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Medicine year 1 semester 1 > Case 5- Diabetes > Flashcards

Case 5- Diabetes Flashcards

1
Q

Difference between testing of type 1 and 2 diabetes

A

Type 1 diabetes will have low insulin, high ketone levels and antibodies in their blood. Type 2 diabetes will have high insulin and no ketones.

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2
Q

What do diabetics have in their urine

A

Sugar due to Hyperglycaemia

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3
Q

Glucose levels in diabetics

A

In fasting plasma glucose diabetes is diagnosed at >7.0mmol/L, in random plasma glucose it is >11.1mmol/L.

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4
Q

How can you diagnose type 1 diabetes

A

Blood or ketones in urine, found in dipstick test

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5
Q

Screening diabetes with no symtpoms

A
  • Overweight
  • Vascular disease
  • Over 40
  • Hypertension
  • Previous gestational diabetes
  • People in a pre-diabetic state
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6
Q

HBA1c test

A

Measures amount of Glucose stuck to a red blood cell. The patient does not have to fast. It is a reflection of chronic hyperglycaemia which shows diabetes and not an unusual rise in Glucose. Used in diagnosis of type 2 diabetes and monitoring established diabetes. A measure of >48 mmol/mol (6.5%) is diagnostic.

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7
Q

Diagnosing pre-diabetic state

A

Oral Glucose tolerance test. You drink 75g of glucose and do a blood test at baseline and after 120 minutes. Diagnosed with impaired glucose tolerance at >7.8 mmol/L but less than 11.1 mmol/L at 120 minutes.

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8
Q

Pre-diabetic fasting glucose levels and HBA1c

A

The fasting glucose for a normal person is <6.1mmol/L for diabetes it’s >7.0 mmol/L, in between its impaired fasting glycaemia (IFG). If IGT or IFT measure HBA1c, 42-47 mmol/mol is prediabetes

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9
Q

Testing for Gestational diabetes

A

The oral glucose tolerance tests is done between 24-28 weeks. It is done in a fasting state. A fasting state plasma glucose level of 5.6mmol/litre or above or a 3 hour plasma glucose level of 7.8mmol/litre or above is indicative of gestational diabetes. Good diabetes control reduces complications at birth

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10
Q

Hallmarks of Type 1 diabetes

A

Acute (symptoms present rapidly), young age, marked symptoms (very obvious symptoms that they are sure of), no family history, no complications when diagnosed, may present as an emergency.

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11
Q

Hallmarks of type 2 diabetes

A

Insidious (don’t know when symptoms started, mild symptoms), older and middle aged, may have no symptoms, usually a family history, may present with or because of symptoms.

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12
Q

General diabetes symptoms

A

Thirst, more urine passed, tiredness, weight loss and blurred vision

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13
Q

Secondary diabetes

A

Occurs as a result of the treatment doctors give patients. Most likely steroid hormones which are prescribed for eczema and cirrhosis. Could be due to pancreatitis or pancreatic surgery which can destroy beta cells leading to diabetes. Endocrine conditions can antagonise insulin, i.e. crushing’s syndrome, acromegaly and phaeochromocytoma.

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14
Q

Polygenic diabetes

A

The majority of type 1 and type 2 diabetes, means they are related to defects in multiple genes. In type 1 susceptibility increases with a genetic trigger and personal or family history of other autoimmune illnesses. Type 2 diabetes is the interaction between inherited genes, the environment and life-style.

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15
Q

Genetic/inherited diabetes

A

Can be monogenic diabetes which is due to the inheritance of a mutation on a single gene. It is very rare occurring in 1-5% of cases. Mostly Neonatal Diabetes Mellitus or MODY (maturity onset diabetes of the young). In this case diabetes often develops before 25 and runs in the family from one generation to the next. May be treated by diet or tablets and does not always need insulin treatment.

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16
Q

Gestational diabetes

A

Diabetes diagnosed in pregnancy. Occurs as a result of pregnancy related hormones increasing insulin resistance. More likely if the woman is overweight, had gestational diabetes before, a large baby in previous pregnancy (4.5kg), family history of diabetes and is from a South Asian, black or African Caribbean or middle Eastern background. It is associated with large babies and difficult labour. Resolves after delivery of the baby but can recur in subsequent pregnancies. It is a risk factor for type 2 diabetes

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17
Q

Diabetes mellitus

A

A metabolic disorder which is characterised by chronic hyperglycaemia and disturbances of carbohydrates, fat and protein metabolism resulting from defects in insulin secretion, insulin action or both.

