Type 1 & Type 2 Diabetes Mellitus Flashcards

1
Q

What is type 1 diabetes?

Who does it affect?

What is type 1 diabetes associated with?

What is the genetic susceptibility?

What is the environment influence?

A

Type 1 diabetes : insulin deficiency due to autoimmune destruction of insulin secreting pancreatic beta cells

Onset: common in adolescent but can affect anyone

Assoc. with other autoimmune disease i.e. coeliac’s, Addison’s and pernicious anaemia.

Genetics: >90% people carry HLA DR3 ± DR4

Environment => most type 1 diabetic don’t have close family hx & only 10% with HLA susceptible gene develop diabetes:

=> maternal factors i.e. gestational infections
=> viral infections i.e. coxsackie B
=> exposure to cow’s milk and deficiency of vitamin D
=> childhood obesity
=> psychological stress

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2
Q

What is type 2 diabetes?

Who does it affect?

What is type 2 diabetes associated with?

What is the genetic susceptibility?

A

Type 2 diabetes = low insulin secretion ± high insulin resistance

Onset: prevalence higher in asians ; men ; >40yrs but teenagers with type 2 increasing

=> pancreatic beta cell function declines with age so incidence of type 2 diabetes increases with age

Assoc. with obesity, lack of exercise, calorie & alcohol excess

Genetics: >80% concordance in twins => higher genetic susceptibility than type 1 diabetes

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3
Q

What are the symptoms of hyperglycaemia?

A

Polyuria

Polydipsia

Unexplained weight loss

Visual blurring

Genital thrush

Lethargy

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4
Q

What are the other causes of diabetes?

A

Steroids ; anti-HIV drugs ; newer anti-psychoticss

Pancreatitis ; pancreatic surgery (>90% pancreas removed) ; trauma ; pancreatic destruction (haemachromatosis, cystic fibrosis) ; pancreatic cancer

Cushing’s disease ; acromegaly ; phaeochromocytoma ; hyperthyroidism ; pregnancy

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5
Q

How do you diagnose diabetes?

A

i) Symptoms of hyperglycaemia AND raised venous glucose once : Fasting >7mmol/L or Random >11.1mmol/L

OR

ii) Raised venous glucose on 2 separate occasions : Fasting >7mmol/L or Random >11.1mmol/L or glucose tolerance test (OGTT) - 2h value >11.1mmol/L

OR

iii) HbA1c >48mmol/mol => Avoid in pregnancy, children, type 1 DM & haemoglobinopathies

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6
Q

What are the features of type 1 diabetes?

A

Weight loss

Persistent hyperglycaemia despite diet & medications

Presence of autoantibodies i.e. islet cell antibodies and anti-glutamic acid decarboxylase antibodies

Ketonuria

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7
Q

Differences between type 1 and type 2 diabetes:

Type 1 DM:
=> Starts before puberty
=> HLA D3 & D4 linked
=> Autoimmune beta-cell destruction
=> Polydipsia, polyuria, weight loss, ketosis 
Type 2 DM:
=> Older patients (usually)
=> No HLA assoc. 
=> Insulin resistance / beta cells dysfunction 
=> Asymptomatic / complications e.g. MI
A

*Not all new onset diabetes in older patients = Type 2 DM

=> If ketotic ± poor response to oral hypoglycaemic
=> Patient slim ± has family or self Hx of autoimmunity
=> Could be latent autoimmune diabetes in adults (LADA)
=> Measure islet cell antibodies

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8
Q

What is the best diet for an obese patient with type 2 diabetes?

A

Dietary carbohydrates = big determinant of post-prandial glucose levels & low carbohydrate diets improve glycemic control

=> low carb ketongenic diet better at maintaining/lowering blood glucose than low glycemic/reduced calorie diet

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9
Q

What preventative measures are taken before starting medications for diabetes?

