Endocrine - Blueprint

diagnosis of DM

• Patient is symptomatic and has a random BG ≥ 200

• If asymptomatic:

  • Fasting BG ≥ 126 on more than one occasion

  • 2 hour (75 g) OGTT plasma glucose value ≥ 200 

  • A1c values ≥ 6.5%

type 1 DM tx

exogenous insulin - long acting first and short acting (i.e. regular insulin, NPH, lispro, glulisine, glargine, or detemir)

DM II tx*

metformin (biguanide) = INC peripheral sensitivity to insulin and low risk for hypoglycemia

thiazolidinediones (pioglitazone, rosiglitazone)

alpha-glucosidse inhibitors (acarbose)

lucagon-like peptide 1 (GLP1) receptor agonists (exenatide, liraglutide),

dipeptidyl peptidase 4 inhibitors (DPP4) (saxagliptin, sitagliptin),

and sodium-glucose cotransporter 2 inhibitors (SGLT2) (canagliflozin, empagliflozin).

metformin SE

diarrhea, abd cramp

vit B12 def

lactic acidosis

fruity smeling breath =

diabetes-related ketoacidosis

hyperglycemia, ketonemia, anion gap

diabetic-ketoacidosis tx

• Tx precipitating cause

• Correct volume depletion with NS, add dextrose to fluids once glucose is < 200 mg/dL

• Replete potassium deficit (usually falsely elevated), do not start insulin if potassium < 3.3 mEq/L

• IV insulin drip until anion gap closes

• DKA is considered resolved when:

  • pH >7.3, serum bicarbonate is ≥ 18, glucose level is < 200

Hyperosmolar Hyperglycemic State

• Glucose > 600

• Minimal or NO ketonuria or ketonemia

• Arterial pH > 7.3

• Serum bicarb > 20

• Altered LOC

• Serum osmolality > 320

• Resolution: normal serum osmolality, vital signs, and baseline mental status

vit A def

night vision loss, xerophthalmia, dry skin (xerosis), growth retardation, Bitot spots on the conjunctivae

bitot spots = collection of keratin in conjunctiva

vit b1 (thiamine) def

beriberi, Wernicke-Korsakoff syndrome, cardiac failure, heavy alcohol use, malnutrition

vit b2 (riboflavin) def

cheilosis, corneal vascularization (the two Cs of B2)

vitamin b3 (niacin) def

dermatitis, dementia, diarrhea, corn-based diet (pellagra)

vit b3 def (pellagra) tx

niacin supplementation

vitamin b6 (pridoxine) def

sideroblastic anemia, convulsions, peripheral neuropathy, INH use

b12 (cobalamin) def

megaloblastic anemia + neurological symptoms, hypersegmented neutrophils

vit c def

scurvy (↑ bleeding, anemia, loose teeth)

hemorrhage, hyperkaratosis, easy bruising

vit d def

rickets (children), osteomalacia, tetanyb12

vit d def dx + tx

dx = serum vit d <12

tx = >12 months vit d 50 mcg/2,000 IU

<12 months = 10 mcg daily vit d

vit e def

anemia, peripheral neuropathy, ataxia

vit k def

↑ bleeding, ↑ PT/INR, ↑ PTT if severe

folate def

megaloblastic anemia, sensory neuropathy

labs for rickets

↓ calcium, ↓ phosphorus, ↓ 25-hydroxyvitamin D, ↑ parathyroid hormone, ↑ alkaline phosphatase

tx for rickets

vitamin d/calcium supplements

if hereditary with LOW SERUM phosphate = calcitriol

wernicke encephalopathy is assoc with a def in _

thiamine

tx for wernicke encephalopathy and korsakoff syndrome

thiamine

korsakoff also gets magnesium

hypomagnesium causes

malnutrition (restricted diet or old)

chronic ppi

assoc with hypocalcemia and hypoK

what cardiac condition is hypomag assoc with

torsades

hypomagnesemia EKG

LONG qt interval

what risk if you correct hyponatremia too fast?

osmotic demyelination syndrome (centrla pontine myelinosis) → dysarthria, dysphagia, paralysis, death

hyperK risks

kidney failure

rhabdo

tumor lysis syndrome

hyperK sx

bradycardia, weakness, paralysis, cardiac dysrhythmia

peaked T waves**, prolonged PR< wide QRS, short QT, no p wave, sine wave

hyperK tx**

calcium gluconate

Causes of Hypercalcemia

• VITAMINS TRAP Families

  • Vitamin A & D intoxication (hypervitaminosis A & D)

  • Immobilization

  • Thyrotoxicosis  (increases bone resorption)

