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Pathophysiology and Pharmacology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Diabetes Mellitus (DM)

A

A multisystem disease related to abnormal insulin production, impaired insulin utilization, or both.

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2
Q

Diabetic ketoacidosis (DKA)

A

An acute metabolic complication of diabetes occurring when fats are metabolized in the absence of insulin; characterized by hyperglycemia, ketosis, acidosis, and dehydration.

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3
Q

Diabetic Nephropathy

A

A microvascular complication of diabetes mellitus associated with damage to the small blood vessels that supply the glomeruli of the kidney.

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4
Q

Diabetic Neuropathy

A

Nerve damage that occurs because of the metabolic derangements associated with diabetes mellitus.

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5
Q

Glycemic Index (GI)

A

The rise in blood glucose levels after a person has consumed a carbohydrate-containing food.

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6
Q

Hyperosmolar hyperglycemic state (HHS)

A

A life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent diabetic ketoacidosis but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion.

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7
Q

Insulin Resistance

A

A condition in which body tissues do not respond to the action of insulin

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8
Q

Lipodystrophy

A

Hypertrophy or atrophy of subcutaneous tissue.

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9
Q

Prediabetes

A

When a fasting or a 2-hour plasma glucose level is higher than normal but lower than that considered diagnostic for diabetes; places the individual at risk for developing diabetes and its complications. Also known as impaired glucose tolerance (IGT) or impaired fasting glucose (IFG).

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10
Q

Somogyi Effect

A

Produces a decline in blood glucose level in response to too much insulin; counter-regulatory hormones are released that cause rebound hyperglycemia and ketosis resulting in high blood glucose levels at morning testing; treatment is a reduction of insulin dosage.

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11
Q

Onset of type 1 DM

A
  • < 30 years old
  • Peak onset about 11-13 years old
  • Long preclinical period, then rapid symptom onset, often emergent (i.e. –DKA)
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12
Q

Insulin is produced by

A

the beta cells of the islets of Langerhans in the pancrea

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13
Q

Basal rate

A

Insulin is produced in continuous small amounts

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14
Q

average insulin rate

A

40-50 u/day

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15
Q

Normal blood sugar ranges

A

4-6 mmol/L

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16
Q

Hormones that work to increase glucose by opposing insulin (counterregulatory)

A

Glucagon, epinephrine, growth hormone, cortisol

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17
Q

How do counterregulatory hormones oppose insulin

A

Stimulate glucose production and output by the liver and decreasing the movement of glucose into the cells

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18
Q

Etiology of DM1

A
  • Autoimmune – autoantibodies in the islet cells cause a
  • 80-90% reduction in normal beta cell function
    genetic predisposition (HLAs)
  • viral trigger causing beta cell destruction
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19
Q

When do clinical manifestations occur in DM1

A

when the pancreas can no longer

produce insulin

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20
Q

When do clinical manifestations occur in DM1

A

when the pancreas can no longer

produce insulin

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21
Q

Clinical Manifestations of DM1

A

sudden weight loss
Polydipsia – excessive thirst
Polyphagia – excessive hunger
Polyuria – frequent urination

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22
Q

Cause of Polyuria and polydipsia

A

secondary to the osmotic effect of hyperglycemia (water is pulled out of the ICF, causing cellular dehydration)

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23
Q

Cause of polyphagia

A

secondary cellular malnourishment – without insulin, the cells cannot use glucose for energy

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24
Q

Cause of weight loss in DM1

A

a body cannot use glucose, so it uses body

fat and protein

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25
Q

Cause of weakness and fatigue in DM1

A

d/t lack of glucose for energy

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26
Q

Sequela of hyperglycemia

A

changes to visual acuity, increased infections, delayed healing

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27
Q

non-insulin dependent diabetes

A

Type 2 diabetes mellitus

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28
Q

Pre-diabetes

A

aka ‘ impaired glucose tolerance’ (IGT) or impaired fasting glucose’ (IFG)
Lower blood glucose than diabetes

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29
Q

‘impaired glucose tolerance’ (IGT) blood glucose

A

7.1-11.0 mmol/L

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30
Q

‘impaired fasting glucose’ (IFG) blood glucose

A

6.1-6.9 mmol/L

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31
Q

Treatment of pre-diabetes

A
  • Monitoring of blood glucose level and HgbA1C
  • Maintaining healthy body weight, regular exercise, healthy diet
  • Some medications may be indicated
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32
Q

What percentage of people with prediabetes progress to being diagnosed with diabetes?

A

25% within 3-5 years

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33
Q

Onset of type 2 diabetes

A
  • Onset > 35 years old
  • Gradual onset, many years with asymptomatic hyperglycemia
  • Progressive disease – even with perfect glycemic control and lifestyle modifications
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34
Q

What is the most prevalent type of diabetes?

