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Diabetes Mellitus Flashcards

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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
mellitus - sweet urine

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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:
- random plasma glucose >11.1mmol/L + clinical features
- HBA1c >48mmol/mol (6.5%)
- fasting glucose >7mmol/L

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 (5.7-6.4%)
  • diabetes: >48mmol/mol (6.5%)
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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
  • if GI adverse effects with metformin, trial modified release
  • 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 (6.5%)
  • >1 antidiabetic drug: 53mmol/mol (7%)
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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
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25
Outline flash glucose monitoring example
- 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
Acute complications of diabetes
**Hyperglycaemia**: - metabolic decomposition - diabetic ketoacidosis in type 1 - hyperosmolar hyperglycaemic syndrome in type 2 . **Hypoglycaemia**: - coma - brain is glucose dependent
27
Chronic complications of diabetes Macro and micro vascular disease
**Macro vascular disease**: - cerebrovascular - stroke - coronary artery - heart attack - peripheral vascular disease > diabetic foot ulcer - hypertension **Micro vascular disease**: - retinopathy - nephropathy - peripheral neuropathy
28
How to recognise diabetic retinopathy
- blurred/fluctuating vision - floaters or dark spots in visual fields - fundoscopy findings
29
Fundoscopy findings of diabetic retinopathy
- **hemorrhages** - red spots - **hard exudates** - yellow plaques - **cotton wool spots** - ischaemia - **micro-aneurysms** - new vessels on retina
30
What is proliferative diabetic retinopathy?
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
Management of diabetic retinopathy
- 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
What does pan retinal photocoagulation on fundoscopy?
clusters of burn marks on retina created by the laser during treatment
33
Drug management of CKD in diabetes patients
**ACR >3**: ACEi - **ACR >30**: SGLT-2 inhibitors
34
Pharmacological options for neuropathic pain in diabetes
- ***amitriptyline***: tricyclic antidepressant - ***duloxetine***: SNRI antidepressant - ***gabapentin***: anticonvulsant - ***pregabalin***: anticonvulsant
35
Management of diabetic foot ulcers
- 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
Infection related complications of diabetes mellitus
- UTIs - pneumonia - skin + soft tissue infections (esp. in feet) - fungal infections *e.g. oral + vaginal candidiasis*
37
What suppressed ketone production?
Insulin
38
What is needed in the presence of ketones?
Immediate insulin therapy
39
Why do patients with type 1 diabetes need immediate referral?
- insulin suppressed ketone production - lack of insulin > ketones produced - ketoacidosis if not treated rapidly
40
What is metabolic syndrome?
Group of the most dangerous risk factors of cardiovascular disease: - diabetes + raised fasting plasma glucose - abdominal obesity - hypertension - high cholesterol
41
What is needed for a person to have metabolic syndrome?
Waist >94 cm for men >80 cm for women PLUS 2 from: - raised triglycerides - reduced HDLs - raised fasting blood glucose - raised blood pressure
42
What causes metabolic syndrome?
Insulin resistance Central obesity Genetics Inactivity Ageing
43
Why does insulin need to been given as an injection not orally?
Insulin is a peptide hormone it would get broken down in GI tract into amino acids if it was taken orally
44
What is hyperosmolar hyperglycaemic state?
- Rare complication of DM2 - Characterised by hyperosmolality, hyperglycaemia + absence of ketones
45
What characterises hyperosmolar hyperglycaemic state?
- **Hyper osmolality** (water loss > very conc. blood) - **Hyperglycaemia** - **Absence of ketones**
46
What distinguishes DKA + hyperosmolar hyperglycaemic state?
Absence of ketones in HHS
47
Presentation of hyperosmolar hyperglycaemic state
- polyuria - Polydipsia - weight loss - dehydration - tachycardia - hypotension - confusion
48
Treatment of hyperosmolar hyperglycaemic state
- IV fluids - careful monitoring - involve seniors
49
What test can be done to work out if insulin is from an endogenous or exogenous source?`
serum **C-peptide**
50
Outline the form insulin is released in by the pancreas to insulin that is used in the body
preproinsulin > proinsulin > insulin + C-peptide
51
Presentation of diabetic ketoacidosis
- sweet smelling breath - abdominal pain - Polyuria - polydipsia - dehydration - deep hyperventilation
52
When should you suspect diabetic ketoacidosis?
- blood glucose >11mmol/L AND - polyuria, Polydipsia, abdominal pain, lethargy, acetonic breath, confusion
53
Diagnosis of DKA
Hyperglycaemia Ketosis >3mmol/L Acidosis
54
Test results which suggest diabetic ketoacidosis
- +++ ketones in urine or blood - venous blood pH <7.3 - HCO3 <15mmol/L - hyperglycaemia >11mol/L - (potassium imbalance)
55
What are possible precipitating factors to diabetic ketoacidosis?
Infection Trauma Non adherence to insulin treatment Drug drug interactions
56
Treatment of diabetic ketoacidosis
FIG PICK - IV **F**luids - **I**nsulin infusion - **G**lucose monitoring - add **P**otassium to fluids + monitor - **I**nfection: treat any underlying cause - **C**hart fluid balance - monitor **K**etones, pH + bicarbonate
57
Complications during DKA treatment
- hypoglycaemia - hypokalaemia - cerebral oedema - pulmonary oedema - arrhythmias - acute respiratory distress syndrome
58
What is the target HbA1c of a someone with type 2 diabetes?
48mmol/mol (6.5%) Or 53mmol/mol (7%) if at risk of hypoglycaemia
59
Screening for diabetic retinopathy How often is this done?
Diabetic eye screening at diagnosis Every 2 years if at low risk, every year otherwise
60
Factors affecting accuracy of HbA1c
- **anything that affects lifespan of RBCs** - **increased HbA1c**: iron deficiency anaemia, folate/B12 deficiency, splenectomy, CKD (due to reduced EPO), alcoholism, high doses of aspirin - **decreased HbA1c**: B12/iron/EPO injection, chronic liver disease, splenomegaly, RA, pregnancy, haemodialysis, haemoglobinopathies *e.g. sickle cell, GP6D deficiency*
61
Autonomic complications of diabetes
- postural hypotension - ED + sexual dysfunction - bloating, nausea, vomiting - reduced sweating - urinary symptoms - hesitancy, reduced frequency, urinary retention
62
What shows DKA resolution ?
pH >7.3 Blood ketones <0.6mmol/L Bicarbonate >15mmol/L
63
Management of hypoglycaemia
_in community_: - **oral glucose 10-20g liquid, gel or tablet** - quick acting carb *e.g. glucogel, dextrogel* - hypokit - IM or SC glucagon . _in hospital_: - quick acting carb if alert - if unconscious or unable to swallow: **IV glucose 20%** if IV access available or **IM or SC glucagon**
64
Screening of diabetic nephropathy
Early morning urinary ACR
65
Features of hypoglycaemia
- sweating - shaking - hunger - anxiety - nausea - weakness - confusions
66
Sick day rules in type 1 diabetes mellitus
- DO NOT stop insulin - check blood glucose more frequently - maintain normal meal papers if possible - aim for 3L of fluid
67
Sick day rules in type 2 diabetes mellitus
- stop metformin if risk of dehydration - lactic acidosis risk - stop SGLT-2 inhibitors if risk of dehydration - euglycaemic DKA risk - stop GLP1 agonstis if risk of dehydration - AKI risk - stop sulfonylureas - risk of hypoglycaemia - continue insulin therapy - monitor blood glucose more frequently - restart meds when feeling better + E+D for 24-48 hours o

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