Exam III: Pituitary, SIADH, DI, Adrenal Disorders Flashcards
Endocrine System (ES)
One of two homeostatic regulating systems
____ and ____ Systems
Work _____ to control response to stress
Nervous and Endocrine
together
ES is regulation of (5)
Behavior, metabolism, growth, fluid & electrolytes
Endocrine Gland: secrete hormones into ____ ____ (6 endocrine glands)
extracellular fluid
Pituitary, thyroid, parathyroid, pancreas, ovaries, adrenal
Exocrine Gland: secretes into ____. (2 types)
ducts
salivary, sweat glands
Hypothalamus controls ____ ____ secretion
pituitary hormone
Anterior Pituitary secretes ___ hormones
six
Hypothalamus sends hormones via ____ ____ ____ connection to anterior pituitary
hypophyseal portal vein
Hypothalamus, Pituitary, Adrenal (HPA) axis
Hypothalamus stimulates or inhibits hormone secretion based on a ___ ___ ___
negative feedback loop
Posterior Pituitary Gland - Terminal neuronal tissue originating in ______
hypothalamus
Two hormones synthesized in hypothalamus, secreted to and stored in the posterior pituitary
Vasopressin (Antidiuretic Hormone)
Oxytocin
Vasopressin (Antidiuretic Hormone)
Causes kidney to reabsorb water (___ receptor)
Secretion based on ____ ____ ____ to increased plasma osmolarity
Potent vasoconstriction (___ receptor)
V2
hypothalmic osmoreceptor response
V1
Oxytocin
causes ____ to contract
causes ____ ____ ejection
uterus
breast milk
Physiological response to surgical stress: (3)
increased CRH, ACTH, and cortisol secretion
Increased cortisol secretion
Increases at ____ ____
Continues through ___ ___ period
surgical incision
post op
ACTH stimulates ____ & ____ secretion
androgens & glucocorticoid
Zona glomerulosa secretes: *not stimulated by ACTH
_____: ______
Mineralocorticoids: aldosterone
Zona fasciculata secretes:
____: ______
Glucocorticoids: cortisol
Zona reticularis secretes:
_____: _____(anabolic steroid)
Androgens:dehydroepiandrosterone
Adrenal medulla:
Chromafin cells secrete:
_____: ____, ____, and ____
Catecholamines: norepi, epi, and dopamine
____ (____): primary glucocorticoid (95%)
Cortisol (hydrocortisone)
Cortisol production: __/__ ____ under normal conditions
Cortisol receptors on all cells: primary target tissues are ____, ____, ____ ____
15-30 mg/day
liver, adipose, skeletal muscle
___ & ____ _____ & ___ ____ levels stimulate release
Hypothalamus (CRH)-> Anterior Pituitary (ACTH)-> blood-> adrenal cortex-> cortisol
Physical & mental stress & low glucocorticoid
Cortisol Stimulates ____, _____ (diabetogenic effect)
Heavily affects ____ causing increased output of glucose
↑Free ___ ___ mobilization
gluconeogenesis, glycogenolysis
liver
fatty acid
Inhibits collagen formation causing collagen loss:
___ and ____ thins
↓Protein synthesis, ↓ ___ ___ ___ by muscles, ↑protein catabolism
Skin and hair
amino acid uptake
Reduced ____/____ response
Reduces ____ release
Lysosomal membrane _____ preventing leaky cells
inflammatory/immune
histamine
stabilizing
Osteoporosis: reduced _____ absorption
calcium
Cortisol - Raises blood pressure:
___ reabsorption, ___ excretion
Na+
K+
Cortisol - Raises blood pressure:
____ effects cause water retention
ADH
Cortisol - Raises blood pressure:
Facilitates ____ synthesis
catecholamine
Cortisol - Raises blood pressure:
___ receptor synthesis, regulation,
Beta
Cortisol - Raises blood pressure:
↑ vascular sensitivity to _____ and exogenous _____
Increased vascular tone, cardiac contractility
Without cortisol, ____ ____ occurs
catecholamines
sympathomimetics
cardiovascular collapse
Produces mineralocorticoid (aldosterone) effects:
Cortisol is molecularly similar to _____
Increased affinity for ______ receptor
