Diabetes I & II, Cushing’s Disease and

Addison’s Disease

By: Cera Jane Paran, McKenzie Schumacher, Jinny Tran, and

Cameron Yee
Type 1 Diabetes
 Diabetes I: Pathophysiology
● Juvenile onset or insulin dependent diabetes
● Autoimmune disorder, in which the
body develops antibodies against
insulin and/or the pancreatic
beta-cells that produce insulin.
 Diabetes i
Causes: Manifestations :
● Genetics ● Ketoacidosis
● *Polydipsia
● *Polyuria
● *Polyphagia
● Weight loss
● Weakness & Fatigue
 “
Diabetes 1: Lab work
1. A1C of 6.5% or higher
2. Fasting plasma glucose level ≥ 126 mg/dL
3. 2 hour plasma glucose level ≥ 200 mg/dL
4. Random plasma glucose ≥ 200 mg/dL
 Diabetes 1: assessments
● Past Medical History ● Glucose levels
○ Fasting
● Medications
○ Random
● Nutrition/Metabolism ○ Oral glucose test

● Musculoskeletal tolerance
 Diabetes 1: Nursing diagnosis
1. Unstable glucose levels related to deficient
knowledge of diabetes management

2. Risk for impaired skin integrity related to

decreased circulation and sensation caused
by peripheral neuropathy and arterial
obstruction as evidence by loss of sensation

3. Risk for injury related to decreased sensation

and weakness
 Diabetes 1
Treatment: Nursing interventions:
● Monitor glucose ● Patient and caregiver teaching
levels
● Med administration
● Drug therapy
● Maintain good hygiene

● Instruct patient to carry medical ID

 Diabetes 1
complication prevention
1. Unstable glucose levels 1. Monitor patient’s glucose levels
regularly, instruct patient to take
medications as directed

2. Ineffective health .
……….management 2. Patient teaching

3. Feet injury 3. Assess skin integrity and sensation

Type 2 Diabetes
 Pathophysiology
The pancreas produces some self-made insulin. In type
2 diabetes, there is inadequate production of this insulin,
insulin resistance, or both. Type 2 diabetes can also be
genetic.
Causes/Risk factors and Manifestations
‐ Genetics ‐ Polyuria, polydipsia,
‐ Sedentary lifestyle polyphagia
‐ Ethnicity ‐ Fatigue
‐ Pregnancy ‐ Recurrent infections
‐ Recurrent vaginal
yeast or candidal
infections
‐ Prolonged wound
healing
‐ Visual changes
 Lab work
‐ Fasting blood sugar of 126 mg/dL
‐ A1C 6.5% or higher
‐ Two-hour blood sugar level greater than or equal to
200 mg/dL
‐ Random blood sugar test greater than or equal to
200 mg/dL
 Subjective and objective data
‐ Family history, pregnancy, ‐ Soft, sunken eyeballs
chronic pancreatitis, ‐ Dry/warm skin, ulcers
Cushing syndrome (feet)
‐ Obesity, thirst, hunger, ‐ Rapid/deep respirations
nausea, vomiting, poor ‐ Hypotension, weak/rapid
healing pulse
‐ Frequent urination, ‐ Dry mouth
nocturia ‐ Altered reflexes,
‐ Muscle weakness, fatigue restlessness, confusion
‐ Blurred vision, numbness, ‐ Muscle wasting
tingling
 Nursing diagnoses
‐ Ineffective health
management
‐ Risk for unstable blood
glucose levels
‐ Risk for injury
‐ Risk for peripheral
neurovascular dysfunction
 interventions
‐ Health promotion
‐ Acute Illness and surgery
‐ Ambulatory care
‐ Insulin therapy
‐ Personal hygiene
‐ Medical ID and travel
‐ Patient and caregiver teaching
 Complications and prevention
‐ Diabetic ketoacidosis ‐ Healthy food choices
‐ Hyperosmolar ‐ Exercising
hyperglycemic ‐ Staying at optimal
syndrome weight
‐ Hypoglycemia
‐ Angiopathy
‐ Retinopathy,
nephropathy,
neuropathy
‐ Infection
Cushing’s Disease
 Cushing’s Disease Pathophysiology
Cushing’s Disease, aka
Cushing’s Syndrome, is a
“clinical condition that results
from chronic exposure to
excess corticosteroids.”
(Lewis, 2018)

‐ Usually glucocorticoids
 Cushing’s Disease: Causes & Manifestations
Causes Manifestations
● Iatrogenic administration
Main Symptoms:
of exogenous
corticosteroids
● Weight Gain
● Endogenous tumors: ● Hyperglycemia
○ ACTH-secreting pituitary
● Muscle Wasting
adenoma
○ Adrenal tumors or ● Skin Weaker/Thinner
ectopic ACTH-producing ● Glycosuria
tumors ● Virilization/Feminization
“ Manifestations in Detail
Cushing’s Disease:
Cushing’s Disease: Lab Work
Three Main Tests: to help Diagnose
1. Midnight or Late-Night Salivary Cortisol Test
2. Low-Dose Dexamethasone Suppression Test
3. 24-Hour Urine Cortisol Test