A

Education and lifestyle choices

  1. Exercise to increase insulin sensitivity
  2. Healthy diet (less saturated fats, sugars, more starch carbs, moderate protein)
  3. Negotiate HbA1c and review 3-6 monthly
  4. Assess vascular risk: control BP, initiate high intensity atorvastatin if needed
  5. Foot care
  6. Advice to not drive if hypoglycaemic spells - inform DVLA
    * Bariatric surgery may be a cure for T2DM in selective patients
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10
Q

How do you manage type 2 diabetes?

A

Lifestyle modification - diet, exercise, weight control => always consider first and then alongside meds

  1. Monotherapy: Metformin - 1st line therapy
  2. If HbA1c >58mmol/mol, start dual therapy
    => Metformin + DPP4 inhibitor e.g. sitagliptin
    => Metformin + pioglitazone
    => Metformin + sulphonylurea (SU)
    => Metformin + SGLT-2i e.g. glifazon
  3. If HbA1c still >58mmol/mol, start triple therapy
    => Metformin + DPP4 inhibitor + SU
    => Metformin + pioglitazone + SU
    => Metformin + SU/pioglitazone + SGLT-2i

If triple therapy doesn’t work, try:
=> Metformin + SU + GLP 1 mimetic
=> Insulin based therapy

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11
Q

What class of drug is metformin?

What is its mechanism of action?

What are its side effects?

A

Biguanide => works by increasing insulin sensitivity & helps weight

Side effect: nausea, diarrhoea (try modified release version), abdominal pain
=> does not cause not hypoglycaemia
=> avoid if eGFR <36ml/min - risk of lactic acidosis

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12
Q

What are DPP4 inhibitors?

What is its mechanism of action?

A

DPP4 inhibitors (aka gliptins) e.g. sitagliptin block the action of DPP4

=> DPP4 is an enzyme which destroys the hormone incretin

=> Incretins decrease blood glucose levels => released after eating and augment secretion of insulin

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13
Q

What are Glitazone?

What is its mechanism of action?

What are its side effects?

A

Glitazone increases insulin sensitivity

Side effects: hypoglycaemia, fractures, fluid retention, raised liver function test (do LFT every 8wks for 1 year)

Contraindications: past/present congestive cardiac failure, osteoporosis => monitor weight & stop if weight increasing or oedema

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14
Q

What are sulphonylurea?

What is its mechanism of action?

What are its side effects?

A

Sulphonylurea increases insulin secretion e.g. gliclazide 40mg/d

Side effects: hypoglycaemia (monitor glucose) ; weight increase

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15
Q

What are SGLTI?

What is its mechanism of action?

What are its side effects?

A

Selective sodium-glucose co-transporter-2 inhibitor => blocks reabsorption of glucose in the kidneys and promotes excretion of excess glucose in the urine

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16
Q

How do you treat type 1 diabetes?

A

Lifelong insulin therapy

Blood glucose monitoring

Eating healthy food ; maintaining weight ; exercising; maintaining blood sugar

17
Q

What are the 4 different types of insulin available?

How is it administered?

A

Short-acting (regular) insulin
Rapid-acting insulin
Intermediate-acting (NPH) insulin
Long-acting insulin

=> administered via subcutaneous injection not orally because insulin gets digested by gastric enzymes

18
Q

How do you assess risk in diabetes?

A

BP control => crucial for preventing macrovascular diseases and mortality

Smoking cessation

Plasma lipids

19
Q

How do you control BP in type 1 and type 2 diabetes?

A

Type 1 DM:

=> Treat BP if >135/85mmHg
=> If albuminuria or two or more features of metabolic syndrome then treat 130/80mmHg
=> ACEi (1st line) or ARB

Type 2 DM:

=> Target BP if <140/90mmHg
OR
=> Target BP <130/80mmHg if kidney, eye or CVS damage
=> ACEi (1st line)
=> African / caribbean give ACEi + diuretic or calcium channel blocker

20
Q

What are the macrovascular complications of diabetes?

How can we prevent these complications?

