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76 Cards in this Set
- Front
- Back
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Embryologically, where does the adrenal cortex come from?
the adrenal medulla? |
cortex: mesoderm
medulla: neural crest |
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Describe adrenal gland drainage (R and L)
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Left adrenal: -> L adrenal vein -> L Renal vein -> IVC
Right adrenal: -> R adrenal vein -> IVC |
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Embryologically, what is the neurohypophysis (post pituitary) derived from?
the adenohypophysis (ant pituitary) |
Posterior: neuroectoderm
Anterior: oral ectoderm |
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Which pituitary hormones have a common alpha subunit
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TSH, LH, FSH, and hCG
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Where are Islets of Langerhans most numerous
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in tail of pancreas
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What effect does insulin have on Na and K
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increases Na retention (kidneys)
increases cellular uptake of K |
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What organs do not need insulin for glucose uptake
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BRICK L
Brain RBCs Intestine Cornea Kidney Liver |
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What is the mechanism of action of insulin
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made in B cells of pancreas in response to ATP from glucose metabolism closing K+ channels and depolarizing cells
depolarization opens Ca channels in cell membrane -> increased intracellular [Ca] -> exocytosis of insulin |
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Where do they act?
GLUT-1 GLUT-2 GLUT-4 |
GLUT-1: RBCs, brain
GLUT-2 (bidrectional): B islet cells, liver, kidney GLUT-4 (insulin responsive): adipose tissue, skeletal muscle |
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Which of the GLUT transporters is birectional?
Which is insulin responsive Which is insulin independent |
GLUT-2 is bidirectional
GLUT-4 is insulin responsive GLUT-1 is insulin independent |
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How does 17alpha-hydroxylase deficiency manifest in a male
in a female? |
male: pseudohermaphroditism from decreased DHT
female: sexual infantilism; NL female, but lacking secondary characteristics |
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17alpha-hydroxylase characteristics
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increased cortisol
decreased sex hormones increased mineralocorticoids (HTN, hypokalemia) |
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21-hydroxylase deficiency characteristics
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decreased cortisol
increased sex hormones decreased mineralocorticoids (increased renin) |
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11-beta hydroxylase deficiency characteristics
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decreased cortisol
increased sex hormones decreased aldosterone and corticosterone |
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What is a consequence of 21-hydroxylase deficiency in newborns
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b/c of decreased mineralocorticoids, salt wasting can lead to hypovolemic shock
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What is a common characteristic of all the congenital adrenal hyperplasias
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adrenal gland enlargement from increased ACTH b/c of decreased cortisol
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What effect does Mg+2 have on PTH
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low serum Mg -> low PTH secretion
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What are common causes of low serum Mg+2
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diarrhea, aminoglycosides, diuretics, EtOH abuse
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What cells make PTH?
What cells make Calcitonin? |
PTH: Chief cells of parathyoid
Calcitonin: parafollicular cells (C cells) of thyroid |
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What is the signaling pathway for GH, Prolactin, Insulin, IGF-1, PDGF, FGF
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tyrosine kinase
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What is the signaling pathway for GnRH, GHRH, Oxytocin, ADH (V1 receptor), TRH
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IP3
("GGOAT") |
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What is the signaling pathway for FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2 receptor), MSH, PTH, Calcitonin, Glucagon
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cAMP
("FLAT CHAMP") |
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What is the signaling pathway for ADH:
V1 receptor? V2 receptor? |
V1 is IP3
V2 is cAMP |
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What is the signaling pathway for ANP and NO (EDRF)
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cGMP
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What effect does an increase in SHBG (sex hormone binding globulin) cause
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increased SHBG lowers free testosterone -> gynecomastia
