Glucagonoma
Clx	Necrolytic migratory erythema –        Erythematous papules/plaques on face, perinueum, extremities –        Lesions enlarged, coalesce over next 7-14 days with central clearing and blistering, crusting &scaling at borders.
	DM –        Mild hyperglycemia controlled easily with oral agents and diet.
	GIT symptoms –        Diarrhea, anorexia, abdominal pain, constipation. Other findings: –        Weight loss –        Neuropsychiatric (such as: ataxia, dementia, proximal muscle weakness) –        Association with venous thrombosis.

	Multiple Endocrine Neoplasia
1	Primary hyperparathyroidism (parathyroid adenomas or hyperplasia) Pituitary (prolactin, visual defects) Pancreatic tumors (especially gastrinomas)
2A	Primary hyperparathyroidism (parathyroid hyperplasia) Pheochromocytoma Medullary thyroid cancer (calcitonin)
2B	Medullary thyroid cancer (calcitonin) Pheochromocytoma Mucosal neuromas/marfanoid habitus

MEN 1
Pituitary adenomas	–        Secretion of prolactin, growth hormone, ACTH (or “nonfunctioning’ tumors) –        Mass effects (eg, headache, visual field defects)
Primary HyperPTH	–        Multiple parathyroid adenomas or parathyroid hyperplasia –        Hypercalcemia (eg, polyuria, Nephrolithiasis, ⤵️ bone density)
Pancreatic/GI Neuroendocrine tumors	–        Gastrinoma – recurrent peptic ulcers –        Insulinoma – hypoglycemia –        VIPoma – secretory diarrhea, hypokalemia, hypochlorhydria –        Glucagonoma – weight loss, necrolytic migratory erythema, –        hyperglycemia

Insulin Physiology
Liver	Glycogenesis ⤴️	Glycogenesis ⤵️
Muscle	Glycogenesis ⤴️	Glycogenesis ⤵️
Fat	Triglyceride storage	Fat breakdown/ketone synthesis

DM Dx
Blood	HgbA1C	Sx + Glu 200
Repeat 2x	Repeat 2x	No need to repeat
>126	≥ 6.5	>200

Routine Evaluation of Patients with T2DM
Retinal exam	At time of dx then annually
HbA1c	Every 3 to 6 months
Blood chemistries and renal function	Every 6 months
Complete foot exam	Annually
Lipids	Every several years
Urine microalbumin/creatinine ratio	At time of dx then annually

Urine dipstick for protenuria
Trace	Between 15 and 30 mg/dL
+1	Between 30 and 100 mg/dL
+2	Between 100 and 300 mg/dL
+3	Between 300 and 1000 mg/dL
+4	>1000 mg/dL

Tx

Start w/ lifestyle changes

If A1c is >7 –> Start meds (Metformin) –(renal failure?)–> GLP-1 (-tide)

—– still >7? Add another med (Sulfonylurea)

—– still >7? Start Insulin / or add another med (TZD)

If A1c >9 (at time of dx) –> Start insulin.

Recommended glycemic control goals for adults w/ DM
Fasting glucose	80-130
Postprandial glucose	<180
Hemoglobin Alc	<7%
-Suitable for most nonpregnant females. -Less strict targets are reasonable for pts with limited life expectancy, comorbid conditions, or ⤴️ hypoglycemia risk.

Diabetic Ketoacidosis
Pt	–        Young age –        Brittle type 1 diabetes –        May be initial manifestation of diabetes
Clx	–        Acute to subacute onset Initial:  Polydipsia/polyuria, blurred vision, weight loss Later: changed mentation, –        hyperventilation, abdominal pain
Dx	–        Glucose 250-500 mg/dL –        Bicarbonate mEq/L –        ⤴️ anion gap –        Positive serum ketones
Tx	–        High-flow IV fluids –        IV insulin –        Follow & replace potassium

