Glucose Regulation Flashcards
(194 cards)
1
Q
Glucose Regulation
A
The process of maintaining optimal blood glucose levels
2
Q
The ultimate end result of glucose metabolism is…
A
Cellular use of glucose for energy synthesis
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
4
Q
Normal insulin metabolism
A
- produced by the B cells
- Released continuously into the bloodstream in small increments with larger amounts released after food
- Stabilizes glucose range 4-6 mmol/L
5
Q
Hypoglycemia
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State of insufficient or low Blood glucose levels, defined as less than 4 mmol/L
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Q
Hyperglycemia
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State of elevated blood glucose levels, defined as more than 6-8 mmol/L when not fasting
7
Q
Insulin is synthesized from
A
proinsulin
8
Q
Insulin secretion is promoted by…
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Increased blood glucose levels, amino acids and GI hormones
9
Q
Insulin facilitates …
A
the rate of glucose uptake into the cells of the body
10
Q
Amylin
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Peptide hormone co secreted with insulin
11
Q
Amylin delays
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Nutrient uptake
12
Q
Amylin suppresses
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Glucagon secretion
13
Q
Glucagon secretion is promoted by
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Decreased blood glucose levels
14
Q
Glucagon stimulates
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Glycogenolysis, gluconeogenesis, and lipolysis
15
Q
Pancreatic somatostatin
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Possible involvement in regulating alpha-cell and beta-cell secretions
16
Q
Hormone to lower glucose
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Insulin
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Q
Counterregulatory hormones to raise glucose
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Glucagon
Cortisol
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Q
Diabetes
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A chronic multi system disease related to abnormal insulin production, Impaired insulin utilization, or both
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Q
links to diabetes
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Genetic
Autoimmune
Viral
Environmental
20
Q
Two most common types of diabetes
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Type 1
Type 2
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Q
Other types of diabetes
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gestational
Prediabetes
Secondary diabetes
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Q
Insulin promotes
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Glucose transport from bloodstream across cell membrane to cytoplasm of cell
Decreases glucose in the bloodstream
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After a meal insulin…
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Increases
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After a meal insulin stimulates storage of …
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glucose as glycogen in the liver and muscle
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after a meal insulin inhibits
glyconeogenesis
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after a meal insulin enhances
fat deposition
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increase in protein synthesis happens ...
after a meal
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skeletal muscle and adipose tissue are...
insulin dependent tissue
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Insulins function as a...
substitute for the endogenous hormone
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Insulin restores the pt ability to
Metabolize carbohydrates, fats and proteins
Store glucose in the liver
Convert glycogen to fat stores
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Common Diagnostic tests
```
Glucose screening
assess antibodies to confirm type 1 diabetes mellitus
Lipid analysis
Microalmuninuria
C-reactive protein
```
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Glycemic goal of treatment
HbA1c of less than 7%
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Fasting Blood glucose goal for diabetic patients
4-7mmol/L
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2 hour postprandial target of...
5-10mmol/L
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Type 1 diabetes mellitus
Formerly known as juvenile onset or insulin dependent diabetes
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End result oflongstanding process of type 1 diabetes mellitus
progressive destruction of pancreatic B cells by body's own T cells
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Causes of type 1 diabetes mellitus
Genetic predisposition - related to human leukocyte antigens
Exposure to a virus
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Type 1 diabetes mellitus has a long ______ period
Preclinical period
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With Type 1 diabetes mellitus antibodies are present _________ befit symptoms occur
Months to year
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Diabetic ketoacidosis
Occurs in absence of exogenous insulin
Life threatening disease
Results in metabolic acidosis
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Classic symptoms of Type 1 diabetes mellitus
```
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
weakness
fatigue
```
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Pre diabetes
Individuals already at risk for diabetes
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In prediabets Blood glucose is...
High but not high enough to be diagnosed as having diabetes
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Prediabets is characterized by
Impaired fasting glucose (IFG)
| Impaired glucose tolerance (IGT)
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IFG & IGT for prediabetes
IFG 6.1-6.9mmol/L
| IGT 7.1-11mmol/L
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Prediabets is usually present with ...
No symptoms
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Type 2 Diabetes mellitus is the...
most prevalent type of diabetes
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With Type 2 Diabetes mellitus pancreas still.
produces some endogenous insulin
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The most powerful risk factor for Type 2 Diabetes mellitus is
obesity
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Type 2 Diabetes mellitus genetic mutations
lead to insulin resistance
| Increased risk for obesity
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Type 2 Diabetes mellitus Four major metabolic abnormalities
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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Insulin resistance
Body tissues do not respond to insulin
Insulin receptors are either unresponsive or insufficient in number
Results in hyperglycaemia
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Pancreas decreased ability to produce insulin
B cells fatigued from compensating
| B cell mast lost
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Inappropriate glucose production from liver
Liver response of regulating release of glucose is haphazard
| Not considered a primary factor in Development of type 2
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Alteration in production of hormones and adipokines
Play a role in glucose and fat metabolism
| - contribute to pathophysiology of type 2 diabetes
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Two main adipokines
Adiponectin and leptin
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Individuals with metabolic syndrome are at an increased risk for...
