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Year 3 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the normal range for plasma glucose?

A

Between 3.9 mmol/L and 5.6 mmol/L

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2
Q

What is the normal range for venous glucose?

A

Between 4 mmol/L and 6 mmol/L

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3
Q

What is an indicator for insulin release?

A

C-peptides which are important for correct folding of insulin and released with insulin by pancreatic beta cells

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4
Q

What are the criteria for diagnosing diabetes according to WHO 2006?

A

Must have diabetes symptoms and either:
* Random venous glucose of 11.1 mmol/L or more
* Fasting blood glucose over 7.1 mmol/L
* Two-hour plasma glucose over 11.1 mmol/L

Evidence from at least two tests must be on two separate days

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5
Q

What are the diagnostic criteria for gestational diabetes?

A

Fasting glucose over 5.6 mmol/L and 2-hour glucose over 7.8 mmol/Ll

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6
Q

What is the cutoff point for HbA1c?

A

Over 48 mmol/L; however it is not used by WHO for diagnosis of diabetes

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7
Q

In which populations is HbA1c not appropriate for diagnosing diabetes?

A

Children and young people
Type 1 diabetics
Acutely ill patients
Those with acute pancreatic damage

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8
Q

What conditions can make HbA1c levels inaccurate?

A

Anaemia
Medications predisposed to hyperglycaemia suc as steroids
Pregnancy
Patients on haemodialysis due to high glucose levels of dialysate fluid

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9
Q

What investigations are included for diabetes?

A

Estimated glomerular filtration rate, lipid profile, serum creatinine, sensation testing

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10
Q

What is the cause of Type 1 diabetes?

A

Autoimmune cell-mediated destruction of beta cells that prevents peripheral uptake of glucose due to
Genetic conditions associated with HLA-DR3 and HLA-DR4
Environmental triggers
Autoimmunity

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11
Q

Which HLA markers are associated with Type 1 diabetes?

A

HLA-DR3 (Coeliacs) and HLA-DR4 (Hashimoto’s disease)

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12
Q

What is the autoantigen associated with Type 1 diabetes?

A

-> Glutamate decarboxylase (GAD65) is the most common
-> Islet cell cyptoplasm
-> Insulin

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13
Q

What are some environmental triggers for Type 1 diabetes?

A

Infectious agents such as cytomegalovirus, enterovirus, influenza, mumps and rubella
Childhood vaccination

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14
Q

What is the clinical presentation of Type 1 diabetes?

A

Hyperglycaemia
Weight loss
Diabetic ketoacidosis
Fruity smelly breath/acetone
Fatigue, polyuria and polydipsia

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15
Q

What characterizes Stage 1 of Type 1 diabetes?

A

Asymptomatic with normal fasting glucose and presence of 2 pancreatic autoantibodies. Beta cell death overwhelms phagocytes and causes buildup in pancreas.

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16
Q

What characterizes Stage 2 of Type 1 diabetes?

A

Asymptomatic with dysglycaemia, raised HbA1c between 5.7 to 6.4, impaired glucose tolerance. There will be auto activation of B and T cells in the pancreatic lymph nodes.

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17
Q

What characterizes Stage 3 of Type 1 diabetes?

A

Symptomatic hyperglycaemia, polydipsia, polyuria, unintentional weight loss. There is movement of auto reactive B and T cells back into the pancreas.

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18
Q

Why is screening recommended for first or second-degree relatives of Type 1 diabetics?

A

Due to the heritability of autoimmune disease

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19
Q

What are common features of both Type 1 and Type 2 diabetes?

A

Polydipsia, polyphagia, polyuria due to glucose being a highly osmotic diuretic that draws water out of the nephrons into the urine.

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20
Q

What causes Type 2 diabetes?

A

Defective insulin secretion of pancreatic B cells and insulin insensitivity which reduces peripheral glucose uptake, associated with metabolic syndrome.

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21
Q

What are the features of metabolic syndrome?

A

Low HDL, high LDL, VLDL, and waist circumference

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22
Q

What happens when glucose levels are high in pancreatic beta cells?

