PANCE Prep- Endocrine Flashcards
Labs:
- increased ACTH and cortisol= ?
- increased ACTH and decreased cortisol = ?
- Decreased ACTH and increased cortisol= ?
- Cushings Disease (pituitary adenoma)
- Addison’s Disease
- Adrenal adenoma
Describe the lab findings for
- primary hypothyroidism
- subclinical hypothyroidism
- TSH-mediated hyperthryoidism
- primary hyperthryoidism
- High TSH, low fT4
- High TSH, normal ft4
- High TSH, high fT4 (2ry or 3ry- same direction)
- Low TSH, high fT4
What do the following thyroid Ab typically mean?
Anti-thyroid peroxidase Ab
Anti-thyroglobulin Ab
Thyroid stimulating Ab (TSH receptor Ab)
- Hashimoto’s or other autoimmune thyroiditis
- Hashimoto’s or other autoimmune thyroiditis
- Specific for Graves disease
RAdioactive iodine test:
- Diffuse uptake
- Decreased uptake
- Hot nodule
- multiple nodules
- cold nodule
- Graves or TSH-secreting pit. adenoma
- Thyroiditis (Hashimotos, postpartum, deQuervain)
- Toxic adenoma
- Toxic Multinodular goiter
- r/o malignancy
- Congential hypothyroidism due to maternal hypothyroidism or infant hypopituitarism
- Macroglossia, hoarse cry, coarse facial features, umbilical hernia, weight gain, mental delay
Cretinism
TX: levothyroxine
How do you dx Euthryoid sick syndrome
Decreased fT4/T3, TSH
Abnormally low T3
Increased reverse T3
How do you treat thyroid storm
- Anti-thyroid meds: IV PTU or Methimazole
- BB for symptomatic tx
- Supportive: IV glucocorticoid (inhibits conversion of T4 into T3), Antipyretics (avoid ASA) , cooling blankets
Tx of Myxedema crisis and who is MC seen in
- extreme form of hypothyroidism
- MC seen in elderly women w/ longstanding hypothyroidism in winter (cold weather)
TX:
- IV levothyroxine
- passive warming w/ blankets- avoid rapid rewarming
- Diffuse, enlarged thyroid
- Thyroid bruits*
- Ophthalmopathy: lid lag, exophthalmos/proptosis
- ***Pretibial myxedema
Grave’s disease
*MC cause of hyperthryoidism
DX: +Thyroid-stimulating immunoglobulins (Ab)
-Low TSH, high fT4/fT3
RAIU: Diffuse uptake
TX: radioactive iodine (MC tx)
- Methimazole or PTU
- BB- sx
- Thryoidectomy
+/- dyspnea, dysphagia, stridor, hoarseness
- No skin/eye changes
- Labs: low TSH, high fT4/T3
- RAIU: PATCHY areas of both increased decreased uptake
Toxic multinodular Goiter
TX: Radioactive iodine
- Methimazole or PTU
- BB
+/- dyspnea, dysphagia, stridor, hoarseness
- No skin/eye changes
- Labs: low TSH, high fT4/T3
- RAIU: increased LOCAL uptake
Toxic adenoma
TX: Radioactive iodine
- Methimazole or PTU
- BB
- Diffuse, enlarged thyroid
- Bitemporal hemianopsia
- Mental disturbance
- Labs: high TSH and fT4/T3
- RAIU: DIFFUSE uptake
TSH secreting pituitary adenoma
TX: Transsphenoidal surgery to remove pit. adenoma
TX of postpartum thyroiditis
- return to euthyroid state in 12-18 months w.o tx
1. ASA
2. No anti-thyoroid meds
*Have + thyroid Ab present
Firm hard, ‘woody’ nodule
Riedels thyroiditis
MC cause of hypothyroidism in the US= ?
MC cause of hypothyroidism in the world = ?
Hashimoto’s Thyroiditis
Iodine deficiency
MC type of benign and malignant thyroid nodules
Benign: Follicular adenoma (colloid)-MC
Malignant: Papillary Carcinoid (80%)
**Only 5% of thyroid nodules are malignant
What thyroid carcinoma?
- Hx of radiation exposure
- young female
- Local cervical lymph node METS
Papillary (MC-80%)
- MC after radiation exposure
* least aggressvie and distant METS are uncommon
* excellent prognosis
What thyroid carcinoma?
- Associated with MEN2
- Secretes Calcitonin
Medullary
What thyroid carcinoma?
