N300 Exam 2

Endocrine, Respiratory, Renal, and Hepatobiliary

hormones

chemical signals that coordinate a range of bodily functions, secreted into the bloodstream

endocrine network contains the following

hypothalamus
pineal gland
pituitary gland
thyroid
parathyroid
thymus
adrenals
pancreas
ovaries
testes

general functions of endocrine system

growth and development
homeostasis
metabolism
reproduction
response to stimuli (stress, injury)

Problems that can occur in endocrine system

-incorrect amount release of hormones
-not a strong enough blood supply
-not enough receptors at target tissue
-targets do no response appropriately to hormonal signal

hypothalamus

maintains homeostasis
link between endocrine and NS
produces releasing and inhibiting hormones, helps stimulate or inhibit key processes:
-HR, BP, T, Fl and lyte balance including thirst, apetite and BW, glandular secretions of stomach and intestines, production of substances that influence the pituitary gland, sleep cycle

hypothalamus location

below the thalamus (relays sensory info), and above the pituitary and brain stem
size of an almond

hypothalamus hormones

highly involved in pituitary gland function by secreting neurohormones: ADH, CRH, GnRH, GHRH, Oxytocin, PRH, TRH

Pituitary gland

master gland (controls thyroid, adrenals, ovaries and testes)
acts after the hypothalamus prompts it

pituitary gland location

base of the brain
1/3 in diameter
connected to hypothalamus by the pituitary stalk= infundibulum
has an anterior and posterior lobe

anterior lobe of pituitary

produces and releases hormones upon receiving releasing or inhibiting hormones from hypothalamus
ACTH, FSH, GH, LH, Prolactin, TSH

posterior lobe of pituitary

does not produce hormones but releases them (from ends of nerve cells coming from the hypothalamus)
ADH, oxytoxin

pineal gland location

third eye
located deep in center of brain
shaped like a pine cone, reddish gray, 1.3 in long

pineal gland hormone

melatonin- circadian rhythm (light stops melatonin production, secreted during dark periods) , reproduction (blocks secretion of LH and FSH from ant pituitary bc these aid in proper development and functioning of ovaries and testes)

thyroid gland

metabolism through action of thyroid hormone, which is made by extracting iodine from the blood and incorporating it into thyroid hormones
cells are highly specialized to absorb and use iodine
controlled by both pituitary and hypothalamus: when thyroid horomone levels are too low, hypothalamus secretes TSHRH which alerts the pituitary to produce TSH

thyroid gland anatomy

greek for shield
butterfly shaped located in front of trachea and below the larynx/adams apple
has two lobes attached by the isthmus

thyroid hormones

T3 (tri-iodothyronine) (20%) (stronger)
T4 (thyroxine) (80%)
calcitonin

parathyroid gland

4 small glands that regulate calcium, help nervous and muscular systems function
found on back side of thyroid, size of grain of rice
maintains calcium and phosphate homeostasis

calcium is important bc

causes muscles to contract
for normal conduction of electrical currents along nerves

parathyroid hormone (PTH)

acts on receptors in bone, kidney and intestine
causes bones to release calcium and phosphate into bloodstream by increasing osteoclast activity and decreased osteoblasts
inc kidney tubular reabsorption of calcium while excreting phosphate
increases the formation of active Vit D= increases intestinal Ca and P absorption which regulates how much Ca is absorbed from your diet

adrenal glands

two glands on top of kidneys
adrenal cortex: outer part produces corticosteroids (glucocorticoids and mineralcorticoids, and sex steroids)
adrenal medulla: inner part produces nonessential hormones like adrenaline

cortisol

helps regulate metabolism and stress response
secreted by adrenal cortex

aldosterone

helps control BP
secreted by adrenal cortex

adrenal cortex hormones

Glucocorticoids:
- hydrocortisone/cortisol
- corticosterone (immune response)
Mineralcorticoids:
-aldosterone
Sex steroids

adrenal medulla hormones

epinephrine/adrenaline (inc BP, inc BG, Inc HR)
norepinephrine/noradrenaline (vasoconstriction, High BP)

