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Multi Choice Exam BN3 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

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

A

DM is complex disturbance of metabolism due to lack of insulin production or a loss of receptor function.
Type1 - characterised by insulin deficiency or total lack off.
Type 2 - presents as a result of insulin resistance where the insulin receptor become insensitive.

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1
Q

After a meal, how long does it take for glucose levels to increase?
When does blood glucose levels peak?
When does it return to normal?

A

Increase immediately after a meal.
Peaks in 3-5mins
Return to normal 2-3 hours.

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2
Q

Facilitation of glucose uptake and usage by cells is one function of insulin in the body. There are five others, what are they?

A

Increasing glycogen synthesis and decreasing gluconeogenesis.
Increasing accumulation of fatty acids into adipose cells -lipogenesis.
Decreases ketogenesis.
Increasing protein synthesis and decreasing protein breakdown.
Moves potassium and phosphates into cells.

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3
Q

Is the function of insulin anabolic?

A

True.

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4
Q

True or false. All cells in the body need insulin to get glucose into the cell.

A

False, as beta cells, RBC and neurons do not insulin.

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5
Q

The insulin receptors on the cell membranes of hepatocytes are called?
a. Glut1
b. Glut2
c. Glut3
d. Glut4

A

D - Glut4- found on liver and somatic cells.

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6
Q

Which of the cells in the Islets of Langerhans in the pancreas are sensitive to hypoglycaemia?
a. beta cells
b. alpha cells.
c. delta cells.
d. gamma cells

A

Alpha cells - secrete glucagon.

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7
Q

What are three methods of administration for insulin?

A

SC / IV / Parenterally

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8
Q

Insulin can be classified based on the time it takes have an effect. What are 4 classifications of insulin and name one that goes with each?

A

Ultra short acting - Humalog, Novorapid
Short acting - Actrapid, Humilin
Intermediate acting - Humulin NPH, protophane
Long acting - ultratard, lantus

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9
Q

Why can insulin not be given orally?
a. salivary amylase will digest insulin.
b. gastric acid and enzymes destroys insulin.
c. insulin cannot be absorbed in the small intestine.
d. insulin will be metabolised by the liver.

A

Gastric acid and enzymes destroys insulin - protein digesting enzymes destroy insulin.

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10
Q

Why can patients with type 1 DM not be treated with oral hypoglycaemic drugs?
a. hypoglycaemic drugs do not replace insulin.
b. in type 1 DM the pancrease must be stimulated to make insulin.
c. the BGL fluctuate to much to be controlled by oral drugs.

A

The hypoglycaemic drugs do not replace insulin.

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11
Q

How do we achieve the fastest rate of absorption of insulin?

A

If insulin is injected into the abdomen.

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12
Q

What molecule can you add to insulin to delay the onset of action?

A

A protein called protamine to the insulin molecule delays the onset of action and duration.

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13
Q

How is insulin transported in the body?

A

Through the blood after absorption.

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14
Q

Where is insulin metabolised?

A

In the liver, by breaking the bonds between A & B chains and then breaking them down further. Only 30-40% of the exogenous insulin is cleared by the liver.

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15
Q

What organ excretes insulin, and how much is excreted?

A

Around 60% of insulin is excreted by the kidneys.

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16
Q

Lipodystrophy is one minor side effect of insulin. What are two others?

A

Weight gain.
Infection at injection site.

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17
Q

Hypoglycaemia is one major effect of insulin. What are three others?

A

Insulin resistance
Allergic reaction
Hypokalaemia

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18
Q

Hypokalaemia may occur as a result of insulin therapy because?
a. insulin destroys potassium.
b. potassium moves into the cells together with glucose.
c. BGL have an inverse relationship with potassium levels.
d. potassium is required to breakdown insulin.

A

Potassium moves into the cells with glucose.

19
Q

How much insulin does the pancreas release per a day to maintain normal BGL?

A

Around 50units of insulin.

20
Q

Where should we store insulin?

A

In the fridge as it a protein.

21
Q

What is the difference in colour between insulin that is fast acting or has a delayed onset of action?

A

Fast acting - clear
Delayed onset of action - cloudy?

22
Q

Do we use insulin in an IV that is cloudy?

A

No, it must be clear.

23
Q

What parameters of a person influences the dose of insulin?

A

Persons weight, age, diet and lifestyle.

24
Q

Where can you administer Insulin that is injected via SC injection?

A

Into abdomen, thighs, upper arms or buttocks - avoid veins.

