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Title: Nurse Licensure Examination Review


1
Nurse Licensure Examination Review
  • Diabetes Mellitus

2
Diabetes Mellitus
  • A group of metabolic diseases characterized by
    elevated levels of glucose in the blood
    resulting from defects in insulin secretion,
    insulin action, insulin receptors or any
    combination of conditions.

3
Diabetes Mellitus
  • A chronic disorder of impaired glucose
    metabolism, protein and fat metabolism

4
Diabetes Mellitus
  • BASIC PATHOLOGY Insulin problem (deficiency or
    impaired action)

5
Diabetes Mellitus
  • Insulin is a hormone secreted by the BETA cells
    of the pancreas
  • Stimulus of insulin- HYPERGLYCEMIA

6
Diabetes Mellitus
  • Action of insulin it promotes entry of Glucose
    into the body cells by binding to the insulin
    receptor in the cell membrane

7
INSULIN Physiology
  • Insulin Metabolic Functions
  • 1. Transports and metabolizes GLUCOSE
  • 2. Promotes GLYCOGENESIS
  • 3. Promotes GLYCOLYSIS
  • 4. Enhances LIPOGENESIS
  • 5. Accelerates PROTEIN SYNTHESIS

8
Diabetes Mellitus
  • RISK FACTORS for Diabetes Mellitus
  • 1. Family History of diabetes
  • 2. Obesity
  • 3. Race/Ethnicity

9
Diabetes Mellitus
  • RISK FACTORS for Diabetes Mellitus
  • 4. Age of more than 45
  • 5. Previously unidentified IFG/IGT
  • 6. Hypertension

10
Diabetes Mellitus
  • RISK FACTORS for Diabetes Mellitus
  • 7. Hyperlipidemia
  • 8. History of Gestational Diabetes Mellitus

11
Diabetes Mellitus
  • CLASSIFICATION OF DM
  • 1. Type 1 DM
  • Insulin dependent Diabetes Mellitus
  • 2. Type 2 DM
  • Non-insulin dependent Diabetes Mellitus
  • 3. Gestational DM
  • Diabetes Mellitus diagnosed during pregnancy
  • 4. DM associated with other conditions or
    syndromes

12
Diabetes Mellitus
  • CLASSIFICATION OF DM
  • 1. Type 1 DM
  • Insulin dependent Diabetes Mellitus

13
Diabetes Mellitus
  • CLASSIFICATION OF DM
  • 2. Type 2 DM
  • Non-insulin dependent Diabetes Mellitus

14
Diabetes Mellitus
  • CLASSIFICATION OF DM
  • 3. Gestational DM
  • Diabetes Mellitus diagnosed during pregnancy

15
Diabetes Mellitus
  • CLASSIFICATION OF DM
  • 4. DM associated with other conditions or
    syndromes

16
Diabetes Mellitus
  • Other types of DM
  • 1. Impaired Glucose Tolerance
  • 2. Impaired Fasting Glucose
  • 3. Pre-diabetes

17
TYPE 1- Diabetes Mellitus
  • This type of DM is characterized by the
    destruction of the pancreatic beta cells

18
TYPE 1- Diabetes Mellitus
  • Etiology
  • 1. Genetic susceptibility- HLA DR3 and DR4
  • 2. Autoimmune response
  • 3. Toxins, unidentified viruses and environmental
    factors

19
TYPE 1- Diabetes Mellitus
  • PATHOPHYSIOLOGY
  • Destruction of BETA cells? decreased insulin
    production ? uncontrolled glucose production by
    the liver? hyperglycemia ? signs and symptoms

20
TYPE 1- Diabetes Mellitus
  • PATHOPHYSIOLOGY
  • CLASSIC Ps
  • Polyuria
  • Polydipsia
  • Polyphagia

21
TYPE 2- Diabetes Mellitus
  • A type of DM characterized by insulin resistance
    and impaired insulin production

22
TYPE 2- Diabetes Mellitus
  • Etiology
  • 1. Unknown
  • 2. Probably genetic and obesity

23
TYPE 2- Diabetes Mellitus
  • PATHOPHYSIOLOGY
  • Decreased sensitivity of insulin receptor to
    insulin ? less uptake of glucose ? HYPERGLYCEMIA

24
TYPE 2- Diabetes Mellitus
  • PATHOPHYSIOLOGY
  • Decreased insulin production ? diminished insulin
    action ? hyperglycemia ? signs and symptoms

25
TYPE 2- Diabetes Mellitus
  • PATHOPHYSIOLOGY
  • BUT () insulin in small amount ? prevent
    breakdown of fats ? DKA is unusual

26
GESTATIONAL Diabetes Mellitus
  • Any degree of glucose intolerance with its onset
    during pregnancy
  • Usually detected between 24-28th week gestation

27
GESTATIONAL Diabetes Mellitus
  • Blood glucose returns to normal after delivery of
    the infant
  • NEVER administer ORAL HYPOGLYCEMIC AGENTS to
    PREGNANT MOTHERS!

