Nova Southeastern University
Ron and Kathy Assaf College of Nursing
NUR 3032
Pathophysiology
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Used to satisfy energy needs in the body
The liver, with hormones from the endocrine pancreas,
regulates energy production
Glucose is metabolized to CO2 and H2O.
◦ Brain can’t synthesize or store glucose
Fat is metabolized to glycerol and fatty acids
Protein is metabolized to amino acids
◦ Amino acids building blocks of protein
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Acini
◦ Secrete digestive juices into the duodenum
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Islets of Langerhans
◦ Secrete hormones into the blood
◦ Composed of
 beta cells that secrete insulin
 alpha cells that secrete glucagon
 delta cells that secrete somatostatin
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Insulin
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Glucagon
◦ Increases glucose transport into skeletal muscle
and adipose tissue
◦ Increases glycogen synthesis
◦ Decreases gluconeogenesis
◦ Promotes glycogen breakdown
◦ Increases gluconeogenesis
◦ Maintains blood glucose between meals and during
fasting
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Anabolic in nature
Promotes glucose uptake by target cells and
provides for glucose storage as glycogen
Prevents fat and glycogen breakdown
Inhibits gluconeogenesis and increases
protein synthesis
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Catabolic in nature
Increases transport of amino acids into
hepatic cells
Increases breakdown of proteins into amino
acids for use in gluconeogenesis
Increases conversion of amino acids into
glucose precursors
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Catecholamine
◦ Epinephrine and norepinephrine
◦ Help to maintain blood glucose levels during
periods of stress
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Growth hormone
◦ Increases protein synthesis in all cells of the body,
mobilizes fatty acids from adipose tissue, and
antagonizes the effects of insulin
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Glucocorticoids
◦ Critical to survival during periods of fasting and
starvation
◦ Stimulate gluconeogenesis by the liver
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Common chronic disease
◦ Abnormality in blood glucose regulation and
nutrient storage
 Absolute deficiency of insulin
 Resistance to the actions of insulin
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Requires lifelong behavioral & lifestyle
changes
Collaborative approach
Nurse’s role as part of team:
◦ plan, organize, coordinate care
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◦ Affects 23.1 million (7.2% of population)
◦ 84.1 million adults have “prediabetes”
◦ More common in American Indians/Alaska
Natives, African Americans, Hispanic Americans
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Percentage ( Natural Breaks )
Source: www.cdc.gov/diabetes/da
Disclaimer: This is a user-generated report. The findings and conclusions are those of the user and do not necessarily represent the views of the CDC.
ta
National Center for Chronic Disease Prevention and Health Promotion
Division of Diabetes Translation
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Pre-diabetes: impaired fasting plasma glucose and impaired
glucose tolerance
Disorder of carbohydrate, protein, and fat metabolism
◦ Results from an imbalance between insulin availability and
insulin need
Can represent:
◦ An absolute insulin deficiency
◦ Impaired release of insulin by the pancreatic beta cells
◦ Inadequate or defective insulin receptors
◦ Production of inactive insulin or insulin that is destroyed
before it can carry out its action
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Normal fasting plasma
glucose (FPG) <100 mg/dL
Impaired fasting plasma
glucose
◦ FPG 100-125 mg/dL= “Prediabetes”
◦ FPG > 126 mg/dL = criteria for
diagnosis of DM
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Glycosylated hemoglobin
(HbA1C)
◦ Reflects glucose control
over last 120 days
 3.9%-5.6%= normal
 5.7-6.4% = increased risk
 > 6.5%= + DM
Random blood glucose
>200 mg/dL with signs of
DM  diagnosis of DM
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Fasting blood glucose test
Casual blood glucose test
Oral glucose tolerance test
Capillary blood tests and self-monitoring of
capillary blood glucose levels
Glycoslylated hemoglobin testing (HbA1C)
Urine tests
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HbA₁c %
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Glucose
mg/dL
126
154
183
212
240
269
298
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Loss of beta cell
function
An absolute insulin
deficiency
◦ Type 1A: immunemediated diabetes
 Genetic predisposition
 Hypothetical triggering
event
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Impaired beta cell
function
Insulin resistance
Relative lack of insulin
or impaired release of
insulin in relation to
blood glucose levels
◦ Type 1B: idiopathic
diabetes
Type 1
Type 2
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Prone to development of
ketoacidosis
◦ Fatty acids converted to
ketones
All clients with type 1
require exogenous insulin
replacement
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1.
2.
3.
Type 1
Older adults
Overweight
Strong genetic component
Increasing in children
(obesity)
Insulin resistance
Increased glucose
production by liver
Deranged secretion of
insulin from beta cells
Type 2
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Insulin resistance initially stimulates increase in insulin
secretion
Increase demand for insulin  beta cell exhaustion and
failure
Increased post-prandial glucose levels
Increased glucose production by liver
Highly associated with obesity and physical inactivity
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Hyperglycemia in patients with type 2
diabetes is frequently associated with
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Intra-abdominal obesity
High level of plasma triglycerides
Low levels of high density lipoproteins (HDLs)
Hypertension
Elevated C-reactive protein (CRP)
Abnormal fibrinolysis
Abnormal function of the vascular endothelium
Macrovascular disease
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Pancreatic disease
Endocrine disease
Medication induced
Infection related
Gestational diabetes
◦ Glucose intolerance with onset or first recognized
during pregnancy
◦ Diagnosis based on results of 100 g oral GTT
during pregnancy
◦ FPG > 126 mg/dL or random > 200 mg/dL
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Polyuria
◦ Excessive urination
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Polydipsia
◦ Excessive thirst
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Polyphagia
◦ Excessive hunger
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Weight loss or gain
Recurrent blurred vision
Fatigue
Paresthesia
Skin infections
Dehydration 
◦ Hemoconcentration
◦ Hypovolemia
◦ Hyperviscosity
◦ Hypoperfusion
◦ Hypoxia (especially to brain cells)
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Diabetic
ketoacidosis (DKA)
Hyperosmolar Hyperglycemic state (HHS)
Hypoglycemia
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Most common in Type 1 DM
◦ Stress; inflammation; infection
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Lack of insulin  increased free fatty acids
from adipose tissue  ketone production
Characteristics
◦ Hyperglycemia
◦ Ketosis (+ urine and serum ketones)
◦ Metabolic acidosis (low serum bicarbonate, low pH)
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Life-threatening
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Characterized by
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Hyperglycemia
Hyperosmolarity (pulls water out of body cells)
Dehydration
Absence of ketoacidosis
Depression of sensorium
Primarily occurs with Type 2 DM
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Secondary to relative excess of insulin in the
blood, failure to eat, increased exercise,
medication changes, change in injection site.
Low blood sugar levels (<70 MG/dL)
Rapid onset
Clinical manifestations:
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Altered level of consciousness
Headache
Hunger, tachycardia, sweating, anxiety
Coma and seizures
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Microvascular changes
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Macrovascular changes
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Norris, T. L. (2020). Porth’s Essentials of Pathophysiology (5th ed.).
Philadelphia, PA: Wolters Kluwer.