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NUR 370 Pathophysiology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Exocrine glands (pancreas)

A

Secretes digestive juice into the duodenum through the pancreatic duct

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2
Q

Endocrine glands (pancreas)

A

Produces hormones to control blood sugar

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3
Q

Islets of Langerhans (2 of main focus)

A

Tiny clusters of cells scattered throughout the pancreas

2 types to focus on:
Alpha cells – secrete glucagon
Beta cells – secrete insulin

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4
Q

Insulin (from beta cells)

A
  • A hormone and major factor in control of carbohydrate, lipid and protein metabolism
  • Allows glucose from food to enter the body’s cells where it is converted into energy needed by muscles and tissues to function
  • Activates glucose uptake (through glucose transporters), metabolism and storage of glucose as glycogen in muscle and fat tissue – glycogenesis
  • Insulin facilitates the transport of potassium, phosphate and magnesium
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5
Q

Glucagon (from alpha cells)

A
  • Released when blood glucose levels are low
  • Acts to increase blood glucose levels by stimulating:
    Glycogenolysis – the break down of glycogen into glucose and release of that glucose into the blood stream
    Gluconeogenesis – converting non-carbohydrate (protein and fat) sources to glucose
  • Glucagon release is inhibited by high glucose levels
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6
Q

Type 1 Diabetes

Describe process of how it develops

A

Absolute insulin deficiency (beta cell destruction)

  • 5-10% of all cases of diabetes mellitus
  • Progressive destruction of pancreatic  cells by body’s own T cells
  • Autoantibodies cause a reduction of 80% to 90% in normal - cell function before manifestations occur.
  • Long preclinical period
  • Without insulin, glucose is present but unable to enter cells for utilization – hyperglycemia
  • Antibodies present for months to years before symptoms occur
  • Manifestations develop when pancreas can no longer produce insulin.

Client becomes dependent on exogenous insulin administration to survive

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7
Q

What are HLAs (human leukocyte antigens)?

A
  • Cell-surface antigens that help the immune system to distinguish self from non-self.
  • These antigens are unique to every person.
  • Damage/mutation in HLAs may be linked to Type 1 DM; causing the body to attack its own cells.
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8
Q

What are ICAs (islet cell antibodies)?

A
  • A virus infection may trigger an autoimmune response. ICAs act against beta cells progressively decreasing insulin.
  • ICAs are found in 85% of patients with Type 1 DM at the time of diagnosis
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9
Q

Describe the progression of type 1 diabetes

A

Genetic predisposition (HLAs) -> Environmental trigger (viral infection) -> Active autoimmunity -> Progressive beta cell destruction -> Overt diabetes mellitus

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10
Q

What are the clinical manifestations of Type 1 diabetes?

A

Polyphagia: Depletion of cellular stores of carbohydrates, protein and fat results in cellular starvation (chronic hunger)
Polydipsia: To compensate for osmotic diuresis (chronic thirst)
Polyuria: Osmotic diuresis – hyperglycemia causes water to leave the cells resulting in cellular dehydration
Glucosuria: Once the kidneys reach a threshold and can no longer keep up with the high glucose, it is excreted into the urine
Fatigue: Glucose in unable to enter the cells for energy production
Weight loss: Fluid loss from osmotic diuresis and loss of body tissue as fats and proteins are used for energy
Blurred vision: Edema of the lens
Ketonuria: Fatty acid metabolism produces ketones as a by-product

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11
Q

How do you manage Type 1 diabetes?

A

Insulin therapy

  • Variety of options exist and will be individually optimized (pen or syringe injections or pumps)
  • Self-monitoring of blood glucose levels (capillary blood glucose monitors, continuous blood glucose monitors, flash glucose monitoring)

Meal planning

  • Involvement of RD
  • Variety of foods

Exercise regimens

  • Improve glucose control
  • 150 minutes/week of aerobic exercise
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12
Q

Type 2 diabetes

A
  • Insulin resistance

- Relative insulin deficiency (beta cell failure)

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13
Q

What is the prevalence of type 2 diabetes? Who is at risk?

