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Endocrine and Metabolic Y3 > Type 1 and 2 diabetes mellitus > Flashcards

Type 1 and 2 diabetes mellitus Flashcards

1
Q

What is diabetes?

A

In diabetes, there is a lack of effectiveness of endogenous insulin

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2
Q

How is diabetes diagnosed in general?

A

DIAGNOSIS
- Symptoms of hyperglycaemia (polyuria/polydipsia/unexplained weight loss/visual blurring/genital thrush/lethargy) AND raised venous glucose detected once (fasting greater than/equal to 7mmol/l or random greater than/equal to 11.1mmol/l) OR
- Raised venous glucose on 2 separate occasions (fasting greater than/equal to 7mmol/l or random greater than/equal to 11.1mmol/l or OGTT 2h value greater than/equal to 11.1mmol/l)
- HbA1c greater than/equal to 48mmol/l but below this does not exclude DM

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3
Q

What are the different types of diabetes

A

Type 1:
- Immune destruction of the pancreas
- Insulin dependent diabetes
- usually young pts (12-16)
- DKA (ketoacidosis)
- Quite high glucose
- acute onset

Type 2:
- Resistance to the action of insulin
- Non-insulin dependent diabetes
- Maturity onset diabetes (30-70)
- Often overweight
- not prone to ketoacidosis
- Very high glucose
- insidious onset

Monogenic diabetes:
- (e.g. MODY “maturity onset diabetes of the young”, mitochondrial diabetes)
- Autosomal dominant inheritance. Family history of early onset diabetes is often present.

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4
Q

How is glucose control monitored?

A
  • Fingerprick glucose if T1DM, and T2DM if on insulin
  • Glycated haemoglobin (Hba1c) relates to mean glucose level over previous 8 weeks
  • Ask about hypoglycaemic attacks and symptoms
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5
Q

What is Type 1 diabetes mellitus?

A

Autoimmune response that triggers the destruction of insulin-producing beta cells in the pancreas leading to an absolute insulin deficiency (⇒ lipolysis and ketogenesis). Commonly manifests in childhood. Associated with HLA DR3/4. May be FH of autoimmune disease.

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6
Q

Explain the cause/ risk factors of type 1 diabetes mellitus

A
  • Caused by destruction of pancreatic insulin-producing beta cells (autoimmune process)
  • Associated with other autoimmune conditions
  • Genetic: >90% carry HLADR3 +/- DR4
  • with an environmental trigger (Enteroviral infections, Cow’s milk protein exposure, Seasonal variation & Changes in microbiota)
  • LADA (latent autoimmune diabetes of adults) is a form of T1DM with slower progression to insulin dependence
  • Autoantigens associated with T1DM:
    *Glutamic acid decarboxylase (GAD)
    *Insulin
    *Insulinoma-associated protein 2
    *Cation efflux zinc transporter
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7
Q

Summarise the epidemiology of type 1 diabetes mellitus

A

0.25% prevalence in the UK

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8
Q

What presenting symptoms of Type 1 DM can be found in the history?

A
  • Excessive urination (polyuria)
  • Nocturian (getting up in the night to pee)
  • Excessive thirst (polydipsia)
  • Blurring of vision
  • Recurrent infections eg thrush
  • Unexplained weight loss
  • Fatigue
  • Polyphagia (Excessive Appetite)
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9
Q

What signs of Type 1 DM can be found on physical examination?

A
  • dehydration
  • cachexia
  • hyperventilation
  • DKA Symptoms (can be triggered by surgery, UTI, MI, pancreatitis, chemotherapy, psychotics, wrong insulin dose/non-compliance):
    *Nausea and vomiting
    *Abdominal pain
    *Polyuria, polydipsia
    *Drowsiness
    *Confusion
    *Coma
    *Kussmaul breathing (rapid, deep breathing at a consistent pace)
    *Ketotic (sweet smelling) breath
    *Signs of dehydration
  • glycosuria
  • ketonuria
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10
Q

What investigations are used to diagnose/ monitor type 1 DM?

A

Investigations to do in order: Urinanalysis 🡪 random glucose 🡪 fasting glucose 🡪 OGTT 🡪 HBA1c
1. Blood Glucose - fasting blood glucose > 7 mmol/L or random blood glucose > 11.1 mmol/L
2. FBC - MCV, reticulocytes
3. U&Es - monitor for nephropathy and hyperkalaemia
4. Lipid profile
5. Urine albumin creatinine ratio - used to detect microalbuminuria
6. Urine - glycosuria, ketonuria, MSU (check for infection)
7. Investigations for DKA:
- Capillary blood glucose 🡪 urine dipstick (check for glycosuria and ketonuria) 🡪 ABG (check for metabolic acidosis) 🡪 plasma osmolality
- FBC (raised WCC without infection in DKA)

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11
Q

What effect does insulin deficiency have on the organs of the body?

