Endocrine 6% Flashcards
Primary Hyperparathyroidism =
MC cause =
excess (inappropriate) PTH production
Parathyroid Adenoma
MEN I
MEN IIa
MEN I = HyperPTH, Pituitary Tumors, Pancreatic Tumors
MEN IIa = HyperPTH, Pheochromocytoma, Medullary Thyroid Carcinoma
Secondary Hyperparathyroidism =
MC cause =
Increased PTH in response to hypocalcemia or vit D deficiency
Chronic kidney failure: d/t hyperphosphatemia –> increased ionized Ca, decreased renal production of active vit D
Primary hyperparathyroidism: (Increased/decreased) DTR (Increased/decreased) Ca (Increased/decreased) PTH (Increased/decreased) phosphate (Increased/decreased) 24 hr urine calcium excretion Increased/decreased) vit D
Primary hyperparathyroidism: DECREASED DTR INCREASED Ca INCREASED PTH DECREASED phosphate INCREASED 24 hr urine calcium excretion INCREASED vit D
Tx of primary hyperparathyroidism
Tx of secondary hyperparathyroidism
Primary: Parathyroidectomy
Secondary: Vit D, Ca supplementation
MC causes of hypoparathyroidism (2)
Postsurgical
Autoimmune
Hypoparathyroidism: (Increased/decreased) DTR (Increased/decreased) Ca (Increased/decreased) PTH (Increased/decreased) phosphate
INCREASED DTR
DECREASED Ca
DECREASED PTH
INCREASED phosphate
Hypocalcemia causes ____ on EKG.
Hypercalcemia causes ____ on EKG.
Hypo: Prolonged QT interval
Hyper: Shortened QT interval
Tx of hypercalcemia
Avoid ___
1st line: Loop diuretics (Furosemide)
Severe: Calcitonin, Bisphosphonates
HCTZ–> caused increased Ca
Elevated calcium, low PTC indicates ___
Secondary HYPERPTH –> malignancy
All pts should be screened for ____ with ____ for ____ before treating hyperparathyroidism
Familial benign hypoclaciuric hypercalcemia
24 hr urine for Ca and Cr
DiGeorge Syndrome
Features (3)
Congential cause of hypocalcemia
Parathyroid hypoplasia
Thymic hypoplasia
Outflow tract defects of heart
Avoid ____ in hypocalcemia
Phenothiazine
Furosemide
Thyroid stimulating Ab
Graves dz (hyperthyroidism)
Abs in Hashimoto’s OR autoimmune thyroiditis
Antithyroid peroxidase Ab
Anti-Thyroglobulin Ab
Decreased radioactive iodine uptake
Thyroiditis
Diffuse radioactive iodine uptake
Grave’s Dz
Pituitary Adenoma
Low TSH, Low FT4
(rare) 2ry/3ry hypothyroidism
Usually pituitary
Drugs: dobutamine, octreotride, high-dose glucocorticoids
Riedel’s thyroiditis =
Presentation =
Tx =
Normal thyroid stroma replaced by fibrotic tissues
Painless fixed nodular that may grow rapidly
Steroids, tamoxifen, levothyroxine
Opthalmopathy w/ lid lag, exophthalmos/proptosis is exclusively seen in ___
Grave’s Dz
Pretibial myxedema =
Seen in__
nonpitting, edematous, pink-brown plaques/nodules on shins
Grave’s Dz
Methimazole and PropylThioUracil (PTU) used to tx ____
SE ____
Safe in pregnancy?
