1
Q
paracrine function
A
hormone acts adjacent to site of origin
2
Q
endocrine function
A
hormone enters blood & acts at distant site
3
Q
autocrine function
A
hormone acts at site of origin
4
Q
Hormones released by hypothalamus
A
- luteinizing hormone-releasing hormone
- corticotropin-releasing hormone
- thyrotropin-releasing hormone
- prolactin-releasing factor
- prolactin-inhibiting factor
- growth hormone-releasing factor
- growth hormone-inhibiting factor
5
Q
Where is the pituitary gland located?
A
- sella turcica
- connected to hypothalamus by pituitary stalk
6
Q
adenohypophysis
A
anterior pituitary gland
7
Q
posterior pituitary gland
A
neurhypophysis
8
Q
hormones released by anterior pituitary gland
A
F- Follicle-stimulating hormone
L- Luteinizing-hormone
A- Adrenocorticotropic hormone
T- Thyroid stimulating hormone
P(i)- Prolacting
G- Growth hormone
9
Q
FSH
A
- stimulates germ cell maturation & ovarian follicle growth
- HYPERSECRETION = early puberty
- HYPOSECRETION = infertility
10
Q
LH
A
- stimulates testosterone production, ovulation
- HYPERSECRETION = early puberty
- HYPOSECRETION = infertility
11
Q
ACTH
A
- stimulates adrenal hormone release
- HYPERSECRETION = cushing’s disease
- HYPOSECRETION = secondary adrenal insufficiency
12
Q
TSH
A
- stimulates thyroid hormone release
- HYPERSECRETION = hyperthyroidism
- HYPOSECRETION = hypothyroidism, cretinism
13
Q
Prolactin
A
- stimulates lactation
- HYPERSECRETION = infertility
- HYPOSECRETION = menstrual dysfunction
14
Q
GH
A
- stimulates cell growth
- HYPERSECRETION = acromegaly, giantism
- HYPOSECRETION = dwarfism
15
Q
Where is ADH synthesized?
A
supraoptic nuclei of the hypothalamus
16
Q
Where is oxytocin synthesized?
A
paraventricular nuclei of hypothalamus
17
Q
Posterior pituitary gland releases:
A
- ADH
- oxytocin
18
Q
ADH
A
- stimulates water retention
- HYPOSECRETION = SIADH
- HYPERSECRETION = DI
19
Q
Oxytocin
A
- stimulates uterine contraction & breast feeding
- HYPERSECRETION = 0
- HYPOSECRETION = uterine atony
20
Q
SIADH
A
- 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
21
Q
DI
A
- 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
22
Q
Acromegaly
A
- 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
23
Q
thyroid anatomy
A
- left & right lobe joined by thyroid isthmus
- RLN runs lateral of each lobe
24
Q
T4
A
- inactive form
- released directly from thyroid
- high concentration in blood
- highly protein bound
- low potency
- 1/2 life = 7 days
25
T3
- active form
- high concentration in target cell
- low protein binding
- high potency
- 1/2 life = 1 day
26
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
27
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
28
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
29
Medical MGMT hyperthyroidism
1. Block synthesis
- PTU, carbimazole, methimazole K+ iodide
2. Block release
- radioactive iodine, K+ iodide
3. Block T4-T3 coversion
- PTU, propanolol
4. Block beta receptors (SNS)
- propanolol, esmolol
30
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
31
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
32
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
33
myxedema coma
complication of severe hypothyroidism
34
cretinism
Complication of neonatal hypothyroidism
35
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
36
osteoblasts
- promote bone deposition
- add Ca+ to bone
37
osteoclast
- promote bone resorption
- remove Ca+ from bone
38
PTH site of production
parathyroid gland
39
PTH site of release
parathyroid gland
40
What stimulates release of PTH?
- decreased ionized Ca+
- increases phosphate
41
PTH release effects
1. increases ionized ca+
- increases bone resorption
- increase ca+ absorption in intestine & kidney
2. decreases phosphate
- decreased phosphate reabsorption in kidney
42
Calcitonin site of production
C cells (parafollicular cells) in thyroid gland
43
Calcitonin site of release
thyroid
44
What stimulates release of calcitonin?
