Endocrinology Flashcards
What are the symptoms of PHEochromocytoma?
*Palpitations
*Headache
*Excessive sweating
What are the names of the two metabolites that will be elevated in PHEochromocytoma? Which is most sensitive?
Metanephrines (more sensitive)
Vanillylmandelic acid
How should PHEochromocytoma be treated?
1) Alpha blocker: PHEnoxybenzamine or PHEnotolamine
2) Beta blocker
3) Complete adrenalectomy
Why are alpha-blockers initated before beta-blockers in treating phenoxybenzamine?
Unopposed alpha-receptor stimulation causes severe vasoconstriction without the counterbalancing vasodilation from beta-2 receptors = a hypertensive crisis.
What is the most specific test for crushing syndrome?
24 hr urinary free cortisol is most specific
nighttime salivary cortisol & low dexamethasone can also be used.
If a pituitary adenoma is suspected what diagnostic imaging is used? What if it comes back as negative?
MRI; if pos conduct a transsphenoidal resection of pituitary tumor
If MRI is negative: inferior petrosal venous sampling
What is the treatment of Addisonian crisis?
1) IV isotonic fluids +/- dextrose (if hypoglycemic)
2) IV hydrocortisone
3) R/O infections and treat.
What is somogyi Effect?
Nocturnal hypoglycemia triggers regulator hormones that increase glucose causing hyperglycemia
What is the treatment of somogyi effect?
Prevent hypoglycemia
1) decrease night NPH insulin dose
2) Move NPH insulin dose to earlier in the evening
3) Have a bedtime snack
What is Dawn Phenomenon?
Normal glucose levels until there is an increased release of Growth hormone at night which increases glucose levels
What is the treatment of Dawn phenomenon?
1) bedtime injection of NPH
2) increased evening NPH
3) Avoid late night snacking
4) insulin pump use early morning
Which lipid lowering medication shoudl be a avoided in a patient with gout?
Niacin it can increase uric acid levels and potentially exacerbate gout attacks. Niacin raises uric acid by reducing its excretion in the kidneys
What is metabolic syndrome?
3 or more of the following: abdominal obesity, increased triglycerides, decreased HDL, HTN, and hyperglycemia. -> increase risk for DM and cardiovascular disease
What is the 1st line managment of prolactinoma
Dopamine agonist: Cabergoline or Bromocriptine
Why is dopamine agonist used to treate prolactinoma instead of transsphenoidal resection?
Dopamine naturally inhibits prolactin secretion via dopamine receptor activation in the pituitary gland
What are increased levels of beta-hydroxybutyrate diagonstic of?
Diabetic ketoacidosis
What is a key component of Metabolic syndrome?
Insulin resistance: increased triglyceride & glucose levels leads to hyperinsulinemia and insulin resistance. -> High insulin inturn causes Na+ reabsorption = HTN
in metabolic syndrome, what are the 5 metabolic abnormalities that increase risk for complication of DM & CVD?
HDL <40 (men & <50 (women)
BP>135/85
Fasting triglyceride levels >150
Fasting blood sugar >100
waist circumference >40inch (men) >35 in women
What are medication that can be used for weight loss?
Phentermine (only 3 months)
Phentermine/topiramate (no duration limts)
What is the difference between acromegaly & gigantism?
Both are a result of increased growth hormone but Gigantism is found in children before the fusion of growth plate and acromegaly is found in adult after growth plate has fused.
What marker is elevated in paget disease of the bone, and why?
Paget disease of the bone is the aggressive breakdown of bone by osteoclast as a result, there is increased bone formation by osteoblast (disorganized and weak structure, prone to breakage)
Alkaline phosphate is released by osteoblast and will be elevated as a result of its activity
What are the phases of paget disease of the bone?
1) lytic phase: osteoclast agressively breaks down bone
2) mixed phase: osteoclast break down and osteoblast disorganizely tries to rebuild bone
3) Sclerotic phase: bone formation exceeds bone break down = weaker than normal healthy bone
What is the diagnosis of T2DM?
1) Fasting plasma >126
2) Random plasma glucose >200
3) OGTT >200 after 2hr
4) HbA1C >6.5%
x2 abnormal test required if asymptomatic
sxs require 1 abnormal test
What are the two T2DM known to decrease ASCVD risk?
GLP1a: Glucagon-like peptide agonist
SGLT2i: Sodium-glucose co-transporter 2 inhibitor
How does GLP1a: Glucagon-like peptide agonist work?
1) Increase insulin
2) decrease the release of glucagon
3) Increase incretin which decreases gastric emptying (promoting fullness & suppressing appetite)
GLP1a: Glucagon-like peptide agonist drug names
Dulaglutide
Semaglutide
SGLT2i: Sodium-glucose co-transporter 2 inhibitor drug names?
empagliflozin, canagliflozin, dapagliflozin
How does SGLT2i: Sodium-glucose co-transporter 2 inhibitor work?
blocks glucose re-absorption in the proximal tubules of kidneys = increased glucose removal via urine.
What are the side effects of metformin?
decreases vitamin B12 (cobalamin)
Increase lactic acid overtime
N/V/D
Which T2DM diabetic drug is known to cause fluid retention?
Thiazolidinediones: increases insulin sensitivity at tissues sites
But known associated with peripheral edema and fluid retention
contraindicated in heart failure and pregnancy.