Hyperosmolar hyperglycemic state
Pt	Type 2 DM Older age
Clx	–        Gradual hyperglycemic symptoms (eg, polyuria, polydipsia) –        Altered mentation
Dx	–        Glucose >1000 –        Normal pH & bicarbonate –        Normal anion gap –        Negative or small serum ketones –        Serum osmolality >320
Tx	–        Excessive hydration with normal saline –        Intravenous insulin –        Careful monitoring & supplementation of potassium

DKA		HHS
Pt	–        Type 1 –        Younger pt	–        Type 2 –        Older pt
Clx	–        Less AMS –        Rapid onset –        ⊕ Hyperventilation & abdominal pain	–        More AMS –        Gradual onset
Labs	–        Glucose 250-500 mg/dL –        Bicarbonate <18 –        Elevated anion gap –        ⊕ serum ketones –        Serum osmolality <320	–        Glucose >600 –        Bicarbonate >18 –        Normal anion gap –        ⊖ or small serum ketones –        Serum osmolality >320

Management of DKA & HHS
IVF	–        High-flow 0.9% normal saline is initially suggested –        Add dextrose 5% when serum glucose is < or equal 200 mg/dL
Insulin	–        Initial continuous IV insulin infusion –        Switch to SQ (basal bolus) insulin for the following: Able to eat, glucose <200 mg/dL, –        anion gap <12 mEq/L, serum HC03 215 mEq/L –        Overlap SQ & IV insulin by 1-2 hours
Potassium	–        Add IV potassium if serum K+ = or < 5.2 –        Hold insulin for serum <3.3 –        Nearly all patients K + depleted, even with hyperkalemia
Bicarbonate	–        Consider for patients with pH <6.9
Phosphate	–        Consider for serum phosphate <1.0 mg/dL cardiac dysfunction, or respiratory depression –        Monitor serum calcium frequently

Tx of DKA & HHS
IVF	–        0.9 NS –        When to add 5% dextrose? if Glucose = or < 200
Insulin	–        IV Reg Insulin –        Switch to SQ, when? 1.     Eating is possible, 2.     glucose <200 3.     anion gap < 12 mEq/L, 4.     serum HCO3 > or = 15 mEq/L –        (Overlap SQ & IV insulin by 1-2 hours)
K+	–        IV potassium if K + < or = 5.2 –        When to stop insulin? K+ < 3.3
Bicarbonate	–        When? If pH <6.9

Tx of DKA & HHS
IVF	0.9 NS Dextrose when GLU <200
Insulin	IV Regular Insulin if the anion gap closes à switch to SQ
K+	Add IV potassium if serum K+ is equal or less than 5.2 Stop insulin for serum K + <3.3
Bicarb	If PH <6.9

Charcot joint (neurogenic arthropathy)
RF	–        Diabetic neuropathy –        Any peripheral neuropathy (Vit B12 def, 30 syphilis, SC injury)
Pathology	–        ⤵️ ROM –        ⤵️ Sensation & proprioception –        changed weight bearing & recurrent trauma -9 deformity + ulcer
clx	–        Impaired mobility / Foot & ankle deformity –        Mild pain –        X-ray: bone & joint destruction, fragmentation, subluxation/dislocation
Tx	–        Mechanical offloading & correction of joint mechanics (Casting, orthotics)

Diabetic foot ulcers
RFs	–        Diabetic neuropathy (loss of protective sensation, small muscle atrophy, abnormal –        vascular tone, ⤵️ sweating with fissures) –        Arterial insufficiency –        End-stage renal disease in a patient on dialysis –        Smoking
Location	Plantar surface, areas under pressure points (bony prominences)
Tx	–        Mechanical offloading –        Debridement –        Wound dressings –        Antibiotics if infected

Class	Generic Name	Brand Name	Doses/Day
Sulfonylureas	Glyburide, glipizide, Glimepiride	Micronase, Diabeta, Amaryl	1-2
Biguanides	Metformin	Glucophage	2-3
Thiazolidinediones	Rosiglitazone, pioglitazone	–	1
Glucosidase inhibitors	Acarbose, miglitol	Precose	With every meal
Meglitinides	Repaglinide, nateglinide	–	–
DPP-IV inhibitors	Sitagliptin, saxagliptin,  linagliptin	Januvia, Onglyza, Tradjenta	–
Subcutaneous agents
GLP-I	Exenatide, liraglutide	Byetta, Victoza	2/day, 1/day

