Unit 10 - Endocrine Flashcards
negative feedback loop
The response is negative (opposite) the initiating stimulus, which returns the parameter to a set point to maintain stability (homeostasis).
positive feedback loop
Provides an unstable cycle in which the system responds in a way that increases the magnitude of the response.
This results in the amplification of the original signal instead of stabilization
what 2 major systems maintain homeostasis in the body
nervous system
endocrine system
hormones released by the posterior pituitary
ADH
oxytocin
hormones released by the anterior pituitary
Follicle-stimulating hormone
Luteinizing hormone
Adrenocorticotropic hormone
Thyroid-stimulating hormone
Prolactin
Growth hormone
“FLAT PiG”
i = ignore
function of hypothalamus in the endocrine system
- monitors hormone concentrations in the systemic circulation
- instructs the pituitary to increase or decrease hormone release (usually through negative feedback)
function of FSH
germ cell maturation
ovarian follicle growth (females)
function of Luteinizing hormone
testosterone (males)
ovulation (females)
function of ACTH
adrenal hormone release
function of prolactin
lactation
where are inhibiting and releasing hormones released from
hypothalamus into hypophysial portal vessels
where is ADH primarily formed
in supraoptic nuclei of hypothalamus
where is oxytocin primarily formed
paraventricular nuclei
where does pituitary gland reside
sella turcica
how is the pituitary connected to the hypothalamus
via pituitary stalk
another name for anterior pituitary
adenohypophysis
another name for posterior pituitary gland
neurohypophysis
what results from FSH hyper hypo-secretion
hyper = early puberty
hypo = infertility
what results from LH hyper and hypo-secretion
hypo = early puberty
hyper = infertility
result of ACTH hyper and hypo-secretion
hyper = Cushing’s
hypo = Addison’s disease
result of TSH hyper and hypo-secretion
hyper = hyperthyroidism
hypo = hypothyroidism, Cretinism
result of prolactin hyper and hypo-secretion
hyper = infertility
hypo = menstrual dysfunctoin
result of growth hormone hyper and hypo-secretion
hyper = acromegaly, gigantism
hypo = dwarfism
result of ADH hyper and hypo-secretion
hyper = SIADH
hypo = diabetes insipidus
result of oxytocin hyposecretion
hypo = uterine atony
regulates TRH release
Triiodothyronine (T3)
regulates CRH release
cortisol
regulate LHRH release
testosterone
estrogen
progesterone
regulate GHRH and GHIG release
growth hormone
insulin growth factor-1
5 systemic hormones affected by negative feedback
- TRH
- CRH
- LHRH
- GHRH
- GHIH
2 hormones not affected by negative feedback
oxytoxin
prolactin
hormone that is part of a positive feedback loop
oxytocin
how is oxytocin release stimulated
uterine contraction
how is prolactin release controlled
under neural control, where increased dopamine decreases prolactin release
why can metoclopramide caue hyperprolactinemia
increased dopamine decreases prolactin release
metoclopramide is a dopamine antagonist
conditions assoc. with SIADH
- TBI (most common)
- cancer (small-cell lung carcinoma)
- noncancerous lung disease
- carbamazepine
most common cause of SIADH
TBI
electrolyte abnormality with SIADH
hyponatremia
plasma volume, osmolarity, and sodium in SIADH
- Volume = euvolemic or hypervolemic
- Osmolarity = hypotonic (< 275 mOsm/L)
- Sodium = low (< 135 mEq/L)
urine volume, osmolarity, and sodium in SIADH
- Volume = low
- Osmolarity = higher than plasma
- Sodium = high
treatment of SIADH
- fluid restriction
- demeclocycline
- +/- treat hyponatremia
use of demeclocycline in SAIDH
decreases responsiveness to ADH
when should sodium be corrected in pt with SIADH
if pt is symptomatic or Na+ < 120 mEq/L, give hypertonic NS
Don’t correct hyponatremia > 1 mEq/L/hr
when should sodium be corrected in pt with SIADH
if pt is symptomatic or Na+ < 120 mEq/L, give hypertonic NS
Don’t correct hyponatremia > 1 mEq/L/hr
conditions assoc with DI
- pituitary surgery (most common)
- TBI
- subarachnoid hemorrhage
most common cause of DI
pituitary surgery
presentation of DI
polyuria
plasma volume, osmolariy, and sodium in DI
- Volume = euvolemic or hypovolemic
- Osmolarity = hypertonic (> 290 mOsm/L)
- Sodium = high (> 145 mEq/L)
urine volume, osmolarity, and sodium in DI
- Volume = high
- Osmolarity = lower than plasma
- Sodium = normal
DI treatment
supportive, DDAVP or vasopressin
what is acromegaly
Results from oversecretion of GH after adolescence
cause of nearly all cases of acromegaly
pituitary adenoma
what causes gigantism
increased GH output before puberty