- Mc in males >65y/o
- rapid growth w/ compressive sx
- May invade trachea
Anaplastic
*Most aggressive
__ is required for intestinal Ca2+ absorption
What hormones regulate Ca2+ levels
Vit. D
PTH and Calcitriol (Vit. D) increased blood Ca++ (via GI, kidney absorption and increased osteoclast activity)
Calcitonin decreased blood Ca++ (via decrease GI, kidney absorption and increased bone mineralization)
MC causes of primary hyperPTH and secondary hyperPTH
primary: parathryoid adenoma (80%)
Parathyroid hyperplasia/enlargement
-Lithium
secondary: hypocalcemia or vit. D def.
- Chronic kidney failure (MC)
S/S of primary hyperparathyroidism
HYPERcalcemia: “stone, bones, abdominal groans, psychic moans” (kidney stones, bone pain/fractures, ileus, constipation, weakness, fatigue)
-decreased DTR
Labs: TRIAD: HyperCa++, increased PTH, decreased phosphate
-increased 24hr urine calcium excretion
S/S of hypoparathryoidism
HYPOcalcemia: carpopedal spasm, Trousseau’s and Chvosteks sign
-Increased DTR
Labs: TRIAD: HypoCa++, decreased PTH, increase phospate
TX: Ca and Vit. D supp.
What is Chvostek’s sign and Trousseau’s sign
Chvosteks: facial spasm with tapping of the facial nerve
Trousseau: inflation of BP cuff above systolic BP causes carpal spasm
*seen in hypocalcemia
MC of hypocalcemia w/ decrease PTH and increased PTH
Decreased PTH: hypoparathyroidism (autoimmune, post surgical)
Increased PTH: chronic renal dz, liver dz, hypomagnesemia
EKG findings of hypoCa++ and hyperCa++
Hypo: prolonged QT
hyper: shorten QT interval
TX of hypercalcemia
Mild: nothing- tx underlying cause
Sever/symptomatic: IV saline–> furosemide 1st line
*avoid hydrochlorothiazide
DEXA scan of what indicates osteoporosis and what is the tx
T score = -2.5
TX:
- Bisphosphonates (inhibits osteoclasts) (Alendronate, Risedronate, Ibandronate)
- Vit D (Ergocalciferol)
- Selective Estrogen Receptor Modulator (SERM)- Raloxifene
- Estrogen
- PTH tx
- Calcitonin (last line tx)
SE of Bisphosphonates
- Pill esophagititis
- jaw osteonecrosis
- pathologic fx of femur
Blue-tinted sclerae and presenile deafness
Osteogenesis imperfecta
- Bone and prox. muscle pain
- Labs: low Ca and high phosphate, PTH
- Radiographs: periosteal erosions, bony cysts, “salt and pepper” appearance of skull
- Cystic brown tumors on biopsy
Renal osteodystrophy
*Osteitits fibrosis cystica and osteomalacia
TX: phosphate binders: Calcium carbonate, calcium acetate, Sevelamer
2. vit. D active forms (Calcitriol)
How can you differentiate osteoporosis and osteomalacia
Osteoporosis: (bone breakdown) mineral and matrix loss is proportional
-“brittle bones”
Osteomalacia: (vit D def) decreased mineralization of bone osteoid only - cortical thinning
-XRAY: looser lines (zones) and “pseudofracture” lines
“soft bones”
Describe what layers of the adrenal cortex produce each hormone
G- glomerulosa (outer)= A-aldosterone
F- fasiculata= C-Cortisol
R- reticularis = E-estrogen/androgen
MC causes of primary and secondary adrenocortical insufficiency
Primary (Addison’s disease) adrenocortical insuff. = lack cortisol AND aldosterone
- Autoimmune- MC in industrialized countries (causes adrenal atrophy)
- Infection- MC worldwide- TB, HIV (adrenal calcifications)
Secondary= lack of cortisol (MC than primary)
1.Exogenous steroid use
- Hyperpigmentation
- Orthostatic hypotension (decreased aldosterone)
- HyperK+, hypoNA+, Hypoglycemia
- Metabolic acidosis
Primary (Addison’s disease) adrenocortical insuff.
How to dx and tx adrenocortical insuff.