Testicular Cancer
#	–        Age 15-35 –        RF: FHx, cryptorchidism
Signs and symptoms	–        (u) nonpainful testicular nodule or swelling –        Dull lower abdominal ache –        Metastatic sx (SOB, neck mass, low back pain)
Dx	–        PEx: firm, ovoid mass or@ swelling –        Scrotal US –        Tumor markers (AFP, ß-hCG)  –        staging (CT/CXR)
Tx	–        Surgery: Radical orchiectomy –        Chemotherapy –        Cure rate is almost 95%

Male hypogonadism
	Primary (testicular disease)	Secondary (pituitary/hypothalamic disease)
?	–       ⤵️Energy/libido, ⤵️ body hair –       Gynecommastia more likely –       ⤴️ LH/FSH –       ⤵️⤵️Testesterone/sperm count	–       ⤵️ Energy/libido, ⤵️ body hair –       Gynecommastia more likely –       ⤵️/ Normal LH/FSH –       ⤵️Testesterone/sperm count
Causes	–        Congenital (Klinefelter syndrome) –        Varicocele –        Acquired –        Radiation –        Infection (mumps) –        Trauma –        Medications (alkylating agents, glucocorticoiods) –        Chronic disease	–        Congenital (Kallman syndrome) –        Gonadotropin suppression –        Hyperprolactinemia –        Glucocorticoids/opiates –        Gonadotroph cell damage –        Benign/malignanat tumers –        Pituitary apoplexy –        Infiltration (eg,hemochromatosis) –        Systemic disease
Dx	Karyotype Others based on clinical suspicion	–        Prolactin –        Transferrin –        +/- MRI

Common causes of hypogonadism in men
Primary (testicular)	–        Congenital (eg, Klinefelter syndrome, cryptorchidism) –        Drugs (eg, alkylating agents, ketoconazole) –        Orchitis (eg, mumps), trauma, torsion –        CKD
Secondary (pituitary/ hypothalamic)	–        Gonadotroph damage: Tumor, cranial trauma, infiltrative diseases (Hemochromatosis), apoplexy –        Gonadotropin suppression : Exogenous androgens, hyperprolactinemia, DM,  morbid obesity
Combined (primary & secondary)	–        Hypercortisolism –        Cirrhosis –        Alcohol

Androgen Abuse
Types	–        Exogenous (Testosterone replacement) –        Synthetic (Stanozolol, nandrolone) –        Androgen precursors (DHEA)
SE	Reproductive: –        Men 🤵🏻à ⤵️ testicular function & sperm production, gynecomastia –        Women 👩🏻 à acne, hirsutism, voice deepening, menstrual irregularities CVS: left ventricular hypertrophy, possible ⤵️HDL & ⤴️ LDL Psychiatric: antagonistic behavior (men), mood disturbances Hematologic: polycythemia, possible hypercoagulability

Cushing Syndrome
Clx	–        Trunk obesity (eg, fat accumulation in the cheeks & dorsocervical & supraclavicular fat pads) –        Skin atrophy & wide, purplish striae –        Proximal muscle weakness/atrophy –        HTN –        Glucose intolerance –        Skin hyperpigmentation (if ACTH excess)
Dx	–        1st: 24-hour free urinary cortisol excretion OR 1 mg dexamethasone suppression test à if abnormal   –        2nd: ACTH if ⤵️ cushing / if ⤴️ Pituitary/ ectopic) –        3rd: high dose (8 mg) dexamethasone suppression test –        If Suppressed? Pituitary –        If Not Suppressed? Ectopic
Tx	–        Surgery –(if u can’t)–> ketoconazole or metyrapone.

