Flashcards
Pituitary adenoma: types, presentation and treatment
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- 1Endocrine system is composed of...A group of glands that maintain body homeostasis
- 2What controls hormone release of endocrine system?Feedback mechanism
- 3How do hormones of endocrine system travel?Via blood
- 4Pituitary adenomaBenign tumor of anterior pituitary cells
- 5Classification of pituitary adenomaFunctional (hormone-producing) or non-functional (silent)
- 6How do nonfunctional pituitary adenomas present?Mass effect
1. Bitemporal hemianopsia (loss of peripheral vision) due to compression of optic chiasm
2. Hypopituitarism due to compression of normal pituitary tissue
3. Headache - 7How do functional pituitary adenomas present?Features based on the type of hormone produced
- 8How does prolactinoma (pituitary adenoma) present?Galactorrhea and amenorrhea (females) or decreased libido and headache (males)
- 9What is the most common type of pituitary adenomaProlactinoma
- 10Treatment of prolactinomaDopamine agonists to suppress prolactin production
Surgery for larger lesions - 11Dopamine agonists used to treat prolactinomaBromocriptine
Cabergoline - 12What inhibits prolactin, and what does prolactin inhibit?DA inhibits
PRL inhibits GnRH release (explaining symptoms in women and men with prolactinoma) - 13How does growth hormone cell pituitary adenoma present?1. Enlarged bones of hands, feet, and jaw
2. Growth of visceral organs leading to dysfunction (cardiac failure)
3. Enlarged tongue - 14What is the most common cause of death in those with growth hormone pituitary adenoma?Cardiac failure (growth of visceral organs leading to dysfunction)
- 15What does GH induce?Liver gluconeogenesis
- 16How do you diagnose growth hormone cell adenoma?Elevated GH and insulin growth factor (IGF-1), along with lack of GH suppression by oral glucose
- 17Where is IGF-1 synthesized?Liver
- 18Treatment of growth hormone pituitary adenoma-Octreotide (somatostatin analogue that suppresses GH release)
-GH receptor antagonist
-Surgery - 19What inhibits GH release?Somatostatin
- 20OctreotideSomatostatin analogue used to treat GH pituitary adenoma
- 21Where is somatostatin normally produced?Hypothalamus, it inhibits GH secretion
- 22Name the types of pituitary adenomas1. Prolactinoma
2. Growth hormone cell adenoma
3. ACTH cell adenoma
4. TSH, LH, FSH producing adenomas are rare (can occur) - 23What does ACTH producing pituitary adenoma cause?Cushing Syndrome
- 24Insufficient production of hormones by the anterior pituitary glandsHypopituitarism
- 25When do symptoms of hypopituitarism arise?Over 75% of pituitary parenchyma is lost
- 26Name causes of hypopituitarism1. Pituitary adenomas (adults) or craniopharyngiomas (children)
2. Sheehan Syndrome
3. Empty sella syndrome - 27How does pituitary adenoma/craniopharyngioma cause hypopituitarismMass effect of pituitary apoplexy (bleeding into an adenoma)
- 28What is sheehan syndrome, how does it cause hypopituitarism, and how does it presentSheehan syndrome is pregnancy related infarction of pituitary gland; gland doubles in size during pregnancy, but blood supply does not increasing, so blood loss during parturition (birthing) precipitates infarction
-Presents as poor lactation, loss of pubic hair (pubic hair is dependent on androgens and androgens arise due to LH, which is produced in the AP), fatigue
"SHE is pregnant" - 29What is empty sella syndrome-Congenital defect or trauma of the sella caused by herniation of the arachnoid and CSF into sella, compressing and destroying pituitary gland
-Pituitary gland absent on imaging
-Could also be caused by trauma - 30What hormones are released from the posterior pituitary gland?Antidiuretic hormone (ADH) and oxytocin (made in the hypothalamus and transported via axons to posterior pituitary for release)
- 31ADH actionActs on distal tubules and collecting ducts of kidney to promote free water retention
- 32Oxytocin actionMediates uterine contraction during labor and release of breast milk (let-down) in lactating mothers (prolactin actually helps produce the milk)
- 33Prolactin vs. oxytocin in breast feedingProlactin: induces milk production