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18
Q

Pathology of type 1 diabetes

A

Insulin deficiency, auto-immune condition, destruction of beta cells in the pancreas. Treatable with insulin.

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19
Q

Pathology of type 2 diabetes

A

Insulin resistance, associated with obesity. More common in some racial groups, interplay between genes and environment

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20
Q

How does insulin normally work

A

Normally insulin binds to the transmembrane receptor, this sets off a signalling cascade resulting GLUT4 transporters being added to the cell membrane allowing glucose to be moved from the plasma into the cell. In type 1 diabetes there is not enough insulin for this to happen.

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21
Q

Microvascular complications of diabetes

A

Glucose accumulates in small blood vessels which damage them causing Microvascular microangiography. This tends to happen to people who have had diabetes for a long time and have poor glucose control.

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22
Q

Complications of diabetes

A
  • A 2-to-4-fold increase in cardio-vascular mortality
  • It’s the leading cause of new cases of end stage renal disease (nephropathy)
  • In the leading cause of new cases of blindness in working aged adults (retinopathy)
  • Leading cause of non-traumatic lower extremity amputations. (neuropathy)
  • Erectile dysfunction
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23
Q

Insulin resistance

A

When there is a decreased ability of target tissues to respond normally to circulating insulin. When you have insulin resistance you get uncontrolled hepatic glucose production and decreased glucose uptake by target tissues. Obesity is the most common cause of insulin resistance.

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24
Q

Obesity and insulin resistance

A

Most people with obesity and insulin resistance will not become diabetic as insulin levels will increase to compensate. Type 2 diabetes will develop when insulin resistant individuals develop impaired beta-cell function meaning that insulin resistance can no longer be compensated by increased insulin production.

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25
Q

Non-pharmacological interventions for diabetes

A

Reduced calory intake, increased exercise and physical activity. Reduced alcohol and smoking

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26
Q

Consequences of over-nutrition

A

People who are obese have their life expectancy reduced by 3 years. More likely to be unemployed, face stigma and discrimination and be hospitalised

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27
Q

What is obesity a risk

A
  • Liver disease
  • Type 2 diabetes
  • Reproductive problems
  • Heart disease
  • Anxiety and depression.
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28
Q

Factors effecting control of appetite

A

Control of human appetite is an extremely complex set of interactions between behavioural, environmental and neurological factors. A number of theories about appetite control exist. One theory involves the interplay between short acting GI derived hormones and factors produced by adipose tissue.

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29
Q

What part of the brain is important for appetite regulation?

A

The CNS in the hypothalamus

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30
Q

Leptin

A

Is secreted by adipocytes, and secretion is in proportion to the level of adipocytes present, when fat stores decrease leptin levels will reduce and increase appetite. So high Leptin levels reduce apetite

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31
Q

Cholecystokinin (CCK)

A

Released mainly by the duodenum and jejunum during a meal. Has local action of inhibiting gastric emptying and acts on hypothalamus to reduce appetite

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32
Q

Glucagon-like peptide (GLP-1)

A

Released from small intestinal and colonic L-cells in proportion to calorie intake. It has a local effect of reducing gastric emptying and acts on the hypothalamus to reduce appetite

33
Q

Peptide YY (PYY)

A

Released by L cells in the GI tract acting on the hypothalamus to reduce appetite when there is high calorie intake.

34
Q

Ghrelin

A

Only known gut secreted orexigenic (appetite stimulant) and is secreted by the stomach in absence of food and will stimulate appetite.

35
Q

Hormones released in fasting state

A

In the fasting state Ghrelin increases in concentration. CCK, PYY, insulin and Leptin decrease in concentration.