Type 2 diabetes mellitus
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Cluster of abnormalities increase risk for...
Cardiovascular disease and diabetes
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Risk Factors for type 2 Diabetes mellitus
Abdominal obesity
sedentary lifestyle
Urbanization
Certain ethnicities
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Gestational Diabetes
Diabetes that develops during pregnancy
| Detected 24-28 weeks
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When do glucose levels return to normal in gestational diabetes
6 weeks postpartum
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Gestational Diabetes increased risks
```
Birth trauma
Hypoglycemia
Hyperbilirubinemia
Respiratory distress syndrome
Increased risk for developing type 2 diabetes in 5-10 years
```
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Therapy for gestational diabetes
First- Nutritional
| Second- Insulin
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Secondary Diabetes
Treatment of a medical condition that causes abnormal blood glucose levels
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Drugs that can cause secondary Diabetes
Corticosteroids (prednisone)
Phenytoin (Dilantin)
Atypical antipsychotics (Clozapine)
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Secondary diabetes usually resolves when..
The underlying condition is resolved
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Secondary Diabetes can result from these conditions
```
Schizophrenia
Cushings syndrome
Hyperthyroidism
Immune suppressive therapy
Parentarel nutrition
Cystic Fibrosis
```
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Diabetes mellitus four methods of diagnosis
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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Hemoglobin A1C test
determines glucose levels over time
| Shows the amount of glucose attached to hemoglobin molecules over RBC lifespan
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Normal A1C reduces risks of
Retinopathy
Nephropathy
Neuropathy
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Diabets Mellitus Goals of management
Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of long-term complications
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Type 1 therapy
Insulin
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Type 2 Therapy
Lifestyle changes
Oral drug therapy
Insulin when nothing else can provide glycemic control
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Insulins function as a substitute for..
The endogenous hormone
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Insulin restores the diabetic clients ability to:
Metabolize carbohydrates, fats and protein
Store glucose in the liver
Convert glycogen to fat stores
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Exogenous Insulin
Insulin from an outside of body source
| Required for type 1 diabetes
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Human insulin
derived using recombinant deoxyribonucleic acid technologies
| Recombinant insulin produced by bacteria and yeast
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Insulin as a rapid acting treatment for..
Type 1 & 2 diabetes
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Insulin Most rapid onset of action
10-15 min
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Insulin peak
1-2 hours
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Insulin duration
3-5 hours
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with insulin the pt must_______ after injection
eat a meal
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Lispro (Humalog)
Action similar to that of endogenous insulin
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Short acting insulins
Humulin R
| Novolin ge Toronto
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Short acting routes of administration
IV Bolus
IV infusion
IM
Subcutaneous
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Short acting insulin onset of subcutaneous route
30 min
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Short acting insulin peak of subcutaneous route
2-3 hours
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Short acting insulin duration of subcutaneous route
6.5 hours
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Intermediate acting insulins
Insulin isophane suspension (NPH)
| Often combined with regular insulin
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Intermediate acting insulins onset
1-3 hours
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Intermediate acting insulins Peak
5-8 hours
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Intermediate acting insulins duration
up to 18 hours
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Long acting insulins
insulin glargine (Lantus)
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Insulin Glargine (Lantus)
clear, colourless solution
| Constant level of insulin in the body
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Lantus can be dosed
Once a day, every 12 hours
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Lantus also referred to as
Basil insulin
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Lantus onset
90 min
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Lantus peak
none
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Lantus duration
24 hr
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Fixed combination insulins
contains 2 different insulins, fixed combination
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Fixed combination insulins
```
Humulin 30/70
Novolin 30/70, 40/60, 50/50
Novomix 30
Humalog Mix25
Humalog Mix50
```
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Two types of insulin included in fixed combination insulins
1. Intermediate acting type
| 2. Either a rapid acting or a short acting
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Sliding- scale insulin Dosing
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
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Sliding- scale insulin Dosing Disadvantages
Delays insulin administration until hyperglycaemia occurs, resulting in large swings in glucose control
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Basal-Bolus insulin dosing
Mimics a healthy pancreas by delivering basal insulin constantly as a basal and then as needed as a bolus
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Basal insulin is a _______insulin
long acting
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Insulin pump
Continuous subcutaneous infusion
Battery operated device
Connected via a plastic tubing to a catheter inserted into subcutaneous tissue in the abdominal wall