Oxytocin: induces milk let down - 34Central Diabetes InsipidusADH deficiency due to hypothalamic or psoterior pituitary pathology (tumor, trauma, infection, inflammation)
- 35Clinical features of diabetes insipidusBased on loss of free water
1. Polyuria and polydipsia with risk of life-threatening dehydration
2. Hypernatremia and high serum osmolality
3. Low urine osmolality and specific gravity
4. High serum osmolality with low urine osmolality - 36How do you diagnosis central diabetes insipidus?Water deprivation test fails to increase urine osmolality
- 37Treatment for central diabetes insipidusdDAVP (desmopressin ADH analogue)
- 38What receptor is dDAVP (desmopressin) specific for?V2 receptor
- 39Nephrogenic diabetes insipidusImpaired renal response to ADH
- 40How do you distinguish nephrogenic diabetes insipidus from central diabetes insipidus?Nephrogenic: no response to dDAVP
Central: response to dDAVP - 41What causes nephrogenic diabetes insipidus?Inherited mutations or drugs (lithium and demeclocycline)
- 42Syndrome of inappropriate ADH (SIADH) secretionExcessive ADH secretion most often due to ectopic production (small cell carcinoma of the lung)
- 43What are the causes of SIADH secretion?Most common: ectopic production of ADH (small cell carcinoma of the lung)
Others: CNS trauma, pulmonary infection, COPD, drugs (cyclophosphamide) - 44Clinical features of SIADHBased on free water retention
1. Hyponatremia and low serum osmolality
2. Mental status changes and seizures (caused by hyponatremia leading to neuronal swelling and cerebral edema) - 45Treatment of SIADH-Free water restriction or demeclocycline (demeclocycline blocks effect of ADH)
-NS or 3% saline + loop diuretics
-Vaptans (V2 antagonists) - 46Thyroglossal duct cystsCystic dilation of thyroglossal duct remnant
- 47Thyroid development, and how pathology can resultThyroid develops at the base of the tongue and then travels along thyroglossal duct to anterior neck; thyroglossal duct normally involutes, but if it does not, thyroglossal duct cyst can develop
- 48How does thyroglossal duct cyst present/Anterior neck mass
- 49Lingual thyroidPersistence of thyroid tissue at the base of the tongue
- 50How does lingual thyroid present?Mass at base of tongue
- 51Increased level of circulating thyroid hormoneHyperthyroidism
- 52How does hyperthryoidism affect basal metabolic rate and sympathetic nervous system activity? how does it do that?Increases BMR due to increased synthesis of Na-K-ATPase
Increases sympathetic nervous system activity (due to increased expression of Beta-1 adrenergic receptors, increasing heart rate and contractility) - 53Syndrome of inappropriate antidiuretic hormone secretionCharacterized by:
Excessive free water retention
Euvolemic hyponatremia with continued
urinary Na+ excretion
Urine osmolality > serum osmolality - 54SIADH causes include:Ectopic ADH (eg, small cell lung cancer)
CNS disorders/head trauma
Pulmonary disease
Drugs (eg, SSRIs, carbamazepine,
cyclophosphamide) - 55Diabetes insipidusCharacterized by intense thirst and polyuria with inability to concentrate urine due to lack of ADH (central) or failure of response to circulating ADH (nephrogenic).
- 56Central DIPituitary tumor, autoimmune, trauma, surgery, ischemic encephalopathy, idiopathic
ADH - 57Nephrogenic DIHereditary (ADH receptor mutation), 2° to hypercalcemia, hypokalemia, lithium, demeclocycline (ADH antagonist)
Normal orADH levels - 58HypopituitarismUndersecretion of pituitary hormones due to:
Nonsecreting pituitary adenoma, craniopharyngioma
Sheehan syndrome
Empty sella syndrome
Pituitary apoplexy - 59Sheehan syndrome—ischemic infarct of pituitary following postpartum bleeding; pregnancy- induced pituitary growthsusceptibility to hypoperfusion.
Usually presents with failure to
lactate, absent menstruation, cold intolerance
- 60Empty sella syndrome—atrophy or compression of pituitary (which lies in the sella turcica), often idiopathic, common in obese women; associated with idiopathic intracranial hyeprtension
- 61Pituitary apoplexyudden hemorrhage of pituitary gland, often in the presence of an existing pituitary adenoma. Usually presents with sudden onset severe headache, visual impairment
- 62AcromegalyExcess GH in adults. Typically caused by pituitary adenoma.
