Endocrinology COPY Flashcards
How is DM dignosis made?
- Two fasting glucose ≥ 126
- One random glucose ≥ 200 with symptoms (polyuria, polydipsia, polyphagia)
- Abnormal glucose tolerance test > 200mg/dL (2-hour glucose tolerance test with 75 g glucose load)
- Hemoglobin A1c > 6.5%
Fischer, Conrad (2012-09-22). Master the Boards: USMLE Step 3 (Kindle Locations 2896-2902). . Kindle Edition.
Best initial therarp for type 2 DM
Diet, exercise and weight loss
Best initial medical therapy for adult onset DM
Metformin
Why is metformin beneficial in obese DM patients?
Because it does not lead to weight gain
How does metformin work?
By blocking gluconeogenesis
What are the advantages of metformin?
- No risk of hypoglycemia
- Does not increase obesity
What are the contraindications to use of metformin?
Renal insufficiency
Use of contrast agents
Name the common DM medications
Metformin
Sulfonylureas
Dipeptidyl peptidase IV (DPP IV)
Thiazolidinidiones
Alpha glucosidase inhibitors
Insulin secretagogues
Glucagon-like peptides (GLP) analogues
Long-acting insulin
Short-acting insulin
Name three examples of sulfonylureas
Glyburide
Glimepiride
Glipizide
What is the mechanism of actions of sulfonylureas
By increasing the release of insulin from the pancreas
Side effects of sulfonylureas
Hypoglycemia
SIADH
Weight gain
Side effect of metformin
Risk of lactic acidosis in patients with renal insufficiency
Name three examples of Dipeptidyl peptidase IV (DPP-IV) inhibitors
Sitagliptin
Saxagliptin
Vildagliptin
Name two examples of thiazolidiones (“glitazones”)
Rosiglitazone
Pioglitazone
Side effects of thiazolidiones
Hepatocellular injury
Anemia
Pedal edema
CHF
Mechanism of action of thiazolidiones
Increasing peripheral insulin sensitivity
Name two examples of alpha-glucosidase inhibitors
Acarbose
Miglitol
Mechanism of action of alpha-glucosidase inhibitors
These agents block the absorption of glucose at the intestinal lining
Side effects of alpha-glucosidase inhibitors
Diarrhea
Abdominal pain
Bloating
Flatulence
Elevated LFTs
Name two examples of Insulin secretagogues (Meglitinides)
Nateglinide
Repaglinide
Mechanism of action of Insulin secretagogues (Meglitinides)
Increased release of insulin from the pancreas (similar to sulfonylureas)
Side effects of of Insulin secretagogues (Meglitinides)
Hypoglycemia
Name two examples of Glucagon-like peptide-1 (GLP-1) analogs
Exenatide
Liraglutide
Mechanism of action of Glucagon-like peptide-1 (GLP-1) analogs
Increase insulin and decrease glucagon
Side effects of Glucagon-like peptide-1 (GLP-1) analogs
Nausea
Vomiting
Weight loss
Hypoglycemia
When is insulin introduced in the Rx of type 2 DM
If other agents do not sufficiently control the level of glucose, then the patient is switched to insulin. A long-acting insulin, such as insulin glargine, which is a once-a-day injection with an extremely steady-state level of insulin, is used in combination with a very short-acting insulin at mealtime.
Name 4 short-acting insulin
Regular insulin
Lispro
Aspart
Glulisine
Name 3 long-acting insulin
NPH (Neutral Protamine Hagedorn): twice a day
Detemir
Glargine: once a day
Name the symptoms and signs of DKA
“Fruity breath”
Kussmaul hyperpnea
Dehydration
Abdominal pain
Increase annion gap
Hyperkalemia
Hyperglycemia
Ketones in blood/urine
Best initial test for DKA
Serum bicarbonate is the best way to determine the severity of illness
Lab findings in DKA
Hyperglycemia
Hyperkalemia
Decreased serum bicarbonate
Low pH, with low pCO2 as respiratory compensation
Acetone, acetoacetate, and beta hydroxybutyrate levels are elevated
Elevated anion gap
How is patient improvement monitored in DKA?