Pancreas

6 in long flat gland that lies deep within abdomen between stomach and spine
connected to duodenum of small intestine
both and endocrine (5%) and exocrine gland

islets of langerhans

pancreatic endocrine cells
produce gastrin, glucagon, insulin, somatostatin, vasoactive intestinal peptide (VIP)

thymus gland

behind sternum and between lungs
only active until puberty, after it shrinks and is replaced by fat
secretes thymosin which stimulates T cell development

Ovaries

estrogen and progesterone

testes

testosterone

common endocrine tests

urine, blood, imaging
measure hormone levels, identify tumors, determine if they are working normally

hyperthyroidism

excessive secretion of thyroid hormone leading to inc basal metabolic rate, inc cardiovascular function, inc GI, inc neuromuscular, weight loss, and heat intolerance

hyperthyroidism causes

excess TSH secretions by pituitary
autoimmune- Graves disease
Thyroiditis (radiation)
tumor
excessive dose of supplemental thyroid hormone

hyperthyroidism sx

palpitations, chest pain, systolic HTN, tachycardia, dysrhythmias
dyspnea
visual changes, eye fatigue, eyelid retraction, exophthalmus, tremors
inc apetite, diarrhea, weight loss, inc BMR, heat intolerance, low grade fever
dec attention span, restlessness, irritability, manic/labile
muscle weakness, wasting, fatigue

thyroid storm/crisis

rare but life threatening
uncontrolled hyperthyroidism d/t untreated Graves disease
triggered by major stressor or infection, or vigorous palpation of thyroid, or ill pt treated with radioactive iodine (toxic to thyroid, can further exacerbate storm)

thyroid storm sx

fever >102
tachycardia, systolic HTN, HF, shock, N/V, agitation, confusion, seizures

thyroid storm tx

maintain airway/ventilation
meds to lower thyroid levels
cardiac monitor for dysrhythmias
IV fl
comfort measure (cooling blanket)

hyperthyroidism interventions

assess resp effort, energy levels and activity tolerance
diet is important (enough calories during hypermetabolic state)
regular eye exams, protect eyes with tinted glasses, moisten eyes, sleep w HOB elevated to dec pressure on optic nerve

danger of removing thyroid gland

also removing the parathyroid leading to hypocalcemia and tetany
hemorrhage
respiratory distress d/t swelling
damage to laryngeal nerves

hyperthyroidism tx

radioactive iodine is treatment of choice (oral , make sure not pregnant)
subtotal thyroidectomy
total thyroidectomy (must take thyroid hormone forever)

post thyroidectomy interventions

inspect neck dressing q hour and then every 4 hours
monitor amount of drainage/bleeding
maintain in semi fowlers w ice to neck
assess for sx of hypocalcemia
keep emergency tracheostomy kit at bedside

hypothyroidism

low circulating thyroid hormones
slow, low, cold
one of most common disorders in US, more common in women >65

hypothyroidism causes

autoimmune
thyroid surgery
radioactive iodine tx
cancer
endemic iodine deficiencies
atrophy r/t chronic thyroiditis (hashimotos), or graves
congenital (Cretinism)
secondary: d/t diseases of pituitary and hypothalamus

hypothyroidism sx

dec production of HCL in stomach, reduced GI motility, dec HR and CO, impaired neuro function, dec heat production, dec lipid metabolism, anemia, inc interstitial fl leading to pleural and cardiac effusions, dec BMR, hypotension, periorbital edema, hypoventilation, dyspnea, cold intolerance, slow slurred speech, paresthesias, anorexia, weight gain, constipation, apathy, depression
MYXEDEMA

myxedema

accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues (non pitting edema)
puffy face, periorbital edema, mask like face
seen in hypothyroidism
complications can lead to myxedema coma and death= hypotension, hypothermia, coma, Resp failure, hyponatremia, hypoglycemia

