Thyroid problems, pituitary, adrenal Flashcards
thyroid location
inferior to laryngeal prominence and anterior to…trachea?
hormones released by thyroid and their functions
where are they made
T4 or thyroxine. and Triiodothyronine T3 -prod in follicular cells of thyroid -act on nearly every cell in body function: inc basal metabolic rate, essential to proper development and differentiation. Regulate CHO, protein and fat metb. T3 also inc HR and resp rate
what stimulates production of T3 and T4
Thyrotropin releasing hormone fromt he hypothalamus triggers the release of TSH from the anterior pituitary. TSH stim the release of t3 and t4
T3 aka
triiodothyronine
T4 aka
thyroxine
diff between T3 and T4
T4 is at 20x conc to T3. T3 is the active form of T4. T4 gets converted to T3 in the cells
goiter is an____
hypertrophy or hyperplasia
hypo or hyperfx
- enlarged thyroid
- can be hypofx or hyperfx
Could be hypertrophy or hyperplasia
2 types of goiters
endemic goiter and toxic goiter
endemic goiter
-iodine def-> dec T3 and T4-> compensatory inc in TSH-> hyperplasia and hypertrophy
iodine is nec to synthesize T3 and T4. (without idodine you can form T3 and T4 but they arent fx. this occurs most in places w dietary def)
toxic goiter
large nodular gland
d/t hyperactivity
hyperthyroidism is mostly d/t _____
does the outcome make sense\?
autoimmunity
this is counterintuitive as you would expect it to cause hypothyroidism. In this case an Ab binds to thyroid receptor and acts as TSH and inc T3 and T4
Graves disease
uncommon?
affects
3 hallmarks
is the most common form (80-90%) of hyperthyroidism
-autoimmunity affcts young women most
3 hallmarks
1=goiter
2=hyperthyroidism
3=exopthalamus
what is exopthalamus
eyeballs protruding forward dt fat deposits
patho of Grave’s disease
TSAbs mimic the action of TSH
- autoimmunity targets TSH receptors on thyroid cells
- TsAbs (TSI) mimic TSH an bind to TSH receptors-> TH secretion
- inc TH inhibits TSH secretion
- dec TSH
- TSAbs avoid enzyme degradation and are active longer
theres no T cell involvement
involves Thyroid stimulating Abs which mimic the action of TSH (it doesnt involve T cells)
(-the TSAbs replace TSH on thyroid cell which inc T3 and T4 levles which through negative feedback inhibits TSH release.)
(normally when TSH has bound to receptors this complex is broken down by enzymes but not for TSAbs which leads to enlargement of gland d/t TSAbs)
what is thyrotoxicosis
patho/what results
-clinical presentation of (Grave’s disease) hyperthyroidism
- inc metb results (altered metb pathways)
- inc protein and lipid metb (wt loss) when metabolizing heat is a product. 70% of heart is to warm the body the other 30% is for ATP. you now have excess heat
- metb heat->compromized heat loss mechanisms-> flushed skin and perspiration
- intolerance to inc Temp
- inc HR and inc Co to meet inc demand for 02 and waste removal
- a byproduct of all of the metb is C02 in order to remove it they will be hyperventilating
- excitable, irritable, insomnia, anxiety
Tx for Grave’s disease
1 of 3 options
- antithyroid drugs (eg tapazole) which suppresses prod of T3 and T4
-radioiodine therapy (binds to thyroid selectivley and local radiation detroys
Sx for large goiters
hypothyroidism. where can the problem be? which is most common
primary thyroid, (95%)
secondary pituitary,
tertiary hypothalamus
what mainly causes hypothyroidism
mainly radiation and surgery for hyperfunction
dec metabolic rate
problems of hypothyroidism
- dec body T
- dec Co d/t def of energy
- very dec CNS fx
- weak muscle action (d/t dec ATP)
- inc wt
how is food intake in hypothyroidism
food intake will be normal but unable to metb->inc storage
leads to inc wt
what is the most common hyposecretory state for thyroid
Hashimoto’s thyroiditis
Hashimoto’s thyroiditis occurs mostly in
90% in middle aged women
hashimotos thyroiditis
most common hypothyroidism
- 90% occurs in middle age women
- autoimmune destr of gland
- antithyroid Abs block TSH binding
- lymphocyte infiltrates (there is some degree of classic autoimmunity
how does the autoimmune destr of Hashimotos thyroiditis take place
The abs bind to TSH receptors and block the receptor which doesnt allow TSH to bind-> atrophy
Graves disease or hashimotos thyroiditis which involves Tc cells
Hashimotos
Tx of hypothyroidism
if they have an endemic goiter
take T4 daily (lookup why it is??)
