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NUR370 Pathophysiology and Pharmacology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Functions of Insulin

A
  • hormone and control of carbohydrate, lipid and protein metabolism
  • allows glucose to enter cells and converted into energy
  • allows glucose uptake, metabolism and storage of glucose as glycogen
  • facilitates transport of potassium, phosphate and magnesium into cells
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2
Q

Type 1 Diabetes

A

5-10% of all cases

characterized by destruction of beta cells of the pancreas by body’s own T-cells, causing inability to produce insulin

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3
Q

How does T1DM cause hyperglycemia?

A

without insulin, glucose is present in the blood but unable to enter cells for utilization

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4
Q

Clinical manifestations of T1DM

A

Polyphagia
(excessive hunger)

Polydipsia
(excessive thirst)

Polyuria
(frequent urination)

Glucosuria
(excretion of glucose in urine)

Fatigue

Weight loss

Blurred vision

Ketonuria

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5
Q

What are the two major metabolic abnormalities associated with T2DM?

A

Insulin Resistance

  • inability of muscle and fat tissues to increase glucose uptake
  • metabolic syndrome
  • reduced glycogen synthesis and storage in liver
  • failure to suppress glucose production
  • hyperinsulinemia

Insulin Deficiency

  • beta cells become fatigued and less efficient
  • produced insulin is insufficient or poorly utilized
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6
Q

Four methods of diagnosis using plasma glucose testing

A
  1. A1C > 6.5%
  2. Fasting plasma glucose level >= 7 mmol/L
  3. Two hour OGTT level >= 11.1 mmol/L when glucose load of 75g is used
  4. Random or casual plasma glucose measurement >= 11.1 mmol/L
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7
Q

Goals of diabetes management

A

a. Normalize blood sugars
b. Prevent/resolve symptoms
c. Prevent acute and chronic complications
d. Avoid negative sequelae of therapy (i.e. hypoglycemia - too much insulin!)

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8
Q

Nutritional therapy for T1DM

A
  • Meal plan is based on individual’s usual food intake and is balanced with insulin and exercise patterns
  • Insulin regimen is managed day to day
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9
Q

Nutritional therapy for T2DM

A
  • Emphasis is based on achieving glucose, lipid and blood pressure goals
  • Calorie reduction
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10
Q

Diabetic Ketoacidosis

A

caused by profound deficiency of insulin

Insufficient insulin shifts carbohydrate metabolism to fat and protein metabolism to produce energy
Body breaks down fat stores causes:
- Ketones are byproducts of fat metabolism
- Alter pH balance, causing metabolic acidosis
- Ketone bodies excreted in urine
- Electrolytes become depleted

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11
Q

Precipitating factors of DKA

A
  • Acute illness
  • Infection
  • Inadequate insulin dosage
  • Undiagnosed Type 1
  • Poor self-management
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12
Q

Clinical manifestations of DKA

A

a. Glucose level of 16-42 mmol/L
b. Polyuria, polydipsia
c. Fruity/acetone odour of ketones on breath
d. Lethargy/weakness (early symptoms)
e. Dehydration
f. Abdominal pain
g. Kussmaul’s Respirations

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13
Q

Kussmaul’s Respirations

A
  • Initially breathing is deep and rapid - hyperventilation
  • As acidosis worsens, breathing gradually becomes deep, slow, laboured and gasping

Associated with severe metabolic acidosis or diabetic ketoacidosis

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14
Q

Managment of DKA

A

a. treat promptly
b. airway management
c. rehydration and correction of acid-base and fluid imbalances
d. restore state of carbohydrate catabolism
e. identify and correct precipitating factors

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15
Q

Hyperosmolar Hyperglycemic Syndrome (HHS)

A
  • life threatening, medical emergency
  • results from any illness or condition that leads to dehydration or inadequate food intake
  • ketoacidosis does NOT occur
  • hyperglycemia leads to osmotic diuresis
  • High glucose plus high sodium and urea lead to high serum osmolarity and subsequent intracellular dehydration
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16
Q

Clinical manifestations of HHS

A

a. Decreased LOC
b. Polyuria, polydipsia
c. Hypovolemia, profound dehydration

d. blood glucose >34 mmol/L
e. increase in serum osmolality
f. absent/minimal ketone bodies