A
  • Most prevalent type of diabetes
  • More than 90% of clients with diabetes
  • Usually occurs in people over 35 years of age
  • Prevalence increases with age
  • Higher risk in certain populations (i.e. black, hispanic etc)
  • Increased risk in obesity
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14
Q

What are the risk factors for type 2 diabetes?

A
  • Obesity
  • Hypertension
  • First-degree relative with type 2 diabetes
  • High levels of blood cholesterol
  • A high BMI
  • Age over 40
  • High-risk populations
  • Prediabetes (impaired glucose tolerance or impaired fasting glucose)
  • Polycystic Ovary Syndrome (PCOS)
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15
Q

What are the major metabolic abnormalities in type 2 diabetes?

A
  1. Insulin resistance
    - Body tissues do not respond to insulin.
    - Insulin receptors are either unresponsive or insufficient in number.
    - Results in hyperglycemia
  2. Pancreas ↓ ability to produce insulin – insulin deficiency
    - β cells fatigued from compensating
    - Pancreas continues to produce some endogenous insulin.
    - Insulin produced is insufficient or is poorly utilized by tissues.
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16
Q

What is insulin resistance?

A
  • Resistance to the biologic activity of insulin in both the liver and peripheral tissues
  • Inability of muscle and fat tissues to increase glucose uptake
  • Some studies suggest fewer insulin receptors in the skeletal muscles, liver and adipose tissue in obese persons; others suggest abnormalities in the signaling pathways to allow glucose into the cell
  • Is associated with central/abdominal obesity in a condition known as metabolic syndrome
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17
Q

What is insulin deficiency?

A
  • Due to limited beta cell response to hyperglycemia
  • Beta cells are chronically exposed to high levels of glucose progressively become less efficient with further glucose elevation to secrete sufficient insulin
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18
Q

What are the clinical manifestations of type 2 diabetes?

A
  • Gradual onset
  • Person may go many years with undetected hyperglycemia
  • Nonspecific symptoms
  • May have classic symptoms of type 1 diabetes
  • Fatigue
  • Recurrent infection
  • Prolonged wound healing
  • Visual changes
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19
Q

How is diabetes diagnosed?

A
  • Physical examination
  • Medical history
  • Ophthalmological examination may show diabetic retinopathy
  • Various lab tests
  • Urinalysis
  • Plasma Glucose Testing
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20
Q

How do you diagnose diabetes through urinalysis?

A
  • There is a finite amount of glucose that can be filtered by the kidneys
  • When that amount has been met, any excess spills out into the urine as is found in in the urine of people with diabetes
  • Generally a person loses undetectable amounts of glucose in the urine
  • Those with diabetes lose small to large amounts in proportion to the severity of disease and intake of carbohydrates
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21
Q

What are the four diagnostic methods for plasma glucose?

A
  • A1C ≥ 6.5%
  • Fasting plasma glucose level ≥7 mmol/L
  • Two-hour OGTT level ≥11.1 mmol/L when a glucose load of 75 g is used
  • Random or casual plasma glucose measurement ≥11.1 mmol/L
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22
Q

What is the Hemoglobin A1C test good for?

A
  • Recommended to be used as a diagnostic test
  • Useful in determining glycemic levels over time
  • Shows the amount of glucose attached to hemoglobin molecules over RBC lifespan
  • Approximately 120 days
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23
Q

What is HbA1C? How does it work?

A
  • Glucose normally attaches to hemoglobin of RBC and cannot dissociate once attached
  • A build-up of glycosylated hemoglobin reflects the average level of glucose to which the RBC has been exposed to during its life-cycle: A1C is stated in percentage
  • The higher the blood glucose, the higher the glycosylated hemoglobin (HbA1C or A1C)
  • The longer hyperglycemia occurs in the blood, the more glucose binds to RBCs and the higher the A1C
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24
Q

What is considered normal A1C levels? What level is diagnostic of diabetes? What does normal levels reduce the risk of?