28
Diabetes Mellitus
  • ASSESSMENT FINDINGS
  • 1. Classic 3 Ps
  • 2. Fatigue
  • 3. Body weakness

29
Diabetes Mellitus
  • ASSESSMENT FINDINGS
  • 4. Visual changes
  • 5. Slow wound healing
  • 6. Recurrent skin and mucus membrane infections

30
Diabetes Mellitus
  • DIAGNOSTIC TESTS
  • 1. FBS- gt 126
  • 2. RBS- gt200
  • 3. OGTT- gt 200

31
Diabetes Mellitus
  • DIAGNOSTIC TESTS
  • 4. HgbA1- for monitoring!!
  • 5. Urine glucose
  • 6. Urine ketones

32
Diabetes Mellitus
  • DIAGNOSTIC CRITERIA
  • 1. FBS equal to or greater than 126 mg/dL
    (7.0mmol/L)
  • (Normal 8 hour FBS- 80-109 mg/dL)

33
Diabetes Mellitus
  • DIAGNOSTIC CRITERIA
  • 2. OGTT value 1 and 2 hours post-prandial equal
    to or greater than 200 mg/dL
  • Normal OGTT 1 and 2 hours post-prandial- is
  • 140 mg/dL

34
Diabetes Mellitus
  • DIAGNOSTIC CRITERIA
  • 3. RBS of equal to or greater than 200 mg/dL PLUS
    the 3 Ps

35
Diabetes Mellitus
  • NURSING MANAGEMENT OF DM
  • The main goal is to NORMALIZE insulin activity
    and blood glucose level by

36
Diabetes Mellitus
  • NURSING MANAGEMENT OF DM
  • 1. Nutritional modification
  • 2. Regular Exercise
  • 3. Regular Glucose Monitoring
  • 4. Drug therapy
  • 5. Client Education

37
Diabetes Mellitus
  • The Patient with DM
  • HISTORY
  • Symptoms and characteristics
  • PHYSICAL EXAMINATION
  • VS, BMI, Fundoscopy, Neuro
  • LABORATORY EXAMINATION
  • FBS, RBS, HgbA1c, lipid profile, ECG, UA
  • REFERRALS
  • Ophthalmologist, Podiatrist, Dietician, etc..

38
Diabetes Mellitus
  • The Patient with DM
  • HISTORY
  • Symptoms and characteristics
  • PHYSICAL EXAMINATION
  • VS, BMI, Fundoscopy, and Neuro assessment

39
Diabetes Mellitus
  • The Patient with DM
  • LABORATORY EXAMINATION
  • FBS, RBS, HgbA1c, lipid profile, ECG, and
    Urinalysis
  • REFERRALS
  • Ophthalmologist, Podiatrist, Dietician, etc..

40
DM Nutritional management
41
Diabetes Mellitus
  • NUTRITIONAL MANAGEMENT
  • 1.Review the patients diet history to identify
    eating habits and lifestyle
  • 2. Coordinate with the dietician in meal planning
    for weight loss

42
Diabetes Mellitus
  • NUTRITIONAL MANAGEMENT
  • 3. Plan for the caloric intake distributed as
    follows- CHO 50-60 Fats 20-30 and Proteins
    10-20
  • 4. Advise moderation in alcohol intake
  • 5. Using artificial sweeteners is acceptable

43
DM Exercise management
44
Diabetes Mellitus
  • EXERCISE Management
  • 1. Teach that exercise can lower the blood
    glucose level
  • 2. Diabetics must first control the glucose level
    before initiating exercise programs.

45
Diabetes Mellitus
  • EXERCISE Management
  • 3. Offer extra food /calories before engaging in
    exercise
  • 4. Offer snacks at the end of the exercise period
    if patient is on insulin treatment.

