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Medicine Phase 2a > Endocrine List 1 - Diabetes > Flashcards

Endocrine List 1 - Diabetes Flashcards

1
Q

Give examples of diseases of the pituitary

A

Benign pituitary adenoma (most common in adults, pituitary produces less and presses on surrounding structures e.g. optic chiasm)
Craniopharyngioma
Trauma
Sheehans - pituitary infarction after labour
Sarcoid/TB

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2
Q

What 3 things can result from a pituitary tumour?

A

Pressure on local structures
Pressure on normal pituitary - hypopituitarism
Functioning tumour - hyperpituitarism

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3
Q

Give examples of pituitary tumour causing symptoms by putting pressure on local structures

A

Optic Chiasm pressed results in bitemporal hemianopia
Can cause hydrocephalus
Can get CSF leak

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4
Q

Give examples of pituitary tumour causing symptoms by putting pressure on normal pituitary (hypopituitarism)

A

Can be fatal in case of cortisol deficiency
Males:
Pale, no body hair (takes 9 months to occur), central obesity, effeminate (female like) skin
Females:
Loose body hair
Sallow complexion

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5
Q

Give examples of functional tumours of the pituitary gland (hyperpituitarism)

A

Prolactinoma (increased prolactin)
Acromegaly (increased GH)
Cushing’s (increased CTH)

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6
Q

Describe features of Prolactinoma

A 
Increased prolactin
Results in increased milk production in breast (some seeps out - galactorrhea)
Reduced fertility
Menstruation stops (Amenorrhoea)
Common in young women
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7
Q

Give example of treatment and drug for Prolactinoma

A

Treated using dopamine agonist which in turn will inhibit prolactin release
e.g. CABERGOLINE

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8
Q

Describe features of Acromegaly

A

Increased GH
Thick, greasy, sweaty skin
Enlarged organs e.g. heart thus increase risk of heart disease and death

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9
Q

Describe features of Cushing’s

A

Increased CTH
Too much Cortisol
Central obesity
Bruising, thin skin, osteoporosis, ulcers, purply stretch marks

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10
Q

Define Diabetes Mellitus

A

Syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both.
Hyperglycaemia results in serious microvascular or macrovascular problems.
DM is a vascular disease.

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11
Q

Give examples of microvascular and macrovascular changes that can occur as a result of Diabetes Mellitus

A

Microvascular - Retinopathy, Nephropathy, Neuropathy

Macrovascular - Strokes, Renovascular disease, limb ischaemia

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12
Q

What is normal blood glucose level?

A

3.5-8.0mmol/L under all conditions

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13
Q

What is the principle organ of glucose homeostasis and why?

A

Liver
• Stores & absorbs glucose as glycogen - in post-absorptive state
• Performs gluconeogenesis from fat, protein and glycogen
• If blood glucose is HIGH then the liver will make glycogen (convert glucose to glycogen) in a process called glycogenesis - in the long term the liver will make triglycerides (lipogenesis)
• If blood glucose is LOW then the liver will split glycogen (convert glycogen to glucose) in process called glycogenolysis - in the longer term the liver will make glucose (gluconeogenesis) from amino acids/ lactate

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14
Q

How much glucose is produced and utilised each day

A

200g

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15
Q

What is most glucose derived from in body (not including glucose eaten/direct from gut)

A

More than 90% is derived from Liver GLYCOGEN and Hepatic GLUCONEOGENESIS
(remainder is Renal gluconeogenesis)

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16
Q

What organ in the body is the major consumer of glucose

A

Brain
its function depends on an uninterrupted supply of this substrate
(glucose is oxidised to CO2 and water)

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17
Q

Why is the brain’s function dependent on just glucose?

A

Free fatty acids CANNOT CROSS the BLOOD BRAIN BARRIER
Therefore brain cannot use free fatty acids to be converted to ketones (which can then be converted to Acteyl-CoA and used in the Kreb’s cycle for energy production)

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18
Q

True or False:

Insulin can affect glucose uptake by the brain

A

False

Glucose uptake by the brain is OBLIGATORY and is not dependent on insulin

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19
Q

What is name of receptors found in muscle and fat tissue that responds to insulin?

A

Insulin-responsive glucose transporters

absorb glucose in response to postprandial peaks in glucose and insulin

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20
Q

What is meant by postprandial peaks in glucose and insulin?