Primary Hyperaldosteronism
Clx	–        HTN, –        Metabolic alkalosis, –        hypokalemia, mild hypernatremia –        No significant peripheral edema due to aldosterone escape
Dx	–        Plasma aldosterone to plasma renin activity ratio >20 suggests Dx –        Adrenal suppression testing after oral saline load à Dx –        Abdominal CT & adrenal venous sampling to ddx b/w (U)adrenal adenoma & (b) adrenal hyperplasia
Tx	–        ⓤ adrenal adenoma à Surgery (preferred) –        Aldosterone antagonists (eg, spironolactone, eplerenone) if patient can’t go for surgery –        ⓑ adrenal hyperplasia: Aldosterone antagonists

	Primary Aldosteronism	Secondary Aldosteronism
Diastolic HTN	+	–
Muscle weakness	+	–/+
Polyuria, polydipsia	+	–/+
Edema	–	–/+
Hypokalemia	+	+
Hypernatremia	+	–
Metabolic alkalosis	+	+
Renin	–	+

Primary vs. Central adrenal insufficiency
Primary		Central
MCC	Autoimmune	Chronic glucocorticoid use
Cortisol	⤵️	⤵️
ACTH	⤴️	⤵️
Aldosterone	⤵️	Normal
Clx	–        Severe symptoms –        Hyperpigmentation –        Hyperkalemia –        Hyponatremia –        Hypotension	–        Less severe symptoms –        No hyperpigmentation –        No hyperkalemia –        Possible hyponatremia

Primary Adrenal Insufficiency
?	–        Autoimmune –        Infections (TB, HIV, Fungal) –        Hemorrhagic infarction –        Metastatic
Clx	–        ⤵️ Aldosterone & Cortisol / ⤴️ ACTH –        Fatigue, weakness, anorexia/weight loss, salt craving –        Postural hypotension –        Hyperpigmentation or vitiligo –        Hyponatremia, hyperkalemia –        Can cause acute adrenal crisis (abdominal pain, shock, fever, reformed mental status)
Dx	–        ACTH, serum cortisol & high-dose (250 mg) ACTH stimulation test –        Primary adrenal insufficiency: Low cortisol, high ACTH –        Secondary/tertiary adrenal insufficiency: Low cortisol, low ACTH

Clx Presentation of Primary adrenal insufficiency
Causes	–        Autoimmune –        Infections (eg, TB, HIV, Disseminated fungal) –        Hemorrhagic infraction (eg, meningococcemia, anticoagulants) –        Metastatic cancer (eg, Lung)
S/S	–        Acute: –        Usually with shock –        Abdominal pain with deep palpation (unclear causes) –        Unexplained fever –        Nausea, vomiting, weight loss, anorexia –        Hyponatremia, hyperkalemia, hypercalcemia, eosinophilia –        Chronic: –        Fatigue, weakness, anorexia
Dx	–        Measures ACTH and serum cortisol with high-dose (250 ug) ACTH stimulation test. –        Primary adrenal insufficiency: Low cortisol, high ACTH –        Secondary/tertiary adrenal insufficiency: Low cortisol, low ACTH

Pheochromocytoma
#	–        25% inherited: VHL gene (von Hippel-Lindau) / RET gene (MET type 2) / NFI gene (NF1) –        sx from ⤴️ catecholamine secretion
Sx	–        EPISODIC –        Headache –        Tachycardia/palpitations –        Sweating –        Severe HTN
10	–        10% ⓑ –        10% extra-adrenal (paragangliomas) –        10% malignant
Dx	⤴️ urinary & plasma catecholamines & metanephrines

	Acute adrenal crisis
Features	·       pts on long-term glucocorticoid therapy who have Cushingoid features (eg, central obesity, moon facies) are at very high risk of adrenal crisis.
S/S	weakness, abdominal pain, loss of appetite, mild hyponatremia. postural hypotension and hyperkalemia. FEVER
Dx	ACTH stimulation test
Tx	Treatment includes hydrocortisone or dexamethasone with aggressive fluid support.

