Endocrine Disorders Flashcards
endocrine
ductless
blood stream
exocrine
ducts for transportation
paracrine
secrete hormones for LOCAL effect
pancreas
an example of a gland that is classified as all three types of glands
pituitary
“master gland”
regulates most levels of hormones
anterior –> adenohypophysis
posterior –> neurohypophysis
thyroid and parathyroid
metabolism
adrenal
fight or flight
pancreas
digestion and sugar metabolism
gonads
sexual characteristics and reproduction
thyroid hormones
thyroxine (T4)
triiodothyronine (T3)
thyroid hormone’s principal effects
increase cellular metabolism
facilitate normal growth and development
parathyroid hormone
parathormone (PTH)
parathyroid hormone principal effects
increase blood calcium
pancreas hormone
glucagon
insulin
pancreas hormone principal effects
increase blood glucose
decrease blood glucose
increase carb, fat and protein storage
adrenal cortex hormone
glucocorticoids
mineralocorticoids
adrenal cortex hormones principal effects
regulate glucose metabolism
enhance response to stress
regulate fluid and electrolyte levels
adrenal medulla
epinephrine
norepinephrine
adrenal medulla principal effect
vascular and metabolic effect that facilitate increased physical activity
gonad hormones
testosterone
estrogens
progesterone
gonad hormones principal effects
spermatogenesis –> male sexual characteristics
female reproductive cycle and sexual characteristics
5 general functions of endocrine system
differentiation of fetus
development
reproduction
homeostasis
fight of flight response
where does the endocrine meet the hypothalamus
hypothalamic-pituitary surface
what does inflammation of a gland result in
hypofunction
hyperthyroidism
excessive secretion of thyroid hormone
increased body metabolism
what is the most common cause of hyperthyroidism
Grave’s disease
increased T4 (autoimmune)
what do high levels of T3/T4 cause
TSH to be suppressed d/t negative feedback loop
hyperthyroidism manifestations
enlargement of thyroid
nervousness
heat intolerance
weight loss w/ increased appetite
sweating
diarrhea
tremor
palpitations
exophthalmos (bulging eyes)
intolerance to exercise
treatment hyperthyroidism
antithyroid medications
radioactive iodine
surgery
beta-adrenergic blockers
hypothyroidism
deficiency of thyroid hormone
decreased body metabolism
type 1 and type 2
type 1 hypothyroidism
thyroid is the issue
low T3/T4 and high TSH
type 2 hypothyroidism
pituitary/hypothalamus is the issue
low T3 and T4 and TSH
hypothyroidism manifestations
fatigue
cold sensitivity
fluid retention
forgetfulness
depression
dry skin/hair
edema
hypothyroidism treatment
increased activity and exercise (need to be cognizant of Rhabdo)
synthetic T3/T4
goiter hyperthyroidism
may be d/t lack of iodine, inflammation, or tumors
an increase in TSH thyroglobulin release into glandular tissue
hypertrophy of gland
thyroiditis
inflammation of the thyroid
types of thyroiditis
active suppurative
subacute granulomatous
lymphatic/chronic
acute suppurative thyroiditis
cause by bacteria pus forming
very rare
subacute granulomatous thyroiditis
caused by viral agents
uncommon
lymphotic/chronic thyroiditis
women are more affected (autoimmune basis)
destruction of thyroid (d/t infiltration of lymphocytes and antithyroid antibodies) decreased serum levels of T3/T4 stimulating the pituitary gland to increase TSH
begins w/ hyperthyroidism, after enough destruction, hypothyroidism develops
thyroid cancer
tumors are usually benign but make up 90% of all endocrine tumors
women are affected more than men
types of thyroid cancer
papillary
follicular
medullary
anaplastic
papillary thyroid cancer
most common
develops IN follicular cells
follicular thyroid cancer
slow
develops FROM follicular cells
medullary thyroid cancer
develops in C cells
5% of thyroid cancers
anaplastic thyroid cancer
rare
fast
poorly differentiated
red flag symptoms of thyroid cancer
vocal cord paralysis
ipsilateral cervical lymphadenopathy
fixation of nodule
treatment of thyroid cancer
removal of thyroid, hypothyroidism or possible damage to laryngeal nerve
when do you refer out for thyroid cancer
if you notice an asymptotic nodule or unusual swelling
what does the parathyroid do
secretes PTH to regulate calcium and phosphate metabolism
calcitonin
vitamin D
what does PTH do
Ca and PO4 from bone (demineralization)
absorption of Ca and excretion of PO4 by kidneys
absorption of Ca in GI tract
targets osteoblasts therefore osteoclast activity
calcitonin and PTH
secreted by parafollicular cells
promote bone mineralization
vitamin D and PTH
increases Ca absorption
calcitonin actions
plasma Ca concentration
cellular uptake of Ca
renal excretion of Ca
bone formation
hyperparathyroidism
overactivity of parathyroid
primary hyperparathyroidism
PTH and serum calcium
secondary hyperparathyroidism
d/t malfunction of another organ
ex: renal failure
tertiary hyperparathyroidism
exclusive to dialysis pts who have secondary hyperparathyroidism
manifestations of hyperparathyroidism
bone damage
hypercalcemia
kidney damage
treatment of hyperparathyroidism
surgical removal
fall/fracture prevention
hypoparathyroidism
insufficient secretion of PTH and low serum calcium
high serum phosphate
TETANY
latrogenic
acquired w/ hypothyroidism d/t accidental removal of gland or infarction
hypoparathyroidism manifestations