36
Q

Biguanides i.e. Metformin

A

First line treatment for T2D (type 2 diabetes), it inhibits liver gluconeogenesis

37
Q

Advantages of Biguanides

A

Weight neutral/ weight loss. Cheap, improves mortality, not likely to cause hypoglycaemia. In overweight people with type 2 diabetes, metoformin is significantly more effective than intensive blood glucose control with sulphonylureas or insulin at reducing diabetes- related outcomes and all-cause mortality

38
Q

Disadvantages of Biguandiess

A

Gastrointestinal upset (nausea, wind, diarrhoea), best to take with or after food. Lactic acidosis, rare but can be fatal. Caution in use with impaired renal function, heart failure, liver disease.

39
Q

Sulphonlyureas i.e Gliclazide, Tolbutamide

A

Binds to Sulphonlyurea receptors on the beta cells of the pancreas, it blocks K+ channels depolarising the beta cell, resulting in increased insulin secretion from the Pancreas
Advantages- cheap, benefits glycaemic control
Disadvantages- Hypoglycaemia, weight gain, hyperinsulinemia

40
Q

Thiazolidenediones/ Glitazones i.e. Pioglitazone, Rosiglitazone

A

It activates the transcription factors ‘PPARy’ which when switched on stimulated the activation of genes involved in the lipid and glucose metabolism pathways. This enhances peripheral lipogenesis, decreases lipolysis, decreases plasma fatty acid levels which are sensitive to insulin. The onset of action is slow and can take 8 weeks for max effect.

41
Q

Thiazolidenediones side effects

A

Fluid retention, cardiac failure, weight gain, bladder cancer and liver dysfunction

42
Q

Rosiglitazon withdrawl

A

Long-term effects Drug withdrawal Rosiglitazone was associated with an increased risk of cardiovascular events, including congestive heart failure, myocardial infarction and stroke. For this reason rosiglitazone was withdrawn from EU market in 2010 and from the New Zealand and South Africa markets in 2011.

43
Q

Incretins

A

There are two main types of Incretins: GLP-1 and GIP. Both are hormones secreted by intestinal endocrine cells (L cells in the small intestine) in response to nutrient intake. Incretins help the body to produce more insulin ONLY when it is needed and reduce the amount of glucose being produced by the liver when it is not needed

44
Q

GLP-1

A

It is released from L cells in the pancreas and is rapidly broken down by the enzyme DPP-1V inactivating it. You presecibe a DPP-1V enzyme inhibitor and GLP-1 mimetics in order to increase the half life

45
Q

DPP-1V inhibitors i.e. sitagliptin

A

Advantages- oral, fewer hypoglycaemic episodes, not associated with weight gain, well tolerated.
Disadvantages- unaware of long term effects, expensive, discontinue if symptoms of acute pancreatitis.

46
Q

GLP-1 Mimetics i.e. exenatide

A

Modified to enhance incretin effects
Advantages- weight loss, low risk of hypoglycaemia
Disadvantages- nausea, vomiting, SC injections, contraindicated at low GFR, expensive, don’t know long term effects.

47
Q

Rapid acting Secretalogues i.e. Repaglinide

A

Meglitinides- non sulphonylurea beta cell stimulators. More expensive than sulphonylurea.
They have been associated with weight gain and hypoglycaemia. They have a rapid onset of action and a short duration of activity; they are taken shortly before each main meal. Although flexible use of these drugs in mealtime regimens may appeal to some people with diabetes (e.g. those with erratic lifestyles), multiple dosing requirements may limit their usefulness in practice

48
Q

SGLT2 inhibitors i.e. canagliflozin and dapagliflozin

A

Inhibits SGLT2 in the proximal renal tubule which is a Glucose specific transporter which usually transports Glucose back in the bloodstream. It prevents reabsorption of Glucose (increases Glucose in the urine), causes Glycosuria and osmotic diuresis.
Advantages- weight loss, low risk of Hypoglycaemia
Disadvantages- urinary tract infections, expensive, limited clinical experience, hypotension.

49
Q

Alpha Glucosidase inhibitors i.e. acarbose

A

Targets postprandial (after a meal) hyperglycaemia by reducing carbohydrate digestion and absorption. Causes adverse Gastrointestinal effects (abdominal bloating, flatulence and diarrhoea), not commonly used in clinical practise.

50
Q

NICE recommendations for type 1 diabetes

A

NICE recommends that patients should be offered multiple daily injection basal-bolus insulin regimens, rather than twice-daily mixed insulin regimens.