	Acute adrenal crisis
causes	Adrenal hemorrhage or infarction Acute illness injury/surgery in pt with chronic adrenal insufficiency or a long-standing Glucocorticoid use.
Features	weakness, abdominal pain, vomiting, Shock/hypotension Nausea FEVER
Tx	hydrocortisone or dexamethasone with aggressive IV fluid support.

Acute adrenal insufficiency (adrenal crisis)
RF	·       Adrenal hemorrhage / infarction ·       Acute illness, injury, or surgery in patients with: ·       Chronic adrenal insufficiency ·       Chronic glucocorticoid use ·       Congenital adrenal hyperplasia
S/S	·       Hypotension shock ·       Nausea & vomiting, ·       abdominal pain ·       Weakness ·       Fever ·       Acute kidney injury
Dx	·       Cortisol ·       Electrolytes, BUN, creatinine, glucose ·       ACTH ·       Renin ·       ACTH stimulation test when stable
Tx	·       Hydrocortisone or dexamethasone ·       High-flow intravenous fluids ·       Monitor serum electrolytes

Classic Cong Adrenal Hyperplasia
Path	–        AR –        21 -hydroxylase deficiency
Clx	–        Salt-wasting syndrome in neonatal boys & girls 1.     Hypotension 2.     Dehydration 3.     Vomiting –        Ambiguous genitalia in girls
Labs	⤵️ Sodium, ⤴️ potassium, ⤵️ glucose ⤴️17-a-hydroxyprogesterone
Tx	–        GCS & MCS –        High-salt diet –        Genital reconstructive surgery for girls –        Psychosocial support

Androgen Abuse
Types	–        Exogenous (Testosterone replacement) –        Synthetic (Stanozolol, nandrolone) –        Androgen precursors (DHEA)
SE	Reproductive: –        Men 🤵🏻à ⤵️ testicular function & sperm production, gynecomastia –        Women 👩🏻 à acne, hirsutism, voice deepening, menstrual irregularities CVS: left ventricular hypertrophy, possible ⤵️HDL & ⤴️ LDL Psychiatric: antagonistic behavior (men), mood disturbances Hematologic: polycythemia, possible hypercoagulability

Prolactinoma overview
Clx	–        Premenopausal women: Oligo/amenorrhea, infertility, galactorrhea, hot flashes, ⤵️ bone density –        Postmenopausal women: Mass effect symptoms (headache, visual field defects) –        Men: Infertility, ⤵️ libido, impotence, gynecomastia
Dx	–        Serum prolactin (often >200 ng/mL) –        Rule out renal insufficiency (creatinine) & hypothyroidism (thyroid-stimulating hormone, thyroxine) –        Magnetic resonance imaging of the brain/pituitary
Tx	–        Dopamine agonist (cabergoline) –        Trans-sphenoidal surgery

Clx features of Acromegaly
Local tumor effect	–        Pituitary enlargement, visual field defects, headache, cranial nerve defects
MSK/Skin	–        Gigantism, maloccluded jaw, arthralgias/arthritis, proximal myopathy, hyperhidrosis, –        skin tags, carpal tunnel syndrome
Cardiovascular	–        Cardiomyopathy, HTN, heart failure, valvular disease (eg, mitral & aortic –        regurgitation
Pulmonary/Gastrointestinal	–        Sleep apnea, narcolepsy, colon polyps/cancer, diverticulosis
Enlarged organs	–        Tongue, thyroid, salivary glands, liver, spleen, kidney, prostate
Endocrine	–        Galactorrhea, ⤵️ libido, diabetes mellitus, hyperparathyroidism, –        hypertriglyceridemia

SIADH
#	–        CNS (Stroke, hemorrhage, trauma) –        (Carbamazepine, SSRIs, NSAIDs) –        Lung (Pneumonia) –        Ectopic ADH secretion (SCLC)
Clx	–        Euvolemic Hyponatremia: Headache, confusion / forgetfulness –        PEx: pt is EUVOLEMIC = no edema –        If Severe hyponatremia: SZ, coma
+	–        Hyponatremia –        Serum osmolality <275 (hypotonic) –        Urine osmolality >IOO / Urine sodium >40
Tx	–        Fluid restriction ± salt tablets –        Demeclocycline (⤵️ responsiveness to ADH) –        Vaptan (ADH receptor ×) –        Hypertonic (3%) saline for severe hyponatremia

In SIADH, when to use Demeclocycline, MoA?

