Endocrine Disorders Flashcards
Anterior Pituitary secretes 6 hormones; what are the two we are focusing on for class?
thyroid stimulating hormone
adrenocorticotropic hormone (ACTH)
Posterior Pituitary secretes what 2 hormones?
antidiuretic hormone (AKA Vasopressin)
oxytocin
Adrenal Gland: location and composition
sit on top of the kidneys
each gland is composed of an inner medulla and an outer cortex
Adrenal Medulla secretes what 2 catecholamines?
epinephrine
norepinephrine
Adrenal Cortex secretes what in response to ACTH? (3)
“the 3 S’s”
glucocorticoids (Cortisol) (SUGAR)
mineralcorticoids (Aldosterone) (SALT)
sex steriods (Androgens) (SEX)
Adrenocortical Hormone Disorders (2)
Cushing Syndrome
Addison Disease
Cushing Syndrome: Definition
a collection of S/S associated with hypercortisolism
Cushing Syndrome: Causes (3)
primary hyperdysfunction
secondary hyperdysfunction
exogenous steroids
Primary hyperdysfunction (Cushing)
disease of the adrenal cortex and adrenal cortex releases too much cortisol
Secondary hyperdysfunction (Cushing)
disease of the anterior pituitary gland, and causes release of too much ACTH, which results in too much cortisol production
Exogenous Steroids
Can cause Cushing Syndrome
used in the management of various diseases
prednisone and dexamethasone are MOST common cause of cushing syndrome in the US
Cortisol: Functions (4)
Raises blood sugar (opposes insulin)
Protects against the physiologic effects of stress
Suppresses immune and inflammatory processes
Breaks down protein and fat
Cushings: Clinical Manifestations (CM) (6)
with increased cortisol:
-Glucose intolerance, hyperglycemia
-HTN, capillary friability (ecchymoses)
-Muscle wasting, muscle weakness, thinning of skin, osteoporosis and bone pain
-Redistribution of fat to abdomen, shoulders, and face
-Impaired wound healing and immune response, risk for infection
-Mood swings, insomnia
Cushings: Drug Therapy
treatment depends on cause
-pituitary or adrenal tumor?: surgery or radiation
-exogenous steroids?: taper the drug slowly if possible
-2 drugs possible
Cushings: Drugs (2)
aminoglutethimide
ketoconazole
aminoglutethimide (Cytadren): Indication and MOA
for Cushings: temporary therapy to decrease cortisol production
blocks synthesis of all adrenal steroids
aminoglutethimide (Cytadren): Effects and SE
reduces cortisol by 50%
does NOT affect the underlying disease process
SE:
-drowsiness
-nausea
-anorexia
-rash
ketoconazole (Nizoral): Indication and MOA
adjunct therapy to surgery or radiation for Cushings
antifungal drug that also inhibits glucocorticoid synthesis
ketoconazole (Nizoral): SE and Safety Issues
MAIN SE: severe liver damage
Do NOT take with alcohol or other drugs that harm liver
Do NOT give during pregnancy (fetal thyroid damage)
Addison Disease: Definition
disease of the adrenal cortex that cause HYPOsecretion of all 3 adrenocortical hormones (cortisol, aldosterone, androgens)
* Most SEVERE effects come from the LACK of cortisol
Addison Disease: Etiology (3)
idiopathic
autoimmune
other
Addison Disease: Pathogenesis
adrenal gland destroyed
symptoms when 90% non-functional
ACTH and melanocyte-stimulating hormone (MSH) are secreted in large amounts
Addison Disease: EARLY CM (7)
anorexia
weight loss
weakness
malaise
apathy
electrolyte imbalances
skin hyperpigmentation
With Addison Disease, why do they appear tan (skin hyperpigmentation)?
MSH secretion- excess melanocyte stimulation
Addison Disease: CM: 2 Main Types
hypoaldosteronism
hypocortisolism
Addison Disease: Hypoaldosteronism CM
hypotension
-decreased vascular tone
-decreased CO
-decreased circulating
blood volume
salt craving
-decreased Na levels
-increased K levels
-dehydration
Addison Disease: Hypocortisolism CM (4)
hypoglycemia
weakness and fatigue
unsuppressed ACTH production
hyperpigmentation
Addison Disease: Pharmacotherapy
Adrenal insufficiency requires lifelong corticosteroid replacement therapy
All patients require a glucocorticoid
-Hydrocortisone (Cortef)
-Prednisone
-Dexamethasone
Some patients require a mineralcorticoid
-Fludrocortisone
(Florinef)
Addison Disease: what is drug of choice for AD?
