Endocrine Disorders
Endocrine Glands
Glands that do not have a duct or outlet and release their hormones (chemicals, secretions)
directly in the bloodstream and affect every cell of the body
Thyroid-Adrenal-Gonadotropins
As opposed to exocrine glands whose secretions enter a duct and either directly or indirectly
reach the outside of the body
Sweat Glands, Parotid Glands
Endocrine Functions
General
Communication
Control
Integration
Specific
Regulate metabolism (Growth and Development)
Reproduction
Stress Responses
Maintain homeostasis in:
Fluid and Electrolytes
Acid-Base Balance
Energy Balance
Major Endocrine Glands
Pituitary Gland- attached to the hypothalmus
Pineal Gland-in the brain
Thyroid Gland- in the throat and encircles the trachea
Thymus- chest area
Adrenal Gland- on kidneys
Pancreas- abdominal cavity
Ovary- pelvis
Testis- scrotum
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Anterior Pituitary- Adenohypophysis- Master Gland
Growth Hormone-Somatotrophic Hormone- Stimulates the buildup of protein and muscle mass
Causes a shift of the use of carbs for fuel to fats. This is why young person has leaner
mass. Can cause elevation in glucose level.
Lactogenic Hormone or Prolactin- to produce milk
Thryotrophin (TH)- also called Thyroid Stimulating Hormone (TSH)
Adrenocorticotrophin (ACTH)- stimulates the cortex of the adrenal glands
Two Gonadotropins:
Female: Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH)- egg release
Male: FSH and ICSH- Interstitial Cell Stimulating Hormone- produce sperm and
testosterone
Melanocyte-Stimulating Hormone- genetically controlled and influences skin color
Posterior Pituitary- Neurohypophysis
Oxytocin- uterine contractions
ADH- Anti-diuretic hormone- affects the kidneys to reabsorb water
Both men and women have some Prolactin and oxytocin- thought needed for sexual maturation
For every hormone produced in the pituitary, there is a releasing gland produced
in the hypothalmus that tell the pituitary gland when to release the needed
hormones.
Hypothalmus-Computer System
Command and control center by manufacturing and releasing hormones that stimulate trophic
hormones from the anterior pituitary gland to stimulate a specific gland to release its own
hormones
Also manufactures oxytocin and ADH and sends it down the capillary system and stored in the
posterior pituitary gland until needed
Anytime you are under stress, the immune system can attack the glands and cause
disorders
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Biologic Feedback Loop
1.
2.
3.
4.
Hypothalmus secretes Thyroid releasing Hormone-TRH
Releasing Hormone causes Anterior Pituitary Gland to secrete Thyroid Stimulating Hormone-TSH
Bullet sent to Thyroid Gland causing Thyroid to secrete its hormones
T3-T4-Calcitonin goes directly into the blood stream to affect every cell in the body
Feedback
The blood level of hormone needed or not needed determines how much stimulation the
hypothalamus receives
Hypothalamus determines blood level is high- less stimulation to the thyroid then T3-T4 level
will drop
Never abruptly stop steroid med like Prednisone- taper dose
Hypo does not differentiate between endogenous (inside body)/exogenous (outside body)
steroids
Hypo goes on vacation and will take time to increase the body’s own production of steroids
Patient will crash!
Hyperpituitarism
Caused by benign adenoma
Secreting tumor- causes more hormone level than is normal
In the brain- space occupying lesion laying on optic chiasma where optic nerve criss-crosses in
brain:
Hemianopia (loss of half of visual field)/visual problems- Seizures- headaches
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Hyperpituitarism- Overproduction of Growth Hormone
Acromegaly- Abraham Lincoln
Large hands, nose, feet, ears, facial bones/jaw- in adult
Giantism (if occurs as child) (8 ft. tall)
May also have: Hyperthyroidism-Cushing’s-Reproductive Problems
Diagnosis
Skull x-rays, CAT scans, MRI’s
Serum and Blood Tests
Treatment:
Surgery
Irradiation
Parlodel-Bromocriptine mesylate which decreases GH production
Growth Hormone causes blood sugar levels to increase by burning fat for metabolism
rather than carbs- glucose stays in the blood
May need to treat with insulin
Surgery
Hypophysectomy- old term
Craniotomy
Transphenoidal Hypophysectomy done above the gum line through the sphenoid sinus
behind the nose into the brain
Nursing Care
I&O- removed pituitary gland- no ADH- Diabetes Insipidus where one excretes large
amount of dilute urine- measure urine specific gravity (1.003- 1.035) and electrolytesshock
Hormone replacement therapy for the rest of their lives
ADH- Desmopressin, Vasopressin tanate, Pitressin either IM or sniffed
Brain surgery- decrease brain edema and increased intracranial pressure
Low fowler’s position reduces cerebral edema and IICP
No bending, coughing, or vomiting
If clear liquid drainage- check for glucose- if present CSF!!! Danger of infectionAntibiotics- Mouth is dirty
No tooth brushing for a short period
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Hypopituitarism
Diagnosis: same way
Sx: headache, visual problems, growth retardation (Premature aging, dwarfism)
Treatment: Replace all hormones- Essential for life
Stress increases demand for hormones and taxes the system
Thyroid Gland
Secretes 3 hormones
Thyroxine- T4
Triiodothyroxine- T3
Calcitonin- reroutes calcium from blood to bones and lowers the blood calcium level
Prevents Hypercalcemia
Normal Calcium 8-10 mg/dL
Shaped like a butterfly over the trachea
Iodine’s Role
Body must have Iodine to make thyroid hormones- T3 and T4
Insufficient Iodine causes goiters
Problem for Iodine deficient soil but is les problematic with Iodized table salt
T4 contains 4 iodine atoms and secreted abundantly
T3 contains 3 atoms of iodine
Both regulate metabolism and growth and development
Diagnosis
T3- 70-22- mg/dL
T4- 4.5-11.5 ug/dL
TSH
RAIU- Radioactive Iodine Uptake Test
Thyroid scan- I-131 given and scanned for density
No iodine before test- no seafood parties- discuss Cardiac cath verses thyroid scan (cardiac cath
can interfere with thyroid test because of the radioactive iodine. Do thyroid test first unless
emergency cath)
? Thyroid med stopped- ask MD (Estrogen and Birth Control can contain Iodine)
T3 Resin Uptake- blood drawn and I 131 is added afterwards- normal RBC uptake is 11-19%
uptake
BMR done- determine amount of O2 consumed by body per minute- No smoking, no activity,
done upon awakening- NPO after MN- clamp nose and breath into a machine
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Mrs. Myxedema has hypothyroidism
Slow burning fire inside the body
Thermostat is set low
Slow metabolism
Decreased metabolic rate
Heart Rate: 50-60 bpm- CHF
Resp rate: 6-8/min
Temp: always cold
Activity: easily fatigued
GI: Constipation
Says: “Turn up the heat! Give me another blanket! Put my socks on, please! Help me out of
bed!”
