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Pharmacology > module 15 > Flashcards

module 15 Flashcards

1
Q

What is Diabetes

A
  • chronic disease characterized by elevated blood glucose
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2
Q

How is diabetes diagnosed

A

when untreated, blood glucose rises so high that proximal tubule kidney transporters are overwelmed
= large amounts of glucose found in urine

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3
Q

Causes of diabetes

A

1) not enough insulin produced in the body

2) body’s cells do not respond to the insulin that is produced

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4
Q

Common symptoms of diabetes (4)

A
  • polyuria
  • polydipsia
  • polyphagia
  • weight loss
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5
Q

Polyuria

A

increased urination

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6
Q

Polydipsia

A

Increased Thirst

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7
Q

Polyphagia

A

Increased hunger

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8
Q

What is insulin?

A

A hormone produced by the pancreas that is involved in tightly regulating blood glucose

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9
Q

Where is insulin synthesized

A

Beta cells of islets of Langerhans (pancreas)

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10
Q

Body’s (normal) response to insulin

A
  • causes glucose uptake into muscle, liver, fat cells
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11
Q

Insulin + liver cells

A

insulin causes glucose uptake –> glycogen synthesis (storage form of glucose)

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12
Q

Insulin + muscle cells

A

insulin causes glucose uptake –> glucose is used as energy and promotes protein synthesis

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13
Q

Insulin + fat cells

A
  • insulin causes increased synthesis of fatty acids, which results in increased triglyceride synthesis
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14
Q

Role of potassium and insulin

A
  • extracellular potassium = helps insulin to drive glucose into the cell
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15
Q

Normal Cycle of the pancreas (from food to blood sugar) (5)

A

1) stomach converts food to glucose
2) glucose enters bloodstream
3) Pancreas produces insulin
4) Glucose enters body effectively
5) glucose levels in balance

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16
Q

Types of Diabetes

A

1) type 1 diabetes
2) Type II diabetes
3) gestational diabetes

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17
Q

Type 1 Diabetes - prevalence

A

10% of diabetics are type I

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18
Q

Type 1 Diabetes - onset/diagnosis

A

usually in children or adolescence

symptoms may not appear until early adulthood

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19
Q

Type 1 Diabetes - cause

A

autoimmune reaction where the body’s own immune cells attack and destroy the insulin secreting beta cells

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20
Q

Type 1 Diabetes - insulin

A

body makes too little or no insulin at all and requires insulin replacement

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21
Q

Type 1 Diabetes - preventable?

A

not preventable…not caused by eating too much sugar

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22
Q

Type 1 Diabetes - cycle (food intake to blood sugar) = 5

A

1) stomach converts food to glucose
2) glucose enteres blood
3) pancreas produces little or no insulin
4) glucose unable to enter body effectively
5) glucose levels increase

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23
Q

Type II Diabetes - prevelance

A

approx 90% of diabetics are type II

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24
Q

Type II Diabetes - cause

A
  • pancreas produces sufficient insulin, however, insulin produced is resistant to use
  • over course of disease, insulin synthesis may also decrease
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25
Q

Type II Diabetes - risk factors (7)

A
  • age
  • family member with diabetes
  • previous gestational diabetes
  • lack of excercise
  • heart disease
  • obesity (80% with type II are overweight)
  • ethnicity (african and native descent have greater risk)
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26
Q

Type II Diabetes - age of onset

A

typically later in life, but is trending toward younger people getting the disease

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27
Q

Type II Diabetes - cycle from food to blood glucose (5)

A

1) stomach converts food to glucose
2) glucose enters bloodstream
3) pancreas produces sufficient insulin but it is resistant to effective use
4) glucose unable to enter body effectively
5) glucose levels increase

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28
Q

Gestational Diabetes

A
  • diabetes that first starts during pregnancy
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29
Q

Gestational Diabetes - onset

A

usually begins approx halfway through pregnancy

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30
Q

Gestational Diabetes - diagnosis

A
  • women shoudl have oral glucose tolerance test between weeks 24 and 28 of pregnancy to test for gestational diabetes
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31
Q

Gestational Diabetes - treatment

A
  • usually diet and exercise are sufficient to keep blood glucose levels within normal ranges
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32
Q

Gestational Diabetes - impact on fetus

A
  • tent to have larger babies + babies with hypoglycemia in the first days of life
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33
Q

Gestational Diabetes - after delivery

A
  • blood sugar of mother usuallly returns to normal

- blood glucose should be continually monitored as many patients develop diabetes 5-10 years later

