endo - patho - E3 Flashcards
synthesis and secretion of pituitary hormones are controlled by what
the hypothalamus
what hormones does the anterior lobe of the pituitary gland secrete
thyroid stimulating hormone (TSH)
adrenocorticotropic hormone (ACTH)
what hormones does the posterior lobe of the pituitary gland secrete
antidiuretic hormone (vasopressin)
oxytocin
ADH
released in response to high serum osmolality and/or hypotension & causes water retention via action in the kidneys
the adrenal medulla secretes
epinephrine and norepinephrine
(catecholamines)
in response to ACTH, the adrenal cortex secretes
Glucocorticoids (Cortisol)
Mineralcorticoids (Aldosterone)
Sex steroids (Androgens)
what do epi and norepi do
fight or flight
enhance/enlong the effect of the sympathetic nervous system
steroid hormones
-secreted by the adrenal cortex
-regulates the body’s response to normal & abnormal levels of stress
-made on demand
-activities: sugar, salt, & sex
what is the principal hormone of glucocorticoids
cortisol
functions of cortisol
-raise blood sugar
-protect against physiologic effects of stress
-suppress inflammatory and immune processes
-release muscle stores of proteins (maintains vascular system)
-increase blood cholesterol (raises our BP)
what is the principal hormone of mineralocorticoids
aldosterone
what regulates mineralocorticoids
renin-angiotensin system in the kidneys
functions of aldosterone
-maintain salt and water balance
-promotes excretion of potassium
-when triggered by angiotensin II, aldosterone promotes sodium retention & thus water retention
the thyroid secretes
triiodothyronine (T3, active form) and thyroxine (T4, either attached to proteins when not needed or freely in the tissues when needed)
T4 is converted to T3 when it reaches organs and tissues to aid in metabolism
what is a necessary component in synthesis of thyroid hormone
iodine
euthyroid
normally functioning thyroid gland
how many glands are in the parathyroid
4
parathyroid function
-produce and secrete parathyroid hormone (PTH) in response to hypocalcemia and break down bone to re-establish normal calcium in the blood
-Promotes vitamin D production
what is the primary use of looking at ACTH
dx of adrenal cortical dysfunction
sympathetic nervous system responses vs parasympathetic
Sym: pupils dilates, inhibits saliva, inc HR, dilates bronchi, inhibs peristalsis & secretion, converts glycogen to glucose, secretes adrenaline, inhibits bladder
Para: constricts pupils, stims saliva, slows HR, constricts bronchi, stims peristalsis & secretion, stims bowels
what is the patho behind why cushing syndrome happens
hypothalamus stimulates the release of ACTH which stimulates the adrenal cortex to produce glucort (cortisol) but there is too much of this process activated and we get increased cortisol levels
cushing syndrome definition
a collection of signs and symptoms associated with hypercortisolism
causes of Cushing’s
1) primary hyperfunction = Cushing’s syndrome
2) secondary hyperfunction = Cushing’s disease
3) exogenous steroids used in the mgt of various disease = Cushing’s syndrome
what is the most common cause of Cushing’s syndrome
exogenous steroids like predisone & dexamethazone
what does a patient lose when they have Cushing’s syndrome in regards to stress
the protective nature of stress -> in a healthy body, increased stress is used a protective mechanism for disease states
if a patient is having surgery, may need to give ACTH or Cortisol prior bc their body can’t respond to natural triggers
what is a byproduct of Cushing syndrome
the pituitary decreases production of ACTH because the adrenal gland isn’t being stimulated so it will often atrophy
clinical manifestations of Cushings
-glucose intol, hypergly
-htn, capollary friability
-muscle wasting/weakness, skin thinning, oesteoporosis & bone pain
-redistribution of fat to abdomen, shoulders and face
-impaired wound healing & immune response, inc risk of infection
-mood swings & insomnia
what will a person physically look like with Cushings
-red cheeks
-fat pads on neck base
-abdominal stretch marks
-bruise easily
-pendulous abdomen
-thin arms and legs
Addison’s disease
disease of the adrenal cortex that causes Hyposecretion of all 3 adrenocortical hormones
the most severe effect coming from the lack of cortisol
Addison’s disease pathogenesis
the adrenal gland is destroyed causing the gland to stops secreting cortisol which causes a lack of negative feedback so the anterior pituitary increases the secretion of ACTH & a hormone called melanocyte to try and stimulate cortisol (which doesn’t happen)
Addison’s Disease CM: early
anorexia, weight loss, weakness, malaise, apathy, electrolyte, skin hyperpigmentation
Addison’s Disease CM: hypoaldosteronism
low aldosterone means we are not retaining sodium or water
hypotension, decreased vascular tone & CO, decreased BV, hypoNa (salt cravings), hyperK, dehydration
Addison’s Disease CM: Hypocortisolism
low levels of cortisol = low levels of energy
hypoglycemia, weakness & fatigue, high levels of ACTH, & hyperpigmentation
