Week 1 CH 48 Diabetes

DIABETES MELLITUS
Chapter 48
Jennel Osborne, PhD
Copyright © 2017, Elsevier Inc. All Rights Reserved.

Diabetes Mellitus
A chronic multisystem disease characterized by
hyperglycemia related to abnormal insulin
production, impaired insulin utilization, or both
■ Affects 29.1 million people
■ Seventh leading cause of death

Diabetes Mellitus
■ Leading cause of
– Adult blindness
– End-stage renal disease
– Non-traumatic lower limb amputations
■ Major contributing factor

– Heart disease
– Stroke

Etiology and Pathophysiology
■ Combination of causative factors
– Genetic
– Autoimmune
– Environmental
■ Absent/insufficient insulin and/or poor utilization of

insulin

■ Normal glucose and insulin metabolism
– Produced by -cells in islets of Langerhans
– Released continuously into bloodstream in small
increments with larger amounts released after food
– Stabilizes glucose level in range of 70 to
110 mg/dL

Normal Insulin Secretion

■ Insulin
– Promotes glucose transport from the bloodstream
across the cell membrane to the cytoplasm of the
cell
■ Cells break down glucose to make energy
■ Liver and muscle cells store excess glucose as
glycogen
■ Skeletal muscle and adipose tissue are
considered insulin-dependent tissues

■ Counter-regulatory hormones
– Glucagon, epinephrine, growth hormone, cortisol
– Oppose effects of insulin
– Stimulate glucose production and release by the
liver
– Decrease movement of glucose into cell
– Help maintain normal blood glucose levels

Classes of Diabetes
■ Type 1
■ Type 2
■ Gestational
■ Other specific types
■ Prediabetes

Type 1 Diabetes Mellitus
Formerly known as juvenile-onset or insulin-dependent
diabetes
■ Accounts for about 5% to 10% of all people with
diabetes
■ Generally affects people under age 40
– Can occur at any age

■ Autoimmune disorder
– Body develops antibodies against insulin and/or
pancreatic β cells that produce insulin
– Results in not enough insulin to survive
■ Genetic link
■ Idiopathic diabetes
■ Latent autoimmune diabetes in adults (LADA)

Onset of Disease
■ Autoantibodies are present for months to years before
symptoms occur
■ Manifestations develop when pancreas can no longer
produce insulin—then rapid onset with ketoacidosis
■ Necessitates insulin
■ Patient may have temporary remission after initial
treatment

Formerly known as adult-onset diabetes (AODM) or non–
insulin-dependent diabetes (NIDDM)
■ Most prevalent type (90% to 95%)
■ Many risk factors: overweight, obesity, advanced age,
family history
■ Increasing prevalence in children
■ Greater prevalence in ethnic groups

■ Pancreas continues to produce some endogenous
insulin but
– Not enough insulin is produced
OR
– Body does not use insulin effectively
■ Major distinction
– In type 1 diabetes there is an absence of
endogenous insulin

■ Genetic link
1. Insulin resistance
2. Decreased insulin production by pancreas
3. Inappropriate hepatic glucose production
4. Altered production of hormones and cytokines by
adipose tissue (adipokines)
5. Research continues on role of brain, kidneys, and gut
in type 2 diabetes

■ Metabolic syndrome increases risk for
type 2 diabetes
– Elevated glucose levels
– Abdominal obesity
– Elevated BP
– High levels of triglycerides
– Decreased levels of HDLs

Onset of Disease
■ Gradual onset
■ Hyperglycemia may go many years without being
detected
■ Often discovered with routine laboratory testing
– At time of diagnosis
■ About 50% to 80% of β cells are no longer
secreting insulin
■ Average person has had diabetes for 6.5 years

Prediabetes
■ Asymptomatic but long-term damage already
occurring
■ Patient teaching important
– Undergo screening
– Manage risk factors
– Monitor for symptoms of diabetes
– Maintain healthy weight, exercise, make healthy
food choices

Gestational Diabetes
Develops during pregnancy

■ Increases risk of need for cesarean delivery and of
perinatal complications
■ Screen high-risk patients first visit; others at 24 to 28
weeks of gestation
■ Usually glucose levels normal
6 weeks post partum

Other Specific Types of Diabetes
■ Results from injury to, interference with, or
destruction of β-cell function in the pancreas
■ From medical conditions and/or medications
■ Resolves when underlying condition is treated or
medication is discontinued