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34
Q

Complications of diabetes mellitus (11)

A
  • cognitive impairment
  • depression
  • cerebrovascular disease
  • visual impairment
  • cardiovascular disease
  • nephropathy
  • weight loss
  • urinary incontinence
  • peripheral vascular disease
  • peripheral neuropathy
  • foot ulcer
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35
Q

Diabetic retinopathy - what/frequency

A
  • most common cause of blindness in people under age 65
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36
Q

Diabetic retinopathy - cause

A
  • hyperglycemia causes damage to retinal capillaries
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37
Q

Diabetic retinopathy - prevention

A
  • tightly controlling blood sugar minimizes risk of retinopathy
  • Patients with type 1 or 2 diabetes should have eye exam once a year
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38
Q

Diabetic nephropathy

A
  • characterized by proteinuria (early sign), decreased glomerular filtration, increased blood pressure
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39
Q

Proteinuria

A

protein in the urine

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40
Q

Diabetic retinopathy - impact

A
  • leading cause of morbidity and mortality in patients with type I diabetes
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41
Q

Diabetic retinopathy - prevention

A
  • tight control of blood glucose both delays and reduces severity of diabetic nephropathy
  • ACE inhibitors and ARBs are useful in preventing diabetic retinopathy = take even if the client has a normal BP
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42
Q

Cardiovascular Disease (Diabetes)

A
  • CVD = heart attack + stroke
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43
Q

Cardiovascular Disease (Diabetes) - impacts

A
  • leading cause of morbidity and mortality in type II diabetes
  • atherosclerosis develops much earlier in diabetic patients than in non-diabetics
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44
Q

Cardiovascular Disease (Diabetes) - cause

A
  • combo of
    • hyperglycemia
    • altered lipid metabolism
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45
Q

Cardiovascular Disease (Diabetes) - prevention

A

Statins reduce cardiovascular events in diabetic patients regardless of LDL cholesterol levels

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46
Q

Diabetic Foot Ulcers - impact

A
  • most common cause of hospitalization for diabetic patients

- diabetes accounts for half of all lower limb amputations every year due to infection

47
Q

Diabetic Foot Ulcers - prevention

A

all diabetics should have regular foot exams

48
Q

Diabetic Foot Ulcers - impact of diabetes (3)

A
  • Diabetes causes nerve damage –> decrease ability to feel pain, heat, cold in foot
  • Poor circulation –> decreased blood flow –> decreased ability to heal and fight infection
  • nerves controlling oil and moisture –> impair skins ability to be moist = dry cracking skin
49
Q

Diagnosis of Diabetes (4)

A

1) Fasting Plasma Glucose Test
2) Casual Plasma Glucose Test
3) Oral Glucose Tolerance Test (OGTT)
4) *** Glycosylated Hemoglobin

50
Q

Fasting Plasma Glucose Test (what, normal values)

A
  • patients fast for at least 8 hours and then have blood drawn to measure blood glucose
  • if fasting plasma glucose is > or = to 7.0 mmol/L then diabetes is diagnosed
  • prefered test for diagnosing diabetes
51
Q

Casual Plasma Glucose Test (what, normal values)

A
  • blood drawn at any time no matter interval since last meal
  • diagnose diabetes - plasma glucose greater than 11.1 mmol/L AND patient displays signs of diabetes (polyuria, polydipsia, weight loss)
  • positive plasma glucose test = follow up with fasting plasma glucose test
52
Q

Oral Glucose Tolerance Test (OGTT) (what, normal values)

A
  • Used when other tests are unable to definitively diagnose diabetes
  • Patients are given oral 75 gram dose of glucose and plasma clucose is measured 2 hours later
  • Plasma glucose > or = to 11.1 mmol/L then the patients will be diagnosed with diabetes
53
Q

Glycosylated Hemoglobin

A
  • when upon prolonged exposure in the blood, glucose interacts with hemoglobin to form glycosylated derivatives (HbA 1C)
  • Useful in providing an index of the average blood glucose over previous 2-3 months
  • good determinant of how well a patient is responding to therapy
  • target level = HbA 1C of <7% of total hemoglobin
54
Q

Treatment Goals of Diabetes

A
  • maintain tight control of plasma glucose levels
  • Tight Control = normal range for entiere day
  • pre meal, peak post meal glucose goals
55
Q

Pre-meal plasma glucose goal

A

4.0 - 7.0 mmol/L

56
Q

Peak post-meal glucose (#)

