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• Endocrine disorders • Adult (II)

○ Julie Mann, NP • Problematic: Type I can occur in adults.


• Case Study #1 ○ Type I and Type II
○ Jimmy Johns a 7-year-old boy presents with • Difference in how it develops and how
recent onset of polydipsia (really thirsty), it presents.
polyuria (has to pee a lot), and polyphagia ○ Gestational Diabetes
(very hungry). He has experienced some • Pregnancy related diabetes
weight loss and n/v despite no change in
his diet. His parents are concerned.
○ What might be going on with Jimmy?
• Maybe diabetes.
• Case Study #2
○ George Glass is a 45-year-old obese man
with a pmh significant for high cholesterol,
high triglycerides, and htn. He presents
with c/o increasing fatigue and thirst.
○ What might be going on with George Glass?
• Diabetes Type II
○ What tests might be ordered for Jimmy and
George?
• Fasting glucose - electrolyte panel
• "Casual sample" of glucose.
○ What do you anticipate these tests to
show?
• Hyperglycemia
• Naming of Diabetes • Pancreas secretes insulin through islet of
○ NIDDM and IDDM langerhans into blood stream.
• Noninsulin dependent Diabetes (II) vs
• Type I Diabetes
insulin dependent diabetes (type I) ○ pancreatic beta cells destroyed, can no
• Problematic: Some of our Type II's need longer form insulin, can't countereffect
insulin. actions of glucose.
○ Juvenile onset and Adult onset ○ Two types:
• Juvenile (I) • immune mediated diabetes
 most common of skin, weightgain) does not stop liver
 autoimmune destruction from producing glucose -->
 total lack of insulin, elevated blood ○ 3. Increased glucose production in liver
glucose, breakdown of body fats (from glycogen)
and proteins • Pathogenesis of Type II
• Ideopathic
 beta cell destruction without
evidence of autoimmune response
 strongly inherited
 African and Asian descent (genetic
history)
 Periods with a lot of insulin
produced followed by periods of
reduced insulin production.
 episodes of ketoacidosis due
varying degrees of insulin
deficiency.
○ http://www.youtube.com/watch?v=_OOWhuC_9L
w
• Type II Diabetes
○ hyperglycemia and insulin deficiency.
○ most commonly found in older overweight
people but becoming more common in
children and older adolescents
○ family history increases risk 2-4x’s! • Criteria for Diagnosis (either/or)
○ Either not making enough insulin, or insulin ○ Symptoms of diabetes (polyuria,
made is not effective. plolydipsia, and unexplained weight loss)
○ http://www.youtube.com/watch?v=VLiTbb6MaEU plus casual blood glucose >200 mg/dL
• What causes Type II? • Yeast infex with women.
○ 1. Insulin Resistance: effect of insulin less • Itchy, visual changes, fatigue.
then expected ○ Fasting blood glucose >126 mg/dL
○ 2. Deranged secretion of insulin by beta • Anythying over 105 puts pt in
cells (cannot be maintained) prediabetic state, will moniter pt.
• Ppl go into a hyperinsulin state ○ Two hour postload blood glucose >200
(hyperinsulinemia, may have darkening during OGTT
• Oral Glucose Tolerance Test endothelium and macrovascular disease
• Signs of Diabetes (Atherosclerosis, heart disease)
• Diagnostic Criteria for Metabolic Syndrome
○ Contains three or more of the following
symptoms
○ Abdominal Obesity: waist >35 in. in women
or 40 in. in men.
○ Triglycerides >150 mg/dL
○ HDL <50 mg/dL in women, <40 mg/dL in
men
○ Blood pressure >130/85 mm Hg
○ Fasting blood glucose >100 mg/dL
○ Greater chance to develop diabetes II
• Case Study con’t
○ Mr. Glass has been relatively non-compliant
with his DM management and manages to
take is BS once or twice a week. He also
frequently misses his Oral Diabetes
medications. He is celebrating his 46th
birthday and decides to go out to dinner
with a group of friends at a local italian
restaurant.
○George Glass’s pmh indicates he has ○ What might happen to Mr. Glass
multiple comorbidities. What are they?
• Hyperglycemia (hypoglycemia is more
• Obesity, HTN, high triglycerides, high
dangerous…) from large CHO meal--
cholesterol >(see pic below)
○ How might this be connected to Type II
diabetes?
• Metabolic Syndrome (Syndrome X)
○ a cluster of abnormalities including:
obesity, high triglycerides, low HDL’s, HTN,
systemic inflammation (CRP - C reactive
protein), abnormal fibrinolysis (higher risk
for clots), abnormal fxn of vascular
electrolytes out with fluid, depressed
sensorium
• Bring down BS slowly, follow neuro
status, tricky to treat.
• Case Study con’t
○ Mr. Glass hasn’t leaned the importance of
managing his dietary intake. He wakes up
late for work, doesn’t check his blood
glucose, skips breakfast,and rushes to his
job stocking the supermarket. 2 hours after
starting work Mr. Glass doesn’t feel so
good, what might be happening?
• Hypoglycemia