–        Acts at renal tubules to ⤵️ responsiveness to ADH –        Use when fluid restriction therapy fails

	Primary polydipsia	Central DI	Nephrogenic DI
Defect	Extra Water intake	low ADH release from pituitary	ADH resistance in kidney
Etiology	• Antipsychotics • Anxious, middle-age women	• Idiopathic • Trauma • Pituitary surgery • Ischemic encephalopathy	• Chronic lithium use • Hypercalcemia • Hereditary (AVPR2 mutations)
Clinical	Low serum Na	High serum Na	Normal serum Na

Secondary Causes of Osteoporosis
Endocrine	–        Hyperthyroidism –        Hyperparathyroidism –        Hypercortisolism –        Hypogonadism
Metabolic/ nutritional	–        Calcium &/or vitamin D deficiency –        Eating disorders
GI/hepatic	–        Malabsorption (Celiac disease, Crohn disease) –        Chronic liver disease –        Bariatric procedures
Renal	–        Chronic kidney disease –        Renal tubular acidosis –        Hypercalciuria
Tx	–        CGS –        Heparin –        Phenytoin, carbamazepine –        Aromatase inhibitors –        Medroxyprogesterone (depot) –
+	–        Inflammatory (Rheumatoid arthritis) –        Multiple myeloma –        Alcoholism –        Immobilization

Clx of Osteomalacia
?	–        Malabsorption –        Intestinal bypass surgery –        Celiac sprue –        Chronic liver disease –        Chronic kidney disease
S/S	–        May be asymptomatic –        Bone pain and muscle weakness –        Muscle cramps –        Difficulty walking, waddling gait
Dx	–       ⤴️ Alkaline phosphatase, ⤴️ PTH –       low serum calcium and phosphorus, low urinary calcium –       low 25 OH-D levels –       X-rays may show thinning of cortex with reduced bone density –       Bilateral and symmetric pseudofractures (Looser zones) are characteristic radiologic finding

Etiology for HyperPTH
HyperPTH	Primary	Adenoma
	Secondary	Renal Failure
	Tertiary	Autonomous PTH
Malignancy	Metastatis (Ostolytic)	Breast Cancer Multiple Myeloma
	Ectopic PTH	Lun SqCC Ovarian cancer

If the patient has a nodule:

Do thyroid function tests (T4 and TSH) If normal à biopsy of the gland.

Papillary	Most Popular –  Psammoma body – Post-radiation – Tx: Surgery / Radiation + Surgery (if big tumor)
Follicular	Spread hematogenously – dont use FNA – Tx: total thyroidectiomy –> Radiation
Medullary	MEN syndrome – Calcitonin – Tx: surgery
Anaplastic	Most aggressive, least common.

Dz	uptake	character
Grave’s	⤴️	diffuse
Toxic adenoma	⤴️	local
Mutinodular goiter	⤴️	nodular patter
thyroiditis	⤵️	⤴️ thryroglobulin
Iodine	⤵️	⤴️ thryroglobulin
Exogenous	⤵️	⤵️ thryroglobulin

Thyrotoxicosis with ⓝ or ⤴️ RAIU	Thyrotoxicosis with ⤵️ RAIU
–        Graves’ disease –        Toxic multinodular goiter –        Toxic nodule	–        Painless (silent) thyroiditis –        Subacute (de Quervain) thyroiditis –        Amiodarone-induced thyroiditis –        Excessive dose (or surreptitious intake) of levothyroxine –        Iodine-induced

