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MEH > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is diabetes mellitus?

A

Elevated blood glucose concentration (hyperglycaemia) which leads to damage of small and large blood vessels causing cardiovascular disease

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2
Q

Three main presentations of diabetes mellitus

A

Polyuria
Polydipsia
Weight loss

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3
Q

Why do people with diabetes present with polydipsia + polyuria?

A
  • hyperglycaemia overwhelms the kidneys
  • glucose levels in urine + draws water out
  • this causes polyuria + dehydration
  • dehydration causes polydipsia
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4
Q

Diagnosis of diabetes

A

Lab tests:
- oral glucose intolerance test
- HBA1c
- fasting glucose

Symptoms + 1 abnormal test or asymptomatic + 2 abnormal tests

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5
Q

What is the difference between [glucose] + HbA1c?

A
  • [glucose]: immediate measure of glucose levels in that current moment in time
  • HbA1c: % of glycated haemoglobin - average blood sugar over the last 3 months
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6
Q

What are the blood glucose levels for:
- non diabetic
- pre diabetic
- diabetic

A
  • non diabetic: <5.5mmol/L
  • pre diabetic: 5.6-6.9mmol/L
  • diabetic: >7mmol/L
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7
Q

Compare and contrast the feature of type 1 and type 2 diabetes

A

Type 1:
- Childhood
- Sudden onset
- Ketoacidosis
- No C peptide - insulin not produced
- Autoimmunity
- Recent weight loss

Type 2:
- Middle age
- Gradual onset
- Non-ketoacidosis
- C-peptide detectable - insulin still produced
- Not autoimmunity
- Often no weight loss

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8
Q

What is type 1 diabetes?

A

Autoimmune disease
Destroys beta cells in pancreas which secretes insulin

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9
Q

Presentation of diabetes mellitus type 1

A
  • Rapid onset weight loss
  • Polyuria
  • Polydipsia
  • Presence of ketones > acetone smell on breath
  • Increased venous plasma glucose
  • Vomiting due to ketoacidosis in late presentation
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10
Q

Management of type 1 diabetes mellitus

A
  • s.c. insulin
  • monitoring dietary carb intake
  • monitor blood sugars upon waking, at each meal + before bed
  • monitor + manage complications - regular clinics
  • pancreas/islet transplant
  • closed loop system/artificial pancreas
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11
Q

What is a closed loop system/artificial pancreas?

A

combination of continuous glucose monitoring + insulin pump
- devices communicate to automatically adjust insulin based on glucose readings

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12
Q

What is the basal bolus regime of insulin?

A

involves a combination of a:
- basal/long acting insulin once a day
- bolus/short acting insulin 30 mins before each meal

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13
Q

Advantages + disadvantages of insulin pumps

A

Advantages:
- better blood glucose control
- more flexibility with eating
- less injections
.
Disadvantages:
- difficulties learning to use the pump
- must be attached at all times
- blockage in infusion set
- risk of infection

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14
Q

Two types of insulin pumps

A
  • tethered pumps: replaceable | attach to patient’s belt or waist with tube connecting to the pump
  • patch pump: disposable | sits directly on the skin
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15
Q

What is type 2 diabetes?

A

combination of insulin resistance + reduced insulin production

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16
Q

Pathophysiology of type 2 diabetes mellitus

A
  • repeated exposure to glucose + insulin makes the cells resistant to the effects of insulin
  • more insulin is required to simulate glucose uptake in cells
  • over time the pancreas becomes fatigued + damaged > reduced insulin output
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17
Q

Risk factors of type 2 diabetes

A
  • older age
  • ethnicity (black african, Caribbean, south asian)
  • family history
  • obesity
  • sedentary life style
  • high carb diet
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18
Q

Presentation of type 2 diabetes

A
  • Polyuria
  • Polydipsia
  • fatigue
  • opportunistic infections e.g. thrush
  • slow wound healing
  • acanthosis nigricans
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19
Q

What is acanthosis nigricans?

A

velvety darkening appearance of the skin
often at the neck, axilla + groin
associated with insulin resistance

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20
Q

What is the HbA1c for pre-diabetes + diabetes?

A
  • pre diabetes: 42-47mmol/mol
  • diabetes: >48mmol/mol
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21
Q

management of type 2 diabetes

A
  • weight loss
  • exercise
  • low glycaemic index, high fibre diet
  • a structed education program
  • antidiabetic drugs
  • monitoring + managing complications - clinics
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22
Q

Pharmacological management of type 2 diabetes - step wise

A
  • first line: metformin
  • add SGLT-2 inhibitor once settled on metformin if existing CVD or heart failure
  • second line: add sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor
  • third line: triple therapy (*metformin + 2 second line drugs) | insulin therapy
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23
Q

Treatment targets of HbA1c for new type 2 diabetics + those with >1 antidiabetic medications

A
  • new: 48mmol/mol
  • >1 antidiabetic drug: 53mmol/mol
24
Q

Monitoring of diabetes

A
  • HbA1c every 3-6 months
  • capillary blood glucose (finger prick test)
  • flash glucose monitoring: e.g FreeStyle Libre
  • continuous glucose monitoring
25
Q

Outline flash glucose monitoring
example

A
  • uses a sensor on the skin that measures glucose level of interstitial fluid in the s.c. tissue
  • 5 min lag behind blood glucose
  • to read results, phone is swiped over sensor to collect reading
  • replacement sensor ever 2 weeks
  • FreeStyle Libre
26
Q

Acute complications of diabetes

A

Hyperglycaemia:
- metabolic decomposition
- diabetic ketoacidosis in type 1
- hyperosmolar hyperglycaemic syndrome in type 2
.
Hypoglycaemia:
- coma - brain is glucose dependent

27
Q

Chronic complications of diabetes
Macro and micro vascular disease

A

Macro vascular disease:
- stroke
- heart attack
- hypertension
- peripheral ischemia > diabetic foot ulcers

Micro vascular disease:
- retinopathy
- nephropathy
- peripheral neuropathy

28
Q

How to recognise diabetic retinopathy

A
  • blurred/fluctuating vision
  • floaters or dark spots in visual fields
  • fundoscopy findings
29
Q

Fundoscopy findings of diabetic retinopathy

A
  • hemorrhages - red spots
  • hard exudates - yellow plaques
  • cotton wool spots - ischaemia
  • micro-aneurysms
  • new vessels on retina
30
Q

What is proliferative diabetic retinopathy?