A

B cells take up glucose from the GLUT2 receptor, undergo glycolysis, causing a rise in ATP which inhibits the K+ channel to prevent K+ efflux. This rise in intracellular K+ causes opening of Ca2”+ channels for Ca2+ influx that causes the release of insulin vesicles.

B cells synthesise pre-proinsulin, which undergoes a maturation process to pro insulin by the endoplasmic reticulum, and trnaslocated into vesicles of insulin in the Golgi apparatus, which are triggered to be released by high blood glucose.

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23
Q

What is Late Autoimmune Diabetes (LADA)?

A

Diabetes onset after age 30, associated with autoantibodies against islet B cells. It shares lifestyle risk factors with type 2 diabetes such as excess body weight, heavy smoking and intake of high carb food. Risk factors for LADA include autoimmune disease and low birth weight.

Patients with LADA may have hyperglycaemia for over 6 months without the need for insulin.

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24
Q

What symptoms are associated with LADA?

A

Polydipsia, polyuria, weight loss, visual changes and neuropathic symptoms

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25
Q

What should be avoided in the management of LADA?

A

Sulphonylureas, as they worsen pancreatic beta cell function.

-> LADA has a risk of cardiovascular disease and small fibre neuropathy.

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26
Q

What is Mature Onset Diabetes of the Young (MODY)?

A

An autosomal dominant condition due to a monogenic mutation disrupting pancreatic beta cell function.

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27
Q

What is the most common mutation associated with MODY?

A

MODY3, due to a mutation of Hepatocytes nuclear factor 1 which is found in liver, pancreas and intestine. It is involved in pancreatic beta cell maturation, mitchochondrial metabolism and insulin secretion, causing a decreased renal threshold for glycosuria. It can lead to vascular complications and risk of metabolic Syndrome.

There is also a mutation of glucokinase, which can at as a sensor of glucose for pancreatic beta cells to stimulate insulin release.

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28
Q

What characterizes MODY2?

A

Only experiences mild hyperglycaemia, requiring lifestyle and dietary modifications

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29
Q

What is the most common medication prescribed for young people with MODY?

A

Metformin and sulphonylurea

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30
Q

What are the key features of MODY?

A

Family history of diabetes, patient does not necessarily require insulin, diagnosis under 25 years old

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31
Q

Which substance inhibits ketogenesis?

A

Insulin.

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32
Q

What is diabetic ketoacidosis (DKA)?

A

Most common complication in Type 1 diabetes with acute onset due to inability to use glucose as energy source. This stimulates liver cells to induce the uptake of fatty acids for beta-oxidation to form ketones which build up and raise blood pH. Ketones will be above 3 and ph will be below 7.3. The body tries to compensate by increasing breathing to get rid of CO2, causing shortness of breath and Kussmaul breathing. Patients present with Hypovolemia, hypotension, Kussmaul breathing and hyperglycaemia.

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33
Q

How do patients present with diabetic ketoacidosis?

A

Patients present with Hypovolemia, hypotension, Kussmaul breathing and hyperglycaemia. They progress from polyuria to volume depletion, with decreased urine output, skin turgor and sweating.

There is hyperkalemia due to shift in potassium from intracellular space to extracellular space due to insulin deficiency and hyperglycaemia.

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34
Q

What is the criteria for diagnosis of diabetic ketoacidosis?

A

Arterial ph below 7.3, serum bicarbonate less than 15 and hyperglycaemia.

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35
Q

Why does diabetic ketoacidosis occur?

A

DKA occurs with:
incorrect insulin management or non-compliance
Pancreatitis
Acute illness such as infection (pneumonia and UTI) trauma and surgery
Alcohol abuse and myocardial infarction
SGLT2 inhibitors

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36
Q

Why do SGLT2 inhibitors cause diabetic ketoacidosis?

A

SLGT2 inhibitors like canagliflozin have a diuretic effect and loss of glucose, promote glucagon secretion and stimulating ketogenesis to compensate.

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37
Q

What are the risks of treatment with diabetic ketoacidosis?

A

Acute respiratory failure due to depletion of potassium and phosphate
Cerebral oedema

38
Q

What is the management of diabetic ketoacidosis?

A

DKA should be managed with IV insulin supplemented with dextrose solution and 1 litre of 0.9% NaCl administered over an hour with 15-20ml per kilogram.