By monitoring anion gap
Outline the management of DKA
Admit ICU/ward
Fluid resuscitation (NS + IV insulin)
Monitor Na+ K+ phosphate and glucose
Change NS to D5NS when glucose level < 250 mg/L
Change IV insulin to an SQ insulin sliding scale once the anion gap normalizes
Continue IV insulin for at least 30 minutes following the administration of the first dose of SQ insulin
Name the complications of DKA
HTN
Retinopathy (proliferative)
Nephropathy
Neuropathy
Erectile dysfunction
Gastroparesis
Rx for gastroparesis in DM
Metoclopromide
Erythromycin
Rx of DM neuropathy
Gabapentin
Pregabalin
LDL goal in DM
< 100
LDL goal in CAD and DM
< 70
Rx of retinopathy in DM
Laser photocoagulation
Diagnostic criteria for hyperglycemic hyperosmolar nonketotic diabetic state/coma
Serum glucose > 600 mg/dL (hyperglycemia)
Serum pH > 7.3
Serum bicarbonate > 15 mEq/L
Anion gap 14 mEq/L (normal)
Serum osmolality > 310 mOsm/kg.
Clinical features of hypothyroidism
Weight Gain
intolerance Cold intolerance
Coarse hair
Dry skin
Depressed
Bradycardia
Diminished reflexes
Muscle weakness
Fatigue
Menstrual changes
Clinical features of hyperthyroidism
Weight loss
Heat intolerance
Fine hair
Moist skin
Anxious
Tachycardia, tachyarrhythmias such as atrial fibrillation
Muscle weakness
Fatigue
Menstrual changes
Best initial tests for hypothyroidism
T4 (decreased)
TSH (elevated)
Rx for hypothyroidism
T4 ot thyroxine replacement. T4 will be converted to T3 in the local tissues as needed
Best initial tests for hyperthyroidism
T4 (increased)
TSH (often decreased)
Name the four forms of hyperthyroidism
Grave’s disease
Silent thyroiditis
Subacute thyroiditis
Pituitary adenoma
Findings in diagnostic testings for Grave’s disease
TSH - low
T4 - high
RAIU(radioactive iodine reuptake) - elevated
Findings in diagnostic testings for “Silent” thyroiditis
TSH - low (not specific for this form of hyperthyroidism)
T4 - high
RAIU(radioactive iodine reuptake) - low
In which form of hyperthyroidism may present with antibodies to thyroid peroxidase and antithyroglobulin antibodies
Silent thyroiditis
Name the only cause of hyperthyroidism with an elevated TSH
Pituitary adenoma
Rx for hypothyroidism
T4 or thyroxine replacement. T4 will be converted to T3 in the local tissue as needed
Outline the Rx of thyroid storm and the role of medications used
Iodine: Blocks uptake of iodine into the thyroid gland
Propylthiouracil or methimazole: Blocks production of thyroxine
Dexamethasone: Blocks peripheral conversion of T4 to T3
Propranolol: Blocks target organ effect
Most common cause of hypercalcemia
Primary hyperparathyroidism
Causes of hypercalcemia
Primary hyperparathyroidism
Malignancy: Produces a parathyroid hormone– like particle
Granulomatous disease: Sarcoid granulomas actually make vitamin D
Vitamin D intoxication
Thiazide diuretics: These increase tubular reabsorption of calcium
Tuberculosis
Histoplasmosis
Berryliosis
Criteria for surgical removal of the parathyroid gland
Any symptomatic disease (“ stones, bones, psychic moans, GI groans”)
Renal insufficiency, no matter how slight
Markedly elevated 24-hour urine calcium
Very elevated serum calcium (> 12.5)
Normal serum calcium level
8.4 - 10.2 mg/dL
Outline Rx for acute severe hypercalcemia
- Hydration: High volume (3– 4 liters) of normal saline
- Furosemide: Only after hydration has been given. Loop diuretics increase calcium excretion by the kidney
- Bisphosphonate (pamidronate) is very potent but slow, taking a week to work.
