Week 7 Flashcards

1
Q

Which hormone has a hypoglycaemic action?

A

Insulin

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2
Q

Which hormones have a hyperglycaemic action?

A

Glucagon, adrenaline, cortisol, growth hormone

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3
Q

What are some causes of hypoglycaemia?

A

1) Exertion/exercise - skeletal muscle uses a lot of glucose
2) Fasting - no glucose entering from the gut
3) Excess exogenous insulin
4) Insulinoma (excess endogenous insulin)
5) Alcohol intake
- Causes an increase in endocrine pancreatic microcirculation, increasing insulin secretion
- Inhibits hepatic gluconeogenesis

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4
Q

What are some actions of insulin?

A

Stimulates glucose transport (muscle, adipose tissue)

Stimulates glycogen synthesis (liver, muscle)

Inhibits gluconeogenesis (liver)

Stimulates protein synthesis; antagonises proteolysis

Facilitates vasodilation

Stimulates K ion uptake into cells

Stimulates Na reabsorption in renal tubule

Activates lipogenesis (Liver, muscle, adipose tissue)

Inhibits fatty acid oxidation (Liver, muscle)

Inhibits lipolysis (Adipose tissue)

Acts as a growth factor and has effects on gene expression

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5
Q

How does the hypothalamus stimulate insulin secretion?

A

Lateral hypothalamus –> motor nuclei of vagus –> parasympathetic nerves to islet –> release of ACh, VIP, PACAP, GRP –> Insulin secretion

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6
Q

How does the hypothalamus inhibit insulin secretion?

A

Medail hypothalamus –> sympathetic motor neurones (cord) –> sympathetic nerves to islet –> release of noradrenaline, galanin, NPY –> Inhibits insulin secretion

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7
Q

What are some causes of hyperglycaemia?

A

Stress: chronically high cortisol and adrenaline
- Both hormones activate glycogenolysis in the liver

Absolute absence of insulin (Type-1 diabetes, T1DM)

  • Autoimmune destruction of the pancreatic β-cells
  • Dawn phenomenon in T1DM due to diurnal surge in cortisol

Relative insufficiency of insulin (insulin resistance leading to T2DM)
- Insulin is secreted, but tissues (or specific pathways) are not sensitive to it

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8
Q

What are the factors involved in the Insulin Resistance Syndrome?

A
  • Decreased incretin effect
  • Increased lipolysis
  • Increased glucose reabsorption
  • Decreased glucose uptake
  • Neurotransmitter dysfunction
  • Increased hepatic glucose production
  • Increased glucagon secretion
  • Decreased insulin secretion
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9
Q

How can you improve control of blood glucose?

A
  • Improve insulin sensitivity (exercise, improved diet, insulin sensitisers)
  • Stimulate endogenous insulin secretion
  • Inhibit hepatic glucose production
  • Prescribe exogenous insulin
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10
Q

What complications can arise from chronic hyperglycaemia in poorly controlled diabetes?

A
  • Non-enzymic modification of proteins by glucose: glycation of haemoglobin (HbA1C)
  • Sorbitol pathway overactivity; formation of osmotically active metabolites
  • Disturbance of cellular redox state
  • Impaired vasodilation
  • Peripheral neuropathy; cataract; blindness; impaired kidney function
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11
Q

What are the actions of metformin?

A

Liver:

  • decrease gluconeogenesis
  • decrease glycogenolysis
  • decrease oxidation of fatty acids

Muscle:

  • Increase glucose uptake and oxidation
  • Increase glycogenolysis
  • Decrease oxidation of fatty acids
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12
Q

Define diabetes mellitus

A

A heterogenous complex metabolic disorder characterised by elevated blood glucose secondary to either resistance to the action of insulin or insufficient insulin secretion or both.

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13
Q

What are the 4 stages in the spectrum of diabetes according to WHO criteria?

A

Normal - HbA1c less that 42mmol/mol, Fasting Plasma Glucose < 6.1mmol/L

Impaired Fasting Glucose - FPG>6.1 mol/L but less than 7mmol/L

Impaired Glucose Tolerance - OGTT 2h glucose greater or equal to 7.8mmol/L but less than 11.1 mol/L (HbA1c of 42-47mmol/mol = high risk of diabetes)

DM - HbA1c 48mmol/mol and above, FPG above 7mmol/L OR OGTT 2h greater than 11.1 mmol/L

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14
Q

Who can you not use HbA1c for?

