Pituitary and Adrenals Flashcards
list homones secreted by the
adrenal cortex
adrenal medulla
Cortext
- glucocorticoids - cortisol
- Mineralocorticoids - Aldosterone
- Androgens - testosterone
Medulla
- Epinephrine (80%)
- Norepinephrine (20%),
- Dopamine catecholamines = Chromaffin cells
fucntions of cortisol
•released at diurnal basal rate with bursts d/t stress response regulated by Anterior pituitary & ACTH via negative feedback loop (hydrocortisone is rx of cortisol)
- Mobilize sugar
- Suppress immune system
- Stimulate Gluconeogenesis = Increase in glucose metabolism and glycogen formation, especially in the liver
- anti-inflammtory effects
Mineralocorticoids (aldosterone)- Production in the Zona ______
Androgens - Production in the Zona_____
Mineralocorticoids (aldosterone)- Production in the Zona Glomerulosa
Androgens - Production in the Zona Reticularis
Adrenal medulla tumor - produce, store, secrete catecholamines
Extra-adrenal originating in ANS
MEN2a/2B
Pheochromocytoma
si/sx of phenochromocytoma
Recurrent episodes that occur suddenly:
- HTN(most common) +/- tachycardia
- HA
- Diaphoresis
- Palpitations
dx phenochromocytoma
24-hour urine metanephrine,
- VMA (vanillylmandelic acid),
- total catecholamines, creatinine
Abnormal THEN image
Abdominal CT/MRI – mRI preferred
dx phenochromocytoma
Surgical resection – Laparoscopic if <8mm preferred
Alpha-adrenergic blockade– 10-14 days
Beta adrenergic blockade 2 days prior to surgical resection to prevent intra-operative HTN crisis to prevent intra-operative HTN crisis
- Phenoxybenzamine HCl (Dibenzyline)
- Propranalol or Nadolol
2 etiologys of Hyperaldosteronism
Primary (Conn’s syndrome)
- Adrenal adenoma
- Bilat cortical nodular hyperplasia - Idiopathic hyperaldosteronism
- Hypersecretion Aldosterone = Renal distal tubular exchange of Na+ K+ and H+ secretion
Secondary: appropriate ↑ aldosterone production d/t RAAS –> low flow through JGA
- Edema (nephrotic syndrome, cirrhosis, CHF)
- Assoc w/ HTN –> Renin overproduction –> ↓ in renal blood flow (ie RAS Renin producing tumor)
si/sx of Hyperaldosteronism
- Diastolic HTN so HIGH - HA
- Hypokalemia == muscle weakness/fatigue
- Hypernatremia
- Metabolic alkalosis –> Excess H+ secretion = ↑HCO3
dx of primary vs secondary Hyperaldosteronism
Primary - DEC plasma renin
Secondary - INC plasma Renin
dx Hyperaldosteronism
Renin hyposecretion w/ volume depletion – STILL ↓renin
- SHOULD - ↑ w/ vol depletion
Failed aldosterone suppression w/ volume expansion – STILL ↑aldosterone
- SHOULD ↓ renin and aldosterone
ECG (flat T-waves, ST depression, U waves)
Hypokalemia / Hypernatremia
CXR
Metabolic alkalosis (↑ HCO3) – Loss of H+ in urine and Shift H+ into cells
tx hyperaldosteronisms
Adenoma – Surgical excision
Hyperplasia
- Diet Na+ restriction
- Spironolactone
criteria for dx of Hyperaldosteronism
Diastolic HTN without edema
↓Secretion of renin when stimulated - Stimulate w/ volume depletion
↑Secretion of aldosterone that cannot suppress - Try to suppress w/ volume expansion
No diuretic use
Cushings endogogenous vs exogenous causes
Endogenous - ↑ cortisol from adrenal cortex
- Pituitary overproduction ACTH (80%) - Cushing’s
- ↓ TSH, FSH, LH, GH, prolactin, and if lrg ?vasopressin(ADH)
- Adrenal adenoma
- Small cell lung ca.
