Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
100 Cards in this Set
- Front
- Back
A hypothyroid pt is currently being treated w/ synthroid. The patient starts HRT. What should be done?
|
Increase the dose of synthroid.
Estrogen increases TBG |
|
What are causes of primary hypothyroidism?
|
problems w/ the thyroid gland
Hashimoto's thyroiditis, idoine deficiency, iatrogenic |
|
What are causes of secondary hypothyroidism?
|
pituitary does not secrete enough TSH
radiation, surgery, pituitary tumor |
|
What is the cause of tertiary hypothyroidism?
|
hypothalamus does not secrete enough TRH
|
|
A pt comes in with normal T3/T4 and elevated TSH. What is the name of the condition and tx?
|
subclinical hypothyroidism
tx with thyroid hromone only is patient develops Sx of hjypothyroidism, goiter, or dyslipidemia |
|
A patient with a severe viral illness has low T3. The normal T3/TSH ratio is preserved. What is the condition and tx?
|
sick euthyroid syndrome
don't treat, it will return to normal after illness clears |
|
A pt present with weight gain, decreased appetite, fatugue, cold intolerance, dry skin, brittle hair, bradycardia, constipation, depression, anemia, carpal tunnel syndrome and nonpitting edema, menstrual cycle abnormalities, osteoporosis, and poor lipid profile. What is the likely cause? What is the dirrect cause of the menstrual cycle abnormalities?
|
hypothyroidism
hypothyroidism --> elevated TRH --> elevated prolactin |
|
A pt comes in with dyslipidemia, fatigue, and constipation. What hormone test would be appropriate?
|
TSH
|
|
A pt comes in low w/ T3/T4, high TSH, high TRH?
|
primary hypothyroidism
|
|
A pt comes in w/ low T3/T4, low TSH, high TRH?
|
secondary hypothyroidism
|
|
A pt comes in w/ low T3/T4, low TSH, low TRH?
|
tertiary hypothyroidism
|
|
What antibodies are present in hypothyroidism?
|
anti-microsomal, anti-thyroid peroxidase, and anti-thyroglobulin antibodies in Hashimoto's
|
|
What is the primary treatment for hypothyroidism?
|
levothyroxine
|
|
What are causes of primary hyperthyroidism?
|
thyroid gland over-secretes
toxic nodule: nodule that has become independent of the pituitary and begins secreting excess thyroid hormone Graves disease: auto autibodies (thyroid stimulating immunoglobulins) bind to the TSH receptors and lead their activation Associated autoimmune diseases- vitiligo, pernicious anemia Amiodarone toxicity |
|
What is the cause of secondary/tertiary hyperthyroidism?
|
pituitary/hypothalamus hyperstimulates thyroid gland
pituitary adenoma/ hyperplasia |
|
What are ectopic site of hormone production?
|
Stuma ovarii: ovarian teratoma that contains thyroidism tissue
|
|
A patient comes in with normal T3/T4 levels w/ decreased TSH. What is the treatment?
|
Subclinical hyperthyroidism
treat as if primary hyperthyroidism t decrease cardiac disease |
|
A patient comes in with heat intolerance, weight loss, increased appetite, tachycardia, a. fib, tremor, nervousness, diaphoresis, diarrhea. What is the condition? The pt also has exopthalmos and pretibial myxedema. What is the specific cause?
|
hyperthyroidism
Graves disease with auto antibodies binding to TSH receptor |
|
A pt comes in w/ high T3/T4 and low TSH? What is the diagnosis?
|
primary hyperthyroidism
|
|
A pt comes in w/ high T3/T4 and high TSH and low TSH? What is the diagnosis?
|
secondary hyperthyroidism
|
|
A pt comes in w/ high T3/T4 and high TRH and TSH?
|
tertiary hypothyroidism
|
|
What is the purpose of radioactive iodine uptake?
|
RAIU correlates to hormone synthesis
|
|
What are the treatments of hyperthyroidism?