- HD ACTH stimulation test–> little/no increase in cortisol levels= Adrenal insuff
- CRH stimulation test–> Increased ACTH levels but LOW cortisol = primary/Addison
OR
low ACTH and low cortisol= secondary
TX:
primary: Glucocorticoids (Hydrocortisone) + mineralocorticoids (fludrocortisone)
secondary: glucocorticoids only
**During illness/surgery/high fever oral dosing needs to be adjusted to recreate the normal adrenal gland response to stress (ie. 3x normal dose)
Tx of Adrenal (Addisonian) Crisis
- IV fluids: normal saline or D5 if hypoglycemic
- IV hydrocortisone
- fx electrolytes
- Fludrocortisone
Causes of Cushing’s Syndrome
*hypercortisolism
Exogenous: LT HD corticosteroid (MC cause overall)
Endogenous:
- Cushings Disease (70%)- Benign pit. adenoma or hyperplasia (secretes ACTH)
- Ectopic ACTH- small cell lung CA (secretes ACTH)
- Adrenal tumor
How do you dx Cushing’s Syndrome
Screen:
- LD dexamethasone suppression test–> No suppression = Cushings syndrome
- 24hr urinary free cortisol levels –> increased urinary cortisol= Cushings syndrome
- Salivary cortisol levels–> increased cortisol = C.S
Differentiating
- HD dexamethasone suppression test –> Suppression = Cushings Disease OR –> no suppression= adrenal or ectopic ACTH producing tumor
- ACTH levels–> decreased ACTH= adrenal tumors OR –> normal/increased ACTH= Cushings disease or ectopic ACTH producing tumor
Tx of
- Cushings DZ
- Ectopic ACTH-secreting or adrenal tumor
- Iatrogenic steroid tx (hypercortisolism)
- Transsphenoidal surgery
- tumor removal
3 .GRADUAL steroid taper
Causes of primary and secondary hyperaldosteronism
Primary: renin-independent
- idiopathic or idiopathic bilateral adrenal hyperplasia
- Conn’s syndrome: Adrenal aldosteronoma
Secondary: due to increased renin
- renal artery stenosis
- decreased renal perfusion (CHF, hypovolemia)
- Proximal muscle weakness, polyuria*, fatigue, constipation
- Hypertension** HA**, flushing of face
- NOT EDEMATOUS
- Labs: HypoK+ w/ metabolic alkalosis
Hyperaldosteronism
DX:
- Labs: hypoK+ w/ metabolic alkalosis
- Aldosterone:renin ratio screening if hypertensive (ARR>20 and plasma aldosteron >20 and *low plasma renin levels= primary)
- DEFINITIVE TEST: saline infusion test: no decrease in aldosterone level= primary
How to tx hyperaldosteronism
- Conn’s syndrome
- Hyperplasia
- Secondary (renovascular HTN)
- excision of adrenal aldosteronoma + spironolactone (blocks aldosterone)
- Spironlactone, ACEI, CCB
- Angioplasty definitive, ACEI
How do you dx and tx PCC
- increased 24hr urinary catecholamines including metanephrine and vanillymandelic acid
- MRI/CT
- S/S= HTN, palpitations, HA, excessive sweating
TX: complete adrenalectomy
***Preoperative nonselective alpha-blockade w/ PHEnoxybenzamine or PHEntolamine x7-14days followed by BB
(do not initiate w/ BB to prevent unopposed alpha-constriction)
s/s of hyperprolatinemia include: amenorrhea, galactorrhea, infertility because prolactin inhibits gonadotropin-releasing hormone (FSH/LH)
TX ?
TX:
- stop offending drugs (dopamine antagonists)
- Dopamine agonists: Cabergoline* or bromocriptine
What is the difference between type 1 and 2 DM
Type 1: Pancreatitc beta cell destruction (inability to produce insulin) (MC dx <30y/o)
Type 2: insulin resistance and relative impairment of insulin secretion (MC dx >40y/o)
What is the first sign of diabetic nephropathy?
microalbuminuria
TX: ACEI
*DM is most common cause of ESRD (HTN is 2nd MC)
DX of DM
- Fasting plasma glucose:
- 2hr GTT:
- HgbA1c:
- Random plasma glucose:
- Fasting plasma glucose: (Gold standard)- 126 or higher (fasting at least 8 hrs on 2 occasions)
- 2hr GTT: 200 or higher (3 hr GTT is GS for gestational DM)
- HgbA1c: 6.5% or higher
- Random plasma glucose: 200 or higher
Management and goals of DM
- Diet, exercise, lifestyle changes (Carbs 50-60%, protein 15-20%, 10%unsaturated fats)
- HgbA1c <7%
- Lipid control LDL<100
- Neuropathy: Gabapentin, podiatrist x1yr
- Retinopathy: opthalmologist x 1yr
- Nephropathy: ACEI, yearly screening for microalbuminemia and BUN/creatinine
What type of anti-hyperglycemic med? Benefits and SE?
MOA: decreased hepatic glucose production and increases peripheral glucose utilization
-decrease GI intestinal glucose absorption, increase insulin sensitivity no effect on pancreatic beta cells
Biguanides
ex. Metformin
Benefits: NO WT GAIN, 1st line PO meds
SE: Lactic acidosis (don’t give w/ hepatic or renal impairment), GI upset, Macrocytic anemia*
What type of anti-hyperglycemic med?
Benefits and SE?
-Stimulates pancreatic insulin release from beta cells
Sulfonylureas (insulin secretagogue)
ex. 1st gen: Tolbutamide
2nd gen: Glipizide, glyburide, glimepiride
Benefits: 2nd gen have less SE
SE: Hypoglycemia** (MC), GI upset, disulfiram reaction*, WT GAIN
What type of anti-hyperglycemic med?
