Endocrinology Flashcards
What is Hypothyroidism
Decreased T3/T4
Sx of Hypothyroidism
Decreased metabolic rate Cold Intolerance Dry, thickened rough skin, Goiter, Hypoactivity like fatigue sluggishness, memory loss, depression, Decreased DTR Bradycardia, Decreased CO Menorrhagia Hypoglycemia
What are causes of Hypothyroidism
Iodine Deficiency
Hashimoto’s Thyroiditis
What is Hyperthyroidism
Increased T3/T4
Sx of Hyperthyroidism
Increased metablic rate
Heat Intolerance
Weight loss, skin warm moist, soft, fine hair
Hyperactivity like anxiety, tremors, weakness
Diarrhea
Tachycardia, Palpitations
Hyperglycemia
What are causes of Hyperthyroidism
Grave’s Disease
Toxic Multinodular Goiter
TSH secreting tumor
What is Grave’s Disease
Hyperthyroidism
Circulating TSH Receptor Antibodies
Sx of Grave’s Disease
Diffuse, enlarged thyroid
Thyroid Bruits
Opthalmopathy: Lid lag, Exophthalmos, Proptosis
Pretibial Myxedema
Dx of Grave’s Disease
Positive TSH Immunoglobulin Antibodies
Increased T4/T3
Decreased TSH
Tx of Grave’s Disease
RAdioactive Iodine
Methimazole/Propylthiouracil
Beta Blockers: Propranolol for sx
Thyroidectomy
What is Toxic Multinodular Goiter
Autonomous functioning nodules
Sx of Toxic Multinodular Goiter
Hyperthyroidism
Dx of Toxic Multinodular Goiter
Increased T3/T4
Decreased TSH
RAIU: Patchy areas of both increased and decreased uptake
Tx of Toxic Multinodular Goiter
Radioactive Iodine
Methimazole/PTU
What is Hashimoto’s
Autoimmune disorder
Sx of Hashimoto’s
Hypothyroidism
Painless, enlarged thyroid
Dx of Hashimoto’s
Positive Thyroid Antibodies present: Thyroglobulin Antibodies, Antimicrosomial and thyroid peroxidase antibodies
Tx of Hashimoto’s
Levothyroxine
What is De Quervain’s
Hypothyroidism that is painful and subacute
Usually post-vira
What is a Thyroid Storm
Potentially fatal complication of untreated thyrotoxicosis usually after a precipitating event
Sx of Thyroid Storm
Hyper Metabolic State
Palpitations, Atrial Fibrillation, Tachycardia, High fevers, N/V, psychosis, delirium, tremors
Dx of Thyroid Storm
Increased T3/T4
Decreased TSH
Tx of Thyroid Storm
Methimazole, PTU
Beta Blockers for x
Supportive IV fluids
Glucocorticoids
What is a Myxedema Crisis
An Extreme form of hypothyroidism
Usually seen in elderly women with long standing hypothyroidism in winter
Sx of Myxedema Crisis
Sever signs of Hypothyroidism
Bradycardia, CNS depression, Respiratory depression, hypothermia, hypotension
Dx of Myxedma Crisis
Decreased T3/T4
Increased TSH
Tx of Myxedema Crisis
IV Levothyroxine
Supportive: Saline, Abx, Steroids
Passive Warming (blankets in warm room)
What are the 4 types of Thyroid Carcinomas in order of least aggressive to most aggressive
Papillary, Follicular, Medullary, Anaplastic
What is Primary Hyperparathyroidism
Excess Inappropriate Increased PTH production
Usually due to a Parathyroid Adenoma
What is Secondary Hyperparathyroidism
Increased PTH response to hypocalcemia or Vitamin D deficiency
Usually due to Chronic Kidney Failure
Sx of Primary Hyperparathyroidism
Signs of Hypercalcemia
Stones, Bones, Groans, Moans
Decreased DTR
Dx of Primary Hyperparathyroidism
Hypercalcemia + Increased PTH + Decreased Phosphate
24 hour urine Calcium Excretion
Osteopenia on bone scan
Tx of Hyperparathyroidism
Surgery: Parathyroidectomy if Primary
If secondary, Vitamin D/Calcium Supplement