Don’t use heating pads- neurovascular response is offset- peripheral nerves die and won’t be
able to feel it burning.
Only increases: weight even on lettuce and heavy menses
Drooping eyes
Non-pitting edema
Sleepy
Cretinism in infants if not corrected
Replacement Meds
Desiccated thyroid- T3 and T4- oral- 15-180 mg per day
Synthroid/Levoid/Cytolen- synthetic T4- Initial dose: 100 mcg per day then 100-400 mcg/day
Euthroid-Cytomel
Action: increases the metabolic rate of body tissue
Meds
Adverse reactions: Weight loss, tachycardia, cardiac arrhythmias, angina, nervousness, cramps,
diarrhea, sweating, insomnia, fever (turned up the furnace too high)
Teaching: Take pulse- if over 100 bpm or change in rhythm, consult dr.
Take before breakfast
May reduce anticoagulant dose (causes more free Warfarin)
Long term therapy
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Hyperthyroidism
Rapidly burning fire inside body
No stored fuel because the body has burned it for energy to run the body
Nervous- boundless energy- tremors
Need extra oxygen because heart is working on overload
HR: 100-120 bpm
RR: 30/min
Graves Disease- Hyperthyroidism
Barney Fife- Barbara Bush and former President Bush and Millie had Graves
“I am burning up! Open the windows! Take the covers off of me! I can’t sleep! I can’t sit still!”
GI tract is rapid- diarrhea- no caffeine or other stimulants
Startled appearance- boggy eyes- Exopthalmus
Runny eyes to dry eyes irritated eyes
Artificial Tears and tape eyes shut at night to prevent corneal damage which may lead to
blindness
Lose weight regardless of how much they eat
Menses- light and scanty amounts
Meds
Adrenergic blocking agents:
Inderal- Propranolol hydrochloride- oral 40-120 mg daily in divided doses
Alleviate sweating, tremor, and tachycardia
Give before meals
Side Effects: Hypotension, Bradycardia, alopecia, depression, CHF
Others: Lasix, Digoxin, Steroids
Anti-thyroid Meds
Tapazole- methimazole
Propacil-propylithiouracil
Inhibit thyroid hormone synthesis
Harmful to liver, bone marrow, leukopenia, alopecia, lymphadenopathy, hypothyroidism
Take 2-3 weeks to see side effects
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Lugol’s Solution- radioactive iodine- I-131- shrinks and destroys the gland and then go for
thyroidectomy which prevents thyroid storm and hemorrhage during surgery
Actions: Inhibits release of thyroid hormone- reduces its vascularity and shrinks the size
of the gland- works in 10-15 days
Adverse reactions: acne, gum soreness, brassy metallic taste, headache, N&V,
radioactive medication
Wear gloves, Mix in juice and use straw to prevent staining of teeth
Excreted in urine- flush commode times 2
No cuddling- spouse sleeps on the couch
No crowded areas
Don’t be around pregnant women
Use common sense
Post-op Thyroidectomy
Semi-Fowler- No neck flexion or hypertension
Check for blood behind neck/back
Trach set in room
Calcium Gluconate in room IV- if parathyroid damaged then will lead to Hypocalcemia,
(hyperirritability, seizures)
Oxygen for 48 hours
Suction
Watch for tetany/convulsions
Check laryngeal nerve damage
Check facial nerve damage
Trousseau’s- carpal spasms when blood pressure cuff- low calcium
Chvostek’s- facial tics when tap on cheek
Monitor calcium level- parathyroid removal- normal is 8-10 mg/dL
Monitor for thyroid storm: Thyrotoxicosis
High fever- over 100F
Extreme tachycardia- 130 bpm
Altered mental state like delirium
No ASA (causes release of T3 and T4), use hypothermia blankets
Dialysis
Grandma with a Goiter
Simple endemic goiter
Used to be common- depending on the soil in which you grew your vegetables
Iodized salt
Thyroid needs iodine to produce T3 and T4
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Thyroid Disorders
Hashimoto Thyroiditis: Chronic Thyroiditis
Women 30-50 years of age
May have goiter
Few symptoms: slow insidious course leading to Myxedema
Autoimmune disease?