A

Post-meal peaks

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21
Q

What are 2 things that can happen to glucose in muscle

A

Stored as glycogen

Metabolised to lactate or CO2 and water

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22
Q

What does fat tissue use glucose for?

A

Substrate for triglyceride synthesis

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23
Q

What is released/produced from Lipolysis of triglycerides

A

Fatty acids and glycerol

Glycerol is then used as a substrate for hepatic gluconeogenesis

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24
Q

What are to 2 keys hormonal regulators of carbohydrate metabolism?

A

Insulin

Glucagon

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25
Q

What are the functions of insulin?

A

Suppresses hepatic glucose output - decreases glycogenolysis and gluconeogenesis
Increases glucose uptake into insulin sensitive tissues:
-Muscle = glycogenesis and protein synthesis
-Fat = Fatty acid synthesis
-Suppresses Lipolysis and Breakdown of muscles (decreased ketogenesis)

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26
Q

What is meant by the biphasic insulin release?

A
  • B-cells can sense the rising glucose levels and aim to metabolise it by releasing insulin - glucose levels are the major controlling factor in insulin release
  • First phase response is the RAPID RELEASE of stored insulin
  • If glucose levels remain high then the second phase is initiated, this takes longer than the first phase due to the fact that more insulin must be synthesised
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27
Q

Where is insulin produced and what chromosome codes for its production?

A

Beta cells of Islets of Langerhans of Pancreas

Chromosome 11

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28
Q

Describe the production of insulin

A

• Proinsulin is the precursor of insulin
• It contains the Alpha & Beta chains of insulin which are joined together
by a C PEPTIDE
• When insulin is being produced, the proinsulin is cleaved from its C peptide and is then used to make insulin which is then packaged into insulin secretory granules
• Thus when there is insulin release there will also be a high level of C peptide in the blood from the cleavage of the proinsulin from it
• Synthetic insulin DOES NOT have C peptide - thus the presence of C peptide in the blood determines whether release is natural (then C peptide will be present) or synthetic (then C peptide will not be present)

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29
Q

What is the main action of insulin in a fasting state?

A

Regulate glucose release by the liver

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30
Q

What is the main action of insulin in the post-prandial state?

A

Promote glucose by fat and muscle

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31
Q

What % of secreted insulin is extracted and degraded in the liver

A

50%

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32
Q

What is function of GLUT-1 transporters

A

Enables basal NON-INSULIN-STIMULATED glucose uptake into many cells

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33
Q

Where are GLUT-2 transporters found?

A

Beta cells of pancreas

Also found in the Renal Tubules and Hepatocytes

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34
Q

What is the purpose of GLUT-2 transporters having a low affinity?

A

only allows glucose in when there is a high concentration of glucose and thus want insulin release

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35
Q

What is purpose of GLUT-2 transporters?

A

Transports glucose into beta cells, thus enabling these cells to sense glucose levels. Low affinity transporter so only detects high glucose levels (to release insulin)

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36
Q

What is function of GLUT-3 transporters?

A

Enables NON-INSULIN-MEDIATED glucose uptake into BRAIN NEURONES and PLACENTA

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37
Q

What GLUT receptors are found on Renal Tubules?

A

GLUT-2

also on beta cells of pancreas and hepatocytes

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38
Q

What GLUT receptors are found on placenta?

A

GLUT-3

Also on brain neurones

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39
Q

What is function of GLUT-4 receptors?

A

Mediates much of the PERIPHERAL ACTION of INSULIN.
It is the channel through which glucose is taken up into MUSCLE and ADIPOSE TISSUE cells, following stimulation of the insulin receptor by INSULIN binding to it

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40
Q

What GLUT receptors are found on adipose tissue?

A

GLUT-4

also muscle

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41
Q

Insulin receptor:

a) What type of molecule is it?
b) Which chromosome codes for it?

A

a) Glycoprotein

b) short Arm of chromosome 19

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42
Q

Insulin receptor:

Describe what happens when insulin binds

A

When insulin binds to the receptor it results in the activation of tyrosine kinase and initiation of a cascade response - one consequence of which is the migration of the GLUT-4 transporter to the cell surface and increased transport of glucose into the cell

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43
Q

What are different actions of insulin?