51
Q

Basal insulin

A

Provides a constant supply of insulin to bring down restring glucose levels, can be an intermediate or long acting Insulin

52
Q

Bolus insulin

A

Provides a short term effect on blood glucose, it is taken at meal times to keep blood glucose levels under control following a meal. Can be short acting or rapid acting insulin

53
Q

Basal-bolus regimen

A

involves taking longer acting form of insulin that keeps blood glucose levels stable through period of fasting and separate injections of shorter/rapid acting insulin to prevent rises in blood glucose levels resulting from meals

54
Q

Twice-daily mixed insulin regimen

A

Considered if a multiple daily injection basal–bolus insulin regimen is not possible. Generally biphasic insulin is injected 15 to 30 minutes before breakfast and the evening meal. Short or rapid acting insulin can be combines with intermediate insulin to produce biphasic combinations.

55
Q

Rapid acting insulin analogues i.e. NovoRapid

A

Onset between 5-15 minutes, peak after 1-2 hours. Lasts for 4-5 hours can be injected with food or post-prandial. Controls post prandial hyperglycaemia and covers mealtime carbohydrate intake. They have the benefit of allowing insulin to be taken immediately before a meal.

56
Q

Short actin Insulins (non-analogue) i.e Actrapid

A

A soluble form of human insulin. Onset 30-60 minutes and lasts 8-10 hours. Addresses post-prandial glucose excursion. The disadvantages are that come have to be injected 20-30 minutes before a meal meaning that meal planning is essential. Patients may need a snack between meals and there is a risk of hypoglycaemia.

57
Q

Immediate acting insulin i.e. Humulin 1

A

1-2 hours onset and lasts for 13-18 hours. It is given twice daily and addresses basal hyperglycaemia. Longer life span than rapid or short acting insulin but is slower to reach its peak.

58
Q

Long acting Insulin analogues i.e. Lantus and Levemie

A

Onset of action is about an hour and lasts the whole day. Has the advantage of greater predictability, potentially less weight gain and lower risk of hypoglycaemia. Can be given as a basal insulin or in a Basal Bolus regimen.

59
Q

Mixed insulin

A

Pre-mixed Insulin is a combination of two insulins mixed together, one short acting and one intermediate or long acting insulin. Thus providing both basal and postprandial coverage with one injection. Premixed analogues can conveniently be administered twice daily directly before the meal. Patients however must eat regular meals or they will be at greater risk of hypoglycaemia. Examples include: NovoMix 30, Humalog Mix 25, Humulin M3, Isuman Comb 25

60
Q

Twice daily injection

A

A twice-daily human mixed insulin regimen can be considered for adults with type 1 diabetes if a multiple daily injection basal–bolus insulin regimen is not possible. It may be considered if an adult using a twice-daily human mixed insulin regimen has hypoglycaemia that affects their quality of life. A twice-daily insulin regimen works on the assumption that the patient will have 3 meals each day hence it may be suitable for patients who have regular daily routines that include three main meals at similar times each day. It may also be appropriate for school children as injections can be given before and after school without the need for a lunchtime injection.

61
Q

Multiple daily injections

A

Involves injecting rapid insulin before meals together with one or more separate injections or intermediate or long acting insulin (twice-daily detemir should be used first line). The intermediate- or long-acting injection is given at the same time each day, commonly at bedtime, but in the case of insulin detemir it should be repeated in the morning, as recommended by NICE. MDI regimens provide tighter glycaemic control, which is associated with reduced rates of diabetic complications compared with twice daily regimens. It is the insulin injection regimen of choice.

62
Q

Multiple daily injections

A

Involves injecting rapid insulin before meals together with one or more separate injections or intermediate or long acting insulin (twice-daily detemir should be used first line). The intermediate- or long-acting injection is given at the same time each day, commonly at bedtime, but in the case of insulin detemir it should be repeated in the morning, as recommended by NICE. MDI regimens provide tighter glycaemic control, which is associated with reduced rates of diabetic complications compared with twice daily regimens. It is the insulin injection regimen of choice.

63
Q

Type 2 diabetes insulin

A

Insulin resistance which leads to Hyper-insulinemia. The insulin resistance causes a decline in beta cell function and you may get no insulin produced at all

64
Q

Type 1 insulin diabetes

A

An immune trigger or another cause results in the destruction of beta-cells in the Pancreas resulting in the absence of Insulin.