25
Q

What is the reason for rotating the injection site?
a. fluctuations in absorption rates.
b. lipodystrophy
c. micovascular disease at the injection site.
d. developing resistance to insulin

A

Lipodystrophy - is a disorder of the adipose tissue - complications of SC insulin injections and occurs because of repeated injections at the same site.

26
Q

True or false. Giving a bolus dose of insulin with a meal mimics the body’s natural rhythm of insulin release.

A

True. Endogenous insulin levels increase immediately after eating.

27
Q

why is insulin given through IV in emergency situations?
a. higher doses can be given
b. there are less side effects.
c. the onset of action is faster.
d. easier to adminster

A

The onset of action is faster.

28
Q

True or false. In older patients, the risk of hypoglycaemia is higher with the use of long acting insulin that with shorter acting preparations?

A

True.

29
Q

What are some drugs that increase BGL?

A

Beta2 agonists
Atypical antipsychotics
Triglyceride antidepressants
Glucocorticosteroids
Oral contraceptives
Thiazide diuretics
Thyroid and growth hormone

30
Q

What are some foods that increase BGL?

A

Processed foods
White rice, bread and pasta
Sugary drinks
maple syrup
honey

31
Q

What are some drugs that decrease BGLs?

A

Alcohol
ACE Inhibitors
Monoamine oxidase inhibitors
high doses salicylates
Dyrsrhythmic drugs
anabolic steroids
sulfonamides

32
Q

What are diagnostic tools for diabetes?

A

Random BGL of greater that 11.1mmol/L.
Fasting plasma glucose of >7
glycated haemoglobin (hbA1c) ?55mmol/L
Oral glucose tolerance test

33
Q

What is HbA1c?

A

Glycated haemoglobin.
It measures the amount of BG attachd to haemoglobin. This shows your average blood glucose over the last 3mths.
Normal 40mmol/mol or below.
Pre diabetes 41-49
Diabetes 50 or above

34
Q

Explain type 1 Dm pathophysiology?

A

caused by an autoimmune response to the beta cells of the pancreas, resulting in total loss of insulin production. If there is not enough insulin in the body, the glucose in the blood cannot enter the cells = results in hyperglycaemia.

35
Q

Why is there gluconeogenesis in the presence of hyperglycaemia in patients with DM?

A

Starving liver cells switch to gluconeogenesis as an energy source for metabolism.

36
Q

What is the pathophysiology of T2DM

A

Condition in which the cells develop an insulin resistance and therefore cannot uptake glucose into the cells. This would lead to hyperinsulinemia.

37
Q

Why would diabetics experience polyuria

A

Due to glucose induced osmotic diuresis due to being hyperglycaemic. Osmotic diuresis it the increased urination due to the presence of certain substances in the fluid filtered by the kidneys. The process of osmosis created by these substances cause additional water to come into urine, increasing its amount.

38
Q

Why do diabetics have impaired wound healing

A

Circulation of blood at the wound site it critical for wound healing. Diabetics can have damaged blood vessels due to excess blood glucose levels. This decreases elasticity of the blood vessels and causes them to narrow, impeding blood flow. This reduces the supply of blood and therefore less oxygen can reach the wound and the tissues cant heal as quickly.

39
Q

Why do diabetics experience polydipsia

A

Caused by loss in fluid therefore thirst response is activated.

40
Q

Why do diabetics experience polyphagia

A

The body cells are starving as they are unable to absorb glucose from the blood, therefore hunger is increased.

41
Q

What is an example of macrovascular damage by high blood glucose?

A

Atherosclerosis resulting in hypertension, MI or decreased cerebral perfusion.
Decreased immune responses impeding wound healing.

42
Q

Why would SOB indicate persistent hyperglycaemia in an acute presentation of a patient with T1DM

A

T1DM pts cannot synthesis insulin. If Their BGL’s remain high for too long without insulin, the cells become starved. The liver will metabolize fats for energy, with acidic ketones being a by-product. This would cause DKA. There would be respiratory compensation to try and restore normal pH and resp rate would increase.

43
Q

What are Kassmaul breaths

A

Rapid and deep breaths that indicate metabolic acidosis.

44
Q

Why would a milky drink not be used to treat hypoglycaemia

A

Fats would slow the metabolism of the sugars in milk. Lower fat content milk would raise BGL’s faster.

45
Q

What is the pathophysiology of diabetic ketoacidosis

A

When someone is hyperglycaemic, the cells are not receiving an adequate fuel source to produce energy and go into starvation mode. This triggers The liver to metabolize fats for energy where
Ketones are released as a by-product of fat being catabolised. Ketones are acidic therefore when they build-up in the blood it leads to a metabolic acidosis called diabetic ketoacidosis.

Multi Choice Exam BN3 (11 decks)

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