|
beta-blockers (symptomatic relief), methimazole (decrease thyroid hormone synthesis)
propylthiouracil (decrease synthesis and peripheral conversion of T4 to T3) curative w/ radioactive iodine or thyroidectomy |
|
What are common causes of thyroiditis?
|
chronic lympocytic --> Hashimoto's thyroiditis
subacute granulomatous --> de Quervain's thyoiditis (painful and tender) subacute lymphocytic (painless) fibrous --> Riedel's thyroiditis (firm fibrous gland) other: radiation, amiodarone toxicity, postpartum thyroiditis |
|
A pt comes in with inflammation of the thyroid gland that intially causes high T3/T4 levels but transitions to low T3/T4. What is the etiology?
|
thyroiditis
|
|
What is the main treatments for thyroiditis?
|
NSAIDS!
steroids, agents to treat hypo/hyperthyroidism |
|
What leads to you suspect a thyroid nodule is malignant?
|
younger pts, history of radiotherapy to neck or neck as child, nodule grows rapidly, growth can't be suprresed by levothyoxine, nodule appears cold on radioactive scan, solid nodule on ultrasound
|
|
How do you diagnose thyroid nodules?
|
fine needle aspiration, TSh followed by serum thyroid hormone and antibody levels, I131 radionuclide scan w/ ultrasound
|
|
What is the treatment of thyroid nodules?
|
Surgery if malignant, conservative management and observation of nodule if warm, biopsy negative, and H&P is nonsuggestive
|
|
A pt presents with slow growing and localized thyroid carcinoma? After a few months it spreads via regional lymph nodes. What is the prognosis?
|
papillary: best prognosis of thyroid cancers and less likely to recur
|
|
A pt present with a thyroid cancer depends on TSH and spreads hematogenously to bone, brain, and lung? Dx?
|
Follicular carcinoma
|
|
A pt presents with a thyroid cancer and elevated levels of calcitonin. Men II syndrome. Dx?
|
Medullary carcinoma
|
|
What is the tx for anaplastic carcinoma of the thyroid?
|
go to God. I'm so sorry. I always loved you.
|
|
What is the Tx for thyroid cancer?
|
• Surgery in most cases except for anaplastic CA
• Radioactive iodine ablation and chemotherapy as adjuvant |
|
How does parathyroid hormone increase calcium concentration?
|
o Stimulates calcium release from bone mineral compartment
o Binds osteoblasts and indirectly effects osteoclasts to cause bone resorption o Increases calcium re-absorption in kidney |
|
What is the net effect of calcitonin on Ca and phosphate?
|
Both decrease
|
|
What is the net effect of vit D on Ca and phosphate?
|
Both increase
|
|
What are the causes of hyperparathyroidism?
|
parathyroid adenoma (single gland)
parathyroid hyperplasia (all 4 glands enlarged), malignancy |
|
A pt comes in with: Renal stones, polyuria, Bone pains, fractures due to Osteitis fibrosa cystic (“brown tumor”), Constipation, abdominal pain, PUD, N/V, Depression, memory deficits, poor concentration, anorexia, anxiety. What is the dx technique and treatment?
|
hyperparathyroidism
o Inappropriately elevated PTH with normal or elevated serum calcium level o ↓PO4, ↑Alkaline Phosphate, ↑urine cAMP, ↑Cl- (effects of excess PTH) o Urine analysis showing hypercalciuria o US and CT to look for adenomas and bone changes o Parathyroidectomy o IV NS for symptomatic hypercalcemia o Loop diuretics to enhance calcium excretion |
|
A pt has chronic RF and hyperparathyroidism. What is the dx? What could also cause their condition? What is the treatment?
|
Secondary hyperparathyroidism
vitamin D deficiency and renal hypercalciuria Treatment: calcitriol, oral calcium supplements, and phosphorus restriction in CKD |
|
A pt tests high for Parathyroid Hormone-related Peptide (PTHrP). What 2 cancers are possible? The pt presents with renal stones, bone weakness, GI problems, and memory deficits. What is their likely level of PTH?
|
Squamous cell carcinoma of lung & Renal cell carcinoma
low |
|
A pt comes in w/ low PTH levels. What are possible etiologies?
