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NSB231 > Diabetes + Endocrinology > Flashcards

Diabetes + Endocrinology Flashcards

1
Q

Define diabetes mellitus

A

A disease in which the body’s ability to produce or respond to the hormone insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated BGLs.

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2
Q

What are 5 common clinical features of diabetes mellitus?

A
  1. Increased thirst/dehydration (polydipsia)
  2. Frequent urination (polyuria)
  3. Hunger
  4. Fatigue
  5. Blurred vision
  6. Polyphagia
  7. Glycosuria
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3
Q

Explain the role of insulin in maintaining homeostasis of blood glucose.

A

Insulin aids in regulating and reducing the BGL. Insulin promotes the transport of glucose into cells from the bloodstream and inhibiting glucose production. Insulin is a hormone that is produced by the pancreas that facilitates glucose transport into cells. By facilitating glucose transport, insulin lowers BGLs. It inhibits glucose production from amino acids, fatty acids and glycogen. Insulin stimulates glycogen formation from glucose.

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4
Q

Explain the role of glucagon in maintaining homeostasis of blood glucose.

A

Glucagon promotes glucose production and release into the bloodstream. Glucagon is a hormone produced by the pancreas that raises BGLs by stimulating the breakdown of glycogen into glucose, stimulating glucose production from amino acids and fatty acids and stimulating the release of glucose from the liver. Glucagon and insulin have antagonistic effects

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5
Q

Explain blood glucose tests used in diagnosis.

A

Finger prick for the blood glucose meter, urine glucose test and a pathology blood test. Oral glucose tolerance test is another primary method of diagnosing diabetes mellitus.

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6
Q

Explain prediabetes

A

Prediabetes is a condition characterized by slightly elevated BGLs, regarded as indicative that a person is at risk of progressing to Type 2 diabetes, lifestyle changes can reduce the risk of diabetes

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7
Q

What is the cause of type 1 diabetes?

A

Usually it’s the body’s own immune system (which normally fights harmful bacteria and viruses) mistakenly destroys the insulin producing cells in the pancreas

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8
Q

What are the clinical features of type 1 diabetes?

A
  1. Increased thirst
  2. Frequent urination
  3. Fatigue
  4. Blurred vision
  5. Hunger
  6. Headache
  7. Weight loss
  8. Sweating
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9
Q

Explain the pathophysiology of type 1 diabetes.

A

Type 1 diabetes is a chronic illness characterized by the body’s inability to produce insulin due to the autoimmune destruction of the beta cells in the pancreas. Although onset occurs frequently in childhood, it can develop in adulthood. T1D is a catabolic disorder wherein circulating insulin is very slow or absent, plasma glucagon is elevated and the pancreatic beta cells fail to respond to all insulin secretory stimuli. The pancreas shows lymphocytic infiltration and destruction of insulin secreting cells of the islets of langerhans causing insulin deficiency. Insulin deficiency can cause disruption of glucose uptake to inhibitory effect on hepatic glucose production, lipolysis and ketogenesis, diureses and dehydration and elevated free fatty acid levels and DKA

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10
Q

What is the cause of type 2 diabetes?

A

Modifiable lifestyle risk factors. The pancreas can’t make enough insulin. The body becomes resistant to insulin or when the pancreas stops producing enough insulin.

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11
Q

What are the clinical features of type 2 diabetes?

A
  1. Excessive thirst
  2. Frequent urination
  3. Excessive hunger
  4. Fatigue
  5. Blurred vision
  6. Weight gain or loss
  7. Poor wound healing
  8. May be no symptoms
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12
Q

Explain the pathophysiology of type 2 diabetes.

A

In T2D the body either produces inadequate amounts of insulin to meet the demands of the body or insulin resistance has developed. Insulin resistance refers to when cells of the body such as the muscle, liver, and fat cells fail to respond to insulin even when levels are high. In fat cells, triglycerides are instead broken down to produce free fatty acids for energy; muscle cells are deprived of an energy source and liver cells fail to build up glycogen stores. This leads to an overall rise in the BGL in the blood. Obesity and inactivity are thought to be major causes of insulin resistance.

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13
Q

What is gestational diabetes?

A

Placental hormones can cause high blood sugar. GDM is a form of diabetes that occurs during pregnancy. Most women will no longer have diabetes after the baby is born. It is diagnosed when higher than normal BGLs first appear during pregnancy.