Grave dz, Toxic multinodular goiter (Plummer Dz)
SE: agranulocytosis, hepatitis –> monitor w/ CBC
PTU safe in pregnancy
Elevated TSH, High FT4
Presentation:
RAIU:
TSH secreting pituitary adenoma
Bitemporal hemianopsia
Diffuse uptake
MC therapy for Grave’s Dz and Plummer Dz
Radioactive Iodine
Antimicrosomial Ab seen in
Hashimoto’s Hypothyroidism
Post viral hypothyroidism =
Presentation =
Hallmark dx findings =
Tx =
De Quervain’s (Granulomatous)
PAINFUL neck/thyroid
Clinical HYPERthyroidism –> hypothyroid
Increased ESR
NO thyroid Ab
Tx: Aspirin, NO anti-thyroid meds
Medications that may induce HYPOthyroidism
Amiodarone*
Lithium*
Alpha interferon
MC cause of hypothyroidism in US =
MC cause of hypothyroidism worldwide =
Hashimoto’s
Iodine deficiency
Myxedema crisis =
MC in ___
Tx =
Extreme form of HYPOthyroidism
MC in elderly women w/ long standing hypothyroidism in cold weather
IV Levothyroxine
PASSIVE warming
Supportive
Best initial test to evaluate a thyroid nodule
Fine Needle Aspiration w/ Biopsy
MC type of benign thyroid nodule
Thyroid adenoma
MC type of thyroid carcinoma
Papillary
type of thyroid carcinoma MC associated w/ MEN2
Medullary
type of thyroid carcinoma MC after radiation exposure
MC in ___
Papillary
Young females
type of thyroid carcinoma MOST aggressive
MC in ___
Anaplastic
Males > 65 y/o
type of thyroid carcinoma w/ good prognosis
Papillary, Follicuar
type of thyroid carcinoma that commonly mets to local/cervical lymph nodes
Papillary
Early Medullary
type of thyroid carcinoma that commonly mets to distant areas via vascular invasion of lung, neck, brain, bone, liver, skin
Follicular
Late Medullary
____ used to monitor if residual dz present after tx or detect recurrence of MEDULLARY thyroid cancer.
Calcitonin levels
HYPERcalcemia stimulates ____
increased calcitonin secretion –> decreases blood Ca via decreased GI/kidney absorption and increased bone mineralization
Symptomatic tx of hyperthyroidism
beta blocker (propranolol)
IV methylprednisolone used to tx ___
Ophthalmopathy in hyperthyroidism
Ab that CAUSES hypothyroidism
Anti-TSH ab
Antiperoxidase, antithyroglobulin ab are disease markers
MC type of thyroid adenoma
Follicular
Osteopenia: T-score =
-1 to -2.5
Osteoporosis: T-score =
< -2.5
Recommended repeat DEXA scan scheduled based on T-score
- 1.0 to -1.5: Q 5 years
- 1.5 to -2.0: Q 3-5 years
Genetic mutation of type 1 collagen =
Associated w/:
Osteogenesis Imperfecta
Severe osteoporosis, *spontaneous fractures in childhood, *blue sclerae, *presenile deafness
Cystic brown tumors
Seen in renal osteodystrophy
NOT an actual tumor
Seen on biopsy d/t appearance of hemosiderin depositis
Osteitis Fibrosis Cystica d/t ___
Xray
d/t osteoclast activity from increased PTH in hypocalcemia in chronic kidney disease
Periosteal erosions
Bony cysts
“salt and pepper” appearance of skull
Looser lines (zones)
Rickets/Osteomalacia in Vit D deficiency
= transverse “pseudo fracture” lines
Osteomalacia:
(Increased/decreased) Ca
(Increased/decreased) Phosphate
(Increased/decreased) ALP
Decreased Ca
DECREASED phosphate
Increased ALP
Renal osteodystrophy:
(Increased/decreased) Ca
(Increased/decreased) Phosphate
(Increased/decreased) ALP
= osteomalacia and osteitis firbrosis cystica in pts w/ CKD
Decreased Ca
INCREASED phosphate
Increased ALP
3 zones of adrenal gland and what they produce
Zona Glomerulosa (outer) --> aldosterone Zona Fasciculata (middle) --> cortisol Zona Reticularis (inner) --> androgen/estrogen
Addison’s Disease =
Deficiency in ____
(Hyper/hypo)natremia
(Hyper/hypo)kalemia
(non/anion gap)metabolic (acidosis/alkalosis)
