phys II Flashcards
what can cause thyrotoxicosis
graces factitious thyrotoxicosis toxic adenoma toxic nodular goiter pituitary overproduction of TSH granulomatous thyroiditis subacute lymphocytic thyroiditis
What is factitious thyrotoxicosis
exogenous thyroid hormone with gland atrophy and low thyroglobulin
what is toxic adenoma
hot nodule, over production of thyroid hormone by the nodule with low TSH and gland atrophy surrounding the nodule
what is granulomatous thyroiditis
subacute, viral in etiology, with painful gland
what is subacute lymphocytic thyroiditis
silent thyroiditis, autoimmune in etiology with non-tender gland, transient
postpartum thyroiditis
what helps to differentiate Dx of causes of thyrotoxicosis
radioactive iodine scan
differentiate primary, secondary tertiary hypothyroidism
primary is problem in thyroid gland
secondary problem in pituitary
tertiary is problem in hypothalamus
examples primary hypothyroidism
hashimotos
T cell mediated
example secondary hypothryoisism
pituitary insufficiency
example tertiary hypothyroidism
hypothalamic disease
zones of the adrenal gland and what they secrete
1) zona glomerulosa- aldosterone
2) zone fasciculata- cortisol and zona reticularis- androgens
3) medulla- epinephrine
what regulates the aldosterone release from adrenal gland
Angiotensin II and K
hence why aldosterone leels normal in hypopituitary situation
what controls release of cortisol and androgens in adrenal gland
ACTH
what occurs if enzyme 21- alpha hydroxylase is deficient
excess adrogens, no glucococorticoids or minerlocorticoids
what occurs is absent 17-alpha hydroxylase
increase in mineralocotricoids and absent androgens and low glucocorticoids
what occurs if absent 11 beta hyroxylase
absent glucocorticoids and mineralocorticoids, escess androgens
what occurs if absent 17,20 desmolase
no androgens
stimualtion for cortisol release
decreased blood cortisol sleep wake transition stress, surgery, trauma pschiatric ADH alpha adrengergics, beta adrengergic antagonists serotonin
inhibitory factors for cortisol secretion
increased blood cortisol
opioids
somatostatin
what negatively feedsback on renin release from kidney
decreased Na excretion and H20 excretion and increased K excretion causing increased circulating volume, increase ECvolume, increased BP
what will a decrease in plasma K in kidney cause
and increase in K plasma which will stimuate the adrenal Cx
actions of glucocotricoids
increase gluconeogenesis increase proteolysis increase liplysis decrease glucose utilizaiton decrease insulin sensitivity
actions of mineralocotricoids
increase Na resorption
increase K secretion
increase H secretion
actions of adrenal androgens in females
stimualte growth of pubic and axillary hair, sitmualte libido
actions of adrenal androgens in males
same as testosterone
what is released in times of stress like falling and dislocating hip
cortisol, epinephrine and norepi
decrease in the insulin/glucoagon ration
what occurs in a chronically elevated cortisol level patient
increase cortisol, increase insulin/glucagon ration
dec epi and norepi
promotes obesity and muscle wasting
how does cotisol affect appetite
stimualtes appetite and increases insulin/glucagon ration
the high levels cortisol antagonize insulin’s effect on GLUT4 mediated glucose uptake into skeletal muscle and adipose tissue
have glucose intolerance
clinical features of addisons
hypoglycemia
anorexia, weight loss, nausea, vomiting, weakness, hypotension, hyperkalemia, metabolic acidosis
decreased pubic and axillary hair in females
hyperpigmentation
ACTH levels in addisons
increased (neg feedback effect of decreased cortisol aka less neg feedback)
Tx for addisons
replacement glucocorticoids and mineralocorticoids
clinical features of cushin syndrome
hyperglycemia, muscle wasting, central obesity, round face, supraclavicular fat, buffalo hump, osteoporosis, striae, virilization and menstrual disorders in females, HTN
ACTH levels in cushing syndrome
decreased (neg feedback from increased cortisol
Tx for cushing syndrome
ketoconazole
metyrapone
ACTH levels in cushing disease
increased
Tx cushings disease
surgical removal ACTH secreting tumor
clinical features of Conn syndrome
HTN, hypokalemia, metabolic alkalosis, decreased renin levels
Tx Conn syndrome
aldosterone antagonists (spironolactone) surgery
clinical features 21-beta hydroxylase deficiency
viralization in females, early acceleration linear growth
early appearance pubic hair
deficient in gluco and mineralocorticoids
ACTH levels in 21-B hydroxylase deficiency
increased (neg feedback decreased cortisol)
Tx 21beta hydroxlyase deficiency
replacement of gluco and mineralocorticoids
clinical features 17a hydroxylase deficiency
lack of pubic and axillary hair in females
Sx for deficient glucocorticoids
Sx excess mineralocorticoids
ACTH levels in 17ahydroxylase deficiency
increased from decreased cortisol
Tx for 17 a hydroxlyase deficiency
replacement of glucocorticoids
aldosterone antagonists like spironolactone
what is test to Dx cushing
overnight DST or late night salivary cortisol or 24 h urine free cortisol
if first line of testing + for cushing what is next step
confirm positive test with 1-2 additional studies
what happens to glucose, aa and fat in fed state
insulin increase
there is energy from oxidaiton, synthesis of nitrogens and membranes form aa and fat
storage of glycogen and TAG
what occurs in 12 hour fasting
TAG broken down to FA–> ketones
gluconeogenesis and glycogenolysis–> glucose
GLUT4 R are where
skeletal m and adipose tissue
where are GLUT2 R
liver
where are GLUT3 R
brain
majority of endocrin pancreatic hormones are what
insulin then glucagon only 5% is somatostatin
action of insulin
increase glucose uptake increase glycogen fomation decrease glycogenolysis and gluconeogensis increase protein syntehsis increase fat deposition decrease lipolysis increas eK uptake
effect of insulin on blood level
decrease blood glucose, decrease blood aa, FA and ketoacid and blood K
stimulatory factors for insulin release
glucose [ [ increase increase aa, FA and ketoacid glucagon, cortisol GIP K vagal stimulation, Ach sulfonylurea drugs obesity
inhibitory factors for insulin secretion
decreased blood glucose, fasting, exercise, somatostatin, a-adrenergic agonists, diazoxide
effects of insulin on fat
increase glucose uptake, increase lipgenesis, decrease liplysis
effects of insulin on skel mm
increase glucose uptake, glycogen synthesis, protein synthesis
effects of insulin on liver
dec gluconeogenesis, inc glycogen synthesis, lipogenesis
actions of glucagon
increase glycogenolysis
increase gluconeogeneis
increase lipolysis
increase ketoacid formation
effects of glucagon on blood levels
increase glucose, FA and ketoacid in blood
stimulatory factors for glucagon release
fasting, decreased glucose [ ]
increased aa [ ]
cholecystokinin CCK
beta adrenergic agonists, Ach
what are the inhibitory factors for glucagon release
insulin, somatostatin, increased FA and ketoacid [ ]
what processes are increased with there is a high Insulin:glucagon ration
glycogen synthesis, muscle protein synthesis
lipogenesis and TAG formation
what processes are increased with a low insulin:glucagon ration
glycogen breakdown, gluconeogensis, muscle proteolysis, lipolysis, FA oxidation, ketone body formation
