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Year 3 TCDs > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Name an anabolic hormone

A

Insulin

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2
Q

Name 4 catabolic hormones

A

Glucagon
Catecholamine
Growth hormone
Cortisol

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3
Q

What causes hyperglycaemia?

A

Inadequate insulin action

  • Reduced insulin production
  • Reduced insulin target organ sensitivity
  • Overwhelming increases in catabolic hormones
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4
Q

What is the definition of diabetes mellitus?

A

A reduction in insulin action sufficient to cause a level of hyperglycaemia that over time will result in diabetes-specific microvascular pathology in eyes, kidneys, and nerves

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5
Q

What is non-diabetic hyperglycaemia (pre-diabetes)?

A

Aka impaired glucose tolerance

Results if insulin action is reduced such that blood glucose is raised above normal but not to a level that will cause microvascular damage

5-10% progress to T2 diabetes each year

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6
Q

What are the WHO definitions of diabetes mellitus in plasma glucose concentration (mmol/L)?

A

Fasting (x2 or + symptoms) ≥ 7

OR

2h post glucose load (or random glucose) ≥ 11.1

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7
Q

What is the WHO definition of impaired glucose tolerance by plasma glucose concentration (mmol/L)?

A

Fasting < 7

OR

2h post glucose load < 11.1 ≥ 7.8

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8
Q

With respect to HbA1c what level diagnoses a patient with DM? With NDH (IGT, pre-diabetes)?

A

≥ 48mmol/mol = diagnosed DM

42-47mmol/mol = NDH

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9
Q

What is the benefit of using HbA1c?

A

Gives an integrated view of what glucose levels have been like over the past 3 months.

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10
Q

Name 4 other types of diabetes

A
  1. Genetic defects of b-cell function or insulin action (Maturity onset diabetes of the young)
  2. Diseases of exocrine pancreas (I.e. pancreatitis, cancer, cystic fibrosis)
  3. Endocrinopathies (i.e. Cushing’s, Acroegaly, phaeochromocytoma)
  4. Drug induced (I.e. steroids, antipsychotics)
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11
Q

What are the main traits of type 1 diabetes?

A
  1. B-cell destruction
  2. Organ specific/autoimmune
  3. Most childhood onset
  4. Early viral trigger
  5. Ketosis prone -> will burn fat inappropriately b/c no insulin thus generate ketones
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12
Q

What are the main traits of type 2 diabetes?

A
  1. Insulin resistance + b-cell dysfunction
  2. Most adult onset
  3. Ketosis resistant -> overweight
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13
Q

What are modifiable and non-modifiable risk factors for type 2 diabetes?

A

Non-Modifiable:

  1. Family history
  2. Ethnicity (Black, Caribbean, South Asian)
  3. Age
  4. Socio-economic deprivation

Modifiable:

  1. Overweight + obesity (intra-abdominal fat)
  2. Diet composition
  3. Lack of exercise
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14
Q

What is the twin cycle hypothesis of diabetes?

A

That chronic calorie excess leads to accumulation of liver fat with eventual spill over into the pancreas. These self-reinforcing cycles between the liver and pancreas eventually cause metabolic inhibition of insulin secretion after meals and onset of hyperglycaemia.

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15
Q

What happens initially for someone with NDH/IGT to maintain normoglycemia?

A

As their insulin sensitivity decreases, their levels of insulin secretion increases to compensate and keep blood glucose levels normal.

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16
Q

What are the key differences between T1 and T2 diabetes?

A 
Age of onset: <30//>30
Autoimmune (associations - thyroid disease, pernicious anemia, Addison’s disease, celiac disease): Yes//No
Prone to ketosis: Yes//No
Family history/Ethnicity: +/-//+++
Obesity a risk factor: No//+++
Inactivity a risk factor: No//+++
Social deprivation a risk: No//++
Insulin-treated: All//Some
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17
Q

What are 3 main causes of polyuria?

A
  1. Diabetes -> sugar build up in bloodstream unable to be filtered out by kidneys.
  2. Diabetes insipidus -> lack of antidiuretic hormone (ADH) from posterior pituitary means kidneys cannot make enough concentrated urine and too much water is passed from the body.
  3. Hypercalcemia -> Too much calcium in blood can affect ADH levels or kidney’s response to it. This can affect the way your kidneys produce urine. Symptoms = constipation, anorexia, N/V, abdominal pain, ileus
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18
Q

Why is infection more likely in diabetes?