(Hyper/hypo)glycemia
PRIMARY adrenocortical insufficiency –> adrenal gland destruction
cortisol AND aldosterone
HYPOnatremia
HYPERkalemia
NON anion gap metabolic ACIDOSIS
HYPOglycemia
2ndary adrenal insufficiency
MC cause =
Deficiency in ____
PITUITARY failure of ACTH secretion
MC caused by exogenous steroid
LOW cortisol, NORMAL aldosterone
Dx of chronic adrenocortical insufficiency
1st: High dose ACTH (Cosyntropin) Stimulation test –> adrenal insufficiency –> little/no increase in cortisol levels
2nd: CRH stimulation test: Differentiates causes –>
Primary/Addision: High ACTH, LOW cortisol
Secondary (pituitary): Low ACTH, Low cortisol
Teritary (hypothalamus): delated, prolonged, exaggerated ACTH response
Tx of Addison’s
Glucocorticoid + mineralocorticoid =
Hydrocortisone + fludrocortisone
MC cause of Adrenal (addisonian) Crisis
Presentation
Tx
Abrupt withdrawal of glucocorticoids
Shock, hypotension, hypovolemia
Normal saline
Dexamethasone (undiagosed) or Hydrocortison (addison’s)
Fludrocortisone
SCREENING tests for dx of Cushing’s Syndrome (Hypercortisolism)
LOW-dose Dexamethasone Suppression test –> NO suppression = Cushing’s syndrome
Increased 24 hr urinary free cortisol
Increased salivary cortisol levels (night time)
DIFFERENTIATING tests for causes of Cushing’s Syndrome
HIGH dose Dexamethasone Suppression Test –>
Suppression = Cushing’s disease
NO suppression = adrenal or ectopic ACTH producing tumor
ACTH levels –>
Decreased ACTH = adrenal tumor (b/c produce high levels of cortisol –> suppress ACTH levels via HPA axis)
Normal/increased ACTH = Cusing’s disease or ectopic ACTH producing tumor (b/c secrete ACTH independent of HPA axis)
Cushing’s Disease =
Cushing’s syndrome caused by PITUITARY increased ACTH secretion
HYPERcortisol
Cushing’s disease tx:
Ectopic/adrenal tumor tx:
Cushing’s: Transsphenoidal sx
Ectopic/adrenal tumor: tumor removal. Ketoconazole if inoperable
Primary hyperaldosteronism caused by = Is renin (independent/dependent)
Idiopathic
Idiopathic bilateral adrenal hyperplasia (60%)
Conn Syndrome = Adrenal aldosteronoma
Renin INDEPENDENT
Secondary hyperaldosteronism caused by = Is renin (independent/dependent)
Renal artery stenosis
Decreased renal perfusion (CHF, hypovolemia, nephrotic syndrome)
Renin DEPENDENT: Increased Renin –> increased aldosterone via RAAS
Hyperaldosteronism:
(Hyper/hypo)kalemia
(Hyper/hypo)tension
Metabolic (alkalosis/acidosis)
HYPOkalemia
HYPERtension: DBP more elevated than SBP
Metabolic ALKALOSIS (d/t dumping of K+ and H+ in exchange for Na+)
Screening test for Hyperaldosteronism
Primary aldosteronism:
ARR = ___ ; plasma aldosterone = ___ ; (high/low) plasma renin
Aldosterone:Renin ratio
Primary: ARR > 20, plasma aldosterone > 20, LOW plasma renin
High plasma renin = 2ndary
Conn’s syndrome tx
Excision of adrenal aldosteronomas + spironolactone
Adrenal hyperplasia hyperaldosteronism tx:
Spiranolactone, ACEI, CCB
Pheochromococytoma = ____ secretes ____
Presentation:
Dx:
Tx:
Catecholamine-secreting adrenal tumor; Norepinephrine, epinephrine
Palpitation, HA, Excessive sweating
HTN
Increased 24 hr urinary catecholamines including metabolites (metanephrine, vanillylmandelic acid)
Complete adrenalectomy
Preoperative nonselective alpha blockade (phenoxybenzamine, phentolamine x 7-14 days) –> beta blockers/CCB
**DO NOT initiate BB before alpha blockade
T/F: Transsphenoidal sx is 1st line tx of prolactinomas.
False: medical tx for prolactinomas. Cabergoline OR bromocriptine (dopamine agonists inhibit prolactin)
TSS for Active or compressive pituitary tumors EXCEPT prolactinomas.
