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Cardiovascular Health > Patho & Treatment - Diabetes > Flashcards

Patho & Treatment - Diabetes Flashcards

1
Q

What is diabetes mellitus?

A

The loss of glucose homeostasis i.e. a failure of plasma glucose levels to remain within a normal homeostatic range of 4 -6 mmol/L

Abnormal fat, carbohydrate and protein metabolism due to defects in insulin secretion and action

Hyperglycaemia = too much glucose 
Dyslipidaemia = too much lipids in the blood (drives atherosclerosis)
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2
Q

How is normal glucose homeostasis maintained?

A

Glucose homeostasis is normally maintained by the interaction between glucagon & insulin which are both stored & released in the Islets of Langerhans in the pancreas

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3
Q

Describe which cells manufacture and secrete insulin and glucagon?

A

Alpha cells - secretes glucagon

Beta cells - manufacture and secrete insulin

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4
Q

Describe how the hormone glucagon works

A

Glucagon is released from the pancreas when blood glucose levels falls
Glucagon acts on the liver to break down glycogen to glucose (glycogenolysis)
Liver releases glucose into the blood system i.e. when this occurs blood glucose levels rise bringing it back into the homeostatic range

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5
Q

Describe how the hormone insulin works

A

Insulin is released from the pancreas when blood glucose levels rise
Insulin promotes the uptake of glucose into adipocytes, cardiac and skeletal muscle cells to be used as an energy source. In the liver it converts glucose to glycogen and stores it there

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6
Q

What is the difference between type 1 and type 2 diabetes?

A

Type 1 diabetes - inability to secrete insulin (beta cells in Islet of Langerhan) - blood glucose levels rise.
Glucose cannot be used as an energy source

Type 2 diabetes: receptors, on cell membrane of adipocytes on skeletal and cardiac muscle cells and liver cells, become less sensitive to insulin which inhibits the ability of cells to remove glucose from the blood. Long term there is beta cell failure. This causes hyperglycaemia

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7
Q

What are the 8 types of diabetes mellitus?

A

Type 1
Type 2
Gestational - mothers are at greater risk of developing type 2 diabetes. Baby can gain too much weight making them at higher risk of developing brain trauma during delivery (they also are at a higher risk of developing obesity and type 2 diabetes later in life)
Congenital - babies are born with no functioning beta cells
CF - related - as CF disrupts functioning of the pancreas
Secondary - e.g. an infection within the pancreas affecting the beta cells
LADA - Latent autoimmune diabetes
Diabetes MODY - maturity onset type 2 diabetes (no obesity)

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8
Q

What are the possible causes of type 1 diabetes?

What aged people does it occur in?

A

Possibly caused by autoimmune, genetic, viral or bacteria causing beta cells in pancreas
Insulin cells in liver, skeletal- cardiac muscle, liver adipocytes are not affected

<40 years - usually manifests in 13 year olds

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9
Q

What are possible causes of type 2 diabetes?

A

Poor lifestyle causing insulin-receptor resistance

Progressive beta cell failure occurs after long-term type 2 diabetes

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10
Q

Can babies and children get obesity?

A

Yes both can

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11
Q

What are the 3 physiological responses that occur due to lack of insulin?

A

The body compensates by increasing beta cell activity (called hyperinsulinaemia)
Later in the disease insulin resistance continues to grow and beta cell exhaustion occurs
1. Excess glucose is converted to fat and stored within adipocytes in the presence of insulin
2. When there is a lack of insulin, accelerated lipolysis occurs liberating free fatty acids and this increases low density lipoproteins (LDLs) in the blood
3. Abnormal release of glucagon (glucagon stimulates liver to break down glucose) which stimulates appetite

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12
Q

How do you prevent diabetes or reverse diabetes to pre-diabetes?

A
  1. Weight management – diet & exercise

2. CRF – exercise – maintains receptor sensitivities

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13
Q

What initiates insulin receptor resistance?