where are the adrenal glands
how are they divided
what do they produce
there are two. they lie superior to the kidneys and inferior to the diaphragm. They are retroperitoneal
divided into the adrneal cortex (on the outside) produces:
mineralocorticoids (aldosterone)
glucocorticoids (cortisol)
androgens (male sex hormones) (in the male body this has little effect as the testes produce androgens)
the medulla which produces NE and E (catecholamines)
fx of mineralocorticoids, namely aldosterone
minerocorticoids reguate sodium (mineral)
In kidneys, aldosterone acts on DCT and CD by inc the reabsorption of sodium and the excretion of both potassium and hydrogen ions
fx of glucocorticoids namely cortisol
inc the circulating levels of glucose
suppress the immune sys
potent anti-inflammatory
other effects on metabolism
what area of the adrenal gland is most commonly affected
what is this area under the control of
the cortex
controlled by pituitary (anterior)
Hyperfx (adrenal)
etiology
cortical tumor or hyperplasia-> inc++cortisol, dec adrenocorticotropic hormone
- tumor or hyperplasia of anterior pituitary->inc++ACTH
- ectopic ACTH sec tumour (eg in lung)
are endocrine gland tumors always fx
no they can be either fx or nonfx
Cushing’s syndrome
glucorticoid hypersecretion-> inc++ hormone action
-protein catabolism (weak muscles) and fat deposition in face, neck, abd
gluconeogenesis
prolonged hyperglycemia
- I resistance
- IGT
Na and water retention (HTN and hypokalemia) it shouldnt have
rounded moon face
susceptible to infections
androgen hypersec??
buffalo hump
see table 41.4 for Cushing
e
s
d
why would someone w Cushing’s get fat deposition to face, neck and abdomen
(buffalo hump and the rounded moon face)
cortisol i involved in gluconeogenesis which would cause fat deposition
why would someone w Cushing’s get Na and water retention and what could this lead to
cortisol in normal levels doenst have fx r/t fluid balance but in excess it does have minero fx and can act like aldosterone.
could lead to HTN and hypokalemia
why is a pt w Cushing’s susceptible to infections
cortisol is a steroid->anti inflm-> problem w defenses-> susceptible to infection
Tx of Cushing’s
(this would be to treat tumors or hyperplasia)
- excise tumor
- irradiate pituitary (2nd line approach)
- use drugs for ectopic tumors
- adrenalectomy
conn syndrome hypo or hypersec of which H un/common inc in men or women which gland is affected
aldosterone hypersec
uncommon
high in women
adrenal gland
etiology of Conn syndrome
- usually cortical adenoma
- idiopathic cortical hyperplasia
- renin secreting renal tumor WHY? RAAS stim the prod of aldosterone by AII. also stim ADH. Renin will stim inc aldosterone
mnfts of Conn syndrome. explanation of them
what is the major problem
major problem: HTN (d/t aldosterone inserting sodium channels-> Na retention and water will follow-> hypervolemia->HTN)
-hypokalemia and alkalosis WHY? (aldosterone excretes K and Hydrogen which inc pH)
Tx of Conn syndrome
-adrenalectomy for adenoma (unilateral)
(w hyperplasia you dont excise, you either suppress H or allow H prod and use receptor blocker)
drugs for hyperplasia
aldosterone receptor antagonist
na restriction
when treating an ectopic Cushing’s syndrom tumor what are the 3 categories of drugs/how do they act
- allow production of the hormone
- enzyme inhibitors to suppress synthesis
- receptor blockers
hypofx disorder of adrenals
addison’s disease
Addison’s disease
- primary def of the cortex of adrenal gland.
- all 3 groups of hormones are affected (Making up for the def is diff because it secretes 3 H)
uncommon
etiology of Addison’s disease
TAIG
tumor,
autoimmunity
infection,
high dose glucocorticoid Tx->dec++ACTH
mnfts of Addison’s
fluid losses (Na, Cl)-> hypovolemia-> dec CO-. HoTn-> weakness, fatigue
-dec GAS? gastric acid sec?
wt loss WHY? LOOKUP!
- if not taking meds. 2. if taking meds and facing stress theyll go into Addisonian crisis: acute insuff d/t stress (can be fatal
Tx of acute vs chronic Adiison’s disease
acute:
- give IV fluids
- IV glucocorticoids
Chronic
-glucocorticoids
mineralocorticoids
pituitary disorders how is it broken down
hyper/hypoactivity
which is more affected by disorders anterior or post. pituitary
what are most disorders d/t
anterior
mostly d/t adenomas
hyperactivity of AP
adenomas (trophic and non trophic Hormones). (if its a trophic hormone youll see impact on target gland if its non-trophic problem will be in body on target cells.
hyperactivity of target gland
SIADH pg 743
l
ADH is secreted by
fx
acts on
secreted by PP but made in hypothalamus
fx: increases water permeability of the CD and DCT by inducing translocation of aquaporin-CD water channels in the plasma membrane of collecting duct cells
also sodium reabsorption
hyperactivity of PP
syndrome of inappropriate ADH (SIADH)
- hypersec of ADH
- ectopic tumor secretes ADH-like substance eg in lungs
- ADH prevents water loss, Na follows-> fluid retention
- dilutional hyponatremia
what condition is the opposite of hyperactivity of PP
Addison’s
How does the RAAS respond to the ++water retention and the dilutional hyponatremia of hyperactivity of PP
RAAS is triggered by dec renal perfusion but the pt has hypervolemia so no renin is released. The RAA would cause an inc in aldosterone but since this does not happen sodium is not retained
Tx of hyperactivity of PP
diuretic (coud cause them to lose more sodium)
-restrict fluid intake if mild
to address cause: ADH antagonists (aquaretics block ADH receptor