neuromuscular irritability
weak bones
hypothyroidism treatment
fall/fracture prevention
adrenal cortex outer cortex
mineralocorticoids
glucocorticoids
androgens
zones
zones of outer cortex
zona glomerulosa –> mineralocorticoids (aldosterone)
zona fasciculata –> corticosteroids (cortisol)
zona reticularis –> androgens
adrenal cortex inner cortex
epinephrine and norepinephrine
primary adrenal insufficiency
Addison’s disease
addison’s disease
insufficient cortisol and aldosterone release d/t disorder w/in adrenal gland
metabolic disturbances and fluid/electrolyte imbalances
how do patients appear with addison’s disease
bronzed or tanned d/t increased skin pigmentation
hallmark –> primary adrenal insufficiency
positive response to synthetic ACTH administration
treatment for primary adrenal insufficiency
DO NOT STRESS PATIENT
aquatic therapy contraindicated d/t low BP
secondary adrenal insufficiency
d/t disorder @ pituitary-hypothalamus unit or too rapid withdrawal of corticosteroid drugs
only cortisol deficient, aldosterone is normal
secondary adrenal insufficiency treatment
synthetic ATCH
adrenocortical hyperfunction
excessive glucocorticoids, mineralocorticoids and androgens
example of adrenocortical hyperfunction
cushing’s syndrome
hypercortisolism
cushing’s syndrome
as a result of hyperfunction of adrenal gland
excess of corticosteroid medication or excess ACTH stimulation from pituitary
cushing’s syndrome manifestations
poor would healing
thinning of skin
muscle weakness
osteoporosis
cushingoid apparence
buffalo hump
thin extremities
skin striations
moon face
high BP
Conn’s syndrome
primary aldosteronism d/t adrenal lesion that results in hypersecretion of aldosterone
tetany
aldosterone effects on the body
tubular reabsorption of sodium and water
excretion of potassium and hydrogen ions
hyperlipidemia
adipose tissue = endocrine gland b/c it stores triglycerides
obesity can lead to diabetes, cancer and inflammation
osteoporosis
most common metabolic bone disease
negative calcium balance (parathyroid affects calcium levels)
pharmacology of endocrine disorders
glucocorticoids
mineralocorticoids
mineralocorticoid antagonists
glucocorticoid pharmacology
effects on glucose, protein and lipids metabolism
adverse effects: adrenocortical suppression drug induced Cushing’s , breakdown of supporting tissues
mineralocorticoid pharmacology
aldosterone involved in maintaining fluid and electrolyte balance
adverse effects; HTN
diabetes mellitus
chronic, systemic disorder characterized by hyperglycemia and disruption of the metabolism of carbs, fats and proteins
insulin defects –> 1st issue is in the blood vessels that leads to other symptoms
leading cause of blindness and renal failure in adults
insulin transports glucose into the cell for use as energy and storage as glycogen
islet of Langerhans (diabetes)
a cells
b cells
d cells
f cells
a cells
secretes glucagon
near periphery
b cells
secrete insulin
central
d cells
secrete somatostatin
f cells
secrete pancreatic polypeptide
type 1 diabetes mellitus
deficiency of insulin production and secretion (may be autoimmune)
metabolic problems w/ DM 1
decreased utilization of glucose
increased fat mobilization
impaired protein utilization
metabolic ketoacidosis
DM1 manifestations
polyuria
polydipsia
weight loss w/ polyphagia
blurred vision
loss of beta cell function w/in 5 years
microvascular complications DM1
nephropathy
retinopathy
type II DM
combination of cellular resistance to insulin action and an inadequate compensatory insulin secretory response
more common in black, native, hispanic, mexican and asian Americans
metabolic symptoms of DM II
not as severe as type I
DM type II manifestations
abnormal thirst
urination
visual blurring
neuropathic complications
infections
significant blood lipid abnormalities
when do microvascular complications occur DM II
much later than type I
blood levels of diabetes
fasting glucose plasma is greater than or equal to 126 mg/dL after 8 hours of fasting
glucose tolerance test: after ingesting a sugary drink, pt is tested after an hour, greater or equal to 200 mg/dL
A1C is equal to or greater than 6.15%
complications of diabetes
atherosclerosis –> lipid accumulation in blood vessels
CV, retinopathy, nephropathy, MS problems, sensory, motor, autonomic neuropathy
limited joint mobilization –> collagen (glucose metabolite) get “stuck” and can lead to vascular disease ischemia
when should you screen for diabetes?
CDC –> 25
ADA –> 45
treatment of diabetes
insulin adverse effects –> hypoglycemia (glucagon is not used to treat)
drugs
treatment of neuropathy
drugs used to treat diabetes
Metformin
Incretin mimetics
Sulfonylureas and Benzoic acid derivatives
Biguanides and Thiazolidinediones
Alpha-glucosidase inhibitors
Immunosuppressants
metformin
lowers blood glucose levels, increases insulin sensitivity
Incretin mimetics
increase insulin secretion by mimicking GI hormones
Sulfonylureas and Benzoic acid derivatives
: act on beta cells to secrete insulin
Biguanides and Thiazolidinediones
: inhibits glucose production
Alpha-glucosidase inhibitors
: delays glucose absorption by inhibiting sugar breakdown
immunosuppressants
: type I to fight autoimmune response that destroys beta cells
A Treatments of neuropathy
Aldose reductase inhibitors, anticonvulsants, selective serotonin reuptake inhibitors
