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Cause/pathophysiology S&Sx Interventions listed in

priority
Hypo- Causes:  muscle weakness,  Steroid
adrenalism   ACTH (secondary) fatigue, lethargy, replacement (IV
 dysfunction of hypotension hydrocortisone)
(Addison’s control/feedback (dehydration)—postural  Vasopressors
disease) (secondary) hypotension, (MAP>60)
 complete/partial gland hypoglycemia,  IV volume and
destruction (primary) hyperpigmentation electrolyte
 symptoms gradually, (bronze skin), salt replacement
accelerate w/ stress craving, A/N/V,
 loss of cortisol abdominal pain/cramps,
( gluconeogenesis, weight loss
hypoglycemia, stress  elevated: K+, BUN,
intolerance) HCT
 loss of aldosterone  Reduced: Na+, glucose,
(hyperkalemia, serum cortisol
hyponatremia, hypovolemia)  ACTH (adrenal
Primary: corticotropin) levels:
 d/t autoimmune disorder, high = primary, low =
TB, cancer, AIDS, adrenal secondary
hemorrhage, sepsis  ACTH stimulation test
 bilateral adrenalectomy, (baseline plasma levels,
abdominal radiation, toxic IV dose cosyntropin,
drugs check for rise
Secondary EXACTLY 30&60
 d/t failure of mins-no rise, suspect
hypothalamus/pituitary insufficiency)
feedback, tumors, long-term  Changes in distribution
steroid RX of body hair
 GI disturbances
 Vascular collapse
 Renal shut down
Hyper-  Prolonged, excessive  Weight gain, fat to trunk  Surgical:
adrenalism cortisol secretion/use w/ small arms/legs pituitary/adrenal
 Pituitary tumor (disease),  Moon face, buffalo tumor removal
(Cushing’s pituitary fails to sense hump (fat deposit on watch for postop
disease) cortisol levelsconstant back), edema shock (reduce
secretion of ACTH  Muscle weakness, steroids)
 Adrenal tumor secrete osteoporosis, fractures  Drugs to inhibit
ACTH (syndrome)  Mood swings, capillary production of
 Protein catabolim (BUN , fragility/easy bruising adrenocorticoids
skinny extremities)  Thin, transparent skin,  Radiation to
 Hyperglycemia (steroid multiple ecchymoses pituitary gland to
insulin resisance &  (purple striae, bruises &  ACTH
gluconeogenesis & glycogen petechiae—small  Diet: low cal?
storage liver) red/purple spot—broken CHO
 Rise lipids (fat distribution cap. vessle) (hypoglycemia) 
in trunk)  Female: K+ (loss)
 Excessive aldosterone (Na+,  hirsutism (excessive  DX: 24hr urine
H20 retention, K+ loss) hairiness, amenorrhea (free cortisolO,
 Loss of bone density (absence or suppression dexamethasone
(osteoporosis, renal stones) of normal menstrual suppression test
 Inhibited inflammatory flow) (dose suppresses
response ( lymphocyte  Male: gynecomastia plasma cortisol by
function =  wound healing) (excessive development 50%)
of breast)
 Personality changes
 CNS irritability
 Hyperglycemia
  susceptibility to
infection
 GI distress-- acid
 Na & fluid retention
 Ateriosclerotic changes
in heart, brain, kidney
 Renal stones, thirst,
polyuria, impotence
 DX: 24hr urine (free
cortisolO,
dexamethasone
suppression test (dose
suppresses plasma
cortisol by 50%)
Hypo-  Inadequate thyroid hormone   T3, T4
(if TSH : primary
thyroidism levels (99%)
 Gland enlarges over time
(myxedema (non-toxic goiter)
hypothyroidism—gland itself;
coma) Hypometabolism: if TSH : pituitary problem
  HCL acid & motility, HR, not secreting enough)
heat  systems depressed: 
 abnormal lipid metabolism BP/HR/UO.