46
Diabetes Mellitus
  • EXERCISE Management
  • 5. Advise that exercise should be done at the
    same time every day, preferably when blood
    glucose levels are at their peak

47
Diabetes Mellitus
  • EXERCISE Management
  • 6. Regular exercise, not sporadic exercise,
    should be encouraged.
  • 7. For most patient, WALKING is the safe and
    beneficial form of exercise

48
Glucose Self Monitoring
49
Diabetes Mellitus
  • GLUCOSE MONITORING
  • Self-monitoring of blood glucose (SMBG) enables
    the patient to adjust the treatment regimen to
    obtain optimal glucose control

50
Diabetes Mellitus
  • GLUCOSE MONITORING
  • Most common method involves obtaining a drop of
    capillary blood applied to a test strip.
  • The usual recommended frequency is TWO-FOUR times
    a day.

51
Diabetes Mellitus
  • When is it done?
  • At the peak action time of the medication to
    evaluate the need for adjustments.
  • To evaluate BASAL insulin ? test before meals

52
Diabetes Mellitus
  • When is it done?
  • To titrate bolus or regular and lispro? test 2
    hours after meals.
  • To evaluate the glucose level of those taking
    ORAL hypoglycemics ? test before and two hours
    after meals.

53
Diabetes Mellitus Monitoring therapy
  • Testing the glycosylated hemoglobin (HbA1c)
  • This glycosylated hemoglobin refers to the blood
    test that reflects the average blood glucose over
    a period of TWO to THREE months.

54
Diabetes Mellitus Monitoring therapy
  • Normal value is 4 to 6
  • No patient preparation is needed for this testing
  • Done to monitor therapy

55
Diabetes Mellitus
  • Urine testing for glucose
  • Benedicts test

56
Diabetes Mellitus
  • Urine testing for ketones
  • Ketones are by-products of fat breakdown

57
Diabetes Mellitus
  • Urine testing for ketones
  • This is performed whenever TYPE 1 DM have
    glucosuria or persistent elevation of blood
    glucose, during illness, and in gestational
    diabetes

58
DM Drug therapy
59
Diabetes Mellitus
  • DRUG THERAPY and MANAGEMENT
  • Usually, this type of management is employed if
    diet modification and exercise cannot control the
    blood glucose level.

60
Diabetes Mellitus
  • DRUG THERAPY and MANAGEMENT
  • Because the patient with TYPE 1 DM cannot produce
    insulin, exogenous insulin must be administered
    for life.

61
Diabetes Mellitus
  • DRUG THERAPY and MANAGEMENT
  • TYPE 2 DM may have decreased insulin production,
    ORAL agents that stimulate insulin production are
    usually employed.

62
Diabetes Mellitus
  • PHARMACOLOGIC INSULIN
  • This may be grouped into several categories
    according to
  • 1. Source- Human, pig, or cow
  • 2. Onset of action- Rapid-acting, short-acting,
    intermediate-acting, long-acting and very long
    acting

63
Diabetes Mellitus
  • PHARMACOLOGIC INSULIN
  • This may be grouped into several categories
    according to
  • 3. Pure or mixed concentration
  • 4. Manufacturer of drug

64
Diabetes Mellitus
  • GENERALITIES
  • 1. Human insulin preparations have a shorter
    duration of action than animal source

65
Diabetes Mellitus
  • GENERALITIES
  • 2. Animal sources of insulin have animal proteins
    that may trigger allergic reaction and they may
    stimulate antibody production that may bind the
    insulin, slowing the action

66
Diabetes Mellitus
  • 3. ONLY Regular insulin can be used INTRAVENOUSLY!

67
Diabetes Mellitus
  • 4. Insulin are measured in INTERNATIONAL UNITS or
    iu
  • 5. There is a specified insulin injection
    calibrated in units

68
Diabetes Mellitus
  • RAPID ACTING INSULIN
  • Lispro (Humalog) and Insulin Aspart (Novolog)
  • Produces a more rapid effect and with a shorter
    duration than any other insulin preparation

69
Diabetes Mellitus
  • RAPID ACTING INSULIN
  • ONSET- 5-15 minutes
  • PEAK- 1 hour
  • DURATION- 3 hours
  • Instruct patient to eat within 5 to 15 minutes
    after injection

70
Diabetes Mellitus
  • REGULAR INSULIN
  • Also called Short-acting insulin
  • R
  • Usually Clear solution administered 30 minutes
    before a meal

