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Medicine Year 2 > Endocrine Topic 2 - Diabetes > Flashcards

Endocrine Topic 2 - Diabetes Flashcards

1
Q

How can T1DM development be predicted?

A

High lysophosphatidylcholine

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2
Q

How are bisphosphonates administered?

A
  • Oral or IV administration, depending on preparation, free drug excreted by kidney
  • Alendronate oral once weekly on an empty stomach with large glass of water, upright, 30 minutes before breakfast
  • Zolendronate IV once weekly
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3
Q

How is T1DM treated?

A

Insulin replacement

Islet transplant

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4
Q

How is DKA treated?

A

IV fluid, insulin, potassium (cardiac monitoring), NG tube (vomiting)

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5
Q

Describe the normal pattern of insulin secretion

A

Natural insulin secretion - basal low, steady background secretion, bolus meal-time insulin

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6
Q

List the sources of replacement insulin

A
  • Human - recombinant DNA technology
  • Human analogues - recombinant DNA technology modified for desired kinetic characteristics
  • Animal insulin - bovine or porcine (no longer initiated)
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7
Q

What is the diabetic response to hyperglycaemia?

A
  • No insulin production
  • No glucose uptake by cells (no GLUT 4 action)
  • Blood glucose remains high
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8
Q

What causes insulin resistance?

A
  • Occurs with age, exacerbated by increasing weight, due to genetic susceptibility (ethnicity, parent/1st degree relative), environmental triggers
  • Adipokines have role e.g. Leptin (acts on hypothalamus to regulate fat stores), adiponectin (reduces free fatty acids, high free fatty acids disrupt insulin signalling), Resistin (increases hypothalamic stimulation of glucose production)
  • Insulin receptor gene mutations
  • Increased inflammatory mediators - CRP, IL6, TNF alpha
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9
Q

What is the normal response to hypoglycaemia?

A
  • Descreased insulin production by beta cells - decreased glucose uptake by fat/muscle/liver
  • Increased glucagon production by alpha cells - increased glycogenolysis and gluconeogenesis
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10
Q

List the possible mechanisms of action of drugs used to treat T2DM

A
  • Decrease glucose absorption (GI tract)
  • Increase glucose uptake (muscle/fat)
  • Decreased glucose reabsorption (renal tubules)
  • Increased insulin production (pancreas)
  • Decreased gluconeogenesis (liver)
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11
Q

How is diabetic retinopathy treated?

A
  • Glycaemic control
  • Ophthalmic reveiw - laser, VEGF inhibitors (bevacizumab), vitrectomy
  • Screening - annual from age 12
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12
Q

What are the symptoms of hypoglycaemia?

A
  • Initital autonomic
    • Sweating
    • Tremor
    • Palpitations
    • Hunger
    • Anxiety
  • Later neuroglycopaenic
    • Confusion
    • Decreased consciousness
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13
Q

Give examples of bisphosphonates

A

End in -dronate e.g. alendronate, zolendronate

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14
Q

What happens to potassium concentration in reponse to hyperglycaemia?

A
  • Increased aldosterone production to increase water retention (counteract water loss due to osmotic diuresis)
  • Hyperaldosteronism - renal K+ loss
  • Lack of insulin - no K+ into cells (KATP)
  • Plasma K+ rises, total body K+ falls
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15
Q

Describe the pathophysiology of T2DM

A
  • Increasing insulin resistance
  • Initial hyperinsulinaemia to compensate (in pre-diabetes/early stage), then reduced secretion
    • Glucotoxicity - impaired beta cell function
    • Glucokinase defects
    • Pancreatic beta cell transcription factor mutations
  • Macrovascular then microvascular complications
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16
Q

What is the diabetic response to hypoglycaemia?

A
  • Increased cortisol
  • Increased adrenaline - tremor, sweating
  • Increased acetyl choline, noradrenaline (sympathetic) - hunger
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17
Q

What stimulates release of mineralocorticoids?

A

Stimulated by angiotensin II, ACTH and potassium

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18
Q

How can macrovascular complications of diabetes be prevented?

