UWorld Endo Flashcards
Metformin management with contrast
When given with large-dose iodine contrast can increase risk for lactic acidosis .
Discontinue on day of IV iodine exposure and restart 48 hours later.
Possible hyperthyroid in pregnancy
Start with TSH compared to trimester specific norms.
If TSH is suppresses confirm with pregnancyT4. If equivocal use T3.
T4/ T3 not suitable as initial due to reduced specificity/ sensitivity in pregnancy
Physiology of Thyroid Hormone in Pregnancy
Thyroid Hormone increases to meet growing physiological demand. & Elevated estrogen increases TBG.
hCG directly stimulates thyroid hormone release.
TBG becomes saturated
TSH levels decline (feedback)
Net effect: significant increase in total serum hormone levels with normal/ slightly elevated free hormone and low/ low-normal TSH.
Lab levels Thyroid in pregnancy
Normal: slight low TSH, normal free T4, elevated total T4
Hyperthyroid: low TSH, increased free T4, increased total T4
Hypothyroid: increased TSH, decreased free T4, variable total T4.
Free T4 can be normal if subclinical
Pathogenesis of gestational transient thyrotoxicosis
Women with particularly high hCG have increased total and free T.
seen with multiple gestations and hyperemesis gravidum .
Self limiting- resolves as hCG declines by week 14-16
Hyperaldosetonism
-Difficult-to-control hypertension
-Hypokalemia & metabolic alkalosis
-low renin
-No extravascular volume overload (aldosterone escape)
- Normal GLucose in primary hyperaldoseton,
Diagnosis hyperaldosteronism
Elevated aldosterone & low plasma renin (ratio >20)
Absence of aldosterone suppression with oral saline load
CT scan of adrenal glands to determine bilateral hyperplasia vs adenoma
Primary hyperaldosteronism Tx
Bilateral: Mineralocorticooid receptor antagonist (spironolactone)
Unilateral: surgical resection preferred
Hyperaldosteronism vs pheochromocytoma
Pheo only has episodic hypertension. Not resistant hypertenton
Pheochromocytoma Sxs
Headache
Palpitations
Tremors
Anxiety
Flushing
Normal labs except metanephrine and catecholamine levels
Best initial step in new hypercalcemia
Serum PTH (always first)
Identifies PTH-dependent vs non PTH dependents.
In non dependent follow up with CXR,PTHRP, Vit D levels,
Renal failure affect on calcium
Hypocalcemia
(^ phos—> ^ calcium binding,—> low calcium —> ^PTH)
Secondary hyperparathyroidism
Compensatory rise in PTH due to HYPOcalcemia
PTH- related protein
Most common cause of non PTH dependent hypercalcemia is humoral hypercalcemia of malignancy.
Elevated PTH-related
Primary vs Secondary vs Tertiary hyperparathyroid
Primary: high PTH causes high Ca
Second: Low Ca causes high PTH
Tertiary: Long term secondary leads to high PTH with very high Ca
Which Congenital Adrenal Hyperplasia causes hypotension
21- hydroxylase deficiency
2 LOW
11B and 17A-
Letter High
Congenital adrenal hyperplasia in “girls”
21Hydroxylase
11B Hydroxylase
Girls are #x1 (ambiguous genitalia in girls.
(17 in girls lacks development)
Congenital Hyperplasia in Boys
17a Hydroxylase
Ambiguous genitalia in boys
Absent puberty
7Boys can’t play
Elevated in 21 Hydroxylase deficiency
17-hydroxyprogesteron
Treatment 21 hydroxylase deficiency
Glucocorticoids & mineralocorticoids
High salt diet
Psychosocial support
Iodine- induces hyperthyroidism features
Most often develops in pts with preexisting nodular thyroid disease
Acute thyrotoxicosis (decreases TSH, ^T3&T4)
Increased vascularity +/- nodules
Iodine induced hyperthyroidism triggers
Radiocontrast agents (hx: angiography, imaging),
Iodine- containing medications (amiodarone),
Iodine- containing topical antiseptic & wound dressings
Kelp-based Diatary supplements
Iodine induced hyperthyroidism Tx
Self-limited. Beta blocker for symptomatic tachycardia
If persistent hyperthyroid (>4 weeks) or older patients with underlying heart disease: methimazole
Subclinical hypothyroidism increased risks
Subclinical hypothyroidism increases risk for:
Recurrent miscarriages
Severe preeclampsia
Preterm birth
Low birth wight
Placental abruption
Subclinical hypothyroidism findings
High TSH
Normal T4
Mild nonspecific symptoms. Or none
MCC: hashimoto (test for anti TPO)
Most common cause of hyperglycemia hyperosmolar nonketotic state
Major illness
Dehydration
Drugs (corticosteroids, antipsychotics, diuretics, sympathomimetic agents, BB)
Insulin management Inpatient
SHort acting human insulin on sliding scale
Short is not alone. Basal insulin/ long acting needs to be added as well.
First step in management of tachycardia due to thyrotoxicosis
Beta blocker recommended to ameliorate hyperadrenergic symptoms and control heart rate. Initiated as soon as hyperthyroid is noted.
Tachycardia results form increased sympathetic activity due to increased catecholamines (a fib)
Evaluation of THyroid nodule
Evaluate HPI and PMH for risks of malignancy and compressive symptoms.
Initial Test: TSH and ultrasound
Low TSH- Iodine uptake
All else FNA
Initial management once diagnosis of thyroid cancer is made
Ultrasound of neck and cervical lymph nodes for initial staging
Thyroid lobectomy vs total thyroidectomy
<1cm: papillary thyroid - lobectomy
> 1cm, extension outside of the thyroid, distant metastases, Hx of head or neck radiation - total thyroidectomy
Congenital hypothyroidism features
normal at birth
< 1 month: jaundice, poor feeding, hypothermia
1-4 months: failure to thrive, constipation
Treatment congenital hypothyroidism
Hormone replacement initiated by age 2 weeks to avoid intellectual disability.
STSRT LEVO IMMEDIATELY
Beneficial effects of combined estrogen/ progesterone menopausal hormone therapy
Reduces menopausal symptoms
Increases bone mass/ fractures
Decreases risk of colon cancer and DM2
Lower All cause mortality (age <60)
Negative effects of combined estrogen/ progesterone menopausal hormone therapy
Increase risk of:
venous thromboembolism
breast cancer
Coronary heart disease
Stroke
Gall bladder disease
Age and use of menopausal hormonal therapy
Women age 50-59 slightly lower risk.
MHT can be safely used for short period (3-5yrs) in younger low risk women.