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Problems with Insulin therapy
```
Hypoglycemia
allergic reaction
lipodystrophy
somogyi effect
Dawn phenomenon
```
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Somogyi effect
Rebound effect in which an overdose of insulin causes hypoglycemia Usually occurs during sleep
Rebound hyperglycemia and ketosis may occur
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Dawn phenomenon
Characterized by hyperglycaemia present on awakening in the morning
Due to release of counter regulatory hormones in predawn hours
Growth hormone/ Cortisol possible factors
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Pharmacotherapy oral agents
not insulin
| work to improve mechanisms by which insulin and glucose are produced and used by the body
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Oral agents work on 3 defects of type 2 diabetes
Insulin resistance
Decreased insulin production
Increased hepatic glucose production
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Types of oral agents
```
Sulphonylureas
Meglitinides
Bigunaides
a-glucosidase inhibitors
Thiazolidinediones
```
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Sulphonylureas increase
Insulin production from pancreas
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Sulphonylureas Decrease
chance of prolonged hypoglycemia
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Examples of Sulphonylureas
Giclazide (Diamicron, Diamicron MR)
| Glimepirdie (Amaryl)
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Meglitinides increase
insulin production from the pancreas
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Meglitinides should be taken how many minutes before a meal
30 min
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Meglitinides should not be taken when
a meal is skipped
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Examples of Meglitinides
Repaglinide (GlucoseNorm)
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Biguanides Reduce
glucose production by liver
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Biguanides Enhance
Insulin sensitivity at tissues
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Biguanides improve
Glucose transport into cells
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Biguanides examples
Metformin (Glucophage)
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a-Glucosidase inhibitors
Starch blockers
| Slow down absorption of carbohydrate in small intestine
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a-Glucosidase inhibitors Example
Acarbose (Glucobay)
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Thiazolidinediones
Improve insulin sensitivity, transport, and utilization at target tissues
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Thiazolidinediones most effective in
those with insulin resistance
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Thiazolidinediones examples
Pioglitazone (Actos)
| Rosiglitazone (Avandia)
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Dipeptidyl peptidase - 4 inhibitor (DDP-4)
Slows the inactivation of incretin hormones
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Dipeptidyl peptidase - 4 inhibitor (DDP-4) adverse effects
potential for hypoglycemia
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Dipeptidyl peptidase - 4 inhibitor (DDP-4) Examples
Sitagliptin (Januvia)
| Saxagliptin (Onglyza)
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Other pharmacotherapy Agents
Glucagon-like peptide 1 receptor agonists
B- adrenergic blockers
Thiazide/ loop diuretics
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Glucagon-like peptide 1 receptor agonists
```
Synthetic peptide
Stimulates release of insulin from B cells
Suppress glucagon secretion
Reduces food intake
Slows gastric emptying
Not to be used with insulin
```
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Glucagon-like peptide 1 receptor agonists examples
Liraglutide (Victoza)
| Exenatide (Byetta)
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B- adrenergic blockers
Mask symptoms of hypoglycemia
| Prolong hypoglycemic effects of insulin
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Thiazide/ loop diuretics
Can potentiate hyperglycemia by inducing potassium loss
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Nutritional therapy Carbohydrates
Sugars, starches and fiber
| Carbohydrate allowance: less than 10% of daily energy should come from sucrose
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Nutritional therapy Fats
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
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Nutritional therapy Protein
Contibute 15-20% of total energy consumed
| Intake should be significantly less than in the general population
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Nutritional therapy Alcohol
```
High in calories
No nutritive value
Promotes hypertriglyceridemia
Detrimental effects on liver
Can cause severe hypoglycemia
```
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Glycemic Index (GI)
Term used to describe rise in blood glucose levels after carbohydrate- containing food is consumed
Should be considered when a meal plan is formulated
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Exercise is an essential
part of diabetes management
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Exercise increases
insulin receptor sites
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Exercise lowers
blood glucose levels
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To prevent hypoglycemia during exercise
several small carbohydrate snacks can be taken every 30 min
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Self monitoring of blood glucose
Enables client to make self management decisions regarding diet, exercise, and medication
Important for detecting episodic hyperglycemia and hypoglycemia
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Hypoglycemia
Low blood glucose
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Hypoglycemia Occurs when
Too much insulin in proportion to glucose in the blood
| blood glucose level less than 4mmol/L
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Hypoglycemia Common Manifestations
```
Anxiety
Nervousness
Diaphoresis
Tremors
Hunger
Pallor
Palpitations
```
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Hypoglycemic unawareness
Person does not experience warning signs/ symptoms, increasing risk for decreased blood glucose levels
Related to autonomic neuropathy
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Causes of Hypoglycemia
