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Anatomy > Endocrine Disorders W4 > Flashcards

Endocrine Disorders W4 Flashcards

1
Q

What is considered the fastest growing chronic disease?

A

Type II Diabetes

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2
Q

What is Diabetes Mellitus defined as?

A

Diabetes mellitus refers to “presence of glucose in the urine”

It is associated with a lack of secretion or a lack of activity of the hormone insulin, which, in uncontrolled diabetes, results in raised blood glucose levels

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3
Q

Explain this diagram. What is the bidirectional relationship between diabetes and periodontitis?

A

The relationship between diabetes and periodontal disease is a two way process. Hyperglycaemia increases risk of periodontitis and poor periodontitis health negatively impacts diabetes.

More specifically:

Higher blood sugar levels in diabetes = increased formation of glycated AGE’s (advanced glycation end products) which are proinflammatory mediators

= more inflammation, increased osteoclasts, destruction of oral tissues

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4
Q

What is the difference between Diabetes Mellitus and Diabetes Insipidus?

A
  • Diabetes mellitus: blood level glucose (blood sugar) = excessively high. The kidneys try to remove the extra glucose by passing it in urine. Associated with deficiency of the hormone, insulin.
  • In diabetes insipidus, your blood glucose levels are normal, but your kidneys can’t properly concentrate urine. Caused by a deficiency of ADH.
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5
Q

What is the main distinction between Type 1 diabetes and Type 2 diabetes?

A

Type 1: genetic condition that shows in early life. Characterised by the destruction of insulin-producing beta cells in the pancreas. An absolute lack of insulin.

Type 2: heterogeneous condition, lifestyle related (unhealthy diet, physical inactivity) shows later in life. Disorder of both insulin levels (insufficient) AND insulin disfunction/resistance = hyperglycaemia results.

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6
Q

Explain the difference between Type 1A and 1B diabetes

A

Type 1A: immune-mediated ie. autoimmune destruction of pancreatic beta cells = NO insulin = evelaveted blood glucose levels & breakdown of body fat and proteins

Type 1B: idiopathic ie. arises spontaneiously (cause unknown) - possible inheritence

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7
Q

If diabetes is not controlled, what is the basic impact of the condition on the metabolism?

A

In uncontrolled Diabetes, a person is unable to transport glucose into fat and muscle cells.

= cells being “starved”

= fat and protein breakdown is increased in order to compensate and provide an energy source for these cells.

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8
Q

What leads to the loss on insulin production with Type I Diabetes?

A

An autoimmune reaction directed at insulin-producing beta cells in the pancreas. Or idiopathic (1b) spontaneous.

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9
Q

If Type 1 diabetes is not carefully managed, sufferers can develop the serious problem of ____.

What causes this problem?

A

Ketoacidosis

Insulin inhibits lipolysis (breakdown of fat) and release of free Fatty Acids (pro inflammation) from adipocytes. Free FA’s convert to ketones in the liver.

Therefore if insulin isn’t present, lipolysis is not inhibited and its effect yields uncontrolled Free FA release- ketoacidosis.

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10
Q

How is Type I and Type II diabetes diagnosed?

A

blood tests…

  • fasting plasma glucose levels
  • casual (random) plasma glucose tests
  • glucose challenge test
  • glycosylated haemoglobin test (long term picture of blood glucose levels)

Hyperglycaemia = above 7mmol/L

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11
Q

What is Type II Diabetes defined as?

A

Heterogeneous, lifestyle disease, progressive condition.

Disorder of both insulin levels (beta cell dysfunction) and insulin function (insulin resistance). Results in hyperglycaemia.

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12
Q

What are some factors that lead to beta-cell dysfunction in the pancreas with Type 2 Diabetes?

What role does a high-fat diet play in this process?

A

Obesity,

Increased Free FA concentration and adipokines, stimulates beta-cells to secrete insulin

Chronic and excess stimulation causes beta-cell failure

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13
Q

What does insulin normally do

A

Induces glucose storage in liver, muscle and aipose tissue = lowering blood glucose levels

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14
Q

What causes insulin resistance in type 2 diabetes

A

Due to inflammatory processes in the dysfunctional visceral adipose tissue

ie. Obestity = inflammation (particularly in adipose tissue)

= dysfunctional adipose tissue ie. adipocytes can’t take more lipids and die an early cell death

= membrane ruptures release of intracellular contents (adipokines: pro-inflammatory ex. free F.A’s)