Goal: slow process to Myxedema (hypothyroidism)
Thyroid Cancer
Risk factor: exposure to radiation to head and neck in childhood to shrink tonsils or adenoids
96% survival rate- 1000 people die annually
Asymptomatic nodule in neck
Most common is papillary adenocarcinoma
Care of a Client with Adrenal Disorders
Ad- next to
Renal- kidneys
Inside layer (Adrenal Medulla)- Adrenalin- fight or flight/controls the emergency response
system that works with the autonomic nervous system
Adrenals
Outer 3 layers- Cortex
Outer Layer- Salt
Middle Layer- Sugar
Inner Layer- Sex
Aldosterone- Mineralocorticoids-Salt-Outer
Commands kidney nephrons to retain Na and kick out K+
Na retained and water retained = normal B/P
Excessive production: fluid and electrolyte imbalance/edema/hypertension
Sodium 134-145 mg
Potassium 3.5- 5.0
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Glucocorticoids- Cortisone- Middle Layer- Sugar
Converts stored glycogen to glucose in emergency situations- elevates blood sugar- monitor BS
levels
Controls internal anti-inflammatory response
Immunosuppressant activity
Given to people with arthritis first- problem demineralization of bone-osteoporosis
Meds
Hydrocortisone-Cortone-Prednisone
Decadron or dexamethasone- good for brain swelling
Fludrocortisones or Forinef- Aldosterone replacement
Side Effects
Retention of Na and water thus hypertension-Moon face-edema-CHF
Causes ulcers- use food or antacids
Reduce high sodium food
Monitor BS
Calcium supplements
Monitor for infections
Inner Layers- Sex
Sex Hormones: all have androgens (male hormone) and estrogens (female hormones)
Too much: Hirsutism (facial hair on female)-acne-mood swings
Magnesium
4th most abundant cation
Most is intracellular
Normal serum level: 1.5-2.5 mEq/L
50% is present in bone
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Function:
Activates many enzyme reactions especially empowering the B vitamins to function
Enzyme activity with carb and protein metabolism
Nucleic acid and proteins require magnesium
Exerts similar neuromuscular activity like Calcium
Sometimes acts synergistically with calcium, while at other times acting antagonistically
Usually antagonistic with Calcium competing for same receptor sites of absorption
Affects skeletal muscle directly by depressing acetylcholine release at the synaptic
junction
Neuromuscular activity is increased when magnesium levels are decreased and vice
versa.
Also aids in transportation of sodium and potassium across cell walls
If magnesium is deficient, the kidneys are likely to excrete more potassium
Magnesium influences the levels of intracellular calcium through its effect on
parathyroid hormone secretions
If magnesium level is low, the action of parathyroid hormone is impaired
Sources
Chlorophyll in green vegetables
Green beans
Nuts
Legumes
Fruit esp. bananas
Peanut Butter
Chocolate
Absorption
Diet- Magnesium intake
Intestines
Amounts of calcium, phosphate and lactose
Lost by kidneys
Kidneys are able to conserve or eliminate magnesium based on levels of
Calcium/Phosphorus in the blood
Hypomagnesemia
Positive Chvostek’s sign
Paresthesia of feet and legs
Convulsions etc
Hypermagnesemia
Stop infusion if you see
Hypotension
Flushing of the face
Calcium Gluconate is antagonistic to the Magnesium. Hopefully and only temporarily.
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Cushing’s disease
Hypersecretion of adrenal hormones
Too much sugar
Moon face-buffalo hump-trunk obesity with thin arms and legs- red/purple striae,
ecchymosis, elevated blood glucose, brittle bones, immunosuppressed- slow wound
healing
Too much salt:
Hypertension-fluid retention with edema-CHF-Hypernatremia-Hypokalemia-fatigue
Too much sex:
Male pattern baldness-Hirsutism-deep voice-acne-hair on chest and chin-decreased
libido
Cushing’s Syndrome is caused by too much steroid medicine
Watch diurnal patterns- highest in AM
If for disease: give in AM
If for replacement: 2/3 in AM and 1/3 in PM
Taper Dose
Symptoms will go away when condition is treated
Adrenalectomy
Post-op
Vital signs- more prone to shock than normal- because of sodium imbalances
Encourage T, C, and Deep B- incision near lungs
Pneumothorax
Adrenal Gland
Hydrocortisone-Cortisone-Prednisone
Decadron or dexamethasone- Good for brain swelling
Fludrocortisone or Florinef- Aldosterone replacement
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Client with Addison’s disease
Hyposecretion of adrenal hormones
Not enough sugar, salt and sex hormones
Can also affect the medulla: No adrenalin or emergency response system
No anti-inflammatory response
No immunosuppressant
Not enough salt: Decreased sodium and water- hypotension- circulatory collapse- shock
Increased potassium-heart arrhythmiasIncreases MSH- Melanocyte stimulating hormone which causes a rusty/tanned/dirty skin
appearance
President John F. Kennedy
Replacement hormones for life: prednisone, Florinef-fludrocrtisone
Addisonian Crisis/Adrenal Insufficiency/Shock
Can occur with client’s who have had nephrectomy
Pheochromocytoma
Usually caused by benign tumor in the adrenal medulla
Causes an increased production of catecholemines
24 hour urine collection for VML and catecholemines (epinephrine and Norepinephrine) or CAT
scan
Hypertension- 300/100- sweating-headache-heart palpitations- tremors- nervousnesstachycardia
Treatment- Vasodilators
Regitine
Nipride
Inderal- beta blocker
Renin- ACE Angiotensin converting enzyme inhibitor- decrease B/P- all the pril’sEnalapril/Vasotec- Catopril- Capoten- Lisinopril/Zestril
Bed rest and Surgical removal
