Endocrine 1 Flashcards
types of glands
pituitary thyroid parathyroid adrenal pancreas ovaries testes
hormones
chemical substances
affect only target cells with receptors
initiate specific “f” or activites
hormone regulation mechs
negative feedback
positive feedback
nervous system
rhythms
negative feedback
high levels of a substance inhibit hormone synthesis/secretion
low levels stimulate
positive feedback
high levels stimulate synthesis and secretion
low level inhibit
nervous system (hormone reg)
causes release of hormones
ie epineph
rhythms (hormone reg)
hormones fluctuate, circadian rhythms
post pit “f”
ADH
oxytocin
ADH
antidiuretic hormone
regs fluid vol, causes H20 retention, dec UO, vasoconstriction (dec BP)
oxytocin
stim. contraction of uterus, lactating milk
SIADH
high levels ADH
etiology of SIADH
tumors, transient after surgery, meds, infections, pulm disease, most often hypoxia
patho of SIADH
ADH released causes H20 retention
Excess fluid volume + dilutional hyponatremia
Renin suppressed causs dec aldo and dec Na reabsorption
net effect of SIADH
hyponatremia, hypoosmolality, H20 retention
CM of SIADH
FEWMACHS Fatigue/lethargy Edema Wt gain Muscle weakness Abdominal cramps Confusion/coma/Change in MS H/A Seizures
DT of SIADH
serum osmolarity dec
urine osmolarity inc
serum Na dec
urine output dec
Treatment for SIADH
H20 restrictions
hypertonic saline solution
if chronic, meds to inhibit ADH
Diabetes Insipidus
Low ADH or dec action
types of diabetes insipidus
neurogenic
nephrogenic
psychogenic
patho of diabetes insipidus
neuro- dec ADH leads to excretion of lrg amounts of dilute urine
nephro- ADH OK but collecting ducts arent responding
CM for diabetes insipidus
PNIFF Polyuria nocturia inc thirst fatigue fluid volume deficit
DT for diabetes insipidus
serum osmolarity inc
urine osmolarity dec
water deprivation study
treatment for diabetes insipidus
fluid
synthetic ADH
meds to enhance ADH
ant pit “f”
GH TSH ACTH PR FSH, LH
Hypopituitarism
absence of 1 hormone to complete failure of all
patho of hypopituitarism
infarctions lead to tissue necrosis and edema
tumors lead to destruction of gland
etiology of hypopituitarism
infarction
tumors
infections
trauma
CM for hypopituitarism-general
WSHDV Weakness/fatigue Sexual dysfunction H/A Dec tolerance to stress Visual changes
CM for hypopituitarism- panhypo
CTDGD Cortisol deficiency Thyroid deficiency Diabetes insipidus Gonadal failure Dec GH
DT for hypopituitarism
radioimmunoassay- ID which hormones affected
Treatment for hypopituitarism
hormone replacement
Excess growth hormone
inc GH
GH promotes
bone/cartilage growth
elev. of BG
protein synthesis
mobilizes glucose and fatty acids
patho of EGH
excess causes soft tissue and bony overgrowth
gigantism
before epiphyses closure
grow proportionately
acromegaly
after epiphyses closure
bones grow wider/thicker/longer
metabolic effects of EGH
hyperglycemia
CM for EGH
EBECO Enlargement of bones Back/joint pain Enlargement of soft tissue Cardiac probs Overactive sebaceous/sweat glands
DT for EGH
GH inc
oral glucose tolerance test- drink sol and GH inc
MRI
Treatment for EGH
radiation
meds to dec GH
Thyroid gland
stores iodine which is needed for thyroid hormone synthesis
thyroxin
T4, 90%, converted to T3
triidothyronine
T3, active form of thyroid hormone
T3 and T4
together, affect metab rate, caloric requirements, 02 consumption, CHO and fat metab, growth/dev’t of brain “f” and NS activity
calcitonin
produced by C cells, helps regulate Ca levels
Hyperthyroidism
inc TH
thyrotoxicosis
hypermetab from excess hormone
patho of hyperthyroidism
graves and toxic goiter
graves disease
autoimmune disease
stim of thyroid with ABs against TSH receptors.
ABs stim prod of T3 and T4,
excess thyroid hormone bc acting on receptors causes thyroid storm (thyrotoxoc crisis) leads to death
age for graves disease
40-50 y.o
toxic goiter
cells/nodules that secrete hormone,
“f” autonomously, continue to prod excess amts.
age for toxic goiter
60-70 y.o, mostly occur in women
CM for hyperthyroidism
WINSHIIP Wt loss Inc HR, RR, palpitations Nervousness/excitability SOB Heat intolerance Insomnia Inc in GI motility Protrusion of eyeballs- exopthalmus
DT for hyperthyroidism
T3, T4 levels inc
TSH dec
iodine uptake test
treatment for hyperthyroidism
remove thyroid followed by replacement pill
radiation
anti-thyroid meds
hypothyroidism
dec production of TH
patho of hypothyroidism- primary
diminished thyroid tissue causes dec TH prod.
patho of hypothyroidism-secondary
dec TSH due to ant pit
cretinism
infancy, stunt growth and mental retardation
myxedema
adults, accumulation of hydrophilic mucopolysaccharides in dermis- puffiness around hands/feet/face
CM for hypothyroidism
DDDWWFFCIS Dec GI motility Dec HR Dec libido/fertility Wt gain Weakness/ muscle aches Fatigue Fluid retention Cold intolerance Impaired memory Sluggishness
Dt for hypothyroidism
T3/ T4 dec
TSH depends on prob:
primary- high
secondary- low
treatment for hypothyroidism
hormone replacement- synthetic thyroid hormone
PTG
secrete PTH, regulates Ca levels
hyperparathyroidism
excess PTH, Ca levels inc
patho of hyperparathyroidism
primary- tumor
secondary- response to chronically low Ca
tertiary- hyperplasia of gland, loss of sensitivity to Ca
CM of hyperparathyroidism
FINMMK Fractures Insulin resistance N/V, constipation Muscle weakness Metab acidosis Kidney stones
DT for hyperparathyroidism
PTH inc serum Ca inc serum phosphate dec urine pH alkalosis bone density scans
treatment for hyperparathyroidism
surgery
diuretics
meds that dec resorption of Ca from bone
hypoparathyroidism
dec PTH, rare,
seen after surgery, hypomagnesium
patho of hypoparathyroidism
dec PTH causes dec in serum Ca
CM for hypoparathyroidism
HDSHTML Hyperreflexes Dry skin Seizures Hair loss Tetany Muscle spasms Laryngeal spasms
DT for hypoparathyroidism
PTH dec
serum Ca dec
serum phosphate inc
magnesium level
treatment for hypoparathyroidism
Ca supplements
Vit D
