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pain, endocrine
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pain is…
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, Pain is whatever the person says it is, existing wherever the person says it does
Opioid tolerance
expected adaptation: a normal physiologic response that can occur with regular administration of an opioid and consists of a decrease in one or more effects of the opioid
Opioid physical dependence
withdrawal if stopped, normal response that occurs with repeated administration of the opioid
opioid addiction
physical + behavioral used for nontherapeutic reasons. influenced by genetic, psychosocial, and environmental factors.
Pseudo addiction
mistaken diagnosis of substance use disorder that occurs when a patient’s pain is not well controlled; the patient may begin to manifest symptoms suggestive of SUD: demanding behavior, escalating demands
Pain relief typically eliminates these behaviors accomplished by increasing opioid doses or decreasing intervals between doses
Pain and brain connection
Nociceptive sensory pain information transmitted to the brain along several pathways with chemical mediators (transduction, transmission, perception, modulation)
Transduction (nociception)
1. Stimulus > electrical signal
2. Mediators: prostaglandins, bradykinins
3. NSAIDs act here
Transmission (Nociception)
1. Peripheral nerves → spinal cord → brain 2. A-delta fibers: fast, sharp 3. C fibers: slow, dull
Perception
1. Occurs in brain 2. Pain becomes conscious
Modulation
1. Descending pathways 2. Endorphins reduce pain 3. Opioids act here
Factors influencing perception of pain
physical factors (disease, rest/fatigue, nutrition), social, spiritual, psychological (support/isolation, mental, emotional, cognitive state)
Acute pain
Known cause ie surgery, fractures, burns
New to a few weeks: normal healing
Localized
Easily Treatable
Has observable physical response: ↑ BP ,heart rate, & respiratory rate Patient looks uncomfortable
Chronic pain
Lasting > 3 months
There is often not a change in BP, HR and patient may just look chronically ill, not “writhing in pain”
Cause and onset may not be known; multiple sclerosis, diabetic neuropathy, tumors, shingles…
intermittent and malignant
chronic intermittent pain
migraine headaches
IBS
chronic malignant pain
cancer with growing tumors, worsening pain
Cutaneous nociceptive pain
local (bee sting) perceived from the skin well localized
Somatic nociceptive pain
muscle, bone, fracture pain. aching throbbing well localized
visceral pain
intestine, gastric, gall bladder pain. tumor involvement may be well localized while obstruction involvement diffuses(poorly localized) pain
Neuropathic pain examples
phantom pain, diabetic neuropathy, shingles, neurological diseases: ALS, AIDS, MS
Phantom pain
Result of peripheral nerve damage
Shingles
postherpetic neuralgia: persistent pain where you had a rash/blisters
nociceptive pain meds
• ASA, APAP • NSAIDs • APAP/Codeine #3 • APAP/Hydrocodone • APAP/Oxycodone • Tramadol • Morphine • Oxycodone • Methadone
Types of nociceptive pain and descriptions
cutaneous, somatic, visceral are more localized: • Cramping • Crushing • Cutting • Gnawing • Pounding • Pressing • Sharp Squeezing • Tender • Throbbing.
types of neuropathic pain descriptions
• Flashing • Lancinating(mix of stabbing/shooting pain)• Numb • Radiating • Burning • Shooting • Stabbing
Neuropathic pain meds
Gabapentin, Pregablin, Tricyclic antidepressants-- desipramine ,Methadone, Corticosteroids
WHO step ladder
step one with mild pain: 2-4/10 ASA APAP NSaIDS +/- adjuvants, step two moderate pain: 5-7/10 (A/Codeine) tylenol/codeine (A/Hydrocodone) Vicodin (A/Oxycodone) Percocet (Tramadol) Ultram step three Severe pain: 8-10 Morphine Hydromorphone (Dilaudid) Methadone (Dolophine) Fentanyl (Duragesic) Oxycodone
Side effects of anticonvulsants
gabapentin/ pregablin: Somnolence: feeling tired wanting to sleep, Dizziness, Depression, suicidal thoughts
Polypharmacy
meds having the same class, same route, same speed, same purpose medication. Not good!! Not acceptable!! ex: Morphine IR15 mg PO and oxycodone IR 30 mg PO
Common adverse opioid effects
Constipation, dry mouth, n/v, sedation, sweats, urinary retention
uncommon adverse opioid effects
bad dreams/hallucinations, dysphoria/delirium, myoclonus/seizures, pruritus/ urticaria, resp depression
Basal medication
The pain medication that is given for continuous pain relief
Anterior pituitary gland
produces hormones that affect the breasts, adrenals, thyroid, ovaries, and testes, as well as several other hormones
Posterior pituitary gland
the kidneys. are to store and release the hormones oxytocin and vasopressin (antidiuretic hormone)
Hyperpituitarism
too much of hormone, resulting in: Cushing’s syndrome Acromegaly: excess growth hormone: growth plates open: heights growth plate closed: hands and feet grow Hyperthyroidism Hypogonadism: no sex gland hormones/very little SIADH Cushing syndrome: too much cholesterol steroid use is most common reason for this to happen + tumors
Tx hyperpituitarism
Meds (hormone replacements), radiation Surgery: Transsphenoidal hypophysectomy
Hypopituitarism
too little of hormone, resulting in: Addison’s disease Stunted growth Hypothyroidism Infertility / irregular Diabetes Insipidus
Transsphenoidal Hypophysectomy
Preferred to open craniotomy as can be done endoscopically Decreased: 1. risk of infection 2. length of stay / recovery 3. pain Assess vision pre & post surgery! Elevate HOB Test packing for glucose!