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Nursing Care
Prevent activities that precipitates attacks
Anxiety
Palpation of the tumor
Vigorous exercise
Trauma
Lying on the tumor
Quiet environment/remain with patient
Client with Parathyroid Disorders
Parathormone prevents Hypocalcemia- breaks down calcium in bone and causes a shift to blood
Calcium needed for normal neuromuscular functioning
Calcium keeps impulses calm and smooth and prevents tremors/seizures
Helps blood clot
Calcium= 8-10 mg/dL
Parathyroid
Overproduction by tumor: Brittle bones and Hypercalcemia
Kidneys deal with renal stones
Encourage mobility
Give Calcitonin to force Calcium back into bones
Hypercalcemic crisis- 15 mg/dL- dialysis
Underproduction caused by autoimmune or removal by surgery
Hypocalcemia: tetany/convulsions/coma- hyperirritability of nervous system
Calcium Gluconate IV and PO
Calcium= 5-6 mg/dL
Diet high in calcium and low in phosphorous. Need Vitamin D for absorption
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Care of the Client with Diabetes Mellitus
Diabetes- large amount of urine
Mellitus- honey or sweet urine
Sugar Diabetes- old name
Pancreas
Large fish shaped organ behind and inferior to the stomach and liver which is both and exocrine
and endocrine gland
Exocrine: trypsin to digest protein, amylase to digest carbs, lipase to digest fats enter duodenum
the out through GI tract
Islets of Langerhan- alpha cells produce glucagon and beta cells produce insulin
Endocrine: insulin produced by beta cells
Glucagon produced by the alpha cells
Tests
Gold standard diagnosis
Oral Glucose Tolerance Test
Fasting urine and blood- 100 gram carbohydrate drink- Blood glucose at 30 min-1hr-2hr-3hr-4hr intervals
Diabetic clients go higher and stay higher than others
FBS- 70-110 mg/dL
2 hour PG- Post Prandial Glucose
0-50 years- 70-140
50-60 years- 70-150
60+ years- 70-160
Glucola or pancakes- 100 gram carbohydrates
Oral Glucose Tolerance Test
Fasting: 70-110
30 min: <200mg
1 hr: <200 mg
2 hr: <140 mg
3 and 4 hour: 70-115
Urine negative for sugar and acetones
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Test
A1C- Glycosalated Hemoglobin blood test
Not a diagnostic test
Normal: 2.2-6% >8% shows poor control
Glucose attaches to RBC’s that live 120 days
“You can’t cheat test”
Routine Screening
Should be done if:
Obese
First degree relative with DM
High risk ethnic population
Delivered baby >9 lb or gestational diabetes history
Hypertensive
HDL < 35mg/dL- Normal is 60 mg
Triglycerides > 250 mg/dL- normal is <200 mg
Impaired glucose tolerance or fasting glucose in the past
Diabetes Mellitus
Chronic Disease
Not a single disorder
Group of metabolic disorders
Characterized by hyperglycemia
Overview
Large number of individuals are not diagnosed
Silent then erupts like a volcano
Cannot be cured
Can be controlled in efforts to control complications
Watch individuals who have constant yeast infections and ingrown toenails that will not heal
Apple shaped individuals at risk
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Complications affect:
Eyes- Diabetic Retinopathy- leading cause of blindness
Changes in the retinal capillaries cause decreased blood flow to the retina, leading to
retinal ischemia and has possible retinal hemorrhage or detachment
Kidneys
Nervous system- peripheral nerves (numbness, tingling, burning/stinging)
Cardiovascular system-** most common vascular complications is atherosclerosis
Leads to affecting micro-vessels that feed the eye and kidneys
Amputation from sores that will not heal
Sugary blood irritates the cell walls and leads to hardening and therefore atherosclerosis
Recommendations
Diabetic need to wear WHITE cotton socks- to be able to see blood or drainage
Look at feet at home with a mirror to inspect feet
Type I Diabetes Mellitus
Insulin Dependant
Usually occurs in children and adolescents
Results from autoimmune disorder that destroys the beta cells of the Islets of Langerhan and
usually had a history of viral episode 4-6 weeks prior to onset of symptoms
Symptoms of diabetes seem to come on abruptly and patient admitted in diabetic KetoacidosisDKA
“My Brown Eye Girl”
BS level 2000
Brown emesis coming out of mouth
Muscles-loose
Skin hot to touch
Remained unconscious
History of increased urination and salt crystals in toilet
Door to cell is locked without key- INSULIN
Without insulin glucose stays in bloodstream and the cells starves to death
In ER situation- can only give Regular insulin (pork) IV
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Insulin
Key to unlock the cell
Eases the active transport of glucose into muscle and fat cells
Energy source- glucose burned
Present for glucose to be stored as glycogen
Assists with protein synthesis
Unused glucose stored first in liver and muscles then as adipose tissue
Somogyi Phenomenon
Blood glucose controlled by insulin and glucagon
Other gland affect BS
Epinephrine- gluconeogenesis- creation of new glucose using amino acids
Adrenal Cortex through Cortisol- taking steroids elevates BS levels due to Cortisol
Anterior Pituitary: Growth Hormone
Times of stress, starvation, or growth
Somogyi Effect
Night time Hypoglycemic episode: Insulin induced
Body converts stored glycogen to glucose and elevates the BS level
Cat chasing its tail
Symptoms: Tremors; Restless, sweats; followed by a morning rise in blood sugar; may cause
nightmares
Different than dawn phenomenon where around 3 am glucagon is over secreted and insulin
under effective and BS level is very high in the morning. Dawn phenomenon will have none of
the above symptoms.