A

young patients (under 18), pregnant, acutely unwell, CKD or anaemia

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15
Q

How do T1DM patients tend to take their insulin?

A

Basal-bolus regime

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16
Q

What are the criteria for DKA?

A

D - diabetic - BM>11.1 (can be normal!)

K - ketonaemia (blood ketones >=3 or urine ketones >=3+)

A - acidosis pH < 7.3 or bicarb <=15

17
Q

What are some causes of recurrent DKA?

A
  • Insulin technique and sites
  • Carb counting
  • Alcohol
  • Pregnancy
  • Psychological and psychosocial difficulties eg. body image, needle phobia
  • Nature of lifestyle
  • Possible organic causes such as gastroparesis
  • Iatrogenic causes eg. surgery
18
Q

What are some oral hypoglycaemic agents?

A
  • Decrease hepatic gluconeogenesis - Biguanides (metformin)
  • Increase insulin secretion - sulfonylureas (eg. Gliclazide)
  • Reduce insulin resistance - Thiazolidinediones (TZDs eg. pioglitazone)
  • Prevent breakdown of GLP - DPP-4 inhibitors
  • Promote glycosuria - SGLT2 inhibitors
  • Decrease carbohydrate absorption - alpha-glucosidase inhibitor
19
Q

What are the 4 key hormones responsible for glucose regulation?

A
Amylin
Pancreatic beta-cells
- Suppresses post-prandial glucagon secretion
- Slows gastric emptying
- Reduces food intake and body weight
Insulin
Pancreatic beta-cells
Promotes:
- Glucose uptake by cells
- Protein and fat synthesis
- Use of glucose as energy
- Suppresses post-prandial glucagon secretion
Glucagon
Pancreatic alpha-cells
Promotes:
- Breakdown of liver glycogen stores
- Hepatic gluconeogenesis
- Hepatic ketogenesis

GLP-1
Small intestine L-cells
Promotes:
- Glucose-dependent insulin production
- Suppresses post-prandial glucagon secretion
- Slows gastric emptying
- Reduces food intake and body weight (increases satiety, hypothalamic level)

20
Q

What is metabolic syndrome?

A

Metabolic syndrome is a cluster of the most dangerous CVD, diabetes and prediabetes, abdominal obesity, high cholesterol and high blood pressure

21
Q

What are the diagnostic criteria for gestational diabetes?

A
  • Fasting plasma glucose level of 5.6 mmol/L or above
    or
  • 2-hour plasma glucose level of 7.8 mmol/L or above on the OGTT
22
Q

What are some of the parameters of the pathophysiology of T2DM?

A
  • Increased hepatic glucose production
  • Increased glucagon secretion by islet alpha cells
  • Decreased glucose uptake
  • Increased lipolysis
  • Impaired appetite regulation
  • Decreased insulin secretion from beta cells
  • Increased glucose reabsorption
  • Decreased incretin effect
23
Q

What is concordance?

A

A negotiated, shared agreement between clinician and patient concerning treatment regime(s), outcomes and behaviours; a more co-operative relationship than those based on issues of compliance and non-compliance

24
Q

What is compliance?

A

The fulfilment by the patient fo the healthcare professional’s recommended course of treatment

25
Q

What is adherence?

A

The extent to which a person’s behaviour - taking medication, following a diet, and/or executing lifestyle changes, corresponds with agreed recommendations from a health care provider

26
Q

How is concordance reached?

A
  • through a therapeutic alliance and negotiation between the prescriber and the patient.
  • the patient is encouraged to discuss concerns about medications that have been prescribed and preferences for treatments and participation in decision making.
  • the health professional gives evidence based information to the patient and shares his or her clinical experience.
27
Q

What are the two main problems of poor concordance?

A
  • for treatment outcomes and direct clinical consequences

- increases financial burden on society

28
Q

What are the factors affecting concordance?

A
  • patient centred
  • therapy related
  • social and economic
  • healthcare system
  • disease
29
Q

How can concordance be improved?

A
  • Patients help design treatment plan
  • detailed explanation re disease and treatment
  • patients need to understand illness and therapy
30
Q

Why do young people find self-management and concordance challenging?

A
  • Working towards independence and autonomy
  • New environments and activities
  • New relationships with peers, family and clinicians
31
Q

At what level is the cricoid found?

A

C6 in women and C7 in men but can range from C5 to T1 in both.