Metabolism:
Hormonal Concept
and Glucose
Regulation
 The sum of all chemical reactions that take place in every cell of the
body, providing energy for the processes of life and synthesis of new
cellular material.
Outcomes
Metabolism/Sensation
Understand and discuss
the concept
of metabolism
Recognize patients with
optimal metabolism,
those at risk, and those
who are experiencing
poor metabolism
Apply knowledge of
pathophysiology to care
of patients with
metabolic disorders.
Analyze physical
assessment findings
of patients with a
selected metabolism
disorder
Outcomes (cont)
Identify and interpret
laboratory studies for
patients with
metabolic disorders
Apply principles of
pharmacologic
management for
metabolic disorders
Discuss nutritional
management with
metabolic disorders
Collaborate with
interdisciplinary teams
for patients with
metabolic disorders
Outcomes (cont)
Plan and
prioritize nursing interventions
for those with metabolic
disorders
Develop individualized teaching
plans for patients with
metabolic disorders
Discuss risk factors for
developing peripheral
neuropathy
Develop a plan of care for a
patient with peripheral
neuropathy
 Hormonal regulation is physiological mechanisms
that regulate the secretion and action of hormones
associated with the endocrine system.
 The scope of hormonal regulation can also be
thought about from the perspective of the hormones
and gland represented.
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 The scope of hormonal regulation ranges from normal range of
circulating hormone (based on physiological need) to abnormal
secretion, either in excess or deficient amounts.
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 Anterior pituitary
gland
 Pancreas
 Adrenal glands
 Posterior pituitary gland
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 Hormonal regulation represents the hormones produced and
secreted from the following:
 Hypothalamus
 Anterior Pituitary
 Posterior Pituitary
 Thyroid
 Parathyroid
 Adrenal Cortex
 Ovary
 Testes
 Pancreas
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
Glands, the hormones they produce, the target
tissue, and the physiological effect, locations of
various adrenal glands
 Four types of feedback control:
 Negative feedback
 Positive feedback
 Biological rhythms
 Central nervous system control
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 Common consequences from impaired hormonal
regulation can include:
 Alterations in growth and development
 Alterations in cognition
 Alterations in metabolism
 Alterations in reproduction
 Changes in growth
 Altered adaptive responses
 The disruption of any hormone production may
result in potential complications associated with the
underlying condition and the potential for lifetime
hormonal replacement therapy.
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 Glucose regulation is the process of maintaining optimal blood
glucose levels
 The ultimate end result of glucose metabolism is cellular use of
glucose for energy (adenosine triphosphate [ATP]) synthesis
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 Hormone to lower glucose
 Insulin
 Counterregulatory hormones to raise glucose
 Glucagon
 Cortisol
 Problems arise when hormones are deficient or
excessive or when production is not balanced with
the blood glucose need
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Glucose Regulation
Definition; the process for maintaining optimal
serum glucose levels
Other terms
◦ Glycogen is the major source of stored glucose found in the liver and
muscles
◦ Glycogenolysis refers of the breakdown of glycogen to glucose
◦ Glucogenesis is the process of producing glucose from non
carbohydrates
Glucose Regulation
Normal Physiological Process
◦ Glucose sources
◦ The role of the hormone Insulin
◦ The body without insulin
◦ Counter regulatory hormone
◦ Glucagon
◦ Cortisol
◦ Epinephrine
◦ Norepinephrine
Role of Hormones
Pancreas produces hormones necessary for metabolism, cellular
utilization of carbohydrates, proteins, fats
◦ Islets of Langerhans
◦ Alpha cells produce glucagon
◦ Decrease glucose oxidation via glycogenolysis
◦ Increase blood glucose levels via gluconeogenesis
◦ Beta cells produce insulin
◦ Facilitates movement of glucose across cell membranes into cells
◦ Prevents excessive breakdown of glycogen in liver, muscle
◦ Facilitates formation of lipid, inhibits breakdown of stored fats
◦ Helps to move amino acids into cells for protein synthesis
◦ Delta cells produce somatostatin
◦ Neurotransmitter that inhibits production of glucagon, insulin
Overview
Diabetes mellitus (DM)
◦ Disorder of hyperglycemia
◦ Results from defects in:
◦ Insulin secretion
◦ Insulin action
◦ Both
◦ Leads to abnormalities in carbohydrate and fat metabolism
Four major types
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Type 1 DM (T1D)
Type 2 DM (T2D)
Gestational diabetes
Other specific types
Etiology/ Types of
Diabetes
•Type 1- An autoimmune disorder in which beta cell destruction occurs
in a genetically susceptible individual approximately under age 30.
•Type 2- A genetically predisposed condition consisting of excessive
glucose production by the liver, impaired insulin secretion, and the
peripheral insulin resistance primarily occurring in liver, adipose and
muscle tissue.