- 63symplarge tongue with deep furrows,
deep voice, large hands and feet, coarsening of facial features with aging A , frontal bossing, diaphoresis (excessive sweating), impaired glucose tolerance (insulin resistance),
hypertension.
risk of colorectal polyps and cancer. - 64dxserum IGF-1
- 65HypothyroidismCold intolerance,sweating, weight gain (basal metabolic ratecalorigenesis), hyponatremia (free water clearance)
Constipation (GI motility),appetite - 66part 2Hypoactivity, lethargy, fatigue, weakness,
depressed mood,reflexes (delayed/slow relaxing)
Bradycardia, dyspnea on exertion (cardiac output) - 67labsTSH (if 1°)
free T3 and T4 - 68HyperthyroidismHeat intolerance,sweating, weight loss (synthesis of Na+-K+ ATPasebasal metabolic ratecalorigenesis)
Warm, moist skin (due to vasodilation); fine hair; onycholysis ( A ); pretibial myxedema in Graves disease - 69part 2Hyperdefecation/diarrhea (GI motility), appetite
Hyperactivity, restlessness, anxiety, insomnia, fine tremors (due toβ-adrenergic activity), reflexes (brisk)
Tachycardia, palpitations, dyspnea, arrhythmias (eg, atrial fibrillation), chest pain and systolic HTN due tonumber and sensitivity of β-adrenergic receptors - 70labsTSH (if 1°)
free T3 and T4 - 71Hashimoto thyroiditisMost common cause of hypothyroidism in iodine-sufficient regions;
an autoimmune disorder with antithyroid peroxidase (antimicrosomal) and antithyroglobulin antibodies.
Associated with HLA-DR3, HLA-DR5 - 72sympnontender thyroid.
- 73Postpartum thyroiditisSelf-limited thyroiditis arising up to 1 year after delivery. Presents as transient hyperthyroidism, hypothyroidism, or hyperthyroidism followed by hypothyroidism.
Thyroid usually painless and normal in size. - 74Congenital hypothyroidism (cretinism)Severe fetal hypothyroidism due to antibody-mediated maternal hypothyroidism, thyroid dysgenesis
- 75Subacute granulomatous thyroiditis (de Quervain)Self-limited disease often following a flu-like illness (eg, viral infection).
Findings:ESR, jaw pain, very tender thyroid. - 76Riedel thyroiditisThyroid replaced by fibrous tissue and inflammatory infiltrate D .
Fibrosis may extend to local structures (eg, trachea, esophagus), mimicking anaplastic carcinoma - 77sympFindings: fixed, hard (rock-like), painless goiter.
- 78Other causesIodine deficiency (with goiter E ),
goitrogens (eg, amiodarone, lithium),
Wolff-Chaikoff effect (thyroid gland downregulation in response toiodide). - 79Graves diseaseMost common cause of hyperthyroidism. Thyroid-stimulating immunoglobulin (IgG, can cause transient neonatal hyperthyroidism;
type II hypersensitivity) stimulates TSH receptors on thyroid (hyperthyroidism, diffuse goiter), - 80Thyroid stormUncommon but serious complication that occurs when hyperthyroidism is incompletely treated/ untreated and then significantly worsens in the setting of acute stress such as infection, trauma, surgery.
- 81Jod-Basedow phenomenonIodine-induced hyperthyroidism.
Occurs when a patient with iodine deficiency and partially autonomous thyroid tissue (eg, autonomous nodule) is made iodine replete.
Can happen after iodine IV contrast or amiodarone use.
Opposite to Wolff-Chaikoff effect. - 82Papillary carcinomaMost common thyroid cancer, excellent prognosis.
Empty-appearing nuclei with central clearing (“Orphan Annie” eyes) A , psamMoma bodies,
Prevalent, Palpable lymph nodes. - 83Medullary carcinomaFrom parafollicular “C cells”;
produces calcitonin, sheets of polygonal cells in an amyloid stroma B (stains with Congo red). - 84HypoparathyroidismDue to injury to parathyroid glands or their blood supply (usually during surgery), autoimmune destruction, or DiGeorge syndrome.
- 85symptetany,
hypocalcemia, hyperphosphatemia.
Chvostek sign—tapping of facial nerve (tap the Cheek)contraction of facial muscles.
Trousseau sign—occlusion of brachial artery with BP cuff (cuff the Triceps)carpal spasm. - 86Primary hyperparathyroidismUsually due to parathyroid adenoma or hyperplasia.
- 87sympHypercalcemia,
hypercalciuria (renal stones),
polyuria (thrones),
May present with bone pain,
weakness, constipation (“groans”), abdominal/flank pain (kidney stones,
acute pancreatitis),
neuropsychiatric disturbances (“psychiatric overtones”). - 88Osteitis fibrosa cysticacystic bone spaces filled with brown fibrous tissue A (“brown tumor” consisting of osteoclasts and deposited hemosiderin from hemorrhages; causes
bone pain).