Clinical Manifestations
■ Classic symptoms
– Polyuria (frequent urination)
– Polydipsia (excessive thirst)
– Polyphagia (excessive hunger)
■ Weight loss
■ Weakness
■ Fatigue

Clinical Manifestations
■ Nonspecific symptoms
– Classic symptoms of type 1 may manifest
■ Fatigue
■ Recurrent infection
■ Recurrent vaginal yeast or candidal infection
■ Prolonged wound healing
■ Visual changes

Case Study (©RyanMcVay/Digital Vision/Thinkstock)
■ R.H. is a 62-year-old woman who comes to the clinic

for a routine physical examination.
■ She works as a banking executive and gets little
exercise.
■ She says she is “just tired.”
■ She has gained 18 pounds over the past year and eats
a high-fat diet.
■ Her BP is 162/98, HR is 92, and RR is 20.

■ R.H. complains of some weakness in her right foot

that began about a month ago.
■ She says it also feels a little numb.
■ A sensory examination reveals diminished sensations
of light touch, proprioception, and vibration in both
feet.
■ R.H. also complains of increased thirst and frequent
nighttime urination.
■ She denies any other weakness, numbness, or
changes in vision.

■ A physical examination reveals an erythematous

scaling rash in both inguinal areas and in axillae.
■ R.H. states the rash has been there on and off for
several years and is worse in the warm weather.

■ What risk factors for diabetes does R.H. have?

■ Which type of diabetes is R.H. at highest risk for
developing?
■ What clinical manifestations of diabetes is she

displaying?
■ What diagnostic tests for diabetes would you
expect the health care provider to order?

■ R.H.’s diagnostic testing results

– Random glucose test: 253 mg/dL
– A1C: 9.1%
– Urine: positive for glucose and negative for protein
– Wet preparation of smear from rash: consistent
with Candida albicans
– ECG: evidence of early ventricular hypertrophy

Interprofessional Care
■ Goals of diabetes management
– Decrease symptoms
– Promote well-being
– Prevent acute complications
– Delay onset and progression of
long-term complications
■ Need to maintain blood glucose levels as near to
normal as possible

■ R.H. receives a diagnosis of type 2 diabetes mellitus.

■ What 3 treatment modalities will you expect to teach
R.H. about?

Types of Insulin

Commercially Available Insulin Preps
Commercially available insulin preparations showing onset, peak, and duration of action. Individual patient responses
to each type of insulin are different and affected by many different factors.
Insulin
■ Storage of insulin
– Do not heat/freeze
– In-use vials may be left at room temperature up to
4 weeks
– Extra insulin should be refrigerated
– Avoid exposure to direct sunlight, extreme heat or
cold
– Store prefilled syringes upright for 1 week if 2
insulin types; 30 days for one

Insulin
■ Administration of insulin
– Given by subcutaneous injection
– Regular insulin may be given IV
– Cannot be taken orally

Insulin
■ Administration of insulin
– Absorption is fastest from abdomen, followed by
arm, thigh, and buttock
– Abdomen is often preferred site
– Do not inject in site to be exercised
– Rotate injections within and between sites

Subcutaneous Injection Sites

Insulin
■ Problems with insulin therapy

– Hypoglycemia
– Allergic reaction
– Lipodystrophy

Somogyi Effect
■ Somogyi effect
– Rebound effect in which an overdose of insulin
causes hypoglycemia
– Release of counter-regulatory hormones causes
rebound hyperglycemia

Dawn Phenomenon
■ Dawn phenomenon
– Morning hyperglycemia present on awakening
– May be due to release of counter-regulatory
hormones in predawn hours
■ Growth hormone and cortisol

Inhaled Insulin
■ Afrezza
– Rapid-acting inhaled insulin
– Administered at beginning of each meal or within
20 minutes after starting a meal
– Not a substitute for long-acting insulin

Oral Agents
■ Work on 3 defects of type 2 diabetes

– Insulin resistance
– Decreased insulin production
– Increased hepatic glucose production
■ Can be used in combination

■ R.H.’s health care provider orders metformin

(Glucophage) 500 mg PO bid.
■ What is the mechanism of action of metformin?
■ What would you teach R.H. about metformin?

