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What is the effect of sex hormones (e.g., estrogen) on bone development? What the effect of estrogen on regions outside of the epiphyseal growth plate?

Initially increase linear growth, but also promote closure of the epiphyseal plate (linear growth stops when epiphysis fuses with the metaphysis)

Outside of the epiphyseal growth plate, estrogen is anabolic because it increases osteoblastic bone deposition and decreases osteoclastic bone resorption. (low estrogen associated with rapid bone loss)


What are the effects of IGF-1 on the epiphyseal growth plate? What is another name for IGF-1?

IGF-1 also called somatomedin C

IGF-1 causes the differentiation and proliferation of chondrocytes int he epiphyseal growth plate, causing an increase in linear growth
but does NOT accelerate epiphyseal closure (as sex hormones do).


What disease does vitamin D deficiency cause in children? In adults?

Rickets in children (bone pain and deformity)
Osteomalacia in adults (bone pain and muscle weakness)


What is the function of vitamin D? What are characteristic lab values in vitD deficiency?

Increases intestinal absorption of calcium and phosphate
Increases bone mineralization

vitD deficiency:
high PTH (secondary hyperparathyroidism)
low Ca2+ (poor GI uptake, exhausted stores)
low phosphate (poor GI uptake, increased urinary excretion from PTH)


What does vitD do to calcium and phosphate levels? PTH?

vitD: increases BOTH calcium and phosphate absorption in the gut

PTH: increased calcium reabsorption and decreased phosphate reabsorption in the kidney


Difference between hypertrophy and hyperplasia? Which happens in Cushing's disease to what layer of the adrenal cortex?

hypertrophy - increase in size of cells
hyperplasia - increase in number of cells / proliferation of cells

increased ACTH causes hyperPLASIA in the zona fasiculata (glucocorticoid hormoes like cortisol) and zona reticularis (secrete small amounts of androgens)


How does PTH increase serum calcium? What suppresses PTH synthesis?

1) increases bone resorption by osteoclastic activation -> Ca2+ efflux
2) increases renal absorption of Ca2+
3) increases formation of 1,25-hydroxy-vitD (kidney 1-a hydroxylase)

Increased serum calcium and increased 1,25-dihydroxy-vitaminD suppresses PTH production


What hormone does prolactin levels regulate? What regulates prolactin level? What does hyperprolactinemia cause?

Prolactin regulates GnRH levels (which determine FSH, LH levels)

Dopamine decreases secretion of prolactin; TRH increases prolactin

High levels of prolactin suppresses GnRH secretion from the hypothalamus, leading to hypogonadism (also causes milk discharge from the breasts/galactorrhea)
Hyperprolactinemia -> hypogonadism -> low estrogen -> accelerated bone loss risk


Features of SIADH? What is total body fluid volume?

- Excessive water retention
- Hyponatremia with continued urinary Na+ secretion
- Urine osmolarity > serum osmolarity

EUVOLEMIC hyponatremia

pt presentation with headache, weakness, dizziness, altered mental status


What are adrenal steroid levels in 21-hydroxylase deficiency? How/when does it present for males vs. females?

mineralocorticoids: LOW
cortisol: LOW
sex hormones: HIGH

Females: present at birth with ambiguous (virilized) genitalia
Males: normal genitalia and present in infancy (salt-wasting) or in childhood (precocious puberty)


What levels are diagnostic for 21-hydroxylase deficiency?

high serum level of 17-hydroxyprogesterone


What are normal prolactin levels and how are they controlled?

Prolactin is under tonic (constant) inhibition by dopamine secretion from the hypothalamus.
Dopamine acts on D2 dopamine receptors on lactotrophs (the prolactin-producing cells of the pituitary).

Destruction of the hypothalamic thus causes hyperprolactinemia via loss of this tonic inhbition.
(Other pituitary hormones are stimulated by hypothalamic activity.)


How do you measure visceral vs. subcutaneous fat? What is visceral obesity associated with?

waist-to-hip ratio indirectly measures visceral to subcutaneous fat
(the abdomen contains mainly viscera and hips have only subcut. fat)

high WHR asscoiated with insulin resistance, metabolic syndrome, and type 2 DM.


Male pt 1wk old with vomiting, low Na, high K, hypotensive? each symptom due to?

21-hydroxylase deficiency
males have normal genitalia, but present with salt-wasting after birth.

low Na, high K - no aldosterone
hypotension - no cortisol


What are adrenal steroid levels in 17alpha-hydroxylase deficiency? What is the presentation in males vs. females?