A

Caused by the hyperglycaemic environment that favours immune dysfunction (I.e. damage to the neutrophil function, depression of the antioxidant system, and humoral immunity), micro and macro-angioplasties, neuropathy, decrease in the antibacterial activity of urine, gastrointestinal and urinary dysmotility, and greater number of medical interventions in these patients

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19
Q

What tests would you perform on someone with suspect diabetes?

A
  1. Capillary glucose (random blood glucose > 13mmol/l is sufficient to make a diagnosis of DM)
  2. HbA1c
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20
Q

What are 5 main symptoms of diabetes?

A
  • Thirst
  • Polyuria
  • Polyphagia
  • Tiredness
  • Weight loss

Remember glucose is an osmotic diuretic

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21
Q

Name 2 hyperglycaemic emergencies

A

Diabetic ketoacidosis (T1DM)

Hyperosmolar Hyperglycemic state (T2DM) -> increased mortality than DKA, more fluids needed
- Can be caused by dehydration, steroids, improper medication use

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22
Q

What are some diabetic complications?

A
  1. Microvascular (neuropathy, retinopathy, nephropathy)

2. Macrovascular (ACS, Stroke, PVD)

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23
Q

What are the treatment goals for diabetes?

A
  1. Minimise treatment side effects (I.e. hypoglycaemia, weight gain)
  2. Maintain glucose levels as near-normal as possible (to minimise acute/long-term complications
  3. Cardiovascular risk management (CV risk increased even with target glucose; diet, exercise, smoking, BP, lipid management)
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24
Q

What are the types of insulin?

A
  1. Quick Acting -> given SC injection/infusion; IV infusion
  2. Slow acting -> slowed entry into bloodstream; SC injection only (I.e. isoprene, lente)
  3. Bi-Phasic -> mixtures of #1 + #2; ratio usually 25/75 or 30/70
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25
Q

Name 3 rapid acting insulin analogues

A
  1. Lispro
  2. As part
  3. Glulisine
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26
Q

Name 1 slow acting insulin analogue

A

Isoprene

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27
Q

Name 3 basal insulin analogues

A
  1. Glargine
  2. Detimir
  3. Deluded
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28
Q

List the 6 main drug categories for type 2 diabetes

A
  1. Reduce insulin resistance
    - Biguanide (metformin) -> work on liver
    - Thiazolidenediones (pioglitazone) -> work on fat + muscle
  2. Increase B cell activity
    - Sulphonylureas (gliclazide, glipizide, glibenclamide)
    - Meglitinides (nateglinide, repaglinide)
  3. Increase GLP1 activity -> glycolipid protein 1, important in metabolism; slows down metabolism of food + increases satiety signal to the brain
    - DPP4 inhibitors (sitagliptin, vildagliptin) -> enzyme responsible for GLP1 metabolism
    - Incretins (exenatide, liraglutide) -> GLP1 agonists
  4. Slow glucose absorption -> not very effective
    - Acarbose (a-glucosidase inhibitor) -> stops metabolism of starches ++ side effects b/c they ferment in bowel
  5. Enhance glucose excretion
    - SGL2 antagonists (dapagliflozin, canagliflozin, empagliflozin)
  6. Insulin supplementation
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29
Q

What are the main side effects of drugs for type 2 diabetes?

A
  1. Weight gain
    - Increase B cell activity
    - Insulin
  2. Hypoglycaemia
    - Increase B cell activity
    - Insulin
  3. GI symptoms (N/V/abdo discomfort)
    - Metformin
    - Incretins
    - Acarbose
  4. Weight loss
    - Metformin
    - Incretins
    - SGLT2 inhibitors
  5. Others
    - Osteoporosis -> pioglitazone
    - UTI -> SGLT2 inhibitors
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30
Q

What is the negotiated treatment escalation plan for type 2 diabetes?

A
  • Lifestyle
  • Lifestyle + metformin
  • Lifestyle + metformin + further drugs
  • Lifestyle + metformin + further drugs + insulin
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31
Q

What are the annual checks for diabetes?

