Glucose Regulation Flashcards

1
Q

Glucose Regulation

A

The process of maintaining optimal blood glucose levels

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2
Q

The ultimate end result of glucose metabolism is…

A

Cellular use of glucose for energy synthesis

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3
Q

Endocrine system Functions

A

Differentiation of reproductive system and CNS in fetus
Stimulation of growth and development
Coordination of the male and female reproductive systems
Maintenance of internal environment
Adaptation to emergency demands of body

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4
Q

Normal insulin metabolism

A
  1. produced by the B cells
  2. Released continuously into the bloodstream in small increments with larger amounts released after food
  3. Stabilizes glucose range 4-6 mmol/L
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5
Q

Hypoglycemia

A

State of insufficient or low Blood glucose levels, defined as less than 4 mmol/L

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6
Q

Hyperglycemia

A

State of elevated blood glucose levels, defined as more than 6-8 mmol/L when not fasting

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7
Q

Insulin is synthesized from

A

proinsulin

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8
Q

Insulin secretion is promoted by…

A

Increased blood glucose levels, amino acids and GI hormones

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9
Q

Insulin facilitates …

A

the rate of glucose uptake into the cells of the body

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10
Q

Amylin

A

Peptide hormone co secreted with insulin

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11
Q

Amylin delays

A

Nutrient uptake

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12
Q

Amylin suppresses

A

Glucagon secretion

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13
Q

Glucagon secretion is promoted by

A

Decreased blood glucose levels

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14
Q

Glucagon stimulates

A

Glycogenolysis, gluconeogenesis, and lipolysis

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15
Q

Pancreatic somatostatin

A

Possible involvement in regulating alpha-cell and beta-cell secretions

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16
Q

Hormone to lower glucose

A

Insulin

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17
Q

Counterregulatory hormones to raise glucose

A

Glucagon

Cortisol

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18
Q

Diabetes

A

A chronic multi system disease related to abnormal insulin production, Impaired insulin utilization, or both

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19
Q

links to diabetes

A

Genetic
Autoimmune
Viral
Environmental

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20
Q

Two most common types of diabetes

A

Type 1

Type 2

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21
Q

Other types of diabetes

A

gestational
Prediabetes
Secondary diabetes

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22
Q

Insulin promotes

A

Glucose transport from bloodstream across cell membrane to cytoplasm of cell
Decreases glucose in the bloodstream

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23
Q

After a meal insulin…

A

Increases

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24
Q

After a meal insulin stimulates storage of …

A

glucose as glycogen in the liver and muscle

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25
Q

after a meal insulin inhibits

A

glyconeogenesis

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26
Q

after a meal insulin enhances

A

fat deposition

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27
Q

increase in protein synthesis happens …

A

after a meal

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28
Q

skeletal muscle and adipose tissue are…

A

insulin dependent tissue

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29
Q

Insulins function as a…

A

substitute for the endogenous hormone

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30
Q

Insulin restores the pt ability to

A

Metabolize carbohydrates, fats and proteins
Store glucose in the liver
Convert glycogen to fat stores

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31
Q

Common Diagnostic tests

A
Glucose screening
assess antibodies to confirm type 1 diabetes mellitus 
Lipid analysis
Microalmuninuria
C-reactive protein
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32
Q

Glycemic goal of treatment

A

HbA1c of less than 7%

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33
Q

Fasting Blood glucose goal for diabetic patients

A

4-7mmol/L

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34
Q

2 hour postprandial target of…

A

5-10mmol/L

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35
Q

Type 1 diabetes mellitus

A

Formerly known as juvenile onset or insulin dependent diabetes

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36
Q

End result oflongstanding process of type 1 diabetes mellitus

A

progressive destruction of pancreatic B cells by body’s own T cells

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37
Q

Causes of type 1 diabetes mellitus

A

Genetic predisposition - related to human leukocyte antigens
Exposure to a virus

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38
Q

Type 1 diabetes mellitus has a long ______ period

A

Preclinical period

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39
Q

With Type 1 diabetes mellitus antibodies are present _________ befit symptoms occur