|
Hypoparathyroidism
o Most commonly iatrogenic, post-thyroidectomy or post-parathyroidectomy o DiGeorge syndrome o Rarely, polyglandular failure (autoantibodies to adrenal and parathyroid tissue) |
|
A pt comes in latent tetany. What 2 signs did you look for? They also display overt tetany, cardiac arrhythmias, rickets, and brittle teeth/skin. What hormone should you test?
|
Positive Chvostek’s sign: tapping anterior to the ear on the facial nerve elicits facial muscle contraction
Positive Trousseau’s sign: carpal tunnel spam is induced by inflated blood pressure cuff on arm for longer than 3 minutes PTH (hypo) |
|
↓Calcium, ↑Phosphate, ↓PTH, ↓urine cAMP. What is the treatment?
|
replace serum calcium orally or IV with vitamin D supplementation
|
|
A pt comes in w/ Tetany, Chvostek’s sign, Trousseau sign, confusion, weakness, prolonged QT, seizures, cataracts, bronchospasm. If their knuckles/facies are abnormal, what is their likely etiology? What hormone will have no effect on their condition despite normally helping in a similar condition w/ low Ca and high PO4?
|
Type 1a pseudohypoparathyroidism
PTH |
|
A pt has an excess in CRH. What type of facies is expected?
|
moon facies. Cushing's
|
|
A pt comes in with poorly developed genitals and anosmia. What is the likely dx?
|
Kallman syndrome: failure of GnRH neurons migration & olfactory bulbs formation
|
|
A pt comes in w/ o Enlarging sinuses, prominent frontal supraorbital ridges
o Enlarged jaw and tongue, wide spacing of teeth, deep voice o Cardiomegaly, hypertension o Thickened skin with enlarged sweat glands o Increasing hand and foot sizes o Glucose intolerance or diabetes What is the dx techniques and prognosis? |
• Diagnosis
o Serum levels of IGF-1 for initial screening o Lack of suppression of GH after injection of glucose o Death from cardiovascular disease, cerebrovascular disease, respiratory disease and cancer is doubled in these patients |
|
A child displays short stature and failure to thrive. What hormone should be tested? What is a mutation related to a deficiency in that hormone?
|
GH
GH receptor mutation = Laron dwarfism |
|
What are signs of GH deficiency in adults?
|
decreased strength, energy, and bone mass
|
|
If connection between hypothalamus and pituitary gland is lost, the only hormone that will not be deficient is __________. What is that hormone inhibited by?
|
prolactin
dopamine |
|
Why breast feeding provide slight protection against pregnancy?
|
PRL inhibits GnRH
|
|
In primary hypothyroidism, what levels of PRL is expected?
|
normal to high.
TSH stimulates PRL |
|
Pt presents with weight gain, galactorrhea, secondary amenorrhea, HA, and papilledema. How would her Sx be different if she was a male? What are other possible sx as the disease progresses?
|
prolactinoma
hypogonadism, gynecomastia, impotence compression of CN --> oculomotor palsies bitemproal hemianopsia from crossing fibers of optic chiasm |
|
A pt experiences a constellation of progressive Sx: fatigue, weight loss, flabby muscles, loss of axillary and pubic hair, breast atrophy, hypotension, amenorrhea, wrinkling of skin. What are possible causes?
|
o Neoplasm (Craniopharyngioma = benign tumor of Rathke’s pouch… presents with triad of DI, bitemporal hemianopia, HA)
o Infarction (Sheehan’s syndrome = postpartum necrosis of pituitary) o Aneurysm o Hypothalamic disease o Head trauma o Irradiation |
|
What is the purpose, mechanism, and trigger of ADH?
|
• Regulates body’s retention of water
• Increases permeability of renal collecting tubules to water via aquaporin channels • ADH release stimulated by dehydration of hypovolemia (ie trauma with blood loss) |
|
A pt comes in w/ lethargy, confusion, HA, and convulsions. You run some tests and discover the following: Hyponatremia (Na <135), Plasma osmolality <270, and extremely concentrated urine.