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Type 1 DM-DKA- Diabetic Ketoacidosis- Insulin Dependent DM
Insulin no longer produced
Leads to hyperglycemia and breakdown of body fat and protein
Cells starve- “Give me glucose!” Body says ok by burning glycogen stores and secreting
glucagon
BS level higher but cells are still not fed
Burning of fat leads to “ketosis”
Ketone bodies accumulate- fatty acids/metabolic acidosis occurs
Lactic acid is produced when the cells can’t get enough oxygen and breakdown. This also
contributes to metabolic acidosis.
When you retain sodium you lose potassium and vice versa- Sugar will be actively transported
with the sodium and water out of the kidney- When the renal threshold (BS of 160) is breachedyou lose sodium, water, and glucose and retain potassium and with that the hydrogen ions
leading to Hypokalemia and metabolic acidosis
Type 1 DM- Pathophysiology
Elevated blood glucose
Excess spills into the urine leading to Glycosuria- renal threshold breached! - Both glucose and
Sodium is lost!
Once hyperglycemia and Glycosuria occur, three manifestations of diabetes are seen: 3 Poly
Sisters
Polyuria
Polydipsia
Polyphagia- hunger
Symptoms
Fluid and Electrolyte imbalance
Hyperglycemia increases the osmotic pressure of the blood and sucks the H2O out of the cells
Dehydration: dry-hot-flushed skin/thirsty
N&V
Weight and strength loss but hungry
Ketones in sugar in urine
Air hunger- Kussmaul’s respirations- lungs are trying to blow off CO2 to resolve acidosis- deep,
intense respirations
Fruity odor to breath- can smell like fresh cut grass or juicy fruit gum
Photophobia
Urine crystallizes when dry
Vulvar itching
Yeast infection
Visual problems noted
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Compensation of DKA
Kidney’s try to pee it off
Lungs try to blow it off- tries so hard to get low CO2 levels= <35-45 mmHg and <22-26 mEq HCO3
GI tract tries to puke it off
If insulin is not replaced, person goes into a coma- Diabetic coma- and dies due to acid in body
from ketones- Also needs fluid/electrolytes- perhaps Sodium Bicarbonate if severe because can
cause an alkalosis rebound
pH: 7.35-7.45 – metabolic acidosis <7.35
Type 2 DM- Most Common Type of Diabetes- NIDDM
Characterized by hyperglycemia due to insufficient insulin production and insulin resistanceLocks on the doors are rusty. Can’t see receptor sites
Not enough insulin to lower blood glucose levels
Enough insulin to prevent the breakdown of fats; ketosis does not develop
Risk factors
Heredity
Obesity
Increasing age
High risk ethnic group
Type 2 DM- Role of Obesity
Reduces available insulin receptor sites, leading to insulin resistance
Three quarters of older adults with type 2 are overweight
All older adults develop some insulin resistance
Weight loss through diet and exercise can reduce insulin resistance and sites reappear
With enough weight loss, may not need oral medications
Controlled not cured
Often undiagnosed for years- drive themselves to the hospital with BS of 600 mg/dl.
Less severe hyperglycemia
Only Polyuria and Polydipsia are present- no Polyphagia- cells already full of sugar
Breeding ground for bacterial infections
Cloudiness of eye lens leading to blurred vision
Destruction of peripheral nerves leading to paresthesia/numbness
Fatigue
Nocturia
Rebound hypoglycemic episodes
Impotence
Foot ulcers
Vulvar itching
Usually older person
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Hyperosmolar Hyperglycemic State (HHS) or (HHNKC)
Seen in type 2 diabetes
Severely elevated blood glucose
Extreme dehydration/shock/death
Altered LOC
Develops over hours to days
Life threatening emergency
HHS
Treatment: Correct fluid and electrolyte imbalances; provide insulin
Manifestations of Type 1 and Type 2 Diabetes Mellitus
Type 1
Polyuria
Polydipsia
Polyphagia
Weight Loss
Fatigue
Malaise
Type 2
Polyuria
Polydipsia
Recurrent Infections
Obesity
Fatigue
Blurred vision
Paresthesia
DKA
Dehydration (From Hyperglycemia)
Thirst
Warm, dry skin with poor turgor
Dry Mucous Membranes
Rapid, Weak pulse
Hypotension
Soft Eyeballs
Metabolic Acidosis (From Ketosis)
Nausea and Vomiting
Lethargy to Coma
Acetone (fruity, alcohol like) breath odor
Other Manifestations
Abdominal Pain
Kussmaul’s respirations (rapid, deep respirations; a
compensatory response to prevent a further decrease
in pH)
Blood Glucose
>250 mg/dL
Blood and Urine Ketones
Positive
Arterial Blood pH
<7.3
Serum Osmolarity
<340 mOsm/L
HHS
Dehydration from high osmolarity
Extreme Thirst
Warm, dry skin with poor turgor
Dry Mucous Membranes
Rapid, weak pulse
Hypotension
Neurologic Manifestations
Depressed Level of Consciousness to coma
Grand Mal Seizures
Other Manifestations
Abdominal Discomfort May be present
Rapid Shallow breathing
Blood Glucose
>600 mg/dL
Blood and Urine Ketones
Negative
Arterial Blood pH
Normal (7.35-7.45)
Serum Osmolality
>340 mOsm/L
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Treatment- Oral Antidiabetic Medications for Type II Diabetes
Sulfonyleureas: stimulate the release of insulin
Glipizide (Glucotrol), glyburide (Diabeta/Micronase)
Severe Side Effects: hypoglycemia, intolerance or Antabuse like effects with alcohol, liver
damage, leukopenia, interacts with ASA
Increases appetite but you need to lose weight- Recipe for failure- Newer meds better
Thiazolidinediones: Improve receptor activity
Avandia and Actos used now but Rezulin off market due to liver damage
Biguanide: reduces hepatic glucose
Metformin-Glucophage
Nursing Implications for Pharmacology: Oral Antidiabetic Agents
Class/Drugs
Purpose
Nursing Responsibilities
Sulfonylureas
Glimepiride (Amayrl)
Increases release of insulin
Assess for allergy to
Glipizide (Glucotrol,
from pancreas and increases
sulfonamides.