A

Months to year

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40
Q

Diabetic ketoacidosis

A

Occurs in absence of exogenous insulin
Life threatening disease
Results in metabolic acidosis

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41
Q

Classic symptoms of Type 1 diabetes mellitus

A
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
weakness
fatigue
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42
Q

Pre diabetes

A

Individuals already at risk for diabetes

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43
Q

In prediabets Blood glucose is…

A

High but not high enough to be diagnosed as having diabetes

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44
Q

Prediabets is characterized by

A

Impaired fasting glucose (IFG)

Impaired glucose tolerance (IGT)

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45
Q

IFG & IGT for prediabetes

A

IFG 6.1-6.9mmol/L

IGT 7.1-11mmol/L

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46
Q

Prediabets is usually present with …

A

No symptoms

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47
Q

Type 2 Diabetes mellitus is the…

A

most prevalent type of diabetes

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48
Q

With Type 2 Diabetes mellitus pancreas still.

A

produces some endogenous insulin

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49
Q

The most powerful risk factor for Type 2 Diabetes mellitus is

A

obesity

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50
Q

Type 2 Diabetes mellitus genetic mutations

A

lead to insulin resistance

Increased risk for obesity

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51
Q

Type 2 Diabetes mellitus Four major metabolic abnormalities

A
  1. Insulin resistance
  2. Pancreas decreased ability to produce insulin
  3. Inappropriate glucose production from liver
  4. Alteration in production of hormones and adipokines
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52
Q

Insulin resistance

A

Body tissues do not respond to insulin
Insulin receptors are either unresponsive or insufficient in number
Results in hyperglycaemia

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53
Q

Pancreas decreased ability to produce insulin

A

B cells fatigued from compensating

B cell mast lost

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54
Q

Inappropriate glucose production from liver

A

Liver response of regulating release of glucose is haphazard

Not considered a primary factor in Development of type 2

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55
Q

Alteration in production of hormones and adipokines

A

Play a role in glucose and fat metabolism

- contribute to pathophysiology of type 2 diabetes

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56
Q

Two main adipokines

A

Adiponectin and leptin

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57
Q

Individuals with metabolic syndrome are at an increased risk for…

A

Type 2 diabetes mellitus

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58
Q

Cluster of abnormalities increase risk for…

A

Cardiovascular disease and diabetes

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59
Q

Risk Factors for type 2 Diabetes mellitus

A

Abdominal obesity
sedentary lifestyle
Urbanization
Certain ethnicities

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60
Q

Gestational Diabetes

A

Diabetes that develops during pregnancy

Detected 24-28 weeks

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61
Q

When do glucose levels return to normal in gestational diabetes

A

6 weeks postpartum

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62
Q

Gestational Diabetes increased risks

A
Birth trauma
Hypoglycemia
Hyperbilirubinemia
Respiratory distress syndrome 
Increased risk for developing type 2 diabetes in 5-10 years
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63
Q

Therapy for gestational diabetes

A

First- Nutritional

Second- Insulin

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64
Q

Secondary Diabetes

A

Treatment of a medical condition that causes abnormal blood glucose levels

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65
Q

Drugs that can cause secondary Diabetes

A

Corticosteroids (prednisone)
Phenytoin (Dilantin)
Atypical antipsychotics (Clozapine)

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66
Q

Secondary diabetes usually resolves when..