  • Addison's disease, Acromegaly

  • Milk alkali syndrome (too much tums), Medications (Lithium)

  • Inflammatory disorders

  • Neoplasm (lytic bone mets, MEN I, MEN IIa, multiple myeloma, Zollinger-Ellison Syndrome (gastronoma))

  • Sarcoidosis (granulomas/macrophages produce vit D-like substances)

  • Thiazide diuretics (will increase Ca2+ resorption)

  • Rhabdomylolysis (muscle break down; Ca released from sarcoplasmic reticulum)

  • AIDS (increased bone resorption)

  • Paget's disease, Parathyroid disease, Parental nutrition, Paraproteinemia, Pheochromocytoma, Paraneoplastic syndrome (tumor producing pth-rp [PTH-related peptide, e.g. squamous cell lung  carcinoma - sCa++mous cell)

  • Familial hypocalciuric hypercalcemia – abnormal (low) set-point of calcium sensing receptors (CASR) in the parathyroid for PTH secretion.  Benign; accompanied by ↑Mg++

causes of hypocalcemia

hypoparathyroid

vit D def

chvostek sign

facial muscle contraction

(hypocalcemia or hypoPTH)

trousseau sign

carpopedal spasm

(hypocalcemia or hypoPTH)

EKG of hypocalcemia (long)

prolonged QT interval

lab results for primary hyperparathyroidism

increased PTH, increased calcium, decreased phosphorous

→ parathyroidectomy

labs for hypoPTH

low PTH, low calcium, high phosphorus

tx for hypoparathyroidism

calcitriol and calcium

paroxysmal/episodic headaches, diaphoresis, palpitations, tremors, and vision changes with hypertension, tachycardia, orthostasis =

Pheochromocytoma

pheochromocytoma dx

24 hr urinary catecholamines and metanephrines (TOC if low risk), or ↑ plasma metanephrine levels (TOC if high risk)

pheochromocytoma tx*

• Alpha-blocker** (phentolamine, phenoxybenzamine) prior to beta-blockade to prevent unopposed alpha-agonism

• CCB

• Surgical resection

main thyroid carcinoma

papillary

papillary thyroid carcinoma dx

fine needle aspiration → psammoma bodies

neuroendocrine tumor from parafollicular C cells (produces calcitonin), may be associated with MEN2

medullary

→ diarrhea, flushing

give calcitonin

thyroid carcinoma dx

U/S

final needle aspiration biopsy

blood work

if low TSH → thyroid scan

normal/high tsh → fine needle aspiration

Suspicious features on US: microcalcifications, irregular borders, hypOechoic regions, increased vascularity, taller than is wide, extrathyroid extension

tx for thyroid carcinoma

• total or partial thyroidectomy and TSH suppression with levothyroxine (T4) replacement, or radioiodine therapy in certain pts

can → hypoCa and recurrent laryngeal nerve injury

hyperthyroidism tx*

methimazole or PTU (propylthiouracil)-preg

methimazole MOA

inhibits synthesis of T3 and T4 by blocking oxidation of iodine in thyroid gland

PTU MOA

nhibit the 5’-monodeiodinase that converts thyroxin (T4 - inactive) to triiodothyronine (T3 - active form) in extrathyroid tissue

graves disease findings

exophthalmos

goiter

tibial myxedema

diffusely INC radioactive iodine uptake

POS thyrotropin receptor stimulating antibodies

thyroid storm occurs in pts with

graves disease

• Sx: hyperpyrexia, tachycardia, agitation, altered mental status

• Tx: beta-blocker, thioamide, iodine, glucocorticoids

(low TSH and high T4)

primary hypothyroidism labs

elevated TSH and low T4

subclinical hypothyroidism labs

elevated TSH and normal T4

what lab to check with hypothyroidism?

TSH 6 weeks after initiating

if impaired T4→T3, may need liothyronine

congenital hypothyroidism

thyroid gland dysgenesis

head size inc d/t myxedema

large fontanels

hypotonio

prolonged physiologic jaundice

Prader Willi Syndrome

• Most common syndromic form of obesity

• Caused by absence of expression of the paternally active genes on lang arm of chromosome 15

• Infancy → risk of neonatal hypotonia (risk of asphyxia), difficulty feeding, etc.

• Late childhood and adolescence → premature pubic and axillary hair (early adrenarche), 2º sex characteristics delayed, menarche delayed, obesity, behavior problems

• Adulthood → obesity, short stature, hypogonadism, osteoporosis, etc.