However, this should be controlled to prevent cerebral oedema.

The risks of treatment can cause hypokalemia and hypophosphataemia to occur so this should be corrected.

39
Q

What is a complication with type 2 diabetes?

A

Hyperosmolar hyperglycaemic state is a complication associated with type 2 diabetes, in the absence of ketoacidosis. It occurs due to insulin insufficiency where hyperglycaemia in the blood draws out K+ and water to be lost through the urine, resulting in polyuria, dehydration and hypokalemia.

40
Q

What is the pathophysiology of hyperosmolar hyperglycaemic state?

A

Insulin deficiency worsens circulating glucose levels, causeing an increase in serum and urine osmolality and a high risk for dehydration and cardiovascular collapse. Lipolysis occurs but maintained minimal levels of insulin inhibits ketogenesis occurring.

Glucose crosses the blood brain and can lead to cerebral oedema, increasing the risk for stroke.

41
Q

What is the clinical presentation of hyperosmolar hyperglycaemia?

A

Polyuria and polydipsia with weakness, malaise and lethargy
Hypovolemia with dry mucous membranes and delayed capillary refill

Complication from cerebral oedema can cause delirium, coma and seizures.

42
Q

What is found on investigation of hyperglycaemic hyperosmolality?

A

High serum osmolality with Pseudohyponatremmia
Hyperkalemia and hyperphosphataemia unless excessive urination causes loss of K+

43
Q

What is the management of hyperosmolar hyperglycaemia?

A

First line treatment is IV fluid with 0.9% saline over 1-2 hours with 15-20ml per kg to correct hydration and insulin with oxygen for Hb desaturation and bicarbonate to correct acidity.

44
Q

What should be avoided in the initial management of hyperglycaemic hyperosmolality?

A

Insulin
-> Rapid drop in blood glucose can cause cerebral oedema

45
Q

What are the 6 Ps of acute limb ischaemia?

A

Pain, pallor, pulseness, paraesthesia, paralysis, perishingly cold

46
Q

What are the macro vascular complications of diabetes?

A

Atherosclerotic plaques, causing
Peripheral vascular disease, transient ischaemic attack, myocardial infarction, angina and chronic mesenteric ischaemia.

47
Q

What is peripheral vascular disease?

A

Atherosclerotic plaques build up in the arteries of the abdominal aorta, iliac arteries and lower limbs, leg muscles. This occurs due to atherosclerotic plaques which result in intermittent claudication, where there is pain on walking due to ischaemia during exertion.

48
Q

What are the complications with peripheral vascular disease?

A

Critical end ischaemia where gangrenous necrosis occurs due to obstruction of the pain at rest and non-healing ulcers.

49
Q

How is peripheral vascular disease managed?

A

PVD is managed with heparin, and surgical intervention through inflation with a balloon or artery bypass graft.

50
Q

What is caused by acute limb ischaemia?

A

Commonly caused by a thrombus/embolus, or in other cases trauma from compartment syndrome which blocks block flow and causes 6 Ps: pain, pallor, pulseness, paraesthesia, paralysis and perishingly cold. Pain is worse at night, especially when the leg is raises

51
Q

What is used to diagnose peripheral vascular disease?

A

Investigations include serum lactate to assess ischaemia, ECG and Doppler ultrasound and CT angiogram.

52
Q

What are microvascular complications of diabetes?

A

Chronic kidney disease, diabetic retinopathy, peripheral neuropathy, cataracts, glaucoma

53
Q

What are the stages of diabetic retinopathy?

A

1) Background retinopathy 2) Non-Proliferative phase 3) Proliferative phase

54
Q

What happens in background retinopathy?

A

Background retinopathy stage with hyperglycaemia causing microaneurysms and hard exudates of lipids due to capillary leakage from damage. This stage can be managed with steroids.

55
Q

What happens in the non-proliferative phase?

A

Non-Proliferative phase, where ischaemia results in cotton wool spots due to retinal arteriole obstruction and and capillary leakage of contents leading to hard exudate, flame haemorrhage and cotton wool spots; haemorrhages occur that cause blurred vision

56
Q

What happens in the proliferative phase?