A

Normal range is <6.0%
A A1C of 6.5mmol/L is diagnostic of diabetes
Normal A1C reduces risks of retinopathy, nephropathy, and neuropathy

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25
Q

What is fasting plasma glucose (FPS) good for? How is it done? What are normal levels? What is diagnostic of diabetes?

A
  • Indicates overall glucose homeostasis
  • A sample is drawn when the client has not ingested any nutrients except water for at least 8 hours
  • Fasting plasma glucose level (normal <6.1 mmol/L) in diabetics is ≥ 7 mmol/L
  • A level of 7mmol/L or greater confirmed by a repeat test on another day generally considered a preferred method for diagnoses
26
Q

What does the oral glucose tolerance test? How does it work? What are normal levels? What is diagnostic of diabetes?

A
  • Measures the body’s ability to handle a glucose load
    Patient fasts for the previous 8 to 14 hours
  • Zero time (baseline) blood sample drawn in the morning
  • Person ingests 1g of glucose per kg of body weight to a maximum 75 g
  • Blood is drawn at intervals, the most important being the 2 hour sample
  • Two hour OGTT ≥ 11.1 mmol/L with glucose load of 75 g usually means diabetes
27
Q

What are the goals of diabetes management?

A
  • Decrease symptoms
  • Promote well-being
  • Prevent acute complications
  • Delay onset and progression of long-term complications
28
Q

What skill do we want to teach the client?

A

Self-monitoring of blood glucose

29
Q

What strategies do we want to teach/implement in the management of diabetes?

A

Nutritional therapy
Drug therapy
Exercise

30
Q

What does nutritional therapy consist of in type 1 diabetes?

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.

31
Q

What does nutritional therapy consist of type 2 diabetes?

A

Emphasis is based on achieving glucose, lipid, and blood pressure goals.

Calorie reduction

32
Q

What does exercise therapy look like for individuals with diabetes?

A

Essential part of diabetes management
- ↑ insulin receptor sites
- Lowers blood glucose levels
- Contributes to weight loss
Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia.
- Best done after meals
- Exercise plans should be started after medical clearance.
- Should be individualized
- Monitor blood glucose levels before, during, and after exercise

33
Q

What causes diabetic ketoacidosis (DKA)? What is it characterized by? Which type of diabetes does it usually occur?

A

Caused by profound deficiency of insulin

Characterized by:
Hyperglycemia
Ketosis
Acidosis
Dehydration

Most likely occurs in type 1

34
Q

What are the precipitating factors of DKA?

A 
Illness
Infection
Inadequate insulin dosage
Undiagnosed type 1
Poor self-management (not taking required insulin doses)
35
Q

What happens in DKA when insulin is insufficient?

A
  • Glucose cannot be properly used for energy.
  • Body breaks down fat stores.
  • Ketones are by-products of fat metabolism.
  • Alter pH balance, causing metabolic acidosis
  • Ketone bodies excreted in urine
  • Electrolytes become depleted
36
Q

What are the clinical manifestations of DKA?

A 
Glucose level 16-42mmol/L
Polyuria, polydipsia
Fruity/acetone odour of ketones on breath
Lethargy/weakness
Early symptoms
Dehydration
- Poor skin turgor
- Dry mucous membranes
- Tachycardia
- Orthostatic hypotension
Abdominal pain
Kussmaul’s respirations
- Rapid deep breathing
- Attempt to reverse metabolic acidosis
37
Q

What are Kussmaul respirations?

A

Deep laboured breathing associated with severe metabolic acidosis/diabetic ketoacidosis

Initially breathing is deep and rapid (hyperventilation)

As acidosis worsens breathing gradually becomes deep, slow, laboured and gasping

38
Q

What are some nursing considerations when managing DKA?

A

Airway management
Oxygen administration
Rehydration, correction of acid-base and fluid imbalances
Isotonic IV infusion
Restore urine output
Raise blood pressure
Restoration of a state of carbohydrate catabolism from a state of fat catabolism and identify and correct the precipitating factors
Insulin therapy
When blood glucose levels approach 14 mmol/L
5% dextrose added to regimen
Prevent hypoglycemia

39
Q

What is Hyperosmolar hyperglycemic syndrome (HHS)?