Types (cont)
•Gestational affects 7% of all women. Dx. done with glucose tolerance
test (24-28 weeks)
•Other/medical or surgical
•Pre-diabetes / impaired glucose tolerance
– Estimated 41 million in US.
– Glucose levels elevated at 100-125 fasting or 140-199 with a 2 hour
glucose tolerance test
Types
 Maturity-onset diabetes of youth (type 2 in children)
 Latent autoimmune diabetes in adults (type 1 in older individuals)
sometimes referred to as 1.5.
Diabetes Risk Factors
•
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•
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•
•
•
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Family history
Obesity
Origin
Age
HTN
HDL < 35
H/o gestational diabetes
Delivery of large babies
Blood Glucose Homeostasis
Body tissues and organs require constant supply of glucose
◦ Brain, liver, intestines, renal tubules do not require insulin to transfer glucose
into their cells
◦ Skeletal muscle, cardiac muscle, adipose tissue require insulin
Normal blood glucose in healthy patients regulated by insulin and
glucagon
In Type 1 diabetes insulin production is lost
In Type 2 diabetes insulin production is altered
Diagnosis of
Diabetes/Symptoms
Classic Symptoms
Hyperglycemia
Elevated glucose leading to fluid and electrolyte imbalances
(osmotic diuresis)
Polyuria- excessive urination
Polydipsia-excessive thirst
Polyphagia-excessive eating
Diagnostic Tests (1 of 3)
Four diagnostic tests used for diagnosis
◦ Hemoglobin A1C ≥6.5% (normal level 4-6%)
◦ Symptoms of diabetes + casual plasma glucose (PG) concentration >200
mg/dL
◦ Fasting plasma glucose (FPG) >126 mg/dL
◦ Two-hour PG >200 mg/dL during oral glucose tolerance test (OGTT)
Each must be confirmed on a subsequent day with a different test
Diagnostic Tests (2 of 3)
Levels for FPG
◦ Normal fasting glucose: 100 mg/dL (6.1 mmol/L)
◦ Impaired fasting glucose: >100 mg/dL (6.1 mmol/L) and <126 mg/dL (7 mmol/L)
◦ Diagnosis of diabetes: >126 mg/dL (7 mmol/L)
Levels used for OGTT
◦ Normal glucose tolerance (GT): 2-hour PG <140 mg/dL (7.8 mmol/L)
◦ Impaired GT: 2-hour PG >140 mg/dL (7.8 mmol/L) and <200 mg/dL (11.1 mmol/L)
◦ Diagnosis of diabetes: 2-hour PG >200 mg/dL (11.1 mmol/L)
Either can be used, FPG recommended in clinical setting for nonpregnant adults
Diagnostic Tests (3 of 3)
Diabetes management monitoring
◦ Fasting blood glucose (FBG): 70–110 mg/dL
◦ Hemoglobin (A1C)
◦ Average blood glucose over 2–3 months
◦ Elevated: >6.5%
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Urine glucose and ketones levels: not as accurate
Urine test for presence of protein as albumin (microalbuminuria) **
Serum cholesterol, triglyceride levels
Serum electrolytes (can be lost in hyperglycemia)
Acute Complications
Hypoglycemia
◦ Common in T1D or T2D
◦ Often called insulin shock, insulin reaction, or the lows
◦ Mismatch between insulin intake, physical activity, carbohydrate availability
◦ Error in insulin dose
◦ Missing a meal
◦ Intake of alcohol
◦ Certain medications
◦ Manifestations
◦ Result from compensatory autonomic nervous system response
◦ Vary, especially in older adults
◦ Sudden onset
◦ Severe hypoglycemia may cause death
Signs and Symptoms of
Hypoglycemia
Hypoglycemia Treatment
Hypoglycemia, continued
◦ Treatment for mild hypoglycemia: ~15 g of rapid-acting sugar
◦ If manifestations continue, follow 15/15 rule
◦ Wait 15 minutes, monitor blood glucose, eat another 15 g carbohydrates
◦ Hospitalized if
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Blood glucose <50 mg/dL
Coma, seizures, or altered behaviors
Hypoglycemia has been treated but a responsible adult cannot be with patient for next 12 hours
Caused by sulfonylurea drug
◦ Conscious, alert patient: administer 10–15 g of oral carbohydrate
◦ Patient with altered level of consciousness: 20–50 mL 25–50% glucose solution
◦ Then continuous IV infusion of glucose 10–20% at 50–200 mL/hr
◦ Severe insulin-induced hypoglycemia: glucagon subcutaneous (SC), intramuscular
(IM), or IV
Diabetic Ketoacidosis (DKA)
Onset: Slow can occur in Type 1 or Type 2 diabetes, most common T1
Cause: Elevated glucose and deficient insulin
Symptoms: Flushed skin, abdominal pain, Fruity breath, < LOC
Diagnosis: Labs show > BS, > urine ketones, <plasma PH (<7.3)
Treatment: Fluids, insulin, electrolytes
More on this in 2nd level
Hyperosmolar Hyperglycemic
State (HHS)
Onset: Slow
Cause: < insulin, older age
Symptoms: Flushed skin, lethargic, severe fluid loss, malaise, seizures
Diagnosis: > glucose, ketones normal, < electrolytes, normal PH
Treatment: Insulin, Fluids, Electrolytes
Lifespan Considerations
Older adults
◦ Besides complications found at younger age, also at high risk for other things
◦ Polypharmacy
◦ Functional disabilities
◦ Cognitive impairment
◦ Depression
◦ Urinary incontinence
◦ Falls
◦ Goals of T2D management similar to those in younger adults
◦ Increased risk for hypoglycemia
Cultural aspects of diabetes
Type 2 diabetes risk is higher in America Indians, African Americans, and
Hispanics.