Glucotrol XL)
the number of receptor cells
Observe for signs and
Glyburide (Dia Beta)
to maintain blood glucose
symptoms of hypoglycemia
levels within normal range
(sweating, hunger, weakness,
dizziness, tremor,
tachycardia, anxiety)
Test client’s blood glucose
level before giving drug.
Assess for side effects of
heartburn, nausea or
diarrhea
Biguanides
Metformin
Reduces liver glucose
Monitor renal function,
(Glucophage)
production and improves
especially in clients at risk for
glucose use in skeletal
kidney disease
muscle to maintain blood
Monitor glucose levels
glucose levels within normal
throughout therapy
Discontinue 48 hours before
injection with any
radiocontrast dyes
Call physician if weakness,
drowsiness, malaise occurs.
These are signs of lactic
acidosis
Alpha-Glucoside Inhibitors
Acarbose (Precose)
Slows digestion and
Do not give to clients with
Miglitol (Glyset)
absorption of carbohydrates
intestinal disorders; acarbose
to maintain normal blood
will worsen these conditions
glucose levels
Meglitinides
Repaglinide (Prandin)
Nateglinide (Starlix)
Thiazolidinediones
Rosiglitazone (Avandia)
Pioglitazone (Actos)
Client Teaching
Take at the same time each
day. Take 30 minutes before
meals, except Glucotrol XL,
which must be taken with
food.
Monitor for hypoglycemia.
Test blood glucose level
before taking drug
Take at same time each day.
If a dose is missed, do not
double doses
Call physician if weakness,
malaise or drowsiness occur
These are signs of lactic
acidosis
Take with the first bite of a
meal.
May cause gas and diarrhea;
tends to decrease with
continued therapy
Stimulates pancreas to
secrete insulin
Monitor for hypoglycemia
Monitor for hypoglycemia
Increases insulin sensitivity at
receptor sites on liver,
muscle, and fat cells.
Assess for signs of liver
toxicity (e.g. anorexia,
jaundice, or dark urine)
Call physician if anorexia,
jaundice, or dark urine
develops
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Self- Monitoring Blood Glucose
Monitor and achieve metabolic control
Useful if ill or pregnant
Useful if symptomatic with hypo or hyperglycemia
On insulin: 3 or more times per day (Anytime if feeling funny)
Not on insulin: 2-3 times per day
Always check when feeling funny
Equipment:
Lancet
Blood glucose monitoring device
Test strip
Follow manufacturer’s instructions
Techniques: use sides of finger tip and warm and wash hands before stick
Non-Invasive Blood Glucose Monitoring
Gluco-watch biographer: worn as a watch
Measure Glucose values in perspiration
Urine Testing for Ketones and Glucose
Has unpredictable results
Should be done with type 1 diabetes
Either acid test/Ketostix
Normal results is no glucose in urine
If are ordered to check urine for glucose make sure you have double voided specimen for fresh
rather than concentrated specimen
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Insulin
Pork or synthetic (man-made)
Short or Fast Acting R-regular or Humulin R
Onset: 20 min Peak: 2-4 hours Dur: 6-8 hours
Intermediate: NPH or Humalin or Novalin N
Onset: 2-4 hours Peak: 6-8 hours Dur: 24-48 hours
Peak: med takes most glucose out of the blood
Type of Insulin
Rapid Acting
Lispro (Humalog)
Short Acting
Regular
Intermediate Acting
NPH
Lente
Novolin NPH
70/Regular 30
Long-Acting
Ultralente
Glargine (Lantus)
Onset (Hours)
Peak (Hours)
Duration (Hours)
0.25
0.5-1.5
4-5
0.5-1
2-4
4-6
1-2
1-3
0.5
6-12
8-12
4-8
18-24
18-24
Up to 24
4-6
1.5
18-24
Unclear Peak
36
24
Insulin Strengths
100 U per mL or 500 U per mL
Administered in a sterile, single-use, disposable syringe
All insulin given parenterally
Regular insulin: either subcutaneous or IV- given 30 minutes before meals
Give RN when mixing- draw up
Regular- First
N:NPH second
Insulinize the tubing: push 10 U of insulin to let drain out of tubing to coat tubing- so that
patient will get the full dose
Regular Insulin Sliding Scale
BS 200-250-----------------------------------------------5 units
BS 250-300-----------------------------------------------10 units
BS 300-350------------------------------------------------15 units
BS 350-400------------------------------------------------20 units and call Doctor
Page 24 of 35
Delivery Methods
Insulin Pen
Jet injector
Continuous or subcutaneous infusion pump
Sites of Insulin Injections Pg 362
Process: pinch skin, inject @ 90 degree angle- unless extremely emaciated- use common sense
Don’t inject into muscle; Don’t massage after injection
Rotate injection site
Minimize painful injection pg 362
Do arm then leg (use all sites then move to extremities
New sites more likely to cause hypoglycemia (due to better absorption)
Techniques to Minimize Painful Injections
Inject insulin at room temperature
Make sure no air bubbles remain in the syringe before injection
Wait until alcohol on the skin dries completely before injection
Teach client to relax muscles in the injection area
Penetrate the skin with the needle quickly
Don’t change the direction of the needle during insertion or withdrawal
Don’t reuse needles
Problems with Insulin Injection (both due to rotating sites)
Lipodystrophy- orange peel skin- edema
Lipoatrophy- due to not rotating site- sunken area
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Nursing Implications for Administering Insulin and Client Teaching
Nursing Implications
Discard vials of insulin whose expiration date has
passed
Discard any vial that is discolored or contains clumps,
granules, or solid deposits on the sides
Check client’s blood glucose level 30 minutes before
giving an insulin injection
When drawing up insulin dose, always check type and
dose with another nurse
If a client’s meal is delayed, hold administration of
rapid-acting insulin
Monitor and maintain a record of blood glucose
readings before each meal and at bedtime or as
ordered
Monitor food intake; notify physician when client eats
an inadequate diet.