causes of myxedema

acute illness
rapid withdrawal from thyroid medication
use of sedatives/narcotics
surgery
hypothermia

interventions for myxedema coma

maintain airway
give replacement thyroid hormone (levothyroxine sodium) IV
administer IV glucose
administer corticosteroids
cover with warm blankets

interventions for hypothyroidism

monitor cardiac status (BP and HR)
assess hemodynamic (urine output, BP)
monitor mental changes
administer hypothyroid meds: synthroid
blankets for temperature
encourage fluids at least 2L and diet high in fiber to promote regular BM

hyperparathyroidism

increased PTH, more common in older adult women
leads to hypercalcemia and hypophosphatemia
kidneys then inc bicarb excretion and dec acid excretion leading to metabolic acidosis and hypokalemia
bones inc rate of ca and P release leading to bone decalcification
hypercalcemia causes calcium deposits in soft tissues, renal calculi, altered neuro, muscle weakness, altered DI, abd pain, anorexia, altered CV function

causes of primary hyperparathyroidism

80-85% from adenomas to gland
hyperplasia
genetic factors
carcinoma
when one or more hyperfunctioning parathyroid glands is unresponsive to normal feedback mechanism of Ca

causes of secondary hyperparathyroidism

d/t hypocalcemia seen in chronic renal disease
vit d deficiency
both of these lead to hyperplasia of parathyroid gland

cause of tertiary hyperparathyroidism

hyperplastic glands eventually develop independent function and do not respond to calcium correction

key features of hyperparathyroidism

polyuria, renal calculi
HA, confusion, drowsy, depressed DTR
generalized bone pain, pathological fx
flank pain, muscle weakness, fatigue
constipation, N/V
HTN, heart block, shortened QT interval and ST, cardiac arrest
(All of these can be cause by excessive PTH or hypercalcemia)

interventions for hyperparathyroidism

fall risk, strain urine to detect stones
2-3L/day, high fiber diet
diuretics and NS IV to increase calcium excretion
analgesics
phosphates (PO or IV) only when rapidly lowering of calcium in necessary
mithramycin= chelating agent, cytotoxic agent that rapidly lower serum calcium within 48 hours but causes thrombocytopenia, hepato/renal toxicity
assess renal status q2-4 hrs
continuous cardiac monitoring
labs: CBC, BUN, Crt, Ca, LFTs

tx of hyperparathyroidism

partial or total parathyroidectomy
if gland on one side is enlarged, a frozen section is done on both
if adenoma is present in one side only, adenoma is removed and other side left intact
if hyperplasia present, 3 glans and 1/2 of 4th is removed and 1/2 left as marker

post parathyroidectomy care

assess bleeding
monitor resp, keep emergency trach
monitor serum calcium q4hr
monitor for hypocalcemia
assess for voice quality and hoarseness

hypoparathyroidism

usually directly r/t lack of PTH secretion or dec effectiveness of PTH on target tissue causing hypocalcemia
Types:
iatrogenic (most common form)
idiopathic (spontaneously in children/adults)
pseudohypoparathryoidism (rare hereditary)

iatrogenic hypoparathyroidism

d/t total parathyriodectomy

Idiopathic hypoparathyroidism

associated with adrenal insufficiency, hypothyroidism, DM, pernicious anemia, gonadal failure, certain skin disorders

pseuodhypoparathyroidism cause

unresponsiveness of body to PTH

key features of hypoparathyroidism

tingling/numbness around mouth, tetany, laryngospasm with possible respiratory arrest, hyperactive DTR, muscle cramps/spasms (Chvostek and trousseau), hyperactive bowel sounds, diarrhea, dry brittle nails and hair, irritability, anxiety, hallucination, seizures, hypotension, dec myocardial contractility, prolonged QT and ST, cardiac arrest