HIGH mineralocorticoids
LOW cortisol
LOW sex hormones

hypertension - high aldosterone
hypokalemia - high aldosterone
low DHT - low sex hormones

Males: appear phenotypically female at birth but no internal female genitalia (absence of virilizing androgens in utero), no secondary sex development
Females: normal genitalia, no secondary sex development


What are adrenal steroid levels in 11beta-hydroxylase deficiency? What is the presentation in males vs. females?

LOW mineralocorticoids (low aldosterone)
but HIGH 11-deoxycorticosterone (results in high BP)
LOW cortisol
HIGH sex hormones

hypokalemic HTN - low renin, due to presence of weak mineralocorticoid 11-deoxycortisone

XX: virilization (ambiguous genitalia)
all individuals: hypertension and hypokalemia early in life


Increased calcium - what happens to PTH? Calcitonin?

decrease in PTH
increase in calcitonin
decrease in 1,25-dihydrocalciferol (vitaminD)


What is the function of calcitonin? Where does it come from? What is it regulated by?

decreases bone resorption of Ca2+ by osteoclasts
opposes activity of PTH, but not important in normal Ca2+ homeostasis

secreted by parafollicular C cells in the thyroid

mainly regulated by serum Ca2+ (high calcium = calcitonin secretion)


How do you distinguish between central and nephrogenic DI?

central DI - deficiency of ADH
nephrogenic DI - resistance to ADH's action on the kidneys

water deprivation test performed; vasopressin injection distinguishes
- when two consecutive urine samples show little change in urine osmolality, five units vasopressin given and values measured 1hr later
- if urine osmolality changes 50% = complete central DI
change of less than 50% = partial central DI (some vasopressin present but not enough to allow normal kidney function)


Describe a water deprivation test - what is it used for?

used in pts with suspected DI; distinguishes between central vs. nephrogenic DI

consecutive similar urine collections - administer vasopressin
if urine osmolality changes less than 10% = nephrogenic DI
if urine osmolality changes more than 10% = central DI
(>50% is complete central DI; <50% is partial central DI/some ADH)


Why does reproductive dysfunction occur with high prolactin levels?

prolactin suppresses gonadotropin-releasing hormone (GnRH) from the hypothalamus leading to hypogonadism, anovulation, and amenorrhea among other things -- low estrogen causes vaginal dryness and bone fractures.


What is the function of somatostatin secreted from the pancreas?

secreted from delta cells of the pancreas
decreases secretion of secretin, cholecystokinin, glucagon, insulin, and gastrin

also secreted by the hypothalamus to inhibit pituitary production of GH
secreted from other parts of the CNS in addition


How do pts with somatostatinomas present?

rare pancreatic islet cell tumors arising from delta cells
- hyperglycemia (greater inhibitory effect on insulin than glucagon), or hypoglycemia
- steatorrhea (excessive fat in feces)
- gallbladder stones (poor gallbladder contractility, secondary to inhibition of CCK release)


Pt with adrenal hyperplasia presenting with weight gain and easy bruising?

Cushing's syndrome (intermediate layer of cortex)
inhibited collagen and matrix GAG synthesis results in weaker, thinner skin and connective tissue = easy bruising


Pt with adrenal hyperplasia presenting with paresthesia, muscle weakness?

Conn's syndrome (outer layer of cortex)
paresthesia = hypokalemic alkalosis
muscle weakness = hypokalemia


Pt with adrenal hyperplasia presenting with excessive hair growth?

innermost layer of the cortex
hirsutism and androgen excess


What is Conn's syndrome? Presentation?

primary hyperaldosteronism
adrenal hyperplasia or an aldosterone-secreting adrenal adenoma, either bilateral or unilateral

- hypokalemia
- metabolic alkalosis
- low renin

no edema due to aldosterone escape (Na+ levels are normal)


Pt with adrenal hyperplasia presenting with sweating and tremulousness? Other symptoms? Findings/diagnosis?

Pheochromocytoma (adrenal medulla)
sweating/tremors due to excess circulating catecholamines

Episodic hyperadrenergic symptoms / 5 P's:
- Pressure (high BP)
- Pain (headache)
- Perspiration
- Palpitations
- Pallor

Findings: urinary VMA (breakdown product of NE and epinephrine) and
increased plasma catecholamines


What are advanced glycosylation end products (AGEs) and why are they detrimental?

attachment of glucose to amino acid residues in various proteins to form reversible glycosylation products that slowly stabilize to irreversible prducts

these products accumulate and crosslink with collagen in BV walls and interstitial tissues
- microangiopathy and nephropathy
- facilitates inflamm. cell invasion and deposition of LDL in vascular walls (atherosclerosis)


What do secreting prolactinomas do to the GnRH-LH-FSH-sexhormones axis and what does this present as? Treatment?

inhibits GnRH and all beyond
impotence in men, amenorrhea in women; infertility, low libido

Tx: dopamine agonists (bromocriptine, cabergoline)