A

is 5.0 - 10 mmol/L

57
Q

HbA 1C goal

A

<7%

58
Q

Other treatment goals of Diabetes - cardiovascular

A
  • BP <130 systolic, <80 diastolic

- lipids = LDL <2.6 mmol/L, triglycerides <1.7 mmol/L, HDL (men) >1.0 mmol/L, HDL (women) >1.3 mmol/L

59
Q

Other treatment goals of Diabetes - kidney

A

Urine albumin to creatinine ration <30 mg/g (albumin/creatinine)

60
Q

Lifestyle Modifications - Type 1 Diabetes - Diet

A
  • type 1 diabetes patients = thin, GOAL = maintain weight

- split total caloric intake throughout the day with meals 4-5 hours apart

61
Q

Lifestyle Modifications - Type 1 Diabetes - Exercise

A
  • exercise increases cellular response to insulin + increases glucose tolerance
  • encourage patients to exercise
  • strenuous exercise may cause hypoglycaemia = close patient oversight
62
Q

Lifestyle Modifications - Type 1 Diabetes - Insulin

A
  • insulin required for survival

- monitor blood glucose 3 or more times per day

63
Q

Lifestyle Modifications - Type II Diabetes - Diet

A
  • dietary modification alone (caloric restriction) often normalizes insulin release and decreases insulin resistance
  • patients with type II dibetes are often obese so losing weight is a treatment goal
64
Q

Lifestyle Modifications - Type II Diabetes - Excercise

A

Exercise stimulates glucose uptake and should be encouraged

65
Q

Insulin - metabolic actions (general)

A
  • is anabolic (building up or conservative)

- promote energy storage and conservation

66
Q

Insulin’s anabolic actions (5)

A
  • cellular uptake of glucose into liver, muscle, fat
    • glucose uptake results from formation of glycogen (liver + muscle) and
      triglycerides (adipose tissue)
  • Decreased hepatic gluconeogenesis (glucose synthesis)
  • cellular uptake of amino acids (mostly muscle)
    • amino acid uptake results in increased protein synthesis
67
Q

Insulin deficiency

A
  • puts the body into a catabolic (“breaking down” state)
  • body favours breakdown of complex molecules into simpler substances
  • these effects contribute to diabetes
68
Q

Insulin Deficiency - catabolic effects (3)

A
  • glycogenolysis
  • gluconeogenesis
  • decreased glucose utilization
69
Q

Glycogenolysis

A

conversion of glycogen to glucose

70
Q

gluconeogensis

A

new glucose synthesis

71
Q

Insulin Therapy - categories (4)

A
  • short duration-rapid acting
  • short duration-slower acting
  • intermediate duration
  • long duration
72
Q

Short Duration Rapid Acting Insulin - types (3)

A
  • Insulin lispro
  • Insulin aspart
  • insulin glulisine
73
Q

Short Duration Rapid Acting Insulin - when used

A
  • in association with meals to control postprandial (after eating) rise in glucose
74
Q

Postprandial

A

after eating

75
Q

Short Duration Rapid Acting Insulin - route of administration

A

subcutaneous (may be used IV if required)

76
Q

Short Duration Rapid Acting Insulin - appearance

A

clear solution

77
Q

Short Duration Slower Acting Insulin - type(s)

A
  • unmodified human insulin
78
Q

Short Duration Slower Acting Insulin - when used

A
  • injected before meals to control postprandial rises in glucose
79
Q

Short Duration Slower Acting Insulin - route of administration

A
  • subcutaneously

- IM (rare)

80
Q

Short Duration Slower Acting Insulin - pathophysiology

A
  • after injection, insulin molecules form small aggregates (dimers) which slows absorption
81
Q

Short Duration Slower Acting Insulin - formulation

A
  • clear solution
82
Q

Intermediate Duration Insulin - types

A
  • Neutral Protamine Hormone (NPH) insulin

- Insulin Detemir

83
Q

Intermediate Duration Insulin - uses

A
  • delayed onset = can’t be used at mealtime to control postprandial rises in blood glucose
  • injected once or twice daily to control blood glucose between meals and in the evening
84
Q

Intermediate Duration Insulin - why is action delayed for NPH insulin?