Benefits and SE?
-Stimulates pancreatic beta cell insulin release
Meglitindies
ex. Repaglinide, Nateglinide
SE: hypoglycemia (less than sulfonylurea), Wt gain
What type of anti-hyperglycemic med?
SE?
-Delays intestinal glucose absorption (inhibits pancreatic alpha amylase and intestinal alpha-glucosidase hydrolase)
Alpha-glucosidase inhibitors
ex. acarbose, Miglitol
SE: Hepatitis (increased LFTs), GI upset
What type of anti-hyperglycemic med?
Benefits and SE?
-Increase insulin sensitivity at peripheral receptor site-adipose and muscle tissue
Thiazolidinediones
ex. Pioglitazone, Rosiglitazone
* no effect on pancreatic beta cells
SE: fluid retention and edema, cardiovascular toxicity w. Avandia, MI
What type of anti-hyperglycemic med?
Benefits and SE?
- Mimics incretin–> increase insulin secretion, decrease glucagon secretion
- Delays gastric emptying
Glucoagon-like peptide (GLP-1) Agonists
ex. Exenatide, Liraglutide
Benefit: no wt gain
SE: hypoglycemia, pancreatitis,
*CI if hx of gastroparesis**, thyroid CA
What type of anti-hyperglycemic med?
Benefits and SE?
-Lowers renal glucose threshold–> increased urinary glucose excretion
SGLT-2 inhibitor
ex. Canagliflozin, Dapaglifozin
SE: thirst, Nausea
Give examples of
- Rapid acting insulin
- Short-acting insulin
- Intermediate acting
- Long acting
- Rapid: Lispro, Aspart (give at the same time of meal- often used w/ long acting)
- Short- regular (given 30-60min prior to meal)
- Intermediate: NPH, Lente (covers insulin for about 1/2day or overnight)
- Long: Detemir, Glargine/Lantus (covers insulin for 1 day, ie. basal insulin)
Normal glucose until rise in serum glucose levels btwn 2am-8am. results from decreased insulin sensitivity and nightly surge of counter regulatory hormones
Dawn Phenomenon
TX: betime injection of NPH (to blunt moring hyperglycemia) aoviding carbs late at night
Noctural hypoglycemia followed by rebound hyperglycemia (due to surge in GH)
Somogyi effect
TX: prevent hypoglycemia by decreasing bedtime NPH dose or give bedtime snack
Progressive rise in glucose from bed to morning
Insulin waning
*seen when NPH dose given before dinner
TX: move insulin dose to bedtime or increase the evening dose
what are kussmaul respirations
deep continuous respirations as lung attempts to blow off excess CO2 to reduce acidemia
**seen w/ DKA
for DKA and HHS, describe:
- plasma glucose
- arterial pH
- Serum bicarb
- ketones
HHS:
- plasma glucose: over 600
- arterial pH: >7.3
- Serum bicarb: >15
- ketones: small
DKA:
- plasma glucose: >250
- arterial pH: <7.3
- Serum bicarb: 15-18
- ketones: Positive
Tx of DKA/HHS
*DKA= DM1, HHS= DM2
- IV fluids** (isotonic 0.9% NS–> then 0.45% NS after hypotension resolves–> then D5 0.45 1/2 NS when glucose reaches 250
- Insulin (regular)
- K+ repletion (despirt serum K elvels, pt always has total K+ def.)
Multiple Endocrine Neoplasia I (MEN I) are rare inherited disorders of 1 or more overactive endocrine gland tumors:
- Parathyroid 90%
- Pancrease 60%
- Pituitary 55%
- Most tumors are benign
- associated w/ Menin gene defect
___ associated w/ presence mucosal neuromas and Marfan-like body habitus
__ have more aggressive form of medullary thyroid carcinoma (presents in infancy)
MEN 2B
MEN 2B
_____ seen only in MEN 2A
____ seen only in MEN 2B
hyperparathryoidism= 2A
Neuromas, marfan-like body habitus= 2B
Multiple Endocrine Neoplasia II (MEN 2) are rare inherited autosomal dominant disorders that are associated w/ what types of tumors?
MEN2 (90%): medullary thyroid carcinoma, PCC, hyperPTH
MEN1 (5%): medullary thyroid carcinoma, PCC, neuromas, Marfanoid
Management of Metabolic Syndrome
- Lifestyle
- weight loss
- phentermine
- Lorcaserin: induces satiety
- Orlistat: inhibits fat absorption - LDL Tx
- TG tx
- Increase HDL
- BP managment
- Insulin resistance: metformin
___ waist circumference of men and __ for women are possible criterias for metabolic syndrome
> 40 inches for men
>35inches for women