A

Inflammatory mediators and adipokines (cytokines released by adipose tissue) arising from VAT decrease insulin receptor sensitivity and increase insulin resistance
VAT (visceral adipose tissue) is an inflammatory tissue and is metabolically active
VAT is created by excess calories which cause adipocytes to increase in size

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14
Q

Describe how inflammatory mediators cause insulin receptor resistance

A

Macrophages become active and release TNF alpha, CRP and IL6 which blunt sensitivity of insulin receptors
Resistin (is an adipokine - i.e. is released from adipocytes). It increases insulin receptor resistance. The more VAT present the more resistin is secreted.It promotes the liver to convert free fatty acids to LDLs causing dislipidoemia
Adiponectin (an adipokine) acts on insulin receptors maintaining their sensitivity levels. As an individual expands their VAT the production of adiponectin is decreased
Lack of insulin, fat cells undergo rapid lipolysis which creates free fatty acids. These FFAs increase insulin receptor resistance. Resistin encourages the liver to breakdown FFAs (free fatty acids) to LDLs. Increased LDLs cause atherosclerosis

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15
Q

How does VAT affect hypertension?

A

VAT secretes leptin and angiotensin 2 which drives up blood pressure

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16
Q

What are the weight features of with type 2 diabetes?

A
  • tend to have high waist circumferences & W:H ratios
  • central adiposity (VAT)
  • tend to have high BMI > 25 black & white populations or > 23 Asians
  • very little subcutaneous adipose tissue (SCAT) but high VAT- common in Asian populations
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17
Q

What occurs when hyperinsulinaemia progresses?

A

The inflammatory mediators released by VAT (CRP, TNF-alpha, IL-6) induce apoptosis of beta cells in the Islets of Langerhan
This continues until there is no functioning beta cells left

18
Q

What is the link between type 2 diabetes and atherosclerosis?

A
  1. VAT & atherosclerosis –> in absence of insulin: FFA conversion to LDLs
  2. Hyperglycaemia causes insulin resistance, abnormal activation of glucagon and endothelial wall damage.
    Excess glucose in the blood comes in contact with and binds to proteins and lipids on the arteriole endothelium which cause an inflammatory response. Hyperglycaemia causes glycosylation of proteins and lipids in capillary endothelium which causes the release of advanced glycation end-products (AGEs). AGEs are pro-inflammatory and cause endothelal damage and dysfunction and also cause atherosclerosis
19
Q

What 3 types of tests are used to diagnose diabetes?

A

Fasting blood glucose test
Random blood glucose test
Oral glucose tolerance test (OGTT) - giving them a bolus of glucose in their mouth. Would expect them to secrete insulin within 2hr and to uptake that glucose very quickly

  • These methods are used to monitor their blood glucose throughout the day
20
Q

How would you monitor the glycaemic health of an individual long term?

A

% of glycosylated haemoglobin in the blood (HbA1c)

The more blood glucose present the higher the % of glycosylated haemoglobin

21
Q

What are the causes of hypoglycaemia?

A

Miscalculation of insulin medication in type 1 diabetes (as they have no insulin production) or in type 2 diabetes who have very poor or no insulin production)

22
Q

What is the signs of hypoglycaemia?

A

Sympathetic n.s. symptoms e.g. anxiety, dizziness, confusion, cloudy vision, headaches, hunger, sweating, tremors
- Convulsions, loss of consciousness, coma, death

23
Q

How do you treat hypoglycaemia?

If exercising a diabetic patient how would you ensure they don’t become hypoglycaemic?

A

Eat/drink carbohydrates
IV glucose
Subcutaneous glucagon injection
Pre-exercise glucose test

24
Q

What does severe hyperglycaemia cause?

A

Diabetic ketoacidosis (DKA)

25
Q

How does severe hyperglycaemia occur?

A

Under-dosing of insulin medication or due to mismanaging their diabetes
Cells cannot access blood glucose so they resort to fat metabolism (free fatty acids) which causes production of ketone bodies

26
Q

What does the production of ketone bodies do to the blood?

A

Causes the blood to become acidotic

27
Q

What are the symptoms of ketoacidosis?

A

Early symptoms: Dehydration, nausea, lethargy

Advanced: dizziness, ketone breath, vomiting, tachycardia, confusion, coma, death

28
Q

What is the difference between macrovascular & microvascular damage? What causes this damage?

