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GP block (Y3) > Week 8: Diabetes > Flashcards

Week 8: Diabetes Flashcards

1
Q

normal reaction to glucose

A

When you eat, your body breaks food down into glucose. Glucose is a type if sugar that is your body’s main energy source.

  • As blood glucose rises, the body sends signals to the pancreas, which releases insulin
  • Insulin (B-cells) binds to insulin receptors, unlocking the cell so glucose can pass into it (bringing GLUT 4 receptors to the surface of cells)
  • Most glucose is used for energy right away
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2
Q

pancreatic islet cells

A

beta- insulin

alpha- glucagon

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3
Q

why does blood glucose rise in diabetes

A

2 fundamental principle mechanisms

  1. Inability to produce insulin due to beta cell failure
  2. Insulin production adequate but insulin resistance prevents insulin working effectively and invariably linked to obesity
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4
Q

types of diabetes related to blood glucose

A
  • Type 1 and 2
  • Gestation
  • Prediabetes
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5
Q

normal blood glucose rnage

A

3.3-7 mmol/l

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6
Q

diagnostic criteria of diabetes based on

A
  • Diagnosis
    • Symptoms (retinopathy, neuropathy etc) plus one abnormal result or
    • Two abnormal results at different times (at least week)
  • Glucose levels
    • Fasting >7.0 mmol/l and/or
    • 2 hours after 75g glucose >11.1 mmol/l
    • Hba1c >6.5%
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7
Q

fasting blood glucose above

A

7.0 mmol/l

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8
Q

Oral glucose tolerance test above

A

11.1 mmol/l 2 hours after 75g

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9
Q

Hba1c above

A

6.5%

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10
Q

General management of DM

*

A
  • Glycaemic control
  • Diet and exercise
  • Oral hypoglycaemic drugs
  • Insulins
  • Limiting cardiovascular risk by targeting risk factors
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11
Q

type 1 diabetes

A
  • Absolute insulin requirement
  • Pathophysiology: Autoimmune destruction of beta cells leading to absolute insulin deficiency
    • Associated with other autoimmune disease- e.g. thyroid
  • Causes
    • Not well understood
    • Genetic predisposition
    • Virus’
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12
Q

presentation of type 1 diabetes

A
  • <30 years old usually
  • Rapid onset (usually weeks)
  • Weight loss
  • Polyuria
  • Polydipsia
  • Ketosis
  • BMI below 35 usually
  • Late presentation- may be vomiting due to ketoacidosis
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13
Q

diagnosis of type 1 diabetes

A
  • Elevated plasma glucose- HbA1C, FBG, random plasma glucose of higher than 11.1mmol/l
  • Presence of autoantibodies
    • Islet cells- GAD65
  • Presence of ketones is an indication for immediate insulin therapy
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14
Q

target Hba1c for T1DM

A

A target HbA1c level of 48 mmol/mol (6.5%) or lower, to minimize the risk of long-term vascular complications

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15
Q

management of T1DM

A
  • Insulin therapy (exogenous)
    • Numerous devices  subcut injection
      • Intermediates
      • Rapid
      • Mixtures
      • Analogues
  • Pt education
    • Exercise
    • Diet
    • Glucose monitoring with BM
  • Regular HbA1ctesting and complications screening
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16
Q

types of insulin and example names

A
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17
Q

type 2 diabetes mellitus

A

relative insulin deficiency

Background

  • Pancreas loses ability to produce insulin or insulin production is adequate but insulin resistance prevents insulin working effectively
  • Cause- environmental
    • Obesity (central obesity)
    • Muscle and liver fat deposition
    • Physical inactivity
    • Genetic influence
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18
Q

RF for T2Dm

A
  • Prediabetes
  • High BMI
  • Genetically inclined
  • Physically inactive
  • Have had gestational diabetes
  • African American, Indian,
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19
Q

presentation of T2DM

A
  • >45 yo usually (getting younger)
  • Onset more gradual
  • Thirst
  • Polyuria
  • Tiredness
  • Infections
  • Change in vision
20
Q

diagnosis of T2DM

A
  • Based on clinical features
  • HbA1c of 48mmol/mol (6.5%) or more
  • FPG of 7 mmol/l or more in presence of symptoms of diabetes
  • Random plasma glucose of 11.1 mmol/l in presence of symptoms or signs of diabetes
    • If pt has no symptoms do a repeat testing of Hba1c
21
Q

management of T2DM

A
  • Lifestyle- weight loss
  • Non-insulin therapies (oral hypoglycaemics)
    • Biguanide i.e. metformin
    • Sulphonylureas
    • GLP1 analogues
    • SGLT2
  • Anti-obesity drugs- orlistat
  • Insulin
  • Patient education
22
Q

pharmacological management fo t2DM

A
23
Q

if patient doesnt tolerate metformin what is the next step

A

modified release metformin

24
Q

when is metformin offered

A

metformin is still first-line and should be offered if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions

25
Q

if whilst taking emtformin the HbA1c increases to 58 mmol/mol (7.5%) then a second drug should be added from the following list:

A
  • sulfonylureas
    • glicazide
  • gliptin
    • saxagliptin
  • pioglitazone
  • SGLT-2 inhibitor
    • canagliflozin
26
Q

if despite double therapy the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then triple therapy with one of the following combinations should be offered:

A
  • metformin + gliptin + sulfonylurea
  • metformin + pioglitazone + sulfonylurea
  • metformin + sulfonylurea + SGLT-2 inhibitor
  • metformin + pioglitazone + SGLT-2 inhibitor
  • OR insulin therapy should be considered
27
Q

Criteria for glucagon-like peptide1 (GLP1) mimetic (e.g. exenatide)

A
  • if triple therapy is not effective, not tolerated or contraindicated then NICE advise that we consider combination therapy with metformin, a sulfonylurea and a glucagon-like peptide1 (GLP1) mimetic if:
    • BMI >= 35 kg/m² and specific psychological or other medical problems associated with obesity or
    • BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
  • only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months
28
Q

Cannot tolerate metformin or contraindicated

A
  • if the HbA1c rises to 48 mmol/mol (6.5%) on lifestyle interventions, consider one of the following:
    • sulfonylurea
    • gliptin
    • pioglitazone
  • if the HbA1c has risen to 58 mmol/mol (7.5%) then a one of the following combinations should be used:
    • gliptin + pioglitazone
    • gliptin + sulfonylurea
    • pioglitazone + sulfonylurea
  • if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then consider insulin therapy
29
Q

Managing risk factors of diabetes

A
  • Regular BM testing, Hba1C
  • Reduce weight / BMI
    • Physical activity
    • DIET
  • Managing CVD risk
    • Statins for high cholesterol (atorvostatin)
    • Antihypertensives
  • Screening for diabetes complications
30
Q

antihypertensives in diabetics

A

ACE inhibitors or angiotensin II receptor blockers (ARB) are first-line

  • an ARB is preferred if the patient has a black African or African–Caribbean family origin
31
Q

Screening in T2DM

A
  • HbA1C monitored every 3-6 months
  • 12 monthly check with diabetic nurse
    • Kidney function
      • U and E
      • Creatinine
      • Albumin
    • Diabetic eye screening
    • Foot ulcer clinics
    • Cholesterol screening
    • BP
32
Q

routine delivery of insulin

A
  • HbA1C monitored every 3-6 months
  • 12 monthly check with diabetic nurse
    • Kidney function
      • U and E
      • Creatinine
      • Albumin
    • Diabetic eye screening
    • Foot ulcer clinics
    • Cholesterol screening
    • BP
33
Q

MOA of insulin

A
  • Insulin binds to insulin receptor
  • Causes cascade of events which causes GLUT4 receptors to translocate from the cytoplasm to the membrane
  • GLUT4 increases uptake of glucose into the cell lowering blood glucose
34
Q

Adverse drug response of insulin

A
  • Hypoglycaemia
  • Lipodystrophy
    • Lipohypertrophy or
    • lipoatrophy
35
Q

contradiction of insulin

A
  • renal impairment- hypoglycaemia risk
36
Q

drug-drug interaction of insulin

A
  • dose needs increasing with systemic steroids (steroids increase blood glucose)
  • caution with other hypoglycaemic agents
37
Q

basal bolus dosin

A

A common dosing schedule for young active TIDM patients which provides some flexibility if adherence is good

  • Basal- long acting e.g. glargine
    • Given once a day
  • Bolus- rapid acting e.g. aspart
    • Given before meals
38
Q

sulphonylureas

A

glicazides

  • stimulates pancreatic insulin secretion
  • beware of hypoglycaemia
  • weight gain
  • PO
39
Q

biguanides

A

metformin

  • reduces hepatic glucose output- stop glucoseneogenesis
  • no risk of hypoglycaemia
  • suppresses appetite
  • PO
40
Q

thiazolidinediones (glitazones)

A

pioglitazone

  • PPAR agonist
  • enhanced insulin sensitivity
  • risk of hypoglycaemia
  • increase weight
41
Q

Dipeptidyl peptidase-5 (DPP-4) inhibitors (gliptins)

A

saxagliptin, sitagliptin

  • prevent breakdown of incretins- incretins promote insulin secretion and suppress glucagon release
  • no risk of hypoglycaemia
  • reduces appetite
42
Q

SGLT-2 inhibitors

A

canagliflozin

  • reduces glucose reabsorption via sodium glucose channel
  • no risk of hypoglycaemia
  • helps decrease weight
43
Q

glucagon-like peptide-1 (GLP1) receptor agonists (incretin mimetic)

A

exenatide, liraglutide

  • mimics incretin- increases glucose-dependant synthesis of insulin
  • no risk of hypoglycaemia
  • increased satiety
  • Sub cut injection
44
Q

Macrovascular complications of DM

A
  • Cerebrovascular
    • stroke
  • Cardiovascular
    • MI
    • Angina
  • Peripheral vascular disease
    • Intermittent claudication
    • Gangrene
    • Peripheral neuropathy leading to
      • Diabetic foot ulceration
      • Charcot’s foot
45
Q

Microvascular complications

A
  • Retinopathy
  • Nephropathy
    • Diabetic nephropathy
  • Neuropathy
    • Erectile dysfunction
    • Foot ulceration
46
Q

acute complications

A

ketoacidosis and HHNS

47
Q

diabetic ketoacidosis triad

A
  • glucose > 11 mmol/l or known diabetes mellitus
  • pH < 7.3
  • ketones > 3 mmol/l or urine ketones ++ on dipstick

GP block (Y3) (39 decks)

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