In some of these groups diet and cultural beliefs play a role in how
diabetes is viewed and treated.
As a nurse you need to be sensitive to the cultural norms to work within
the groups.
Glucose Regulation
Clinical Management
Primary Prevention
◦ Body Weight
◦ Exercise
◦ Diet
◦ Glucose Monitoring
◦ Education
Glucose Regulation
Collaborative Interventions
◦ Patient Education for Self Management
• Sick Days Rule
• Ongoing Lab assessments
•
Routine examinations
• Diabetic Foot Care
◦ Pharmacologic Therapy
◦ Insulin
◦ Oral Antidiabetic Agents page 1119
◦ Statin Agents
◦ Insulin preps. page 1114
Mixing Insulin
Slide inserted by Lori Martone-Roberts
Oral Agents
 Short-term consequences
 Inadequate glucose reaching the cells
 Dehydration
 Long-term consequences
 End-organ disease due to microvascular damage
 Retinopathy
 Nephropathy
 Peripheral neuropathy
 Macrovascular angiopathy
 Hypertension
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 Cardiovascular and peripheral vascular disease
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Glucose Regulation
Consequences
◦ Physiological consequences of Hyperglycemia
◦ Macrovascular
◦ Microvascular
◦ Neuropathy
◦ Fluid and Electrolyte imbalance
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Chronic Complications of
Diabetes
Macrovascular/microvascular disease
Retinopathy (vision problems)
Nephropathy (kidney dysfunction)
Neuropathy (nerve dysfunction)
Macrovascular Complications
(large vessel disease)
Cardiovascular disease
◦ CAD
◦ Hypertension
Cerebrovascular disease
PVD
Microvascular Complications
(small vessel disease)
Eye and vision complications
Diabetic neuropathy
Diabetic nephropathy
Male erectile dysfunction
Diabetic Retinopathy
Diabetic retinopathy is the most
common cause of new cases of
blindness among adults 20-74
years of age.
Patient Education
Retinal Blood Vessels
Optic Nerve
Macula
Normal Retina
Diabetic Retinopathy and
Macular Edema
Vitreous and Preretinal
Hemorrhage
Peripheral neuropathy
Weakness, numbness, and pain from nerve damage, usually in the
hands and feet.
Can be caused by:
•Diabetes (#1 cause)
•Chemotherapy/Toxins
•Anemia or poor perfusion
•Injury or infection
•Autoimmune disorders such as MS or Lupus
Incurable, but there are treatments available that can help.
Symptoms include nerve pain, “pins and needles”, weakness or
numbness.
Overview
Peripheral neuropathy results when trauma or a disease process
interferes with innervation of peripheral nerves
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Effectiveness of blood vessels decreases
Superficial blood vessels constrict to divert blood to larger vessels
Peripheral nerve endings suffer from decreased blood flow
Neuropathy develops
Collaboration
Peripheral neuropathy can involve multiple body systems
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Urinary (impotence)
Gastrointestinal (gastroparesis)
Sensory (paresthesia)
Orthostatic hypotension
Primary goal: correct or manage underlying cause to control symptoms,
minimize further nerve damage
Pharmacologic Treatment
Individualized
◦ Comorbidities
◦ Extent of nerve damage
◦ Nerve affected
No single drug to treat pain
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Pain relievers
Anticonvulsants (gabapentin)
Antidepressants
Lidocaine patch
Nonpharmacologic Therapy
Complementary health approaches
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Acupuncture
Biofeedback
Massage
Transcutaneous electrical nerve stimulation (TENS)
Nonpharmacologic Therapy
Physical and occupational therapy
Changes in daily life
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Adherence to therapeutic regimen by managing blood glucose
Healthy, well-balanced diet
Maintain optimal weight
Avoid smoking
Limit alcohol
Regular exercise
Daily foot care
Maintaining patient safety
through patient education
Patients need to be taught:
•To inspect areas affected daily to catch injury/chafing early
•Always wear socks and closed-toe shoes (no going barefoot at the
beach)
•Maintain proper moisture of skin (prevent dry skin/cracked skin)
•Avoid extreme temperatures/always check temperature of bath water
or dish water with elbow first
•Keep areas free of clutter