Tx of Acromegaly
Transsphenoidal sx + Bromocriptine (dopamine agonist –> decreases GH production)
Octreotride: somatostatin analogue that inhibits GH secretion
Gold standard of dx for DM
Other dx of DM
Fasting plasma glucose >126 mg/dL
HA1C >6.5%
Plasma glucose >220
GGT: 2 hr plasma glucose >200
Gold standard of dx for gestational DM
3hr oral glucose tolerance test
Plasma glucose > 200 mg/dL
Screening of DM recommended for:
Pts >45 y/o w/ BP > 135/80
Younger adults w/ BMI >25
>1 additional RF: FHX, low HDL, Polycystic ovarian syndrome, NON-caucasian
1st sign of diabetic nephropathy
Microalbuminuria
Kimmelstiel-Wilson
Nodular glomerulosclerosis; pink hyaline material* around glomerular capillaries
Seen in DM
Type of insulin:
Lispro (Humalog)
Aspart (Novolog)
Insulin coverage?
Onset? Peak? Duration?
Rapid-acting
Given at same time of meals
Onset: 5-15 min
Peak: 1 hr
Duration: 3 hrs
Type of insulin:
Ultralente (U)
Insulin Glargine (Lantus)
Detemir (Levemir)
Insulin coverage?
Onset? Peak? Duration?
Long acting
Covers insulin 1 full day (basal insulin)
Onset: 6-8 hr
Peak: 12-16 hr
Duration: 20-30 hrs
T/F: Lantus (insulin glargine) causes more hypoglycemic episodes than NPH.
T/F: Lantus should not be mixed with other types of insulin
False. Causes less.
True.
Type of insulin:
REgular (humulin-R)
Insulin coverage?
Onset? Peak? Duration?
Short-acting
Given 30-60 mins prior to meals
Onset: 30 min-1 hr
Peak: 2-3 hr
Duration: 4-6 hrs
Type of insulin:
NPH
Lente
Insulin coverage?
Onset? Peak? Duration?
Intermediate
Overs 1/2 day (or overnight)
Onset: 2-4 hrs
Peak: 4-12 hrs
Duration: 16-20 hrs
Dawn phenomenon =
d/t ___
Management:
Normal glucose until 2-8 am when it rises
d/t decreased insulin sensitivity and nightly surge of counter regulatory hormones
Bedtime injection of NPH
Avoid carbohydrate snake late at night
Somogyi effect =
d/t ___
Management:
nocturnal hypoglycemia followed by rebound hyperglycemia
d/t surge in growth hormone
Decrease nighttime NPH dose
OR give bedtime snack
Insulin waning =
Management:
Progressive rise in glucose from bed to morning
Move insulin dose to bedtime or increase dose
Biguanides =
MOA:
SE:
T/F: Causes hypoglycemia and weight gain.
T/F: Decreases HDL
Metformin, Phenformin
MOA:
- decrease hepatic glucose production **
- increase peripheral glucose utilization **
- decrease GI intestinal glucose absorption
- increase insulin sensitivity
SE:
- Lactic acidosis* –> do not give in hepatic/renal impaired pts
- Macrocytic anemia
- Metallic taste
False: Does not effect pancreatic beta cells
False: Decreases triglycerides
Tolbutamide, Chlorpropramide
Glipizide, Glyburide, Glimepiride =
MOA:
SE:
Sulfonylureas (1st gen, 2nd gen)
Stimulates pancreatic beta cell insulin release
SE:
- Hypoglycemia**
- Disulfuram reaction (sulfa allergy)
- Weight gain
- Cardiac dysrhythmias
Repaglinide, Nateglinnide =
MOA:
SE:
Meglitinides
Stimulates pancreatic beta cell insulin release
SE:
- Hypoglycemia (< sulfonylureas)
- Weight gain
Acarbose, Miglitol =
MOA:
SE:
Caution in pts w/ ___
Alpha-glucosidase inhibitors
Delays intestinal glucose absorption
Inhibits pancreatic alpha amylase and intestinal alpha-glucosidase hydrolase
- Does NOT affect insulin secretion
SE:
- Hepatitis (increase LFTs)
- Flatulence, diarrhea, abd pain
- Caution in pts w/ gastroparesis, IBD
Pioglitazone, Rosiglitazone =
MOA:
SE:
Thiazolidinediones
Increase insulin sensitivity at peripheral receptor site adipose and mm.
