• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/97

Click to flip

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;

97 Cards in this Set

  • Front
  • Back
MCC of Cushing's syndrome
exogenous (iatrogen) steroid use (decreased ACTH)
Cushing's disease
70% of endogenous causes; due to ACTH secretion from pituitary adenoma (increased ACTH)
ectopic ACTH as cause of Cushing's
15%; nonpituitary tissue making ACTH ex. small cell lung cancer, bronchial carcinoids (increased ACTH)
adrenal cause of Cushing's
15%; adenoma, carcinoma, nodular adrenal hyperplasia (decreased ACTH)
dexamethasone suppression test - healthy person
decreased cortisol level after low dose
dexamethosone suppression test - ACTH producing pituitary tumor (Cushing's disease)
increased cortisol after low dose; decreased cortisol after high dose
dexamethosone suppression test - ectopic ACTH producing tumor
increased cortisol after both low and high doses
dexamethasone suppression test - cortisol-producing tumor
increased cortisol after low and high dose
clinical findings in Cushing's syndrome
HTN, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia, skin changes, osteoporosis, amenorrhea, immune suppression
primary hyperaldosteronism (Conn's syndrome)
unilateral/bilateral aldosterone-secreting tumor
findings in Conn's syndrome
hypertension (Na+ and H20 retention), hypokalemia, metabolic alkalosis (H+, K+ secretion), low plasma renin
treatment of Conn's syndrome
(1) surgery to remove tumor (2) spirinolactone - K+ sparing diuretic that is an aldosterone antagonist
secondary hyperaldosteronism
kidney perception of low IV volume results in overactive renin-angiotensin system; associated with high plasma renin
causes of secondary hyperaldosteronism
CHF, renal artery stenosis, chronic renal failure, cirrhosis, nephrotic syndrome
Addison's disease
chronic primary adrenal insufficiency due to adrenal atrophy or destruction by disease resulting in deficiency of aldosterone and cortisol
findings in Addison's disease
hypotension, hyperkalemia, metabolic acidosis, skin hyperpigmentation, adrenal atrophy of all 3 layers
secondary adrenal insufficiency
decreased pituitary ACTH production which has no skin hyperpigmentation and no hyperkalemia
waterhouse-friedrichson syndrome
acute primary adrenal insufficiency due to adrenal hemorrhage
causes of waterhouse friedrichson syndrome
Neisseria meningitidis, DIC, endotoxic shock
MC tumor of adrenal medulla in adults
pheochromocytoma
which cells does a pheochromocytoma arise from?
chromaffin cells (neural crest)
findings in pheochromocytoma
(1) episodic HTN - due to E, NE and DA release (2) urinary VMA elevated (3) plasma catecholamines elevated
pheochromocytomas are associated with..
neurofibromatosis, MEN types 2a and 2b
rule of 10s (pheochromocytoma)
10% malignant, 10% bilateral, 10% extraadrenal, 10% calcify, 10% kids, 10% familial
pheochromocytoma symptoms
episodic: Pressure (BP), Pain (headache), Perspiration, Palpitations (tachycardia), Pallor
breakdown productions of DA (1), NE (2) and E (3)
(1) DA - HVA (2) NE - VMA (3) E - metanephrine
MC tumor of adrenal medulla in children
neuroblastoma
neuroblastoma
can occur anywhere along sympathetic chain, elevated HVA in urine, overexpression of N-myc oncogene associated with rapid tumor progression
signs/symptoms of hypothyroidism
cold intolerance, weight gain (decreased appetite), lethargy/fatigue, constipation, decreased reflexes, myxedema, dry cool skin, bradycardia, dyspnea on exertion
signs/symptoms of hyperthermia
heat intolerance, weight loss, increased appetite, hyperactivity, diarrhea, increased reflexes, pretibial myxedema, warm moist skin, fine hair, chest pain, palpitations, arrhythmias
lab findings in hypothyroidism
increased TSH, decreased total T4, free T4, T3 uptake
lab findings in hyperthyroidism
decreased TSH, increased total T4, freeT4 and T3 uptake
MCC of hypothyroidism
Hashimoto's thyroiditis
Hashimoto's thyroiditis
autoimmune disorder; antimicrosomal and antithyroglobulin ab's with association to HLA-DR5
histology in Hashimoto's
Hurthle cells, lymphocytic infiltrate with germinal centres
findings in Hashimoto's
moderately enlarged, nontender thyroid
Cretinism
severe fetal hypothyroidism
endemic Cretinism
endemic goiter is prevalent ex. lack of dietary iodine
sporadic cretinism
defect in T4 formation or developmental failure in thyroid function
findings in Cretinism
pot bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue; mental retardation
subacute thyroiditis (de Quervain's)
self-limited hypothyroidism following a flu-like illness; may initially be hyperthyroid
histology of subacute thyroiditis