A

BP/cholesterol control and not smoking

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19
Q

How do bisphosphonates function?

A
  • Carbon substituted pyrophosphate
  • Bind to bone and inhibit osteoclast activity
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20
Q

Compare DKA and HHS (hyperosmolar hyperglycaemic state)

A
  • DKA - short history, HHS - insidious
  • DKA - young T1DM, HHS - old T2DM
  • DKA - no residual insulin, HHS - residual insulin
  • DKA - hyperglycaemia, HHS - profound hyperglycaemia
  • DKA - dehydration, HHS - significant dehydration
  • DKA - acidosis, HHS - no acidosis (no increased in lipolysis, no ketones)
  • DKA - patient usually alert, HHS - patient often drowsy
  • HHS - hypernatraemia
  • HHS - high mortality (comorbities)
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21
Q

How is an oral glucose tolerance test performed?

A

75g anhydrous glucose, blood glucose concentration taken every 30-60 minutes

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22
Q

Describe the 3rd line treatment of T2DM

A
  • Add different oral agent or injectable agent
    • BMI > 30 - GLP1 agonist
    • BMI < 30 - basal insulin
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23
Q

What treatments are used for osteoporosis other than bisphosphonates?

A
  • Calcium and Vitamin D - essential for bone formation
  • Denosumab - monoclonal antibody, inhibits RANK ligand which signals to osteoclasts, therefore reduces resorption, subcutaneous injection every 6 months
  • Teriparatide - recombinant parathyroid hormone, binds to osteoblasts to increase bone formation, requires subcutaneous injection as it is a peptide
  • Strontium ranclate stimulates osteoblasts and inhibits osteoclasts
  • HRT for menopause related bone loss
  • SERMs - bind to oesteogen receptor and decreases bone resorption
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24
Q

What is the function of DPP-4?

A

Breaksdown GLP-1

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25
Q

List the types of diabetes mellitus

A
  • Type 1
  • Type 2
  • Maturity onset diabetes of the young (MODY)
  • Gestational
  • Secondary - pancreatitis, cystic fibrosis, haemachromatosis, steroid induced
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26
Q

List the types of diabetic neuropathy

A
  • Peripheral neuropathy
  • Autonomic neuropathy
  • Mononeuritis multiplex - painful motor/sensory, 2+ nerves
  • Diabetic amyotrophy - painful proximal neuropathy (thigh/buttock)
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27
Q

What causes MODY?

A
  • Autosomal dominant
    • Mutations - HNF1 alpha, glucokinase, HNF4 alpha, HNF1 beta, neonatal (K+ channel deficiency)
  • Insulin produced but not secreted by beta cells
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28
Q

Describe the pharmacokinetics and pharmacodynamics of thiazolidinediones

A
  • Pharmacokinetics
    • Rapidly absorbed
    • Extensive hepatic metabolism
    • Pioglitazone excreted in bile
  • Pharmacodynamics
    • PPAR alpha agonists - increase transcription of insulin sensitising genes
    • PPAR alpha is a nuclear receptor expressed in adipose tissue, muscle and liver
  • Increased insulin sensitivity over weeks-months
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29
Q

How is MODY treated?

A

Sulphonylureas e.g. Glicazide

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30
Q

Which drugs are used to treat T2DM by increasing insulin secretion by the pancreas?

A

Insulin, sulphonylureas, meglitinides, GLP-1 receptor agonists, DPP4 inhibitors

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31
Q

Describe the clinical features of DKA

A
  • Metabolic acidosis (pH < 7.3, bicarbonate < 15mmol/L)
  • Usually hyperglycaemia (>13.9 mmol/L)
  • Ketosis
  • Dehydration
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32
Q

How must insulin be administered? Why?