A

Proliferative phase causes vascular endothelial growth factor to be produced and new blood vessels to be formed. Vitreous haemorrhage can occur, where blood leaks into the vitreous space between the lens and retina that causes vision loss, worsened by retinal detachment. This can be managed with anti VEGF inhibitors and laser photocoagulation

57
Q

What is the treatment of diabetic retinopathy?

A

Treatment of diabetic retinopathy includes:
corticosteroids
Anti-VEGF therapy
Laser photocoagulation to shrink abnormal areas and removal of virtuous fluid to be replaced with saline

58
Q

Why do diabetic foot ulcers occur?

A

Diabetic foot ulcers occur typically due to diabetic nephropathy where there is paraesthesia. This is combined with vessel disease from hyperglycaemima impairing blood supply that results in increased susceptibility to unnoticed injury and infection with a complication being osteomyelitis.

59
Q

What is diabetic nephropathy?

A

Non-enzymatic glycation causes damage to the renal vessels, causing mesangial cell hypertrophy due to the hypertension and resulting in glomerulosclerosis over time. Ths can lead to albuminuria and inappropriate RAAS ACTIVATION.

60
Q

What is the criteria for diabetic nephropathy?

A

Elevated blood pressure, progressive decline in GFR and persistent albuminuria.

61
Q

What is the management of diabetic nephropathy?

A

Glycaemic control
ARBs and ACE inhibitors to manage hypertension

62
Q

What are the differences between arterial and venous leg ulcers?

A

Arterial leg ulcers are deeper, smaller with well-defined borders; venous leg ulcers are more superficial with irregular borders

63
Q

What is the role of Metformin in diabetes management?

A

Inhibits hepatic gluconeogenesis and promotes peripheral glucose uptake and glycolysis

64
Q

What risks are associated with Metformin in patients with nephropathy?

A

Can lead to lactic acidosis and cause B12 deficiency and GI disturbances

65
Q

What is the action of Sulphonylureas?

A

Sulphonylureas work by blocking the K+ channel pancreatic beta cell to stimulate the activation of the Ca2+ channel for influx of Ca2”+ which causes the release of insulin.

66
Q

What are the adverse effects of Sulphonylureas?

A

Adverse effects include a disulfiram-like reaction of coming, flushing, weakness and headache.

It causes weight gain, hyperkalemia, and SIADH so discontinue with renal impairment.

67
Q

What is the effect of DPP-4 inhibitors in diabetes treatment?

A

Inhibit dipeptidyl peptidase-4, promoting insulin release and inhibiting glucagon release

68
Q

What can lead to lactic acidosis when nephropathy occurs?

A

Certain medications should be discontinued when kidney disease occurs

This includes drugs that may contribute to lactic acidosis.

69
Q

What is the mechanism of action of meglitinides?

A

Increase the effect of peripheral glucose on pancreatic beta cells, to increase closure of K+ channels and stimulate opening of Ca2+ for insulin release.

Meglitinides potentiate the closure of K+ channels, leading to Ca2+ influx.

70
Q

How do DPP-4 inhibitors function?

A

Inhibit the enzyme dipeptidyl peptidase-4, increasing GLP-1 availability which promotes insulin release and inhibits glucagon release.

This promotes insulin release and inhibits glucagon release.

71
Q

What are gliptins, and what do they do?

A

GLP-1 agonists that promote insulin release and inhibit glucagon release

Examples include Exenatide and liraglutide.

72
Q

What are common adverse effects of gliptins?

A

Nausea, vomiting, and severe pancreatitis

These effects are important considerations in treatment.

73
Q

What is the action of SGLT-2 inhibitors?

A

Inhibit the SGLT-2 channel on the PCT to prevent glucose uptake

This leads to glucosuria and can increase the risk of UTIs and yeast infections.

74
Q

What are the adverse effects of SGLT-2 inhibitors?

A

Glucosuria which increases the risk of UTI’s like yeast infections, dehydration, and increased risk of ketoacidosis

Glucose is a highly osmotic agent that can draw water.

75
Q

What class of medication do glitazones belong to?

A

Thiazolidinedione drugs

They are agonists of PPAR-alpha and improve insulin sensitivity.

76
Q

What are the potential side effects of glitazones?