High Levels of Cortisol → Cushing’s Disease Diagnosis

Other tests to help indicate disease

● Plasma ACTH Levels
● CBC with WBC differential
● Blood chemistry of electrolytes: Na, K, Glucose
● CT Scan or MRI
 Cushing’s Disease: assessments
Assessment
A. Subjective Data
a. Past Medical History
b. Medications
c. Nutritional-Metabolic
B. Objective Data
a. Truncal Obesity
b. Plethora (excessive of bodily fluids)
c. Hypokalemia
 Cushing’s Disease Nursing Diagnosis
Nursing Diagnosis
1. Risk for Infection
a. Related to lowered resistance to stress and suppression of
Immune System
2. Risk for Overweight
a. Related to increased appetite, high caloric content, and
inactivity
3. Disturbed Body Image
a. Change in appearance in Disease was Process
4. Impaired Skin Integrity
a. Excess corticosteroids, immobility and altered skin fragility
 Cushing’s Disease: Interventions
Interprofessional Care
1. Transphenoidal Resection
2. Radiation Therapy
3. Adrenalectomy
a. (Open/Laparoscopic)
4. Drug Therapy
5. Treatment of Tumor
6. Discontinue or alter dose of exogenous
corticosteroids
Complications:
1. Bone Loss
“
Cushing’s Disease: Complications
Treatment:
1. Increase Ca
(Osteoporosis) 2. Take BP meds
2. High BP 3. Manage Diabetes
3. Type 2 Diabetes 4. Assess WBC count
4. Unusual Infections and signs/symptoms
5. Loss of Muscle mass of infections ASAP
and Strength 5. Exercise
Addison’s Disease
 Addison’s Disease Pathophysiology
Addison disease is
“characterized by
inadequate corticosteroid
and mineralocorticoid
synthesis and elevated levels
of serum ACTH (loss of
negative feedback)”
(Huether 484)
Huether, Sue, Kathryn McCance. Understanding Pathophysiology, 6th
Edition. Mosby, 02/2016. VitalBook file.
 Addison’s Disease Causes & Manifestations
Risk Factors/ Causes
● 30-60 years
● Female
● Tuberculosis
● Idiopathic Addison’s Disease
○ Childhood (type 1) adulthood (type 2)
○ Associated with autoimmune diseases:
Hashimoto/ idiopathic
hypoparathyroidism, pernicious anemia
■ Can be inherited as an autosomal
recessive trait
 ●
Addison’s Disease lab values
Serum and urine levels of cortisol: low
● ACTH stimulation test: high
● Serum potassium: > 5 mEq/L → mild hyperkalemia high
● Plasma glucose, fasting < 50 mg/dL (< 2.78 mmol/L) low
● BUN > 20 mg/dL (> 7.1 mmol/L) high
● Lymphocytes and Eosinophil count: high
Imaging
X-ray or CT: Evidence of
● Calcification in adrenal area
● Renal TB
● Pulmonary TB
 Addison’s Disease NDX/assessment/intervention
1. Risk for Imbalanced Nutrition
Assessment:
‐ Appetite, nausea, vomiting, or diarrhea
‐ Monitor trends in weight
Interventions:
‐ High protein, low carbohydrate and high sodium diet
‐ Encourage rest periods after eating
 Addison’s Disease NDX/assessment/intervention
2. Risk for Deficient Fluid Volume
Assessment:
‐ Skin turgor, mucous membranes, and trends in weight
‐ BP and HR
‐ Color, concentration, and amount of urine
‐ Fatigue, sensory deficits, or muscle weakness
‐ Electrocardiogram rhythm
Interventions:
‐ Encourage oral fluids
‐ Instruct patient to ingest salt additives when hot or humid
 Addison’s Disease NDX/assessment/intervention
3. Risk for decreased Cardiac Output
Assessment:
‐ Skin temp. And peripheral pulses
‐ LOC
‐ BP (orthostatic hypotension)
‐ Monitor for dysrhythmias
‐ Monitor urine output
Interventions:
‐ Minimize stress- quiet environment
‐ Provide rest periods
‐ Assist patient with activities as needed
 Addison’s Disease Collaborative Care
Treatment:
‐ Oral corticosteroids

‐ Corticosteroid injections
 Addison’s Disease complications/prevention
Complication: Prevention:
1. Stroke 1. Increase fluid → lower
serum potassium levels

2. Hypovolemic Shock 2. Increase fluids

3. Hypoxia/ Cerebral 3. Immediately check

Ischemia SaO2 and administer
O2 if <90%