A
  • Injected - subcutaneous, usually into abdomen or outer thigh/buttocks
  • Peptide hormone - inactivated by GI enzymes, can’t be given orally
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33
Q

Describe the 1st line treatment of T2DM

A
  • Lifestyle and metformin/sulphonyurea
  • Targe = <7% HbAlc
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34
Q

List the genes which cause type 1 diabetes susceptibility

A
  • HLA - DR3/4 and DR2/8 - largest genetic effect
  • Protein tyrosine phosphatase PTPN 22
  • CTLA-4 - cytotoxic T lymphocyte associated protein 4
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35
Q

How does bone resorption occur?

A

Preosteoclasts –> osteoclasts –> acid and lysosome secretion –> bone resorption at ruffled membrane

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36
Q

List the risk factors for T2DM

A
  • Age >40 (or 25 if south Asian)
  • Parent/1st degree relative with T2DM
  • Overweight/obese
  • South Asian, Chinese, Afrocaribbean or black African origin
  • Hypertension
  • High waist circumference
  • Schizophrenia, bipolar illness, depression or treatment with anti-psychotic medication
  • Women with polycystic ovaries, gestational diabetes or baby weighing >10 lbs
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37
Q

Describe the types of insulin replacement regimens

A
  • Basal-bolus insulin regimens - 1/2 daily long or intermediate-acting insulin with bolus
  • Mixed biphasic - short and intermediate, short-acting before meals
  • Continuous subcutaneous insulin infusion (pump) - continuous short acting
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38
Q

How is hypoglycaemia treated?

A
  • Mild (blood glucose < 4 mmol/L)
    • 15-20g fast-acting carbohydrate
    • Retest 15-20 minutes later
  • Severe (requiring help from another person)
    • 15-20g fast-acting carbohydrate, retest 15-20 minutes later
    • If decreasing consciousness - IM glucagon, IV dextrose
    • Retest
    • Follow with long-acting carbohydrate
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39
Q

What leads to activation of the T1DM susceptibility genes?

A

Precipitating event:

  • Enterovirus, rotavirus
  • Bacteria
  • Environmental - cows milk, wheat proteins
  • Vitamin D deficiency
  • Puberty, pregnancy
  • Psychological stress (adult-onset)
40
Q

What are the compensatory mechanisms for metabolic acidosis?

A

Hyperventilation - Kussmaul’s breathing

41
Q

Describe the 2nd line treatment of T2DM

A
  • If not reaching target after 3-6 months
  • Add sulphonylurea/pioglutazone/DPP-4 inhibitor/SGLT2 inhibitor
42
Q

Where is GLP-1 produced?

A

Produced by intestinal epithelial L cells in response to the ingestion of food

43
Q

List the types of preparations of insulin

A
  • Short-acting - 15-30 minutes before meal (or in diabetic emergencies e.g. DKA
    • Soluble, rapid acting
  • Intermediate-acting - 1/2 daily with short acting or as part of biphasic insulin
  • Long-acting - mimics endogenous basal insulin secretion
44
Q

Why is diabetic retinopathy difficult to manage?

A

Symptoms don’t appear until damage has been done and it is too late to reverse

45
Q

How is HHS treated?

A

IV fluid (slow and steady), insulin, potassium

46
Q

Describe the endocrine pancreas

A
  • Functional unit = islets of Langerhans
    • Alpha cells secrete glucagon
    • Beta cells secrete insulin
    • Delta cells secrete somatostatin
    • Gamma cells secrete pancreatic polypeptide
47
Q

Describe the pathophysiology of microvascular complications of diabetes

A
  • Capillary damage - increased blood flow, increased pressure, thickening and damage to walls
  • Metabolic damage - retina/kidneys/nerves don’t need insulin to take up glucose, glucose is converted to sorbitol by aldose reductate
    • High sorbitol causes oxidative stress, sorbital is converted to fructose (L-sorbose 1 dehydrogenase), then to advanced glycation end products
48
Q

Describe the pathophysiology of type 1 diabetes

A
  • Autoimmune disease, destruction of Beta cells in the pancreas
  • T cell mediated, type IV hypersensitivity
  • Pathogenic T cells have specificity for pancreatic islet antigens
  • Disease results from inflammation causes by cytokines produced by CD4+, Th1 + Th1/17 cells or killing of self cells by CD8+ T cells
49
Q