A
  • Accelerate diffusion of glucose INTO cells
  • Speed up the conversion of glucose into glycogen
  • Increase the uptake of amino acids and increase protein synthesis • Speed up the synthesis of fatty acids
  • Slow glycogenolysis (breakdown of glycogen to glucose)
  • Slow gluconeogenesis (formation of new glucose)
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44
Q

True or False:

Hypoglycaemia stimulates the release of glucagon

A

True

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45
Q

What are functions of glucagon on the liver?

A

Convert glycogen into glucose
Form glucose from lactic acid and amino acids
(Glycogenolysis and gluconeogenesis)

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46
Q

Give examples of diseases that can result in secondary diabetes

A

• Pancreatic pathology e.g. total pancreatectomy, chronic pancreatitis, haemochromatosis
• Endocrine disease e.g. acromegaly and Cushing’s disease
• Drug induced commonly by thiazide diuretics and corticosteroids
• Maturity onset diabetes of youth (MODY):
- Autosomal dominant form of type 2 diabetes - single gene defect altering beta cell function
- Tends to present <25 yrs with a positive family history

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47
Q

What type of diabetes is described here:
Has insulin deficiency with no resistance and immunogenic markers
Most prevalent in Northern European countries, particularly Finland and the incidence is increasing in most populations - particularly in young children

A

Type 1 primary diabetes

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48
Q

Which type of primary diabetes is described here:
Common in all populations enjoying an affluent lifestyle and is also increasing in frequency - particularly in adolescents

A

Type 2

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49
Q

What is LADA

A

Latent autoimmune diabetes in adults

50
Q

Describe LADA (Latent autoimmune diabetes in adults)

A
  • A ‘slow burning’ variant of type 1 diabetes mellitus with slower progression to insulin deficiency occurs in later life
  • May be difficult to differentiate from type 2 diabetes (which also presents in later life) - clinical clues include; leaner build, rapid progression to insulin therapy following an initial response to other therapies and the presence of circulating islet autoantibodies)
51
Q

What is diabetes mellitus type 1

A

Disease of insulin deficiency caused by autoimmune destruction of beta cells of the pancreas

52
Q

Epidemiology of diabetes mellitus type 1

A

Typically manifests in childhood, reaching a peak incidence around the time of puberty - but can present at any age
Usually younger - < 30yrs
Patient is usually lean
Increased in those of Northern European ancestry, especially in Finland Incidence is increasing in most populations - particularly children
(Also latent autoimmune diabetes in adults)

53
Q

Aetiology of diabetes mellitus type 1

A

AUTOIMMUNE - Auto-antibodies forming against insulin and islet beta cells - INSULITIS
Idiopathic (spontaneously arises/unknown cause)
Genetic susceptibility - HLA-DR3-DQ2 or HLA-DR4-DQ8

54
Q

Risk factors of diabetes mellitus type 1

A

Northern European - especially Finnish
Family history - HLA-DR3-DQ2 or HLA-DR4-DQ8 in > 90%
Associated with other autoimmune disease
Environmental factors

55
Q

What other autoimmune diseases associate with Diabetes Mellitus type 1

A
  • Autoimmune thyroid
  • Coeliac disease
  • Addison’s disease (low cortisol)
  • Pernicious anaemia
56
Q

What environmental factors associate with diabetes mellitus type 1

A
  • Dietary constituents
  • Enteroviruses such as Coxsackie B4
  • Vitamin D deficiency
  • Cleaner environment may increase type 1 susceptibility
57
Q

Give example of enterovirus

A 
Coxsackie B4
(DM type 1)
58
Q

Pathophysiology of diabetes mellitus type 1

A

Results from autoimmune destruction by autoantibodies of the pancreatic insulin-secreting Beta cells in the Islets of Langerhans
Causing insulin deficiency and thus the continued breakdown of liver glycogen (producing glucose and ketones) leading to glycosuria and ketonuria as more glucose is in the blood
In skeletal muscle and fats there is impaired glucose clearance
Blood glucose is increased - when it reaches 10mmol/L body can no longer absorb glucose - you become thirsty and get polyuria (as body attempts to remove excess glucose)
Must have insulin since patient prone to diabetic ketoacidosis
Eventual complete Beta cell destruction results in absence of serum C-peptide
Present VERY LATE (often only 10% beta cells remaining)

59
Q

At what glucose concentration can body no longer absorb glucose as too high and what is result of this

A

10mmol/L

Get thirsty and get polyuria (as body tries to remove glucose)