-NO effect on pancreatic beta cells
SE:
- Fluid retention, edema**
Cardiovascular toxicity w/ Rosiglitazone (MI)**
Hepatotoxicity, Bladder CA, Fractures
Exenatide, Liraglutide =
MOA:
SE:
CI in:
Glucagon-like peptide 1 (GLP-1) Agonists
- Lowers bloos sugar by mimicking incretin
- Increase insulin secretion, decrease glucagon secretion
- Delays gastric emptying
SE:
- Hypoglycemia
- Pancreatitis
CI if h/o gastroparesis*
Sitagliptin (Januvia), Linagliptin =
MOA:
SE:
DPP-4 Inhibitor
Inhibitior of degradation of GLP-1
SE:
- Pancreatitis
- Renal failure
- GI sx
Canagliflozin, Dapagliflozin =
MOA:
SE:
SGLT-2 Inhibitor
(SGLT = Sodium-glucose transport)
-Lowers renal glucose threshold –> Increase urinary glucose excretion **
SE:
-Thirst, Nausea, Abd pain, UTIs
(Hyper/hypo)kalemia is DKA and HHS
HYPOkalema
*Despite serum K levels, patient is always total body potassium deficient
MEN1 =
MEN2a =
MEN2b =
MEN1 = Parathyroid, Pancreas, Pituitary
MEN2a = Medullary thyroid carcinoma, Pheochromocytoma, Hyperparathyroidism
MEN2b = Medullary thyroid carcinoma, Pheochromocytoma, Neuromas/Marfanoid
Gene involved in MEN1:
Gene involved in MEN2:
MEN1: menin gene
MEN2: RET proto-oncogene
Necrolytic migratory erythema associated w/ ___
Glucagonomas (MC @ head of pancreas)
Seen in MEN1 (pancreatic tumor)
MC presenting feature of MEN1
Hyperparathyroidism
vs. MEN2a
MC presenting feature of MEN2
Medullary thyroid carcinoma
VIPomas =
Presentation:
Vasoactive INtestinal peptide tumors
Watery diarrhea, HYPOkalemia, Achlorhydria
Hypovolemia
Dehydration
Seen in MEN1 (pancreatic tumor)
USPSTF recommends screening for hyperlipidemia in ____.
National Cholesterol Education Program recommends screening for hyperlipidemia in ____.
35 y/o if no evidence CVD and no other RF
20 y/o regardless of RF
Monitor recurrence of papillary thyroid cancer with ___
Neck US
Whole body scan
Serum thyroglobulin
Tx of choice for multinodular goiter
Iodine ablation
Type 1 DM may present with ____abs
Beta cell ab: insulin ab, glutamic acid decarboxylase
Islet cell ab
Catecholamines are synthesized in ____
adrenal medulla
Low testosterone w/ low gonadotropin (LH/FSH) suggests ___
secondary hypogonadism = pituitary and/or hypothalamus dysfunction
Low testosterone w/ elevated gonadotropin (LH/FSH) suggests ___
Primary hypogonadism (testicular dysfunction)
SE of carbamazepine include ____
SIADH –> enhance release/potentiate effects of ADH
Tx of Paget disease of bone
Bisphosphate*
Tiludronate
Screening dx of gigantism and acromegaly w/ ____.
Insulin-like growth hormone factor 1 (IGF-1)
GH is pulsatile –> bad for random level check
Pts w/ DM1 w/ recurrent hypoglycemic spells and goor glycemic control despite attention to dietary intake and insulin administration should be evaluated for ___
Celiac disease
Kids w/ DM1 commonly have coexisting Celiac disease
Orthostatic hypotension w/o compensatory increase in heart rate when BP decreases is indicative of ____. MC caused by ___.
Sympathetic autonomic dysfunction
Diabetic autonomic neuropathy