A

90% of diabetes is type II

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35
Q

Risk factors for type 2 diabetes

A
  • High BMI: > 25 – overweight > 30 - obese
  • 80-90% of type II DM are overweight at the time of diagnosis
  • Aboriginal, Hispanic, South Asian, African ancestry
  • Insulin resistance (HTN, dyslipidemia, overweight,
    abdominal obesity – apple shape – PCOS)
  • History of IGT (impaired glucose tolerance) or IFG
    (impaired fasting glucose)
  • History of gestational diabetes and delivery of
    macrosomic infant
  • History of bipolar disorders (d/t medications)
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36
Q

Medications that Increase Blood Glucose:

A
  • Certain medicines to treat schizophrenia and psychosis
  • Beta-blockers
  • Corticosteroids
  • Estrogens
  • Lithium
  • Oral contraceptives
  • Phenytoin
  • Salicylates
  • Thiazide diuretics
  • Tricyclic antidepressants
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37
Q

What does insulin do?

A

lowers blood glucose by increasing the transportation of glucose into cells and promotes conversion of glucose to glycogen; also promotes conversion of amino acids to protein in muscles.

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38
Q

Type II Diabetes

A

Pancreas produces some insulin BUT it may not be
enough insulin and/or the insulin may be poorly utilized
by the body tissues

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39
Q

4 Metabolic Abnormalities Contribute to type II diabetes

A
  1. Insulin Resistance (major factor)
  2. Beta Cell Fatigue (major factor)
  3. Inappropriate glucose production by liver (minor factor)
  4. Altered hormone/cytokine production in adipose tissue (minor factor?)
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40
Q

Insulin Resistance in Type 11 diabetes

A
  • Unresponsive and/or low numbers of insulin receptors
    (mostly fat, skeletal muscle, liver cells)
  • Results in glucose not entering cells and hyperglycemia
  • In early type II DM: pancreas responds to this hyperglycemia by producing ++ insulin (in the presence of normal beta cell function), resulting to hyperinsulinemia
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41
Q

Beta Cell Fatigue in Type II diabetes

A
  • Due to the hyperinsulinemia!
  • Results in IFG and IGT (Prediabetes) – can be corrected back to euglycemic states with lifestyle modifications and sometimes meds
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42
Q

Inappropriate glucose production by liver in type II diabetes

A

Poor regulation, in proper response

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43
Q

Altered hormone/cytokine production in adipose

tissue in type II diabetes

A

Adipokines (adiponectin and leptin) – role in glucose and fat metabolism – contribute to type II DM

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44
Q

Metabolic Syndrome

A

Cluster of abnormalities that synergistically increase the risk for CVD

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45
Q

Risk factors for metabolic syndrome

A 
central obesity (apple shape); sedentary
lifestyle; urbanization/Westernization; Aboriginal, Hispanic, African ancestry, Abdominal obesity, HTN, dyslipidemia, insulin resistance, dysglycemia
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46
Q

Metabolic syndrome results in what?

A

significant risk for development of type II DM

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47
Q

Clinical Manifestations of Type II diabetes

A
  • Symptoms often nonspecific
  • Sometimes similar to Type I (3 P’s)
  • More commonly: fatigue, recurrent infections, prolonged wound healing, changes in visual acuity, peripheral neuropathy
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48
Q

Age of onset Type I vs. Type II Diabetes

A

Type I Diabetes: <30yo; peaks at 11-30

Type II Diabetes: >35yo

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49
Q

Type of onset Type I vs. Type II Diabetes

A

Type I Diabetes: Rapis onset

Type II Diabetes: Gradual onset

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50
Q

Prevalence Type I vs. Type II Diabetes

A

Type I Diabetes: 5-10%

Type II Diabetes: 90%

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51
Q

Environmental Factors Type I vs. Type II Diabetes

A

Type I Diabetes: Virus; toxins
Type II Diabetes: Insulin resistance, decreased insulin
production, altered adipokin production

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52
Q

Islet-Cell Antibodies Type I vs. Type II Diabetes

A

Type I Diabetes: Often present at onset

Type II Diabetes: None

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53
Q

Endogenous Insulin Type I vs. Type II Diabetes

A

Type I Diabetes: Minimal or absent

Type II Diabetes: Possibly excessive, reduced utilization, diminishes over time

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54
Q

Nutritional Status Type I vs. Type II Diabetes

A

Type I Diabetes: Thin, catabolic state

Type II Diabetes: Obese or normal

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55
Q

Symptoms Type I vs. Type II Diabetes

A

Type I Diabetes: 3 P’s and fatigue
Type II Diabetes: Often none, fatigue, recurrent
infection + 3 P’s

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56
Q

Ketosis Type I vs. Type II Diabetes

A

Type I Diabetes: Prone at onset or during insulin deficiency

Type II Diabetes: Resistant except infection or stress

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57
Q

Nutritional Therapy Type I vs. Type II Diabetes

A

Type I Diabetes: Essential

Type II Diabetes: Essential

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58
Q

Insulin Type I vs. Type II Diabetes

A

Type I Diabetes: Required for all

Type II Diabetes: Required for some

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59
Q

Oral Hyperglycemic Agents Type I vs. Type II Diabetes

A

Type I Diabetes: Not Indicated

Type II Diabetes: Often Beneficial

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60
Q

Vascular and neurological complications Type I vs. Type II Diabetes

A

Type I Diabetes: Frequent

Type II Diabetes: Frequent

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61
Q

Type II diabetes diagnostic studies
Three methods of diagnosis; must be confirmed with
additional test (any method) on another day