What is an eventual complication if you do not treat? What is the treatment? What are causes? |
coma
o Treat underlying cause o Fluid restriction of 500-1000 ml/day o If sodium is critically low (<125 and symptomatic), treat with hypertonic saline Watch out for central pontine myelinolysis o Vasopressin receptor antagonist (Tolvaptan, Conivaptan) o Demeclocycline: inhibits effect of ADH on renal tubules o Small cell carcinoma of the lung that secretes ADH (paraneoplastic syndrome) Less commonly, pancreatic, prostate, bladder, lymphoma, leukemia o CNS disorders or trauma o Drugs: SSRI’s, carbamazepine, desmopressin o Others: pulmonary disease (TB, sarcoidosis), major surgery, |
|
A pt comes in with a head injury. They notice they are constantly thirsty, urinate more often, and excrete dilute urine. What do you suspect? What would you test for to confirm your diagnosis?
|
neurogenic DI
o Initial labs: hypernatremia, high plasma osmolality, low urine osmolality o Water deprivation test: urine osmolality does not increase with dehydration o Response to IV ADH kidney function restored (neurogenic) |
|
A pt taking lithium and demeclocycline comes in with chronic thirst, polydipsia, and dilute urine. Initial labs confirm hypernatremia, high plsma osmolaity, and low urine osmolality. What 2 tests could you also perform? What would be the treatment? What would the tx be if the etiology was destruction of pituitary?
|
Water deprivation test
Response to IV ADH thiazide diuretics desmopression |
|
What cells make glucagon, insulin, and somatostatin?
|
alpha, beta, and delta islet cells
|
|
What hormone lowers blood glucose levels by increasing glucose uptake for glycogen synthesis and increase fatty acid synthesis and decrease proteolysis/lipolysis?
|
insulin
|
|
What hormones increase blood glucose levels?
|
glucagon, growth hormone, hydrocortisone, and epinephrine
|
|
What hormone stimulates glycogenolysis, ketogenesis, and gluconeogenesis to increase blood glucose levels?
|
glucagon
|
|
What hormone is secreted when insulin is secreted and acts to block glucagon release?
|
amylin
|
|
A pt comes in with glucose levels below 50 mg/dL. What organ is most affected? What happens to the levels of insulin, glucagon, epinephrine, and cortisol?
|
decrease insulin, increase the others
|
|
How would you advise a diabetic pt afraid of hypoglycemia about risk factors?
|
risk factors: previous episodes, dosing errors, dietary inconsistency
|
|
A diabetic pt comes in diaphoresis, tremors, increased BP, tachycardia, palpitations, irritability, drowsiness, HA, confusion, and convulsions. The pt smells like alcohol and looks malnourished. What test do you run and what tx do you give?
|
serum glucose, serum insulin, C-peptide (insulinoma = high, factitious hypoglycemia = low), sulfonylurea levels, anti-insulin Ab (factitious hypoglycemia)
give thiamine, then oral (or IV) glucose |
|
What are the 2 defects in Type 2 DM?
|
insulin resistance and impaired insulin secretion
|
|
A pregnant woman was screened with an oral glucose tolerance test and was positive for gestational DM. What should the pt be advised about concerning risks?
|
increased risk of type 2 DM for mother and baby
baby: hypoglycemia, macrosomia, cardiac defects, fetal respiratory distress, dystocia |
|
A pt displays polyuria, polyphagia, polydipsia, and weight loss. The pt also has increased infections and poor wound healing. what test should be performed on the pt?
|
fasting glucose and oral glucose tolerance test or random glucose (Sx are present)
|
|
A lean pt with sudden onset polyuria, polyphagia, polydipsia, and weight loss, and no family hx of any similar disorder comes into the office. What do you expect with future ketosis episodes, presence of HLA-DR3/DR4, and what tests should you perform?
|
ketosis prone, associated w/ HLA-DR3/DR4
test islet cell antibodies, glutamic acid decarboxylase antibodies, and insulin antibodies |
|
What is metabolic syndrome?
|
central obesity, dyslipidemia (TG>150, HDL-C <40), hypertension >130/85, impaired fasting glucose (>110)
|
|
What is the long term tx monitor of diabetes? What is the target?
|
Hb A1C<6.5 or 7
|
|
What is the tx of diabetes?
|
D&E, oral medication (metformin), insulin for long standing DM Type 2
|
|
What is the Somogyi effect and Dawn phenomenon? How do you differentiate them?
|
They cause early morning hyperglycemia.