Hyperthyroidism Clx manifestations
Sx	–        Anxiety & insomnia –        Palpitations –        Heat intolerance –        ⤴️ perspiration –        Weight loss without ⤵️ appetite
PEx	–        Goiter –        HTN –        Tremors including fingers/hands –        Hyperreflexia –        Proximal muscle weakness/atrophy –        Lid lag –        Atrial fibrillation

Hypothyroidism effects

⤴️ lipids ⤵️ Na ⤴️ CK ⤴️ LFTs

·       Clx of Grave’s disease
General	Heat intolerance, weight loss, sweating
Eyes	Lid lag, proptosis, diplopia
Skin	Hair loss, infiltrative dermopathy (pretibial myxedema)
Cardiovascular	Tachycardia, HTN, atrial fibrillation
Nails	Onycholysis, clubbing (acropachy)
Endocrine	Hyperglycemia, hypercalcemia, bone loss, menstrual irregularities
Gastrointestinal	Diarrhea
Neurology	Tremors, hyperreflexia, proximal muscle weakness

Graves Tx complications
Antithyroid drugs	·       Agranulocytosis ·       Methimazole: First trimester teratogen, cholestasis  ·       Propylthiouracil: Liver failure, ANCA- related vasculitis
Radioiodine ablation	·       Permanent Hypothyroidism ·       Worsens Ophthalmopathy ·       Possible Radiation side effects
Surgery	·       Permanent Hypothyroidism ·       Risk Of persistent laryngeal nerve damage ·        hypoparathyroidism

	TSH	Sx/PE findings	Tests	Tx
Graves’ disease	⤵️	Exophthalmos, visual deficits, pretibial myxedema, Autoimmune diseases	Thyroid- stimulating Ig (+)	Propranolol, PTU/ methimazole, RAI ablation. subtotal thyroid removal
Toxic nodular goiter	⤵️	Nodules	RAIU scan	RAI ablation
Thyroiditis	⤵️	subacute Pain, postpartum (< I year)	RAIU scan (low uptake); among them It differs	Propranolol for symptoms; differs depending on nature
Factitious hyperthyroidism	⤵️	Absence of goiter	Thyroglobulin (low)	Psychotherapy
Struma ovarii	⤵️	Abdominal mass	Abdominal CT	Resection
2ndry hyperthyroidism	⤴️	Bitemporal hemianopsia	MRI	Resection
Amiodarone-induced hyperthyroidism	⤴️	On amiodarone	Clinical Dx.	D/c

Thyroiditis Types
Autoimmune (Hashimoto)	–        Main hypothyroid features –        Diffuse goiter	(+ve) Anti-TPO antibody
Painless (silent thyroiditis)	–        Chronic autoimmune thyroiditis –        Mild, short-term hyperthyroid phase –        Small, nontender goiter –        Spontaneous recovery	Positive TPO antibody RAIU: Low uptake
Subacute (de Quervain)	–        Possible post-viral inflammatory process –        Prominent fever & hyperthyroid symptoms –        Sore/tender goiter	Elevated ESR & CRP RAIU: Low uptake

Thyroiditis
	Clx	Tests
Chronic autoimmune thyroiditis (Hashimoto thyroiditis)	–        Major hypothyroid features –        Diffuse goiter	–        TPO antibody –        Variable radioiodine uptake
Painless thyroiditis (Silent thyroiditis)	–        Different of chronic autoimmune thyroiditis –        Minor, brief hyperthyroid stage –        Small, nontender goiter –        Self-limited	–        (+ve) TPO antibody –        ⤵️radioiodine uptake
Subacute Thyroiditis (de Quervain thyroiditis)	–        Possible post-viral inflammatory process –         Protruding fever & hyperthyroid s/s –        Sore/tender goiter	–        ⤴️ ESR & CRP –        ⤵️ radioiodine uptake

Causes of Thyroiditis
	Subacute granulomatous thyroiditis	Hashimoto thyroiditis
Clx	–        Usually following a viral illness –        Painful thyroid expansion –        Transient hyperthyroid symptoms	–        Autoimmune causes –        nontender thyroid enlargement –        Major hypothyroid features
Dx	–        ⤴️ ESR & CRP(C-reactive protein) –        ⤵️ radioiodine uptake	–        (+ve) TPO antibody –        Variable uptake of radioiodine
Path	–        macrophages & giant cells infiltration.	–        Lymphocytic infiltration with  well-developed germinal centers –        Hürthle cells (eosinophilic epithelial cells)