A
  • Increased proteinolysis (breakdown of muscle) to gain amino acids- used for fuel
  • Increased hepatic glucose output (HGO)- Counterintuitive- blood glucose is high but it is not being used, so the body gets confused and increases production
  • Increased lipolysis (breakdown of fat/ adipose tissue) to gain non-esterified fatty acids/ NEFA’s for fuel
    = Formation of ketone bodies
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12
Q

Why are ketone bodies formed as a result of insulin definicency?

A
  • Breakdown of fat:
  • Fatty Acyl-Co A into the ketone bodies
  • Used as fuel during starvation
  • Acidic: accumulation= acidosis
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13
Q

How is Type 1 DM managed?

A
  1. Glycaemic Control:
    - Advice and patient education – vital to educate to self-adjust doses in the light of exercise, fingerprick glucose and calorie intake
    –Basal-Bolus Insulin ⇒ long acting (eg. insulin glargine, subcutaneous injection OD) + short acting (eg. insulin lispro or aspart, before meals) note: insulin is given subcutaneously
    a. Short-acting insulin (three times daily before meals):
    - Lispro
    - Aspart
    - Glulisine
    b. Long-acting insulin (once daily):
    - Isophane
    - Glargine
    - Detemir
  2. Insulin pumps/ disposable pens
  3. DAFNE courses (dose adjustment for normal eating)
  4. Monitor (Regular capillary blood glucose tests, HbA1c every 3-6 months)
  5. Treatment of hypoglycaemia:
    - If reduced consciousness: 50 ml of 50% glucose IV, intravenous dextrose OR 1 mg glucagon IM
    - If consciousness and cooperative: 50 g oral glucose + starchy snack
  6. DKA Management
  7. Management of cardiovascular risk factors
  8. Management of complications: Thyroid disease is most commonly associated with type 1 diabetes, as both are autoimmune conditions. This can be easily screened for with routine thyroid function tests.
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14
Q

Identify possible complications of type 1 diabetes mellitus

A
  1. Diabetic ketoacidosis
    - Can be precipitated by infection, errors in management of diabetes, newly diagnosed diabetes, idiopathic
  2. Microvascular complications:
    - Retinopathy
    - Nephropathy
    - Neuropathy
  3. Macrovascular complications:
    - Peripheral vascular disease
    - Ischaemic heart disease
    - Stroke/TIA
  4. Increased risk of infection
  5. Complications of treatment:
    - Weight gain
    - Fat hypertrophy at insulin injection sites
    - Hypoglycaemia:
    *Personality changes
    *Fits
    *Confusion
    *Coma
    *Pallor
    *Sweating
    *Tremor
    *Tachycardia
    *Palpitations
    *Dizziness
    *Hunger
    *Focal neurological symptoms
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15
Q

Summarise the prognosis for patients with type 1 diabetes mellitus

A
  • Depends on early diagnosis, good glycaemic control and compliance with treatment and screening
  • Vascular disease and renal failure are the main causes of increased morbidity and mortality
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16
Q

What is Type 2 DM?

A

“A condition in which the combination of insulin resistance and beta-cell failure result in hyperglycaemia”
- Body makes insulin but tissues don’t respond to it (reason not fully understood)
- INSULIN RESISTNACE
- obesity and genetic risk factors of T2DM
- Body makes excess insulin to try to move the glucose out of blood
- Eventually puts strain on beta cells (overworked)- beta cell damage
- Insulin starts to go down (depending on time of diagnosis, insulin levels will vary)

17
Q

Explain the aetiology of type 2 DM

A

Genetic & environmental:
- Obesity: possible increases rate of release of NEFAs causing post-receptor defects in insulin’s actions
- Genetics: mutations in genes encoding insulin receptors. There are a few monogenic causes e.g. MODY, mitochondrial diabetes
- Pancreatic disease (e.g. chronic pancreatitis)
- Endocrine disease (e.g. Cushing’s syndrome, acromegaly, phaeochromocytoma, glucagonoma)
- Drugs (e.g. corticosteroids, atypical antipsychotics, protease inhibitors)
- Circulating autoantibodies to the extracellular domain of the insulin receptor

18
Q

What are the risk factors for insulin reistance?

A
  • Metabolic syndrome
  • Obesity
  • Asian ethnicity
  • TB drugs
  • SSRIs (Selective serotonin reuptake inhibitors)
  • Pregnancy
  • Acromegaly
  • Renal failure
  • Cystic fibrosis
  • PCOS
  • Werner’s syndrome
  • Age
  • high BMI
  • Family History
  • Inactivity
19
Q

Summarise the epidemiology of type 2 diabetes mellitus

A
  • UK Prevalence: 5-10%
  • Asian, African and Hispanic people are at greater risk
  • Incidence has increased over the past 20 yrs
  • This is linked to an increasing prevalence of obesity
20
Q

What presenting symptoms of type 2 diabetes mellitus can be found in the history?