(hi chol & triglycerides) Sluggishness, extreme
 deficiencies of B12 & folate, fatigue,  sleep periods,
anemia weakness, anorexia,
 accumulation of interstitial constipation, weight
fluids (pleual, cardiac, gain, cold intolerance, 
abdominal effusions) libido
Causes:  apathy, lethargy
 thyroid surgery  muscle aches &
 radioactive iodine Rx weakness
 chronic thyroiditis  menstrual disturbances
 cancer  coarse facial features,
 idiopathic atrophy periorbital edema, dry
 cretinism skin, thinning hair (loss),
 inadequate TSH from brittle hair & nails,
pituitary blank/staring expression,
slowed memory, thick
tounge—slow speech
 Rx: life long thyroid
replacement
Late:
 subnormal temp
 bradycardia
 wight gain
 LOC
 thickened skin
 cardiac complication

Myxedema Coma
 Rare but serious
hypothyroidism
 Precipitatedby acute
illnesss, Hashimoto’s
thyroiditis, rapid
withdrawal of thyroid
meds, anesthesia,
surgery, hypothermia
 Absence of hormone:
bradycardia,
hypotension,
hypventilationm AMS,
coma, hyporeflexia,
hyponatremia,
hypoglycemia
 Rx: IV thyroxine,
steroids, passive
rewarming, volume &
lytes replacement,
ventilator for respiratory
failure
Hyper- Excessive secretion:  Systems accelerated:  Block/interfer w/
thyroidism  Hypermetabolism, tachycardia (AFIB), excessive
stimulation S.N.S agitation, nervousness, secretion
(thyroid storm) Causes: muscle tremors,   Est normal thyroid
 Grave’s disease, toxic diarrhea, fever, levels
goiter, cancer, TSH- excessive sweating,  Treat/manage Sx
secreting tumors, pituitary, enlarged thyroid gland, (tachycardia,
radiation-induced exophthalmos, heat HTN)
inflammation, iodine intolerance, weight loss  Surgery: goiter,
administration despite  appitite, subtotal/total
hypotension (hi-output thyroidectomy
heart failure)  Observe: airway
 Finger clubbing obstruction &
 Menstrual changes tetany d/t
(amenorrhea) injury/accidental
 Fine-straight hair removal
 Bulging eyes parathyroid glands
 Facial flushing  Hi-cal diet, avoid
  systolic BP stimulants,
 breast enlargement cool/quite room,
 localized edema protect stress,
 thyrotoxicosis: life monitor for
threatening cardiac, thyroid storm
renal, hepatic failure Anti-thyroid drugs:
 Dx: thyroid scans, USN,  Thionamides
ECG (tachycardia/afib) block synthesis
(propythiouracil-
PTU/Methrimazol
e)
 Potassium iodide
inhibits synthesis
& release (SSKI
or Lugol’s)
 Lithium inhibits
release
 Steroids inhibit
conversion of T4
to T3 & replace
cortisol
 Beta blockers
(diaphoresis,
anxiety, tachy,
palpations)
 Oral I 131 picked
up by thyroid
cells, some
destroyed over 6-8
weeks).
Dx: thyroid scans, USN,
ECG (tachycardia/afib)
Hypo-  Lack of PTH or ineffective  Low Ca+  Correct low Ca+
parathyroidis on target organs  Paresthersia (perioral & Mg+
 Removal of thyroid gland tingling & numbness in  Vitamin D
m  Low Mg+ (ETOH, hands & feet) deficiencies
malabsorption, ESRD)  Tetany (muscle cramps,
carpopedal spasm,
seizures)
 Irritability, psychosis
Hyper-  Hyperplasia of glands  excessive PTH  Surgical removal
parathyroidis  cancer   (high) Ca+/ (low) of some tissue (4
PO4+renal stones glands)
m  GI: A/N/V, constipation,  Hyradtion and
weight loss lasix (renal
excretion Ca+)
 Oral phosphates
 Calcitonin,
Mithramycin
Hypo-  Deficiency anterior pituitary  Based on deficient  Replacement
pituitarism hormones hormone hormone therapy
 Most life-threatening are  Support for client
ATCH & TSH to adapt to
Causes alterations in body
Primary: image an
 Tumors, radiation, infertility
metastasis, trauma, surgical
hypophysectomy
Secondary:
 Infections, trauma, brain