71
Diabetes Mellitus
  • REGULAR INSULIN
  • ONSET- 30 minutes to 1 hour
  • PEAK- 2 to 3 hours
  • DURATION- 4 to 6 hours

72
Diabetes Mellitus
  • INTERMEDIATE ACTING INSULIN
  • Called NPH or LENTE
  • Appears white and cloudy

73
Diabetes Mellitus
  • INTERMEDIATE ACTING INSULIN
  • ONSET- 2-4 hours
  • PEAK- 4 to 6-12 hours
  • DURATION- 16-20 hours

74
Diabetes Mellitus
  • LONG- ACTING INSULIN
  • UltraLENTE
  • Referred to as peakless insulin

75
Diabetes Mellitus
  • LONG- ACTING INSULIN
  • ONSET- 6-8 hours
  • PEAK- 12-16 hours
  • DURATION- 20-30 hours

76
Diabetes Mellitus
  • HEALTH TEACHING
  • Regarding Insulin SELF- Administration
  • 1. Insulin is administered at home subcutaneously

77
Diabetes Mellitus
  • HEALTH TEACHING Regarding Insulin SELF-
    Administration
  • 2. Cloudy insulin should be thoroughly mixed by
    gently inverting the vial or ROLLING between the
    hands

78
Diabetes Mellitus
  • HEALTH TEACHING Regarding Insulin SELF-
    Administration
  • 3. Insulin NOT IN USE should be stored in the
    refrigerator, BUT avoid freezing/extreme
    temperature

79
Diabetes Mellitus
  • 4. Insulin IN USE should be kept at room
    temperature to reduce local irritation at the
    injection site

80
Diabetes Mellitus
  • 5. INSULIN may be kept at room temperature up to
    1 month

81
Diabetes Mellitus
  • 6. Select syringes that match the insulin
    concentration.
  • U-100 means 100 units per mL

82
Diabetes Mellitus
  • 7. Instruct the client to draw up the REGULAR
    (clear) Insulin FIRST before drawing the
    intermediate acting (cloudy) insulin

83
Diabetes Mellitus
  • 8. Pre-filled syringes can be prepared and should
    be kept in the refrigerator with the needle in
    the UPRIGHT position to avoid clogging the needle

84
Diabetes Mellitus
  • 9. The four main areas for insulin injection are-
    ABDOMEN, UPPER ARMS, THIGHS and HIPS

85
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86
Diabetes Mellitus
  • Insulin is absorbed fastest in the abdomen and
    slowest in the hips
  • Instruct the client to rotate the areas of
    injection, but exhaust all available sites in one
    area first before moving into another area.

87
Diabetes Mellitus
  • 10. Alcohol may not be used to cleanse the skin
  • 11. Utilize the subcutaneous injection technique-
    commonly, a 45-90 degree angle.

88
Diabetes Mellitus
  • 12. No need to instruct for aspirating the needle
  • 13. Properly discard the syringe after use.

89
Diabetes Mellitus
  • T-I-E
  • Test blood? Inject insulin ? Eat food

90
Diabetes Mellitus
  • COMPLICATIONS OF INSULIN THERAPY
  • 1. Local allergic reactions
  • Redness, swelling, tenderness and induration
    appearing 1-2 hours after injection
  • Usually occurs in the beginning stage of therapy

91
Diabetes Mellitus
  • COMPLICATIONS OF INSULIN THERAPY
  • 1. Local allergic reactions
  • Disappears with continued use
  • Antihistamine can be given 1 hour before
    injection time
  • Porcine and bovine insulin preparations have a
    higher tendency to produce this reaction.

92
Diabetes Mellitus
  • 2. SYSTEMIC ALLERGIC REACTIONS
  • Very rare
  • Generalized urticaria is the manifestation
  • Treatment is desensitization

93
Diabetes Mellitus
  • COMPLICATIONS OF INSULIN THERAPY
  • 3. INSULIN DYSTROPHY
  • A localized reaction in the form of lipoatrophy
    or lipohypertrophy

94
Diabetes Mellitus
  • Lipoatrophy- loss of subcutaneous fat usually
    caused by the utilization of animal insulin

95
Diabetes Mellitus
  • Lipohypertrophy- development of fibrofatty
    masses, usually caused by repeated use of
    injection site

96
Diabetes Mellitus
  • 4. INSULIN RESISTANCE
  • Most commonly caused by OBESITY
  • Defined as daily insulin requirement of more than
    200 units
  • Management- Steroids and use of more concentrated
    insulin