Mineralocorticoid target tissue enzyme prohibits overstimulation of the receptor by cortisol
aldosterone
mineralocorticoid
cortisol - alteration in ____
mood
cortisol - increased ____
apetite
Glucocorticoid Excess (Cushing’s Syndrome)
ACTH ____:
↑ACTH by ___ ____(75% of endogenous causes)
dependent
pituitary adenoma
Glucocorticoid Excess (Cushing’s Syndrome)
ACTH independent:
adrenal tumor, adrenal carcinoma
Superphysiologic doses of ___ ____ (most common cause)
used for controlling inflammatory or autoimmune conditions such as ___, ____, ____, ____
exogenous steroids
asthma, bronchitis, arthritis, lupus, MS
Glucocorticoid Excess (Cushing’s Syndrome)
Ectopic production:↑ACTH from __-___ ____
non-pituitary tumors
Glucocorticoid Excess (Cushing’s Syndrome)
Increased glucocorticoids can also produce some mineralocorticoid effects:
____, ____
Hypokalemia, Hypertension
Glucocorticoid Excess (Cushing’s Syndrome)
Inability to tolerate stress of ___ ___
normal activity
Glucocorticoid Excess (Cushing’s Syndrome)
____ intolerance
glucose
Glucocorticoid Excess (Cushing’s Syndrome)
___ ____ change
mental status
Glucocorticoid Excess (Cushing’s Syndrome)
catabolic effects (4)
Catabolic effects:
muscle atrophy & wasting, thin skin, osteoporosis
Anesthesia Mgmt of Glucocorticoid Excess
Usually ____, ____, _____
_____: reduces intravascular volume, ↑’s K+
hypertensive, hyperglycemic, hypokalemic
Spironolactone
Anesthesia Mgmt of Glucocorticoid Excess
Positioning concerns:
Pathological ____ risks: careful positioning
___ ___ skin: don’t pinch, tear, use paper tape
fracture
Frail thin
Anesthesia Mgmt of Glucocorticoid Excess
Increased risks of ____: immunosuppressed, aseptic technique
infection
Anesthesia Mgmt of Glucocorticoid Excess
___ ___ weakness:
Mechanical ____ is indicated due to profound weakness
Potential increased sensitivity to ____ due to ↓K+
Skeletal muscle
ventilation
paralytics
Anesthesia Mgmt of Glucocorticoid Excess
Realize increased risks of ____ event (DVT, PE)
thromboembolic
Anesthesia Mgmt of Glucocorticoid Excess
__ ____ may temporarily suppress cortisol release
IV Etomidate
Adrenocortical Insufficiency (AI) (Addison’s Disease)
___ types
3
Adrenocortical Insufficiency (AI) (Addison’s Disease)
Type 1 - ___ ___ insufficiency:
Destruction of the adrenal gland
TB, HIV, malignancy, autoimmune diseases
___ ACTH secretion from pituitary
Both mineralocortoid and glucocorticoid are ____
Clinical signs due to ____ deficiency
Primary adrenal
Normal
deficient
aldosterone
Adrenocortical Insufficiency (AI) (Addison’s Disease)
Type 2 - Secondary adrenal insufficiency:
Inadequate ___ ___ from pituitary
Most often from negative feedback from administration of ___ ____ (adrenal suppression)
Mineralocorticoid secretion _____ (Na+ K+ & volume are normal)
ACTH secretion
exogenous glucocorticoids
unaffected
Adrenocortical Insufficiency (AI) (Addison’s Disease)
Type 3 - Acute adrenal insufficiency:
____-____ patients not receiving glucocorticoids during stress (surgery, trauma, infection)
Patients receiving ____
Steroid-dependent
etomidate
Signs of Acute Adrenal Crisis
____ collapse - ____ instability and hypotension
CV
hemodynamic
Signs of Acute Adrenal Crisis
Severe ___ ___ weakness
skeletal muscle
Signs of Acute Adrenal Crisis
Hypo____, Hyper____
Hyponatremia, Hyperkalemia
Signs of Acute Adrenal Crisis
Nausea,(due to _____) Fever
hypovolemia
Signs of Acute Adrenal Crisis
____ mental status
Declining
Anesthesia Mgmt of Adrenocortical Insufficiency
Correct __, ___, and glucose abnormalities
Na+, K+
Anesthesia Mgmt of Adrenocortical Insufficiency
Avoid ____ (even single dose affects susceptible pts.)