A

Life-threatening syndrome
Less common than DKA
Often occurs in older clients with type 2 DM
Results from any illness that leads to dehydration or inadequate food intake (burns, surgery, sepsis, not eating/drinking, vomiting/diarrhea)
Client has enough circulating insulin that ketoacidosis does not occur.
Produces fewer symptoms in earlier stages.

Hyperglycemia leads to osmotic diuresis and subsequent dehydration with high serum sodium and urea levels

High glucose plus high sodium and urea lead to high serum osmolarity and subsequent intracellular dehydration

40
Q

What are the clinical manifestations of HHS?

A

Decreased LOC, polyuria and polydipsia, hypovolemia, profound dehydration
Neurological manifestations occur because of ↑ serum osmolality.

41
Q

What should be adminstered in HHS? What should be assessed?

A

Administration
IV fluids
Insulin therapy
Electrolytes

Assessment 
Renal status
Cardiopulmonary status
Level of consciousness
Signs of potassium imbalance
Cardiac monitoring 
Vital signs
42
Q

What is hypoglycemia? When does it occur?

A

Low blood glucose

Occurs when:
Too much insulin in proportion to glucose in the blood
Blood glucose level less than 4 mmol/L

43
Q

What are common manifestations of hypoglycemia? What happens if it is untreated?

A 
Anxiety
Nervousness
Diaphoresis
Tremors
Hunger
Pallor
Palpitations

Untreated can progress to loss of consciousness, seizures, coma, and death

44
Q

At first sign of hypoglycemia, what actions should be taken?

A

Check blood glucose

  • If <4 mmol/L, begin treatment
  • If >4 mmol/L, investigate further for cause of signs/symptoms
  • If monitoring equipment not available, treatment should be initiated
45
Q

How do you treat hypoglycemia?

A

If alert enough to swallow
15–20 g of a simple carbohydrate
175 mL of fruit juice
Regular soft drink

Recheck blood sugar 15 minutes after treatment.
Repeat until blood sugar >4 mmol/L.
Client should eat regularly scheduled meal/snack to prevent
rebound hypoglycemia.
Check blood sugar again 45 minutes after treatment.

In acute care settings
20–50 mL of 50% dextrose IV push

46
Q

What can occur in unrecognized nocturnal hypoglycemia? How do you treat this?

A

Unrecognized nocturnal hypoglycemia results in fasting hyperglycemia (somogyi effect)
Hypoglycemia induced by insulin causes a counter-regulatory hormone response that produces hyperglycemia – rebound effect

Blood glucose checked in the morning indicates hyperglycemia and the patient or HCP may increase the insulin dose
Encourage a bedtime snack
Reduce insulin dosage

47
Q

What is the dawn phenomenon? How do you treat this?

A

Rise in blood sugar between the hours of 4-8 am in people with diabetes
Caused by the overnight release of counter-regulatory hormones
Cortisol
Growth hormone
Glucagon
Epinephrine

Adjust timing or increase insulin dose

48
Q

How do you determine the difference between the dawn phenomenon and the somogyi effect?

A

Measurement of bedtime, nighttime (between 2-4 am) and morning BG levels on several occasions:

  • If BG level is LOW, suspect the Somogyi effect
  • If the BG level is Normal or HIGH it’s likely the dawn effect.
49
Q

What are macrovascular complications?

A
  • Diseases of large and medium-sized blood vessels
  • Occur with greater frequency and with an earlier onset in diabetics
  • Development promoted by altered lipid metabolism common to diabetes
50
Q

What are some examples of macrovascular complications in diabetes?

A

Coronary artery disease (2 to 4x more likely)
Hypertension (40% of diabetics)
Cerebrovascular disease
Peripheral vascular disease (ulcers in feet & lower extremities)

51
Q

What are microvascular complications?

A

Result from thickening of vessel membranes in capillaries and arterioles
In response to chronic hyperglycemia
Is specific to diabetes, unlike macrovascular

52
Q

What are examples of microvascular complications in diabetes?