A

Weight gain, fluid retention, liver dysfunction, and increased risk of bladder cancer

These side effects must be monitored in patients.

77
Q

Which diabetic medications cause weight gain?

A

Sulphonylureas and piaglitazones/ thiazolidinediones.

78
Q

Which diabetic medication is ideal for patients with cardiovascular risk?

A

SGLT-2 inhibitors can be used in addition to metformin. SGLT-2 inhibitors are ideal at preventing hypoglycaemia and cardiovascular risk factors. The tolerability to metformin must be established, before then starting SGLT-2.

79
Q

What is the first-line treatment for diabetic patients with intolerance to metformin?

A

DPP-4 inhibitors, followed by
Piaglitazones
Sulphonylureas
SGLT-2 inhibitors

This treatment increases GLP-1 levels.

80
Q

What should be monitored every 5 years for those under 140/90 mmHg?

A

Blood pressure

Regular monitoring is essential for cardiovascular health.

81
Q

What is ambulatory blood pressure monitoring?

A

Continuous monitoring of blood pressure for 24 hours

It investigates organ damage and cardiovascular risk.

82
Q

What are the NICE recommendations for Type 1 diabetes treatment?

A

Insulin injection twice daily, blood glucose management, and carb counting measuring HbA1c every 6 months and continuous glucose monitorings 4x a day, with more frequent monitoring during infection.

Those with BMI over 25 should receive metformin.

Type 1 diabetics should check their blood sugars 2 hours before and after eating.

Also includes managing cardiovascular risk factors and family planning.

83
Q

What are the NICE reccomendations for diabetic renal disease?

A

NICE recommendations for Diabetic renal disease for testing albumin:creatinine ratio, estimation of GFR and urinalysis for protein. Initiate ACE inhibitor and SGLT-2 inhibitor with the use of metformin for CKD and achieve blood pressure target.

84
Q

What are the NICE reccomendations for diabetic foot care?

A

NICE recommendations for Diabetic renal disease for testing albumin:creatinine ratio, estimation of GFR and urinalysis for protein. Initiate ACE inhibitor and SGLT-2 inhibitor with the use of metformin for CKD and achieve blood pressure target.

85
Q

What is the peak action time for rapid-acting insulin?

A

30-60 minutes after administration. This is Humalog, Aspart and Lisopro.

Examples include Humalog, Aspart, and Lispro.

86
Q

What is the peak action time for short-acting insulin?

A

1-3 hours after administration. This is Bovine and Porcine.

It is given 15-30 minutes prior to meals.

87
Q

What is the peak action time for intermediate and short acting insulin?

A

Intermediate acting insulin (NPH) has a peak for 4 to 6 hours to mimic endogenous basal insulin or Long acting insulin between meals to maintain insulin as an endogenous basal insulin. This includes isophane.

88
Q

What is the target blood glucose range before meals for diabetes patients?

A

4-7 mmol/L

This is an important target for managing diabetes effectively.

89
Q

What are the clinical features of hypoglycaemia?

A

Sweating, pallor, tachycardia, tachypnoea, and reduced consciousness

Recognizing these symptoms is crucial for timely treatment.

90
Q

What is the first-line treatment for conscious patients experiencing hypoglycaemia?

A

Oral glucose monitoring capillary blood glucose and monitor glucose every 1-2 hours until stable; if no improvement, provide intravenous glucose with 10% dextrose solution for conscious patients.

If no improvement, intravenous glucose may be necessary.

91
Q

What were the findings of the Diabetes Control and Complications Trial (DCCT)

A

Diabetes Control and Complications trial (DCCT) found that in Type 1 diabetics, managing insulin intensely with 3 or more njections daily and frequent glucose monitoring as early as possible following diagnosis reduced the incidence of diabetes related complications of the eye and kidneys after 6 years, compared with those who received conventional treatment.

Before meals and at night patients should aim for a target between 4-7 mmol/L. 2 hours following a meal, patients should aim for a target between 5-9mmol/L

The study demonstrated the benefits of early and frequent insulin management.

92
Q

What is the mechanism of action for sulphonylureas?

A

Stimulate insulin release from pancreatic beta cells

They are often used in diabetes management.

Year 3 (31 decks)

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