Etomidate
Anesthesia Mgmt of Adrenocortical Insufficiency
Correct volume depletion with ____ ___
normal saline
Anesthesia Mgmt of Adrenocortical Insufficiency
Inotropic or vasopressor support if ____ ____
hemodynamically unstable
Anesthesia Mgmt of Adrenocortical Insufficiency
Glucocorticoid replacement:
Replace if on____ prednisone equivalent for > 2 weeks during the last ___ ____
100 mg Hydrocortisone q8hr followed by ____ over _____
This dosing is adequate to correct mineralocorticoid deficiency
≥ 5mg/day
12 months
100-200mg over 24 hrs
Mineralocorticoids (Aldosterone)
Aldosterone: primary mineralocorticoid (90%)
Produce ____ ____
100-150 mcg/day
Mineralocorticoids (Aldosterone)
Extracellular ___ & ____ regulation
K+ ____ coupled with Na+ ____
sodium & potassium
secretion
reabsorption
Mineralocorticoids (Aldosterone)
Maintains total body ___ balance
fluid
Mineralocorticoids (Aldosterone)
Secretion by adrenal cortex but NOT primarily based on ____
ACTH
Mineralocorticoids (Aldosterone)
Secretion based on 4 stimulants (greatest to least)
Angiotension II (decreased blood pressure, hypovolemic states)
Hyperkalemia
Hyponatremia
ACTH
Circulatory support by the Renin system
Renin is released from the granular cells of the afferent arteriole of kidney in response to: (3)
Pressure decrease hypovolemia beta-1 adrenergic stimulation
Circulatory support by the Renin system
____ converts angiotensinogen to angiotensin I
Renin
Circulatory support by the Renin system
Angiotensin-converting enzyme (ACE) from the ____ converts angiotensin II (potent ____)
lungs
vasoconstrictor
Circulatory support by the Renin system
Angiotensin II stimulates ____ ____ directly from the adrenal cortex
aldosterone release
Circulatory support by the Renin system
Angiotensin II also stimulates _____ release from posterior pituitary
vasopressin
Primary Aldosteronism (Conn’s Syndrome)
↑secretion ____ stimulation (adrenal hypersecretion)
Usually adenoma, hyperplasia or rarely carcinoma
Renin levels are ____ due to ___ ____ from HTN
without
low due to negative feedback
Secondary Aldosteronism:
Stimulation comes from ____ the adrenal gland
Usually because of increased circulating ____ levels
Some conditions stimulate renin-angiotensin system leading to ↑ aldosterone secretion:
CHF, HoTN, hepatic cirrhosis, ascites, nephrotic syndrome
outside
renin
Treat HTN and fluid volume overload:
Na+ levels are usually NOT elevated due to ↑water retention
Spironolactone: ____ antagonist
Antihypertensive properties
Helps with ___ ____
aldosterone
K+ correction
Consider presence of LV ____, LV _____
hypertrophy
dysfunction
Evaluate electrolytes:
Replace ___ ___ slowly IV
May have increased sensitivity to ___-____ agents
Muscle weakness and cramps
Evaluate EKG for presence of __ ____
Avoid ___ventilation
depleted K+
non-depolarizing
U wave
hyper
Aldosterone Deficiency
extremely ___
rare
Aldosterone Deficiency
____ without renal insufficiency usually indicates hypoaldosteronism
Deficiency of aldosterone synthetase
Hypo____
ACE inhibitor-induced reduction in angiotensin
Hyperkalemia
reninemia
Aldosterone Deficiency - hypo____, hypo_____
Hypotension, Hyponatremia
Aldosterone Deficiency
Treatment with ___ and _____
Na+ and corticosteroids
Growth Hormone Hypersecretion
Usually caused by ____ ___
GH promotes growth, promotes a ____ effect
pituitary adenoma
diabetogenic
Growth hormone hypersecretion -
___ ___ deposited on existing bone
↑Hands, feet, vertebrae, kyphoscoliosis, arthritis
Entrapment neuropathy: ___ ___ syndrome
___ ___ collateral flow impediment
New bone
carpal tunnel syndrome
Radial artery
Growth Hormone Hypersecretion
___ ___ ___ occurs
↑Nose, mandible, supraorbital ridge
Dental ____
Soft tissue overgrowth
malocclusion
Growth Hormone Hypersecretion
Organ overgrowth occurs
↑___, ____, ____
Increased pulmonary volumes
Liver, heart kidney, spleen
Growth Hormone Hypersecretion Symptoms
____ intolerance
exercise
Growth Hormone Hypersecretion Symptoms
Symptomatic _____ disease
Biventricular concentric hypertrophy
Diastolic dysfunction, CHF, arrhythmias
cardiac
Growth Hormone Hypersecretion Symptoms
↑glucose: GH ____ resistance effects
insulin
Growth Hormone Hypersecretion Symptoms
Enlarging tumor: ↑___, ___ ___ compression
ICP, optic nerve compression
Anesthesia Management of Acromegally