post op for transsphenoidal hypophysectomy
Monitor for: 1. CSF on nasal packing 2. Neuro changes Decreased LOC > Cushing’s Triad Pupil changes Seizure activity Oral care! Meds: Phenytoin - seizure prevention Mannitol - reduce cerebral edema Lasix - decrease fluid retention Dexamethasone - decrease inflammation (iv > po, taper!!) Antibiotics - reduce risk of infection
Thyroid gland Goiter
enlarged thyroid with - / + thyroid function. Produces: T4 (thyroxine) with iodine. T4 goes to liver (80% and not activated produced in thyroid gland) where T3 (triiodothyronine) is produced. (majority gets produced in the liver 20% in thyroid gland and it is active)
T3 and T4 regulate: Respiratory / cardiac function, temperature, carbs / fats/ protein metabolism, erythropoiesis, gut motility, growth development in fetus of major organs / nervous tissue / bones
Hypothyroidism
Hashimoto’s disease: autoimmune disease usually diagnosed when woman wants to get pregnant, irradiation, idiopathic (we dk) Dx: Central: Pituitary / hypothalamus - ↓TSH, ↓ T3, ↓T4 Primary hypothyroidism: thyroid gland - ↑ TSH, ↓ T3, ↓T Tx: lifelong treatment (Levothyroxine Sodium). Slowly increase dose. Symptoms decrease over several weeks. TSH, T4, T3 prn.
Hyperthyroidism
Grave’s disease, toxic nodular goiter, inflammation, drugs Dx: - ↓TSH, ↑ T3, ↑ T4 - ↓ Cholesterol Tx: meds, radioiodine therapy, surgery Complications: Exophthalmos (from Grave’s) = abnormal protrusion of the eye Thyroid Storm - extreme increase in basic metabolic rate (BMR)
Myxedema
Undiagnosed or undertreated hypothyroidism Dry, waxy swelling with abnormal deposits of mucin in skin and other tissues
Management of excessive thyroid hormone:
Anti-thyroid Medication (Methimazole preferred) < 18 y/o and pregnant women get Propylthiouracil (PTU) instead: impairs thyroid hormone synthesis - alleviates Graves symptoms in 4-8 weeks - agranulocytosis- increased risk of infection Radioiodine Therapy - Contraindicated in pregnancy and rarely used in children - Hypothyroidism as a complication Surgery
Thyroid Storm
extremely high metabolism High fever (104-106F) Tachycardia (>140) Hypertension Hyperreflexia Arrhythmias (AF), Heart failure, Angina Severe agitation / delirium GI distress Dyspnea EMERGENCY
Myxedema Coma
extremely low metabolism Hypothermia Bradycardia Hypotension Hyponatremia Hypoglycemia Hypoventilation
Post-op management for Total Thyroidectomy
Lifelong hormone replacement
Subtotal Thyroidectomy post-op management
+/- hormone replacement Risks tetany, respiratory obstruction, laryngeal edema, vocal cord injury, aspiration Post-op: airway, O2, electrolytes, aware of effect on parathyroid gland (calcium depletion)
Hypoparathyroidism: Causes
Inadvertent removal during thyroidectomy, Idiopathic, Autoimmune
Hypoparathyroidism Pathophysiology
PTH unable to regulate calcium & phosphorus Resulting in: Tetany, painful muscle spasms Labs: ↓ Ca, ↑ Phos Tx: 10% calcium gluconate solution oral calcium and Vit D
Thyroid cancer
Rising incidence Women : men = 3:1, 5-year survival >98% Benign adenomas Most slow growing and palpable in exam Hard, irregular, painless, enlarged thyroid gland Dx: Fine needle aspiration, scans to find mets, TFT’s Tx: Supportive, chemotherapy, and surgery
DM T1: What
Autoimmune destruction of pancreatic beta cells. Absolute insulin deficiency. Glucose cannot enter cells, stays in bloodstream, and causes hyperglycemia. Body switches to fat breakdown which produces ketones which leads to metabolic acidosis. Signs & symptoms: polyuria, polydipsia, polyphagia. Also weight loss, fatigue, blurred vision. Dx: Fasting glucose >126 mg/L, random glucose > 200 mg/L, A1C >6.5%
Acute Complications DM1
1. Diabetic Ketoacidosis (DKA) Tx: IV fluids!! IV insulin, monitor & replete potassium, cardiac monitoring. 2. Hypoglycemia Tx: Conscious > 15g fast carbs! Unconscious > glucagon IM or IV dextrose Chronic Complications: 1. Microvascular changes 2. Macrovascular changes Tx: lifelong insulin therapy
Managing DM1:
Blood glucose monitoring: Before meals & bedtime (or more often) Continuous glucose monitors Nutrition: Carb counting Consistent meals Balance insulin w/ intake Insulin therapy: Rapid (Lispro) Short (regular) Intermediate (NPH) Long-acting (glargine) insulin pump FOOT CARE Inspect feet daily No barefoot walking Proper footwear Report wounds early Exercise Lowers glucose - ? snack before exercise