A
  • Diabetic retinopathy (80% have some form within 15 years of diagnosis)
    Related to HTN, stress from increased blood viscosity, protein breakdown, impaired healing of damage
    Causes intraretinal hemorrhages that can be progressive and impair visual acuity
  • Diabetic nephropathy – kidney disease resulting from diabetes
  • Diabetic neuropathy - neural tissue damage, numbness, and tingling
53
Q

What is diabetic retinopathy? What causes it?

A

Diabetic retinopathy results from ischemia as a result of blood vessel changes and red blood cell aggregation
- Stress on the retina vessels from an increase in blood viscosity, protein breakdown as well as impaired healing leads to intra-retinal hemorrhages which
- This condition can damage blood vessels in the retina and begin to leak fluid and small amounts of blood into the eye
- Sometimes deposit of cholesterols of fats can leak from the blood into the retina and can cause changes in the eye including micro aneurysms where there are small bulges in blood vessels of the retina that often leak fluid
- Hemorrhages in the retina, macular edema where there is swelling or thickening of the macula caused by leaking of the blood vessels
Macular ischemia where small blood vessels and capillaries close – vision blurs occur because the macula is not receiving enough blood supply to function properly

54
Q

What is diabetic nephropathy? What are the risk factors?

A

Most common cause of end-stage renal disease (ESRD)
Involves damage and eventual obliteration of the capillaries that supply the glomeruli of the kidneys
Leads to nephrosis and gross albuminuria

Risk factors include poor glycemic control, longer duration of the disease, and HTN

55
Q

What is peripheral neuropathy?

A

Diabetic neuropathy
40% to 50% of clients with diabetes have some degree of neuropathy.
Nerve damage due to metabolic derangements of diabetes
Insensitivity or loss of ability to feel pain, heat, and cold.
Minor injures can become severe if untreated.

56
Q

What is infection in the context of diabetes?

A

Those with diabetes are more susceptible to infection
Defect in mobilization of inflammatory cells
Impairment of phagocytosis by neutrophils and monocytes
Loss of sensation (nephropathies) may delay detection
WBCs are impaired in their ability to get to affected areas
Vascular insufficiencies
Increased blood viscosity
Treatment must be prompt and vigorous.

57
Q

What is gestational diabetes? What is the incidence?

A

Pregnancy = a state of insulin resistance due to placental hormones on maternal circulation
High levels of counter-regulatory hormones released from the placenta – (block insulin and thus raise the mother’s blood sugar)
Pancreas needs to create more insulin; when the pancreas cannot make enough insulin to overcome the effects of the counter-regulatory hormones  increased blood sugars = gestational diabetes
Occurs in 3-5% of pregnancies
Screened at 24-28th week gestation

58
Q

How does gestational diabetes affect the fetus?

A
  1. Extra glucose from mother’s blood enters into fetal circulation.
  2. Fetus makes more insulin to handle extra glucose.
  3. Extra glucose gets stored as fat leading to high birth weight

Large babies are usually over 4kg, this may lead to complications during delivery such as damaged shoulders, prolonged delivery, higher risk of breathing problems as well as potential hyperglycemia at birth
Greater risk of obesity and developing type II diabetes

59
Q

What is metabolic syndrome? What is it caused by?

A

Term used to describe a group of conditions that puts people at higher risk of developing type 2 diabetes, heart disease and other heart-related problems

Caused by unhealthy lifestyle (poor diet, lack of exercise, weight gain)  insulin resistance  type 2 diabetes

60
Q

What are the factors that characterize metabolic syndrome?

A

If you have 3 or more of the following conditions, you are considered to have metabolic syndrome:

High fasting blood glucose levels (5.6 mmol/L or higher)
High blood pressure (systolic 130 mmHg or higher and/or diastolic 85 mmHg or higher)
High level of triglycerides(1.7 mmol/L or higher)
Low levels of HDL (lower than 1.0 mmol/L in men or 1.3 mmol/L in women)
Abdominal obesity [a waist circumference of greater/equal to 90-102 cm in men and 80-88 cm in women [population specific]

NUR 370 Pathophysiology (3 decks)

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