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aa Step 3 World & MTB & cases > UWorld Endo > Flashcards

UWorld Endo Flashcards

1
Q

Metformin management with contrast

A

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.

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2
Q

Possible hyperthyroid in pregnancy

A

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

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3
Q

Physiology of Thyroid Hormone in Pregnancy

A

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.

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4
Q

Lab levels Thyroid in pregnancy

A

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

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5
Q

Pathogenesis of gestational transient thyrotoxicosis

A

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

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6
Q

Hyperaldosetonism

A

-Difficult-to-control hypertension
-Hypokalemia & metabolic alkalosis
-low renin
-No extravascular volume overload (aldosterone escape)
- Normal GLucose in primary hyperaldoseton,

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7
Q

Diagnosis hyperaldosteronism

A

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

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8
Q

Primary hyperaldosteronism Tx

A

Bilateral: Mineralocorticooid receptor antagonist (spironolactone)

Unilateral: surgical resection preferred

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9
Q

Hyperaldosteronism vs pheochromocytoma

A

Pheo only has episodic hypertension. Not resistant hypertenton

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10
Q

Pheochromocytoma Sxs

A

Headache
Palpitations
Tremors
Anxiety
Flushing
Normal labs except metanephrine and catecholamine levels

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11
Q

Best initial step in new hypercalcemia

A

Serum PTH (always first)

Identifies PTH-dependent vs non PTH dependents.

In non dependent follow up with CXR,PTHRP, Vit D levels,

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12
Q

Renal failure affect on calcium

A

Hypocalcemia

(^ phos—> ^ calcium binding,—> low calcium —> ^PTH)

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13
Q

Secondary hyperparathyroidism

A

Compensatory rise in PTH due to HYPOcalcemia

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14
Q

PTH- related protein

A

Most common cause of non PTH dependent hypercalcemia is humoral hypercalcemia of malignancy.

Elevated PTH-related

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15
Q

Primary vs Secondary vs Tertiary hyperparathyroid

A

Primary: high PTH causes high Ca

Second: Low Ca causes high PTH

Tertiary: Long term secondary leads to high PTH with very high Ca

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16
Q

Which Congenital Adrenal Hyperplasia causes hypotension

A

21- hydroxylase deficiency

2 LOW

11B and 17A-
Letter High

17
Q

Congenital adrenal hyperplasia in “girls”

A

21Hydroxylase
11B Hydroxylase

Girls are #x1 (ambiguous genitalia in girls.

(17 in girls lacks development)

18
Q

Congenital Hyperplasia in Boys

A

17a Hydroxylase

Ambiguous genitalia in boys
Absent puberty

7Boys can’t play

19
Q

Elevated in 21 Hydroxylase deficiency

A

17-hydroxyprogesteron

20
Q

Treatment 21 hydroxylase deficiency

A

Glucocorticoids & mineralocorticoids

High salt diet

Psychosocial support

21
Q

Iodine- induces hyperthyroidism features

A

Most often develops in pts with preexisting nodular thyroid disease
Acute thyrotoxicosis (decreases TSH, ^T3&T4)

Increased vascularity +/- nodules

22
Q

Iodine induced hyperthyroidism triggers

A

Radiocontrast agents (hx: angiography, imaging),
Iodine- containing medications (amiodarone),
Iodine- containing topical antiseptic & wound dressings
Kelp-based Diatary supplements

23
Q

Iodine induced hyperthyroidism Tx

A

Self-limited. Beta blocker for symptomatic tachycardia

If persistent hyperthyroid (>4 weeks) or older patients with underlying heart disease: methimazole

24
Q

Subclinical hypothyroidism increased risks

A

Subclinical hypothyroidism increases risk for:
Recurrent miscarriages
Severe preeclampsia
Preterm birth
Low birth wight
Placental abruption

25
Q

Subclinical hypothyroidism findings

A

High TSH

Normal T4

Mild nonspecific symptoms. Or none

MCC: hashimoto (test for anti TPO)

26
Q

Most common cause of hyperglycemia hyperosmolar nonketotic state

A

Major illness
Dehydration
Drugs (corticosteroids, antipsychotics, diuretics, sympathomimetic agents, BB)

27
Q

Insulin management Inpatient

A

SHort acting human insulin on sliding scale

Short is not alone. Basal insulin/ long acting needs to be added as well.

28
Q

First step in management of tachycardia due to thyrotoxicosis

A

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)

29
Q

Evaluation of THyroid nodule

A

Evaluate HPI and PMH for risks of malignancy and compressive symptoms.

Initial Test: TSH and ultrasound

Low TSH- Iodine uptake
All else FNA

30
Q

Initial management once diagnosis of thyroid cancer is made

A

Ultrasound of neck and cervical lymph nodes for initial staging

31
Q

Thyroid lobectomy vs total thyroidectomy

A

<1cm: papillary thyroid - lobectomy

> 1cm, extension outside of the thyroid, distant metastases, Hx of head or neck radiation - total thyroidectomy

32
Q

Congenital hypothyroidism features

A

normal at birth

< 1 month: jaundice, poor feeding, hypothermia

1-4 months: failure to thrive, constipation

33
Q

Treatment congenital hypothyroidism

A

Hormone replacement initiated by age 2 weeks to avoid intellectual disability.

STSRT LEVO IMMEDIATELY

34
Q

Beneficial effects of combined estrogen/ progesterone menopausal hormone therapy

A

Reduces menopausal symptoms
Increases bone mass/ fractures
Decreases risk of colon cancer and DM2
Lower All cause mortality (age <60)

35
Q

Negative effects of combined estrogen/ progesterone menopausal hormone therapy

A

Increase risk of:

venous thromboembolism
breast cancer
Coronary heart disease
Stroke
Gall bladder disease

36
Q

Age and use of menopausal hormonal therapy

A

Women age 50-59 slightly lower risk.

MHT can be safely used for short period (3-5yrs) in younger low risk women.

aa Step 3 World & MTB & cases (13 decks)

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