A

Insufficient retinal perfusion results in the production of vascular endothelial growth factor (VEGF) which results in the development of new vessels on the retina (neovascularisation).

31
Q

Management of diabetic retinopathy

A
  • control blood glucose
  • control blood pressure
  • regular follow up
  • smoking cessation
  • injections of anti-vascular endothelial growth factor into the eye
  • pan retinal photocoagulation
32
Q

What does pan retinal photocoagulation on fundoscopy?

A

clusters of burn marks on retina created by the laser during treatment

33
Q

Drug management of CKD in diabetes patients

A

ACR >3: ACEi
- ACR >30: SGLT-2 inhibitors

34
Q

Pharmacological options for neuropathic pain in diabetes

A
  • amitriptyline: tricyclic antidepressant
  • duloxetine: SNRI antidepressant
  • gabapentin: anticonvulsant
  • pregabalin: anticonvulsant
35
Q

Management of diabetic foot ulcers

A
  • assess wound + classify
  • control blood glucose
  • offloading pressure e.g. total contact cast
  • ensure wound is kept clean + moist
  • antibiotics if infected
  • daily foot inspection
  • encourage well fitting shoes
  • regular foot clinics
36
Q

Infection related complications of diabetes mellitus

A
  • UTIs
  • pneumonia
  • skin + soft tissue infections (esp. in feet)
  • fungal infections e.g. oral + vaginal candidiasis
37
Q

What suppressed ketone production?

A

Insulin

38
Q

What is needed in the presence of ketones?

A

Immediate insulin therapy

39
Q

Why do patients with type 1 diabetes need immediate referral?

A
  • insulin suppressed ketone production
  • lack of insulin > ketones produced
  • ketoacidosis if not treated rapidly
40
Q

What is metabolic syndrome?

A

Group of the most dangerous risk factors of cardiovascular disease:
- diabetes + raised fasting plasma glucose
- abdominal obesity
- hypertension
- high cholesterol

41
Q

What is needed for a person to have metabolic syndrome?

A

Waist >94 cm for men >80 cm for women
PLUS 2 from:
- raised triglycerides
- reduced HDLs
- raised fasting blood glucose
- raised blood pressure

42
Q

What causes metabolic syndrome?

A

Insulin resistance
Central obesity
Genetics
Inactivity
Ageing

43
Q

Why does insulin need to been given as an injection not orally?

A

Insulin is a peptide hormone
it would get broken down in GI tract into amino acids if it was taken orally

44
Q

What is hyperosmolar hyperglycaemic state?

A
  • Rare complication of DM2
  • Characterised by hyperosmolality, hyperglycaemia + absence of ketones
45
Q

What characterises hyperosmolar hyperglycaemic state?

A
  • Hyper osmolality (water loss > very conc. blood)
  • Hyperglycaemia
  • Absence of ketones
46
Q

What distinguishes DKA + hyperosmolar hyperglycaemic state?

A

Absence of ketones in HHS

47
Q

Presentation of hyperosmolar hyperglycaemic state

A
  • polyuria
  • Polydipsia
  • weight loss
  • dehydration
  • tachycardia
  • hypotension
  • confusion
48
Q

Treatment of hyperosmolar hyperglycaemic state

A
  • IV fluids
  • careful monitoring
  • involve seniors
49
Q

What test can be done to work out if insulin is from an endogenous or exogenous source?`

A

serum C-peptide

50
Q

Outline the form insulin is released in by the pancreas to insulin that is used in the body

A

preproinsulin > proinsulin > insulin + C-peptide

51
Q

Presentation of diabetic ketoacidosis

A
  • sweet smelling breath
  • dehydrated
  • hyperglycaemia
  • potassium imbalance
  • metabolic acidosis
  • N+V
  • altered consciousness
  • hypotension
52
Q

When should you suspect diabetic ketoacidosis?

A
  • blood glucose >11mmol/L
    AND
  • polyuria, Polydipsia, abdominal pain, lethargy, acetonic breath, confusion
53
Q

Diagnosis of DKA

A

Hyperglycaemia
Ketosis >3mmol/L
Acidosis

54
Q

Test results which suggest diabetic ketoacidosis

A
  • +++ ketones in urine or blood
  • venous blood pH <7.3
  • HCO3 <15mmol/L
  • hyperglycaemia >11mol/L
  • (potassium imbalance)
55
Q

What are possible precipitating factors to diabetic ketoacidosis?

A

Infection
Trauma
Non adherence to insulin treatment
Drug drug interactions

56
Q

Treatment of diabetic ketoacidosis

A

FIG PICK
- IV Fluids
- Insulin infusion
- Glucose monitoring
- add Potassium to fluids + monitor
- Infection: treat any underlying cause
- Chart fluid balance
- monitor Ketones, pH + bicarbonate

57
Q

Complications during DKA treatment

A
  • hypoglycaemia
  • hypokalaemia
  • cerebral oedema
  • pulmonary oedema

MEH (23 decks)

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