97
Diabetes Mellitus
  • 5. MORNING HYPERGLYCEMIA
  • Elevated blood sugar upon arising in the morning
  • Caused by insufficient level of insulin
  • DAWN phenomenon
  • SOMOGYI effect
  • INSULIN WANING

98
Diabetes Mellitus
  • DAWN PHENOMENON
  • Relatively normal blood glucose until about 3 am,
    when the glucose level begins to RISE
  • Results from the nightly surges of GROWTH HORMONE
    secretion
  • Management Bedtime injection of NPH

99
Diabetes Mellitus
  • SOMOGYI EFFECT
  • Normal or elevated blood glucose at bedtime,
    decrease blood glucose at 2-3 am due to
    hypoglycemic levels and a subsequent increase in
    blood glucose (rebound hypergycemia)

100
Diabetes Mellitus
  • SOMOGYI EFFECT
  • Nocturnal hypoglycemia followed by rebound
    hyperglycemia

101
Diabetes Mellitus
  • SOMOGYI EFFECT
  • Due to the production of counter regulatory
    hormones- glucagon. cortisol and epinephrine
  • Management- decrease evening dose of NPH or
    increase bedtime snack

102
Diabetes Mellitus
  • INSULIN WANING
  • Progressive rise in blood glucose from bedtime to
    morning
  • Seen when the NPH evening dose is administered
    before dinner
  • Management Move the insulin injection to bedtime

103
Diabetes Mellitus
  • ORAL HYPOGLYCEMIC AGENTS
  • These may be effective when used in TYPE 2 DM
    that cannot be treated with diet and exercise
  • These are NEVER used in pregnancy!

104
Diabetes Mellitus
  • ORAL HYPOGLYCEMIC AGENTS
  • There are several agents
  • Sulfonylureas
  • Biguanides
  • Alpha-glucosidase inhibitors
  • Thiazolidinediones
  • Meglitinides

105
Diabetes Mellitus
  • SULFONYLUREAS
  • MOA- stimulates the beta cells of the pancreas to
    secrete insulin
  • Classified as to generations- first and second
    generations

106
Diabetes Mellitus
  • SULFONYLUREAS
  • FIRST GENERATION- Acetoheximide, Chlorpropamide,
    Tolazamide and Tolbutamide
  • SECOND GENERATION- Glipizide, Glyburide,
    Glibenclamide, Glimepiride

107
Diabetes Mellitus Sulfonylureas
  • The most common side effects of these
    medications are Gastro-intestinal upset and
    dermatologic reactions.
  • HYPOGLYCEMIA is also a very important side-effect

108
Diabetes Mellitus Sulfonylureas
  • Chlorpropamide has a very long duration of
    action. This also produces a disulfiram-like
    reaction when taken with alcohol
  • Second generation drugs have shorter duration
    with metabolism in the kidney and liver and are
    the choice for elderly patients

109
Diabetes Mellitus
  • BIGUANIDES
  • MOA- Facilitate the action of insulin on the
    peripheral receptors
  • These can only be used in the presence of insulin

110
Diabetes Mellitus
  • BIGUANIDES formin
  • They have no effect on the beta cells of the
    pancreas
  • Metformin (Glucophage) and Phenformin are examples

111
Diabetes Mellitus Biguanides
  • The most important side effect is LACTIC
    ACIDOSIS!
  • These are not given to patient with renal
    impairment

112
Diabetes Mellitus Biguanides
  • These drugs are usually given with a sulfonylurea
    to enhance the glucose-lowering effect more than
    the use of each drug individually

113
Diabetes Mellitus
  • ALPHA-GLUCOSIDASE INHIBITORS
  • MOA- Delay the absorption of glucose in the GIT
  • Result is a lower post-prandial blood glucose
    level
  • They do not affect insulin secretion or action!
  • Side-effect DIARRHEA and FLATULENCE

114
Diabetes Mellitus
  • Examples of AGI are Acarbose and Miglitol
  • They are not absorbed systemically and are very
    safe
  • They can be used alone or in combination with
    other OHA

115
Diabetes Mellitus
  • Side-effect if used with other drug is
    HYPOGLYCEMIA
  • Note that sucrose absorption is impaired and IV
    glucose is the therapy for the hypoglycemia

116
Diabetes Mellitus
  • THIAZOLIDINEDIONES
  • MOA- Enhance insulin action at the receptor site
  • They do not stimulate insulin secretion