Describe the process which leads to ketosis

A
  • Low insulin
  • Increased lipolysis - triglycerides broken down into fatty acids and monoglycerides
  • Fatty acids converted to fatty acid carnitine, which is transported into mitochondria and converted into acetyl coA, then acetoacetate, then ketone bodies
  • Ketone bodies are acidic, so build up leads to decreasing pH
50
Q

List the clinical features of HHS

A
  • Hypotension
  • Tachycardic
  • Hypernatraemia
  • Hyperglycaemia
  • Dehydration
  • Drowsiness
51
Q

Give examples of insulin sensitisers

A
  • Biguanides e.g. metformin
  • Thiazolidinediones e.g. pioglitazone
52
Q

Describe the pharmacokinetics and pharmacodynamics of sulphonylureas

A
  • Pharmacokinetics
    • Well absorbed, peak plasma concentration within 2-4 hours
    • Metabolised by liver
    • Duration of action up to 24 hours
  • Pharmacodynamics
    • Bind to receptor on beta cells, inhibit KATP channels and permit increased insulin secretion
    • Increased circulatory insulin
53
Q

How diabetes mellitus be categorized in terms of insulin?

A

Insulin resistant - high BMI

Insulin deficient - low BMI

54
Q

Describe diabetic autonomic neuropathy

A
  • CV - postural hypotension
  • GU - erectile dysfunction
  • GI - gustatory sweating, gastroparesis
55
Q

Which drugs are used to treat T2DM by decreasing glucose absorption in the GI tract?

A

Acarbose

56
Q

What is the kidney’s response to high glucose?

A
  • Osmotic diuresis
    • Glucose (+ ketones) freely filtered at glomerulus
    • Maximum reabsorption threshold exceeded
    • High solute concentration in tubular lumen = osmotic gradient
    • Water dragged out, excreted in urine
57
Q

Describe the pharmacokinetics and pharmacodynamics of metformin

A
  • Pharmacokinetics
    • Rapidly absorbed
    • Half life 2-5 hours
    • Excreted unchanged by kidneys
  • Pharmacodynamics
    • Inhibits mitochondrial glycerophosphate dehydrogenase in liver, activates AMPK
    • Reduced hepatic gluconeogenesis, insulin sensitiser
58
Q

How do insulin deficiency and counteregulatory hormones lead to ketoacidosis?

A
  • Low glucose uptake = hyperglycaemia
  • Hyperglycaemia leads to osmotic diuresis and increased lipolysis
  • Increased free fatty acids, glycogenolysis and gluconeogenesis = ketones and acidaemia - causes vomiting
  • = profound dehydration, ketoacidosis and K+ depletion
59
Q

Give examples of drugs which increase glucose in urine

A

SGLT2 inhibitors e.g. dapagliflozin

60
Q

What is the closest therapeutic preparation to cortisol?

A

Hydrocortisone

61
Q

What is the incretin system? How is it used clinically?

A
  • Gut hormones GLP-1 and GIP enhance insulin secretion in response to oral glucose, broken down by DPP-4
  • GLP-1 agonist - exenatide and liraglutide
    • Subcutaneous injection (peptide)
    • Based on exendin-4 from gila monster venom
  • Increased insulin secretion and weight loss
  • DPP-4 inhibitors - sitagliptin, linagliptin etc.
    • Oral administration, prevent endogenous GLP-1 breakdown
62
Q

What is the normal response to hyperglycaemia?

A
  • Beta cells release more insulin - increased glucose uptake by fat, muscle and liver
  • Alpha cells release less glucagon - decreased gluconeogenesis, decreased glycogenolysis
63
Q

How are glucocorticoids administered?

A
  • Oral
  • Topical
  • Nasal
  • Inhaled
  • Subcutaneous
  • Intramuscular
  • Intravenous
64
Q

Describe the mechanism of action of DPP-4 inhibitors

A

E.g. Vildagliptin, reduce breakdown of GLP-1 - reduction in blood glucose concentration

65
Q

What diseases are associated with T1DM?

