Endocrine Flashcards
paracrine function
hormone acts adjacent to site of origin
endocrine function
hormone enters blood & acts at distant site
autocrine function
hormone acts at site of origin
Hormones released by hypothalamus
- luteinizing hormone-releasing hormone
- corticotropin-releasing hormone
- thyrotropin-releasing hormone
- prolactin-releasing factor
- prolactin-inhibiting factor
- growth hormone-releasing factor
- growth hormone-inhibiting factor
Where is the pituitary gland located?
- sella turcica
- connected to hypothalamus by pituitary stalk
adenohypophysis
anterior pituitary gland
posterior pituitary gland
neurhypophysis
hormones released by anterior pituitary gland
F- Follicle-stimulating hormone
L- Luteinizing-hormone
A- Adrenocorticotropic hormone
T- Thyroid stimulating hormone
P(i)- Prolacting
G- Growth hormone
FSH
- stimulates germ cell maturation & ovarian follicle growth
- HYPERSECRETION = early puberty
- HYPOSECRETION = infertility
LH
- stimulates testosterone production, ovulation
- HYPERSECRETION = early puberty
- HYPOSECRETION = infertility
ACTH
- stimulates adrenal hormone release
- HYPERSECRETION = cushing’s disease
- HYPOSECRETION = secondary adrenal insufficiency
TSH
- stimulates thyroid hormone release
- HYPERSECRETION = hyperthyroidism
- HYPOSECRETION = hypothyroidism, cretinism
Prolactin
- stimulates lactation
- HYPERSECRETION = infertility
- HYPOSECRETION = menstrual dysfunction
GH
- stimulates cell growth
- HYPERSECRETION = acromegaly, giantism
- HYPOSECRETION = dwarfism
Where is ADH synthesized?
supraoptic nuclei of the hypothalamus
Where is oxytocin synthesized?
paraventricular nuclei of hypothalamus
Posterior pituitary gland releases:
- ADH
- oxytocin
ADH
- stimulates water retention
- HYPOSECRETION = SIADH
- HYPERSECRETION = DI
Oxytocin
- stimulates uterine contraction & breast feeding
- HYPERSECRETION = 0
- HYPOSECRETION = uterine atony
SIADH
- TOO MUCH ADH
- Associated w/ *TBI, small cell lung CA, carbamazepine
- HYPOnatremia (< 135)
- plasma osmo = hypotonic = < 275
- low UOP
- high urine omso & Na+
- Tx:
1. fluid restriction
2. demeclocylcidine
3. hypertonic NaCl if Na+ < 120
DI
- TOO LITTLE ADH
- Associated w/ *pituitary surgery, TBI, SAH
- polyuria
- plasma omso = hypertonic = > 290
- hypernatremia ( > 145)
- high UOP, low urine osmo
- Tx:
1. DDAVP/vasopressin
Acromegaly
- secretion of GH after adolescence
- associated w/ pituitary adenoma
- difficult mask (distorted facial features)
- difficult laryngoscopy (large tongue, teeth, epiglottis)
- difficult ETT placement - use smaller tube (subglottic narrowing
- epistaxis - avoid nasal intubation (turbinates enlarged)
- OSA
- HTN, CAD, rhythm disturbances
- glucose intolerance
- skeletal muscle weakness
thyroid anatomy
- left & right lobe joined by thyroid isthmus
- RLN runs lateral of each lobe
T4
- inactive form
- released directly from thyroid
- high concentration in blood
- highly protein bound
- low potency
- 1/2 life = 7 days
T3
- active form
- high concentration in target cell
- low protein binding
- high potency
- 1/2 life = 1 day
Production & release of TH
Anterior pituitary releases TSH
1. stimulates thyroid to produce T3, T4 (+iodine)
2. stimulates follicular tissue to produce thyroglobulin colloid
3. stimulates iodide pump
Hyperthyroidism
- increased TH + BMR + O2 consumption + CO2 production
- Etiologies: **Grave’s, MG, goiter, carcinoma, pregnancy, pituitary adenoma
- Dx: ** Low TSH, High T3, T4
- HTN, tachyarrhythmias, afib, increased Ve, goiter, weight loss, muscle weakness, warm, fine hair, heat intolerance, diarrhea, tremor, exophthalmos, hypercalcemia
Hyperthyroidism anesthesia considerations
- Do NOT proceed to elective surgery until pt
euthyroid - Goiter = awake intubation
- Avoid sympathomimetic, anticholinergics,
- ketamine, pancuronium
- risk of corneal abrasion
- increased incidence of MG - careful w/ NMBs
- careful positioning
- MAC unchanged
Medical MGMT hyperthyroidism
- Block synthesis
- PTU, carbimazole, methimazole K+ iodide - Block release
- radioactive iodine, K+ iodide - Block T4-T3 coversion
- PTU, propanolol - Block beta receptors (SNS)
- propanolol, esmolol
Hypothyroism
- Etiology: **Hashimoto, iodine deficiency, HPA dysfx, neck radiation, thyroidectomy, amiodarone
- Dx: **High TSH, Low T3,T4
- decreased HR, decreased contracility, HF, pericardial effusion, decreased Ve, pleural effusion, goiter, weight gain, fatigue, dry thick skin, brittle hair, cold intolerance, constipation, delayed gastric emptying