○ Should stay hydrated, reeducate on diet


measures, take meds, use up glucose
(walk).
• Hyperosmolar Hyperglycemic State
○ Extreme Hyperglycemia (blood glucose
>600 mg/dL)
○ Hyperosmolarity (plasma osmolarity >3210
mOsm/L)
○ Dehydration, absence of ketoacidosis (no
breakdown of fats/proteins), pull
head to the local ice cream shop. All his
friends are having the “Kitchen sink” so he
orders one too. He doesn’t have his insulin
with him so he skips it, eats the whole ice
cream treat and heads home. The next
morning his mom finds him in his room
lethargic and complaining of nausea and
abdominal pain. His mom brings him to the
ED.
• The Kitchen Sink
○ What might be going on with him?
• Hyperglycemia, ketoacidosis (metabolic
acidosis) seen more with Type I.
• Muscle does not take up glucose
because there is no glucose-->muscle
breaks down protein & fat for energy,
raise ketones (acidic). (See diagram
below)
• Need to work with pt carefully, insulin
IV (monitor blood glucose,
fluid/electrolyte replacements, manage
metabolic acidosis).
• Kussmal's respirations to compensate.

○ Can pass out and die!


○ Raise blood sugar fast with glucose tablet,
then something that will sustain
(complicated carbs).
• Case Study con’t
○ Jimmy Johns has done a great job learning
how to manage his diabetes. He is now 16
and decides to hang out with his friends on
Saturday night. They all go to the movies
and share popcorn and soda’s and then Screen clipping taken: 8/2/2009, 10:00 PM
• Almost all type I will have these
complications, about 60% of type II's.
• More complications = more
uncontrolled.