A
  1. MI 4x more common
  2. Stroke 2x more common

=> women at higher risk because diabetes removes protection from oestrogen

Prevention : Address risk factors i.e. diet, smoking, hypertension

=> Smoking cessation

=> Control BP

=> Statin e.g. atorvastatin 20mg even if no overt IHD, vascular disease, microalbuminuria

=> Aspirin 75mg reduces vascular complications (secondary prevention)

21
Q

Good control of hyperglycaemia is key to prevent microvascular complications in diabetes.

What are the microvascular complications of diabetes?

A

Retinopathy - microalbuminuria

Nephropathy

Neuropathy - loss of sensation in a ‘glove & stocking’ distribution => infections => ischaemia => gangrene => amputation

*For details pg 210-212 ox handbook

22
Q

What is the emergency state in uncontrolled type 1 diabetes?

A

Diabetic ketoacidosis

=> Ketoacidosis: alternative metabolic pathway used in starvation ; less efficient ; produces acetone = sweet pear drop smell

=> Diabetes: excess glucose due to lack of insulin - cannot be taken up into cells - starvation like state => diabetic ketoacidosis

=> Gradual drowsiness, vomiting,

23
Q

Good control of hyperglycaemia is key to prevent microvascular complications in diabetes.

What are the microvascular complications of diabetes?

A

Retinopathy

Nephropathy

Neuropathy

*For details pg 210-212 ox handbook

24
Q

What happens in diabetic nephropathy?

What do the investigations show?

A

Hyperglycaemia => diabetic nephropathy (albuminuria + glomerulonephropathy) => CKD => End stage kidney disease

Investigations:

Microalbuminuria => urine dipstick -ve for protein but urine albumin:creatinine ratio >3mg/mmol => renal disease + high vascular risk

=> ACEi or ARB to protect kidneys

25
Q

Diabetic neuropathy:

Amputations are common but preventable in diabetes.

What happens in diabetic neuropathy?

A

Neuropathy : Loss of sensation in a ‘glove & stocking’ distribution

=> caused by loss of pain sensation leading to increased mechanical stress & repeated joint injury

=> swelling, instability, deformity

=> sensory loss is patchy, absent ankle jerks, neuropathy deformity i.e. charcot joint

26
Q

Diabetic neuropathy:

When do you suspect ischaemia?

How do you investigate ischaemia?

A

Foot pulses cannot be felt

=> doppler pressure measurement

=> neuropathy or vascular disease increases risk of ulceration

=> educate patients to daily inspect feet

=> remove calluses regularly as haemorrhages & tissue necrosis can hide under

27
Q

Diabetic neuropathy:

What are the characteristics of a foot ulcer in diabetes?

A

Painless, punched out ulcer in an area of thick callus ± infection

28
Q

What is the emergency state in uncontrolled type 1 diabetes?

What are the assoc. symptoms?

A

Diabetic ketoacidosis

=> Ketoacidosis: alternative metabolic pathway used in starvation ; less efficient ; produces acetone = sweet pear drop smell

=> Diabetes: excess glucose due to lack of insulin - cannot be taken up into cells - starvation like state => diabetic ketoacidosis

=> Gradual drowsiness, vomiting, dehydration

*check glucose in everyone presenting with unexplained vomiting, abdominal pain, polyuria, polydipsia, lethargy, anorexia, ketotic breath

29
Q

How do you diagnose diabetic ketoacidosis?

A

Acidaemia : pH <7.3

Hyperglycaemia >11mmol/L

Ketoaemia or significant ketonuria

30
Q

How do you manage diabetic ketoacidosis?

A

=> 1L 0.9% saline fluid over 1h

=> Venous blood gas for pH, bicarbinate ; bedside and lab glucose & ketones, U&E’s, FBC, CRP, CXR, ECG

=> 0.1 unit/kg/h insulin continuously

=> Continue patients long-acting insulin at usual dose & time

=> Aim for a fall in ketones of 0.5mmol/L/h

=> Check capillary blood glucose hourly

=> Glucose <14mmol/L start 10% glucose alongside saline to prevent hypoglycaemia

=> Add K+ replacement from 2nd bag fluid onwards (insulin drives K+ in cell)