Hypothyroidism anesthesia considerations
- levothyroxine
- cancel surgery for severe hypothyroidism
- airway obstruction (tongue, swollen VC, goiter)
- increased risk aspiration (delayed emptying)
- increased risk hypotension (hypodynamic circ)
- inhalation induction faster
- corticosteroids
- increased sensitivity to NDNMBs
- MAC unchanged
thyroid storm
- increased TH in r/t stressful events
- can occur w/ hyper/euthyroid pt
- 6-18 hours postop
- S/S
1. fever, tachycardia, HTN, CHF, shock, AMS, n/v - Tx: 4 B’s
1. Block synthesis (methimazole, carbimazole, PTU,
K+ iodide)
2. Block release (radioactive iodine, K+ iodide)
3. Block T4 to T3 conversion (PTU, propanolol,
glucocorticoids)
4. Block beta receptors (propanolol, esmolol)
Cooling
glucocorticoids
myxedema coma
complication of severe hypothyroidism
cretinism
Complication of neonatal hypothyroidism
subtotal/total thyroidectomy
- treatment for hyperthyroidism
- complications
1. hypothyroidism
2. hemorrhage
3. RLN injury (NIM tube)
4. hypocalcemia (PTH removal) - tetany, laryngospasm, AMS, hypotension, prolonged QTi, paresthesia, chvostek, trousseau
osteoblasts
- promote bone deposition
- add Ca+ to bone
osteoclast
- promote bone resorption
- remove Ca+ from bone
PTH site of production
parathyroid gland
PTH site of release
parathyroid gland
What stimulates release of PTH?
- decreased ionized Ca+
- increases phosphate
PTH release effects
- increases ionized ca+
- increases bone resorption
- increase ca+ absorption in intestine & kidney
- decreases phosphate
- decreased phosphate reabsorption in kidney
Calcitonin site of production
C cells (parafollicular cells) in thyroid gland
Calcitonin site of release
thyroid
What stimulates release of calcitonin?
increased ionized ca+
Calcitonin release effects
- decreased ionized ca+
- increased ca+ bone deposiiton
- increased phosphate
Primary hyperPTH
- most common cause of hyperca+
- cause = PTH adenoma
- high PTH level, hyperca+, hypophos
- Tx: parathyroidectomy
- S/S:
1. HTN, short QTi, confusion/lethargy/psychosis, bone pain, osteopenia, pathologic fx, anorexia, n/v, PUD, abd pain, pancreatitis, polyuria, polydipsia, kidney stones
Secondary hyperPTH
- most common cause = CKD
- renal osteodystrophy = bone disease caused by increased PTH 2nd to CKD
HypoPTH
- cause = iatrogenic removal during thyroidectomy
- S/S
1. hypotension, myocardial depression, long QTi, tentany, paresthesias, SZ, muscle spasms, abd cramping
Adrenal cortex synthesizes/releases
G - Salt
F - Sugar
R - Sex
- zona Glomerulosa = (Salt) mineralcorticoids (aldosterone)
- zona Fasciculata = (Sugar) glucocorticoids (cortisol)
- zona Reticularis = (Sex) androgens
Adrenal medulla synthesizes/releases
- Epi (80%)
- NE (20%)
Aldosterone release is increased by
- RAAS
- Hyperkalemia
- Hyponatremia
Aldosterone
- Fx: resorption of Na+/H2O, excretion of K+ & H+
- regulates IV volume
Cortisol
- glucocorticoid
- production = 15-30 mg/day, 12 mcg/dL
- Fx:
- gluconeogenesis
- protein catabolism
- fatty acid mobilization
- anti-inflammatory effects
- improves myocardial fx by increasing # & sensitivity of beta receptors in myocardium
Most to least glucocorticoid effect potency
- dexamethasone, betamethasone (25)
- fludrocortisone (10)
- methylprednisolone, triamcinolone (5)
- prednisone, prednidisolone (4)
- cortisol (1)
- cortisone (0.8)
- aldosterone (0)
Conn’s syndrome
- too much mineralocorticoid (aldosterone)
- Causes:
- too much aldosterone release (pheo, hyperthyroid)
- renovascular HTN
- licorice ingestion (glycyrrhizic acid) resembles conn’s
- S/S
- HTN (Na+/H2O retention)
- Hypokalemia (K+ excretion)
- Metabolic alkalosis (H+ excretion)
-Tx: remove tumor, spironolactone (aldosterone antagonist), K+, Na+ restriction
- Anesthesia
- low K+ = sensitive to NMBs, U wave on EKG, avoid hyperventilation
- HTN
Cushing’s syndrome
- too much cortisol
- Causes: pituitary tumor (Cushing’s Dz) too much ACTH, adrenal tumor releases cortisol
- Glucocorticoid effects
- hyperglycemia
- weight gain (central obesity, buffalo hump, moon
face) - increased infection risk
- osteoporosis
- muscle weakness
- Mineralocorticoid effects
- HTN
- hypokalemia
- metabolic alkalosis
- Androgenic effects
- women become masculinized
- men become feminized
- Tx
- transsphenoidal resection pituitary gland
- adrenalectomy
- pituitary radiation
- MGMT
- aseptic technique
- careful positioning
- steroids
- DI following pituitary resection
A patient w/ adrenal insufficiency & sepsis requires an emergency intubation in ICU. Which drug should be avoided?