why are pts with acromegaly at risk for difficult mask ventilation and DL
mask: distorted facial features, poor seal
DL: large tongue, teeth, and epiglottis
why should you use a smaller ETT in a pt with acromegaly
subglottic narrowing & vocal cord enlargement
why should nasal intubation be avoided in pts with acromegaly
risk epistaxis d/t turbinate enlargement
common comorbidities with acromegaly
- OSA
- HTN
- CAD
- rhythm disturbances
- glucose intolerance
- skeletal muscle weakness
- entrapment neuropathies
source of T4
Directly released from thyroid
source of T3
Mostly extrathyroid conversion of T4 to T3
Small amount released from thyroid
where is concentration of T4 the highest
In the blood
where is the concentrtion of T3 the highest
In the target cell
T4 converted to T3
where is the concentrtion of T3 the highest
In the target cell
T4 converted to T3
which is more protein bound - T4 or T3
T4
which is more potent - T4 or T3
T4
half-life of T3
1 day
half life of T4
7 days
TSH release from anterior pituitary affects the thyroid gland in 2 key ways:
1) Tells the thyroid gland to produce T3 & T4 (requires iodine)
2) Tells follicular tissue to produce thyroglobulin colloid (does not require iodine)
TSH release from anterior pituitary affects the thyroid gland in 2 key ways:
1) Tells the thyroid gland to produce T3 & T4 (requires iodine)
2) Tells follicular tissue to produce thyroglobulin colloid (does not require iodine)
substrate thyroid requires to synthesize T3 & T4
iodine
TSH in pt with hypoactive thyroid
chronically elevated
there isn’t enough thyroid hormone to suppress TSH
TSH in pt with hypoactive thyroid
chronically elevated
there isn’t enough thyroid hormone to suppress TSH
stimulates follicles to make thyroglobulin colloid
TSH
required for follicles to make thyroglobulin colloid
iodine
what causes goiter in hypoactive thyroid
Since TSH is chronically elevated, follicles continue to produce thyroglobulin colloid - causes thyroid gland to increase in size
3 hormones stored and released by the thyroid gland
- T4 = thyroxine
- T3 = Triiodothyronine
- calcitonin
nerve at risk for injury in thyroid or parathyroid surgery
RLN
how does thyroid hormone affect VO2 & CO2 consumption
both increased
effects of increased thyroid hormone on ANS
- ↑ number & sensitivity of # receptors
- ↓ number of cardiac muscarinic receptors
CV effects of increased thyroid hormone
- Increased myocardial performance independent of the ANS
- ↑ chronotropy, contractility, lusitropy
- ↓ SVR
respiratory effects of increased thyroid hornone
↑ BMR = ↑ CO2 production = ↑ Vm (↑ Vt & RR)
increased thyroid hormone = increased O2 consumption in all tissues except:
CNS
how does thyroid hormone affect MAC
hyper- and hypothyroidism do NOT affect MAC
O2 consumption increased in all tissues except CNS
how does thyroid hormone affect MAC
hyper- and hypothyroidism do NOT affect MAC
O2 consumption increased in all tissues except CNS
GI effects of increased thyroid hormone
intestineal hypermotility, diarrhea
how does increased thyroid hormone affect fat
↑ utilization of fat stores = weight loss
how does increased thyroid hormone affect protein
↑ catabolism = skeletal muscle weakness
effect of thyroid hormone on carbohydrates
↑ gluconeogenesis, ↑ insulin release, ↑ glucose uptake
what causes tremors with increased thyroid hormone
↑ sensitivity of neuronal synapses in the spinal cord
etiologies of hyperthyroidism
- Grave’s (autoimmune - most common)
- myasthenia gravis
- multimodal goiter
- carcinoma
- pregnancy
- pituitary adenoma
- amiodarone (less common)
TSH, T3, & T4 in hyperthyroidism
low TSH + high T3 & T4
CV s/s of hyperthyroidism
HTN
Tachyarrhythmias
Atrial fibrillation
pulmonary s/s hyperthyroidism
Increased minute ventilation
electrolyte imbalance associated with hyperthyroidism
hypercalcemia
medical management of hyperthyroidism
Thionamides
Beta blockers
potassium iodide
radioactive iodine
mechanism of thionamides
Inhibits thyroid synthesis by blocking iodine addition to tyrosine residues on thyroglobulin
meds that inhibit peripheral conversion of T4 to T3
PTU
Propranolol
glucocorticoids
thiopental
how long does it take to achieve a euthyroid state with thionamides
6-7 weeks
available routes of thionamides
Only available PO
serious side effects of thionamides
hepatitis
agranulocytosis
mechanism of potassium iodide in management of hyperthyroidism
Reduces thyroid hormone synthesis and release
when should potassium iodide be given in relation to surgery time
Administer 10 days before surgery
mechanism of radioactive iodine in hyperthyroidism
destroys thyroid tissue
