Additional Flashcards
Increased PTH drives ____ (? increase, decrease) in sr. Ca2+ and ____ (? increase, decrease) in sr. PO4 levels in ______.
↑ PTH –> ↑ sr. Ca2+ & ↓ sr. PO4 in primary HyperPTH
*primary HyperPTH seen in
-single hyper-functioning adenoma (80%)
-Parathyroid hyperplasia (15%)
-PTH carcinoma (~5%)
Secondary hyperPTH is driven by ___.
hypocalcemia that may be caused by
-Dietary calcium deficiency
-dietary/pathological Vit D deficiency
-*renal insufficiency (sr. PO4 levels are ↑)
*renal insufficiency–> ↓ Vit D production–> ↓ dietary ca2+ absorption
Tertiary Hyper PTH due to ______ seen in _____, and is marked by __ in sr. levels of ca2+, PO4, and PTH.
d/t hyperplasia and autonomous hyperactivity of PTH gland seen in pts. with long standing secondary hyperPTH on dialysis;
marked by ↑ serum levels of all three (PTH, calcium and phosphate); phosphate is high because kidneys are unable to execute increased excretion of phosphate under PTH influence.
In ectopic PTHrP secretion (lung or breast malignancy), serum PTH levels are ____ in setting of very high sr. ca2+ and normal/low sr. PO4.
serum PTH levels are ↓ in setting of ↑↑ sr. Ca2+ and normal/↓ sr. PO4.
What are the s/s a/w hypercalcemia?
stones, bones, moans, groans, and psychiatric overtones.
What is the initial m/m of acute hypercalcemia?
IV fluids (first-line t/t),
and IV calcitonin
____ is used for long term t/t of hypercalcemia.
IV bisphosphonates.
Hypercalcemia d/t malignancy is usually t/t with _____.
bisphosphonates.
What is the first-line t/t of symptomatic/moderate-severe Paget’s disease of the bone?
Bisphosphonates
Pts. with Paget’s disease of the bone who are intolerant to first-line bisphosphonates, can be t/t with ____.
Calcitonin.
In addition to osteoarthritis and pathologic fractures, what are some other serious complications of Paget’s disease of the bone?
-High-output cardiac failure (d/t AV connections),
-Osteosarcoma (1% cases).
Increased sr. Alkaline phosphatase with increased sr. Gamma-glutamyl transpeptidase (GGT) are suggestive of _____ (? liver, bone) pathology.
Bone pathology e.g. Paget’s disease of the bone.
In Paget’s disease of the bone, Sr. Ca2+ and Sr. phosphate levels are ___ (? increased, normal, decreased).
normal;
Abnormal in Paget’s disease
-Sr. Alkaline phosphatase
-Sr. GGT levels
What are some medications other than the best initial t/t agents bisphosphonates that can be used in t/t of osteoporosis?
-PTH analogues (Teriparatide) act as PTH proxy, and reduce bone resorption.
-Denosumab: monoclonal Ab to RANK-L
-Raloxifene: selective estrogen R modulator.
Osteoporosis is the most common cause of pathological fractures in women with _____, and men over age ____ yrs.
-in women with low-body weight, and
-in men over age 60 yrs.
What are the s/s of Paget disease of the bone?
Mostly asymptomatic and require no t/t;
for s/s remember MNEMONIC: Paget’s PANICS!
-Pain: bone pains
-Arthralgia
-Nerve compression (e.g. deafness)
-Increased bone density
-Cardiac failure (high-output)
-Skull involvement/Sclerotic vertebra/e
Osteoporosis is confirmed with a DEXA T-score of _____.
2.5 SDs less than normal.
DEXA T-score of 1-2.5 below normal is indicative of ____.
Osteopenia.
DEXA screening scan is recommended for _____.
-women > 65 yrs age,
-men > 70 yrs. of age
-pts. with other risk factors for osteoporosis.
Distal radius fracture (Colles fracture) following minimal trauma in an elderly pt. is suggestive of ___.
Osteoporosis.
Defect in bone mineralization often caused by severe Vit D deficiency leads to ____, manifested by bone pains, _____ serum Ca2+ and PO4, and ____ PTH levels.
Osteomalacia; manifested by bone pains, low serum Ca2+ and PO4, and elevated PTH (Secondary HyperPTH).
How do TRH and or TSH affect PRL hormone secretion?
TRH directly stimulates PRL, whereas
TSH *indirectly stimulates PRL via dopamine pathway.
*TSH –> inhibits dopamine —> relieves dopamine’s inhibitory effect on PRL.
GnRH is inhibited by which anterior pituitary hormone?
PRL (thus causing lactational amenorrhea).
What is the effect of somatostatin (SS) on GH and TSH?
Both are inhibited by SS.
A pt. with familial hypocalciuric hypercalcemia (FHH) will have ___ lab profile.