Food intake and peak action of insulin or oral hypoglycemic agents
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Untreated Hypoglycemia can progress to
Loss of consciousness, seizures, coma death
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If blood glucose <4 mmol/L
begin treatment for hypoglycemia
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If blood glucose >4mmol/L
no treatment
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If pt has hypoglycemia and is alert enough to swallow give
15-20g of simple carbohydrate
175 mL of fruit juice
Regular soft drink
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If pt has hypoglycemia and is not alert enough to swallow
Administer 1 mg of glucagon IM or subcutaneously
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Diabetic Ketoacidosis (DKA)
Caused by profound deficiency of insulin
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Diabetic Ketoacidosis (DKA) Characterized by
Hyperglycemia
Ketosis
Acidosis
Dehydration
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Diabetic Ketoacidosis (DKA) mostly occurs with
Type 1 diabetes
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Diabetic Ketoacidosis (DKA) precipitating factors
```
Illness
Infection
Inadequate insulin dosage
Undiagnosed type 1
Poor self management
```
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Diabetic Ketoacidosis (DKA) signs and symptoms
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Polyuria
polydispasia
Lethargy
weakness
Dehydration
Poor skin turgor
Dry mucous membranes
Tachycardia
Orthostatic hypotension
abdominal pain
Rapid deep breathing
sweet fruity odour
```
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Diabetic Ketoacidosis (DKA)Treatment
Correct fluid electrolyte imbalance
| Insulin therapy
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how to correct fluid/ electrolyte imbalance in Diabetic Ketoacidosis (DKA)
IV infusion 0.45% or 0.9% NaCl
Restore urine output
Raise BP
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When blood glucose levels approach 14 mmol/L
5% dextrose added to regimen
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Hyperosmolar Hyperglycemic Syndrome (HHS)
Client has enough circulating insulin that ketoacidosis does not occur
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Hyperosmolar Hyperglycemic Syndrome (HHS) Usually history of
Inadequate fluid intake
Increasing mental depression
Polyuria
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Hyperosmolar Hyperglycemic Syndrome (HHS) Lab values
Blood glucose > 34 mmol/L
Increase in serum osmolality
Absent/Minimal ketone bodies
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Macrovascular Angiopathy
Disease of large and medium sized blood vessels
| Occurs with greater frequency and with an earlier onset in diabetics
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Macrovascular Angiopathy Development promotes
altered lipid metabolism common to diabetes
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Macrovascular Angiopathy Risk factors
```
Obesity
Smoking
Hypertension
High fat intake
sedentary lifestyle
```
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Microvascular Angiopathy
Results from thickening of vessel membranes in capillaries and arterioles
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Macrovascular Angiopathy Areas most noticeably affected
Eyes (retinopathy)
Kidneys (nephropathy)
Nerves (Neuropathy)
Skin (Dermopathy)
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Two types of Diabetic Retinopathy
1. Nonproliferative
| 2. Proliferative
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Diabetic Retinopathy
Microvascular damage to retina- result of chronic hyperglycemia
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Nonproliferative Diabetic Retinopathy
Partial Occlusion of small blood vessels in retina
| Most common form
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Proliferative Diabetic Retinopathy
When retinal capillaries become occluded
| Most severe form involves retina and vitreous
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Diabetic Retinopathy Treatment
Laser photocoagulation
| Vitrectomy
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Laser photocoagulation
Laser destroys ischemic areas of retina
| Prevents further visual loss
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Vitrectomy
Aspiration of blood, membrane and fibres inside the eye
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Diabetic Nephropathy
Associated with damage to small blood vessels that supply the glomeruli of the kidney
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Critical factors to delay/ prevent Diabetic Nephropathy
```
Tight glucose control
Blood pressure management
-ACE inhibitors
- Angiotensin II receptor agonists
Yearly screening
-Microalbuninuria in urine
-Serum creatinine
```
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Sensory Neuropathy
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
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Characteristics of Sensory neuropathy
Loss of sensation, abnormal sensations, pain and parenthesias
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Treatment of Sensory neuropathy
Tight blood glucose control
| Drug therapy
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drug therapies for sensory Neuropathy
Topical creams
Tricyclic antidepressants
Selective serotonin and norepinephrine reuptake inhibitors
Antiseizure drugs
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Autonomic Neuropathy
Affects all body systems
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Autonomic Neuropathy Complications
Gastroparesis
Cardiovascular abnormalities
Sexual function
Neurogenic bladder
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Foot Complications
Most common cause of hospitalization in diabetes
| Result from combination of microvascular and macrovascular diseases
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Foot and lower extremity Risk factors
Sensory neuropathy
| Peripheral arterial disease
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Integumentary Complications
Acanthosis nigricans
Necrobiosis lipoidica diabeticorum
Granuloma annulare
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Acanthosis nigricans
Dark, coarse, thickened skin
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Necrobiosis lipoidica diabeticorum
Associated with type 1
Forms partial rings of papules
Often on the dorsal surface of hands and feet
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Infections
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