Inspect injection sites for signs of lipdystrophy
Monitor for signs and symptoms of hypoglycemia or
hyperglycemia and take appropriate action
Client/Family Teaching
Know the manifestations of diabetes mellitus
Store opened insulin vials in a cool place for up to 4
weeks, avoid exposure to extreme temperatures or
sunlight
Refrigerate unopened extra insulin vials; do not freeze
them
Refrigerated insulin should be brought to room
temperature before using it
Demonstrate self-administration of insulin
Know how to mix two types of insulin
Discard outdated or discolored insulin
Keep a regular insulin vial available for emergencies
Check blood glucose before meals, at bedtime, and as
prescribed
If breakfast is delayed, also delay giving rapid-acting
insulin
Know the signs of hypoglycemia and hyperglycemia
Keep candy or sugar available to treat hypoglycemia
Avoid alcoholic beverages to prevent hypoglycemia
Observe injection site for hardness, dimpling, or sunken
areas; develop a plan for rotating injection sites
Page 26 of 35
Insulin Regimen
Individualized (trial and error)
Mix short and longer acting
Timing depends on feed, exercise, glucose level, type of insulin
Tight glucose control results in fewer long term complications
Insulin Pump- Basal is 0.5 units- 1 unit
Looks like a pager
Hold 2-3 days worth of insulin with preservatives
Battery driven plunger pushes out small amounts of insulin based on basal rate
Up and down keys to increase dose and given bolus injection
Cannula in abdomen- watch peritonitis (hard, ridge like stomach- inflammatory)
Change sites every 2-3 days- look for signs and symptoms of infection
Costly
Requires training
Cap it off to go swimming or bathing
Hypoglycemia- pg 369
Causes:
Too much insulin
Overdose of oral antidiabetic medication
Too little food
Excess physical activity (acts like insulin- pushes glucose into the cell and lowers blood
glucose level)
Sudden onset; blood glucose <50 mg/dL
Signs and Symptoms
Shakiness, convulsion, slurred speech, cool and clammy skin, perspiration, staggering
gait, double/blurred vision
Headache
Brain requires a constant supply of glucose so a hypoglycemic episode alters brain
function
Page 27 of 35
Manifestations of Hypoglycemia
Caused by responses of the autonomic nervous system
Hunger
Nausea
Anxiety
Pale, cool skin
Sweating
Shakiness
Irritability
Rapid pulse
Hypotension
Caused By Impaired Cerebral Function
Strange or unusual feelings
Headache
Difficulty in thinking
Inability to concentrate
Change in emotional
Blurred vision
Decreasing levels of consciousness
Seizures
Coma
Slurred speech
Laboratory Findings
Blood Glucose
Blood and urine ketones
Plasma pH
Serum Osmolality
<50 mg/dL
Negative
Normal
Normal
Hypoglycemia Awareness
Automatic response
May develop in some people with long standing type 1 diabetes
No symptoms of hypoglycemia in the urine of a low blood glucose level
Page 28 of 35
Glycemic Index
Varies with age and weight
Some foods raise your blood sugar level higher than others
High glycemic index
Refined carbs/sugar
White bread-white bagels- white rice- white pasta- cornflakes
Low index:
Broccoli
Leafy greens
Plums
Fruits and veggies
Fiber
Ice cream and yogurt?? Fat slows BS increase
Better use sugar free ice cream
Macrovascular Complications: pg 371
Macrocirculation: Large blood vessels undergo changes due to atherosclerosis
Complication
Coronary Artery Disease
Stroke
Peripheral Vascular Disease
Risk factor for an MI
High cholesterol and high triglycerides
Page 29 of 35
Manifestations of Peripheral Vascular Disease
Loss of hair on lower leg, feet, and toes
Atrophic skin changes: shininess and thinning
Cool to cold feet
Legs become red when dependant; legs become white when elevated
Thick toenails
Diminished or absent peripheral pulses
Intermittent claudication- pain with walking
Pain at rest, usually at night
Complication: Diabetic Retinopathy
Changes in the retinal capillaries; lead to retinal ischemia, retinal hemorrhage, or detachment
Retinopathy stages: nonproliferative and proliferative
Leading cause of blindness in people ages 20-74
Yearly eye exams are recommended
Somogyi Effect
A morning rise in blood glucose to hyperglycemic levels following an episode of night time
hypoglycemia
Other organs kick in to help raise blood sugar level
Signs and symptoms: nocturnal hypoglycemia: tremors, night sweats, and restlessness
Page 30 of 35
Hypoglycemia Treatment
Remember to assess 1st and then treat:
Mild:
Immediate treatment
15g rapid acting sugar by mouth if conscious
Example: ½ cup of juice, cola, 3 glucose tablets, 3-4 packets of sugar, 1 tube of glucose
gel- frosting. No diet drink
Squirt gel between check and gums for rapid absorption
Severe- if can’t swallow
Intravenous glucose- 50% Dextrose/Glucose injection
No IV access use glucagon IM/SC reconstitute
When in doubt always treat for hypoglycemia
After pain is conscious:
Follow up with protein to hold blood sugar up
Example: cheese and crackers or peanut butter and crackers
Don’t give insulin to the person who is NPO before surgery or special procedure without
consulting the doctor
Severe hypoglycemia may develop if a person is not eating but receives the usual dose of insulin
Page 31 of 35
Diet
Role of diet with control of blood glucose level
Complex carbohydrates and foods high in fiber
Limit sugar, fat, sodium, and alcohol