A
  1. Lipids
  2. UACR (urine albumin-to-creatinine ratio)
  3. eGFR
  4. Foot exam
  5. Diabetic eye screening program
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32
Q

What are the 4 systems that can be affected by long-term type 2 diabetes?

A
  1. Eyes
  2. Kidneys
  3. Feet
  4. CVS
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33
Q

What increases the risk of microvascular diabetic complications?

A
  1. Hyperglycaemia
  2. Hypertension
  3. Insulin resistance
  4. Certain genes
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34
Q

What is the pathophysiology of diabetic eye disease leading to loss of central vision?

A
  1. Capillary leakage
  2. Intra-retinal haemorrhages
  3. Intra-retinal oedema
  4. Intra-retinal hard exudates
  5. Peripheral retina (non-sight threatening)
  6. Macular area (maculopathy)
    —> Loss of central vision
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35
Q

What is the pathophysiology of total blindness due to diabetic eye disease?

A
  1. Capillary occlusion
  2. Retinal ischemia
  3. Retinal new vessels formation
  4. Intra-vitreal haemorrhage
  5. Intro-vitreal fibrosis
  6. Traction retinal detachment
  7. Secondary new vessel glaucoma
    —> total blindness
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36
Q

How many stages are there of chronic kidney disease?

A

5

1 -> microproteinuria -> GFR > 90ml/min/1.72m2
2 -> mic/macroproteinuria -> 60-90
3 -> macroproteinuria -> 30-59
4 -> macroproteinuria -> 15-29
5 -> macroproteinuria -> <15
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37
Q

What is the salvage therapy used for minimising blindness?

A

Vitrectomy

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38
Q

What is the salvage therapy for end stage kidney disease?

A
  • Diet, Epo, Calcium + Vitamin D, bicarbonate
  • Early AVF (atriovenous fistula), early transplantation
  • Dialysis + transplantation
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39
Q

What are symptoms of neuropathy?

A
  • Burning, cold, tingling
  • Stabbing, toothache
  • Walking on glass
  • Contact sensitivity
  • Allodynia (Pain from stimuli which normally don’t provoke pain)
  • Numbness, restlessness
  • Worse at night, eased by exercise or counter irritation
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40
Q

What are some signs of autonomic neuropathy?

A
  1. Sudomotor (sweating abnormalities)
  2. Pupils (sluggish pupillary reflexes)
  3. GI (reduced motility, Diarrhea, enlarged gall-bladder)
  4. CVS (postural hypotension, tachycardia)
  5. GU (bladder dysfunction, impotence)
  6. Vasomotor (peripheral vascular changes, oedema, Charcot joint, osteopathy)
  7. Glucose metabolism (hypoglycaemic unawareness)
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41
Q

What is Charcot’s joint?

A

A condition causing the weakening of the bones in the foot that can occur in people who have significant nerve damage. The bones are weakened enough to fracture and with continued walking, the foot eventually changes shape

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42
Q

What is the salvage therapy to minimise risk of amputation?

A

Revascularisation or local amputation

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43
Q

What are some complications of diabetic pregnancy?

A
  1. Congenital anomalies

2. 2nd/3rd trimester accelerated growth

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44
Q

What is cheiroarthropathy and give an example condition

A

A syndrome of limited joint mobility that occurs in patients with diabetes. It’s characterised by thickening of the skin resulting in contracture of the fingers

I.e. Dupuytren’s contracture

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45
Q

What are the measures to minimise cardiovascular disease and premature death as a complication of diabetes?

A

Primary prevention:

  • Lifestyle (diet, weight, exercise, smoking, alcohol)
  • Metabolic control (glucose, BP, lipids)
  • ACEI, A2RB, Aspirin, Statins/Fibrates

Secondary Prevention:

  • Post angina, ACS, MI, TIA, CVA, Claudication, ED
  • Aspirin, thrombolysis, DIGAMI, beta blockers
  • As for primary

Salvage Therapy
- Revascularisation

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46
Q

What is the goal blood pressure for a diabetic?

A

< 130/85mmHg

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47
Q

What is DKA?