A

The underlying condition is resolved

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67
Q

Secondary Diabetes can result from these conditions

A
Schizophrenia
Cushings syndrome 
Hyperthyroidism 
Immune suppressive therapy
Parentarel nutrition
Cystic Fibrosis
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68
Q

Diabetes mellitus four methods of diagnosis

A
  1. HbA1C >= 6.5%
  2. Fasting plasma glucose level >= 7mmol/L
  3. Random or casual plasma glucose measurement >= 11.1 mmol/L plus classic symptoms
  4. Two hour OGTT level >= 11.1mmol/L when a glucose load of 75 g is used
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69
Q

Hemoglobin A1C test

A

determines glucose levels over time

Shows the amount of glucose attached to hemoglobin molecules over RBC lifespan

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70
Q

Normal A1C reduces risks of

A

Retinopathy
Nephropathy
Neuropathy

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71
Q

Diabets Mellitus Goals of management

A

Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of long-term complications

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72
Q

Type 1 therapy

A

Insulin

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73
Q

Type 2 Therapy

A

Lifestyle changes
Oral drug therapy
Insulin when nothing else can provide glycemic control

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74
Q

Insulins function as a substitute for..

A

The endogenous hormone

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75
Q

Insulin restores the diabetic clients ability to:

A

Metabolize carbohydrates, fats and protein
Store glucose in the liver
Convert glycogen to fat stores

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76
Q

Exogenous Insulin

A

Insulin from an outside of body source

Required for type 1 diabetes

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77
Q

Human insulin

A

derived using recombinant deoxyribonucleic acid technologies

Recombinant insulin produced by bacteria and yeast

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78
Q

Insulin as a rapid acting treatment for..

A

Type 1 & 2 diabetes

79
Q

Insulin Most rapid onset of action

A

10-15 min

80
Q

Insulin peak

A

1-2 hours

81
Q

Insulin duration

A

3-5 hours

82
Q

with insulin the pt must_______ after injection

A

eat a meal

83
Q

Lispro (Humalog)

A

Action similar to that of endogenous insulin

84
Q

Short acting insulins

A

Humulin R

Novolin ge Toronto

85
Q

Short acting routes of administration

A

IV Bolus
IV infusion
IM
Subcutaneous

86
Q

Short acting insulin onset of subcutaneous route

A

30 min

87
Q

Short acting insulin peak of subcutaneous route

A

2-3 hours

88
Q

Short acting insulin duration of subcutaneous route

A

6.5 hours

89
Q

Intermediate acting insulins

A

Insulin isophane suspension (NPH)

Often combined with regular insulin

90
Q

Intermediate acting insulins onset

A

1-3 hours

91
Q

Intermediate acting insulins Peak

A

5-8 hours

92
Q

Intermediate acting insulins duration

A

up to 18 hours

93
Q

Long acting insulins

A

insulin glargine (Lantus)

94
Q

Insulin Glargine (Lantus)

A

clear, colourless solution

Constant level of insulin in the body

95
Q

Lantus can be dosed

A

Once a day, every 12 hours

96
Q

Lantus also referred to as

A

Basil insulin

97
Q

Lantus onset

A

90 min

98
Q

Lantus peak

A

none

99
Q

Lantus duration

A

24 hr

100
Q

Fixed combination insulins

A

contains 2 different insulins, fixed combination

101
Q

Fixed combination insulins

A
Humulin 30/70
Novolin 30/70, 40/60, 50/50
Novomix 30
Humalog Mix25
Humalog Mix50
102
Q

Two types of insulin included in fixed combination insulins

A
  1. Intermediate acting type

2. Either a rapid acting or a short acting

103
Q

Sliding- scale insulin Dosing

A

Subcutaneous rapid acting or short acting insulins are adjusted according to blood glucose test results
Subcutaneous insulin is ordered in an amount that increases as the blood glucose increases

104
Q

Sliding- scale insulin Dosing Disadvantages

A

Delays insulin administration until hyperglycaemia occurs, resulting in large swings in glucose control

105
Q

Basal-Bolus insulin dosing

A

Mimics a healthy pancreas by delivering basal insulin constantly as a basal and then as needed as a bolus

