Diabetes Mellitus - Putting Theory into Practice - Flashcards in University Pharmacy

State a short history of DM and the statistics/cost

Describe as linked to constant thirst, excessive urination, loss of weight. Cost implications of £14 billion and treating diabetes. First non-infectious disease that is increasing at epidemic rates

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What is diabetes mellitus?

Chronic metabolic disorder. Caused by - insulin deficiency (reduced secretion) or insulin resistance (reduced effectiveness), both. Characterised by persistent rise in blood glucose concentration (hyperglycaemia). Acute symptoms/chronic complications

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What is type 1 diabetes?

Develops as a child/young adult, autoimmune destruction of pancreatic beta cells. Sudden onset associated with rapid weight loss. No insulin produced

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What is type 2 diabetes?

Affects people > 45 yrs old. Insulin resistance and insulin deficiency. Slow onset associated with being overweight (insulin not used effectively, reduced production of insulin)

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What is type 1.5 (LADA) diabetes?

Latent autoimmune diabetes in adults. Gradual autoimmune destruction of pancreatic beta cells. Slower onset in patients >30 yrs old. Not linked to insulin resistance

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What is MODY?

Maturity onset diabetes of the young. Hereditary condition - autosomal gene mutation. Ineffective insulin production. Slow onset in patients <30 yrs old

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What are the secondary forms of diabetes?

Gestational diabetes. Drug-induced e.g. corticosteroids. Severe pancreatitis. Pancreatectomy. Cystic fibrosis

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What are the risk factors for type 1 diabetes?

Family history, genetics, environmental factors

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What are the risk factors for type 2 diabetes?

Family history, ethnicity, age, high blood pressure, obesity, sedentary lifestyle, gestational diabetes, polycystic ovary syndrome

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What is the role of insulin? (1)

Secreted by beta cells of pancreas. Secretion is stimulated by high blood glucose levels and inhibited by low blood glucose levels. Effects on - glucose breakdown, storage/release, storage and breakdown of fat, synthesis and breakdown of proteins

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What is the role of insulin? (2)

Essential for use and storage of energy. High blood glucose levels (beta cells release insulin into blood, liver converts glucose to glycogen/fats/protein, muscles used glucose/convert to glycogen), blood glucose levels fall

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What is the role of insulin? (3)

Low blood glucose levels (alpha cells release glucagon into blood, liver converts glycogen into glucose, blood glucose levels rise). Homeostasis (normal blood glucose levels <110 mg/dL)

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Describe features of insulin deficiency (1)

Cells think there are low glucose levels, response – methods to increase glucose levels, results in hyperglycemia

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Describe features of insulin deficiency (2)

Effects on glucose - reduce glucose uptake in cells, reduce glycolysis, reduce glycogenesis, increase gluconeogenesis, increase glycogen breakdown

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How do the effects of insulin deficiency cause symptoms of hyperglycaemia?

Increased plasma osmolarity, H2O moves out of cells into plasma, tissue dehydration, CNS depression. Polydipsia. Glucosuria, polyuria, loss of Na and K, hypovolaemia, polydipisia

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What are the body's sources of energy?

Glucose, lipids and proteins

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If glucose is not available in cells what does the body do? (1)

Glycogen is broken down for energy production. Once glycogen is utilised fat then protein are broken down. Lipolysis - reduce storage, catabolism, weight loss, ketoacidosis

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If glucose is not available in cells what does the body do? (2)

Protein - reduced amino acid uptake into cells, reduced synthesis, catabolism, muscle wasting and weight loss

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State the process of lipolysis

Free fatty acids - acetyl CoA, metabolised. Ketones - ketonuria, acidosis, reduced pH/HCO3-, increased lactate/respiration

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What are the main symptoms of diabetes?

Polydipsia, polyphagia, lethargy, stupor, blurred vision, breath smells of acetone, weight loss, hyperventilation, nausea, vomiting, abdominal pain, polyuria, glycosuria

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What are the signs and symptoms of hyperglycaemia? (1)

Thirst (polydipsia). Excessive urination (polyuria, nocturia), Glycosuria - UTI, vaginal thrush, urethritis, balanitis vulvitis (restrictions on use of anti-fungals - ongoing thrush could be a symptom of hyperglycaemia)

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What are the signs and symptoms of hyperglycaemia? (2)

Visual disturbances. Fatigue, muscle ache, nausea

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What are the signs and symptoms associated with fat and protein catabolism? (1)

Weight loss, ketonuria, sweet smelling breath (pear drops), acidosis (reduced pH/HCO3, increased lactate/respiratory rate). In severe cases - coma (dehydration/acidosis)