• Mr. Glass the saga continues


○ Poor Mr. Glass he never did embrace the
management of his diabetes. He is now 67
years old and continues to be a poorly
controlled diabetic now on insulin therapy. • Chronic Complications
○ what chronic complications are in store for ○ Somatic Neuropathy (peripheral
Mr. Glass? neuropathy): diminished perception of
• Blindness, neuropathy, cardiac arrest, vibration, pain, &temperature.
amputation (bad peripheral vascular • Use tuning forks on different bony
disease), renal failure. (see pic below) prominences on foot to see if can sense
vibrations. Test for pain in foot using ○ What does this indicate?
monofilament (bendable wire). Test • Gestational diabetes.
temp with test tubes of warm/cold ○ What nursing considerations do you have
water. for her and her unborn baby?
○ Autonomic Neuropathy: disorders of • Macrosomia (big babies), spontaneous
vasomotor function, impaired GI fxn, GU abortion, cardiac anomalies can
fxn, and cranial nerve involvement (ie optic develop, greater risk of development of
nerve) diabetes, hypoglycemia at birth.
○ Nephropathies: changes to the glomerulus
• Gestational Diabetes
(capillary basement membrane thickening ○ Any degree of glucose intolerance first
in glomerulus leading to chronic kidney detected in pregnancy
disease) ○ Risk factors: family history of DM; history of
○ Retinopathies: abnormal retinal vascular
stillbirth or spontaneous abortion, fetal
permeability, microaneurysm, anomalies in previous pregnancy, or
neovascularization and hemorrhage, previous large-for-gestational age infant;
scaring and retinal detachment obesity, advanced maternal age (over 35),
• Recommend diabetes see an >5 pregnancies.
ophthalmologist annually. ○ Screening at first prenatal visit in high risk
• Macrovascular Complications mom’s and at week 24-28 gestation for
○ CAD normal mom’s.
○ Cerebral Vascular Disease ○ GDM means higher risk of complications,
○ Peripheral Vascular Disease mortality and fetal abnormalities
○ Risk: obesity, Htn, hyperglycemia, (macrosomia, hypoglycemia, hypocalcemia,
hyperinsulinemia, hyperlipidemia, altered polycythemia, and hyperbilirubinemia)
platelet fxn, endothelial dysfxn, systemic • Case Study #4
inflammation, elevated fibrinogen levels ○ Peggy Sams is an 22 year old female with
• Case Study #3 no significant pmh. She develops a fullness
○ Julie Mann is a 32-year-old overweight in her throat and has trouble swallowing.
female with a pmh significant for polycystic She brags she can eat what ever she likes
ovarian syndrome (hyper insulin state and not gain weight and states that she is
affecting the reproductive tract) and a glad she lives in Michigan because she
family history significant for DM in both hates to be hot. The NP notices she is
parents. She presents to the clinic for her 5 restless and seldom blinks.
month check up and with results of her one ○ What might be going on with Peggy?
hour OGTT which is 183 mmol/L.
• Hyperthyroidism ○ most common cause is graves disease
• Exophthalmos (protrusion of the eyes) ○ manifestations are related to increased O2
consumption, increased metabolic state,
and increased SNS activity
○ (see below) Fine shiny hair, hair loss.

• Hypothalamus-->TRH-->ant pit-->TSHThyroid-- • Graves Disease


>T3&T4 ○ A state of hyperthyroidism, goiter, and
• Hyperthyroidism ophthalmopathy (eye changes).
○ high levels of circulating thyroid hormone ○ Onset between ages 20-40, more common
(regulates metabolism) in women
○ Autoimmune disorder ○ Manifestations result from slowed
○ abnormal stimulation of the thyroid gland metabolic processes or myxedematous
by TSH-receptor antibodies, which keep process in the tissues
secreting thyroid hormone.
• Thyroid Storm • Myxedematous Coma
○ Life threatening condition, extreme ○ Life threatening, end-stage hypothyroid
hyperthyroidism state, rare
○ precipitated by stress, infection, DKA ○ manifested by coma (possibly d/t body no
(Diabetic Ketoacidosis [autoimmune longer able to metabolize medications),
condition]), or manipulation of thyroid in hypothermia, CV collapse, hypoventilation,
thyroidectomy and severe metabolic disorders (lactic
○ Manifestations: very high fever, extreme acidosis, hyponatremia, hypoglycemia)
○ most often in elderly women, in the winter.
cardiac effects (tachycardia, CHF, angina),
severe CNS effects (aggitation, • Case Study #5
restlessness, and delirium). ○ Ms. Puffer is a 60 year old female s/p
• Put into ICU, cooling blankets, bilateral lung transplant. She is taking her
supportive measures until thyroid anti-rejection regime which includes high
hormone out of system. dose Solumedrol and then Prednisone.
• Case Study Con’t ○ Mr. Kase is a 40 year-old male with a benign
○ Peggy has a thyroidectomy. And now has adrenal tumor.
hypothyroidism. ○ What are they both at risk of developing?
○ What kind of management will she need? • Cushing Syndrome
• Synthetic thyroid hormone. • Hypothalamus-->CRF-->Ant Pit-->ACTH--
○ What manifestations might you see with >adrenal cortex-->Cortisol
her? • Cushing Syndrome
• Weight gain, fatigue ○ excess in cortisol
• Hypothyroidism ○ causes: pituitary tumors, benign or
○ general slowing of metabolic processes and malignant adrenal tumors, ACTH secreting
myxedema (non-pitting mucous edema in tumors, or excessive glucocorticoid
connective tissue) administration,
○ dysfunction or destruction of the thyroid ○ exaggeration of actions of cortisol (see
gland below)
○ Most common cause is Hashimoto’s
Thyroiditis: autoimmune process
○ Severe thin skin like parchment paper.