surgical management of hyperthyroidism
subtotal or total thyroidectomy
complications of thyroidectomy
- hypothyroidism
- hemorrhage (tracheal compression)
- RLN injury
- hypocalcemia
etiologies of hypothyroidism
- Hashimoto’s thyroiditis (autoimmune – most common)
- iodine deficiency
- hypothalamic-pituitary dysfunction
- neck radiation
- thyroidectomy
- amiodarone (more common)
TSH, T3, & T4 in hypothyroidism
high TSH + low T3 & T4
CV s/s of hypothyroidism
Peripheral vasoconstriction
Decreased HR & contractility
Decreased CO
Heart failure
Pericardial effusion
pulmonary s/s hypothyroidism
Decreased minute ventilation
Reduced response to hypoxia
Reduced response to hypercarbia
Pleural effusion
GI effects of hypothyroidism
delayed gastric emptying, constipation
medical management of hypothyroidism
synthetic T4 (levothyroxine)
initial response to levothyroxine therapy
natriuresis & decreased TSH
complication of neonatal hypothyroidism that leads to limited physical and mental development
Cretinism
airway complications of hypothyroidism
Airway obstruction due to large tongue, swollen vocal cords, and/or goiter
Goiter = awake intubation
how does hypothyroidism affect circulation
Hypodynamic circulation: ↓ HR, SV, contractility, CO, and baroreceptor responsiveness
best way to support hemodynamics in hypothyroidism
sympathomimetics that improve myocardial performance (not neo)
management of hypotension unresponsive to catecholamines in pts with hypothyroidism
corticosteroids
Decreased adrenal function is common
management of hypotension unresponsive to catecholamines in pts with hypothyroidism
corticosteroids
Decreased adrenal function is common
when is thyroid storm most likely to happen
6-18 hours after surgery
Can occur in hyper- and euthyroid patients
when is thyroid storm most likely to happen
6-18 hours after surgery
Can occur in hyper- and euthyroid patients
s/s thyroid storm
- fever
- tachycardia/tachyarrhythmias
- HTN
- CHF
- shock
- confusion & agitation
- N/V
4 B’s of thyroid storm management
- Block synthesis
- Block release
- Block T4 to T3 conversion
- Block beta receptors
meds that block synthesis of thyroid hormone
- methimazole
- carbimazole
- PTU
- potassium iodide
meds that block release of thyroid hormone
- radioactive iodine
- potassium iodide
beta blockers used in treatment of thyroid storm
esmolol
propranolol
use of glucocorticoids in thyroid storm treatment
blocks conversion of T4 to T3 and supports stress response
hypermetabolism consumes endogenous steroids
why should aspirin be avoided in thyroid storm
can dislodge T4 from plasma proteins and ↑ free fraction of T4
preparing for a hyperthyroid patient needing emergency surgery
- administration of a beta-blocker, potassium iodide, and glucocorticoids
- PTU should be started
how long may medical management of hyperthyroidism take to be euthyroid
6-8 weeks
airway management in a patient with goiter
1 - awake intubation
Next bet - technique that maintains spontaneous ventilation
meds to avoid in hyperthyroidism
- sympathomimetics
- anticholinergics
- ketamine
- pancuronium
why might pts with hyperthyroid be at higher risk for corneal abrasion
exopthalmos
why is positioning important with hyperthyroid pts
increased bone turnover increases risk of osteoporosis
s/s unilateral RLN injury
hoarseness
ipsilateral vocal cord is positioned midline on inspiration
s/s unilateral RLN injury
hoarseness
ipsilateral vocal cord is positioned midline on inspiration
s/s bilateral RLN injury
airway obstruction
both cords are positioned midline on inspiration
s/s bilateral RLN injury
airway obstruction
both cords are positioned midline on inspiration
cause of hypocalcemia after thyroid surgery
resection of parathyroid glands
how is thyroxine synthesized
from tyrosine
why should NMBs be used carefully in hyperthyroid pts
increased incidence of myasthenia gravis and myopathy
things thyroid storm can mimic under GA
- MH
- pheochromocytoma
- neuroleptic malignant syndrome
- light anesthesia
Chvostek’s sign
tapping on anlge of jaw (facial n./masseter muscle) = ipsilateral facial contraction
Trousseau’s sign
upper extremity BP cuff inflated above SBP for 3 min = dec blood flow accentuates neuromuscular irritability = muscle spasm of hand and forearm
2 CV side effects of hypocalcemia
hypotension
prolonged QT
when does hypocalcemia most commonly occur after thyroid surgery
24-48 hrs postop
If it happens to occur sooner, it’s typically no earlier than 6- 12 hours after surgery
common electrolyte abnormality in a pt with myxedema
dilutional hyponatremia
–left off on page 7–