Thiazolidinediones drug names
Pioglitazone, rosiglitazone
Explain why hirsutism and hyperpigmentation is seen in corticotroph pituitary adenoma (cushing disease)?
1) ACTH and melanocyte-stimulating hormone shares a precursor molecule which leads to increased release of SMH with ACTH.
2) ACTH stimulates the adrenal cortex, not only increasing cortisol but also adrenal androgens like dehydroepiandrosterone (DHEA) = excess facial hair.
diabetic nephropathy is defined as a lab reading of?
albuminuria >300mg/day or >300 mg/g creatinine on random urine sample
What electrole findings are common in primary adrenal insufficiency?
Hyponatremia is seen in primary AI because the adrenal gland is affected = no aldosterone release to hold on to Na+ during Na+ deficit. As a result K+ is elevated
Hyperpigmentation can be seen in which endocrine disorders?
Primary Adrenal insufficiency & and Cushing disease in both conditions the negative feedback on ACTH is disrupted leading to increased ACTH release and melanocyte stimulating hormone is also release since they are derived from the same precurose.
What are drugs for neurpathic pain
Amitriptyline and nortriptyline (TCA) -> increased serotonin & norepinephrine signalling
duloxetine ( SNRI) -> block reuptake of serotonin & norepinephrine
Gabapentin (anticonvulsants
Capsaicin (topical)
Why is methimazole preferred over propylthiouracil when treating hyperthyroidism?
Propylthiouracil has a increased risk of hepatotoxicity
What is the most common presentation of diabetes insipidus?
Sevre polyuira and mild hypernatremia
What is the difference between central DI and Nephrogenic DI?
Central DI: decreased antididuretic hormone production
Nephrogenic DI: renal resistance to ADH
What are common causes of nephrogenic diabetes insipidus?
Hypercalcemia, hypokalemia, interstitial renal disease & medications (lithium, amphotericin)
What are common lab finding for diabetes insipidus?
Hypernatremia
Increased serum osmolality (normal range 275-295)
Decreased urine osmolality <300
(normal range 300-900)
Long acting insulins
Glargine, Detemir, Degludec
The body produces low levels of insulin continuously (basal insulin). long-acting insulin mimics this process but has no peak inactivity during meals. that is why short acting insulin are often paired with long acting insulin to prevent postprandial hyperglycemia.
True or false, metformin is metabolized by the liver.
False; Instead of liver metabolism, metformin is excreted unchanged by the kidneys through active tubular secretion
Rapid acting insulin
aspart, lispro, glulisine
Amiodarone adverse effects on the endocrine system and cardiac system
cards: bradycardia, QT prolongation
Endocrine: hyperthyroidism or hypothroidism
what is the most common type of thyroid nodule?
follicular adenoma (benign tumor)
what is the most common clinical presentation of a patient with a thyroid nodule?
a palpable nodule on the anterior of the neck.
asymptomatic of thyroid-related sxs & most are euthyroid.
What are key presentations that distingiushes a benign thyroid nodule from a malignant thyroid nodule?
benign: smooth, soft, moble
Malginant: rapid growth, firm, hard, fixed, non-moblie or no movement with swallowing
What is the inital testing for a supected thyroid nodule?
TSH level & thyroid US
(U/S finding showing high risk nodules: hypoechoic nodule, irregular margin, central vascularity, microcalcification)
most are asymptomatic but should always get a TSH & US
Performance enhancing drugs
In the evaluation of thyroid nodules, a low TSH levels is shown on lab work. What is the next step?
Radioactive iodine scintigraphy
-> Hyofunctional (cold) nodules should get worked up for malignancy
->hyperfunctional (hot) nodule is depictive of hyperthyroidism and should be treated as such.
Growth hormone elevation is known to stimulate the grow of which major organ?
Cardiac growth leading to left ventricular hypertrophy
Subacute (de Quervain) thyroiditis is known to follow a
Upper respiratory illness
Subacute (de quervain) thyroiditis is known to have a ___
Subacute thyroiditis is self-limiting. It presents w hyperthyroid sxs the follows a hypothyroid phase before returning to euthyroid.
Subacute (de Quervain) thyroiditis presentation
Evaluation of hyperthyroidism
Always conduct a radioactive iodine uptake id no sxs of Graves disease
What are complications of hyperthyrodism?
Osteoporosis (thyroid hormones increase osteoclastic bone resorption), arrhythmia and cardiomyopathy
What is the managment of DKA
Hallmarks of Dequrvain (subacute thyroiditis)
DequerPAINS
Diffuse decreased uptake on radioactive scan
Painful thyroid
After viral illness
Increased CRP & ESR
Negative thyroid antibodies
Self-limiting. Salicylates or NSAID for pain
Which thyroid antibody is specific for hashimoto thyroditis?
Anti-thyroid peroxidase Ab
Anti-thyroglobulin Ab
Which thyroid antibody is specific for Graves Disease?
Thyroid stimulating Antibody (TSH receptor Ab)
Radioactive uptake scan will show what for each disorders; Graves disease, multinodular goiter, Toxic adenoma, thyroditis
Thyroiditis, Hashimoto’s, deQuervain: diffused decreased or absent uptake. This is due to the release of already-made thyroid hormones, The inflammation prevents the production of new hormones.
Toxic multinodular goiter: multiple areas of increased & decreased uptake
Toxic adenoma (hot nodule): increased uptake in a focal point
