Exam III: Pituitary, SIADH, DI, Adrenal Disorders Flashcards by Linsley Lloyd

Endocrine System (ES)

One of two homeostatic regulating systems
____ and ____ Systems
Work _____ to control response to stress

Nervous and Endocrine
together

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ES is regulation of (5)

Behavior, metabolism, growth, fluid & electrolytes

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Endocrine Gland: secrete hormones into ____ ____ (6 endocrine glands)

extracellular fluid
Pituitary, thyroid, parathyroid, pancreas, ovaries, adrenal

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Exocrine Gland: secretes into ____. (2 types)

ducts
salivary, sweat glands

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Hypothalamus controls ____ ____ secretion

pituitary hormone

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Anterior Pituitary secretes ___ hormones

six

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Hypothalamus sends hormones via ____ ____ ____ connection to anterior pituitary

hypophyseal portal vein

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Hypothalamus, Pituitary, Adrenal (HPA) axis
Hypothalamus stimulates or inhibits hormone secretion based on a ___ ___ ___

negative feedback loop

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Posterior Pituitary Gland - Terminal neuronal tissue originating in ______

hypothalamus

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Two hormones synthesized in hypothalamus, secreted to and stored in the posterior pituitary

Vasopressin (Antidiuretic Hormone)
Oxytocin

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Vasopressin (Antidiuretic Hormone)
Causes kidney to reabsorb water (___ receptor)
Secretion based on ____ ____ ____ to increased plasma osmolarity
Potent vasoconstriction (___ receptor)

V2
hypothalmic osmoreceptor response
V1

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Oxytocin
causes ____ to contract
causes ____ ____ ejection

uterus
breast milk

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Physiological response to surgical stress: (3)

increased CRH, ACTH, and cortisol secretion

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Increased cortisol secretion
Increases at ____ ____
Continues through ___ ___ period

surgical incision
post op

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ACTH stimulates ____ & ____ secretion

androgens & glucocorticoid

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Zona glomerulosa secretes: *not stimulated by ACTH
_____: ______

Mineralocorticoids: aldosterone

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Zona fasciculata secretes:
____: ______

Glucocorticoids: cortisol

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Zona reticularis secretes:
_____: _____(anabolic steroid)

Androgens:dehydroepiandrosterone

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Adrenal medulla:
Chromafin cells secrete:
_____: ____, ____, and ____

Catecholamines: norepi, epi, and dopamine

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____ (____): primary glucocorticoid (95%)

Cortisol (hydrocortisone)

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Cortisol production: __/__ ____ under normal conditions
Cortisol receptors on all cells: primary target tissues are ____, ____, ____ ____

15-30 mg/day
liver, adipose, skeletal muscle

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___ & ____ _____ & ___ ____ levels stimulate release
Hypothalamus (CRH)-> Anterior Pituitary (ACTH)-> blood-> adrenal cortex-> cortisol

Physical & mental stress & low glucocorticoid

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Cortisol Stimulates ____, _____ (diabetogenic effect)
Heavily affects ____ causing increased output of glucose
↑Free ___ ___ mobilization

gluconeogenesis, glycogenolysis
liver
fatty acid

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Inhibits collagen formation causing collagen loss:
___ and ____ thins
↓Protein synthesis, ↓ ___ ___ ___ by muscles, ↑protein catabolism

Skin and hair
amino acid uptake

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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

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

Exam III: Pituitary, SIADH, DI, Adrenal Disorders Flashcards

(119 cards)