Biquanides
Metformin
■ Withhold if patient is undergoing surgery or
radiologic procedure with contrast medium
– Day or two before and at least 48 hours after
– Monitor serum creatinine
■ Contraindications
– Renal, liver, cardiac disease
– Excessive alcohol intake

Sulfonylureas
■ ↑ Insulin production from pancreas

■ Major side effect: hypoglycemia
■ Examples
– Glipizide (Glucotrol)
– Glyburide (Glynase)
– Glimepiride (Amaryl)

Meglitinides
■ ↑ Insulin production from pancreas

■ Rapid onset: ↓ hypoglycemia
■ Taken 30 minutes to just before each meal
■ Should not be taken if meal skipped
■ Examples
– Repaglinide (Prandin)
– Nateglinide (Starlix)

α-Glucosidase Inhibitors
■ “Starch blockers”
– Slow down absorption of carbohydrate in small
intestine
■ Take with first bite of each meal
■ Example
– Acarbose (Precose)
– Miglitol (Glyset)

Thiazolidinediones
■ Most effective in those with insulin resistance

■ Improve insulin sensitivity, transport, and utilization
at target tissues
■ Examples
– Pioglitazone (Actos)
– Rosiglitazone (Avandia)
■ Rarely used because of adverse effects

Dipeptidyl Peptidase–4 (DDP-4) Inhibitor
■ Blocks inactivation of incretin hormones

– ↑ Insulin release
– ↓ Glucagon secretion
– ↓ Hepatic glucose production
■ Examples (gliptins)
– Sitagliptin (Januvia)
– Saxagliptin (Onglyza)
– Linagliptin (Tradjenta)

Sodium-Glucose Co-Transporter 2 (SGLT2)
Inhibitors
■ SGLT2 inhibitors work by

– Blocking reabsorption of glucose by kidney
– Increasing glucose excretion
– Lowering blood glucose levels
■ Canagliflozin (Invokana)
■ Dapagliflozin (Farxiga)
■ Empagliflozin (Jardiance)

Dopamine Receptor Agonist
■ Bromocriptine (Cycloset)
■ Mechanism of action unknown
■ Thought that patients with type 2 diabetes have
low levels of dopamine
■ Increases dopamine receptor activity
■ Alone or in combination

Glucagon-like Peptide-1 Receptor Agonists
■ Simulate glucagon-like peptide–1 (GLP-1)

– Increase insulin synthesis and release
– Inhibit glucagon secretion
– Slow gastric emptying
– Increases satiety

Drug Therapy
Amylin Analog
■ Pramlintide (Symlin)
■ Slows gastric emptying, reduces postprandial
glucagon secretion, increases satiety
■ Used concurrently with insulin
■ Subcutaneously in thigh or abdomen before meals
■ Watch for hypoglycemia

Drug Therapy
■ Combination oral therapy
– Blend two different classes of medications to treat
diabetes
– Improves adherence because patient takes fewer
pills
■ Other drugs affecting blood glucose levels
– Drug interactions can potentiate hypoglycemia and
hyperglycemia effects

Diabetes
Nutritional Therapy
■ Counseling
■ Education
■ Ongoing monitoring
■ Inter-professional team
– Registered dietitian with expertise in diabetes
management

Diabetes
Nutritional Therapy Goals
■ ADA healthy food choices
– Maintain blood glucose levels to as close to normal as
safely possible
– Normal lipid profiles and blood pressure
– Prevent or slow complications
– Individual needs; personal, cultural preferences
– Maintain pleasure of eating

Diabetes
Nutritional Therapy: Type 1 DM
■ Meal planning
– Based on usual food intake and preferences
– Balanced with insulin and exercise patterns
■ Day-to-day consistency makes it easier to
manage blood glucose levels
■ More flexibility with rapid-acting insulin,
multiple daily injections, and insulin pump

■ What would you teach R.H. about her dietary needs

in relation to her type 2 diabetes?
– Food composition
– Carbohydrates
– Fats
– Protein
– Alcohol

MyPlate for People With Diabetes

■ R.H. realizes that she needs to start exercising in

order to gain her health back.
■ She asks you what she should be doing.
■ How would you respond?