106
Q

Basal insulin is a _______insulin

A

long acting

107
Q

Insulin pump

A

Continuous subcutaneous infusion
Battery operated device
Connected via a plastic tubing to a catheter inserted into subcutaneous tissue in the abdominal wall

108
Q

Problems with Insulin therapy

A
Hypoglycemia
allergic reaction
lipodystrophy
somogyi effect
Dawn phenomenon
109
Q

Somogyi effect

A

Rebound effect in which an overdose of insulin causes hypoglycemia Usually occurs during sleep
Rebound hyperglycemia and ketosis may occur

110
Q

Dawn phenomenon

A

Characterized by hyperglycaemia present on awakening in the morning
Due to release of counter regulatory hormones in predawn hours
Growth hormone/ Cortisol possible factors

111
Q

Pharmacotherapy oral agents

A

not insulin

work to improve mechanisms by which insulin and glucose are produced and used by the body

112
Q

Oral agents work on 3 defects of type 2 diabetes

A

Insulin resistance
Decreased insulin production
Increased hepatic glucose production

113
Q

Types of oral agents

A
Sulphonylureas
Meglitinides
Bigunaides
a-glucosidase inhibitors
Thiazolidinediones
114
Q

Sulphonylureas increase

A

Insulin production from pancreas

115
Q

Sulphonylureas Decrease

A

chance of prolonged hypoglycemia

116
Q

Examples of Sulphonylureas

A

Giclazide (Diamicron, Diamicron MR)

Glimepirdie (Amaryl)

117
Q

Meglitinides increase

A

insulin production from the pancreas

118
Q

Meglitinides should be taken how many minutes before a meal

A

30 min

119
Q

Meglitinides should not be taken when

A

a meal is skipped

120
Q

Examples of Meglitinides

A

Repaglinide (GlucoseNorm)

121
Q

Biguanides Reduce

A

glucose production by liver

122
Q

Biguanides Enhance

A

Insulin sensitivity at tissues

123
Q

Biguanides improve

A

Glucose transport into cells

124
Q

Biguanides examples

A

Metformin (Glucophage)

125
Q

a-Glucosidase inhibitors

A

Starch blockers

Slow down absorption of carbohydrate in small intestine

126
Q

a-Glucosidase inhibitors Example

A

Acarbose (Glucobay)

127
Q

Thiazolidinediones

A

Improve insulin sensitivity, transport, and utilization at target tissues

128
Q

Thiazolidinediones most effective in

A

those with insulin resistance

129
Q

Thiazolidinediones examples

A

Pioglitazone (Actos)

Rosiglitazone (Avandia)

130
Q

Dipeptidyl peptidase - 4 inhibitor (DDP-4)

A

Slows the inactivation of incretin hormones

131
Q

Dipeptidyl peptidase - 4 inhibitor (DDP-4) adverse effects

A

potential for hypoglycemia

132
Q

Dipeptidyl peptidase - 4 inhibitor (DDP-4) Examples

A

Sitagliptin (Januvia)

Saxagliptin (Onglyza)

133
Q

Other pharmacotherapy Agents

A

Glucagon-like peptide 1 receptor agonists
B- adrenergic blockers
Thiazide/ loop diuretics

134
Q

Glucagon-like peptide 1 receptor agonists

A
Synthetic peptide
Stimulates release of insulin from B cells
Suppress glucagon secretion 
Reduces food intake 
Slows gastric emptying 
Not to be used with insulin
135
Q

Glucagon-like peptide 1 receptor agonists examples

A

Liraglutide (Victoza)

Exenatide (Byetta)

136
Q

B- adrenergic blockers

A

Mask symptoms of hypoglycemia

Prolong hypoglycemic effects of insulin

137
Q

Thiazide/ loop diuretics

A

Can potentiate hyperglycemia by inducing potassium loss

138
Q

Nutritional therapy Carbohydrates

A

Sugars, starches and fiber

Carbohydrate allowance: less than 10% of daily energy should come from sucrose

139
Q

Nutritional therapy Fats

A

Reduce combined saturated fats and trans- fats to less than 7% of energy intake
Include foods rich in polyunsaturated omega-3 fatty acids and plant oils