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14
Q

Explain the causes of acute diabetes mellitus

A

Uncontrolled high and low BGL.
High = lifestyle factors, ie diet, inactivity.
Low = genetic, not eating regularly

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15
Q

Explain the clinical features of acute diabetes mellitus

A
  1. Polyuria
  2. Thirst
  3. Blurred vision
  4. Weight loss
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16
Q

Explain the treatment of acute diabetes mellitus.

A

T1D = goal is to maintain BGL through regular monitoring, insulin therapy, diet and excercise.

T2D = diet, exercise, medication and insulin therapy.

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17
Q

Explain the complications of acute diabetes mellitus.

A
  1. Cardiovascular disease
  2. Nerve damage (neuropathy)
  3. Kidney damage (nephrology)
  4. Eye damage (retinopathy)
  5. Skin conditions,
  6. Hearing impairment
  7. Alzheimer’s disease
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18
Q

Explain long term complications of diabetic nephropathy.

A

High BGL can injure nerves throughout the body, particularly nerves in the legs and feet. Symptoms can range from pain, numbness, to problems with the digestive system, urinary tract, blood vessels and heart.

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19
Q

Explain long term complications of visual disturbances/retinopathy

A

The increase in BGL can cause visual impairment/loss. Including glaucoma (macular degeneration), cataracts, and contrast sensitivity.

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20
Q

Explain long term complications of macro/microvascular

A

Impacts muscle, skin, brain, and kidneys. Glycation end product accumulation, impaired vasodilatory response attributable to nitric oxide inhibition, smooth muscle cell dysfunction, chronic inflammation, enhanced platelet aggregation.

21
Q

Explain long term complications of peripheral vascular disease

A
  1. Diabetic ulcers,
  2. Critical limb ischaemia
  3. Peripheral artery disease (pad)
  4. Atherosclerotic occlusive disease of the lower extremities
22
Q

Explain long term complications of coronary heart disease

A

This primarily impacts T2D due to other risk factors that contribute to the development of both T2D and cardiovascular heart disease. E.g. lifestyle factors, diet, exercise

23
Q

Explain long term complications of infection

A

Malignant external otitis, rhinocerebral mucormycosis and gangrenous cholecystitis are diabetic specific infections. Hypoglycaemia, ketoacidosis and coma are other metabolic complications for DM.

24
Q

What are some methods of monitoring glycaemic control and what is the importance of glycaemic control?

A
  1. Self monitoring BGL (allow for adjustment of food intake, excercise or medication dose)
  2. Urine tests (glycosuria, albuminuria)
  3. BGL tests
25
Q

What are some diabetic management strategies?

A
  1. Meal planning with dietitian
  2. Increase physical activity
  3. Monitor BGL
  4. Plan medications (hypoglycaemics - metformin, glucose, antihypertensives and lipid lowering drugs)
  5. Reduce other lifestyle factors that may impact BGL levels
26
Q

What are some diabetic treatment strategies?

A

T1D = medication/insulin, dietary and exercise

T2D = dietary changes, weight reduction, exercise, insulin/non insulin

27
Q

What are some diabetic prevention strategies?

A

Altering lifestyle factors, including diet, and exercise.

28
Q

What are BGL goals? Normal / impaired fasting glucose (IFG) / Impaired glucose tolerance (IGT) / DM

A 
Normal = <6.1mmol/L
IFG = 6.1 - 6.9
IGT = <7.0
DM = >7.0
29
Q

What are glycated haemoglobin goals? Normal / impaired fasting glucose (IFG) / impaired glucose tolerance (IGT) / DM

A 
Normal = <7.8
IFG = <7.8
IGT = 7.8 - 11
Diabetes = >11.1
30
Q

What are causes of obesity?

A
  1. Sedentary lifestyle
  2. Poor diet
  3. Genetics
  4. Stress
  5. Smoking
  6. Socioeconomic factors
31
Q

What are characteristics of obesity?

A

Pain in the back or joints, excess fat, BMI 30+

32
Q

Describe adipose tissue function

A

Adipose tissue or fat is an anatomical term for loose connective tissue composed of adipocytes. Its main role is to store energy in the form of fat, although it also cushions and insulates the body as well. It produces hormonse e.g. leptin (endocrine function). Produces cytokines and pro-inflammatory factors that may contribute to atherosclerosis.