What is Hypoparathyroidism
Low PTH or insensitivity to its action
Due to Postsurgical damage (like thyroidectomy), or autoimmune destruction of parathyroid gland
Sx of Hypoparathyroidism
Signs of Hypocalcemia
Carpopedal Spasms, Trousseau and Chvostek Sign, Perioral Parasthesias, Increased DTR
Dx of Hypoparathyroidism
Hypocalcemia, Decrased PTH, Increased Phosphate
Tx of Hypoparathyroidism
Calcium Supplements + Vitamin D (Ergocalciferol or Calcitriol)
What is Chronic Adrenocortical Insufficiency
Disorder where adrenal gland does not produce enough hormones
What is Primary (Addison’s Disease) Adrenocortical Insufficiency
Adrenal Gland destruction which causes a lack of Cortisol and Alodsterone
What causes Primary Adrenocortical Insufficiency
Autoimmune
Infection like TB
Thrombosis or Hemorrhage
Meds like Ketoconazole, Rifampin
What is Secondary Adrenocortical Insufficiency
Pituitary failure of ACTH secretion, leads to lack of Cortisol only
Aldosterone is intact because it is controlled via RAAS system
What causes Secondary Adrenocortical Insufficiency
Exogenous Corticosteroid use
Sx of Primary Adrenocortical Insufficiency
Hyperpigmentation due to increased ACTH stimulation, which in turn stimulates melanocytes
Decreased Aldosterone marked by orthostatic hypotension, severe hyponatremia, hyperkalemia and non-anion gap metabolic acidosis, hypoglycemia
Decreased sex hormone in women leads to loss of libido, amenorrhea, loss of axillary and public hair
Sx of Secondary Adrenocorticol Insufficiency
Sx due to lack of Cortisol
Weakness, muscle ache, myalgias, fatigue, weight loss, anorexia, N/V
Dx of Adrenocortical Insufficiency
Get baseline ACTH first
- High dose ACTH stimulation test
- Normal response is rise in blood/urine cortisol levels after ACTH is given
- If no increase in cortisol after ACTH given = Adrenal Insufficiency - CRH Stimulation Test
- If high levels of ACTH but low Cortisol = Primary
- If Low ACTH and low Cortisol = Secondary (pituiatiry can’t produce enough ACTH)
Tx of Adrenocortical Insufficiency
Primary: Glucocorticoids + Mineralocorticoids
Secondary: Only Glucocorticoids
Glucocorticoids: Hydrocortisone, Presdnisone, Dexamethasone
Mineralocorticoids: Fludrocortisone
What is Adrenal (Addisonian) Crisis
Sudden worsening of adrenal insufficiency due to a “stressful” event like surgery, trauma, volume loss, MI, fever, sepsis
What causes Addisonian Crisis
Abrupt withdrawal of glucocorticoids
Previously undiagnosed patients with Addison’s disease
Exacerbation of known ADdison Disease (who didn’t increase glucocorticoid during stress)
Sx of Addisonian Crisis
Shock, Decreased BP, Hypotension, Hypovolemia, Abdominal Pain, N/V, fever, weakness, lethargy, coma
Dx of Addisonian Crisis
BMP: Hyponatremia, Hyperkalemia, Hypoglycemia
Cortisol levels, ACTH, CBC
Tx of Addisonian Crisis
IV fluids (NS) Glucocortoids, Reverse electrolyte abnormalities, Fludrocortisone
What is Cushing’s Syndrome vs. Cushing’s Disease
Syndrome: Signs and sx related to cortisol excess
Disease: Cortisol excess caused by pituatiry increased ACTH secretion
Sx of Cushing’s
Central trunk obesity, moon facies, buffalo hump, supraclavicular fat pads, wasting of extremities, skin atrophy, striae, HTN, weight gain, osteoporosis, hypokalemia, acanthosis nigricans, depression, mania, psychosis, Hirsuitism, oily facial skin
What causes Cushing’s