A
  1. Fasting glucose > 7 mmol/L
  2. Random glucose ≥11.1 mmol/L plus symptoms
  3. Two hour OGTT (oral glucose tolerance test) with 75 g glucose load
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62
Q

Glycosylated Hemoglobin

A
  • aka HgbA1C
  • Determines glycemic control over time
  • Last three months (really last 6-8/52); usually assessed q3/12
  • Test shows the amount of glucose that has been attached to Hgb molecules
  • Target: 7% - lower is not better, demonstrates increased risk of CV events
  • For older adults – should match their age i.e. – 80 y.o.
    should be 8% - if too low increases risk for hypoglycemia
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63
Q

Goals of collaborative care for type II diabetes

A
  • Glycemic control:
    ~ Fasting blood sugar 4-7 mmol/L
    ~ Post prandial 5-10 mmol/L (within 1-2h after meals)
  • Prevent acute and chronic complications
  • Empower patients via education to promote self-management of disease
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64
Q

Team members involved in care of DMII

A
  • Primary care practitioner
  • Diabetic educator
  • Dietitian
  • Pharmacist
  • Endocrinologist
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65
Q

Nutritional Therapy in DM

A
  • Cornerstone of DM therapy
  • Education essential
  • Although labeled a diabetic diet – truly, it is just a healthy diet we should all be eating
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66
Q

Highlights of nutritional therapy for DM

A
  • Three meals per day at regular times, no longer than 6 hours apart
  • Limit sugar (pop, dessert, candy, jam, honey)
  • Limit high-fat foods
  • Eat more high-fiber foods
  • Drink water
  • Add physical activity
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67
Q

Type I Nutritional Therapy

A

Meals based on preferred foods and balanced with insulin and exercise pattern

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68
Q

Type II Nutritional Therapy

A
  • 80-90% of type II DM are overweight
  • Nutritional therapy is focused on glucose, lipid, BP control and weight loss
  • Weight loss of 5-7% of body weight improves glycemic control
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69
Q

Alcohol considerations in Diabetes

A
  • High calories, no nutritive value, contributes to increased triglycerides
  • High risk for hypoglycemia, may be delayed in type I by up to 24 h
  • 1-2 drinks per day or <14/wk for men and <9/wk for women
  • Decreased risk for hypoglycemia by having drink with food
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70
Q

Evaluation of Nutritional Therapy

A
  • lab work – HgbA1C, lipid profile, eGFR urine ACR
  • Blood pressure
  • Body weight, BMI, waist circumference
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71
Q

Benefits of exercise for diabetic patients

A
  • Once again – not just for diabetics!
  • Great way to burn off excess sugar
  • ↑ insulin sensitivity = ↓blood glucose
  • Contributes to weight loss
  • ↓need for diabetic medicines
  • ↓triglycerides and LDL and ↑ HDL
  • ↓ blood pressure and improves circulation
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72
Q

How much exercise should someone with Type II diabetes be getting after medical clearance?

A

Type II 150 min/week over at least three sessions – only counts if
you sweat, should include weight bearing exercise

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73
Q

Risk of exercise in person with diabetes

A

↑risk for hypoglycemia if on medications that can cause

hypoglycemia

74
Q

How to prevent hypoglycemia after exercise?

A

time 1 h after meals, or have a snack prior to exercise; carry fast-acting sugar

75
Q

How to evaluate for symptoms and titration of

medicines?

A

Blood glucose monitoring

76
Q

Fasting Glucose Target Value

A

4-7 mmol/L

77
Q

Post Prandial (1-2 hours after meals) Target Values

A

5-10 mmol/L

78
Q

Indication of Insulin in Type I diabetes

A

Required from diagnosis

79
Q

Indication of Insulin in Type II diabetes

A
  1. Required when lifestyle modifications (diet, exercise)
    and oral anti-hyperglycemics are inadequate for
    glycemic control.
  2. Required when HgbA1c is markedly increased at
    diagnosis.
  3. Required with acute episodic health challenges –
    increased stress, illness, infection = hyperglycemia; also
    may not be able to tolerate usual oral medications d/t
    nature of illness, surgery etc.
80
Q

Classifications of insulin

A 
Rapid
short
intermediate
long
mixes
81
Q

Long-Acting (Basal) Background Insulin

A
  • i.e. - Lantus and Levemir
  • extended long-acting insulin with steady release over 24 h period
  • no peak; ↓↓ risk of hypoglycemia
  • OD administration; cannot be mixed with any other
    insulin
82
Q