Due toPTH - 89Secondary hyperparathyroidism2° hyperplasia due toCa2+ absorption 3−
and/orPO4 ,
most often in chronic kidney disease (causes hypovitaminosis D and hyperphosphatemiaCa2+). - 90sympHypocalcemia,
hyperphosphatemia in chronic kidney disease - 91Diabetes mellitus AcUte mAniFestAtionsPolydipsia,
polyuria,
polyphagia,
weight loss, DKA (type 1),
hyperosmolar hyperglycemic state (type 2). - 92Type 1 DMAutoimmune T-cell–mediated destruction of β cells (eg, due to presence of glutamic acid decarboxylase antibodies)
< 30 yr
Yes, HLA-DR4 and -DR3 (4 – 3 = type 1) - 93Type 2 DMresistance to insulin, progressive pancreatic β-cell failure
> 40 yr - 94Diabetic ketoacidosisInsulin absent, ketones present (complications).
Insulin noncompliance orrequirements fromstress (eg, infection)excess fat breakdown andketogenesis fromfree fatty acidsketone bodies (β-hydroxybutyrate > acetoacetate). - 95sympDKA is Deadly:
Delirium/psychosis,
Kussmaul respirations (rapid, deep breathing),
Abdominal pain/nausea/vomiting,
Dehydration.
Fruity breath odor (due to exhaled acetone). - 96labsHyperglycemia,H ,HCO3
- 97Hyperosmolar hyperglycemic stateInsulin present, ketones absent.
- 98sympThirst, polyuria, lethargy, focal neurologic deficits, seizures
- 99Cushing syndrome Exogenous corticosteroidsACTHbilateral adrenal atrophy. Most common cause.
Primary adrenal adenoma, hyperplasia, or carcinomaACTHatrophy of uninvolved adrenal gland.
- 100part 2ACTH-secreting pituitary adenoma (Cushing disease); paraneoplastic ACTH secretion (eg, small cell lung cancer, bronchial carcinoids)bilateral adrenal hyperplasia. Cushing disease is responsible for the majority of endogenous cases of Cushing syndrome.
- 101sympCUSHING Syndrome:
Cholesterol,
Urinary free cortisol,
Skin changes (thinning, striae A ), Hypertension,
Immunosuppression,
Neoplasm (a cause, not a finding),
Growth retardation (in children),
Sugar (hyperglycemia, insulin resistance). - 102part 2Also, amenorrhea, moon facies B , buffalo hump, osteoporosis,weight (truncal obesity), hirsutism.
- 103dxScreening tests include:
free cortisol on 24-hr urinalysis,
late night salivary cortisol, and no suppression with overnight low-dose dexamethasone test. - 104Adrenal insufficiencyInability of adrenal glands to generate enough glucocorticoids +/− mineralocorticoids for the body’s needs.
- 105sympweakness, fatigue, orthostatic hypotension, muscle aches, weight loss, GI disturbances, sugar and/or salt cravings.
- 106Primary adrenal insufficiencygland functioncortisol,aldosterone hypotension (hyponatremic volume contraction),
hyperkalemia,
metabolic acidosis,
skin/mucosal hyperpigmentation
A (melanin synthesis due toMSH, a byproduct of ACTH production from POMC). - 107typesAcute—sudden onset (eg, due to massive
hemorrhage). May present with shock in
acute adrenal crisis.
Chronic—Addison disease - 108sympPrimary Pigments the skin/mucosa. Associated with autoimmune polyglandular
syndromes.
Waterhouse-Friderichsen syndrome—acute 1° adrenal insufficiency due to adrenal hemorrhage associated with septicemia (usually Neisseria meningitidis), DIC, endotoxic shock. - 109Secondary adrenal insufficiencySeen withpituitary ACTH production. No skin/mucosal hyperpigmentation (ACTH is not elevated), no hyperkalemia (aldosterone
- 110HyperaldosteronismIncreased secretion of aldosterone from adrenal gland.
- 111symhypertension, +or normal K ,
metabolic alkalosis.
1° hyperaldosteronism does not directly cause edema due to aldosterone escape mechanism - 112Primary hyperaldosteronismSeen with adrenal adenoma (Conn syndrome) or bilateral adrenal hyperplasia.
aldosterone, renin. - 113Secondary hyperaldosteronismSeen in patients with renovascular hypertension,
juxtaglomerular cell tumors (renin-producing),
and edema (eg, cirrhosis, heart failure, nephrotic syndrome). - 114PheochromocytomaMost common tumor of the adrenal medulla in adults A .