A

Hyperglycaemia + hyperketonemia + acidosis

Severe insulin deficiency + increased catabolic hormones (glucagon, catecholamines, cortisol, GH) -> high glucose (glycogenolysis, gluconeogenesis) + ketones (lipolysis) + impaired/saturated disposal (muscle, brain) -> hyperglycaemia + hyperketonemia -> metabolic acidosis

48
Q

What are the 5 clinical features of DKA?

A
  1. Hyperventilation (metabolic acidosis)
  2. Vomiting (ketosis +. Hyperglycemic gastric stasis)
  3. Dehydration (osmotic diuretics + vomiting)
  4. Hypotension with warm peripheries (dehydration + vasodilation)
  5. Decreased conscious level (severe hypotension -> cardiovascular shock)
49
Q

What are the metabolic characteristics of DKA?

A
  1. Water deficiency - 5L
  2. Na+ deficiency - 500mmol
  3. K+ deficiency - 300-1000mmol (NaK ATPase doesn’t function properly so leaks out)
  4. Hyperglycaemia > 25mmol/l
  5. Metabolic acidosis - low pH, low HCO3

** 1-4 similar/more severe in hyperosmolar Hyperglycemic state but no keto-acidosis

50
Q

What are the typical presenting test results for DKA?

A
  1. Hyperglycaemia, glycosuria
  2. Ketonemia, ketonuria (not in HHS)
  3. Na+ = 125-160mmol/l (higher in HHS)
    - Low -> increased fat in blood diluting out Na
    - High -> osmotic diuretics results in more water than sodium being lost from kidneys
  4. K+ = 3-7mmol/l (losing K+ from cells but not excreting it so may be high circulating level even tho total body level is low)
  5. Urea, creatinine raised (hypotension AKI + muscle breakdown b/c of insulin deficiency)
  6. Lipids raised
  7. Leucocytosis (whole process is inflammatory)
51
Q

What are 6 ways to prevent disaster in DKA or HHS?

A
  1. NEVER STOP BASAL INSULIN
  2. Hypovolemic shock -> fluid resuscitation
  3. Aspiration pneumonitis -> airway protection if comatose (GCS < 9)
  4. Fatal arrhythmia -> monitor/replace K+
  5. Pulmonary embolism -> prophylactic LMWH
  6. Cerebral oedema (more common in Females) -> careful IV fluids
52
Q

What are the symptoms of severe hypoglycaemia?

A
  1. Adrenergic symptoms (sweating, trembling, hunger)
  2. Neuroglycopenia (paraesthesia, blurred vision, confusion)

“Loss of warning” can occur where neuroglycopenia precedes adrenergic symptoms. May be iatrogenic (in recurrent hypoglycaemia) but also linked to long duration diabetes.

53
Q

What diabetes treatment can cause excess insulin in the body and a severe hypoglycaemic state?

A

Insulin OR sulphonylurea/glinide treatment

54
Q

When are patients more likely to experience severe hypoglycaemia?

A
  1. Alcohol excess
  2. Very young/old
  3. Long-standing diabetes
  4. Recent severe hypoglycemia
  5. Pregnancy
  6. Autonomic neuropathy
  7. Renal/hepatic impairment
55
Q

What is the treatment for severe hypoglycemia?

A
  1. 30ml lucozade or equivalent (able to cooperate)
  2. Glucose gel (glucogel) on buccal membrane (unable to cooperate, but conscious)
  3. Glucagon SC/IM/IV (comatose, fitting)
    - try to avoid IV glucose as it destroys veins
56
Q

What 2 hormones regulate the extra cellular concentration of glucose?

A

Insulin + glucagon

57
Q

What occurs after a carbohydrate containing meal?

A

Serum glucose concentration rises, glucose enters the pancreatic beta cells, initiating a sequence of intracellular events leading to insulin release into the portal circulation.

Insulin restores normoglycemia by diminishing hepatic glucose production (reducing glycogenolysis + gluconeogenesis) and by increasing glucose uptake in skeletal muscle + adipose tissue. Insulin also reduces the level of circulating glucagon, which contributes to the decline in hepatic glucose production. This effect is mediated by inhibition of both glucagon secretion and of the glucagon gene in the pancreatic alpha cells.