65
Q

How diabetes effects metabolism

A

The absence of Insulin or loss of effect on tissues will leave to derangement of metabolism. There will be increased protein breakdown of proteins from the skeletal muscle and increased Gluconeogenesis. There will be increased Glycogenolysis, decreased cellular Glucose uptake. There is no rapid reduction in blood Glucose after a meal because there is no Insulin. There will be increased Glucose in the blood as it is not taken into the cells so there will be Hyperglycaemia. The increased TAG breakdown will cause increased blood FA’s and ketogenesis causing Ketoacidosis. This is more common in type 1 diabetes because in even a small amount of Glucose will prevent the breakdown of TAG’s.

66
Q

MCADD

A

Medium and long chain FA’s can not be oxidised as you are missing the medium chain Acetyl CoA dehydrogenase, it may also be deficient. So you can not use fat stores properly. Beta oxidation will stop when you get to chain which is 12 carbons long. This means you cant make ketone bodies or undergo Gluconeogenesis so you will very quickly become hypoglycaemic once you have metabolised your ingested Glucose and Glycogen stores.

67
Q

Effects of MCADD

A

Defects in FA oxidation lead to:
• An overreliance on Glucose because FA’s are not utilised for energy and ketone bodies are not produced
• Gluconeogenesis is inhibited because of a reduction in energy produced by FA
• Accumulation of unusual medium chain FA derived C8 acylcarnitine’s and C6 and C10 acylcarnitine’s may inhibit gluconeogenic enzymes.

68
Q

Diagnosing MCADD

A

Diagnosed due to elevated C8 acylcarnitine with lesser elevation of C6 and C10 acylcarnitine’s. Normally diagnosed in Blood spot screening program

69
Q

MCADD treatment

A

Stopping the patients from entering a fasting state and having to use their fat stores, so they have regular meals at regular intervals. You may have to be put on a glucose drip in hospital if you are severely unwell

70
Q

Isovaleric anaemia

A

Defective leucine catabolism which causes a build-up of Isovaleryl-CoA. Causes a sweaty smell. Treatment is limitation of proteins in the diet, picked up in the neonatal blood spot screening programme.

71
Q

Phenylketonuria (PKU)

A

It is the most common error of amino acid metabolism. It is caused by a deficiency in phenylalanine hydroxylase (PAH) that converts phenylalanine to Tyrosine. This causes an accumulation of phenylalanine and a lack of Tyrosine. As well as the build up of phenylactate, phenylacetate and phenylpyruvate. There are lots of reasons for the deficiency it could be due to a mutation or a lack of expression. Tyrosine when present is converted into Melanin and neurotransmitters (Serotonins and catecholamines.

72
Q

Treatment for PKU

A

Limited phenylalanine intake through dietary means. Do not over-restrict phenylalanine below the bodies requirements (essential AA). Supplement the diet with Tyrosine. Avoid the sweetener aspartame.

73
Q

Effects of PKU

A

If not treated IQ will decrease. You can get brain damage in untreated PKU babies as the failure to produce proteins correctly results in a reduction of neurotransmitters

74
Q

Congenital PKU

A

When the mother has untreated PKU and the fetus does not

75
Q

Inherited PKU

A

When you have the PKU mutation

76
Q

Diagnosis of PKU

A

Phenylpyruvate in the urine

77
Q

PKU in the fetus

A

It’s especially important to have a limited phenylaline diet in pregnant woman because its harmful to the CNS of the postnatal human infant. There is competition between Phe and other amino acids for uptake by foetal tissue and perhaps by the placenta. In uncontrolled PKU the foetus will have embryopathy and fetopathy, low birth rate, reduced microphaly, congenital heart disease and Dysmorphic facial features.

78
Q

What metabolic diseases does the neonatal bloodspot test for

A
  • phenylketonuria (PKU)
  • medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
  • maple syrup urine disease (MSUD)
  • isovaleric acidaemia (IVA)
  • glutaric aciduria type 1 (GA1)
  • homocystinuria (pyridoxine unresponsive) (HCU)

Medicine year 1 semester 1 (44 decks)

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