117
Diabetes Mellitus
  • THIAZOLIDINEDIONES
  • Examples- Rosiglitazone, Pioglitazone
  • These drugs affect LIVER FUNCTION
  • Can cause resumption of OVULATION in
    peri-menopausal anovulatory women

118
Diabetes Mellitus
  • MEGLITINIDES
  • MOA- Stimulate the secretion of insulin by the
    beta cells
  • Examples- Repaglinide and Nateglinide

119
Diabetes Mellitus
  • MEGLITINIDES
  • They have a shorter duration and fast action
  • Should be taken BEFORE meals to stimulate the
    release of insulin from the pancreas

120
Diabetes Mellitus
  • MEGLITINIDES
  • Principal side-effect of meglitinides-
    hypoglycemia
  • Can be used alone or in combination

121
Diabetes Mellitus
  • ACUTE COMPLICATIONS OF DM
  • Hypoglycemia
  • Diabetic ketoacidosis
  • Hyperglycemic hyperosmolar non-ketotic syndrome
    (HHNS)

122
Diabetes Mellitus
  • CHRONIC COMPLICATIONS OF DM
  • Macrovascular complications- MI, Stroke,
    Atherosclerosis, CAD, and Peripheral vascular
    disease
  • Microvascular complications- micro-angiopathy,
    retinopathy, nephropathy
  • Peripheral neuropathy

123
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124
Diabetes Mellitus
  • HYPOGLYCEMIA
  • Blood glucose level less than 50 to 60 mg/dL
  • Causes Too much insulin/OHA, too little food and
    excessive physical activity
  • Mild- 40-60
  • Moderate- 20-40
  • Severe- less than 20

125
HYPOGLYCEMIA
  • ASSESSMENT FINDINGS
  • 1. Sympathetic manifestations- sweating, tremors,
    palpitations, nervousness, tachycardia and hunger

126
HYPOGLYCEMIA
  • ASSESSMENT FINDINGS
  • 2. CNS manifestations- inability to concentrate,
    headache, lightheadedness, confusion, memory
    lapses, slurred speech, impaired coordination,
    behavioral changes, double vision and drowsiness

127
HYPOGLYCEMIA
128
HYPERGLYCEMIA
129
HYPOGLYCEMIA
  • DIAGNOSTIC FINDINGS
  • RBS- less than 50-60 mg/dL level

130
HYPOGLYCEMIA
  • Nursing Interventions
  • 1. Immediate treatment with the use of foods with
    simple sugar- glucose tablets, fruit juice, table
    sugar, honey or hard candies

131
HYPOGLYCEMIA
  • Nursing Interventions
  • 2. For unconscious patients- glucagon injection 1
    mg IM/SQ or IV 25 to 50 mL of D50/50

132
HYPOGLYCEMIA
  • Nursing Interventions
  • 3. re-test glucose level in 15 minutes and
    re-treat if less than 75 mg/dL
  • 4. Teach patient to refrain from eating
    high-calorie, high-fat desserts

133
HYPOGLYCEMIA
  • Nursing Interventions
  • 5. Advise in-between snacks, especially when
    physical activity is increased
  • 6. Teach the importance of compliance to
    medications

134
Diabetic Ketoacidosis
  • This is cause by the absence of insulin leading
    to fat breakdown and production of ketone bodies
  • Three main clinical features
  • 1. HYPERGLYCEMIA
  • 2. DEHYDRATION electrolyte loss
  • 3. ACIDOSIS

135
DKA
  • PATHOPHYSIOLOGY
  • No insulin? reduced glucose breakdown and
    increased liver glucose production ? Hyperglycemia

136
DKA
  • PATHOPHYSIOLOGY
  • Hyperglycemia? kidney attempts to excrete glucose
    ? increased osmotic load ? diuresis ? Dehydration

137
DKA
  • PATHOPHYSIOLOGY
  • No glucose in the cell? fat is broken down for
    energy ? ketone bodies are produced? Ketoacidosis

138
DKA
  • Risk factors
  • 1. infection or illness- common
  • 2. stress
  • 3. undiagnosed DM
  • 4. inadequate insulin, missed dose of insulin

139
DKA
  • ASSESSMENT FINDINGS
  • 1. 3 Ps
  • 2. Headache, blurred vision and weakness
  • 3. Orthostatic hypotension

140
DKA
  • ASSESSMENT FINDINGS
  • 4. Nausea, vomiting and abdominal pain
  • 5. Acetone (fruity) breath
  • 6. Hyperventilation or KUSSMAULs breathing