58
Q

What 2 hormonal abnormalities are largely responsible for the development of DKA and HHS in patients with uncontrolled diabetes?

A
  1. Insulin deficiency/resistance

2. Glucagon excess due to removal of the normal suppressive effect of insulin

59
Q

Other than insulin and glucagon levels, what other factors contribute to increases in glucose and ketoacid production (from uncontrolled lipolysis)?

A

Increased secretion of catecholamines, cortisol, and growth hormone which all oppose the actions of insulin

60
Q

What are signs of DKA?

A
  1. Dry mouth
  2. Hypotension
  3. Tachycardia
  4. Abdominal tenderness
  5. Fruity smell of breath (ketones)
61
Q

What are signs of HHS?

A
  1. Profound dehydration
  2. Tachycardia
  3. Hypotension
  4. Altered mental status
62
Q

Why is there no ketoacidosis in HHS but there is in DKA?

A

Suppression of lipolysis + ketogenesis is more sensitive to insulin than the inhibition of gluconeogenesis, thus systemic activity of even small amounts of insulin secretion is sufficient in HHS to minimise the development of ketoacidosis but not adequate to control hyperglycaemia

63
Q

What are the advantages to using VBG over ABG?

A

Less painful for the patient
Provides potassium and glucose levels
pH and bicarbonate levels are similar to ABG

VBG does NOT show an accurate representation of O2 and CO2 levels

64
Q

What are the relevant antibody tests for type 1 diabetes?

A
  1. Islet cell antibodies

2. Anti-GAD antibodies

65
Q

What insulin therapy should be provided for children/young people with type 1 diabetes?

A

Multiple daily injection basal–bolus insulin regimens from diagnosis.

If a multiple daily injection regimen is not appropriate for a child or young person with type 1 diabetes, consider continuous subcutaneous insulin infusion (CSII or insulin pump) therapy.

66
Q

What is the HbA1c target for young people with type 1 diabetes?

A

≤ 48mmol/mol to minimize long-term complications

They should perform at least 5 capillary blood glucose tests/day

67
Q

What are symptoms of type 1 diabetes?

A
  1. Polyuria
  2. Polydipsia
  3. Hyperglycemia (random glucose > 11mmol/L)
  4. Weight loss
  5. Excessive tiredness
68
Q

What are the 3 basic types of insulin regimens used for type 1 diabetics?

A
  1. Multiple daily injection basal–bolus insulin regimens: injections of short‑acting insulin or rapid‑acting insulin analogue before meals, together with 1 or more separate daily injections of intermediate‑acting insulin or long‑acting insulin analogue.
  2. Continuous subcutaneous insulin infusion (insulin pump therapy): a programmable pump and insulin storage device that gives a regular or continuous amount of insulin (usually a rapid‑acting insulin analogue or short‑acting insulin) by a subcutaneous needle or cannula.
  3. One, two or three insulin injections per day: these are usually injections of short‑acting insulin or rapid‑acting insulin analogue mixed with intermediate‑acting insulin.
69
Q

What are the target blood glucose levels for a young person with type 1 diabetes?

A

fasting plasma glucose level of 4–7mmol/L

a plasma glucose level of 5–9 mmol/L after meals

70
Q

What is the treatment for a young person with severe hypoglycaemia?

A

10% IV glucose. Give a maximum dose of 500 mg/kg body weight (equivalent to a maximum of 5 ml/kg) - if in hospital

1mg/500ug glucagon IM (in buccal cavity) - if in community

71
Q

What are the symptoms of DKA?

A
  1. N/V
  2. Abdominal pain
  3. Hyperventilation
  4. Dehydration
  5. Reduced level of consciousness
72
Q

When do you start the insulin infusion for children with DKA and how much do you give?

A

1-2h after fluid therapy (0.9% NaCl + 40mmol KCl)

IV insulin infusion of 0.05-0.1units/kg/hr

Once plasma glucose concentration < 14mmol/L change fluids to 0.9% NaCl + 5% glucose + 40mmol KCl

73
Q

What is the gold standard of insulin treatment for adults with type 1 diabetes?

A

Multiple daily injection basal–bolus insulin regimens

74
Q

When would you add metformin to a type 1 diabetic’s treatment regimen?