-Elevated sr. Ca2+, elevated Sr. Mg2+
-Low ur. Ca2+ (unlike other abnormal hypercalcemic states in which the kidneys filter out ↑↑ Ca2+ –> hypercalciuria).
-Normal/mildly ↑ PTH
*FHH is a rare AD disorder d/t LOF mutation of calcium sensing receptors (CaSR) in PTH gland, kidneys etc, reducing their sensitivity and thus increasing their set point for Ca2+ sensing. So increase in PTH occurs at higher levels of sr. calcium; kidneys keep on reabsorbing Ca2+ and Mg2+ until their higher levels in serum –> maintaining hyperCa2+ and HyperMg2+.
In _____, an inherited disorder, both the PTH gland and kidneys are insensitive to increase in sr. Ca2+ levels d/t decreased sensitivity of the Ca2+ sensing R’s in the same.
FHH.
Severe hemorrhage (anywhere in the body) leading to pituitary infarction causing panhypopituitarism is known as _____, and is commonly seen after _____ hemorrhage.
Sheehan syndrome; postpartum hemorrhage.
Pituitary apoplexy results d/t ___.
Pituitary hemorrhage.
Which pituitary hormones are usually affected first in hypopituitary pathology?
Gonadotropins and GH.
*p/w hypogonadism in adults/adolescents, and growth retardation in children.
MN: GnRH and GH are Gone first in hypopituitarism!
What is the normal A.M. serum cortisol range?
3-25 mcg/dL.
Adrenal insufficiency is likely at serum cortisol levels of less than ____.
3 mcg/dL–> confirm etiology with ACTH levels.
lack of hyperpigmentation is characteristic of _______ adrenal insufficiency as ACTH levels are low.
Secondary adrenal insufficiency.
*unlike in primary adrenal insufficiency, ACTH levels are high leading to hyperpigmentation as ACTH is co-stimulatory of MSH.
ACTH stimulation test (aka Cosyntropin test) is indicated when AM cortisol levels are between ____ mcg/dL.
3-18 mcg/dL.
____ is the test of choice to diagnose hypothyroidism d/t hypopituitarism (aka secondary hypothyroidism).
Free T4;
TSH must be checked concurrently but TSH is not diagnostic as its levels may be normal or even high in sec. hypothyroidism.
Before starting levothyroxine for secondary hypothyroidism d/t TSH deficiency, ____ must be tested to rule out ______ to prevent adrenal crisis.
sr. ACTH levels must be tested to rule out ACTH deficiency because levothyroxine increases cortisol clearance, and can precipitate adrenal crisis in pts. who are already ACTH deficient.
___ should be suspected in a new onset HTN pt. with hypokalemia.
Primary hyperaldosteronism.
A pt. with new onset HTN develops hypokalemia upon initiation of t/t with diuretics. What is the most likely cause of his HTN.
Primary hyperaldosteronism.
The best screening test for primary hyperaldosteronism is _____. Positive tests must be confirmed with _____.
Early morning *PAC: PRA > 20 (& PAC > 15 mg/dL) is suggestive of primary hyperaldosteronism.
Confirm positive tests with aldosterone suppression (salt loading) test. In absence of local adrenal pathology, salt should suppress aldosterone secretion. If Sr. PAC still high–> confirm adrenal pathology with imaging (CT).
*plasma aldosterone conc. to plasma renin activity
In a pt. with PAC/PRA > 20, and an abnormal aldosterone suppression test, what is the next step in confirming the diagnosis of primary hyperaldosteronism.
adrenal CT scan.
In a pt. with suspected of primary hyperaldosteronism in whom CT scan does not reveal a discrete unilateral mass (adenoma)_____ must be done to differentiate between an adenoma and hyperplasia.
Adrenal venous sampling.
In a pt. with hyperosmolar hyperglycemic state (HHS), pH, sr. HCO3 and anion gap are ______ (? elevated, decreased, normal).
normal pH,
normal sr. HCO3, and
normal anion gap.
-normal/slightly ↑ serum ketones.
ABNORMAL:
-RBS > 600 mg/dL (frequently > 1000 mg/dL)
-Sr. osmolality > 320 mOsm/kg
What is the initial/immediate step in m/m of a pt. in HHS?
-Rehydration with IV *NS, and
-start Insulin infusion if **sr. K+ > 3.3 mEq/L
-add K+ to IVF if sr. K+ < 5.3 mEq/L
*use 0.45% NS if corrected sr. Na+ levels are normal/high after the second/third hour, or the pt. is eunatremic/hypernatremic at presentation.
Corrected Sr. Na+ =
Measured Sr. Na+ (mEq/L) + 2 mEq/L for every 100 mg/dL of glucose level at sr. glucose levels of > 100 mg/dL.
** If sr. K+ < 3.3 mEq/L, then withhold Insulin until Sr. K+ levels are raised to > 3.3 mEq/L through IV K+ replacement.
K+ replacement must continue so that levels are > 5.3 mEq/L. Insulin can be started at sr. K+ levels > 3.3 mEq/L.
