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Medicine year 4 CDM > Block 1: diabetes > Flashcards

Block 1: diabetes Flashcards

1
Q

Diabetes symptoms

A

Polyuria, fatigue, blurred vision, polydipsia, weight loss, nocturia

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2
Q

Diagnosing diabetes if asymptomatic

A
  • fasting glucose greater than or equal to7.0 mmol/l
  • random glucose greater than or equal to11.1 mmol/l(or after 75g oral glucose tolerance test)
  • If patient is asymptomatic needs two blood results to confirm
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3
Q

Using HbA1c to diagnose diabetes

A
  • When greater than or equal to 48mmol/mol
  • If less does not exclude diabetes
  • In asymptomatic patient test must be repeated to confirm diagnosis
  • Misleading HbA1c can be caused by high red cell turnover: haemoglobinopathies, haemolytic anaemia, iron deficient anaemia, gestational diabetes
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4
Q

Prediabetes

A
  • HbA1c is 42-47
  • Fasting glucose is 6.1-6.9
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5
Q

Impaired fasting glucose and impaired glucose tolerance

A
  • Fasting glucose between 6.1-7 is impaired fasting glucose (IFG)
  • Impaired glucose tolerance (IGT) is a fasting plasma glucose less than 7 and a OGTT between 7.8 and 11.1
  • Patients with IFG should be offered an OGTT to rule out diabetes of IGT
  • In IFG OGTT is <7.8
  • In IGT and IGT HBa1c is 42-47
  • Incidence increases with age
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6
Q

General principles of medication in T2D

A

You can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)

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7
Q

Dietary advice T2D

A
  • Reduce saturated fats but include low fat dairy products and oily fish
  • Encourage high fibre, low-glycaemic index carbohydrates
  • Initial target weight for an overweight person is 5-10%
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8
Q

HbA1c targets

A
  • Should be checked every 3-6 months till stable, then 6 monthly
  • Can be relaxed for elderly
  • If patient wants to try lifestyle treatment first, HbA1c target is 48
  • If patient on metformin target is 48
  • If 6 months after starting metformin HbA1c has risen to 51, to increase metformin from 500mg bd to 500mg td and reinforce lifestyle
  • If already on one drug but HbA1c has risen to 58 then target is 53
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9
Q

Initial drug therapy for T2D

A
  • If high risk of CVD, established CVD or chronic heart failure then prescribe metformin and once established an SGLT-2 inhibitor
  • If no cardiovascular risk prescribe metformin
  • Metformin should be titrated slowly to reduce gastro side effects
  • If metformin not tolerated prescribe modified release
  • If cardiovascular risk increases an SGLT-2 inhibitor can be prescribed at any time
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10
Q

What to do if metformin is contraindicated

A
  • If risk of CVD/Heart failure: SGLT-2 (empagliflozin) montherapy
  • If no risk prescribe an DPP-4 inhibitor (Sitagliptin) or Pioglitazone or Sulfonylurea. SGLT-2 can be used occasionaly
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11
Q

Further drug therapy if HbA1c targets aren’t met

A
  • If HbA1c has risen to 58 then further treatment is indicated
  • Add one of: DPP-4 inhibitor (Sitagliptin), Pioglitazone, Sulfonylurea (Gliclazide), SGLT-2 inhibitor (empagliflozin) i.e. Metformin + X
  • Add another drug from the same list i.e. Metformin + x + z. OR start insulin based treatment
  • Further therapy= if triple therapy is not effective switch one of the drugs for a GLP-1 mimetic if BMI >35 or insulin has occupational implications. GLP-1 mimetic is only added to insulin in specialist care. Only continue if there is a reduction of 11 mmol HbA1c and weight loss of 3% in 6 months
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12
Q

Starting insulin

A
  • Metformin should be considered
  • Start with human NPH insulin (isophane, intermediate acting) taken at bed time or twice daily
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13
Q

Microvascular complications of diabetes

A
  • Diabetic retinopathy: damage to retinal vasculature leading to microaneurysms, haemorrhage and neovascularisation. Treatment is laser therapy and anti-VEGF injections
  • Diabetic Nephropathy: common cause of CKD. Characterised by albuminuria, declining GFR and renal failure. Management is blood glucose and pressure control, use of ACEI’s or ARBs and dietary modification
  • Diabetic Neuropathy: includes peripheral neuropathy, autonomic neuropathy, and focal neuropathies. Peripheral neuropathy presents with pain, numbness and tingling in the extremities increasing the risk of foot ulcers and amputation. Autonomic neuropathy affects the autonomic nervous system leading to GI, cardiovascular and GU dysfunction. Focal neuropathies affects specific nerves resulting in localised weakness or pain. Management is tight glycaemic control, pain management and appropriate foot care
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14
Q