- Thyroid neoplasm
- Pancreatic neoplasm
Exogenous (most common)
- Chronic steroid use —> HPA suppression
- prednisone, decadron, hydrocortisone
si/sx of cushings
- Weight gain – central adiposity
- Skin Δ (purple striae, buffalo hump, moon face)
- Proximal muscle weakness
- Neuropsych (depression, cognitive dysfunction)
- DM ( infections, poor wound healing)
- Sexual dysfunction
- Hyperpigmented “healthy glow”
dx cushings
Stepwise Approach
24-hour urine cortisol >300 diagnostic
1mg Dexamethasone suppression test
- Nl < 5 mcg/dL
CRH/Dex suppression test – >50 is diagnostic
ACTH (independent vs. dependent)
- ACTH level (should be low normally in early afternoon 4p)
- ACTH high? = cranial MRI & high dose dex-suppression test
- ACTH nl or low? = Abd CT/MRI
tx cushings
Surgical resection (transphenoidal resection) +/- radiation
- Adrenalectomy w/ failed pituitary resection
Medical Mgt:if surgery fails
Ketoconazole: ↓ cortisol production
- Side effects Headache, sedation, nausea, decreased libido, impotence, gynecomastia, elevated LFT’s, irregular menses
Metyrapone: Blocks final step of cortisol synthesis
- Used w/ ketoconazole should it fail to be fully effective
Adrenal insufficency (Addisons) shows an overall decrease of ???
↓aldosterone
↓cortisol
list primary and secondary addisons (adrenal insufficency)
Primary – destruction of adrenal cortex
- Anatomic destruction or metabolic failure of the adrenal cortex INCREASE ACTH
Secondary
- Suppression or disease of the HPA axis DECREASE ACTH
- exogenous steroids
si/sx of primary addisons (adrenal insuff)
- Weakness/fatigue (initially asthenia)
- Dehydration–> hypotension/orthostasis
- Weight loss/anorexia
• Hyperpigmentation
- N/V/D
- Abd pain
si/sx of secondary addisons (adrenal insuff)
- Weakness/fatigue (initially asthenia)
- Dehydration –> hypotension/orthostasis
- Weight loss/anorexia
- N/V/D
- Abd pain
(NO hyperpigmentation)
Panhypopituitarism
dx of addisons (adrenal insuff)
Cortosyn stimulation test (Cosyntropin)
- ACTH stimulation test
- Tests functional ability of adrenal cortex to synthesize cortisol
Hyponatremia / Hyperkalemia
↑urine Na, BUN/Cr
ECG (hyperkalemia - TWiFP)
Abd CT
- Calcified adrenals- Tb, histoplasmosis
- Atrophic adrenals- Idiopathic autoimmune
Tx of addisons (adrenal insuff)
Glucocorticoid - Hydrocortisone +
Mineralocorticoid - Fludrocortisone
Ample sodium intake
define adrenal crisis
complciation od addisons
Rapid/Severe adrenal collapse
exacerbation of chronic adrenal insufficiency –> Stress precipitant OR Sudden withdrawal/ noncompliance of chronic steroid
Acute hemorrhagic destruction of bilateral adrenal glands
- Waterhouse-Friderichsen syndrome –> Pseudomonas, Meningococcemia septicemia
Anticoagulation
Pregnancy complication
dx of adrenal criss
Hypoglycemia
Hyponatremia
Hyperkalemia
metabolic acidosis
tx adrenal criss
Treat underlying cause
IVF resuscitation - 2L NS followed by D51/2NS
Stress dose hydrocortisone or Dexamethasone
Sx management (ex. vasopressors)
Stressors for adrenal crisis Infection
need to ↑ steroid doses, usually do not
- Trauma
- Surgery
- Vomiting/Diarrhea
- Emotional turmoil
adrenal carcinoma classifications of MEN1
3Ps
Hyperparathyroid (most common)
- Hyperplasia or adenoma
- Symptom’s hypercalcemia
- Elevated ionized serum Ca++ and PTH normal
Pancreatic islets
- Occurs in parallel w/ hyperparathyroid
- Hyperplasia, adenoma, or carcinoma