In addition to the initial m/m with IV NS, what is the mainstay t/t of HHS?
IV Regular Insulin.
Serum K+ must be replaced during m/m of HHS with insulin, if levels are below ____. Why?
If sr. K+ levels are < 5.3 mEq/L;
because Insulin will rapidly drive K+ into the cells inducing hypokalemia in an already total K+ deficit state seen in HHS.
____ modality of t/t leads to a transient worsening of Graves opthlamopathy d/t increase in the titers of ____ after t/t initiation.
RAI;
d/t increase in titers of Thyrotropin receptor antibodies (TRAb) on TSH receptors on retro-orbital fibroblasts and adipocytes, during initial t/t phase.
____ can be used to prevent RAI-induced worsening of opthalmopathy in graves disease.
Glucocorticoids
In m/m of DKA, serum pH, electrolytes, and anion gap must be monitored every _____ hourly, and serum glucose must be monitored every ___ hours.
serum pH, electrolytes, and anion gap must be monitored every 2-4 hours, and
serum glucose must be monitored hourly.
_____ is the best index to monitor the response to t/t in DKA.
serum anion gap.
After initial infusion of IV NS in DKA, half NS (0.45%) can be started when sr. Na+ levels are _____.
≥ 135 mEq/L.
Dextrose can be added to infusion when sr. glucose levels reach ____ in t/t of DKA with IV insulin.
Add Dextrose when Sr. glucose < 200 mg/dL.
In m/m of DKA, Insulin infusion must be put on hold if sr. ____ levels are ______.
Withhold Insulin infusion, if Sr. K < 3.3 mEq/L.
Sr. K+ must be replaced if serum levels are below ___ in DKA.
< 5.3 mEq/L.
Insulin infusion must be reduced when sr. glucose levels reach ___.
below 200 mg/dL.
In DKA m/m, IV Insulin can be switched to subcutaneous Insulin when _____.
resolution of DKA achieved evident by normal AG, and pt. is able to eat.
When is sodium-bicarbonate administration indicated in t/t of DKA?
in severe DKA with blood pH ≤ 6.9.
*normal pH is 7.35-7.45.
Trans-sphenoidal resection of a prolactinoma is considered in pts. with _____.
very large tumors (size > 3 cm) or in symptomatic pts. who responded poorly to medical t/t with dopamine agonist such as cabergoline or bromocriptine.
A pituitary adenoma with sr. PRL levels > 200 ng/dL or repeat level > 200 ng/dL, suggest a ____.
Prolactinoma.
A pituitary microadenona is ___ in size, and macroadenoma is ___ in size.
pituitary microadenona: < 10 mm;
pituitary macroadenoma ≥ 10 mm (1 cm).
Initial t/t with dopamine agonists such as cabergoline or bromocriptine is considered in pts. with a ___ prolactinoma.
macro-prolactinoma, or symptomatic pts.
Which CNS tumor that p/w headache, visual disturbances along with s/o hypopituitarism d/t anatomic compression has a bimodal age distribution?
Craniopharyngiomas
*present between 5-14 yrs, and 50-75 years.
*Adamantinomous type in pediatric populations, and papillary type in adults.
What is the difference between Somogyi effect vs Dawn phenomena?
Somogyi effect is
-A.M. rebound hyperglycemia d/t midnight hypoglycemia in diabetics.
-t/t by reducing evening insulin dose.
-3 am blood glucose levels will be low.
Dawn phenomena is
-A.M. hyperglycemia d/t normal diurnal ↑ in counter regulatory hormone secretion (GH, cortisol) after midnight.
-3 am blood glucose is normal/↑.
Bradycardia, irregular respirations, and a widened pulse pressure in a pt. with neurological s/s are indicative of ___, and termed _____.
High ICP (intracranial pressure);
termed Cushing’s triad.
____ is the leading cause of death in children with DKA, and occurs in about ___ % of presenting cases.
Cerebral edema; 0.2-1 %
*AVOID/PREVENT by SLOW administration of IVF and insulin so as to correct effective osmolarity over a 36-48 hr period.
Cerebral edema in DKA results from ?
-rapid reversal of hyperglycemia induced osmolar shifts with IVF + Insulin
-cerebral vasoconstriction d/t acidosis and hypercapnia
-cytotoxic edema
-reperfusion injury with vasogenic edema during rehydration phase of DKA t/t.
What factors increase the r/o cerebral edema in DKA pts.?
pts. with
-High initial BUN
-Low initial PCO2
-t/t with *bicarbonate
-refractory hyponatremia even as blood glucose levels are improving.
*some experts recommend administering bicarbonate only if pH is < 7.0
In absence of oral or IV access, ___ can be given to t/t severe hypoglycemia in a pt.
IM Glucagon.