Acromegaly #1 cause

pituitary adenoma

Acromegaly tx

transsphenoidal resection of tumor

MC of pituitary adenoma

prolactinoma

cushing syndrome finding

purple striae

moon face (facial adipose)

buffalo hump (INC adipose tissue in neck and back)

HTN

cushing syndrome dx

1. HIGH 24 hour free urinary free cortisol

2. late night salivary cortisol (if cortisol is high)

3. low dose dexamethasone supp test (elevated cortisol and AM)

4. high ACTH → pituitary tumor → high dose dexamethasone test

5. low ACTH → adrenal tumor

cushing syndrome tx

ketoconazole

Most common noniatrogenic cause of cushing syndrome

hypercortisolism from ACTH_secreting pituitary tumor

Primary Adrenal Insufficiency (aka Addison Disease)

deficiency of cortisol and HIGH ACTH

fatigue

SALT CRAVING

hyperpigmentation

hypotension

addisons disease labs

hyponatremia, hyperK and hyperCa

serum ACTH and MSH HIGH

addisons dx

cosyntropin test

addison tx

primary = daily steroids (corticosteroid → hydrocortisone, mineralcorticoid replacement → fludrocortisone)

Zona Glomerulosa (outermost)

produces mineralocorticoids, i.e. aldosterone (salt)

Zona Fasciculata (middle)

produces glucocorticoids, i.e. cortisol,(sugar)

Zona Reticularis (innermost)

produces androgens, i.e. dehydroepiandrosterone and androstenedione (sex hormone)

screening for DM

1. fasting plasma glucose

2. glycated hemoglobin (A1C)

3. 2 hour plasma glucose w/ oral glucose test (no common)

when is biguanides/metformin CI?

lactic acidosis

liver impairment

Cr >1.5

SGLT2 CI

GFR <45

TZD CI

III or IV heart failure

what laboratory value is associated with addisons?

DEC cortisol level

INC ACTH

DEC ADH level is assoc with

arginine vasopressin disorder (central DI)

thyroid sterm tx

BB!

can add PTU, steroid, and potassium iodide normally if ENDOGENOUS hyperthyroid, if exogenous only do BB

pt is on metformin and you want to add insulin. how?

continue PO med and add LONG ACTING insulin

prolactinoma suspected, next step?

treat with dopamine agonist (cabergoline, bromocriptine)

if that doesn’t work THEN → transsphenoidal surgical resection

incidental thyroid nodule found - what do you do FIRST?

1. TSH titer - if high → fine needle aspiratio biopsy, if low → radioactive iodine scan

Subacute thyroiditis

results from URI/viral

enlarged, painful thyroid gland.

sx like hyperthyroidism but eventually → hypothyroidism

tx - NSAID

toxic multinodular goiter

Plummer syndrome, is characterized by an enlarged, nontender, irregularly nodular thyroid gland

hyperthryoidism with NO exophthalmos

ANION GAP metabolic acidosis causes (MUDPILES)

1. methanol

2. uremia

3. DM ketoacidosis

4. propylene glycol

5. iron/isoniazid

6. lactic acidosis

7. ethylene glycol

8. salicylates

NON ANION gap metabolic acidosis

1. addisons

2. diarrhea

3. renal tubula necrosis

4. saline infusion

most common precipitating factor of thyroid storm (extra hyperthyroid)

infection

first step of hyperthyroidism management

block sympathetic activity (think about the HR) → BB for sx control!

A 29-year-old woman presents with dry eyes. Which of the following would indicate the need for testing for a systemic illness?

dry mouth

(sjogrens)

complete androgen insensitivity syndrome (AIS) (testicular feminization)

genetically male individuals appear female

terus absent

ntimüllerian hormone by the testes

At puberty, the diagnosis is suspected by the development of breasts but absent menstruation and sexual hair

gynecomastia, small testicles, infertility, mild delays, and a low upper-to-lower segment ratio

klinefelter syndrome (XXY)

mullerian agenesis

underdevelopment or absence of the uterus and the upper portion of the vagina in female individuals, while the ovaries and external genitalia are typically normal

breast buds, short stature, pedal edema, and widely spaced nipples

turner syndrome

(also have primary amenorrhea from streak ovaries and ovarian failrue)

sjogren syndrome tx

pilocarpine or cevimeline (to stimulate saliva)

Hyperaldosteronism (conn syndrome) labs (aka opposite of addisons)

resistant HTN

hypokalemia

hypernatremia

Metabolic alkalosis,

hypomanesium

dx = CT or MRI to look for adrenal adenoma

Treatment is with high-dose spironolactone or eplerenone (aldosterone antagonist)

you suspect addisons. what’s the FIRST lab you want to look at?

morning free cortisol level

(if low, THEN you can do cosyntropin stimulation test)