interventions for hypoparathyroidism

long term correction: vit d replacement, calcium replacement, magnesium
IV calcium
vit d PO
magnesium IV or PO
foods high in Ca but low in PO4 (yogurt, processed cheese)
monitor same labs as hyper

disorders of posterior pituitary gland

SIADH and DI

SIADH

syndrome of inappropriate antidiuretic hormone
excessive ADH increases permeability or renal distal tubules which leads to resabsorption of water into the plasma, and suppression of RAAS mechanism causing renal excretion of Na resulting in water intoxication, dilutional hyponatremia, and cellular edema

causes of SIADH

primarily malignancies (small cell lung CA)
hypersecretion of ADH by hypothalamus d/t head trauma, CVA, meninigitis, encephalitis, pituitary surgery, brain hemorrhage, medications
guillain-barre
hypothyroidism
pneumonia
TB
adrenal insufficiency

SIADH sx

fl retention (inc BP, crackles, JVD, taut skin, imbalanced I/O)
HA, fatigue, anorexia
muscle cramps, weakness
hypochloremia
concentrated urine w low output
cerebral edema, loc changes
weight gain without edema (high fowlers will not help)

SIADH lab findings

high urine osm, and specific gravity
low serum osm
dec Hct, BUN, Na

Na 116-125

LOC changes, N/V, muscle cramping

Na

seizures, coma, death

SIADH interventions

fl restriction (800-1000ml/day)
monitor urine and serum osm, serum lytes, hct
lithium- blocks affect of ADH
lasix only if Na> 125
hypertonic IV or salt tabs
frequent vitals, heart and lung sounds
monitor LOC
ID hidden sources of water (ice chips, soups)

diabetes insipidus

deficiency in production or secretion of ADH= polyuria up to 4-30L in 24 hr
leads to dec water reabsorption in renal tubules, dec intravascular fl volume, and inc urine output and serum osmolarity

causes of DI

lesions of hypothalamus and pituitary (central)
lithium use and nephrogenic DI (dec response to ADH, also caused by hypokalemia and hypercalcemia)
psychogenic DI= lesions in thirst center leading to excessive water intake

DI sx

polyuria (5-20L/day)
polydipsia
dry tenting skin, muscle fatigue/twitching
agitation, hallucinations, seizures, coma
n/v, dry mucous membranes
fl vol deficit leading to= hypotension, tachycardia, constipation, weight loss, shock d/t hypovolemia

DI interventions

water replacement (oral or IV D5W which is hypotonic)
daily weights
report if specific gravity decreases
hormone replacement for central DI= desmopressin acetate nasal spray
nephrogenic DI= kidneys unable to respond to adh so pt will need thiazide diuretics, low sodium and low protein diet

disorders of adrenal cortex

cushing syndrome
addison's disease

cushing's syndrome

hyperfunciton of adrenal cortex- inc cortisol or ACTH
more common in women, 30-40 yr
causes: prednisone use, ACTH secreting pituitary tumor or adrenal tumors

cushings syndrome sx

HTN, fl overload, weight gain, truncal obesity, moon face, thinning hair, hirsutism, purple striae on abd, emotional lability, edema in lower extremities, skin infections and slow wound healing, muscle wasting and weakness, hyperglycemia, thin skin w easy bruising

cushing's syndrome labs

inc cortisol, Na, Glucose, Ca
dec K

cushing syndrome tx

med to suppress ACTH or cortisol
radiation
surgery( if you remove adrenal glands you may need replacement ACTH or cortisol post op)
prevent infection

post op care for cushing syndrome

CDB, IS use
explain mouth breathing d/t nasal packing
turn q2hr
keep HOB >30 degrees
examine pituitary surgical wound for cerebrospinal fl leak

addison's disease

hypofunction of adrenal cortex or lack of ACTH secretion by pituitary
more common in women under age of 60

causes of addisons disease

autoimmune destruction of adrenal tissue in industrialized countries
TB
AIDs or its tx
anticoagulant therapy
sudden stoppage of long term high doses steroids