Thyroid Storm
Causes	–        Surgical procedure Thyroid or non-thyroid –        Acute sickness (eg, trauma, infection), child delivery –        Acute iodine load (eg, iodine contrast)
S/S	–        High grade fever. –        Tachycardia, HTN, CHF, cardiac arrhythmias (eg, atrial fibrillation) –        Anxiety, delirium, seizure and coma –        Goiter, lid lag, tremor –        Nausea, vomiting, diarrhea, jaundice

Neonatal Thyrotoxicosis
Path	–        Transplacental passing of maternal anti- TSH receptor antibodies –        Antibodies bind to infant’s TSH receptors & cause excessive thyroid hormone release
S/S	–        Warm, moist skin –        Tachycardia –        Poor feeding, irritability, poor weight gain –        preterm birth or low birth weight
Dx	–        Maternal anti-TSH receptor antibodies equal or more than 500% normal
Tx	–        Self-resolves within 3 months (disappearance of maternal antibody) –        Methimazole PLUS ß blocker

CVS Effects of Thyrotoxicosis
Rhythm	–        Sinus tachycardia. –        Premature atrial & ventricular complexes –        Atrial fibrillation/flutter
Hemodynamic effects	–        Systolic HTN & ⤴️ pulse pressure –        ⤴️ Contractility & cardiac output –        ⤵️Systemic vascular resistance –        ⤴️ Myocardial oxygen demand
Heart failure	–        High-output failure –        Exacerbation of pre-existing low-output failure
Angina symptoms	–        Coronary vasospasm –        Pre-existing coronary atherosclerosis

Congenital Hypothyroidism
Clx	Initially NORMAL at birth Symptoms develop after maternal T4 ⤵️: –       Lethargy –       Enlarged fontanelle –       Protruding tongue –       Umbilical hernia –       Poor feeding –       Constipation –       Dry skin –       Jaundice
Dx	–       ⤴️ TSH & ⤵️ free T4 levels –       Newborn screening (mandatory)
Tx	Levothyroxine

• Dosing:
• Gradual increase in elderly
• Increase w/ Estrogen or SERM
• ⤴️ in pregnancy
• ⤵️  w/ Glucocorticosteroids
• Check TSH in 6 weeks, DO NOT CHANGE THE DOSE BEFORE THAT
• if normal –> Maintain the dose
• If ⤴️ –> Suboptimal –> Increase
• If ⤵️ –> too much dose –> decrease

• presence of anti-TPO antibodies 
• clinical symptoms of hypothyroidism
• hyperlipidemia
• menstrual dysfunction
• TSH >10

Thyroditis	Pain	Hx/PEx/Labs/Dx	RAIU	Tx
Subacute	YES	⤴️ ESR T4/T3 (⤴️ → ⤵️) Self-limited	LOW	Aspirin Severe: prednisone
Lymphocytic Postpartum	NO!!	Ⓝ ESR T4/T3 (⤴️ → ⤵️) Symmetrical enlargement Self-limited	LOW	BB (Propanolol)
Hashimoto’s	NO	⤴️ TSH ⤵️ T3/T4 ⤴️ risk of lymphoma ⊕ Anti-TPO	LOW	Levothyroxine
Reidel’s	NO	Fibrotic thyroid + other parts of the body Compression sx ⤵️  PTH (hypoPTH), Dx: Surgical Bx	LOW	Levothyroxine prednisone
Grave’s	NO	⊕ Exophthalmos Hyperthyroid can be dx clx	HIGH (DIFFUSE)	1˚ BB 2˚ Anti-thyroid 3˚ RAIU 3˚ Thyroidectomy
Drug-induced	NO	when you suspect a drug	variable	Stop the drug