141
HYPERGLYCEMIA
142
Hyperglycemia
143
DKA
  • LABORATORY FINDINGS
  • 1. Blood glucose level of 300-800 mg/dL
  • 2. Urinary ketones

144
DKA
  • LABORATORY FINDINGS
  • 3. ABG result of metabolic acidosis- LOW pH, LOW
    pCO2 as a compensation, LOW bicarbonate
  • 4. Electrolyte imbalances- potassium levels may
    be HIGH due to acidosis and dehydration

145
DKA
  • NURSING INTERVENTIONS
  • 1. Assist in the correction of dehydration
  • Up to 6 liters of fluid may be ordered for
    infusion, initially NSS then D5W
  • Monitor hydration status
  • Monitor I and O
  • Monitor for volume overload

146
DKA
  • NURSING INTERVENTIONS
  • 2. Assist in restoring Electrolytes
  • Kidney function is FIRST determined before giving
    potassium supplements!

147
DKA
  • NURSING INTERVENTIONS
  • 3. Reverse the Acidosis
  • REGULAR insulin injection is ordered IV bolus
    5-10 units
  • The insulin is followed by drip infusion in units
    per hour
  • BICARBONATE is not used!

148
HHNS
  • A serious condition in which hyperosmolarity and
    extreme hyperglycemia predominate
  • Ketosis is minimal
  • Onset is slow and takes hours to days to develop

149
HHNS
  • PATHOPHYSIOLOGY
  • Lack of insulin action or Insulin resistance ?
    hyperglycemia
  • Hyperglycemia? osmotic diuresis ? loss of water
    and electrolytes

150
HHNS
  • PATHOPHYSIOLOGY
  • Insulin is too low to prevent hyperglycemia but
    enough to prevent fat breakdown
  • Occurs most commonly in type 2 DM, ages 50-70

151
HHNS
  • Precipitating factors
  • 1. Infection
  • 2. Stress
  • 3. Surgery
  • 4. Medication like thiazides
  • 5. Treatment like dialysis

152
HHNS
  • ASSESSMENT FINDINGS
  • 1. Profound dehydration
  • 2. Hypotension
  • 3. Tachycardia
  • 4. Altered sensorium
  • 5. Seizures and hemiparesis

153
HHNS
  • DIAGNOSTIC TESTS
  • 1. Blood glucose- 600 to 1,200 mg/dL
  • 2. Blood osmolality- 350 mOsm/L
  • 3. Electrolyte abnormalities

154
HHNS
  • NURSING INTERVENTIONS
  • Approach is similar to the DKA
  • 1. Correction of Dehydration by IVF
  • 2. Correction of electrolyte imbalance by
    replacement therapy

155
HHNS
  • NURSING INTERVENTIONS
  • 3. Administration of insulin injection and drips
  • 4. Continuous monitoring of urine output

156
MACROVASCULAR CX
  • Nursing management
  • 1. Diet modification
  • 2. Exercise

157
MACROVASCULAR CX
  • Nursing management
  • 3. Prevention and treatment of underlying
    conditions such as MI, CAD and stroke
  • 4. Administration of prescribed medications for
    hypertension, hyperlipidemia and obesity

158
MICROVASCULAR CX
  • Retinopathy- a painless deterioration of the
    small blood vessels in the retina, may be
    classified as to background retinopathy,
    pre-proliferative and proliferative retinopathy
  • Permanent vision changes and blindness can occur

159
MICROVASCULAR CX
  • Retinopathy-ASSESSMENT FINDINGS
  • Blurry vision
  • Spotty vision
  • Asymptomatic

160
MICROVASCULAR CX
  • Retinopathy Diagnostic findings
  • 1. Fundoscopy
  • 2. Fluorescein angiography
  • Painless procedure
  • Side-effects- discoloration of the skin and urine
    for 12 hours, some allergic reactions, nausea
  • Flash of camera may be slightly uncomfortable

161
MICROVASCULAR CX
  • NURSING INTERVENTIONS
  • 1. Assist in diagnostic procedure
  • 2. Assist in the preparation for surgery- laser
    photocoagulation

162
MICROVASCULAR CX
  • NURSING INTERVENTIONS
  • 3. Health teaching regarding prevention of
    retinopathy by regular ophthalmic examinations,
    good glucose control and self-management of eye
    care regimens
  • 4. Maintain client safety