Intermediate–Acting (Basal) Insulin

A
  • i.e. NPH
  • More often administered BID, total daily dose divided 2/3 with BF and 1/3 with supper
  • Often used in combination with mealtime insulin
83
Q

Mealtime Insulin (Bolus)

A
  • i.e. – Humalog and Novorapid
  • Onset of action 10-15min
  • Best mimics natural insulin secretion r/t meals
  • Give when food is insight
  • Often used in combination with long or intermediate
    acting insulin for more consistent glycemic control
  • Titrated by glucose readings
  • ALSO: Regular insulin – action 30-60 minutes, so
    administration should be timed 30-35 min prior to meal
84
Q

Insulin Mechanism of Action:

A

Substitute for endogenous insulin; allows for metabolism of carbohydrates, fats, and proteins; for the storage of insulin in the liver, and conversion of glycogen to fat stores

85
Q

Insulin Contraindications

A

Allergy; hypoglycemia

86
Q

Insulin Adverse Reactions

A

Hypoglycemia (d/t too much insulin!); also tachycardia,
palpitations, headache, lethargy, tremors, weakness, fatigue, delirium, sweating, blurred vision, dry mouth, hunger, nausea, flushing, rash, urticaria, anaphylaxis

87
Q

Insulin Interactions

A

Numerous drug-drug that result in hypo or hyperglycemia

88
Q

Insulin Allergic Reaction

A
  • Generally local – erythema, pruritus at injection site
  • Self-limiting – first 1-3 months of therapy
  • Low dose antihistamine
  • True anaphylaxis or urticaria very rare - r/t use of animal insulins
89
Q

Lipodystrophy

A
  • Hypertrophy or atrophy of SC tissue at injection sites
  • d/t using the same site repeatedly
  • Thickening of tissues = inconsistent absorption
  • Mostly with animal insulins
90
Q

Somogyi Effect

A
  • Characterized by wide difference in early morning low and fasting high glucose levels
  • Generally occurs during hours of sleep
    } First, decline in blood glucose in response to too much insulin
  • Second, counter-regulatory hormones stimulates lipolysis,
    gluconeogenesis, glycogenolysis – result: rebound
    hyperglycemia and ketosis
  • PROBLEMATIC! Morning glucose readings are high so MORE INSULIN gets administered
91
Q

Somogyi Effect Manifestations:

A

headache, nightmares, night sweats

92
Q

Somogyi Effect Treatment

A

checking blood glucose between 0200-0400h,

titrate insulin accordingly (reduce hs insulin, ensure bedtime snack, monitor ETOH use)

93
Q

Dawn Phenomenon

A

Hyperglycemia upon waking d/t the release of counterregulatory hormones in the predawn hours (body’s normal way to kick your behind out of bed!)

94
Q

Dawn Phenomenon Contributory Factors

A

– cortisol and growth hormones

- Affects most people with DM, esp. when growth hormone is at its peak in adolescence and young adulthood

95
Q

Dawn Phenomenon Treatment

A

checking blood glucose between 0200-0400h

(make sure this is not Somogyi effect); increase insulin dose, monitor diet, quality/quantity of hs snack

96
Q

Acute complications of DM

A
  • Hypoglycemia
  • Diabetic Ketoacidosis (DKA)
  • Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHS)
97
Q

Chronic complications of DM

A 
Microvascular:
- Retinopathy
- Nephropathy
- Neuropathy (Peripheral and Autonomic)
Macrovascular:
- Atherosclerosis (CAD, PAD)
ALSO:
- Foot Complications
- Integumentary Complications
- Infection
98
Q

Target fasting blood glucose

A

4-7 mmol/L

99
Q

Target postprandial (1-2 hours pc meals)

A

5-10 mmol/L

100
Q

Hypoglycemia

A

Occurs when too much insulin vs. glucose

Low Blood glucose

101
Q

Hypoglycemia Objective assessment

A

blood glucose < 4 mmol/L

102
Q

Hypoglycemia Subjective assessment

A

individual symptoms of hypoglycemia vary

- some people tolerate lower sugars better, other not so much

103
Q

Causes of Hypoglycemia

A
  • Too much insulin (also occurs with oral antihyperglycemics)
  • Not enough food (meals to small or omitted)
  • Mismatch in timing of insulin administration and food intake
  • Excessive exercise
  • Medication side effects
  • Weight loss without adjustment of diabetic medications
  • ETOH intake without food
104
Q

Signs and symptoms of hypoglycemia

A
  • Cold clammy skin
  • Numbness fingers, toes, mouth
  • Rapid heartbeat
  • Emotional changes
  • Nightmares, disrupted sleep
  • Headache
  • Nervousness, tremors
  • Faintness, dizziness
  • Unsteady gait, slurred speech
  • Hunger
  • Vision changes
  • Seizures, coma
105
Q

Treatment of Hypoglycemia

A
  • Test blood sugar if able
  • 15-20g of simple carbohydrates and repeat blood sugar in 15 minutes – what is the target value?
  • Repeat until relief obtained
  • If meal is > 1 hour away snack of starch and protein
    (cheese and crackers, cereal and milk, PB sandwich)
  • Avoid overtreatment to prevent rebound hyperglycemia
106
Q