acute side effect of glucocorticoid replacement
remember w/ addison’s since deficient, show present as homeostatic person
-increased intraocular pressure
-fluid retention
-high BP
-mood swings
-hunger
chronic side effect of cocorticoid replacement
clouded eye lens, weight gain (moon face & buffalo hump), high BS, increased risk for infection, thinning bones & fractures, suppressed adrenal gland hormone production (fatigue, loss of appetite, N/v, muscle weakness), thin skin, bruising, slow wound healing, hirsutism, striae
Severe Cushing’s Syndrome
presents as an acute emergency and is defined by a massively elevated random serum cortisol at anytime or a 24 hr urine free cortisol more than 4 fold the upper limit + present w/ severe hypokalemia
Severe Cushing’s Syndrome is typically associated with the onset of
sepsis, opportunistic infection, uncontrolled hypertension, heart failure, + more
Severe Cushing’s Syndrome treatment
manage metabolic and electrolyte disturbances in rapid resolution and try to figure out cause
Addisonian Crisis
a sudden insufficiency of serum corticosteroids (like you just got stabbed in your adrenal gland) or a sudden increase of stress or a sudden cessation of the corticosteroid drug
a medical emergency & if the body needs even more stress hormone, they just don’t have it
Pheochromocytoma
Rare tumor of the adrenal medulla that produces excessive catecholamines
-90% of time it is benign
-risk factor: young - middle age
Pheochromocytoma patho
excessive release of epi and norepi in response to SNS stimulation
epi stimulates
alpha and beta receptors which are located in the heart, lungs and vessels
norepi stimulates
alpha receptors
what is the hallmark clinical manifestation of Pheochromocytoma
hypertension which presents w/ headaches, diaphoresis & tachycardia
-sporadic episodes can occur w/ anything that stimulates the SNS (stress, excitement, exercise or smoking)
BP can get to extremely high levels like 250/200)
what environment should a person with Pheochromocytoma be in as they wait for treatment
a low stimulus environment
what is our main concern with someone who has Pheochromocytoma
stroke risk d/t the high BP
treat as quickly as possible -> #1 treatment is surgery
what can we give to patients w/ Pheochromocytoma as they wait to get surgery
alpha blockers bc the cause of the HTN is activation of alpha 1 receptors
-give 14 days prior & a little after
Syndrome of Inappropriate AntiDiuretic Hormone (SIADH)
“An abnormal production or sustained secretion of ADH”
characterized by: fluid retention, serum hypoosmolality & hypoNa and concentrated urine
our body is inappropriately holding onto all the water it can
SIADH etiology
-most common cause is a malignant tumor (Ex: Small cell carcinoma of the lung [Adenocarcinoma])
-CNS disorders like head trauma, stroke, brain tumor
-drug therapy: morphine, SSRIs, chemo drugs
-misc: hypothyroidism, infection
SIADH patho
increasd ADH -> increased water reabsorption in the renal tubules -> increased intravascular fluid volume -> dilutional hypoNa & decreased serum osmolality
SIADH osmolality labs
serum osmolality: low
urine osmolality: high
urine specific gravity: high
serum Na: low
urine output: low
weight: gain
SIADH clinical manifestations
same as hypoNa
-dyspnea, fatigue
-neuro: lethargy, confusion, dulled sensorium, musical twitching, convulsions
-GI: impaired taste, anorexia, vomiting, cramps
if Na = 100-115, irreversible neurologic damage
water intoxication in SIADH
When serum levels of NA become lower than what is INSIDE the cells (so vascular space Na levels are lower than the cell) -> cells will try and take in that water and they will swell causing further neurologic symptoms (confusion, lethargy, coma & death) b/c it is happening in the brain
diabetes insipidus
“a deficiency of ADH or a decreased renal response to ADH”
characterized by excessive loss of water in the urine -> two forms
1) neurogenic (central)
2) nephrogenic
neurogenic DI etiology
-cause: hypothalamus or pituitary gland damage
-associated w/ stroke, traumatic brain injury, brain surgery, cerebral infections
-has a sudden onset and is usually permanent
nephrogenic DI etiology
-cause: loss of kidney function, often drug related (lithium -> bipolar med)
-associated w/ chronic kidney disease
-onset is slow and the disease is progressive
DI patho
decreased ADH -> decreased water reabsorption in renal tubules -> decreased intravascular fluid volume -> increased serum osmolality (hyperNa) & excessive urine output
DI osmolality labs
serum osmolality: high
urine osmolarity: low
urine specific gravity: low
serum Na: high
urine output: high
weight: loss
DI clinical manifestations
-polyuria (up to 15L per day)
-polydipsia
-dehydration
-electrolyte imbalances
-if severe, hypovolemic shock (can lead to death)
DI treatment for neurogenic
synthetic ADH replacement (desmopressin)
DI treatment for nephrogenic DI
give thiazide (htcz) diuretic because it has a paradoxical effect so it decreases polyuria and increases urine osmolality