= attracts more pro-inflam cytokines

= low-grade systemic inflammation

= impaired insulin signalling

= insulin resistance

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15
Q

What is the disease process/propogation of type 2 diabetes

A
  1. Obestity = chronic systemic inflammation = insulin resistance
  2. Initially insulin production in beta cells is upregulated to combat diminised insulin action
  3. Beta cells dysfunction and exhaustion = insulin deficiency
  4. Blood glucose levels continue to rise
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16
Q

What is the condition associated with insulin resistance and the associated symptoms

A

Metabolic syndrome

hyperglycaemia

central obestiy

abnormal blood lipids

hypertension

insulin resistance

Inflammation

Requires 3 of the above symptoms for diagnosis

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17
Q

Insulin resistance not only contributes to hyperglycaemia, but plays a role in other metabolic abnormalities. What are these called, and what are the signs of this?

A

Metabolic Syndrome- Insulin Resistance Syndrome

High LDLS,

Low HDLS,

Hypertension

Systemic inflammation

Vascular Disease

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18
Q

What are the main symptoms of Diabetes?

A
  • Polyuria- excessive urination
  • Polydispia- excessive thirst
  • Polyphagia- excessive eating
  • Weight loss, blurred vision, skin infections, fatigue, paraestheisa
19
Q

What are some complications/comorbities associated with diabetes

A

cardiovascular disease, hypertension, hyperlipidemia, kidney damage, eye damage, foot damage (ulcers), skin conditions, neuropathy (nerve damage), depression, stroke

20
Q

Why do increased free fatty acid concentrations trigger insulin resistance and increase blood glucose

A

FFA’s stimulate insulin secretion from beta cells (insulin normally has a rold in the uptake FFA’s into cells)

therfore chronic and excessive stimulation

= beta cell failure

= reduced glucose uptake and glycogen storage (hyperglycaemia)

21
Q

Give an example of an anti-inflammatory and pro-inflamatory adipokines released from adipose tissue

A

Adiponectin = anti-inflammatory

  • Antidiabetic, anti-atherogenic
  • downregulated in obestiy and insulin resistance
  • positive regulation of B-cells

Lepetin apelin = pro-inflammatory

  • Negative regulation of B-cells
22
Q

What is gestational diabetes?

A

Any degree of glucose intolerance first detected during pregnancy

  • usually effects women with family history of diabetes
  • associated with pregnancy complications
  • high risk of deveoping type 2 diabeted 5-10 years later
23
Q

What is the treatment for Type 1?

A

Type 1: Insulin replacement in order to stop fat and protein catabolism (and ketoacidosis)

Both cannot be cured once established, they can only be managed.

24
Q

What is the prevention of Type 2 diabetes

A

Healthy diet for example a mediterranean diet and exercise (150min/week) dramatically reduces the risk

25
Q

How is Type I Diabetes treated?

A

Normalise blood glucose levels by insulin replacment therapy

Good routine: balance between insulin administration, carb intake and glucose levels.

Insulin IV (mix of short and intermediate acting) and pancreatic islet cell transport.

26
Q

How is Type 2 Diabetes treated?

A

Glucose, lipid and blood pressure goals as well as weight loss by…

  • Metformin tablets. Increase glucose uptake in muscle, inhibits hepatic glucose output and decrease GI absorption. Low risk of hypoglycaemia, but can cause anorexia and encourage weight loss.
  • Sulfonylureas. Stimulates insulin secretion and appetite. May cause hypoglycemaia and weight gain.
  • GLP-1 Therapy (glucagon like peptide incretin). Usually increases insulin secretion and decreases glucagon secretion - released in response to food but reduced levels in diabetics. Treatment can be Inhibiting the enzyme that inactivates GLP-1
27
Q

What is involved in the management of BOTH Type 1 and Type 2 diabetes

A

Normalise blood glucose levels by…

  • dietary managment
  • exercise
  • oral anti-diabetic agents (type 2) or insulin replacement (mostly type 1)
  • pancreatic islet cell transplantation
28
Q

What is a potential complication when administering insulin in the case of type 1 diabetes

A

Hypoglycaemia (insulin coma)

  • too much insulin = blood glucose levels drop too low - brain deprived of energy source, can cause permanent brain damage if severe.
29
Q

What are some of the commmon oral signs of diabetes

A

Dentists have potential to pick up undiagnosed type 2 diabetes

  • increased rates of periodonatal disease
  • xerostomia
  • root caries
  • high salivary glucose levels
  • impaired immune function = more prone to oral infections
  • vascular and immune dysfunction = poor wound healing
  • high risk of oral mucosal disorders ie. lichen planus and burning mouth syndrome
30
Q

What plays a role in the development of periodontitis, and particularly, alveolar bone loss?