Etomidate
Propofol
Ketamine
Thiopental
Etomidate. Inhibits 11-beta-hydroxylase & causes adrenocortical suppression for > 8 hours.
Adrenal Insufficiency (Addison’s Disease)
- destruction of all cortical zones
- decreased production of mineralocorticoids, glucocorticoids, & androgens
- muscle weakness, fatigue, hypotension, hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis, n/v, hyperpigmentation
- Tx: steroids (15-30 mg cortisol/day)
Acute adrenal crisis
- medical emergency
- caused by chronic AI faced w/ stress
- HD instability/collapse, fever, hypoglycemia, AMS
- Tx: steroids, D5NS, HD support
alpha cells
glucagon
beta cells
insulin
delta cells
somatostatin
PP cells
pancreatic polypeptide
Things that stimulate insulin release
- PNS & SNS stimulation
- glucagon
- catecholamines
- cortisol
- GH
- beta agonists
Things that reduce insulin release
- insulin
- VA
- beta antagonists
insulin receptor
- 2 alpha & 2 beta subunits joined together by disulfide bonds
- insulin binds to receptor & activates tyrosine kinase which activates insulin receptor substrates
Things that stimulate glucagon release
- hypoglycemia
- stress
- trauma
- sepsis
- beta agonists
Things that reduce glucagon release
- somatostatin
- insulin
What are uses for glucagon other than increasing blood sugar?
- increases myocardial contractility, HR, AV node conduction by increasing intracellular cAMP
- Useful in: BB OD, CHF, low CO after CPB, improving MAP after anaphylaxis, relaxing sphincter of Oddi (ERCP)
- SE: N/V
Diagnostic criteria for diabetes
- fasting glucose > 126
- random glucose > 200 + classic symptoms
- 2 hour glucose > 200 during oral glucose tolerance test
- Hgb A1C > 6.5%
Type 1 DM
- lack of insulin production from beta cell destruction
- causes = **autoimmune, genetic, viral
- presents in childhood
- thin
- low insulin levels, high glucagon but can be suppressed
- Tx: insulin
- Associated w/ DKA
Type 2 DM
- lack of insulin + insulin resistance
- cause = obesity
- presents in adulthood
- android obesity
- insulin level normal to high, glucagon high & resistant to suppression
- Tx: weight loss, diet, oral hypoglycemic, insulin
- Associated w/ hyperglycemia hyperosmolar syndrome
Metabolic syndrome
At least 3 of the following:
- fasting glucose > 100-110
- abdominal obesity (waist > 40 in M, > 35 in F)
- triglyceride > 150
- HDL < 40 M, < 50 F
- BP > 130/85
DKA
- *More common in DM Type 1
- Not enough insulin –> ketoacidosis,
- hyperosmolarity, dehydration
S/S:
Labs:- *CBG > 250 mg/dL
- pH < 7.3
- bicarb < 18
- anion gap > 10
- hyperosmolarity > 300
- ketones > 5
- Metabolic acidosis
- Kussmaul’s respirations
- Fruity-smelling breath
- Tx:
- fluids
- insulin
- K+
Hyperglycemic Hyperosmolar State
- More common w/ DM Type 2
- Caused by insulin resistance or inadequate
production - Labs:
- CBG > 600 mg/dL
- osmolarity > 330 mOsm/L
- mild metabolic acidosis
- pH > 7.3 , no anion gap
- Tx:
- fluids
- insulin
- correct electrolytes
DM Anesthetic MGMT
- painless MI
- tachycardia (reduced vagal tone)
- dysrhythmias
- ortho hypotension
- aspiration risk
- hypothermia
- difficult intubation (stiff joint syndrome-Prayer’s sign)
- neuropathy
- LR may contribute to hyperglycemia
- GA , BB, & DM autonomic neuropathy may mask hypoglycemia
Carcinoid syndrome
- GI tumor
- secretion of vasoactive substances from enterochromaffin cells
- Most common s/s = flushing, diarrhea
- Histamine release
- bronchoconstriction
- vasodilation
- hypotension
- flushing
- kinins & kallikrein
- bronchoconstriction
- vasodilation
- hypotension
- flushing
- serotonin
- bronchoconstriction
- vasoconstriction
- HTN
- SVT
- diarrrhea
Carcinoid crisis
- tachycardia
- hypo/hypertension
- flushing
- abd pain
- diarrhea
Drugs to give carcinoid syndrome
- somatostatin (octreotide)
- antihistamines
- 5HT3 antagonists
- steroids
- phenylephrine, vasopressin
Drugs to avoid carcinoid syndrome
- histamine-releasing drugs = morphine, meperidine, atracurium, thiopental, sux
- catecholamines
- ephedrine, ketamine (stimulate SNS)