Diabetes: Macrovascular complications

A
  • Coronary artery disease: management is risk factor modification of blood glucose, lipid and blood pressure control, using antiplatelet therapy and revascularisation procedures
  • Cerebrovascular disease: diabetic patients are at increased risk of stroke and TIA. Stroke prevention includes blood glucose, lipid and blood pressure control, antiplatelt therapy and lifestyle modification such as smoking cessation, exercise and weight management
  • Peripheral artery disease: can cause intermittent claudication, critical limb ischaemia and amputation. Management includes risk factor modication, exercise therapy, revascularisation procedures when needed and diligent food care to prevent ulcers and infection
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15
Q

Other diabetes complications

A
  • Diabetic foot: due to combination of neuropathy, PAD and impaired wound healing. Can result in foot ulcers, infections and ultimately amputations
  • Infections: T2DM patients are more susceptible to infections due to immune dysfunction, impaired wound healing, and increased colonization of pathogens. Common infections include urinary tract infections, skin and soft tissue infections, and respiratory infections.
  • Hyperglycaemic emergencies: DKA is rare in T2DM but may occur in cases of severe insulin deficiency. Hyperosmolar hyperglycemic state (HHS) is more common in T2DM patients and is characterized by severe hyperglycemia, hyperosmolarity, and dehydration. Both conditions require prompt recognition and management with fluid resuscitation, insulin therapy, and electrolyte replacement.
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16
Q

Hypoglycaemia defenition

A

Occurs when glucose concentrations fall below 3.3mmol. Occurs more commonly in diabetics

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17
Q

Diabetes and Hypoglycaemia

A
  • Hypoglycaemia is caused by excess insulin by either taking too much or not eating enough after administering insulin
  • Sulfonylureas i.e. gliclazide increase secretions of insulin from beta cells and cause Hypoglycaemia
  • More likely to occur in diabetics with a viral illness, have drunk alcohol, exercised more than usual or started/changed medication
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18
Q

Non diabetic causes of hypoglycaemia

A
  • Iatrogenic: indomethacin, pentamidine, quinine, sulfonamide, IGF-1 and lithium.
  • Alcohol consumption due to its inhibitory effect on gluconeogenesis and glycogenolysis.
  • Rare causes: Hypopituitarism and Addisons disease
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19
Q

Hypoglycaemia physiology

A
  • Low blood glucose increases production of glucagon from alpha cells and reduced production of insulin from the beta cells of the pancreas. Causes liver gluconeogenesis and glycogenolysis
  • Reduced blood glucose increases adrenaline secretion from the adrenal medulla
  • Reduced blood glucose stimulates secretion of GH from the pituitary, ACTH is also secreted from the pituitary stimulation cortisol secretion from the adrenal cortex
  • All this increases blood glucose
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20
Q

Symptoms of hypoglycaemia

A
  • Autonomic symptoms (<3.3): release of glucagon and adrenaline causes sweating, shaking, hunger, anxiety and nausea
  • Neuroglycopenic symptoms (<2.8); due to inadequate glucose supply to the brain causes weakness, vision change, confusion and dizziness
  • Severe and uncommon symptoms: convulsion and coma
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21
Q

Whipples triad

A
  • Aids diagnosis of hypoglycaemia
  • Symptoms or signs of hypoglycaemia
  • Low blood glucose
  • Resolution of symptoms with correction of blood glucose
22
Q

Further tests for hypoglycaemia

A
  • Serum insulin: elevated in insulinoma.
  • Serum C-peptide: elevated in insulinoma or sulfonylurea use.
  • Serum cortisol: reduced in adrenal insufficiency or hypopituitarism.
  • 48 to 72-hour fast with serial blood glucose, serum proinsulin, C-peptide and insulin levels: the gold standard investigation for insulinoma.
  • TSH, U&E, LFTs: abnormalities help identify secondary causes of hypoglycaemia such as hypothyroidism, chronic liver disease or kidney disease.
23
Q

Management of hypoglycaemia in the community

A
  • Initially oral glucose 10-20g given in liquid form or sugar lumps, done in the community
  • Alternatively a quick acting carbohydrate i.e. Glucogel or Dextrogel
  • A ‘Hypokit’ can be prescribed which contains glucagon for IM or SC injections
24
Q

Management of Hypoglycaemia in the hospital setting and further management

A
  • If patient is alert give a quick acting carbohydrate
  • If patient is unconscious or unable to swallow, give SC or IM injections of glucagon
  • Alternatively 20% glucose solution in a large vein