tumors, congenital defects
Hyper-  Excessive stimulation,  Based on excessive Dx: Hormone assays and
tumors, hyperplasia, NOT hormone suppression tests, imaging for
pituitarism
associated w/absence of  Physical S&Sx tumors, physical symptoms
regulatory feedback
Causes Rx: drug therapy to 
 Pituitary adenoma (benign, circulating hormones,
epithelial tumor) surgical resection of tumor
compresses tissue (visual (trans-sphenoid
defects, headaches, elevated hypophysectomy)
ICP)
Syndrome of  Vasopressin (ADH) secreted  Water  DX: water
inappropriate even in presence of low retensiondilutional retention low
plasma osmolarity hyponatremia,  GFR, serum Na+, low
anti-diuretic Causes: inhibition rennin & serum osmolarity
hormone  Altered feedack pathways aldestrone w/urine
(SIADH)  CA of lung, pancreas,  A/N/V, acute, rapid hyperosmolar
duodenum, GU weight gain  ADH plasma
 Thymomas, Ewing’s  NO EDEMA (free water assays (IvI
sarcoma, lymphoma not Na+ retained) inappropriate to
 CNS: trauma, infections,  Dilutional hyponatermia osmo)
CVA, tumors, SLE (<115 mEq/L) Management:
 Drugs: chlorpropamide,  Headache, hostility,  Restrict fluids
chemo, anesthetics, opioids, uncooperative, (500-700mL/day)
tricyclic antidepressants disoriented  Monitor I&O,
 ALOC (lethargy, daily weights
 Eptopic production ADH seizures, coma)  Diuretivs to
malignant tumors   deep tendon reflexes promote excretion
 CNS disorders (infections, of H20,  heart
trauma, hemmorage)   U.O. failure &
 Drugs: chlorproramide,   weight, BP, CVP, pulmonary
vincristinem thiazide PCWP d/t water vascular
diuretics, isoproferonal, retention congestion
morphine  A/N/V  Drugs to block
 MISC: + pressure  CNS changes d/t ADH action
ventilation, pulmonary hyponatremia (lithium,
infections Lab Tests: demeclocyclin)
 Hyponatremia w/ renal  Replace lost Na+
sodium wasting (careful use of
  urinary osmolarity & hypertonic saline)
specific gravity
  serum osmolarity  Fluid restiction to
correct
hyponatremia
 Hypertonic saline
(3%) for sever
hyponatremia
 Demeclocyclin to
block action ADH
in kidney’s
 If drug induced,
D/C drug
Complications:
 Water intoxication
Diabetes  Disorder of water metaolism  Dehydration (skin  SQ/IV doses of
Insipidus (DI) (ADH deficiency) results in turgor, dry mucous aqueous
excretion og huge volume of membranes) vasopressin
dilute  Hemoconcentration,  DDAVP nasal
urinedehydrationhemoc tachycardia, hypotension sprays
oncentration, hyperosmolar  U/O 4-8 L/day,  urine  Monitor effects of
serum, stimulation of thirst specific gravity (<1.005) EVC depletion
Causes:   urine osmolarity (50-  Supplement P.O.
 Nephrogenic (genetic lack 200 mOsm/kg/H20 w/ to match I&O
response to ADH, sickle serum Na+ and  Fluid replacement
cell, obstructive renal osmolarity) (D5W restore H20
(disease)  polyuria not related to loss)
PRIMARY: intake  Hormonal
 Posterior pituitary  loss of diurnal patterns replacement
insufficiency urination (aqueous
SECONDARY:  urine pale vasopressin ot
 Tumor (in sella turcica) or  thirst desmopressin
local ishemia, head trauma,  weight losss, fatigue acetate =
severe infections, TB,  hypovolrmis if fluid DDAVP)
meningitis, metastasis, CVA intake impaired  For nephrogenic
w/ ICP   BP, tachycardia, poor DI: remove
 Drug induced (lithium, skin turgor, orthostatic causative agent,
demeclocycline) changes thiazide diuretic;
 CNS changes from fluid restriction
hypernatremia Complications:
LAB TESTS:  Hypertonic
 Hypernatremia encephalopathy
  urine osmolarity and  Bladder distention
specific gravity  Hydronephrosis

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