163
MICROVASCULAR CX
  • DIABETIC NEPHROPATHY
  • Progressive deterioration of kidney function

164
MICROVASCULAR CX
  • DIABETIC NEPHROPATHY
  • HYPERGLYCEMIA? causes the kidney filtration
    mechanism to be stressed ? blood proteins leak
    into the urine
  • Pressure in the kidney blood vessels increases?
    stimulate the development of nephropathy

165
MICROVASCULAR CX
  • ASSESSMENT findings for diabetic nephropathy
  • 1. Albuminuria
  • 2. Anemia
  • 3. Acidosis

166
MICROVASCULAR CX
  • ASSESSMENT findings for diabetic nephropathy
  • 4. Fluid volume overload
  • 5. Oliguria
  • 6. Hypertension
  • 7. UTI

167
MICROVASCULAR CX
  • NURSING MANAGEMENT1. Assist in the control of
    hypertension- use of ACE inhibitor
  • 2. Provide a low sodium and low protein diet
  • 3. Administer prescribed medication for UTI

168
MICROVASCULAR CX
  • NURSING MANAGEMENT
  • 4. Assist in dialysis
  • 5. Prepare patient for renal transplantation, if
    indicated

169
MICROVASCULAR CX
  • Diabetic Neuropathy
  • A group of disorders that affect all type of
    nerves including the peripheral, autonomic and
    spinal nerves

170
MICROVASCULAR CX
  • Diabetic Neuropathy
  • Two most common types of Diabetic Neuropathy are
    sensori-motor polyneuropathy and autonomic
    neuropathy

171
MICROVASCULAR CX
  • Peripheral neuropathy- ASSESSMENT findings
  • 1. paresthesias- prickling, tingling or
    heightened sensation
  • 2. decreased proprioception
  • 3. decreased sensation of light touch
  • 4. unsteady gait
  • 5. decreased tendon reflexes

172
MICROVASCULAR CX
  • Peripheral neuropathy- Nursing Management
  • 1. Provide teaching that good glucose control is
    very important to prevent its development
  • 2. Manage the pain by analgesics, antidepressants
    and nerve stimulation

173
MICROVASCULAR CX
  • Autonomic Neuropathy- ASSESSMENT findings
  • 1. Silent, painless ischemia
  • 2. delayed gastric emptying
  • 3. orthostatic hypotension
  • 4. N/V and bloating sensation
  • 5. urinary retention
  • 6. sexual dysfunction

174
MICROVASCULAR CX
  • Autonomic Neuropathy-Nursing management
  • 1. Educate about the avoidance of strenuous
    physical activity
  • 2. Stress the importance of good glucose control
    to delay the development

175
MICROVASCULAR CX
  • Autonomic Neuropathy-Nursing management
  • 3. Provide LOW-fat, small frequent feedings
  • 4. Administer bulk-forming laxatives for diabetic
    diarrhea
  • 5. Provide HIGH-fiber diet for diabetic
    constipation

176
MICROVASCULAR CX
  • MANAGEMENT OF FOOT AND LEG PROBLEMS
  • Soft tissue injury in the foot/leg? formation of
    fissures and callus ? poor wound healing ?
    foot/leg ulcer

177
MICROVASCULAR CX
  • RISK FACTORS for the development of foot and leg
    ulcers
  • 1. More than 10 years diabetic
  • 2. Age of more than 40
  • 3. Smoking
  • 4. Anatomic deformities
  • 5. History of previous leg ulcers or amputation

178
MICROVASCULAR CX
  • MANAGEMENT of Foot Ulcers
  • Teach patient proper care of the foot
  • Daily assessment of the foot
  • Use of mirror to inspect the bottom

179
MICROVASCULAR CX
  • MANAGEMENT of Foot Ulcers
  • Inspect the surface of shoes for any rough spots
    or foreign objects
  • Properly dry the feet
  • Instruct to wear closed-toe shoes that fit well,
    recommend use of low-heeled shoes

180
MICROVASCULAR CX
  • MANAGEMENT
  • Instruct patient NEVER to walk barefoot, never to
    use heating pads, open-toed shoes and soaking
    feet
  • Trim toenails STRAIGHT ACROSS and file sharp
    corners
  • Instruct to avoid smoking and over-the counter
    medications and home remedies for foot problems

181
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