How to read food labels
Eating away from house- yes, but in moderation
Relationship between diet, exercise, medication
ADA- Diet
Carbs: 50-60%-- complex carbohydrates
Protein: 12-20%
Fats: 20-30% less with <10% saturated fat
1800 calorie diet gets:
Carbs: 225 gms (x4)
Protein: 90 gm (4)
Fats: 60 gm (9)
3 meals and 2 snacks—especially HS
Diabetic Exchange List
Don’t forget snacks to prevent hypoglycemia
Complication: Diabetic Nephropathy- Kionmelstiel- Wilson:
Type I is at greater risk for this complications
Disease of the kidneys
Characterized by albumin in the urine (too big, should see—not normal)
Hypertension, edema, renal insufficiency
Most common cause of renal failure
First indication: Microalbuminaria
Treatment: (beyond insulin and blood glucose control)
ACE inhibitors- the pril’s Enalapril- Vasotec- Catopril- Capoten- Lisinopril- Zestril
These are to keep BP down
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Complication: Diabetic Neuropathy
Disorder of the peripheral nerves and automatic nervous system
Results: sensory and motor impairments, postural hypotension, delayed gastric emptying,
diarrhea, impaired genitourinary function
Results from the thickening of the capillary membrane and destruction of myelin sheath
Bilateral sensory disorders:
Appears first in toes, feet, and progress upward in fingers and hands
Treatment
None specific
Focus on controlling neuropathic pain with Tricyclic antidepressants/topical creamCapsaicin (Zostrix)---Neurotin medication
Complication: Autonomic Neuropathy
Involves numerous body systems such as cardiovascular, gastrointestinal, genitourinary
Teaching Plan Contents
Medications
Diet
Exercise
Foot Care
Awareness: Have patient wear med alert bracelet/necklace
No smoking
No alcohol- affects glucose levels and tends to cause hypoglycemia
Medications
Types of medication- oral/insulin
Insulin- Type, dosage, mixing instruction, times of onset, peak, obtaining and care of
equipment, self injections, locations for injections
Diet review: teaching for patient
Exercise:
Purpose
Importance
Types
Personal exercise choices
Increase food intake before exercising- 15 gm carb snack
Carry glucose tabs, candy, have soda drink/juice available
If type 1, think about where you are going to put insulin injection- “Remember don’t
inject into the legs”
Page 33 of 35
Foot Care
Wash feet daily and dry between toes
Inspect feet daily
Wear white cotton socks
Buy shoes in the afternoon
Wear shoes that completely cover the feet
Wear shoes with hard soles- no flip flops
Have special training and specific order to cut toenails and cut straight across- above the
quick
Do not shave legs without a specific order
Concern for Young and Middle aged adult
Assess the young adult’s lifestyle including eating habits/patterns, exercise
Provide teaching to address the need for scheduled eating patterns and exercise regime
Concern for Older Adult
If obese, might need diet, exercise, and weight reduction program
Consider: dietary likes/dislikes, eating habits, meal preparation, age related changes in taste and
smell, dental health
Consider: age-related decline in calorie needs and reduced physical activity
Might be on a fixed income
Coexisting illness and multiple medications can decrease appetite and reduce energy to plan,
cook, or eat
Dietary restriction can lead to avoidance of social gathering
Decreased thirst mechanism can lead to dehydration
Exercise should be individualized depending on physical limitation
Withdrawal from social situations can lead to depression
Visual and fine motor skills deficits can make insulin administration, glucose monitoring, food
preparation, exercise and foot care difficult or impossible
Page 34 of 35
Assessing for Diabetes Mellitus
Subjective Data
Presence of hyperglycemia manifestations: Polyuria,
Polydipsia, Polyphagia
Weight loss or gain; changes in appetite
Changes in vision or speech
Presence of numbness and/or tingling or burning in
feet
Presence of slow healing wounds
Pain or burning with urination
Problems of vulvular itching in females
Family history of type 1 or type 2 diabetes mellitus
Use of insulin or oral antidiabetic medications
Any recent surgery
Objective
Vital signs (blood pressure- standing and lying, pulse,
respirations, temperature)
Weight and Height
Assess for DKA, HHS, and/or hypoglycemia
Assess visual acuity
Assess sensations of touch and position, pain, and
temperature
Observe mental status for signs of confusion or
disorientation; slurred speech
Observe gait patterns, use of assistive devices for
walking, and abnormal wear patterns on shoes
Inspect oral cavity for bad breath, bleeding, red gums,
and tooth pain
Inspect skin for dryness or excessive perspiration;
presence of hair on lower extremities; presence of
lesions, redness over pressure points, cellulitis, or
gangrene
Palpate peripheral pulses for decrease or absence
Palpate lower extremity for capillary refill, color, and
temperature of skin, and edema
Monitor and report blood glucose levels above or below
expected range
Evaluation
Collect data related to chronic complications
Identify frequency of DKA, HHNS, hypoglycemia
Document VS, LOC, skin integrity, complications
Notify MD of client’s response to treatment Reinforce teaching related to medications, diet and
self-care
document
Page 35 of 35