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What effect does SHBG (sex hormone binding globulin) cause
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decreased SHBG raises free testosterone -> hirsutism
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What are the main functions of T3
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4 Bs
Brain maturation Bone growth Beta-adrenergic effects increased BMR |
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What condition is there low TBG
is there high TBG? |
Low TBG: hepatic failure
High TBG: pregnancy or OCP use (estrogen increases TBG) |
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Where is most T3 made
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in the blood (from T4 in peripheral tissue)
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When do you see a negative Ca+2 balance
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women during pregnancy or lactation
(intestinal Ca absorption less than excretion) |
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What is the most common cause of primary hyperparathyroidism
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parathyroid adenoma
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What happens in primary hyperparathyroidism
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hypercalcemia, hypophosphatemia, phosphaturia, increased urinary cAMP, increased bone resorption, increased PTH
also, increased URINARY Ca excretion b/c of increased filtered load of Ca+2 |
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What happens in HHM (Humoral Hypercalcemia of Malignancy)
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caused by PTH-related peptide (PTH-rp)
hypercalcemia, hypophosphatemia, phosphaturia, decreased PTH (feedback inhibition from increased Ca) |
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What is the most common cause of hypoparathyroidism
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thyroid surgery, or congenital
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What increases 1alpha-hydroxylase activity
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decreased serum Ca
increased PTH levels decreased serum Phosphate |
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What cells secrete anti-mullerian hormone
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Sertoli cells
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What initiates the onset of puberty in both males and females
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pulsatile GnRH release from hypothalamus
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During lifespan, when is FSH > LH and when is LH > FSH
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FSH > LH: childhood, when hormone levels are the lowest; in senescence, when hormone levels are the highest
LH >FSH: at puberty and during reproductive years, when hormone levels increase from childhood |
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How does prolactin inhibit ovulation
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1. inhibits hypothalamic GnRH secretion
2. inhibits action of GnRH on ant pituitary (and as a result inhibits LH and FSH secretion) 3. antagonizes LH and FSH action on ovaries |
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Regarding cushing's syndrome, what causes have an increase in ACTH?
a decrease in ACTH? |
increase ACTH: Cushing's disease (ACTH secretion from a pit adenoma), Ectopic ACTH
decrease ACTH: exogenous steroids, adrenal adenoma |
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How do you treat Conn's syndrome
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spironolactone
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What is secondary hyperaldosteronism
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kidney perception low intravascular volume -> overactive RAAS
from renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome assoc w/HIGH plasma renin (primary or Conn's has LOW renin) |
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Addison's dz
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chronic adrenal insufficiency
primary deficiency of aldosterone and cortisol -> hypotension, skin hyperpigmentation (high ACTH) characterized by Adrenal Atrophy and Absense of hormone production involves All 3 cortical divisions different from 2ndary adrenal insufficiency which has low ACTH, no hyperpigmentation and no hyperkalemia |
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What is Waterhouse-Friderichesen syndrome
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Acute adrenocortical insufficiency
from adrenal hemorrhage assoc w/N. meningitidis septicemia, DIC, an endotoxic shock |
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Pheochromocytoma?
What are the main characteristics of pheochromocytoma |
most common adrenal tumor in adults. urinary VMA and plasma catecholamine levels elevated. assoc w/neurofibromatosis and MEN Types 2A and 2B
episodic (relapse and remit); 5 Ps Pallor Palpitations (tachycardia) Pain (HA) Pressure (HTN) Perspiration |
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How do you trx pheochromocytoma
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alpha-antagonists, esp phenoxybenzamine (irreversible alpha-blocker)
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What is the most common adrenal tumor in kids?