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What are the signs and symptoms associated with fat and protein catabolism? (2)

Asymptomatic patients - symptoms of chronic complications, incidental discovery during routine medical examination, more likely in T2DM patients

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Describe features of diagnosing diabetes (1)

Symptoms (will prompt investigations). Blood glucose level measurements (fasting - >7 mmol/L, random venous - >11.1 mmol/L, blood glucose level >11 mmol/L 2h after 75 g oral glucose tolerance test). HbA1c (cut off, >48 mmol/L, 6.5%)

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Describe features of diagnosing diabetes (2)

HbA1c measured for type 2 diabetes (sugar control over past 2-3 months), not good for rapid changes (e.g. diabetes during pregnancy, type 1 diabetes)

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State features of the natural history of type 2 diabetes

Microvascular changes, non-diabetes hyperglycaemia (step before diagnosis of type 2 diabetes)

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What is non-diabetic hyperglycaemia? (1)

Defined as fasting plasma glucose 5.5-6.9 mmol/L or HbA1c level of 42-47 mmol/mol (6.0-6.4%)

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What is non-diabetic hyperglycaemia? (2)

Offer lifestyle change programme (National Diabetes Prevention Programme, other interventions - increase physical activity, achieve/maintain weight loss, in dietary fibre, reduction of fat intake (especially saturated fat). Regular follow up

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What is non-diabetic hyperglycaemia? (3)

Repeat HbA1c/FPG at least yearly or sooner if indicated

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Describe features of monitoring

Signs/symptoms of hypo-/hyperglycaemia. Signs/symptoms of chronic complications. Measure blood glucose levels instantly (CBGs). HbA1c (glycosylated Hb) in long term. CV monitoring e.g. BP, cholesterol. Urine proteins. (Care processes, annual check)

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Describe features of HbA1c

Glycosylated Hb. Reflects what blood glucose control has been like over the last few months. Aim for level of <48 mmol/mol (<6.5). Measure every 3-6 months. Treatment targets/decisions made on an individual basis. Differs in type 1 and type 2 DM

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Describe features of glucose level tests - urine testing

Only detects hyperglycaemia not hypoglycaemia, retrospective, simple, cheap, quick. Renal threshold varies

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Describe features of glucose level tests - blood testing

Detects hypo-/hyperglycaemia. Tells you current blood glucose level. More expensive than urine testing. Can be painful. Easy to read

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What are acute complications caused by?

Disturbances in glycaemic control (reversible, not long term)

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Describe features of hyperglycaemia (1)

Acute hyperglycaemia can be life threatening. Infection, illness, missed doses, medications. Presenting symptoms - confusion, lethargy, dehydration, excessive thirst, urination

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Describe features of hyperglycaemia (2)

Diabetic ketoacidosis, hyper-osmolar hyperglycaemic state, require hospital admission

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What is the DKA diagnosis?

Hyperglycaemia (blood glucose >11 mmol/L) or known diabetes. Ketosis - urinary ketones >2+ or plasma ketones >3 mmol/L. +/- ketoacidosis: venous pH <7.35 and/or bicarbonate <18 mmol/L. DKA - type 1

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What is the HHS diagnosis?

Characteristic features - hypovolaemia, marked hyperglycaemia (30 mmol/L or more) without significant hyperketonaemia (<3 mmol/L) or acidosis (pH >7.3, bicarbonate >18 mmol/L). Osmolarity usually >320 mosmol/kg. Mixed HHS/DKA can occur. HHS - type 2

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Describe features of hypoglycaemia (1)

Acute hypoglycaemia (<4 mmol) can be life threatening. Adrenergic signs/symptoms - sweating, shaking/trembling, tingling in hands/lips, hunger, palpitations, pallor, headache, blurred vision, dizziness

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Describe features of hypoglycaemia (2)

Neuroglycopaenic signs/symptoms - difficulty in concentration, slurred speech, odd behaviour, aggression, anxiety, confusion, altered conscious state/drowsiness, loss of consciousness, fitting

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What are the causes of hypoglycaemia? (1)

Taking insulin at the wrong time. Missing insulin doses/overcompensating later. Inaccurate doses. Missing meals. Dietary changes without dose adjustments. Problems with injection technique/site. Failure to re-suspend premixed or intermediate insulin

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What are the causes of hypoglycaemia? (2)

Alcohol/drugs, exercise, other illnesses, deteriorating renal function

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Describe features of chronic complications

Irreversible, occurs after years of poorly controlled hyperglycaemia. Main cause of morbidity/mortality in diabetes. Widespread micro-/macrovascular effects

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What are the causes of chronic complications?