Further management= Diazoxide can be given in chronic hypoglycaemia with excess endogenous insulin secretion

25
Q

Complications of hypoglycaemia

A
  • Short term: coma and seizures, can cause permanaent neurological sequelae and should be managed in intensive care
  • Long term: recurrent episodes can cause ‘hypoglycaemic unawareness’ where patients dont have autonomic symptoms of low blood glucose. More common in T2D and increases chances of neuroglycopenic complications
26
Q

Definition and risk factors for hypertension

A

Definition: chronically raised blood pressure. Important risk factor for developing cardiovascular disease such as ischaemic heart disease and stroke. Unlikely to have symptoms

Risk factors for primary hypertension: age, family history, obesity, high salt intake, sedentary lifestyle and alcohol consumption.

27
Q

Causes of secondary hypertension

A
  • Renal: Glomerulonephritis, Chronic pyelonephritis, Acute polycystic kidney disease, Renal artery stenosis
  • Endocrine: Primary hyperaldosteronism, Phaeochromocytoma, Crushing’s syndrome, Liddle’s syndrome, Congenital adrenal hyperplasia, Acromegaly
  • Other causes: Glucocorticoids, NSAID’s, Pregnancy, Coarctation of the aorta, COCP
28
Q

Symptoms of very high blood pressure

A

Headache, visual disturbance, seizures

29
Q

Further tests for newly diagnosed hypertension

A
  • fundoscopy: to check for hypertensive retinopathy
  • urine dipstick and U&E’s: to check for renal disease, either as a cause or consequence of hypertension
  • ECG: to check for left ventricular hypertrophy or ischaemic heart disease
  • HbA1c: to check for diabetes
  • Lipids: to check for hyperlipidaemia
30
Q

Diagnosing hypertension

A
  • 24 hour blood pressure monitoring is now recommended
  • After blood pressure is recorded in clinic ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) confirms the diagnosis
  • Take blood pressure from both arms, if difference of 20mmHg then repeat. If difference remains then record the high reading
  • A second reading during the consultation should be done, if the first reading is > 140/90 mmHg. The lower reading of the two should determine further management.
31
Q

Blood pressure classification

A
  • Stage 1: Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
  • Stage 2: Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
  • Stage 3: Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg
32
Q

What to do if blood pressure is >= 180/110

A
  • Consider immediate treatment
  • If signs of papiloedema or retinal haemorrhage, same day assessment by specialist
  • Referral is phaeochromocytoma is suspected (labile or postural hypertension, headache, palpitations, pallor and diaphoresis)
33
Q

ABPM

A
  • at least 2 measurements per hour during the person’s usual waking hours (for example, between 08:00 and 22:00)
  • use the average value of at least 14 measurements
  • If not tolerated offer HBPM
34
Q

HBPM

A
  • For each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated
  • BP should be recorded twice daily, ideally in the morning and evening
  • BP should be recorded for at least 4 days, ideally for 7 days
  • discard the measurements taken on the first day and use the average value of all the remaining measurements
35
Q

When to treat stage 1 hypertension

A
  • If <80 AND any of the following: target organ damage, cardiovascular disease, renal disease, diabetes or a 10% QRISK score
  • If <60 and QRISK score <10%
  • If <40 consider specialist evaluation
36
Q

Hypertension: lifestyle management

A
  • A low salt diet of less than 6g/day and ideally 3g/day
  • Reduce caffeine intake
  • Stop smoking, drink less alcohol, eat a balanced diet, exercise more, lose weight
37
Q

Step 1 in treatment for hypertension

A
  • patients < 55-years-old or a background of type 2 diabetes mellitus:(ACE-i orARB):(A). Angiotensin receptor blockers should be used where[ACE inhibitors] are not tolerated (e.g. due to a cough)
  • Patients >= 55-years-old or of black African or African–Caribbean origin:Calcium channel blocker(C)
38
Q

Step 2 and 3 for treatment in hypertension

A
  • If already on an ACE-i or ARB add a CCB or a thiazide like diuretic (Indapamide, Bendroflumethiazide)
  • If already taking a Calcium channel blocker add an ACE-i or ARB or a thiazide like diuretic
  • (A+C) or (A+D) or (C+A) or (C+D)

Sep 3: add a third drug. If already taking A+C then add a D. If already on A+D then add a C