A

If they have a BMI of 25 kg/m2 (23 kg/m2 for people from South Asian and related minority ethnic groups) or above and wants to improve their blood glucose control while minimising their effective insulin dose.

75
Q

What could be the explanation of rising blood glucose results 15mo after diagnosis with type 1 diabetes?

A
  1. First term/examination stress
  2. Complacency/non-adherence (missing some insulin doses)
  3. Emerging from the honeymoon phase (phase during which there is a very small amount of residual endogenous insulin secretion)
76
Q

When should a continuous subcutaneous insulin pump be used for type 1 diabetes?

A
  1. attempts to achieve target haemoglobin A1c (HbA1c) levels with multiple daily injections (MDIs) result in the person experiencing disabling hypoglycaemia.

OR

  1. HbA1c levels have remained high (that is, at 8.5% [69 mmol/mol] or above) on MDI therapy (including, if appropriate, the use of long-acting insulin analogues) despite a high level of care.
77
Q

What blood glucose levels warrant a diagnosis of gestational diabetes? And what is used for their treatment?

A

a fasting plasma glucose level of 5.6 mmol/L or above

OR

a 2‑hour plasma glucose level of 7.8 mmol/L or above

Metformin (or another form of insulin if metformin is contraindicated)

78
Q

What are the normal blood glucose levels of someone with gestational diabetes?

A

fasting: 5.3 mmol/L

and

1 hour after meals: 7.8 mmol/L OR 2 hours after meals: 6.4 mmol/L

79
Q

What are women with diabetes prescribed in addition to taking their diabetes medication during pregnancy?

A

Folic acid (5mg/day) from at least 3 months before conception

80
Q

Which 3 hormones oppose the action of insulin?

A
  1. Glucagon
  2. Cortisol
  3. Noradrenaline (adrenaline, dopamine - all catecholamines)
81
Q

A 32yr old man of south Indian ethnicity presents with thirst, polyuria, tiredness and 8kg weight loss. BMI is now 29. Random blood glucose is 23mmol/l.

What additional information is required to make a precise diagnosis?

A
  1. Urine test
  2. Family history
  3. Anti-GAD antibodies
82
Q

What is the usual dose of sitagliptin?

A

100mg daily

83
Q

A 72yr old woman with Type 2 diabetes for 11yr is admitted urgently with rigors, jaundice and severe abdominal pain. She is hypotensive and has renal impairment (eGFR 32 on admission, 56 5 months ago). Usual diabetes treatment is Metformin 500mg tds, gliclazide 80mg bd and sitagliptin 100mg daily. HbA1c 5months ago was 60mmol/mol. Blood glucose on admission is 32mmol/l. She is diagnosed with cholecystitis and septicaemia.

What 3 things should be done?

A
  1. IV insulin infusion should be started
  2. Target blood glucose should be between 4-9mmol/L
  3. All diabetes tablets should be suspended
84
Q

What is a side effect of irbesartan? What type of drug is this and what is it used for?

A

Hyperkalemia

Angiotensin II Receptor Antagonist

Used to treat hypertension

85
Q

Prescribe a regular treatment of blood glucose for type 2 diabetes mellitus. The patient has no known drug allergies and is not on any treatment for his diabetes at present. His renal function is stable.

A

Metformin 850mg, oral

Taken with meals

86
Q

What is gentamicin and why does it require therapeutic drug monitoring?

A

Aminoglycoside antibiotic active against gram negative and some gram positive bacteria.

It is nephrotoxic and ototoxic - excreted largely unchanged by the kidneys.

87
Q

Name the common drugs that need therapeutic drug monitoring and an indication for their use

A
  1. Digoxin -> maintenance for atrial fibrillation/flutter
  2. Phenytoin -> Tonic-clonic seizures, focal seizures, status epilepticus
  3. Carbamazepine -> Focal/generalised tonic-clonic seizures, trigeminal neuralgia, prophylaxis of bipolar disorder unresponsive to lithium, adjunct to acute alcohol withdrawal
  4. Gentamicin -> Bacterial eye infections, Bacterial otitis externa, Gram-positive bacterial endocarditis, septicaemia, meningitis, HAP
  5. Vancomycin -> C. diff infection, CAP/HAP
  6. Teicoplanin -> C. diff infection, Gram-positive bacterial infections, strep/enterococcal endocarditis
  7. Lithium -> Bipolar disorder
  8. Aminophylline/Theophylline -> Severe acute asthma, Severe acute exacerbation of COPD
88
Q

What are the 4 autoantibodies that are markers of b-cell autoimmunity in type 1 diabetes?