Examples of Simple Carbohydrates:

A
  • Juice box
  • Glucose tabs
  • ½ roll of lifesavers
  • Hard candies
  • Cake icing tubes
    NOT:
  • Cupcakes, cookies, ice cream (fat delays absorption of glucose)
107
Q

Prevention Focused Education

A
  • S & S of hypoglycemia
  • Treatment of hypoglycemia (at home and away)
  • Education of family, friends, coworkers re: hypoglycemia
  • Review recent blood sugar readings (look for patterns and changes)
  • Review medication regimen (dose vs. food, insulin
    administration)
  • Review diet, use of food diary, importance of snacks
  • Review compensation for exercise
108
Q

Treatment of Hypoglycemia in hospital

A
  • Follow facility hypoglycemic protocol
  • 15-20g of simple carbohydrates and repeat blood sugar in 15 minutes
  • Repeat until relief obtained
  • Use pudding/baby food for patients with dysphagia
  • Glucagon I mg IM/SC (hepatic response, converts glycogen to glucose; can result in rebound hypoglycemia)
  • Dextrose 50% via IV infusion
109
Q

Follow up of hypoglycemia

A
  • Document, notify MRP as per facility protocol
  • Generally, adjustment of medication regimen is made
  • Blood sugar target may be adjusted to decrease risk of hypoglycemia in high-risk populations (older adults,
    brittle diabetics)
110
Q 
Diabetic Ketoacidosis (DKA)
aka diabetic acidosis or diabetic coma
A
  • No insulin so body metabolizes fats instead
  • Characterized by hyperglycemia, ketosis, acidosis, and dehydration
  • More common in type I; also in type II with severe
    illness/stress
111
Q

Contributing factors of Diabetic Ketoacidosis (DKA)

A
  • Illness (esp. with dehydration, N/V)
  • Infection
  • Inadequate insulin, insulin omission
  • Undiagnosed type I DM (often presenting episode)
  • Poor self-management
  • Change in diet, medications, exercise
112
Q

Pathophysiology of Diabetic Ketoacidosis (DKA)

A
  • No insulin means glucose can not be used for fuel
  • Body uses fat for fuel – acidic by-product of fat metabolism is ketones
  • Ketones alters body’s pH balance – metabolic acidosis
  • Ketonuria – ketone bodies secreted in urine; cations also excreted in an effort to maintain electrical neutrality
113
Q

Is Diabetic Ketoacidosis (DKA) a medical emergency

A

YES!

114
Q

What does lack of insulin do?

A
  • Impairs protein synthesis and ++ protein degradation = nitrogen loss from tissues
  • Stimulates production from amino acid (from protein) in liver – compounds hyperglycemia
  • Hyperglycemia causes osmotic diuresis – depletes Na, K, Mg, PO4
115
Q

How does Diabetic Ketoacidosis (DKA) lead to death?

A
  • Acidosis causes N & V and more fluid and lyte loss
  • Progresses to hypovolemia and shock
  • Hypovolemic shock = acute renal failure (ARF) – causes retention of ketones and glucose and progresses metabolic acidosis
  • Untreated – comatose d/t dehydration, lyte imbalance and acidosis - DEATH
116
Q

Clinical manifestations of Diabetic Ketoacidosis (DKA)

A
  • Early – lethargy and weakness
  • Polyuria and polydipsia – contribute to dehydration
  • Dehydration: poor skin turgor, dry mucous membranes, tachycardia, pulse weak, orthostatic hypotension; skin dry and flushed, eyes sunken, fever
  • Nausea, vomiting, abd pain
  • Oral or vaginal candida albicans (yeast infection)
  • Restlessness, confusion
  • Kussmaul’s Respirations (rapid, deep, breathing with dyspnea
  • Acetone breath – sweet, fruity odour
  • Hyperglycemia
  • ABG’s – ph < 7.35 HC03 < 15 mmol/L
  • Ketones in blood and urine
117
Q

Emergency Management of Diabetic Ketoacidosis (DKA)

A
  • ABC’s – ensure patent airway, O2 prn
  • Establish IV access for:
    • Fluid resuscitation - what solution and why?
    • Goal to increase urine output to _______ mL/H
    • IV insulin bolus followed by infusion
    • IV KCL to prevent/correct hypokalemia (K+ may be
      normal but with insulin administration K+ will shift
      into cells)
    • IV NaHCO3 for severe acidosis (<7 mmol/H)
118
Q

Nursing Interventions for Diabetic Ketoacidosis (DKA)

A
  • Establish diabetic history, last dose of insulin, last PO
    intake
  • Monitor VS and SpO2, LOC, cardiac rhythm (ECG
    monitoring)
  • Monitor in & outs (fluid balance)
  • Assess respiratory status
  • Assess cardiovascular status
  • Monitor serum glucose, electrolytes, and ABG’s
  • Assess blood and urine for ketones
119
Q

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHS) occurs when?