A

Other autoimmune diseases

  • Thyroid problems
  • Coeliac
  • Addison’s
  • Pernicious anaemia
  • Inflammatory bowel disease
  • Premature ovarian failure
66
Q

Give examples of drugs which increase insulin

A
  • Sulphonylureas e.g. glicazide
  • GLP-1 agonists e.g. exenatide, liraglutide
  • DPP-4 inhibitors e.g. sitaglipin, linagliptin
  • Insulin
67
Q

List the metabolic complications of diabetes

A
  1. Diabetic ketoacidosis
  2. Hyperosmolar hyperglycaemia (non-ketotic) state
  3. Hypoglycaemia
68
Q

What is hypoglycaemic unawareness?

A
  • Frequent hypoglycaemic episodes, particularly noctural
  • Early autonomic symptoms diminished
  • High morbidity/mortality
  • Driving restrictions
69
Q

Describe ‘diabetic foot’

A

Neuropathy + peripheral vascular disease = infection, ulcers, ischaemia

70
Q

Which drugs are used to treat T2DM by decreasing glucose reabsorption in the renal tubules?

A

SGLT2 inhibitors e.g. dapagliflozin

71
Q

What are the effects of GLP-1?

A
  • Beta cells - increased insulin secretion
  • Alpha cells - decreased glucagon secretion
  • Liver - decreased hepatic glucose output
  • Stomach - decreased rate of gastric emptying
  • Brain - decreased appetite
  • Decreases blood glucose concentration
72
Q

How can microvascular complications of diabetes be prevented?

A

Good glycaemic control (Hba1c consistently within specified limits)

73
Q

Which drugs are used to treat T2DM by increasing glucose uptake in muscle and fat?

A

Metformin (biguanide), pioglitazone (thiazolidinedione), concentrated insulin, insulin/GLP-1 combinations

74
Q

List the autoantibodies involved in type 1 diabetes

A
  • Islet cell antibodies
  • Insulinoma associated antigen-2 (I-A2)
  • Glutamic acid decarboxylase 6 (GAD65)
  • Zinc transporter ZnT8
75
Q

Describe the pathogenesis of diabetic nephropathy

A
  • Renal enlargement and hyperfiltration
    • Renal hypertrophy, increased GFR, afferent arteriole vasodilation, increased glomerular pressure, thickened glomerular basement membrane, capillary damage, stress on endothelial cells = leakage of proteins
  • Microalbuminuria - not detected by normal dipstick (30-300mg/24hrs, normal <20)
  • Macroalbuminuria - detected by dipstick
  • Endstage renal failure - glomeruli destroyed
76
Q

What are the potential complications of HHS?

A

Risk of central pontine myelinosis and cerebral oedema

77
Q

List the chronic complications of diabetes

A
  • Microvascular
    • Retinopathy
    • Nephropathy
    • Neuropathy
  • Macrovascular
    • Ischaemic heart disease
    • Peripheral vascular disease
    • Cerebrovascular disease
78
Q

List the typical symptoms of T1DM

A
  • Polyuria
  • Polydipsia
  • Weight loss
  • Fatigue
  • Blurred vision
79
Q

What is addressed during a diabetic annual reveiw?

A
  • HbA1c
  • Cholesterol, HDL, triglycerides
  • Creatinine
  • Microalbuminuria
  • Retinal screening
  • Foot sensation
  • BP
  • Contraception
  • Lifestyle - exercise, diet, smoking
  • Drug therapy
  • Mental well being
  • Visual acuity
  • Pedal pulses
  • BMI
  • Erectile dysfunction
80
Q

List the types of mineralocorticoid receptor agonists

A
  • Spironolactone
    • Competitive antagonist at mineralocorticoid receptor, androgen and progesterone receptors
    • Side effects = gynaecomastia, hyperkalaemia
  • Eplerenone
    • Selective mineralocorticoid receptor antagonist
  • Clinical uses - primary aldosteronism, heart failure, hypertension
81
Q