A
  1. ICA (Islet cell antibodies) -> against cytoplasmic proteins in b-cells
  2. GAD65 (glutamic acid decarboxylase)
  3. IAA -> against insulin
  4. IA-2A -> against tyrosine phosphatase protein
89
Q

Give an example of a sulphonylureas drug and its mechanism of action

A

Chlorpropamide, Glipizide, Gliclazide

Inhibit K+ channels causing cells to depolarize + insulin to be released. Increases glucose uptake into muscle tissues. Increases insulin sensitivity. Can cause weight gain + severe hypoglycaemia. Taken orally

90
Q

Give an example of a biguadine and its mechanism of action

A

Metformin

Acts on mitochondria to increase AMP:ATP ratios which activate AMP-activated protein kinase to inhibit gluconeogenesis + glucagon signalling from liver. Taken orally + can be combined with other hypoglycaemic drugs. Suppresses appetite = weight loss

91
Q

Give an example of a a-glucosiddase inhibitor and its mechanism of action

A

Acarbose

Saccharide that’s a competitive inhibitor of a-glucosidase in the intestine. Delays absorption of carbs from small intestine. Can be used in combo with other drugs. SE = flatulence + diarrhea

92
Q

Give an example of a thiazolidinedione/glitazone and its mechanism of action

A

Pioglitazone

PPAR-y (peroxidase progenitor activated receptor-y) agonists. Induce the transcription of insulin secretary signals (i.e. GLUT4, lipoprotein lipase, fatty acid transporters). SE = weight gain, fluid retention, bladder cancer, heart failure, osteoporotic fractures. Increases glucose uptake into muscle + increase insulin sensitivity.

93
Q

Give an example of a GLP1 agonist/incretin and its mechanism of action

A

Exanitide

Act to increase insulin secretion, decrease glucagon secretion, delay gastric emptying, increase CO2 and brain satiety signals. Rapidly broken down by DPP-4. SC injections. Can be used in combo with other drugs. SE = hypoglycaemia + GI effects.

94
Q

Give an example of a DPP-4 inhibitor/gliptin and its mechanism of action

A

Sitagliptin, Vildagliptin

Inhibit breakdown of endogenous incretins by DPP-4. Increase insulin secretion + decrease blood glucose levels. Increase glucose absorption into tissues. SE = headache, pancreatitis, URTI with vildagliptin

95
Q

Give an example of a SGLT2 inhibitor and its mechanism of action

A

Canagliflozin, dapagliflozin, empagliflozin

Inhibit reabsorption of glucose from the PCT in the kidney (not involved in the insulin pathway!) = therapeutic glucosuria. No hypoglycaemia, weight loss, lowers SBP. SE = UTI

96
Q

Give an example of an insulin and its mechanism of action

A

Insulin lipro, insulin detemir, isophane insulin

Use in type 2 diabetes if blood sugars still uncontrolled after using other medications

97
Q

What are the features of DKA?

A

Hyperglycemia:

  • Dehydration
  • Tachycardia
  • Hypotension
  • Decreased consciousness

Acidosis:

  • Kussmaul’s breathing
  • Abdominal pain
  • Vomiting
  • Acetone on breath
98
Q

What are symptoms of hypoglycaemia?

A

Adrenergic:

  • Tachycardia
  • Palpitations
  • Sweating
  • Tremor
  • Hunger

Neuroglycopaneic:

  • Dizziness
  • Confusion
  • Sleepiness
  • Coma
  • Seizure
99
Q

What is the treatment for a hypoglycaemic event?

A

IV 50% dextrose

Glucogel IM

100
Q

What is the treatment for hyperosmolar hyperglycaemic state?

A

IV dextrose 5% + anticoagulation (i.e. heparin)

B/c so dehydrated they’re at increased risk of thrombosis.