addisons disease sx

only occur once 90% of adrenal cortex is destroyed
hyperpigmentation of skin is exposed to sun and jts (eternal tan)
hyponatremia, hyperkalemia
n/v, irritability, depression
delayed wound healing
hypovolemia, weight loss
muscle weakness
tachycardia, dysryhthmias, orthostatic hypotension

addisons crisis

occurs when steroids are abruptly stopped or exposure to stress
hypotension leading to shock
tachycardia, dehydration

labs in addisons disease

dec serum cortisol, Na, Glucose
inc K, BUN, ACTH

addisons disease tx

steroid replacement therapy
tx underlying cause
assess LOC frequently
asses orthos
watch for low BG
encourage 3L of fl
may need added sodium in diet
protect from infection

B-Cells in the Islets of Langerhans

produce insulin at a basal rate with boluses released when food is ingested

stable BG

70-120 mg/dL
normal adult secretes 40-50 units of insulin /day

hormones that counteract effects of insulin

glucagon, epinephrine, GH, cortisol

insulin is used by

2/3 of bodys cells (except brain, liver, and blood cells)
used to absorb glucose from the blood for use as fuel, or conversion to other molecules or for storage

principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle

insulin

diabetes

heterogeneous group of diseased involving the disruption of the metabolism of carbs, fats and proteins. if uncontrolled, serious vascular and neuro changes may occur

long term complications of diabetes

blindness (diabetic retinopathy)
ESRD
nontraumatic lower limb amputation
heart disease higher risk
risk of stroke 2-4x higher
73% also have HTN
diabetic emergencies
peripheral neuropathy
acid-base imbalances
fluid and electrolye imbalances (Glucose pulls water)

Type 1 DM

insulin dependent DM (IDDM)/ juvenile onset
requires insulin to prevent ketosis, unstable
caused by insulin deficiency d/t destruction of pancreatic beta cells by T cells
autoantibodies present for months to years before onset of sx
once a majority of b cells are destroyed, the sx are abrupt
usually present in ER with pending or actual ketoacidosis
present with weight loss, 3Ps

type 2 DM

non-insulin dependent (NIDDM), adult onset
may be controlled with diet, oral hypoglycemics, or insulin
caused by insuline resistance or reduced sensitivity combined with reduced insulin secretion due to secondary factors such as chronic hyperglycemia, B cell fatigue, or inappropriate release of glucose by liver
same sx of type 1 but occur more gradually, subtle sx of fatigue, recurrent infections, prolonged wound healing, visual changes

gestational DM (GDM)

caused by glucose intolerance
may require tx and then return to pre preg state
combo of inadequate insulin secretions and responsiveness
20-50% get type II later
can damage health of fetus or mother: macrosomia, congenital cardiac and CNS anomalies, skeletal muscle malformations, inhibits fetal surfactant production, hyperbilirubinemia from RBC destruction

3 P's of diabetes

polyuria, polydipsia, polyphagia

risk factors for diabetes type 2

BG >100 but

type II DM labs

FBG >126 mg/dl
random measurement of >200 mg/dl plus 3 Ps accompanied by unexplained weight loss
glucose tolerance test with >200 mg/dl
hgb a1c= bodys ability to control BG in last 3 mo

fluid imbalance in DM

glucose concentration in blood is raised beyond renal threshold, reabsorption of glucose in proximal renal tubule is incomplete and part of glucose remains in the urine (glycosuria)
this increases osmotic pressure of urine and inhibits reabsorption of water in kidney-> polyuria and fl loss
lost blood volume will be replaces osmotically from water held in body cells, causing dehydration and inc thirst
K is pulled out of cells and into bloodstream so pt may have inc K**

assessment of acute hyperglycemia

blurred vision
pruritus
paresthesias, lethargy, weakness, irritability
3 Ps
nonhealing wounds
inc RR, kussmauls respirations