A

Occurs in diabetics who have enough insulin to prevent DKA, but not enough insulin to prevent severe
hyperglycemia, osmotic diuresis, and ECF depletion

120
Q

Which is more common, HHS or DKA?

A

DKA

121
Q

Primary difference between Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHS) and Diabetic Ketoacidosis (DKA)

A
  • Primary difference between DKA and HHS – enough
    insulin to prevent ketoacidosis
  • Has fewer symptoms, so hyperglycemia quite significant prior to recognition
122
Q

Clinical Manifestations of Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHS)

A
  • Hyperglycemia causes increase in serum osmolarity,
    causing severe neurological manifestations
  • Somnolence, coma, seizures, hemiparesis, aphasia
  • Commonly occurs in older adults with type II DM –
    presenting as:
    • impaired thirst and/or functional inability to replace
      fluids
    • History of inadequate fluid intake, mental
      depression, polyuria
  • Lab Work reveals: blood glucose > 23 mmol/L, increased serum osmolarity and minimal to no ketone bodies in serum/urine
123
Q

Emergency Management of Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHS)

A
  • Similar to DKA
  • IV administration of 0.9 % or 0.45 % NaCL
  • Regular insulin via bolus followed by continuous infusion
  • IV fluids changed when blood glucose about 14 mmol/L to prevent rebound hypoglycemia (what solution will they use?)
  • Electrolytes monitored and replaced; K loss not as profound as in DKA
124
Q

Nursing interventions of Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHS)

A
  • Monitor VS, blood glucose readings, laboratory values, in and outs (fluid balance), ECG monitoring
  • Medication administration and IV therapy
  • Assess neurovascular, cardiovascular, respiratory status
125
Q

Macrovascular

A

large and medium sized vessels

126
Q

Dislipidemia

A
  • ↑LDL (bad cholesterol) – diet related
  • ↓HDL (good cholesterol) – increases with exercise
  • ↑ triglycerides - from diet high in sweets and ETOH
127
Q

Dislipidemia can result in:

A 
Cerebrovascular Disease (CVA)
Cardiovascular Disease (HTN, angina, MI),
Peripheral vascular disease (intermittent claudication, lower extremity amputation)
128
Q

Macrovascular complications are further complicated

by many modifiable lifestyle factors, such as:

A
  • High BP
  • Smoking
  • Overweight
  • High fat and cholesterol levels
  • Sedentary lifestyle
129
Q

Treatment of Macrovascular complications

A
  • Routine Screening: BP (target <130-80 mmHg), serum
    lipid profile
  • Tight glycemic control (HgbA1c <7)
  • Lifestyle modifications: low-fat diabetic diet, weight loss, exercise, ETOH in moderation, smoking cessation
  • Low dose ASA
  • Medications for dyslipidemia: statins, also fibrates, EFA’s like salmon oil capsules
130
Q

Microvascular Complications

A
  • Persistent hyperglycemia causes thickening of vessel
    membranes in the capillaries and arterioles
  • These complications are specific to DM
131
Q

Three main microvascular complications

A
  1. Eyes – retinopathy
  2. Kidneys – nephropathy
  3. Feet and lower extremities – neuropathy
132
Q

Retinopathy

A
  • Microvascular damage to the vessels of the retina from chronic hyperglycemia
  • DM for 15 years: 100% in type I and 80% type II
  • Most common cause of new-onset blindness in people of working age
133
Q

Two types of retinopathy

A

Proliferative: more severe – risk of blindness 50 % with
no treatment
Non-Proliferative: more common – risk of blindness if macula involved

134
Q

Proliferative Retinopathy

A
  • retinal capillary occlusion result in new vessels being
    formed, BUT these new vessels are ++ fragile and hemorrhage easily
  • vessels tear and bleed – see ‘floaters’ black or red spots or lines
  • can result in retinal tear or detachment (eye emergency!)
135
Q

Non-proliferative Retinopathy

A
  • partial occlusion of vessels causes microaneurysms in
    capillary walls
  • resulting in fluid leaking out and retinal edema,
    progressing to exudates or intraretinal hemorrhage
136
Q

Collaborative Interventions of retinopathy

A
  • Prevention!

- Annual dilated eye exam by ophthalmologist

137
Q

Treatment of retinopathy

A
  1. Photocoagulation
  2. Cryotherapy
  3. Vitrectomy
138
Q

Photocoagulation

A

laser destruction of ischemic areas of retina to prevent the formation of new fragile vessels

139
Q

Cryotherapy

A

for peripheral retina that cannot be reached

by laser; topical anesthetic and freezing of trouble spots

140
Q

Vitrectomy

A

aspiration of blood, membrane, fibres from the eye via a small incision just behind the cornea

141
Q

Nephropathy in Diabetes

A
  • Microvascular damage to the small blood vessel that
    supply the glomeruli of the kidney
  • Leading cause of end-stage kidney disease
  • Similar risk regardless of type of diabetes
142
Q