A

May be an incidental finding/ many patients are asymptomatic.
- Some may present with hyperosmolar hyperglycaemic state (HHS)
- Polyuria
- Polydipsia
- Tiredness
- Infections (e.g. infected foot ulcers, candidiasis, balanitis)
- Assess cardiovascular risk factors: hypertension, hyperlipidaemia and smoking

21
Q

How does the liver react to the reduced insulin levels seen after T2DM?

A

Hepatic glucose production is increased due to both a reduction in insulin action and increase in glucagon action
“excessive glucagon-mediated glucose output” (but reduced clearance of glucose- still not being removed from circulation)

22
Q

What consequences do other body tissues face from T2DM?

A

Skeletal muscle:
- Reduced glucose uptake
- Impaired glycogen synthesis

Adipocytes:
- Reduced glucose uptake
- Increased lipolysis
- Reduced lipogenesis

Liver:
- Increase in hepatic glucose production
- Increased lipogenesis

23
Q

What signs of type 2 DM can be found on physical examination?

A
  • Calculate BMI (overweight: 25.0-29.9 kg/m2, obese: 30 - 39.9 kg / m2)
  • Increased waist circumference
  • High blood pressure
  • Diabetic foot (ischaemic and neuropathic signs):
    *Dry skin
    *Reduced subcutaneous tissue
    *Ulceration
    *Gangrene
    *Charcot’s arthropathy (chronic/ destructive disease of the bone structure and joints in patients with neuropathy)
    *Weak foot pulses
  • Skin changes (RARE):
    *Necrobiosis lipoidica diabeticorum (well-demarcated plaques on shins or arms with shiny atrophic surface and red-brown edges)
    *Granuloma annulare (flesh-coloured papules coalescing in rings on the back of hands and fingers)
    *Diabetic dermopathy (depressed pigmented scars on shins)
24
Q

What investigations are used to diagnose/ monitor type 2 DM?

A

Investigations in order: Urinanalysis 🡪 random glucose 🡪 fasting glucose 🡪 OGTT 🡪 HBA1c
1. T2DM is diagnosed if one or more of the following are present:
- Symptoms of diabetes and a random plasma glucose ≥ 11.1 mmol/L
- Fasting plasma glucose ≥ 7 mmol/L
- Two-hour plasma glucose ≥ 11.1 mmol/L after 75 g oral glucose tolerance test
2. Monitor:
- HbA1c
- U&Es
- Lipid profile
- eGFR
- Urine albumin: creatinine ration (look out for microalbuminuria)

25
Q

How is type 2 DM managed?

A

Glycaemic control - there is a step-wise approach to the management of T2DM:

(Initial:)
1. Lifestyle advice: smoking cessation, diet, exercise
2. METFORMIN – a biguanide, increases insulin sensitivity and helps weight
- If HbA1C >53mmol/l after 16 weeks, add SULPHONYLUREA e.g. gliclazide – increases insulin sensitivity
- If HbA1c >57mmol/l at 6 months, consider
2. INSULIN – first basal, then premeal rapid-acting insulin
3. GLITAZONE (thiazolidinedione) e.g. pioglitazone
4. SULPHONYLUREA RECEPTOR BINDERS
5. GLP ANALOGUES and DPP4 INHIBTORS
6. A-GLUCOSIDASE INHIBITORS e.g. acarbose
- NOTE: sulphonylurea may be given as a monotherapy if patients cannot tolerate metformin
- NOTE: pioglitazone (thiazolidinedione) may also be given alongside metformin and a sulphonylurea
7. Screening for complications:
- Retinopathy
- Nephropathy
- Vascular disease
- Diabetic foot
- Cardiovascular risk factors (e.g. blood pressure, cholesterol)
8. Pregnancy - requires strict glycaemic control and planning of conception
9. Hyperosmolar Hyperglycaemic State - management is similar DKA
- Except use 0.45% saline if serum Na+ > 170 mmol/L

26
Q

Identify possible complications of type 2 diabetes mellitus

A
  1. Hyperosmolar hyperglycaemic state
    - Due to insulin deficiency
    - Marked dehydration
    - High Na+
    - High glucose
    - High osmolality
    - No acidosis
  2. Neuropathy:
    - Distal symmetrical sensory neuropathy
    - Painful neuropathy
    - Carpel tunnel syndrome
    - Diabetic amyotrophy
    - Mononeuritis
    - Autonomic neuropathy
    - Gastroparesis (abdominal pain, nausea, vomiting)
    - Impotence
    - Urinary retention
  3. Nephropathy:
    - Microabuminuria
    - Proteinuria
    - Renal failure
    - Prone to UTI
    - Renal papillary necrosis
  4. Retinopathy:
    - Background
    - Pre-proliferative
    - Proliferative
    - Maculopathy
    - Prone to glaucoma, cataracts and transient visual loss
  5. Macrovascular complications:
    - Ischaemic heart disease
    - Stroke
    - Peripheral vascular disease
27
Q