Culturally Competent Care
■ Culture can have a strong influence on dietary

preferences and meal preparation
■ High incidence of diabetes
– Hispanics
– Native Americans
– African Americans
– Asians and Pacific Islanders

Nursing Assessment
■ Subjective Data
– Past health history
■ Viral infections, trauma, infection, stress,
pregnancy, chronic pancreatitis, Cushing
syndrome, acromegaly, family history of
diabetes
– Medications
■ Insulin, OAs, corticosteroids, diuretics,
phenytoin
– Recent surgery

Nursing Assessment
■ Objective Data
– Dry mouth
– Vomiting
– Fruity breath
– Altered reflexes, restlessness
– Confusion, stupor, coma
– Muscle wasting

Nursing Assessment
■ Objective Data
– Serum electrolyte abnormalities
– Fasting blood glucose level of 126 mg/dL or higher
– Oral glucose tolerance test and/or random glucose
level exceeding 200 mg/dL
– Leukocytosis
– ↑ Blood urea nitrogen, creatinine

Nursing Assessment
■ Objective Data
– ↑Triglycerides, cholesterol, LDL, VLDL
– ↓ HDL
– Hemoglobin A1C value > 6.0%
– Glycosuria
– Ketonuria
– Albuminuria
– Acidosis

Planning
■ Overall Goals
– Active patient participation
– Few or no hyperglycemia or hypoglycemia
emergencies
– Maintain normal blood glucose levels
– Prevent or minimize chronic complications
– Adjust lifestyle to accommodate diabetes plan with
a minimum of stress

Nursing Implementation
■ Health Promotion
– Identify, monitor, and teach patients at risk
– Obesity: primary risk factor
– Routine screening for all overweight adults and
those older than 45
– Diabetes risk test
■ www.diabetes.org/risk-test.jsp

■ Acute Care
– Hypoglycemia
– Diabetic ketoacidosis
– Hyperosmolar hyperglycemic nonketotic
syndrome

■ Acute illness and surgery
– ↑ Blood glucose level secondary to
counterregulatory hormones
– Frequent monitoring of blood glucose
■ Ketone testing if glucose level exceeds 240
mg/dL
■ Report glucose levels exceeding 300 mg/dL
twice or moderate to high ketone levels
– Increase insulin for type 1 diabetes
– Type 2 diabetes may necessitate insulin therapy

■ Ambulatory Care
– Frequent oral care
– Foot care
■ Inspect daily
■ Avoid going barefoot
■ Proper footwear
■ How to treat cuts
– Travel needs
■ Medication, supplies, food, activity

Medical Alert

Nursing Management
Evaluation
■ Expected Outcomes
– Knowledge
– Self-care measures
– Balanced diet and activity
– Stable, safe, and healthy blood glucose levels
– No injuries

ACUTE
COMPLICATIONS
OF DIABETES
MELLITUS

Acute Complications
■ Diabetic ketoacidosis (DKA)
■ Hyperosmolar hyperglycemic syndrome (HHS)
■ Hypoglycemia

Diabetic Ketoacidosis (DKA)
■ Caused by profound deficiency of insulin

■ Characterized by
– Hyperglycemia
– Ketosis
– Acidosis
– Dehydration
■ Most likely to occur in type 1 diabetes

■ Precipitating factors
– Illness
– Infection
– Inadequate insulin dosage
– Undiagnosed type 1 diabetes
– Poor self-management
– Neglect

■ Clinical manifestations
– Dehydration
■ Poor skin turgor
■ Dry mucous membranes
■ Tachycardia
■ Orthostatic hypotension
– Lethargy and weakness early
– Skin dry and loose; eyes soft and sunken

■ Clinical manifestations
– Abdominal pain, anorexia, nausea/vomiting
– Kussmaul respirations
– Sweet, fruity breath odor
– Blood glucose level of ≥ 250 mg/dL
– Blood pH lower than 7.30
– Serum bicarbonate level < 16 mEq/L
– Moderate to high ketone levels in urine or serum

■ Less severe form may be treated on outpatient basis
■ Hospitalize for severe fluid and electrolyte
imbalance, fever, nausea/vomiting, diarrhea, altered
mental state
■ Also if communication with health care provider is
lacking

■ Ensure patent airway; administer O2
■ Establish IV access; begin fluid resuscitation
– NaCl 0.45% or 0.9%
– Add 5% to 10% dextrose when blood glucose level
approaches 250 mg/dL
■ Continuous regular insulin drip 0.1 U/kg/hr
■ Potassium replacement as needed

Hyperosmolar Hyperglycemic Syndrome
(HHS)
■ Life-threatening syndrome
■ Occurs with type 2 diabetes
■ Precipitating factors
– UTIs, pneumonia, sepsis
– Acute illness
– Newly diagnosed type 2 diabetes
– Impaired thirst sensation and/or inability to replace
fluids

Hyperosmolar Hyperglycemic
Syndrome (HHS)
■ Enough circulating insulin to prevent ketoacidosis
■ Fewer symptoms lead to higher glucose levels (>600
mg/dL)
■ More severe neurologic manifestations because of ↑
serum osmolality
■ Ketones absent or minimal in blood and urine

Hyperosmolar Hyperglycemic
Syndrome (HHS)
■ Medical emergency
■ High mortality rate
■ Therapy similar to that for DKA
– IV insulin and NaCl infusions
– More fluid replacement needed
– Monitor serum potassium and replace as needed
■ Correct underlying precipitating cause

■ Despite intense patient teaching, R.H. presents to the

ED with hyperglycemic hyperosmolar syndrome.
■ She has been ill with the flu and has not taken her
metformin as prescribed.