increased ionized ca+
45
Calcitonin release effects
1. decreased ionized ca+
- increased ca+ bone deposiiton
2. increased phosphate
46
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
47
Secondary hyperPTH
- most common cause = CKD
- renal osteodystrophy = bone disease caused by increased PTH 2nd to CKD
48
HypoPTH
- cause = iatrogenic removal during thyroidectomy
- S/S
1. hypotension, myocardial depression, long QTi, tentany, paresthesias, SZ, muscle spasms, abd cramping
49
Adrenal cortex synthesizes/releases
G - Salt
F - Sugar
R - Sex
- zona Glomerulosa = (Salt) mineralcorticoids (aldosterone)
- zona Fasciculata = (Sugar) glucocorticoids (cortisol)
- zona Reticularis = (Sex) androgens
50
Adrenal medulla synthesizes/releases
1. Epi (80%)
2. NE (20%)
51
Aldosterone release is increased by
1. RAAS
2. Hyperkalemia
3. Hyponatremia
52
Aldosterone
- Fx: resorption of Na+/H2O, excretion of K+ & H+
- regulates IV volume
53
Cortisol
- glucocorticoid
- production = 15-30 mg/day, 12 mcg/dL
- Fx:
1. gluconeogenesis
2. protein catabolism
3. fatty acid mobilization
4. anti-inflammatory effects
5. improves myocardial fx by increasing # & sensitivity of beta receptors in myocardium
54
Most to least glucocorticoid effect potency
1. dexamethasone, betamethasone (25)
2. fludrocortisone (10)
3. methylprednisolone, triamcinolone (5)
4. prednisone, prednidisolone (4)
5. cortisol (1)
6. cortisone (0.8)
7. aldosterone (0)
55
Conn's syndrome
- too much mineralocorticoid (aldosterone)
- Causes:
1. too much aldosterone release (pheo, hyperthyroid)
2. renovascular HTN
- licorice ingestion (glycyrrhizic acid) resembles conn's
- S/S
1. HTN (Na+/H2O retention)
2. Hypokalemia (K+ excretion)
3. Metabolic alkalosis (H+ excretion)
-Tx: remove tumor, spironolactone (aldosterone antagonist), K+, Na+ restriction
- Anesthesia
1. low K+ = sensitive to NMBs, U wave on EKG, avoid hyperventilation
2. HTN
56
Cushing's syndrome
- too much cortisol
- Causes: pituitary tumor (Cushing's Dz) too much ACTH, adrenal tumor releases cortisol
- Glucocorticoid effects
1. hyperglycemia
2. weight gain (central obesity, buffalo hump, moon
face)
3. increased infection risk
4. osteoporosis
5. muscle weakness
- Mineralocorticoid effects
1. HTN
2. hypokalemia
3. metabolic alkalosis
- Androgenic effects
1. women become masculinized
2. men become feminized
- Tx
1. transsphenoidal resection pituitary gland
2. adrenalectomy
3. pituitary radiation
- MGMT
1. aseptic technique
2. careful positioning
3. steroids
4. DI following pituitary resection
57
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.
58
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)
59
Acute adrenal crisis
- medical emergency
- caused by chronic AI faced w/ stress
- HD instability/collapse, fever, hypoglycemia, AMS
- Tx: steroids, D5NS, HD support
60
alpha cells
glucagon
61
beta cells
insulin
62
delta cells
somatostatin
63
PP cells
pancreatic polypeptide
64
Things that stimulate insulin release
- PNS & SNS stimulation
- glucagon
- catecholamines
- cortisol
- GH
- beta agonists
65
Things that reduce insulin release
- insulin
- VA
- beta antagonists
66
insulin receptor
- 2 alpha & 2 beta subunits joined together by disulfide bonds
- insulin binds to receptor & activates tyrosine kinase which activates insulin receptor substrates
67
Things that stimulate glucagon release
- hypoglycemia
- stress
- trauma
- sepsis
- beta agonists
68
Things that reduce glucagon release
- somatostatin
- insulin
69
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
70
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%
71
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
72
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
73
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
74
DKA
- *More common in DM Type 1
- Not enough insulin –> ketoacidosis,
- hyperosmolarity, dehydration
S/S:
Labs:
1. *CBG > 250 mg/dL
2. pH < 7.3
3. bicarb < 18
4. anion gap > 10
5. hyperosmolarity > 300
6. ketones > 5
- Metabolic acidosis
- Kussmaul’s respirations
- Fruity-smelling breath
- Tx:
1. fluids
2. insulin
3. K+
75
Hyperglycemic Hyperosmolar State
- More common w/ DM Type 2
- Caused by insulin resistance or inadequate
production
- Labs:
1. CBG > 600 mg/dL
2. osmolarity > 330 mOsm/L
3. mild metabolic acidosis
4. pH > 7.3 , no anion gap
- Tx:
1. fluids
2. insulin
3. correct electrolytes
76
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
77
Carcinoid syndrome
- GI tumor
- secretion of vasoactive substances from enterochromaffin cells
- Most common s/s = flushing, diarrhea
- Histamine release
1. bronchoconstriction
2. vasodilation
3. hypotension
4. flushing
- kinins & kallikrein
1. bronchoconstriction
2. vasodilation
3. hypotension
4. flushing
- serotonin
1. bronchoconstriction
2. vasoconstriction
3. HTN
4. SVT
5. diarrrhea
78
Carcinoid crisis
- tachycardia
- hypo/hypertension
- flushing
- abd pain
- diarrhea
79
Drugs to give carcinoid syndrome
- somatostatin (octreotide)
- antihistamines
- 5HT3 antagonists
- steroids
- phenylephrine, vasopressin
80
Drugs to avoid carcinoid syndrome
- histamine-releasing drugs = morphine, meperidine, atracurium, thiopental, sux
- catecholamines
- ephedrine, ketamine (stimulate SNS)
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