Hydrocortisone (Cortef)
Has glucocorticoid and mineralcorticoid activity
Addison Disease: Pharmacotherapy: Important Issues
Dosing mimics natural release of hormones
-timing is important-
CONSISTENT
-doses are small
NEVER abruptly stop therapy
Dose will need to be increased during stress
-example: infection,
surgery, trauma
-“3x3 Rule”: 3x usual
dose for 3 days
Always maintain emergency supply
Wear a medical alert bracelet
Adrenal Crises: 2 Types
Severe Cushing Syndrome
Addisonian Crisis
Pheochromocytoma: Definition
adrenal medulla disorder
90% of the time benign
rare tumor of the adrenal medulla that produces excessive catecholamines
Pheochromocytoma: Risk Factor and Pathogenesis
young-middle age
SNS stimulation–> excessive release of epi, norepi
Pheochromocytoma: CM (4)
HYPERTENSION: stroke risk
tachycardia
headache
diaphoresis
Pheochromocytoma: Drug Therapy
*Principal cause of hypertension is activation of the alpha 1 receptors on blood vessels
Preferred treatment: surgery
Alpha-adrenergic blockers may be used (1):
-inoperable tumors
-pre-operatively to
reduce risk of acute HTN
Pheochromocytoma: Drug
phenoxybenzamine HCl (Dibenzyline)
phenoxybenzamine HCl (Dibenzyline): Indication and MOA
pheochromocytoma
long-lasting, irreversible blockage of alpha-adrenergic receptors
phenoxybenzamine HCl (Dibenzyline): Drug Effects and SE
DE: lowers BP
SE:
-orthostatic hypotension
-reflex tachycardia
-nasal congestion
-sexual SE in men
Antidiuretic Hormone (ADH)
Function: causes water retention via action in the kidneys
Released in response to high serum osmolality and/or hypotension
ADH Disorders (2)
SIADH
Diabetes Insipidus
SIADH: Definition
Syndrome of Inappropriate AntiDiuretic Hormone
An abnormal production or sustained secretion of ADH
SIADH: Characterized by (3)
fluid retention
serum hypoosmolality and hyponatremia
concentrated urine
SIADH: Etiology (4)
Malignant Tumors
-ex: small cell carcinoma
of the lung
(Adenocarcinoma)-
MOST common cause of
SIADH
Central Nervous System Disorders
-ex: head trauma, stroke,
brain tumors
Drug Therapy
-ex: morphine, SSRIs,
some chemo drugs
Miscellanous Conditions
-ex: hypothyroidism,
infection
SIADH: Pathogenesis
increased antidiuretic hormone–> increased water reabsorption in renal tubules–> increased intravascular fluid volume—> dilutional hyponatremia and decreased serum osmolality
SIADH: Osmolality
Serum Osmolality= LOW
Urine osmolality and specific gravity= HIGH
Serum Na= LOW
Urine output= LOW
Weight= GAIN
*Remember: pt. is retaining pure water without salt
SIADH: CM (11)
Symptoms of HYPOnatremia:
-dyspnea, fatigue
-Neurologic: lethargy,
confusion, dulled
sensorium
-muscle twitching,
convulsions
-GI: impaired taste,
anorexia, vomiting,
cramps
Manifestation depends on severity and rate of onset of hyponatremia
Severe Symptoms: Na= 100-115 mEq/L–> IRREVERSIBLE neurologic damage
Water Intoxication: Definition and Symptoms
When serum levels of Na become lower than what is INSIDE the cells
Cells SWELL
Symptoms: neurologic primarily–>confusion, lethargy, coma, death
SIADH: Pharmacotherapy
Not the first line of treatment–> instead directed at the underlying cause: ex: discontinue offending medication, head trauma: might wait it out, etc.
Chronic SIADH= demeclocycline (Declomycin)
demeclocycline (Declomycin): Classification and MOA
tetracycline broad-spectrum antibiotic
interferes with renal response to ADH
demeclocycline (Declomycin): Indication and SE
chronic SIADH
antibiotic therapy
photosensitivity
teeth staining
NEPHROTOXIC
Diabetes Insipidus (DI): Definition
A deficiency of ADH or a decreased renal response to ADH
Characterized by: excessive loss of water in the urine
Diabetes Insipidus: Two Forms
NEUROgenic (Central)
NEPHROgenic
DI NEUROgenic: Etiology
Neuro origin (Central DI)
CAUSE: hypothalamus or pituitary gland damage
Associated disorders:
-stroke, traumatic brain
injury
-brain surgery
-cerebral infections
Sudden onset
Usually permanent
DI NEPHROgenic: Etiology
Renal origin
CAUSE:
-loss of kidney function
-often drug-related
(ex: Lithium)
Associated Disorders: CKD
SLOW onset
PROGRESSIVE course of disease
DI: Pathogenesis
decreased ADH–> decreased water reabsorption in renal tubules–> decreased intravascular fluid volume–> increased serum osmolality (hypernatremia) AND excessive urine output
DI: Osmolality
Serum osmolality= HIGH
Urine osmolality and specific gravity= LOW
Serum Na= HIGH
Urine output= HIGH
Weight= LOSS
DI: CM (5)
polyuria
polydipsia
dehydration
others based on severity
-electrolyte imbalances
-hypovolemic shock–>
death
DI Pharmacotherapy: NEUROgenic
synthetic ADH replacement
Desmopressin (DDAVP)
Desmopressin (DDAVP)
NEUROgenic DI
synthetic ADH replacement, anti-diuretic effects
Delivery: nasal spray, PO, IV, SQ
SE:
-small doses: none
-nasal spray: nasal
irritation
-large doses:
hyponatremia, water
inoxication
DI Pharmacotherapy: NEPHROgenic
thiazide diuretics
paradoxical effect:
-decreases polyuria
-increases urine
osmolality
DI: D-I-L-U-T-E
Dry
I & O, daily weight
Low specific gravity
Urinates lots
Treat= desmopressin
rEhydrate