■ R.H.’s admitting blood glucose level is 832 mg/dL.

■ She is admitted to the ICU for IV hydration and insulin
therapy.
■ What will be your priority nursing
assessments/interventions for R.H.?

Hypoglycemia
■ Too much insulin in proportion to glucose in the
blood
■ Blood glucose level < 70 mg/dL
■ Neuroendocrine hormones released
■ Autonomic nervous system activated

■ As you administer IV insulin to R.H., for which clinical

manifestations of hypoglycemia will you assess R.H.?

Hypoglycemia
■ Hypoglycemia unawareness
– No warning signs/symptoms until glucose level
critically low
– Related to autonomic neuropathy and lack of
counter-regulatory hormones
– Patients at risk should keep blood glucose levels
somewhat higher

Hypoglycemia
■ Causes
– Too much insulin or oral hypoglycemic agents
– Too little food
– Delaying time of eating
– Too much exercise
■ Symptoms can also occur when high glucose level
falls too rapidly

Hypoglycemia
■ Check blood glucose level
– If < 70 mg/dL, begin treatment
– If > 70 mg/dL, investigate further for cause of
signs/symptoms
– If monitoring equipment not available, treatment
should be initiated

■ Several days after being admitted for hyperglycemia,

R.H.’s blood glucose level drops to 56 mg/dL.
■ R.H. remains alert and oriented.
■ What are your priority nursing interventions?

CHRONIC
COMPLICATIONS OF
DIABETES MELLITUS

Chronic Complications

Angiopathy
Damage to blood vessels secondary to chronic
hyperglycemia
■ Leading cause of diabetes-related death
■ Macrovascular and microvascular
■ Tight glucose levels can prevent or minimize
complications

Macrovascular Angiopathy
Diseases of large and medium-sized blood vessels
■ Greater frequency and earlier onset in patients with
diabetes
■ Cerebrovascular disease
■ Cardiovascular disease
■ Peripheral vascular disease

Macrovascular Angiopathy
■ Decrease risk factors (yearly screening)
– Obesity
– Smoking
– Hypertension
– High fat intake
– Sedentary lifestyle
■ Screen for and treat hyperlipidemia

Microvascular Angiopathy
Thickening of vessel membranes in capillaries and
arterioles
■ Specific to diabetes and includes
– Retinopathy
– Nephropathy
– Dermopathy
■ Usually appear 10 to 20 years after diagnosis

Diabetic Retinopathy
Microvascular damage to retina
■ Most common cause of new cases of adult
blindness
■ Nonproliferative: more common
■ Proliferative: more severe

Diabetic Retinopathy
■ Non-proliferative
– Partial occlusion of small blood vessels in retina
causes micro aneurysms
■ Proliferative
– Involves retina and vitreous humor
– New blood vessels formed (neovascularization):
very fragile and bleed easily
– Can cause retinal detachment

Diabetic Nephropathy
Damage to small blood vessels that supply the glomeruli of
the kidney
■ Leading cause of end-stage renal disease
■ Risk factors
– Hypertension
– Genetics
– Smoking
– Chronic hyperglycemia

Diabetic Nephropathy
■ Annual screening
■ If albuminuria present, drugs to delay progression:
– ACE inhibitors
– Angiotensin II receptor antagonists
■ Control of hypertension and blood glucose levels in a
healthy range: imperative

Diabetic Neuropathy
Nerve damage due to metabolic derangements of
diabetes
■ 60% to 70% of patients with diabetes have some
degree of neuropathy
■ Reduced nerve conduction and demyelinization
■ Sensory or autonomic
■ Sensory neuropathy
– Loss of protective sensation in lower extremities
– Major risk for amputation
Diabetic Neuropathy
■ Distal symmetric polyneuropathy
– Most common form
– Affects hands and/or feet bilaterally
– Loss of sensation, abnormal sensations, pain,
and paresthesias