granulomatous inflammation
findings in subacute thyroiditis
increased ESR, jaw pain, early inflammation, very tender thyroid
Reidel's thyroiditis
thyroid replaced by fibrous tissue (hypothyroid)
findings in Riedel's thyroiditis
fixed, hard (rock-like) and painless goiter
Grave's disease
type II HS, autoimmune hyperthyroidism with thyroid stimulating/TSH receptor antibodies
signs/symptoms of Grave's disease
ophthalmopathy - proptosis, EOM swelling; pretibial myxedema, diffuse goiter; often presents during stress
thyrotoxicosis
stress-induced catecholamine surge leading to death by arrhythmia; serious complication of Grave's disease
toxic multinodular goiter
focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation of TSH receptor; increased release of T3/T4
Jod-Basedow phenomenon
thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete
treatment strategy for type 1 DM
low sugar diet, insulin replacement
tx strategy for type 2 DM
dietary modification, exercise, oral hypoglycemics, insulin replacement
rapid acting insulin (3)
Lispro, Aspart, Regular
intermediate acting insulin (1)
NPH
long-acting insulin (2)
glargine, detemir
MOA of insulin
(1) liver - increases glucose stored as glycogen (2) muscle - increases glycogen and protein synthesis; K+ uptake (3) fat - aids in TG storage
clinical uses of insulin
(1) type 1 DM/type 2 DM (2) DKA (3) gestational diabetes (4) stress-induced hyperglycemia
toxicities of insulin
(1) hypoglycemia (2) hypersensitivity - very rare
first generation sulfonylureas
tolbutamide, chlorpropamide
second generation sulfonylureas
glyburide, glimepiride, glipizide
MOA of sulfonylureas
close K+ channel in B-cell membrane which depolarizes cells and insulin is released via influx of Ca2+
clinical use of sulfonylureas
stimulate release of endogenous insulin in DM2
side effects of first generation sulfonylureas
disulfuram-like effects
side effects of second generation sulfonylureas
hypoglycemia
ex of biguanide drug
metformin
MOA of metformin
unknown - decreases gluconeogenesis, increases glycolysis and peripheral glucose uptake
clinical uses of metformin
taken orally; can be used in pts without islet function
side effects of metformin
(1) lactic acidosis (2) C/I in renal failure
glitazones/thiazolidinediones
pioglitazone, rosiglitazone
MOA of glitazones
increase insulin sensitivity in peripheral tissue; bind to PPAR-y nuclear transcriptor regulator
clinical use of glitazones
monotherapy in type 2 DM or combined with above agents
side effects of glitazone drugs
(1) weight gain (2) edema (3) hepatotoxicity (4) CV toxicity
alpha-glucosidase inhibitors
acarbose, miglitol
MOA of acarbose/miglitol
inhibit intestinal brush border a-glucosidase = delayed sugar hydrolysis and glucose absorption = decreased post-prandial hyperglycemia
clinical uses of acarbose/miglitol
monotherapy in type 2 DM or combined with above agents
side effects of acarbose/miglitol
GI disturbance - flatulence, diarrhea; potentially hepatotoxic
pramlintide
mimetic that decreases glucagon
clinical uses of pramlintide
type 2 DM
side effects of pramlintide
hypoglycemia, nausea, diarrhea
exenatide
GLP-1 analog that increases insulin and decreases glucagon release
clinical uses of exenatide
type 2 DM
side effects of exenatide
nausea, vomiting, pancreatitis
MOA - propylthiouracil/methimazole
inhibit organification of iodide and coupling of thyroid hormone synthesis; PTU decreased peripheral conversion of T4 to T3
clinical uses of propylthiouracil/methimazole
hyperthyroidism
toxicity of propylthiouracil/methimazole
(1) skin rash (2) agranulocytosis (3) aplastic anemia (4) methimazole = teratogen
which drugs can be used for thyroxine replacement?
levothyroxine/ triiodothyronine
clinical uses of levothyroxine/triiodothyronine
hypothyroidism, myxedema
toxicity of levothyroxine/triiodothyronine
tachycardia, heat intolerance, tremors, arrhythmias
clinical use of GH
GH deficiency, Turner's syndrome
clinical use of somatostatin (octreotide)
acromegaly, carcinoid, gastrinoma, glucagonoma
clinical use of oxytocin
stimulates labor, uterine contractions and milk-letdown; controls uterine hemorrhage
clinical use of desmopressin
ADH analog used to treat central/pituitary diabetes insipidus
demeclocycline - MOA
ADH antagonist (member of tetracycline family)
MOA of glucocorticoids
decreases production of leukotrienes and PGs by inhibiting PLA2 and expression COX2
clinical uses of glucocorticoids
Addison's disease, inflammation, immune suppression, asthma
Iatrogenic Cushing's syndrome
buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes
toxicity of glucocorticoids
adrenal insufficiency if drug stopped abruptly after chronic use