33
Q

Describe adipose tissue changes with weight gain & loss

A

Obesity = impairment of adipose tissue function: hypertrophy, hypoxia, increased lipid storage and impaired insulin sensitivity, increased number of macrophages in adipose, increased adipocyte secretions (fatty acids, proinflammitory, procoagulant, atherogenic, diabetogenic, hypertensive).

34
Q

Identify the role of leptin in regulating food intake

A

Inhibits food intake. There is very high secretion of leptin in obese individuals.

35
Q

Identify the role of ghrelin in regulating food intake

A

Stimulates food intake

36
Q

Discuss the risk factors for obesity.

A
  1. Poor diet
  2. Sedentary lifestyles
  3. Genetics
  4. Age
  5. Certain medications
  6. Medical problems
  7. Socioeconomic status
  8. Distribution of fat
  9. Alcohol consumption
37
Q

Explain BMI, waist circumference measurements and their use to indicate obesity-related health risks

A

BMI = is an internationally recognized standard for classifying overweight and obesity in adults.

Waist Circumference = a higher waist measurement is associated with an increased risk of chronic disease

38
Q

Describe central vs peripheral obesity

A

Central = visceral fat, combo of disorders that increase risk of diabetes and cardiovascular disease; raised triglycerides, reduced HDL cholesterol, raised BP, raised fasting plasma glucose are commonly seen in conjunction. Occurs mainly with ageing due to hormonal changes.

Peripheral = subcutaneous fat around the hips & buttocks, lower risk of obesity related complications

39
Q

What is the importance of visceral abdominal fat

A

Visceral adipose tissue (VAT) is a hormonally active tissue that releases different bio-active molecules and hormones such as adiponectin, leptin, tumour necrosis factor, resistin and interleutin.

40
Q

Identify the main health complications associated with obesity

A
  1. Heart disease
  2. Stroke
  3. Diabetes
  4. Cancer
  5. Gallbladder disease and gallstones
  6. Osteoarthritis
  7. Gout
  8. Breathing difficulties i.e. sleep apnea, and asthma
  9. Psychological problems
41
Q

What are the causes of sleep apnoea?

A

The most common cause of obstructive sleep apneoa is excess weight and obesity, which is associated with soft tissue of the mouth and throat. During sleep, when the throat and tongue muscles are more relaxed this soft tissue can cause the airway to become blocked causing a loud snore and blocking the airway.

42
Q

What are the clinical features of sleep apnoea?

A
  1. Excessive daytime sleepiness
  2. Insomnia
  3. Nightmares
  4. Sleep deprivation
  5. Loud snoring
  6. Fatigue
  7. Mood swings
  8. Weight gain
  9. Depression/irratibility
  10. Episodes of no breathing
43
Q

What is the treatment for sleep apnoea?

A
  1. Physical exercise/weight loss
  2. Continuous positive airway pressure (CPAP)
  3. Tonsillectomy
  4. Adenoid removal
  5. Palatoplasty
44
Q

Describe the characteristics of metabolic syndrome

A
  1. Abdominal obesity
  2. Hypertension
  3. Hyperglycaemia
  4. Dyslipidaemia
  5. Smoking
  6. Genetic susceptibility
45
Q

Discuss meal replacements, drug treatments for weight loss including limitations for their use.

A

Meal replacements = very low calorie diets, effective short term; doesn’t teach good eating habits, weight gain after meal replacements.
Drug Treatments = should only be considered after dietary, exercise and behavioral approaches have been attempted; absorption blocking drugs, and appetite suppressing drugs

46
Q

What is the problem surrounding fad diets?

A
  1. Are difficult to sustain,
  2. Result in rebound weight gain
  3. May restrict essential nutrients
  4. May make it harder to achieve and maintain a health weight in the long term
47
Q

Discuss surgical options for treating obesity.

A
  1. Gastric Bypass
  2. Gastric Sleeve
  3. Gastric banding
48
Q

What are 2 acute complications of DM?

A
  1. Hypoglycaemia

2. Hyperglycaemia (diabetic ketoacidosis, hyperglycaemic hyperosmolar state)

NSB231 (7 decks)

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