Risk factors for nephropathy

A
  • HTN
  • Genetic predisposition
  • Smoking
  • Chronic hyperglycemia
143
Q

Treatment of nephropathy

A
  • Routine screening: urine for ACR (albumin-creatinine
    ratio); serum for eGFR, creatinine
  • Tight glycemic control (HgbA1c <7)
  • Lifestyle modifications: weight loss, exercise, smoking
    cessation, ETOH in moderation
  • Aggressive management of HTN: target BP < 120/70; ACE or ARB (even in absence of HTN d/t renal protective properties that prevent progression of nephropathy)
144
Q

Neuropathy in diabetes

A
  • Occurs in 60-70% of people with diabetes (= in both type I and II)
  • Most commonly – peripheral sensory neuropathy – causes loss of protective sensation in feet and lower extremities – can result in lower limb amputation
  • Also autonomic neuropathy – affects CNS
145
Q

Etiology of Neuropathy

A
  • Not well understood
  • Theories include metabolic, vascular, and autoimmune
    causation
  • Most accepted theory– hyperglycemia
    • Bathes nerves in sorbitol and fructose resulting in reduced nerve conduction and demyelination
    • Contributes to ischemia that supply peripheral nerves
146
Q

Sensory Neuropathy

A
  • Most common – distal symmetrical neuropathy
  • Affects the hands, the feet, or both
  • aka ‘stocking-glove neuropathy’
147
Q

Sensory Neuropathy Clinical Manifestations

A
  • Paresthesias: tingling, burning, itching
  • Pain: burning, cramping, crushing, tearing – worse at night, may only occur at night
  • Loss of sensation: complete or partial
  • Unable to determine hot or cold temperature
  • Feeling of walking on pillows or numb feet
  • Hyperesthesia – hyper-sensitive skin – bothered by light pressure i.e. – bed linen
  • Atrophy of small muscle of hands or feet secondary to
    neuropathy can cause deformity and limit ROM
148
Q

Sensory Neuropathy Potential Risks

A
  • LOPS – loss of protective sensation = foot ulcer or injury unknown to patient d/t lack of sensation
  • Infection (cellulitis), amputation vs. poor wound healing
  • Falls d/t lack of sensation, altered gait
  • Limits activity level and tolerance
149
Q

Treatment of Sensory Neuropathy

A
  • Tight glycemic control

- Prevention!

150
Q

Medications for Sensory Neuropathy

A
  • Topical creams (Capsaicin)
  • TCA’s (Amitriptyline, Nortriptyline)
  • SSRIs and SNRIs (i.e. – Effexor, Cymbalta)
  • Anticonvulsants ( i.e. –Gabapentin, Lyrica)
151
Q

Prevention Strategies for Sensory Neuropathy

A

10 point monofilament exam, tuning fork, checking pulses, skin inspection

152
Q

Patient education for Sensory Neuropathy

A
  • Wash feet daily and inspect; check water temperature
  • Lotion application to prevent drying
  • Avoid open-toed, open heel, high heel shoes
  • Wear slippers to avoid injury
  • Clean absorbent socks (cotton, wool); keep feet dry
  • No heating pads or hot water bottles
  • Trim nails evenly, no foot blades
  • Go to diabetic foot care nurse
  • Exercise, ROM, elevate, avoid crossing
153
Q

Manifestations of Autonomic Neuropathy

A
  • Hypoglycemic unawareness
    GI
  • Bowel incontinence and diarrhea
  • Gastroparesis – delayed gastric emptying – can lead to anorexia, Nausea, vomiting, GERD, persistent fullness; can trigger hypoglycemia d/t delayed food absorption
    GU
  • Neurogenic bladder – decreased sensation of inner bladder wall – urinary retention (dysuria, weak stream)
  • urinary incontinence
  • ED(often first manifestation of autonomic failure); decreased libido; vaginitis
    CVS
  • Postural hypotension, resting tachycardia, silent MI
154
Q

Most common cause of hospitalization for people with DM

A

Lower Extremity Complications

155
Q

Lower Extremity Complications Multifactorial Etiology

A
  • DM micro and macrovascular disease – LOPS –
    injury/infection – amputation
  • Sensory neuropathy
  • Peripheral vascular disease (PVD)
  • Poor glycemic control
  • Smoking
  • Clotting abnormalities
  • Impaired immune function (delayed healing)
  • Improper footwear, bare feet, stepping on foreign body common injury
156
Q

Peripheral Vascular Disease (PVD)

A
  • Reduced blood flow to lower extremities
  • Decreased oxygen, WBC’s, vital nutrients
  • Delayed wound healing and increased infection
  • DM: blood is more viscous
157
Q

Clinical Manifestations of Peripheral Vascular Disease (PVD)

A
  • Intermittent claudication (pain with walking)
  • Pain at rest, dependent rubor
  • Cold feet, loss of hair
  • Delayed cap refill
158
Q

Treatment of Peripheral Vascular Disease (PVD)