17
Q

Hypoglycemia

A

low blood glucose of <4 mmol/L

occurs when too much insulin in proportion to glucose in blood

18
Q

Manifestations of Hypoglycemia

A 
Anxiety, nervousness
Diaphoresis
Tremors
Hunger
Pallor
Palpitations
19
Q

Somogyi Effect

A

Hypoglycemia induced by insulin causes body to break down glycogen causing hyperglycemia

BG level is low at 2-4am

Requires reduction of insulin dosage

20
Q

Dawn phenomenon

A

rise in blood sugar between 4-8am caused by overnight release of counter-regulatory hormones

BG level is normal or high at 2-4am

Requires insulin timing adjustment or increase in insulin

21
Q

Macrovascular Complications of Diabetes

A

a. coronary artery disease
b. hypertension
c. cerebrovascular disease
d. peripheral vascular disease

22
Q

Microvascular Complications of Diabetes

A

specific to diabetes

a. diabetic retinopathy
b. diabetic nephropathy
c. diabetic neuropathy

23
Q

What are the conditions used to screen for metabolic syndrome?

A
  • high fasting BG (>5.6 mmol/L)
  • high bp (>130/85)
  • high levels of triglycerides (>1.7 mmol/L)
  • low levels of HDL (<1.0-1.3 mmol/L)
  • abdominal obesity
24
Q

Hormone that increases glucose in blood

A

Glucagon

25
Q

Counter-regulatory hormones (CRH) (4)

A
  1. glucagon
  2. epinephrine
  3. growth hormone
  4. cortisol
26
Q

2 mechanism of hepatic glucose production

A
  1. Glycogenolysis: breakdown of glycogen into glucose

2. Gluconeogenesis: synthesis of glucose from breakdown of proteins or TG

27
Q

What are the ABCDES of DM?

A 
A1C
Bp
Cholesterol
Drugs to protect heart
Exercise/eating
Smoking cessation
28
Q

Therapeutics of glycemic control

A

a. diet
b. exercise
c. oral hypoglycemic agents
d. insulin

29
Q

Glycemic Targets

A

A1C <= 7.0%
Preprandial (fasting) PG = 4.0-7.0mmol/L
2hr postprandial PG = 5.0-10.0mmol/L
(5.0-8.0mmol/L if A1C not at target)

30
Q

Drugs that cause hyperglycemia

A 
Corticosteroids
Diuretics (i.e. thiazides)
Protease inhibitors
Sympathomimetics
Cyclosporine, tacrolimus
phenytoin
31
Q

Drugs that complicate hypoglycemia management

A

Alcohol

Beta-blockers by masking symptoms (blunt rapid heart rate)

32
Q

Symptoms of hypoglycemia

A

Tremor, weakness, palpitations, tachycardia, sweating, tingling lips, hunger, blurred vision, agitation
Nightmares, restless sleep, morning HA or hangover

33
Q

What complication can arise when diabetic patient has an infection?

A

stress can cause the release of CRH, which predisposes one to hyperglycemia

34
Q

Which regimen has best prandial and fasting control?

A

Basal-bolus insulin (intensive)

  • rapid/regular controls prandial BG
  • long acting controls overnight and between meal fasting
35
Q

Which type of diabetes is basal-bolus most recommended for?

A

T1DM

36
Q

What is the effect of exercise and insulin?

A

Exercise increases insulin sensitivity during and after
- risk of hypoglycemia

especially with T1DM

37
Q

Management strategies for patients with DM exercising

A
  • extra carbohydrate consumption

- reduce pre-meal bolus insulin dose and basal insulin infusion rate

38
Q

Which non-insulin agents reduce glucose production in the liver?

A

a. metformin
b. glitazones
c. DPP-4 inhibitors
d. GLP-1 agonists

39
Q

Patient Education regarding SMBG

A
  1. How and when to perform SMBG
  2. How to record the results
  3. Meaning of various BG levels
  4. How behaviour and actions affect SMBG results

NUR370 Pathophysiology and Pharmacology (20 decks)

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