Long term high dose corticosteroid therapy
Cushing’s Disease: Pituitary Adenoma that secretes ACTH
Ectopic ACTH: ACTH screting tumor like small cell lung cancer, medullary thyroid cancer
Adrenal Tumor: Cortisol secreting adrenal adenoma
Dx of Cushing’s
- First test for Cushings by doing one of the 3 below
A. Low dose dexamthasone suppression
-No suppression = Cushing’s Syndrome
B.Increased 24 hour urine cortisol evels
-Elevated urinary cortisol = Cushing’s Syndrome
C. Increased Salivary Cortisol levels
-Increased in Cushing’s Syndrome (done at night) - What is causing Cushing’s
A. High Dose Dexamethasone Suppression
-If suppressed = Cushing’s Disease = Pituitary Tumor that is secreting ACTH
-No Suppression = Adrenal or Ectopic ACTH producing tumor
B. ACTH Levels
-If decreased ACTH: Adrenal Tumor
-If normal or increased ACTH: Cushing’s Disease or Ectopic ACTH producing tumor
Tx of Cushing’s Syndrome
If Pituitary Tumor: Transsphenoidal Surgery
If Ectopic or Adrenal TUmor: REmove Tumor or Ketoconazole in inoperable patients
If due to Excess Steroid Intake: Stop taking steroids GRADUALLy
What is Diabetes Insipidus
Inability of kidney to concentrate urine which leads to production of large amounts of dilute urine
Due to Vasopressin Deficiency (Central)
or
Due to Insensitivity to ADH (Nephrogenic)
Sx of Diabetes Insipidus
Polyuria, Polydipsia, Nocturia
Hypernatremia if severe or decreased oral water intake
Dx of Diabetes Insipidus
Fluid Deprivation Test
-Normal response is progressive urine concentration
-DI will show continued production of dilute urine
Desmopressin (ADH) Stimulation Test
-Central: Reduction in urin output indicates response to ADH
-Nephrogenic: Continued production if dilute urine
Tx of Diabetes Insipidus
Central: Desmopressin, Carbamazepine
Nephrogenic: Na/Protein Restriction, Hydrochlorothiazide, Indomethacin
If sx: Pure water orally, D5w, or 1/2 NS
What is Diabetic Ketoacidosis
Insulin deficiency leads to Hyperglycemia, Dehydration, Ketonemia (anion gap metabolic acidosis), and Potassium Deficit
Sx of DKA
Hyperglycemia: Thirst, Pollyuria, Polydipsia, Nocturia, Weakness, Fatigue, Confusion, N/V, Abdominal Pain
Tachycardia, Ketotic Breath, Kussmaul’s Respiration
Dx of DKA
Plasma Glucose >250 Arterial pH <7.3 Serum Bicarbonate 15-18 Positive Ketones Variable Serum Osmolarity
Tx of DKA
IV Fluids, usually Isotonic NS
Regular Insulin
Potassium
Bicarbonate only in severe acidosis
What is Diabetes Mellitus
Hyperglycemia due to inability to produce insulin and insulin resistance or both
What is DM type I
Pancreatic Beta-Cell Destruction
The patient can’t produce insulin
Usually presents in kids
What is DM Type II
Insulin Resistance with eventual imparment to insulin secretion
Common risk factors are family hx, AA, HTN, Hyperlipidemia, Obesity, Atherosclerosis, Strokes
Sx of DM Type I
Polyuria, Polydipsia, Polyphagia, Weight Loss, DKA
What are complications of DM
Stcoking Glove proprioception pattern, pain, Decreased DTR, Parasthesias, Orthostatic Hypotension, Constipation
Retinopathy: Microaneurysms, Cotton Wool Spots, REtinal VEnous Beading, Neovascularization, Central Vision Loss
Nephropathy: Microalbuminuria
Dx of DM
Fasting Glucose <126 is GOLD STANDARD
HgA1C >6.5%
2 hour plasma gluocse >200
Plasma glucose >220
Tx of DM
Diet, Exercise, Lifestyle Changes
Glucose Control, Lipid Control