Somogyi = rebound response to nocturnal hypoglycemia Dawn pheonemon: increase in nocturnal secretion of GH 3AM glucose levels are high in Dawn and low in Somogyi |
|
A type I DM pt comes in with N/V, abdeominal pain, decreased level of conscoiusness, deep rapid breathing (Kussmaul's respirations), fruit acetone breath, and dehydration. The pt had a previous viral illness and has been noncompliant with his insulin shots. What are the lab findings and tx?
|
hyperglycemia, anion gap metabolic acidosis, ketonemia/ketonuria, total body potassium (osmotic diuresis)
tx: fluid resuscitation & IV insulin, K replacement, HCO3 (for severe acidemia, controversial) |
|
A type II DM pt presents with dehydration, abnormal sensorium, and seizures. The pt lacks fruit acetone breath. What are the lab findings and tx?
|
Hyperglycemic hyperosmolar nonketotic syndrome
severe hyperglycemia, lack of significant ketosis due to B-cell function vigours fluid resuscitation, insulin |
|
A pt wants to know the microvascular complications of DM?
|
Eye: retinopathy, cataracts, glaucoma, bindness
Kidney: nephropathy, kidney failure Nerves: peripheral neuropathy, cranial nerve neuropathy, autonomic neuropathy |
|
What are the macrovascular complication of DM?
|
risk factors: family history, HTN, dyslipidemia, smoking, obesity, physical inactivity, hyperglycemia
Heart: acute coronary syndrome, CHF brain: TIA, CVA, cognitive impairment extremities: peripheral vascular disease --> ulcers, gangrene, amputation |
|
What is the purpose of aldosterone? What produces it? What stimulates it?
|
Na reabsorption & K/H secretion via collecting tubules --> increased BP, volume expansion, hypokalemia, and metabolic acidosis
stimulated by RAAS released by zona glomerulosa |
|
What produces cortisol? What stimulates cortisol? What does cortisol do? Why does Cushing's cause hyperpigmentation?
|
zona fasciculata
regulates stress response, increases bp, decreases immune sstem, decreases bone formation stimulated by ACTH POMC is precursor to ACTH and will also produce MSH |
|
What does the zona reticularis produce?
|
sex hormones
|
|
What does the adrenal medulla produce? What do these hormones do? What are their breakdown products?
|
EPI, NE (Catecholamines)
fight or flight metanephrines, AMA |
|
What are the causes of adrenal excess?
|
exogenous steroid use (MCC), pituitary adenoma/hyperplasia = Cushing's disease (increased cortisol and ACTH), adrenal neoplasm/hyperplasia (increased Cortisol, decreased ACTH), ectopic production of ACTH from small cell ung CA (increased cortisol, greatly increased ACTH)
|
|
A pt comes in w/ central obesity, moon facies, buffalo hump, purple abdominal striae, mild HTN due to Na retention, impaired glucose tolerance, acne, hirsuitism/oligomenorrhea (women), impotence (men), osteoporosis, psychiatric disturbances, hyperpigmentation. What tests should you run? What is the treatment?
|
Overnight low dose dexamethasone suppression test or 24 free urine cortisol levels [Cushing's syndrome = unable to suppress cortisol levels or elevated 24 hour levels]
ACTH [adrenal Cushing's will have low ACTH levels] High dose dexamethasone suppression test [pituitary Cushing's =high dose will suppress, ectopic = high dose will not suppress] Petrosal sinus catheterization [pituitary Cushing's = high petrosal ACTH, ectopic = regular levels of petrosal ACTH] CT adrenals and MRI pituitary Iatrogenic: taper steroids pituitary: surgery, irridation, adrenalectomy w/ steroid replacement adrenal: surgical resection w/ post-op cortisol replacement |
|
What are causes of primary hyperaldosteronism?