Neuropathy: Neurotrophic
Ulceration

Diabetic Neuropathy
■ Treatment for sensory neuropathy
– Managing blood glucose levels
– Drug therapy
■ Topical creams
■ Tricyclic antidepressants
■ Selective serotonin and norepinephrine
reuptake inhibitors
■ Anti-seizure medications
Diabetic Neuropathy
■ Autonomic neuropathy
– Can affect nearly all body systems
– Gastroparesis
■ Delayed gastric emptying
– Cardiovascular abnormalities
■ Postural hypotension, resting tachycardia,
painless myocardial infarction

Diabetic Neuropathy
■ Autonomic neuropathy
– Sexual function
■ Erectile dysfunction
■ Decreased libido
■ Vaginal infections
– Neurogenic bladder → urinary retention
■ Empty frequently, use Credé’s maneuver
■ Medications
■ Self-catheterization
Foot Complications
■ Microvascular and macrovascular diseases increases risk
for injury and infection
■ Sensory neuropathy and PAD are major risk factors for
amputation
■ Also clotting abnormalities, impaired immune function,
autonomic neuropathy
■ Smoking increases risk

Foot Complications
■ Sensory neuropathy → loss of protective sensation
→ unawareness of injury
– Monofilament screening
■ Peripheral artery disease
– ↓ Blood flow, ↓ wound healing, ↑ risk for infection

Foot Complications
■ Patient teaching to prevent foot ulcers
– Proper footwear
– Avoidance of foot injury
– Skin and nail care
– Daily inspection of feet
– Prompt treatment of small problems
■ Diligent wound care for foot ulcers
■ Neuropathic arthropathy (Charcot’s foot)

Necrotic Toe Before and After
Amputation

Infection
■ Defect in mobilization of inflammatory cells and
impaired phagocytosis
■ Recurring or persistent infections
■ Treat promptly and vigorously
■ Patient teaching for prevention
– Hand hygiene
– Flu and pneumonia vaccine

Gerontologic Considerations
■ Increased prevalence and mortality
■ Glycemic control challenging
– Increased hypoglycemic unawareness
– Functional limitations
– Renal insufficiency
■ Meal planning and exercise
■ Patient teaching must be adapted to needs

Audience Response Question
A patient with type 1 diabetes calls the clinic with

complaints of nausea, vomiting, and diarrhea. It is
most important that the nurse advise the patient to
a. Withhold the regular dose of insulin.
b. Drink cool fluids with high glucose content.
c. Check the blood glucose level every 2 to 4 hours.
d. Use a less strenuous form of exercise than usual
until the illness resolves.

The nurse plans a class for patients who have newly
diagnosed type 2 diabetes mellitus. Which goal is most
appropriate?
a. Make all patients responsible for the management
of their disease.
b. Involve the family and significant others in the care
of these patients.
c. Enable the patients to become active participants
in the management of their disease.
d. Provide the patients with as much information as
soon as possible to prevent complications.

A patient screened for diabetes at a clinic has a fasting
plasma glucose level of 120 mg/dL (6.7 mmoL/L). Which
statement by the nurse is best?
a. “You will develop type 2 diabetes within 5 years.”
b. “You are at increased risk for developing diabetes.”
c. “The test is normal, and diabetes is not a problem.”
d. “The laboratory test result is positive for type 2
diabetes.”

The nurse is caring for a patient with type 1 diabetes

mellitus who is admitted for diabetic ketoacidosis.
The nurse would expect which laboratory test result?
a. Hypokalemia
b. Fluid overload
c. Hypoglycemia
d. Hyperphosphatemia

Week 1 CH 48 Diabetes

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DIABETES MELLITUS

Jennel Osborne, PhD

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■ Major contributing factor

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■ Absent/insufficient insulin and/or poor utilization of

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Develops during pregnancy

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■ R.H. is a 62-year-old woman who comes to the clinic

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■ R.H. complains of some weakness in her right foot

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■ A physical examination reveals an erythematous

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■ What risk factors for diabetes does R.H. have?

■ What clinical manifestations of diabetes is she

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■ R.H.’s diagnostic testing results

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■ R.H. receives a diagnosis of type 2 diabetes mellitus.

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■ Problems with insulin therapy

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■ Work on 3 defects of type 2 diabetes

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■ R.H.’s health care provider orders metformin

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■ ↑ Insulin production from pancreas

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■ ↑ Insulin production from pancreas

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■ Most effective in those with insulin resistance

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