Summarise the prognosis for patients with type 2 diabetes mellitus

A
  • Good prognosis with good control
  • Pre-diabetes can be diagnosed based on fasting blood glucose and oral glucose tolerance test:
    *Impaired Fasting Glucose (IFG) = fasting blood glucose 5.6-6.9 mmol/L
    *Impaired Glucose Tolerance (IGT) = plasma glucose level of 7.8-11.0 mmol/L measured 2 hrs after a 75 g oral glucose tolerance test
  • People with IFG or IGT are at high risk of developing type 2 diabetes
28
Q

What is hyperosmolar hyperglycaemic state?

A

EXTREME DEHYDRATION
Osmotic diuresis leads to severe fluid loss “Hypovolaemic shock” insulin for suppression of lipolysis and ketogenesis.
Symptoms:
- Polyuria
- Dehydration
- (if left untreated): lethargy, seizures, coma, death

treat with intravenous fluids immediately
(CAUTION: rectifying fluids too quickly can cause Central pontine myelinolysis (brain depletion) rapid rise in Na+ conc

29
Q

What are the drug treatments for T2DM? What do each drug tackle?

A
  1. Metformin (Reduces hepatic glucose production + Improves insulin sensitivity + Increases peripheral glucose disposal)
  2. Thiozolidinediones
  3. Pioglitazone (2/3 Improves insulin sensitivity)
  4. Sulphonylureas
  5. DPP4-inhibitors
  6. GLP-1 Agonists (4-6 boost insulin secretion)
  7. Alpha glucosidase inhibitor
  8. SGLT-2 inhibitor (7/8 Inhibit carbohydrate gut absorption + Inhibit renal glucose reabsorption)

Weight loss help to achieve all of these solutions

30
Q

What are some cons of taking metformin?

A
  • GI side effects
  • Contraindicated in severe liver, severe cardiac or moderate renal failure
31
Q

How does Sulphonyleuras work?

A

“Boosts insulin secretion”
Normal insulin release requires closure of the
ATP-sensitive potassium channel
- Sulphonylureas binds to the ATP-sensitive potasssium channels and closes them (independent of glucose/ ATP)

32
Q

How does Pioglitazone work?

A

“Improves insulin sensitivity”
- Adipocyte differentiation modified
- weight gain but peripheral not central
- Improvement in glycaemia and lipids
- Evidence base on vascular outcomes
- Side effects of older types hepatitis, heart failure

33
Q

What is the role of Glucagon like peptide-1 (GLP-1)

A
  • Gut hormone
  • Secreted in response to nutrients in gut
  • Transcription product of pro-glucagon gene, mostly from L-cell
  • Stimulates insulin, suppresses glucagon
  • ↑ satiety (feeling of ‘fullness’)
  • Short half life due to rapid degradation from enzyme dipeptidyl peptidase-4 (DPP4 inhibitor)
  • Used in treatment of diabetes mellitus
34
Q

How do GLP-1 Agonists work?

A

“Boost insulin secretion”
- Injectable –daily, weekly
- Decrease [glucagon]
- Decrease [glucose]
- Weight loss
e.g: Liraglutide, Semaglutide

35
Q

How do DPP4-inhibitors work?

A
  • Increase half life of exogenous GLP-1
  • Increase [GLP-1]
  • Decrease [glucagon]
  • Decrease [glucose]
  • Neutral on weight
    e.g: Gliptins
36
Q

How do SGLT-2 inhibitors work?

A

“Inhibit carbohydrate gut absorption + Inhibit renal glucose reabsorption”

  • Inhibits Na-Glu transporter, increases glycosuria
  • HbA1c lower
  • 32% lower all cause mortality
  • 35% lower risk heart failure
  • Improve CKD (chronic kidney disease)
    E.g: Empagliflozin, dapagliflozin, canagliflozin
37
Q

What are the adverse drug effects of anti-diabetic drugs?

A
  1. Metformin (Activation of AMPK)=
    Lactic acidosis
  2. Sulfonylureas (Inhibits the VGKCs of the pancreatic beta cells)
    = Hypoglycaemia, Weight gain
  3. SGLT-2 inhibitors (Prevents reabsorbtion of glucose in PCT)=
    UTIs

Endocrine and Metabolic Y3 (22 decks)

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