60
Q

Describe diabetic ketoacidosis

A
  • Results from a reduced supply of glucose (since there will be a significant decline in circulating insulin) and an increase in fatty acid oxidation (due to an increase in circulating glucagon)
  • The increased production of Acetyl-CoA leads to ketone body production that exceeds the ability of peripheral tissues to oxidise them. Ketone bodies are relatively strong acids (pH 3.5), and their increase lowers the pH of blood
  • This acidification of the blood can have many consequences but most critical is the fact that it IMPAIRS THE ABILITY OF HAEMOGLOBIN TO BIND TO OXYGEN - note if a patient is in diabetic ketoacidosis, the excess ketones in the blood will result in their BREATH SMELLING OF PEAR DROPS (KETONES)
  • As a result of excess fat breakdown and can result in patient becoming acidotic, anorexic (weight loss) dehydrated leading to AKI and hyperglycaemia and eventual death
61
Q

What is Diabetes Mellitus type 2

A

Results from a combination of insulin resistance and less severe insulin deficiency

62
Q

Describe epidemiology of diabetes mellitus type 2

A
  • Common is all populations enjoying an affluent lifestyle - has increased in incidence due to the ageing population and increasing obesity in the Western world
  • Older - usually >30 yrs of age - but teenagers are starting to get it
  • Often overweight around the abdomen
  • More prevalent in South Asian, African and Caribbean ancestry
  • Middle eastern and Hispanic Americans also more at risk
63
Q

Aetiology of diabetes mellitus type 2

A
  • Decreased insulin secretion +/- increased insulin resistance
  • Associated with obesity, lack of exercise, calorie and alcohol excess
  • No immune disturbance
  • No HLA disturbance but there is a stronger genetic link
  • Polygenic disorder
  • More common in MALES than females
64
Q

Risk Factors of diabetes mellitus type 2

A
  • Family history - genetics
  • Increasing age
  • Obesity and poor exercise - can trigger DMT2 in genetically susceptible individuals
  • Ethnicity - Middle Eastern, South-east Asian and Western pacific
  • Low birth weight (due to poor nutrition impairing beta-cell development and function)
65
Q

Give environmental risk factors of diabetes mellitus type 2

A
  • Association between low weight (as a result of poor nutrition) at birth and/or at 12 months of age, with glucose intolerance later in life
  • Thought to be caused because poor-nutrition early in life impairs beta- cell development and function - predisposing to diabetes later in life
  • Low birth weight also shown to predispose the heat disease and hypertension
66
Q

Pathophysiology of diabetes mellitus type 2

A

Type 2 diabetes is associated with central obesity, hypertension, hypertriglyceridaemia, a decreases high-density lipoprotein (HDL) cholesterol, disturbed homeostatic variables and modest increases in a number of pro-inflammatory markers

67
Q

Which of these does not associate with DM type 2:
Central obesity
Hypotension
Hypertriglyceridaemia
Decreases high-density lipoprotein (HDL) cholesterol
Disturbed homeostatic variables
Modest increases in a number of pro-inflammatory markers

Do they associate with insulin resistance

A

Hypotension
(Hypertension associated with DM2)

A lot of these are strongly associated with insulin resistance as well as an increased CVS risk

68
Q

True or False:

Diabetes mellitus type 2 - insulin binds normally to receptor and so insulin resistance develops post-receptor

A

True

DM2 is not caused by a problem with insulin binding to receptor

69
Q

What other symptoms or things associate with insulin resistance?

A

Central obesity
Accumulation of intracellular triglycerides in muscle and liver
Non-alcoholic fatty liver disease in many

70
Q

Why are circulating insulin levels higher in DM2 compared to normal

A

(Hypersecretion of insulin by a depleted beta cell mass, but still inadequate to restore glucose homeostasis.)
Due to increased glucose production from liver as there is inadequate suppression of gluconeogenesis and reduced glucose uptake by peripheral tissues - insulin resistance

71
Q

Describe the Starling curve of pancreas

A

Circulating insulin levels are typically higher than in non-diabetics following diagnosis and tend to rise further, only to decline again after months or years due to eventual secretory failure

72
Q

DM2 typically progresses from a preliminary phase of IGT or IFG - what do these stand for and what is their importance?

A

Impaired glucose tolerance
Impaired fasting glucose
A unique window for lifestyle intervention to prevent full DMT2 progression

73
Q

What abnormalities of glucose regulation do IGT and IFG denote?