Derived from chromaffin cells (arise from neural crest).
rule of 10 - 115Rule of 10’s:10% malignant
10% bilateral
10% extra-adrenal (eg, bladder wall, organ of
Zuckerkandl)
10% calcify
10% kids - 116sympEpisodic hyperadrenergic symptoms (5 P’s): Pressure (BP)
Pain (headache)
Perspiration
Palpitations (tachycardia) Pallor - 117txPhenoxybenzamine for pheochromocytoma.
- 118Multiple endocrine neoplasias MEN 1Pituitary tumors (prolactin or GH)
Pancreatic endocrine tumors—Zollinger-
Ellison syndrome, insulinomas, VIPomas,
glucagonomas (rare)
Parathyroid adenomas
Associated with mutation of MEN1 - 119MEN 2AParathyroid hyperplasia
Pheochromocytoma (secretes catecholamines)
Associated with mutation in RET (codes for
receptor tyrosine kinase) - 120MEN 2BPheochromocytoma
Associated with marfanoid habitus; mutation in
RET gene - 121MEN 1 = 3 P’s: Pituitary, Parathyroid, and Pancreas MEN 2A = 2 P’s: Parathyroid and Pheochromocytoma MEN 2B = 1 P: Pheochromocytoma.
- 122Adrenal hemorrhage, hypotension, DICWaterhouse-Friderichsen syndrome (meningococcemia)
- 123Skin hyperpigmentation, hypotension, fatigue1° adrenocortical insufficiency → ↑ ACTH, ↑ α-MSH (eg, Addison disease)
- 124Cutaneous flushing, diarrhea, bronchospasmCarcinoid syndrome (right-sided cardiac valvular lesions, ↑ 5-HIAA)
- 125Cold intolerance, weight gain, brittle hairHypothyroidism
- 126Cutaneous/dermal edema due to deposition of mucopolysaccharides in connective tissueMyxedema (caused by hypothyroidism, Graves disease [pretibial])
- 127Facial muscle spasm upon tappingChvostek sign (hypocalcemia)
- 128No lactation postpartum, absent menstruation, cold intoleranceSheehan syndrome (postpartum hemorrhage leading to pituitary infarction)
- 129Deep, labored breathing/hyperventilationDiabetic ketoacidosis (Kussmaul respirations)
- 130Pancreatic, pituitary, parathyroid tumorsMEN 1 (autosomal dominant)
- 131Thyroid tumors, pheochromocytoma, ganglioneuromatosis, Marfanoid habitusMEN 2B (autosomal dominant RET mutation)
- 132Thyroid and parathyroid tumors, pheochromocytomaMEN 2A (autosomal dominant RET mutation)
- 133Hypertension hypokalemia metabolic alkalosis1° hyperaldosteronism (Conn syndrome)
- 134Enlarged thyroid cells with ground-glass nuclei with central clearing“Orphan Annie” eyes nuclei (papillary carcinoma of the thyroid)
- 135ProlactinomaCabergoline/bromocriptine (dopamine agonists)
- 136Diabetes insipidusDesmopressin (central); hydrochlorothiazide, indomethacin, amiloride (nephrogenic)
- 137SIADHFluid restriction,
IV hypertonic saline,
conivaptan/tolvaptan,
demeclocycline - 138Diabetes mellitus type 1Dietary intervention (low carbohydrate) + insulin replacement
- 139Diabetes mellitus type 2Dietary intervention, oral hypoglycemics, and insulin (if refractory)
- 140Carcinoid syndromeOctreotide
- 141Congenital adrenal hyperplasia, hypotension21-hydroxylase deficiency
- 142HypopituitarismPituitary adenoma (usually benign tumor)
- 143CretinismIodine deficit/congenital hypothyroidism
- 144Thyroid cancerPapillary carcinoma (childhood irradiation)
- 145HypoparathyroidismAccidental excision during thyroidectomy
- 1461° hyperparathyroidismAdenomas, hyperplasia, carcinoma
- 1472° hyperparathyroidismHypocalcemia of chronic kidney disease
- 1481° hyperaldosteronismAdrenal hyperplasia or adenoma
- 149Tumor of the adrenal medulla (kids)Neuroblastoma (malignant)
- 150Tumor of the adrenal medulla (adults)Pheochromocytoma (usually benign)
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