- Increase production pancreatic islet cell hormones
Pituitary
- Prolactin = prolactinoma (most common)
- Growth hormone = acromegaly
- ACTH = Cushing’s disease
most common P from MEN 1
most common pituitary presentation
Hyperparathyroid (most common P)
Pituitary: Prolactin = prolactinoma (most common)
tx of MEN 1 & MEN 2a
Surgical resection (often multiple required)
- Transphenoidal approach w/ pituitary tumors (often difficult b/c multicentric)
- Parathyroidectomy + thyroidectomy
- Subtotal or total pancreatectomy
Medical management
- Dopamine agonists (bromocriptine) for prolactinoma
- H2 receptor antagonist, PPI for ZES
Dx of MEN 1 and MEN 2a
Hormone/electrolyte assays
- Gastrin level & Glucagon level
- Ca++ and PTH levels
- Hypokalemia, hypochloremia, metabolic acidosis
- Growth hormone
- Prolactin level
- ACTH level
Provocative testing
- Secretin stimulation test w/ gastrin levels
- Short or 72hr fast w/ serum insulin & C-peptide levels
- Dexamethasone suppression test
Radiologic testing –> CT/MRI
- Annual screening basal and post-prandial pancreatic polypeptides
etiology of MEN 2a
most common manifestation?
MTC, Pheo (50%)
Hyperparathyroidism (15-20%) –> Most common manifestation
MTC typically develops in childhood
and >1cm tumor assoc w/ local and distant metastasis
etiology MEN 2b
- MTC, Pheo (>50%), mucosal neuromas, marfanoid body habitus
- Childhood marfanoid morphology and mucosal neuromas most distinctive
•MTC develops earlier and is more aggressive than 2a
si/sx of MEN 2b
Angiofibroma skin findings – on nares
dx MEN 2b
- Genetic testing
- Annual 24-hour urine - metanephrine/VMA
- Serum Ca++ - PTH q 2-3yrs
Tx MEN 2b
Thyroidectomy w/ central LN dissection -> mortality prevented
Pheo = unilateral vs bilateral resection?
Hyperparathyroidism
- Excise 3 ½ w/ remnant in neck
- Full excision w/ remnant implanted back in forearm
location of pituitary
Pea sized gland at base of brain
- below hypothalamus within the sella turcica
- inferior to optic chiasm
- Laterally by c_avernous sinu_s
- Receives blood from ophthalmic veins and cerebral veins
- Cranial nerves travel through (III, IV, V1, V2, VI)
- Internal carotid arteries
function of anterior vs posterior pituitrayr
Anterior Pituitary Gland/Lobe (adenohypophysis)
- Synthesizes and secretes hormones (6)
- Controlled by hormones from the hypothalamus
Posterior Pituitary Gland/Lobe (neurohypophysis)
- Does NOT make hormones
- Stores and secretes hormones (2) synthesized in the hypothalamus
- Controlled by nerve impulses from the hypothalamus
ant pit hormines
post pit hormones
Anterior: GH (FSH, LH, prolactin, TSH, ACTH)
Posterior: ADH (oxytocin, vasopressin)
ADH — ____ hydration
ADH - ADDS hydration
Anterior pit dz
Posterior pit dz
Ant : Dwarfism
Posterior: DI, Psychogenic polydypsia, SIADH
define dwarfism and 2 types
Adult ≤ 4’10”
Disproportionate Dwarfism
- Some average-sized parts of the body and some shorter than average parts of the body
- Achondroplasia (70% of all dwarfism)à Disproportionately short limbs, average sized torso, disproportionately large head
Proportionate Dwarfism
- Short stature condition with arms, legs, trunk and head being in same proportion (relative size to one another) as in an average-sized person
- Pituitary Dwarfism
dx dwarfism
Provocative GH Testing-
- GH is low even with provocation of pituitary gland
↓ IGF-1
tx dwarfism
Recombinant Human Growth Hormone à Somatotropin injections daily