A

IGT & IFG denote different abnormalities of glucose regulation (post- prandial and fasting) - there may be a lower risk of progression to DMT2 in IFG than IGT
IGT:
- Fasting plasma glucose < 7mmol/L
- Oral glucose tolerance of 2hrs glucose > 7.8mmol/L but < 11mmol/L
IFG:
- Fasting plasma glucose > 6.1mmol/L but < 7mmol/L

74
Q

Summarise pathophysiology of type 2 diabetes mellitus

A

Insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors (obesity and lack of physical activity)

75
Q

Why doesn’t diabetic keto-acidosis occur in type 2 diabetes?

Give example of when could occur

A

Rare because the low insulin levels are sufficient to suppress catabolism and prevent ketogenesis.
It can occur if hormones such as adrenaline rise to high levels (eg during an MI).

76
Q

Why does obesity cause type 2 diabetes mellitus?

A

Obesity (particularly central) impairs insulin action. In those, already insulin resistant due to genetic factors and who have progressive impairment in insulin secretion this brings out diabetes at an early stage.

77
Q

Why does insulin secretion become impaired in Type 2 diabetes mellitus

A

Not entirely clear, but related to:

  • genetic predisposition (ie abnormalities of insulin secretion in first degree relatives)
  • deposition of peptides within the beta cell (‘amilyn’)
  • ‘glucotoxicity’ hyperglycaemia inhibits insulin secretion
  • **Probably main factor is lipid deposition in the pancreatic islets which prevent normal function
78
Q

What can result from impaired insulin action?

A

Reduced muscle and fat uptake after eating
Failure to suppress lipolysis and high circulating FFAs
Abnormally high glucose output after a meal

79
Q

What other conditions associate with DM2

A

Central obesity
Hypertension
Hypertriglyceridaemia
Decreased High Density Lipoprotein cholesterol
Disturbed homeostatic variables
Modest increases in a number of pro-inflammatory markers

80
Q

True or False:

Hyperglycaemia and lipid excess are toxic to beta cells in pancreas

A

True
Cause glucotoxicity
Result in further deterioration of beta cells and glucose homeostasis

81
Q

Risk factors for diabetic ketoacidosis

A
  • Stopping insulin therapy - Infection e.g. UTI
  • Surgery
  • MI
  • Pancreatitis
  • Undiagnosed diabetes
82
Q

Clinical presentation of DMT1

A

Tend to be leaner and present more marked polydipsia, polyuria, weight loss and ketosis

83
Q

Clinical presentation of DMT2

A

Tends to be overweight in the abdominal area and also presents with polydipsia, polyuria and weight loss and ketosis (only when very advanced with absolute insulin deficiency) but less marked

84
Q

What triad of symptoms would you see in an acute presentation (2-6 week history) of DMT1 (and sometimes 2) in a young person

A

Polyuria and Nocturia
Polydipsia
Weight loss

85
Q

Acute presentation of DM (T1)

Why do you get polyuria/nocturia

A

Since glucose draws water into the urine by osmosis - not enough glucose can be reabsorbed as kidneys have reached the renal maximum reabsorptive capacity
This results in high levels of glucose in tubule urine and thus lots of water resulting in polyuria and nocturia

86
Q

Acute presentation of DM (T1)

Why do you get polydipsia

A

Due to the loss of fluid and electrolytes from excess glucose and thus water being in the urine

87
Q

Acute presentation of DM (T1)

Why do you get Weight loss

A

Due to fluid depletion and the accelerated breakdown of fat and muscle secondary to insulin deficiency

88
Q

Describe subacute presentation (months to years) of DM and which people more likely to show this

A
  • Onset may be over several months or years, particularly in older patients
  • Polyuria, polydipsia and weight loss are typically present but tend to be less marked
  • Patients may complain of such symptoms as lack of energy, visual blurring (due to glucose-induce changes in refraction) or pruritus vulvae (itchy vulva) or balanitis (skin irritation) that is due to Candida infection
89
Q

What complications can be presenting features of DM

A
  • Staphylococcal skin infection
  • Retinopathy found during visit to optician
  • Polyneuropathy causing tingling and numbness in the feet
  • Erectile dysfunction
  • Arterial disease resulting in MI or peripheral gangrene
90
Q

True or False:

Glycosuria is diagnostic for diabetes

A

False

Glycosuria (alone) is not diagnostic for diabetes but indicates the need for further investigation