39
Q

Step 4 for treatment in hypertension

A
  • Step 4 is resistant hypertension and they suggest adding a 4th drug or seeking specialist advice
  • First check for: confirm elevated clinic BP with ABPM or HBPM, assess for postural hypotension, discuss adherence
  • If potassium <4.5 add low dose spironolactone
  • If potassium >4.5 then add an alpha or beta blocker
  • If blood pressure remains uncontrolled after 4 drugs seek expert advice
40
Q

Blood pressure targets

A
  • Age <80: clinic BP is 140/90 and ABPM/HBPM is 135/85
  • Age >80 clinic BP is 150/90 and ABPM/HBPM is 145/85
41
Q

Hypertension complications 1

A
  • Cardiovascular: CAD by acceleration atherosclerosis leading to an MI and angina. Heart failure due to increased workload on the heart causing left ventricular hypertrophy (LVH) and heart failure. Atrial fibrilation which can cause stroke
  • Cerebrovascular: Stroke (ischaemic and haemorrhagic) by causing atherosclerosis, arterial stiffness, endothelial dysfunction. Vascular dementia due to cerebral small vessel disease and impaired blood flow to the brain
42
Q

Hypertension complications 2

A
  • Renal: CKD as it damaged the glomeruli and renal vasculature, reducing kidney function
  • Peripheral vascular complications: Peripheral arterial disease (PAD) causes reduced blood flow and potentially ischaemia in the limbs. Aortic aneurysm, weakens the aortic wall, can increase risk of rupture and life threatening bleed
  • Metabolic syndrome: obesity, dyslipidaemia and insulin resistance
43
Q

Impaired glucose tolerance importance

A
  • 50% of people with IGT will develop T2D.
  • Increased risk of cardiovascular disease.
  • Intervention can prevent T2D: diet and exercise with modest weight loss +/- Metformin
  • NHS England has a National Diabetes Prevention Programme: at least 13 sessions over 9 months with health care professionals. If lifestyle changes ineffective then trial metformin or acarbose. Address other CV disease risk factors Blood pressure, plasma cholesterol, smoking, alcohol
44
Q

What is diabetes

A

Diabetes mellitus: a net deficiency of insulin leading to an imbalance in glucose production and utilisation

T2D gene: TCF7L2

Prevalence in UK: 6.5%, about 50% undiagnosed

45
Q

T1D

A
  • usually occurs <40 years of age,
  • peak incidence adolescence but getting younger.
  • Strong genetic and autoimmune basis.
  • Always requires insulin
  • Autoantibodies: Glutamic acid decarboxylase (GAD 65), Islet cells (not specific or sensitive), Insulin, Tyrosine phosphatases (IA2 & IA2beta), Zinc transporter (ZnT8)
  • Genetic: >90% have DR4, DQB0302 and/or DR3, DQB0201
46
Q

Latent autoimmune diabetes in adults (LADA)

A
  • Up to 10% adults in Scandinavia have autoantibodies to b cell antigens, similar to T1D but occurs in adults >40
  • Share genetic features with Type 1 (HLA) and Type 2 (TCF7L2)
  • Variable phenotype but unlikely to be overweight compared to T2D
  • Many develop insulin dependence
47
Q

Diabetes mellitus: other types

A
  • Secondary – due to pancreatic disease e.g. pancreatitis (acute, chronic and calcific)
  • Monogenic – Maturity Onset Diabetes of the Young (MODY) (1-4% young adults with diabetes in UK). 37% glucokinase mutations; 63% transcription factors. Slow presenting but under 25 and dont need insulin. Due to one gene
  • Congenital & neonatal
48
Q

Diabetes mellitus: other types 2

A
  • Syndromic e.g. lipodystrophies, Prader-Willi syndrome, myotonic dystrophy, Wolfram (DIDMOAD)
  • Chromosomal e.g. Down and Turner syndrome increased Type 1 diabetes
  • Mitochondrial – maternal inheritance with deafness and cardio-neural problems ( around 1% of those with Type 2 diabetes in Japan). Be concerned in patients with bilateral sensorineural deafness
49
Q

Secondary diabetes

A
  • Cystic fibrosis - now more common with increased survival
  • Haemachromatosis due to iron deposition in pancreas, have sun tan like physical appearance
  • Drug induced e.g. chronic steroid use, calcineurin inhibitors, statins, major anti-psychotic agents, HAART
50
Q

Diabetes: Associated Endociopathies

A
  • Cushing’s including iatrogenic - Glucocorticoids
  • Acromegaly – Growth Hormone
    Phaeochromocytoma – Catecholamines
  • Glucagonomas
  • Somatostatinomas
  • Hyperthyroidism (NB autoimmune link with Type 1)

Medicine year 4 CDM (44 decks)

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