140
Q

Nutritional therapy Protein

A

Contibute 15-20% of total energy consumed

Intake should be significantly less than in the general population

141
Q

Nutritional therapy Alcohol

A
High in calories 
No nutritive value
Promotes hypertriglyceridemia
Detrimental effects on liver 
Can cause severe hypoglycemia
142
Q

Glycemic Index (GI)

A

Term used to describe rise in blood glucose levels after carbohydrate- containing food is consumed
Should be considered when a meal plan is formulated

143
Q

Exercise is an essential

A

part of diabetes management

144
Q

Exercise increases

A

insulin receptor sites

145
Q

Exercise lowers

A

blood glucose levels

146
Q

To prevent hypoglycemia during exercise

A

several small carbohydrate snacks can be taken every 30 min

147
Q

Self monitoring of blood glucose

A

Enables client to make self management decisions regarding diet, exercise, and medication
Important for detecting episodic hyperglycemia and hypoglycemia

148
Q

Hypoglycemia

A

Low blood glucose

149
Q

Hypoglycemia Occurs when

A

Too much insulin in proportion to glucose in the blood

blood glucose level less than 4mmol/L

150
Q

Hypoglycemia Common Manifestations

A
Anxiety 
Nervousness
Diaphoresis
Tremors 
Hunger 
Pallor 
Palpitations
151
Q

Hypoglycemic unawareness

A

Person does not experience warning signs/ symptoms, increasing risk for decreased blood glucose levels
Related to autonomic neuropathy

152
Q

Causes of Hypoglycemia

A

Food intake and peak action of insulin or oral hypoglycemic agents

153
Q

Untreated Hypoglycemia can progress to

A

Loss of consciousness, seizures, coma death

154
Q

If blood glucose <4 mmol/L

A

begin treatment for hypoglycemia

155
Q

If blood glucose >4mmol/L

A

no treatment

156
Q

If pt has hypoglycemia and is alert enough to swallow give

A

15-20g of simple carbohydrate
175 mL of fruit juice
Regular soft drink

157
Q

If pt has hypoglycemia and is not alert enough to swallow

A

Administer 1 mg of glucagon IM or subcutaneously

158
Q

Diabetic Ketoacidosis (DKA)

A

Caused by profound deficiency of insulin

159
Q

Diabetic Ketoacidosis (DKA) Characterized by

A

Hyperglycemia
Ketosis
Acidosis
Dehydration

160
Q

Diabetic Ketoacidosis (DKA) mostly occurs with

A

Type 1 diabetes

161
Q

Diabetic Ketoacidosis (DKA) precipitating factors

A
Illness
Infection 
Inadequate insulin dosage 
Undiagnosed type 1
Poor self management
162
Q

Diabetic Ketoacidosis (DKA) signs and symptoms

A
Polyuria
polydispasia
Lethargy
weakness
Dehydration 
Poor skin turgor
Dry mucous membranes 
Tachycardia
Orthostatic hypotension 
abdominal pain 
Rapid deep breathing 
sweet fruity odour
163
Q

Diabetic Ketoacidosis (DKA)Treatment

A

Correct fluid electrolyte imbalance

Insulin therapy

164
Q

how to correct fluid/ electrolyte imbalance in Diabetic Ketoacidosis (DKA)

A

IV infusion 0.45% or 0.9% NaCl
Restore urine output
Raise BP

165
Q

When blood glucose levels approach 14 mmol/L

A

5% dextrose added to regimen

166
Q

Hyperosmolar Hyperglycemic Syndrome (HHS)

