Management of type 2 diabetes: A handbook for general practice. https://www.diabetesaustralia.com.au/wp-content/uploads/Available-here.pdf This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Bibliography Australian Institute of Health and Welfare. (2023, June 30). Diabetes: Australian facts. https://www.aihw.gov.au/reports/diabetes/diabetes/contents/about Burchum, J.R. & Rosenthal, L.D. (2019). Lehne’s Pharmacology for Nursing Care E-Book : Lehne’s Pharmacology for Nursing Care E-Book: Vol. 10th edition. Saunders. Neal, M. J. (2015). Medical Pharmacology at a Glance. John Wiley & Sons, Incorporated. PBS analytics and strategic insight section pricing and PBS policy branch technology assessment and access division, Australian Government | Department of Health and Aged Care. (2022). PBS expenditure and prescriptions report 1 July 2021 to 30 June 2022. http://www.pbs.gov.au/info/brose/statistics The Royal Australian College of General Practitioners. (2020). Management of type 2 diabetes: A handbook for general practice. https://www.diabetesaustralia.com.au/wp-content/uploads/Available-here.pdf This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  Diabetes: Case studies This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  Learning outcomes 1. What is HbA1c, blood glucose level, and what are the normal levels? 2. Describe the mechanism of action of Diabex and Janumet in the management of diabetes and link this to physiology and pathophysiology of blood glucose control 3. Identify key side effects of Diabex and Janumet, and link these to their pharmacology 4. What are the important history questions and examination required for diabetic patients in optometry? 5. What are the common ocular effects from diabetes? 6. What is diabetic retinopathy? This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  54-year-old diabetic female Presents with blurry vision >1/12. Wears distance specs full-time – don’t work anymore. Can see clearer without them. -no double vision – no flashes/floaters + Headaches only when tired. + Eyes are gritty at end of the day, doesn’t use any eyedrops. GH: Diabetes Dx 2018. Last HbA1c was 9% and BGL would go as high as 14mmol/L in the mornings. On Diabex – GP changing her medication to Janumet. +HTN – controlled with Avapro. – no HChol – no allergies. POH: LEE >2 years. No ocular injuries, infections, surgeries. FOH: Family history of diabetes on paternal side. No blindness. This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Diabetic history taking 1. Type of diabetes (Type 1 or 2?). 2. Duration (when were they diagnosed). 3. Glucose control (last HbA1c, or fasting BGL). 4. Medications/treatment. 5. GP/endocrinologist – and last blood test done (record the date if possible). 6. Complications e.g., renal disease, peripheral neuropathy etc. 7. Co-existing hypertension or hypercholesterolaemia. This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  HbA1c – haemoglobin A1c What is the In DM, high blood glucose oxidises haemoglobin in red blood cells (RBCs) and changes configuration. HbA1c? What HbA1c = no. of oxidised RBCs in the body. is normal RBCs live 120 days. HbA1c is a measure of blood glucose control over the last 3 months. blood glucose ≥ 6.5% or higher diagnostic of DM. Normal 20 retinal haemorrhages in each 4 quadrants. month (communicate with - Venous beading 2+ quadrants ophthalmologist) - Intraretinal microvascular abnormalities (IRMA) in 1+ quadrant PDR One of the following: Urgent ophthalmology referral - Neovascularisation within days- weeks - Vitreous/pre-retinal haemorrhage Macula oedema Appears as intraretinal thickening or hard exudates Refer in 1-2 months depending on distance from/not involving or involving the macula. severity and VA This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Management 1. Sudden ~1.50-2.00D hyperopic shift from variable blood glucose control. Should subside, no need to prescribe new specs. 2. Anterior – mild cataracts (monitor). Dry eyes advised Systane qid OU. 3. Posterior – moderate NPDR OU, no DMO (DFE again in 6 months). 4. Review 1/12 to re-check refraction with better DM control + report to GP. https://www.optometry.org.au/wp-content/uploads/Professional_support/Guidelines/clinical_guideline_diabetes_revised_sept_2018_final_designed.pdf Wilkinson et al. Proposed International Clinical Diabetic Retinopathy and Diabetic Macular Edema Disease Severity Scales. 2003. American Academy of Ophthalmology. This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Diabetic ocular complications Lids/lashes – xanthelasma, blepharitis. Conjunctiva – conjunctivitis. Cornea – dry eyes (superficial punctate keratopathy), loss of sensitivity due to peripheral neuropathy. Iris – rubeosis. Pupil – sluggish reaction, miotic due to weaker reaction to dilating drops. Loss of nerve terminals from dilator muscle. Lens – refraction change, early onset cataracts. Vitreous – floaters formation. Retina – diabetic retinopathy, tractional retinal detachment, neovascular glaucoma. Macula – oedema. Optic nerve – neuropathy, papillopathy, anterior ischemic optic neuropathy. Cranial nerve palsies e.g. CN6, CN3 most common. This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Explained complications of diabetes Refraction changes Lens shape due to sorbitol pathway in water being drawn into the lens à changes lens curvature, thickness and refractive index. Myopic shifts are typical, but also hyperopic especially on initiation of treatment. Prescription normalises within weeks of treatment. Dry eyes Lower tear film break up associated with peripheral neuropathy and uncontrolled disease. Reduced goblet cells – reduces tear stability. Damage to lacrimal gland. May not cause discomfort due to reduced corneal sensitivity (cranial nerve V). Superficial punctate keratitis. Cataract 4- fold in prevalence in diabetics. Posterior subcapsular cataracts is common. Diabetic retinopathy Presence of microvascular signs in a person with diabetes. These signs include: microaneurysms, haemorrhages, exudates, oedema, angiogenesis (new vessel growth), tractional retinal detachments, etc. Two main forms: non-proliferative and proliferative. Macula oedema occurs at any stage. This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  33-year-old male Diabetic eye exam. No concerns with vision. - No double vision/HAs – no flashes/floaters - No itchy/sore eyes. GH: Diabetes Dx at 8 years old. Last HbA1c was 7.5% 6 months ago. Insulin pump- NovoRapid regulates BGL (doesn’t check BGL that often). Is not too good with diet and exercise and under lot of stress. – no HChol – no HTN – no allergies. POH: LEE 2021 at FMC eye clinic (told he has something at back of eye). Never worn glasses. No ocular injuries, infections, surgeries. FOH: Sister is also diabetic. This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. What’s the pharmacology? Look up the monographs for this medication. Determine the key pharmacology & pharmacotherapeutics, including: Indication(s) NovoRapid Mechanism of action Side effects (3 common, 1 rare, ANY ocular) Precautions This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Examination Unaided VA R 6/4.8 L 6/6 (no change on pinhole R/L) Cover test ortho D&N, motility F&S, confrontation FTFC, pupils –RAPD + D&C response normal. Anterior – open angles OU, L/L, conj, cornea, lens clear OU IOP R 18 L 21mmHg (icare) @ 2:05pm. Posterior: dilated with 0.5% TROP and 2.5% Phenyl @ 2:10pm – (Images of fundus photos). This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  Right fundus – no DR/DMO Left Fundus – see image This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. OCT imaging Right macula – no DMO Left macula – see OCT below This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Now your turn! What are the risk factors for diabetic complications? What is the ocular diagnosis of this patient? How would you manage this patient? (review/referral and time period). This material has been reproduced and communicated to you by or on behalf of Flinders University in Accordance with section 113P of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.