and what are some characteristics |
Neuroblastoma
can happen anywhere along the sympathetic chain; less likely to get HTN HVA (breakdown product of dopamine) in urine N-myc oncogene |
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What is the most common cause of hypothyroidism
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Hashimoto's thyroiditis
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Main features of Hashimoto's thyroiditis
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autoimmune, Anti-microsomal and anti-TG antibodies
-assoc w/HLA-DR5 and Hurthle cells -lymphocytic infiltrate w/germinal centers -slow course, may be hyperthyroid early on (thyrotoxicosis during follicular rupture) |
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Cretinism
What causes sporadic cretinism |
severe fetal hypothyroidism
child is pot-bellied, pale, puffy face, protruding umbilicus, and protuberant tongue sporadic caused by defect in T4 formation or developmental failure in thyroid formation still common in China |
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Subacute thyroiditis (deQuervain's)
Lymphocytic subacute thyroiditis |
Subacute: self-limited HYPOthyroidism, often following flu-like illness
high ESR, jaw pain, very tender thyroid, granulomatous inflammation Lymphocytic: painless |
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Riedel's thyroiditis
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thyroid replaced by fibrous tissue -> hypothyroid
hard, pain-less goiter |
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Grave's dz
When does it often present? What is a serious complication of it? |
autoimmune hyperthyroidism; Type 2 hypersensitivity
often presents during times of stress (like childbirth) Stress-induced catecholamine surge -> death by arrhythmia (serious complication in Graves and other hyperthyroid disorders) |
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Jod-Basedow phenomenon
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thyrotoxicosis if patient w/iodine deficiency goiter is made iodine replete
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Toxic multinodular goiter
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focal patches of hyperfunctioning follicular cells working independently of TSH b/c of a mutation in TSH receptor
increased release of T3 and T4 nodules are not malignant |
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What cancer is assoc w/Hashimoto's thyroiditis
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lymphoma
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What are the 3 main features of hyperparathyroidism
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stones, bones, and groans
hypercalciuria -> renal stones hypercalcemia (bones) groans: constipation (and weakness) |
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osteitis fibrosa cystica
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part of von Recklinghausen's syndrome
cystic bone spaces filled w/brown fibrous tissue (bone pain) |
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renal osteodystrophy
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secondary hyperparathyroidism
secondary to renal dz (chronic renal failure) hypovitaminosis D -> decreased Ca absorption (but hyperphosphatemia) increased PTH b/c of low Ca |
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What is Chvostek's sign
What is Trousseau's sign What condition are they seen in |
Chvostek: tapping on facial nerve -> contraction of facial muscles
Trousseau: brachial artery occlusion w/BP cuff -> carpal spasm both seen in HYPOparathyroidism |
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What is pseudohypoparathyroidism
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Albright's hereditary osteodystrophy
autosomal dominant kidney unresponsiveness to PTH hypocalcemia, shortened 4th/5th digits, short stature |
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What is used to dx acromegaly
What drugs is used to trx it |
dx: failure to suppress serum GH following oral glucose tolerance test
trx: octreotide, after pit adenoma resection |
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Sheehan's syndrome
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postpartum hypothyroidism
enlargedment of anterior pituitary (increased lactotrophs) w/o corresponding increase in blood supply -> increased risk of infarction following severe bleeding + hypoperfusion after delivery can cause fatigue, anorexia, poor lactation, loss of public/axillary hair |
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What can cause central DI
What can cause nephrogenic DI |
pituitary tumor, trauma, surgery, histiocytosis X
nephrogenic: hereditary or secondary to hypercalcemia, lithium, demeclocycline (ADH antagonist) |
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How do you dx central vs nephrogenic DI
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administer desmopressin. If urine osmolarity increases, then its central DI; if not, then it's nephrogenic DI
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How do you treat central DI
how do you treat nephrogenic DI |
central: intranasal desmopressin (ADH analog)
nephrogenic: HCTZ, indomethacin, amiloride |
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What are the major complications of DKA
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life-threatening mucormycosis, Rhizopus infections
cerebral edema, arrhythmias, heart failure |
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How do you treat DKA
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fluids, insulin, K+ (to replete intracellular stores)
glucose if necessary to prevent hypoglycemia |
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what can cause carcinoid syndrome
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carcinoid tumor, especially metastatic small bowel tumors that secrete high levels of serotonin 5-HT
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What is the most common tumor of the appendix
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carcinoid tumor
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What are the characteristics of carcinoid syndrome
How do you treat it |
flushing, diarrhea, wheezing, R-sided valvular dz
Treat with octreotide |
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MEN Type 1
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Wermer's syndrome
Parathyroid tumors Pituitary tumors (prolactin or GH) Pancreatic endocrine tumors (ZES, VIPomas, insulinomas) commonly present w/kidney stones and stomach ulcers |
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MEN Type 2A
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Sipple's syndrome
Medullary thyroid carcinoma Pheochromocytoma Parathyroid tumors |
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MEN Type 2B
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Medullary thyroid carcinoma
Pheochromocytoma oral/intestinal ganglioneuromatosis (assoc w/marfanoid habitus) |
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What is the inheritance for all MEN syndromes
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autosomal dominant
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What gene is associated w/MEN Type 2A and 2B
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ret gene
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