101
Q

Name some microvascular and macrovascular complications of diabetes

A

Microvascular: Neuropathy, Nephropathy, Retinopathy

Macrovascular: Atherosclerosis, MI, Heart failure, Stroke

102
Q

What kind of nephropathy is associated with diabetes?

A

Kimmelstiel-Wilson lesions

Affects the microvasculature in the glomerulus of the kidney.

103
Q

What is abnormal on a foot examination in diabetes?

A
  1. General appearance: plantar ulcer common -> infection -> osteomyelitis
  2. “Architecture”: diabetics walk on metatarsal heads
  3. Pulses: Absent in diabetes
  4. Sensation: Poor/absent with vibration sensor + monofilament
104
Q

Which retinopathy is common in type 1 diabetes? In type 2 diabetes?

A

Proliferative = DM1

  • Retina becomes blocked causing the growth of abnormal blood vessels on the retina
  • These can bleed into the eye, cause the retina to detach, and seriously damage vision

Maculopathy = DM2

  • Exudative, Oedematous, Ischemic
  • Fat + protein deposited around central macula -> can lose fine vision

Both can lead to blindness

105
Q

What indicates a type 2 diabetic needs to be put on supplemental insulin? Pathophysiologically why is this happening?

A

Weight loss

Decrease in b-cell function

106
Q

What is diabetic lens osmosis?

A
  • Benign
  • Osmotic lens fills with fluid b/c of increased glucose
  • Leads to blurring of vision
107
Q

What are the 2 main signs of diabetic retinopathy and what is the grading system of retinopathy?

A 
R0 = no problems
R1 = background retinopathy
R2 = pre-proliferative
R3 = proliferative

Blot hemorrhages, cotton wool spots (retinal ischemia)

108
Q

Compare the composition of soft and hard exudates

A

Soft exudate = cotton wool spot -> retinal ischemia

Hard exudate = lipids

109
Q

What 2 things in the eye would cause complete blindness?

A
  1. Retinal hemorrhage

2. Retinal detachment

110
Q

Name 4 things that can cause renal failure

A
  1. Dehydration
  2. Infection
  3. Hyperglycemia
  4. N/V
111
Q

Give 2 drug classes of diabetic drugs that can have prolonged metabolism in renal/hepatic failure

A
  1. Sulphonylureas

2. Injected insulins

112
Q

Why are diabetics more prone to infections?

A

Hyperglycemia prevents immune system from properly dealing with infections

113
Q

Name an intermediate acting insulin

A

Isophane insulin (NPH)

  • Precipitates into suspensions which slowly dissolve
  • Duration (12-20h)
114
Q

Name 3 short-acting insulins

A

Insulin Lipro, Aspart, Glulisine

  • Rapid onset (10-20min), short duration (2-5h)
  • Prevent dimer formation allowing more active monomer to be bioavailable
115
Q

Name 3 long-acting insulins

A

Insulin Glargine, Detemir, Degludec

Glargine: decreased solubility at neutral pH, forms aggregates that slowly dissolve (duration 24-36h)

Detemir: insulin + fatty acid; confers albumin binding which slowly dissociates prolonging its circulation (duration 24h)

Degludec: insulin + fatty acid; multi-hexamer formation at injection site with slow release (duration > 42h)

116
Q

Explain/differentiate the 3 types of insulin therapy for diabetics in terms of:

  • # of injections
  • Time of injections
  • Suitability
  • Formulations
  • Meal time/content
  • Required patient understanding
A
  1. 1, 2, 3 injections/day
    # of injections: 1-3
    Time of injections: morning/at meals
    Suitability: T2D
    Formulations: Rapid-acting or short-acting insulin is mixed with intermediate-acting insulin
    Meal time/content: Fixed
    Required patient understanding: More basic
2. Basal-bolus
# of injections: multiple
Time of injections: throughout day
Suitability: T1D, some T2D
Formulations: Intermediate/long-acting with short-acting insulin
Meal time/content: Flexible
Required patient understanding: High
  1. Insulin Pump (CSII)
    # of injections: semi-automated (as needed)
    Time of injections: throughout day
    Suitability: T1D
    Formulations: short-acting insulin
    Meal time/content: Flexible
    Required patient understanding: Medium/high

Year 3 TCDs (24 decks)

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