A

Client has enough circulating insulin that ketoacidosis does not occur

167
Q

Hyperosmolar Hyperglycemic Syndrome (HHS) Usually history of

A

Inadequate fluid intake
Increasing mental depression
Polyuria

168
Q

Hyperosmolar Hyperglycemic Syndrome (HHS) Lab values

A

Blood glucose > 34 mmol/L
Increase in serum osmolality
Absent/Minimal ketone bodies

169
Q

Macrovascular Angiopathy

A

Disease of large and medium sized blood vessels

Occurs with greater frequency and with an earlier onset in diabetics

170
Q

Macrovascular Angiopathy Development promotes

A

altered lipid metabolism common to diabetes

171
Q

Macrovascular Angiopathy Risk factors

A
Obesity 
Smoking 
Hypertension 
High fat intake 
sedentary lifestyle
172
Q

Microvascular Angiopathy

A

Results from thickening of vessel membranes in capillaries and arterioles

173
Q

Macrovascular Angiopathy Areas most noticeably affected

A

Eyes (retinopathy)
Kidneys (nephropathy)
Nerves (Neuropathy)
Skin (Dermopathy)

174
Q

Two types of Diabetic Retinopathy

A
  1. Nonproliferative

2. Proliferative

175
Q

Diabetic Retinopathy

A

Microvascular damage to retina- result of chronic hyperglycemia

176
Q

Nonproliferative Diabetic Retinopathy

A

Partial Occlusion of small blood vessels in retina

Most common form

177
Q

Proliferative Diabetic Retinopathy

A

When retinal capillaries become occluded

Most severe form involves retina and vitreous

178
Q

Diabetic Retinopathy Treatment

A

Laser photocoagulation

Vitrectomy

179
Q

Laser photocoagulation

A

Laser destroys ischemic areas of retina

Prevents further visual loss

180
Q

Vitrectomy

A

Aspiration of blood, membrane and fibres inside the eye

181
Q

Diabetic Nephropathy

A

Associated with damage to small blood vessels that supply the glomeruli of the kidney

182
Q

Critical factors to delay/ prevent Diabetic Nephropathy

A
Tight glucose control
Blood pressure management
-ACE inhibitors
- Angiotensin II receptor agonists
Yearly screening 
-Microalbuninuria in urine
-Serum creatinine
183
Q

Sensory Neuropathy

A

Affects hands and/ or feet bilaterally
Foot injury and ulcerations can occur without the client having pain
Can cause atrophy of small muscles of hands/feet

184
Q

Characteristics of Sensory neuropathy

A

Loss of sensation, abnormal sensations, pain and parenthesias

185
Q

Treatment of Sensory neuropathy

A

Tight blood glucose control

Drug therapy

186
Q

drug therapies for sensory Neuropathy

A

Topical creams
Tricyclic antidepressants
Selective serotonin and norepinephrine reuptake inhibitors
Antiseizure drugs

187
Q

Autonomic Neuropathy

A

Affects all body systems

188
Q

Autonomic Neuropathy Complications

A

Gastroparesis
Cardiovascular abnormalities
Sexual function
Neurogenic bladder

189
Q

Foot Complications

A

Most common cause of hospitalization in diabetes

Result from combination of microvascular and macrovascular diseases

190
Q

Foot and lower extremity Risk factors

A

Sensory neuropathy

Peripheral arterial disease

191
Q

Integumentary Complications

A

Acanthosis nigricans
Necrobiosis lipoidica diabeticorum
Granuloma annulare

192
Q

Acanthosis nigricans

A

Dark, coarse, thickened skin

193
Q

Necrobiosis lipoidica diabeticorum

A

Associated with type 1
Forms partial rings of papules
Often on the dorsal surface of hands and feet

194
Q

Infections

A

Diabetics are more susceptible to infection
Defect in mobilization of inflammatory cells
Impairment of phagocytosis by neutrophils and monocytes
Loss of sensation may delay detection
Treatment must be prompt and vigorous