In some cells glucose uptake is not reliant on insulin. In hyperglycaemia these cells take up excess amount of glucose (protein glycosylation, osmotic damage to cells, H2O travels in causing cell lysis). Accelerated atherosclerosis

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Summarise the chronic complications (1)

Macrovascular (CVD, HTN, peripheral vascular disease - annual check, albuminuria/BP/lipid profile/abdominal adiposity/smoking). Microvascular - retinopathy, nephropathy, peripheral neuropathy (annual check, eyes/albumin:creatinine ratio/symptoms)

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Summarise the chronic complications (2)

Macro/microvascular conditions - diabetic foot (foot examination annually)

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Describe features of microvascular complications

Macroangiopathy (large vessel disease). Cause - atherosclerosis. Effect is increased with risk of - IHD (angina/MI), stroke, HTN, peripheral vascular disease. Pain in calf/legs/arms due to poor blood supply. Ulcers, amputation

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Describe features of CV risk - lipids

Patients with type 1 diabetes, modify risk factors, offer 20 mg atorvastatin. Patients with type 2 diabetes, QRISK2 calculation – lifestyle advice/review for <10%, 10-20%, lifestyle/offer 20 mg atorvastatin. Secondary prevention, adjust dose

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Describe features of CV risk - BP (1)

Offer drug treatment in addition to lifestyle to adults (any age) if persistent stage 2 HTN

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Describe features of CV risk - BP (2)

Start treatment/lifestyle changes in ages <80 years with persistent stage 1 HTN when 1+ present: target organ damage, established CVD, diabetes, estimated 10-year CVD risk of 10% or more

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Describe features of CV risk - BP (3)

Discuss with the person - individual CVD risk, preferences for treatment, risks and benefits, lifestyle interventions

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What are the target levels and review according to NICE? (1)

Type 1 (135/85 mmHg, 130/80 mmHg if albuminuria or 2 or more features of metabolic syndrome). Type 2 (140/90mmHg if aged under 80 yrs, 150/90mmHg if aged 80+, use clinical judgement if frailty or multi-morbidity)

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What are the target levels and review according to NICE? (2)

CKD/diabetes (Keep below 130/80mmHg. Systolic target range 120- 129mmHg). At least annual review (depends on BP and CKD level)

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What are the target levels and review according to NICE? (3)

Type 2 diabetes - diagnosed with HTN prior to T2DM, diagnosis, review choice of agents. Only change if poor control or metabolic problems or microvascular complications necessitate

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What is the BP treatment choice for type 2 diabetes? (1)

ACEi (or ARB for Afro-Caribbean patients or persistent cough). Discuss adherence, occur CCD or TLD. Review medication, offer either CCB or TLD (if not added already)

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What is the BP treatment choice for type 2 diabetes? (2)

If BP not controlled take optimal doses of 3 medications, regardless of resistant HTN. If confirmed resistant HTN, consider low dose spironolactone (caution for eGFR), beta blocker or alpha blocker (K < or > 4.5 mmol/L)

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What is the BP management for type 1 diabetes? (1)

Lifestyle - provide information on potential to improve BP. Offer assistance in achieving their aims. Medication - start trail of renin-angiotension blocking drugs as first line for HTN

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What is the BP management for type 1 diabetes? (2)

Do not allow concerns over potential side effects to inhibit advising and offering the necessary use of any class of drugs, unless the side effects become symptomatic or otherwise clinically significant

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What is the BP management for type 1 diabetes? (3)

Selective beta adrenergic blockers (don't avoid where indicated in adults or insulin). Low dose thiazides (may be combined with beta blockers). CCBs (use only long acting preparations)

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Describe features of microvascular complications (1)

Microangiopathy (small vessel disease). Cause (protein glycosylation, osmotic damage). Effect - eyes (retinopathy, cataracts, glaucoma, blindness), kidneys (nephropathy, leading to chronic renal failure and HTN)

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Describe features of microvascular complications (2)

Nerves (sensory neuropathy - numbness, tingling, neuropathic pain, autonomic neuropathy - impotence, GI disturbance (gastroperesis), postural HTN

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What are the benefits of a lower HbA1c?

Reduces the risk of - microvascular disease, PVD, MI, stroke, CHF, cataract extraction, (retinopathy) death related to diabetes

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What is diabetic neuropathy? (1)

Diabetes affecting the kidney (protein leaking, leads to protein in urine). Can cause tingling/burning sensation, numbness, sensitivity and even sharp jabbing pain

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What is diabetic neuropathy? (2)

Increased susceptibility to infection, impaired immune response. Diabetic foot. Caused by PVD, neuropathy, increased susceptibility to infection

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Diabetes Mellitus - Putting Theory into Practice

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