- Calcitonin: If hydration and furosemide do not control the calcium and you need something faster than a bisphosphonate, then calcitonin is the answer.
- Steroid: Use if the etiology is granulomatous disease.
Name the clinical features of acute severe hypercalcemia
Confusion
Constipation
Polyuria and polydipsia from nephrogenic diabetes insipidus
Short QT syndrome on the EKG
Renal insufficiency, ATN, kidney stone
Clinical presentation of Cushing syndrome
Fat redistribution: Truncal obesity, “moon face,” buffalo hump, thin arms and legs
Easy bruising and striae: Loss of collagen from the cortisol thins the skin
Hypertension: From fluid and sodium retention (look for hypokalemia in hyperaldosteronism)
Muscle wasting
Hirsutism: From increased adrenal androgen levels
Anosmia with hypogonadism (low GnRH, FSH, and LH)
Kallman’s syndrome
Clinical features of Klinefelter’s syndrome
Insensitivity of the FSH and LH receptors on their testicles
XXY on karyotype
The FSH and LH levels are very high, but no testosterone is produced from the testicles.
Features common to all forms of congenital adrenal hyperplasia (CAH)
Elevated ACTH
Low aldosterone and cortisol levels
Treatable with prednisone, which inhibits the pituitary.
What forms of CAH has HTN
11 and 17 hydroxylase deficiencies
Virilization is seen in which of the CAH
21 and 11 hydroxylase deficiencies
Diagnosis: CAH with increased 17 hydroxyprogesterone level
21 hydroxylase deficiency
Cause of Hirsutism in 21 and 11 hydroxylase deficiencies
Increased andrenal androgens
Most accurate diagnostic test for prolactinoma
MRI of the brain
Best initial therapy for prolactinoma
Dopamine agonists:
- Bromocriptine
- Cabergoline
Why is DM common among those with acromegaly?
Because growth hormone acts as an anti-insulin
Best initial test for acromegaly
Insulin-like growth factor (IGF)
Why is GH not the best initial test for acromegaly?
Growth hormone (GH) level is not done first, because GH has its maximum secretion in the middle of the night during deep sleep. GH also has a short half-life.
Most acurate test to diagnose acromegaly
Suppression of GH by giving glucose excludes acromegaly.
What is the place of MRI in the diagnosis of acromegaly?
To locate the lesion
Outline the Rx of acromegaly
Surgical resection with transphenoidal removal cures 70 percent of cases
Octreotide: Somatostatin has some effect in preventing the release of growth hormone
Cabergoline or bromocriptine: Dopamine agonists inhibit growth hormone release
Pegvisomant: This is a growth hormone receptor antagonist.
Clinical features of Turner’s syndrome
Short stature
Webbed neck
Wide-spaced nipples
Scant pubic and axillary hair
The XO karyotype prevents menstruation.
Fischer, Conrad (2012-09-22). Master the Boards: USMLE Step 3 (Kindle Locations 3488-3490). . Kindle Edition.
What is the etiopathogenesis of testicular feminization syndrome?
The absence of testosterone receptors results in no penis, prostate, or scrotum.
Fischer, Conrad (2012-09-22). Master the Boards: USMLE Step 3 (Kindle Location 3492). . Kindle Edition.
Name two causes of primary amenorrhea
Turner’s syndrome
Testicular feminization syndrome
Enumerate the causes of secondary amenorrhea
Pregnancy
Exercise
Extreme weight loss
Hyperprolactinemia
Polycystic ovary syndrome
Best initial tests for pheochromocytoma
High plasma and urinary catecholamine levels
Plasma-free metanephrine and VMA levels
Most accurate test for pheochromocytoma
CT or MRI of the adrenal glands
Rx outline for pheochromocytoma
Phenoxybenzamine (alpha blockade) first to control blood pressure. Without alpha blockade, patients’ blood pressure can significantly drop intraoperatively
Propranolol is used after an alpha blocker like phenoxybenzamine.