A

Reducing risk factors (tight glycemic control, smoking

cessation, proactive foot care)

159
Q

Oral Anti-Hyperglycemics

A 
Biguanides
Sulfonylureas
Meglitinides
Thiazolidinediones
a–Glucosidase Inhibitors
Dipeptidyl Peptidase-4 (DPP-4) Inhibitor
160
Q

The only drug in the class Biguanide

A

Metformin (glucophage)

161
Q

‘ the key to open cells so they can use glucose’

A
  1. ↓ glucose production by the liver
  2. ↓ intestinal absorption of glucose
  3. ↑ insulin receptor sensitivity in liver, skeletal muscle, and adipose tissue = ↑ glucose uptake
162
Q

Metformin is used in which type of diabetes?

A

Ty II Diabetes

163
Q

Pros of Biguanide

A
  • No weight gain
  • No hypoglycemia – does not ↑ insulin secretion from
    pancreas
  • Improves lipid profile - ↑ glucose uptake = ↓ liver production of triglycerides and cholesterol
  • Can be used in pre-diabetes, esp. if obese and IFG; can reduce risk of progression to type II DM by 30%
164
Q

Cons of Biguanide

A
  • Terrible GI side fx: diarrhea, cramping, bloating, nausea – usually self-limiting; give with food
  • Risk for lactic acidosis and ARF: with radiological contrast with iodine; held prior to such exams; kidney function evaluated prior re-start of Metformin
165
Q

Sulfonylureas; Examples and what does it do?

A
  • e.g. – Diamicron (glicazide), DiaBeta (glyburide)
    2nd generation
  • ‘the anchor’ or oral therapy fro type II DM for 30+ years ‘squeeze the insulin out of the pancreas’
  • ↑ beta cell insulin production from the pancreas (requires some beta cell function)
    Also
  • Enhances action of insulin = ↑glucose uptake
  • Slows insulin degradation in liver
166
Q

Cons of Sulfonylureas

A
  • Hypoglycemia, esp. with renal impairment and older adults; also r/t drug interactions
  • Decreased effectiveness with prolonged use (r/t beta cell function)
167
Q

Two drugs in the class Meglitinides

A

GlucoNorm (repaglinide) & Starlix (nateglinide)

168
Q

How do Meglitinides work?

A
  • ↑ insulin production from pancreas
  • Very similar action to sulfonylureas BUT faster action and excretion= ↓ r/f hypoglycemia
  • Taken prior to meals
169
Q

Pros of Meglitinides

A
  • ↓hypoglycemia

- Good for people with irregular mealtimes

170
Q

Cons of Meglitinides

A
  • Side fx: headache, weight gain, hypoglycemia, dizziness, joint pain,
  • Drug interactions: ↑ r/f hypoglycemia and hyperglycemia
171
Q

Exemplar Thiazolidinediones

A

aka insulin sensitizing drugs, glitazones,

  • Actos (pioglitazone)
  • Avandia (rosiglitazone)
172
Q

Pros of Thiazolidinediones

A
  • Improve insulin sensitivity, transport, and utilization at target tissues
  • Stimulate peripheral glucose uptake
  • ↓ glucose and triglyceride production in the liver
  • Most effective for people with insulin resistance
173
Q

Cons of Thiazolidinediones

A
  • Moderate weight gain, edema, fluid retention, mild anemia (concerns re use in CHF)
  • Concerns re: liver toxicity - LFTs monitored
174
Q

What drug falls under the class a-Glucosidase Inhibitors, aka ‘starch blockers’

A

Glucobay (Arcabos)

175
Q

How do a-Glucosidase Inhibitors work? and other need to knows.

A
  • Less commonly used
  • Enzyme inhibitor – enzyme a-glucosidase found on brush border of small intestine
  • Slows the absorption of carbohydrates (glucose!) in the small intestine
  • Taken with first bite of main meals
  • Lowers postprandial glucose; no impact on fasting hyperglycemia
176
Q

Pros of a-Glucosidase Inhibitors

A
  • Reduce the risk of progression to type II DM by 30%

- No hypoglycemia or weight gain

177
Q

Cons of a-Glucosidase Inhibitors

A
  • GI side fx: flatulence, diarrhea, abd pain
  • Hugh dose = ↑LFTs
  • Drug interactions that cause hyperglycemia
178
Q

Dipeptidyl Peptidase-4 (DPP-4) Inhibitor exemplar drug

A

Januvia (Sitagliptin)

179
Q

How do Dipeptidyl Peptidase-4 (DPP-4) Inhibitor work?

A
  • Inhibition of DPP-4 slows the inactivation of incretin
    hormones
  • Incretin increases the synthesis and release of insulin
    from the pancreas
180
Q

Pros of Dipeptidyl Peptidase-4 (DPP-4) Inhibitor?

A
  • Glucose dependent – only respond in the presence of
    hyperglycemia – thus decreased hypoglycemia
  • Absence of weight gain

Pathophysiology and Pharmacology (17 decks)

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