|
Conn's syndrome (aldosterone secreting tumor)
Bilateral adrenal hyperplasia |
|
A pt comes in w/ HTN, muscle cramps, HA, and mental status changes. Lab confirm hypernatremia/hypokalemia. what do you expect for pH, aldosterone, and renin levels? What is the tx?
|
primary hyperaldosteronism
metabolic acidosis, Aldosterone high, and renin low surgery for adenoma, spironolactone for bilateral adrenal hyperplasia |
|
What is a pheochromocytoma? What are the signs/Sx?
|
catecholamine secreting tumor of the adrenal medulla
fight/flight: HA, palpitations, sweating, tremor, feeling of impending doom vasoconstriction: severe episodic HTN and facial pallor |
|
What are the rule of 10?
|
bilateral (MEN type II)
malignant not adrenal gland familial |
|
fight/flight: HA, palpitations, sweating, tremor, feeling of impending doom
vasoconstriction: severe episodic HTN and facial pallor What is the dx and tx? |
pheochromocytoma
elevated 24 hour urine excretion of metanephrine and VMA CT/MRI for adrenal imaging tx: surgical resection, alpha and beta blocker (have to be together) |
|
What are causes of primary adrenal insufficiency? What is the level and response to ACTH?
|
Addison's disease, autoimmune/idiopathic, TB, Waterhouse-Friederichsen syndrome, infectious disease (cryptococcus, toxoplasmosis, CMV), iatrogenic (bilateral adrenalectomy), metastatic disease
high level, low response |
|
What are the causes of secondary adrenal insufficiency? What is the level and response to ACTH?
|
pituitary glands do not produce ACTH
Long term steroid use (suppress adrenal-pituitary axis and ACTH release, especially during stress) hypopituitarism low, normal |
|
What is tertiary adrenal insufficiency? What is the level and response to ACTH?
|
Hypothalamus does not produce CRH
decreased ACTH, normal response |
|
A pt present w/ fatigue, weakness, low bp, hypoglycemia, orthostatic hypotension, hyperkalemia, hypoglycemia, skin hyperpigmentation, feer, vomitting, decreased sensorium, abdominal tenderness, and vascular collapse. How do you diagnose? What is the tx?
|
Plasma cortisol levels [increased ACTH, decreased aldosterone, and increased renin = primary AI, decreased ACTH, normal aldosterone/renin - secondary AI)
cosyntropic test: infusion of ACTH w/ measurement of plasma cortisol at end of infusion [primary:fail to raise cortisol sufficiency, secondary: delayed response to ACTH] Labs: hyponatremia, hyperkalemia, metabolic acidosis ECG: high peaked T-waves may be present due to elevated K CT/MRI Tx: glucocorticoid/mineralcoticoid replacement fluid resuscitation |
|
What are the causes, presentation, and diagnostic techniques of congenital adrenal hyperplasia?
|
21-hydroxylase deficiency: low cortisol and mineral corticoids, high sex hormones
11-hydroxylase deficiency: low cortisol, high mineralocorticoids, high 17-hydroxylase deficiency: low cortisol, high mineralocorticoids, low sex hormones Dx: serum horomone levels, imaging |
|
What is the best imaging for the pituitary gland? What is the area that does not enhance on MRI?
|
MRI
adenoma |
|
What is the effect of adrenal adenoma?
|
increased androgens and adrenal virilism
|
|
What is the tumor of the medulla? What types of cells does the medulla contain?
|
pheiochromocytoma, cells of neural crest cell origin
|
|
What scan is used to image palpable nodule of the thyroid? What does it directly measure?
|
scintigraphy
iodine uptake = activity and thyroid function hot= benign, cold = malignant |
|
What is the scan for parathyroid adenoma? What does a positive scan look like?
|
Sestambi parathyroid scan
increased uptake and prolonged activity in hyperactive gland causing hyperparathyroidism |