List the symptoms of diabetes

A
  • Polyuria
  • Nocturia
  • Polydipsia
  • Fatigue
  • Unexplained weight loss
  • Cuts/wounds taking longer to heal
  • Blurred vision
  • Genital itching/thrush
82
Q

Describe the pathogenesis of retinopathy

A
  • Capillary wall damage - microaneurysms
  • Vessel wall breached - dot haemorrhages
  • Protein and fluid left behind - hard exudates
  • Microinfarcts - cotton wool spots
  • Damage to veins - venous budding, blockage
  • Ischaemia - VEGF and other growth factors - neovascularisation, proliferative retinopathy, vitreous haemorrhage
  • Fluid not cleared from macular area - macular oedema
83
Q

Which T1DM patients have increased risk of hypoglycaemia?

A

Those on intensive insulin treatment

84
Q

How is diabetic nephropathy managed?

A
  • Screen for microalbuminuria every year
  • ACE inhibitor/angiotensin II receptor blocker - lower BP if microalbuminura
  • Aggresive CV risk reduction - BP<125/75 - statin, quite smoking
  • Improve glycaemic control - HbAlc < 7%
85
Q

Give examples of SGLT2 inhibitors

A

End in -gliflozin, e.g. dapagliflozin

86
Q

What are bisphosphonates used for?

A

Used to treat osteoporosis, Paget’s disease, metastatic bone disease - reduce bone resorption

87
Q

What are the signs/symptoms of diabetic peripheral neuropathy?

A
  • Reduced vibratory sensation
  • Reduced pressure sensation
  • Reduced reflexes - knee and ankle
  • Aching/burning/lancinating pain
  • Reduced sensation of pressure, temperature and pain
88
Q

Give examples of GLP-1 receptor agonists

A

End in -(glu)tide e.g. liraglutide

89
Q

What are the systemic effects of glucocorticoids?

A
  • Anti-inflammatory by inhibiting transcription of genes for pro-inflammatory cytokines
  • Reduced T-lymphocytes
  • Counter-regulatory metabolic effects - gluconeogenesis, increase adiposity
  • Improve alertness (circadian rhythm)
90
Q

How does diabetes cause neuropathy?

A
  • Capillary damage, occlusion of vasa nervosa
  • Reduced blood supply to neural tissue - impaired signalling
  • High glucose - inability to transmit signals through nerves
  • Metabolic (sorbitol), vascular (capillary damage) and structural changes
91
Q

Describe the 4th line treatment of T2DM

A
    • additional oral agent
  • Prandial insulin/twice daily mixed biphasic insulin
92
Q

Which drugs are used to treat T2DM by decreasing gluconeogenesis in the liver?

A

Metformin, GLP-1 receptor agonists, DPP4 inhibitors, insulin

93
Q

How is diabetes diagnosed?

A
  • 2 abnormal tests or 1 + symptoms
  • Fasting blood glucose
    • < 6 = normal
    • 6.1-6.9 = impaired
    • > 7 = diabetic
  • Oral glucose tolerance test 2hr glucose
    • < 7.7 = normal
    • 7.8 - 11 = impaired
    • > 11.1 = diabetic
  • HbA1c - 3 month average plasma glucose concentration
    • 42-47 = pre-diabetes
    • >48 = diabetes
  • C peptide
94
Q

What is an artificial pancreas?

A

Continuous blood glucose monitor transmits information to insulin pump which calculates and releases the correct dose of insulin - just as the pancreas does

95
Q

Describe the pharmacokinetics and pharmacodynamics of SGLT2 inhibitors

A
  • Pharmacokinetics
    • Oral administration
    • Half-life 10-13 hours
  • Pharmacodynamics
    • Inhibit SGLT transporter which normally reabsorbs glucose in proximal convoluted tubule
  • Potential risk of volume depletion and UTI
  • Lowers glucose without causes hypoglycaemia
96
Q

When does DKA typically occur?

A
  • Presenting episode of T1DM
  • Compliance issue
  • Intercurrent infections
97
Q

Give examples of DPP-4 inhibitors

A

End in -gliptide e.g. saxagliptide

Medicine Year 2 (41 decks)

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