Surgical or laparoscopic resection
What is the strongest indication for screening for DM
HTN
Name the characteristics of MEN syndrome type 1 (Wermer’s syndrome)
Parathyroid hyperplasia
Pancreatic islet cell tumor
Pituitary adenoma
Name the characteristics of MEN syndrome type 2A (Sipple’s syndrome)
Parathyroid hyperplasia
Thyroid medullary cancer
Pheochromocytoma
Name the characteristics of MEN syndrome type 2B
Thyroid medullary cancer
Pheochromocytoma
Mucocutaneous neuromas
Ganglioneuromatosis of the colon
Marfan-like habitus
Presentation of severe hypocalcemia
Seizures
Neural twitching (Chvostek’s sign and Trousseau’s sign)
Arrhythmia: prolonged QT on ECG
Rx outline for hypocalcemia
Replace calcium
Calcium + Vit D (for Vit D def and hypoparathyroidism)
Name the anterior pituitary hormones and the hypothalmic hormones that control their release
- ACTH controlled by CRH
- GH controlled by GHRH
- TSH controlled by TRH
- LH controlled by GnRH
- FSH controlled by GnRH
- PRL controlled by Dopamine (inhibits)
Diagnosis: HTN + Low renin + Low potassium
Hyperaldosteronism
Confirmatory diagnostic test for hyperaldosteronism
CT scan of the adrenals
Risk factors for osteoporosis
Menopause
Low BMI
Family hx of osteoporosis
Early ovarian failure
Low calcium intake
Smoking
Nulliparity
Alcohol
High caffeine intake
(Source: S95)
What are implications of prebreakfast, prelunch, predinner and bedtime glucose levels?
Prebreakfast glucose level: Reflects predinner NPH dose.
Prelunch glucose level: Reflects prebreakfast regular insulin dose.
Predinner glucose level: Reflects prebreakfast NPH dose.
Bedtime glucose level: Reflects predinner regular insulin dose.
What are the time of onset, peak effect and duration of regular insulin
Onset: 30-60 minutes
Peak effect: 2-4 hours
Duration: 5-8 hours
What are the time of onset, peak effect and duration of lispro
Onset: 5-10 minutes
Peak effect: 0.5-1.5 hours
Duration: 6-8 hours
What are the time of onset, peak effect and duration of aspart
Onset: 10-20 minutes
Peak effect: 1-3 hours
Duration: 3-5 hours
What are the time of onset, peak effect and duration of glulisine
Onset: 5-15 minutes
Peak effect: 1.0-1.5 hours
Duration: 1.0-2.5 hours
What are the time of onset, peak effect and duration of NPH (Neutral Protamine Hagedorn)
Onset: 2-4 hours
Peak effect: 6-10 hours
Duration: 18-28 hours
What are the time of onset, peak effect and duration of detemir
Onset: 2 hours
Peak effect: No discernible peak
Duration: 20 hours
What are the time of onset, peak effect and duration of glargine
Onset: 1-4 hours
Peak effect: No discernible peak hour
Duration: 20-24 hours
Possible diagnoses:
- TSH - low
- T4 - high
- RAIU - decrease
Subacute thyroiditis (hyperthyroid stage)
Hashimoto thyroiditis (hyperthyroid stage)
Exogenous T3/T4: levothyroxine
Postpartum thyroiditis
Possible diagnoses:
- TSH - low
- T4 - high
- RAIU - increase
- Graves’ disease
- Toxic adenoma
- Multinodular goiter
Possible diagnoses:
TSH - low
T4 - decrease
Pituitary hypothyroidism
Hypothalamic hypothyroidism
What are the predominant estrogens in reproductive years and during menopause?
Under the stimulation of the stimulizing leutinizing hormone (LH), the theca cells of the post-menopausal ovary produce androstenedione and testosterone.
Estrone, a product of androstenedione conversion in adipose tissue, is the predominant estrogen in menopause.
Estradiol is the most prevalent estrogen in the reproductive years, and estriol is made by the placenta during pregnancy.
Estrane is a minor estrogen
What is hungry bone syndrome?
Hypocalcemia following surgical correction of hyperparathyroidism in patients with severe, prolonged disease, as calcium is rapidly taken from the circulation and deposited into the bone.