Sick day rules DM1
Never stop insulin Check glucose every 3–4 hrs Check ketones if glucose >250 Drink fluids Call HCP if: Persistent hyperglycemia Ketones present Vomiting IV use because of dehydration 250/hr usually. Insulin iv, glucose and potatssium. Look up how potassium decreases in the body in DKA so you give potassium to prevent arrhythmias. Insulin drip check on them every hour. Normal range 70-100 rn
Burns priority care immediately following injury
extinguish
cool the burn
remove restrictions
cover the wound
irrigate chemical burns
What to do with burns at facility/ambulance
start IV (central line may be indicated)
infuse LR
cover with a clean sheet
coordinate care w a burn center
call report
Burns phases of care
emergency, acute/intermediate, rehabilitation
Emergent care burns
onset to completion of fluid resuscitation
acute/intermediate care burns
begginning of diuresis to near completion of wound closure (initiated w/in 48-72 hours)
Rehabilitation care burns
from wound closure to development of pts baseline/optimal performance
Fluid resuscitation for thermal/chemical burns equation
2mL LR x pt weight in kg x %TBSA (for 2nd, 3rd, 4th degree) within 24 hours (give first half 8 hrs second half remaining in 16 hrs)
Fluid resuscitation for electrical burns equation
Or 4mL LR x pt weight in kg x %TBSA (for 2nd, 3rd, 4th degree) within 24 hours (give first half 8 hrs second half remaining in 16 hrs)
Urinary output/changes in color what are we watching for
rhabdomyolysis
Palmar method
better for smaller/scattered/irregular burns
Palm including fingers closed together is considered approximately 1% of their TBSA
Rule of 9’s
best for large quick assessments in adults body’s divided into equal 9%
1st degree burn
superficial:
Sunburn, superficial scald, low-intensity flash.
· Epidermis, possibly a portion of dermis.
· Tingling, peeling, itching, pain. Reddened, blanches with pressure.
· Minimal edema, Possible blisters.
· Recovery is quick and complete (unless infection develops).
2nd degree burn
partial-thickness:
· Scalds, flash flame, contact
· Epidermis, portion of dermis
· Pain, sensitivity to air
· Blisters, mottled base, disrupted epidermis, weeping surface, edema.
· Recovery 2-3 weeks. Scarring & depigmentation possible. May require grafting.
3rd degree burn
full thickness:
· Prolonged exposure to hot liquid, electrical current, chemical, contact
· Epidermis, dermis, sometimes subcutaneous tissue. May involve fascia
· Often insensate. Dry: pale, white, eschar, edema. Eschar may slough. Grafting necessary. Scarring, loss of function.
· Shock, possible hemolysis, myoglobinuria.
4th degree burn
full thickness
· Prolonged exposure or high voltage electrical injury
· Deep tissue, muscle, bone
· Shock, myoglobinuria, hemolysis
· Charring evident
· Amputation likely; grafting non-beneficial
Electrical burns
· Types: Flash, conductive (travels through body), lightning
· Visual exam not predictive of size and severity
· Deep muscle injury may be present without obvious superficial injury
· Compartment syndrome is common due to edema from fluid resuscitation
· Vasculature & heart may be affected
Inhalation Burns
o Can result from thermal or chemical irritants. Damage from smoke: heat, particulates, systemic toxins.
o 6-30% of burn center admissions have inhalation injury & doubles chances of mortality from thermal burns.
o Mechanisms of injury: thermal damage, asphyxiation, irritation of pulmonary tissue
early lab values/critical/abnormalities
Hyperkalemia from massive cell destruction, hyponatremia from plasma loss
later lab values/critical/abnormalitites
18+ hrs afterwards Hypokalemia & hyponatremia with fluid shifts
o Fluids, UOP, Pain, GI
Foley catheter to monitor for kidney function and rhabdo.
NGT for TBSA > 20-25% -- paralytic ileus is common in patients with large burns
IV analgesia Cutaneous, SQ, PO not effective in burn patients
Debridement
o : removal of devitalized tissue. Natural, mechanical, chemical, surgical
grafting
o Autografts (full or split thickness).
Homograft’s & xenografts are considered biologic dressings
o Biosynthetic & synthetic dressings, mesh