A
  • insulin is conjugated to protamine (large protein) which makes the molecule less soluble and decreases the absorption
85
Q

Intermediate Duration Insulin - why is the action delayed Insulin Determir

A

Insulin detemir molecules bind strongly to each other which delays absorption

86
Q

Intermediate Duration Insulin - route of administration

A

subcutaneous injection

87
Q

Intermediate Duration Insulin - appearance - NPH insulin

A
  • cloudy suspension
88
Q

Intermediate Duration Insulin - appearance - insulin detemir

A

clear solution

89
Q

Long Acting Insulin - type(s)

A
  • Insulin glargine
90
Q

Long Acting Insulin - use

A
  • long duration of action - administered once daily at bedtime
91
Q

Long Acting Insulin - route of administration

A

subcutaneous injection

92
Q

Long Acting Insulin - why is it a long duration of action

A
  • low solubility at physiological pH (injected it forms microprecipitates that slowly dissolve and slowly release insulin glargine in small amounts over an extended time)
93
Q

Long Acting Insulin - formulation

A

clear solution

94
Q

Glucagon

A
  • hormone produced by pancreas

- causes conversion of glycogen to glucose, reverses hypoglycemia

95
Q

Glucagon - uses (3)

A
  • when a hypoglycaemic patient is unconscious (once patient regains consciousness you should use oral sugar solution)
  • IV glucose is prefered to glucagon but is impractical outside medical supervision
  • ineffective in starving/malnourished patients (as they do not have any glycogen stores)
96
Q

Oral Antidiabetic Drugs - target disease

A
  • type 2 diabetes
97
Q

Oral Antidiabetic Drugs - classes (6)

A
  • biguanides
  • sulfonylureas
  • meglitinides
  • thiazolidinediones (glitazones)
  • alpha-glucosidase inhibitors
  • gliptins
98
Q

Biguanides

A
  • drug of choice for type II diabetes
99
Q

Biguanides - mechanism of action (3)

A

1) increase sensitivity and number of insulin rceptors
2) decrease hepatic gluconeogenesis
3) decrease intestinal glucose absorption

100
Q

Biguanides - advantage

A

does not increase insulin levels = no risk of hypoglycemia

101
Q

Biguanides - adverse effects (5)

A
  • nausea
  • decreased apetite
  • diarrhea
  • decreased absorption of vitamin B12 and folic acid
  • lactic acidosis (rare, but mortality of 50% in those who get it)
102
Q

Sulfonylureas - mechanism of action

A
  • act by stimulating release of insulin from pancreas

- inhibit glycogenolysis (breakdown of glycogen to glucose

103
Q

Sulfonylureas - Classes, and differences between classes

A

1st generation and 2nd generation

- difference =2nd generation are much more potent and cause fewer drug interactions

104
Q

Sulfonylureas - adverse effects (2)

A
  • hypoglycemia

- prolonged use –> pancreatic burnout (pancreas has reduced capacity to synthesize insulin)

105
Q

Meglitinides - mechanism of action

A
  • stimulate insulin release form the pancreas
  • short half life (treat postprandial rises in glucose
  • less likely to cause hypoglycemia
  • less likely to cause pancreatic burnout
106
Q

Meglitinides - adverse effects

A
  • less likely to cause hypoglycemia than sulfonylureas

- less likely to cause pancreatic burnout

107
Q

Thiazolidinediones (Glitazones) - mechanism of action (4)

A
  • increasing insulin sensitivity in target tissues and decreasing hepatic gluconeogenesis
  • activate the PPAR(gamma) receptor (intracellular) –> turns on genes that regulate carb metabolism –> increases sensitivity of insulin by increasing number of glucose transporters
  • also increase HDL and decrease triglyceride level via activation of PPAR(alpha)
108
Q

Alpha-glucosidase inhibitors - mechanism of action

A
  • act in intestine to delay carbohydrate absorption
    • blocks alpha glucosidase (enzyme in intestine that breaks down carbs
      to monosaccharides) –> decrease in carbohydrate metabolism
109
Q

Gliptin - mechanism of action

A
  • inhibit an enzyme called dipeptidyl peptidase 4 (DPP-4)
    • DPP-4 breaks down incretin hormones GLP-1 and GIP
    • Incretin hormones are released from GI tract after a meal and cause
      increased release of insulin and decreased release of glucagon
  • inhibit DPP-4 –> more GLP-1 adn GIP reach pancreas = increased insulin release and suppression of glucagon release
110
Q

Gliptin - adverse effects

A

no known major adverse effects

111
Q

Incretin Mimetics - mechanism of action

A
  • synthetic incretin analogs that mimic actions of incretin hormones
  • increase in insulin release, decrease in glucagon relase
112
Q

Incretin mimetics - route of administration

A

subcutaneous injection

113
Q

incretin mimetics - use

A

in combination with biguanides or sulfonylureas

Pharmacology (6 decks)

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