Identify the relationship with periodontitis and diabetes.

A
  • High Blood Glucose in Diabetes patients increase the production of AGE’s.
  • AGE’s are proteins that have become glycerinated after sugar exposure and function as pro-inflammatory mediators.
  • AGE’s bind to inflammatory cells- cytokines- and trigger further inflammation.
  • This inflammation causes increased activation of osteoclasts- which results in destruction of oral tissues.
  • Uncontrolled diabetes is strongly correlated to increased alveolar bone loss. While good glycemic control reduces oral problems.
31
Q

What are AGE’s?

A

Advanced Glyceration End Products.

Proteins that become glycerinated after exposure to sugars.

They are produced through normal metabolism

32
Q

What causes the overproduction of AGE’s in diabetes?

A

Diabetes, cells can’t control their glucose uptake, the hyperglycaemia causes oxidative stress and AGE formation is overproduced.

Effect of diabetes on periodontitis has been attributed to AGE’s overproduction.

33
Q

Which diabetic patients are more at risk of developing periodontal disease, or having more severe periodontitis?

A

Type 1 and 2 are both at risk of periodontitis.

However, Type II are more prone and more severe because of hyperglycaemia levels increasing excessive production of AGEs. (pro inflammatory mediators- osteoclast activity increased- oral tissue damage).

34
Q

What are the major potential side effects with insulin therapy?

Are you more likely to see a Type I or Type II diabetic in emergency room?

How do you manage the situation?

A
  • Hypoglycemia, severe, can cause brain damage.
  • Type I because if they inject too much insulin it results in low blood glucose.
  • Treatment is sweet drink or snack or IV glucose.
35
Q

What are some of the factors that lead to beta-cell dysfunction in the pancreas with Type II diabetes?

What role does a high-fat diet play in the process?

A
  • Obesity
  • Increased FFA concentration, stimulate beta cells to secrete insulin
  • Chronic and excess stimulation causes beta cell failure
36
Q

What is glycosylated haemoglobin (HbA1c)?

A

It is made when the glucose (sugar) in your body sticks to your red blood cells. Your body can’t use the sugar properly, so more of it sticks to your blood cells and builds up in your blood.

This test is used in the dental clinic and provides an assessment of risk for hypoglycemic emergencies. FOR THAT DAY ONLY as blood glucose fluctuates.

37
Q

What is the significance of impaired glucose tolerance to a person? (List two things)

A

The person has an increased risk of developing diabetes

Increased risk of cardiovascular issues

38
Q

What products would a urine test for an undiagnosed diabetic show?

A

Ketones and Glucose

39
Q

What is the basic, underlying problem in diabetes, and what causes the production of the large volumes of urine?

A

In diabetes blood glucose is excessively high (due to lack of secretion or activity of insulin hormone). The kidneys try to remove the extra glucose by passing it in urine. This has an osmotic effect and water is taken with it- which results in polyuria- production of large volumes of urine

40
Q
  1. What is the parathyroid’s role in the body?
  2. What is the difference between hyperparathyroid and hypoparathyroid disorder? Symptoms, cause and dental effects.
A
  1. Regulates blood Calcium levels and is released in response to a fall of Ca2 levels. Increases reabsorption of Calcium in kidneys.
  2. Hyper= neoplasia, uncontrolled growth of gland. Bone lesions with excessive osteoclast activity and associated hypercalcaemia. Malocclusion and teeth mobility.
  3. Hypo= affects nerve and muscle activity. Prone to dental caries.
41
Q

Explain insulin resistance.

A

Increased Free Fatty Acids (because insulin regulates uptake of FFAs which are pro inflammation) and increased blood glucose, which trigger insulin resistance.

FFAs stimulate insulin secretion from beta cells-excess stimulation of beta cells- beta cell failure.

42
Q

What diabetic patient would have immune deficiency, and what does this mean in the clinic?

A

Type 1A- autoimmune.

Susceptible to infection and poor wound healing.

At risk of hypoglycaemia.

43
Q

What are incretins?

A

Peptides in the GIT that have a dual action of increasing insulin secretion and decreasing glucagon secretion. Therefore lower blood glucose.

44
Q

When insulin is still present, what drug is best to increase glucose uptake and lower blood glucose?

A

Metformin.

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