Consider existence of ___ disease ___, hypertrophy
cardiac
CAD
Anesthesia Management of Acromegally
Thorough Airway Assessment:
Dyspnea, stridor,hoarseness indicate ____ ____
↑tongue, teeth, pharyngeal tissue, epiglottis:
Fiberoptic or glidescope (diff airway__-__ ____ occurrence)
___ have sleep apnea
↑Facial features: difficult mask fit
Subglottic narrowing, ↑vocal cords: use smaller ETT
↑Nasal turbinates: caution with ___ ____ or nasal trumpets
airway difficulty
4-5x higher
60%
nasal intubation
Anesthesia Management of Acromegally
Blood glucose level (glucose ____, _____)
intolerance
prediabetic
Anesthesia Management of Acromegally
Wrist positioning & ___ ____ ____ concerns
Radial artery circulation
Antidiuretic Hormone (ADH)
ADH: primary regulator of ___ ___
Plasma ____ regulates release
water balance
osmolarity
Antidiuretic Hormone (ADH)
ADH acts on ___ and ___ receptors:
V1 and V2
Antidiuretic Hormone (ADH)
High levels of ADH stimulate V1 receptors:
Potent vasoconstriction: (3)
coronary, splanchnic, renal vascular beds
Antidiuretic Hormone (ADH)
___ ___ of ADH stimulate V2 receptor on renal collecting ducts:
Increases water reabsorption through channels (aquaporins)
Collecting duct impermeable to water reabsorption ___ ___
Increased water loss -> ____ occurs
Low levels
without ADH
dehydration
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Hypersecretion of ADH/vasopressin not caused by ___ ____
increased osmolarity
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Causes:
Hypothyroidism, head trauma, intracranial tumors
Pituitary surgery
Pulmonary infection
Small-cell carcinoma of lung (common)
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Increased renal reabsorption of water:
Hypo____ & plasma hypotonicity
Increased ___ & ____ fluid volumes
Hemodilution and water weight gain
Urine is ____ with low urine output
natremia
intra and extracellular
hypertonic
Clinical Signs of SIADH
No ____ and no peripheral edema
hypertension
SIADH
Clinical signs result from water intoxication:
Hyponatremia
Brain edema
Primarily CNS signs
Lethargy, headache, AMS, seizure
Anesthesia Management of SIADH
Assess and manage volume status:
Fluid restriction: ________
____ saline solutions
800-1000ml/day
Isotonic
Anesthesia Management of SIADH
Severe _____:
Hypertonic saline (3%) infusion if Na+ ____ & ____
Infuse slow to prevent ____ ____ ____ syndrome
hyponatremina
<115 & symptomatic
central pontine demyelination
Anesthesia Management of SIADH
_____ (____) antagonizes vasopressin on renal tubules
Demecloycycline (tetracycline)
Anesthesia Management of SIADH
Prevent nausea: Nausea potent stimulant of ____
ADH
Neurogenic (central DI):
Inadequate secretion of ADH/vasopressin from ___ ___ ___.
Causes (2)
posterior pituitary lobe
Severe head trauma,brain tumors
Pituitary surgery - Temporary: usually resolves in 5-7 days
Nephrogenic DI:
Inability of renal collecting duct receptors to respond to ADH: ___ ___ ____
reduced receptor sensitivity
Nephrogenic DI:
causes:
Genetic mutations
Hypercalcemia, hypokalemia,
Medicine induced nephrotoxicity
Ethanol inhibits response or release (alcohol consumption ↑’s urine output)
Demeclocycline, dilantin, chlorpromazine (thorazine), lithium inhibit ADH response or release
Diabetes Insipidus (DI)
Response to ___ (____ ____) distinguishes between the two
____ corrects neurogenic cause and concentrated urine but will not correct nephrogenic cause
DDAVP (vasopressin analogue)
DDAVP
Diabetes Insipidus (DI)
primary sign
Polyuria is the primary sign
Diabetes Insipidus (DI) signs:
Dehydration, hyper____
____ urine osmolarity
High plasma osmolarity (> ______)
natremia
Low
290 mOsm/L
Diabetes Insipidus (DI) signs:
___dipsia
Polydipsia (increased thirst)
Diabetes Insipidus (DI) CNS signs (4)
Hyperreflexia, weakness, lethargy, seizures
Anes Mngmnt Diabetes Insipidus (DI)
Neurogenic:
DDAVP: ____ analogue
Desmopressin _____
vasopressin
intranasally
Anes Mngmnt Diabetes Insipidus (DI)
Nephrogenic:
____: an oral sulfonylurea hypoglycemic (Diabinese) enhances effects of ADH on renal tubules
Chlorpropamide
Anes Mngmnt Diabetes Insipidus (DI)
____ fluid volume status
Evaluate
Anes Mngmnt Diabetes Insipidus (DI)
Evaluate electrolytes ___ & ____
Na+ and K+
Anes Mngmnt Diabetes Insipidus (DI)
Monitor ____
UOP