91
Q

Describe physical signs of DM

A

Evidence of weight loss and dehydration
Breath may smell of ketones (esp DMT1)
Older patients may present with established complications, e.g. retinopathy
Patients with severe insulin resistance (i.e. DMT2) may have acanthosis nigricans - characterised by blackish pigmentation at the nape of the neck and in the axillae

92
Q

True or False:

Retinopathy characteristic of DM, is diagnostic in diabetes

A

True

93
Q

Describe diagnosis of DM

A

Random plasma glucose > 11.1mmol/L = DIABETES DIAGNOSIS
Fasting plasma glucose > 7mmol/L = DIABETES DIAGNOSIS
- For both tests one abnormal value is DIAGNOSTIC in symptomatic individuals (Hyperglycaemia symptoms e.g. polyuria, polydipsia, unexplained weight loss, visual blurring, genital thrush, lethargy)
- Two abnormal values are required in asymptomatic individuals

Haemoglobin A1c (measures amount of glycated haemoglobin)
HbA1c > 6.5% normal (48mmol/mol) = DIABETES DIAGNOSIS
94
Q

For borderline cases of DM, what test can be done to decide on DM diagnosis and describe the test

A

Oral glucose tolerance tests (OGTT):
• Fasting > 7mmol/L = DIABETES DIAGNOSIS
• 2 hrs after glucose > 11.1 mmol/L = DIABETES DIAGNOSIS

95
Q

What conditions can diabetes be secondary to?

A
  • Pancreatitis
  • Trauma/pancreatectomy
  • Neoplasia of pancreas
  • Acromegaly
  • Cushing syndrome
  • Addisons
96
Q

What drugs can diabetes be secondary to?

A
  • Thiazide diuretics
  • Beta-blockers
  • Immunosuppressives e.g. ciclosporin and tacrolimus
  • Thyroid hormone
97
Q

What % of patients present with hypertension in DMT2

A

50%

a higher proportion of African and Caribbean patients

98
Q

In diabetic treatment, describe diet with good glycemic control

A
  • Low in sugar
  • High in starchy carbohydrates with low glycaemic index e.g. pasta
  • High in fibre
  • Low in fat
99
Q

Diabetic treatment - what would give for treatment of hypertension (give example)

A

ACE-inhibitor

e.g. Ramipril

100
Q

Diabetic treatment - what would give for treatment of hyperlipidaemia (give example)

A

Statin

e.g. Simvastatin

101
Q

How would you administer synthetic (recombinant) human insulin?

A 
Subcutaneous injection
(in abdomen, thighs or upper arm)
102
Q

Why do you need to change injection site of insulin?

A

Prevent lipohypertrophy

103
Q

What are 3 types of insulin

A

Shorting-acting (soluble) insulins
Short-acting insulin analogues
(intermediate or) Longer-acting insulins

104
Q

How long do Shorting-acting (soluble) insulins take to work and when would they be used

A

Start working within 30-60 minutes and last for 4-6 hours
Given 15-30 minutes before meals in patients on multiple dose regimens and by continuous IV infusion in labour, during medical emergencies, at the time of surgery and in patients using insulin pumps

105
Q

When would you use Short-acting insulin analogues

A

Used with the evening meal in patients who are prone to nocturnal hypoglycaemia
Reduced carry-ver effect compared to soluble insulin, but overall does NOT improve diabetic control

106
Q

What are different types of Longer-acting insulins?

A

Intermediate (12-24 hrs) or long-acting (more than 24hrs)
Insulin premixed with retarding agents (either protamine or zinc) precipitate crystals
Protamine insulins are also known as isophane or NPH
insulins
The zinc insulins are also known as LENTE insulins

107
Q

Complications of insulin treatment

A
  • Hypoglycaemia - most common (also caused by SULFONYLUREA)
  • Injection site - lipohypertrophy
  • Insulin resistance - mild and associated with obesity
  • Weight gain - insulin makes people feel hungry
108
Q

Describe first line treatment of DMT2

A
  • Lifestyle and dietary changes essential - exercise, weight loss
  • Dietary factors e.g. low sugar, high in starch carbohydrates with low glycaemic index e.g. pasta, high in fibre, low in fat (esp. sat. fat)
  • Nutrient load should be spread throughout the day (three main meals with snacks in between and at bedtime) - which reduces swings in blood glucose
  • Blood pressure control e.g. RAMIPRIL
  • Hyperlipidaemia control e.g. STATINS
  • Can give ORLISTAT in obesity which is an intestinal lipase inhibitor and reduces the absorption of fat from the diet - it promotes weight loss
109
Q