A

Macrovascular damage = damage to the endothelium of the larger arteries & arterioles. Combination of cytokine, AGE and dyslipidaemia damage.
Microvascular damage = damage to smaller arteries and capillaries

AGE - advanced glycolytic end products and inflammatory cytokines from VAT which contribute to atheroma formation and cause damage

29
Q

How does diabetic cardiomyopathy occur in the diabetic population?

A

The inflammatory process of diabetes causes structural changes in the myocardial wall, hypertrophy and fibrosis on the myocardial walls which decreases compliance of the myocardium and contributes to heart failure

30
Q

What are the medical complications that are associated with diabetes?

A
  1. Retinopathy → visual loss / blindness
  2. Atherosclerosis - peripheral - intermittent claudication
  3. Progressive nephropathy → renal dysfunction → kidney failure
  4. Peripheral neuropathy – mainly feet, mainly sensory → neuropathic foot ulceration → enhanced falls risk and risk of amputation
  5. ANS neuropathy
31
Q

Why would a minor blister potentially cause a sensory neuropathy in a peripheral limb in the diabetic population?
What kind of rehab would you do with this kind of patient?

A

Poor oxygen supply through the obstructed arteries
The tissues cannot heal/there is delayed healing and the wound will expand Sensation may be poor in the limb
May also have a motor neuropathy (causing drop foot - treat with an ankle-foot orthosis (AFO)
Wouldn’t do stepper with them - could do proprioceptive exercises with them

32
Q

What are the symptoms of peripheral sensory neuropathy?

A

Often in the fingers & toes:

numbness, tingling, pins & needles, prickling, burning, coldness, pinching , buzzing

33
Q

What needs to happen, physiologically, with the patient in order for diabetic remission to occur?

A
  1. Lose weight in order to reduce adipose tissue infiltrating the visceral organs - mainly liver and pancreas
  2. Patient needs functioning beta cells. Chances of remission are no longer available if all beta cells have been destroyed (which occurs in well-established type 2 diabetes)
34
Q

Which type of exercise should diabetics engage in?

A

Both but mainly aerobic exercise
Increasing insulin receptor sensitivity (type 1 fibres) - aerobic exercise
Hypertrophy of type 2 muscle fibres will be achieved through strength training

35
Q

Describe how the mechanism of action of metformin

A
  • Beta cells are still active when this drug will be given - it is a first line medication for type 2 diabetes
  • Increases insulin receptor sensitivity to insulin - allows glucose to move across the GLUT4 transporter and into the cell to be used as glycogen or to be stored fat in adipocytes
  • Suppresses gluconeogenesis in the liver (formation of new glucose)
  • Inhibits some of the absorption of glucose from food to reduce blood glucose levels
36
Q

Describe how sulfonylureas works

A
  • Used for type 2 diabetes
  • Increases production and release of insulin in the beta cells in the Islets of Langerhan in the liver
  • Are being phased out, new patients are not usually put on this drug
37
Q

Describe the mechanism of action of SGLT2 inhibitors

A
  • Act on the kidney to reduce glucose reabsorption
38
Q

Describe the mechanism of action of (the drug) insulin

A
  • Used in all people with type 1 diabetes (as their beta cells have been supplied so they cannot produce their own insulin)
  • Used in type 2 diabetes who have progression to significant beta cell failure. This drug will be used in conjunction with metformin or sulfonyureas
  • Has a high risk of hypoglycaemia (risk of this increases after exercise)
  • Its action is to raise plasma insulin levels
39
Q

What other drugs would diabetics need?

A

Statins for high LDLs

Anti-hypertensives for the high amount of VAT as it increases hypertension

40
Q

What is the link between mental health and diabetes?

A

The rate of depression is two times higher in people with diabetes
41% of people with diabetes experience poor mental well-being

41
Q

What is the effect of exercise on blood glucose levels?

How often should diabetic patients exercise?

A

Aerobic exercise reduces blood glucose for 24-48hrs
Every 48hrs at a minimum
Resistance exercise causes a slight increase in blood glucose

Cardiovascular Health (9 decks)

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