Describe second line treatment of DMT2

A

-Used in association with diet & lifestyle changes when this alone has failed to control hyperglycaemia
-Initially give a biguanide e.g. ORAL METFORMIN
-If HbA1c > 53mmol/L 16 weeks later then add a sulfonylurea e.g. ORAL GLICLAZIDE (safest drug in the very elderly is ORAL TOLBUTAMIDE since it has a very short duration of action)
-If at 6 months the HbA1c > 57mmol/L consider adding:
-Insulin may be needed
e.g. ISOPHANE INSULIN or a long-acting analogue
or a glitazone e.g. ORAL PIOGLITAZONE which replaces
metformin or sulfonylurea (to increase insulin sensitivity)
Or GLP e.g. incretins

110
Q 
A 50yo Asian man is referred to the diabetes clinic after presenting with polyuria and polydipsia. His BMI = 30, BP = 137/88, Fasting plasma glucose = 7.7mmol/L (high). The most appropriate first-line treatment is:
Dietary advice and exercise
Sulphonylurea
Exenatide
Thiazolidinediones
Metformin
A

Dietary advice and exercise

Metformin is a 1st line drug but comes after lifestyle change

111
Q

A 6yo girl presents to accident and emergency with severe abdominal pain, nausea and vomiting. Patient has a sweet (fruity) odour from her breath and is breathing fast (tachypnoeic). The most likely diagnosis is:
Diabetic ketoacidosis
Hyperglycaemia hyperosmolar state
Gastroenteritis (Infection of intestine)
Pancreatitis
Addisonian crisis

A

DKA

Diabetic ketoacidosis – Presence of sweet breath & other presentations & patient’s age suggest T1DM
Hyperglycaemia hyperosmolar state – For T2DM patient
Gastroenteritis – No sweet breath
Pancreatitis – No sweet breath
Addisonian crisis – No sweet breath

112
Q 
A 57yo woman presents with dull grey-brown patches in her mouth and the palms of her hand which she has noticed in the last week. She has also noticed she gets very dizzy when rising from a seated position and is continually afraid of fainting. The most likely diagnosis is:
SIADH
Hyperthyroidism 
Hypothyroidsim 
Addison’s disease 
Diabetes insipidus
A

Addisons disease

none of other diseases cause pigmentation

113
Q

Briefly outline treatment of DMT2

A
  1. Lifestyle modification: Diet, Weight control, Exercise
  2. Monotherapy: Metformin (1st line biguanide drug)
  3. If HbA1C rises to 58mmol/mol, consider dual therapy:
    Metformin + DPP4 inhibitor (eg: sitagliptin)
    Metformin + pioglitazone
    Metformin + sulphonylurea (SU)
    Metformin + SGLT-2i (glifazon)
  4. If still no HbA1C change, consider triple therapy:
    Metformin + DPP4 inhibitor + SU
    Metformin + pioglitazone + SU
    Metformin + pioglitazone/SU + SGLT-2i
    Insulin-based therapy
  5. If still not working, either give insulin or ‘Metformin + SU + GLP 1 mimetic’
114
Q

Treatment of DMT1

A

Insulin supplementation

115
Q

*Define pre-diabetic (also diagnosis)

A

Fasting plasma glucose 5.5-7

116
Q

What is metformin

A

Biguanide
Metformin works by reducing the amount of sugar your liver releases into your blood. It also makes your body respond better to insulin. Insulin is the hormone that controls the level of sugar in your blood.
For DMT2

117
Q

Best test for long term diabetes diagnosis

A

HbA1c - measures amount of glycated haemoglobin

not in children, <2 months symptoms, very ill, pregnant, some DMT1

118
Q

DPP4 inhibitors/gliptins

A

Sitagliptin

Block action of DPP4 - an enzyme that destroys the hormone incretin

119
Q

What do glitazones do

A

Increases insulin sensitivity

120
Q

Sulphonylurea

A

Increase insulin secretion

121
Q

SGLT1

A

Selective sodium-glucose co-transporter 2 inhibitor

Blocks reabsorption of glucose in the kidneys and promotes excretion of excess glucose in urine

Medicine Phase 2a (22 decks)

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