Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
34 Cards in this Set
- Front
- Back
|
What causes an increase in Thyroid Binding Globulin (TBG)? A decrease? How does this effect thyroid levels during pregnancy? |
TBG ↑ w/ Pregnancy and OCP use TBG ↓ w/ liver failure and nephrotic synd Pregnancy = ↑ TBG, ↑ Total T3/T4, Normal Free T3/T4, ↓ TSH |
|
|
What medications can cause hypothyroidism? |
Amiodarone Lithium Tyrosine Kinase Inhibitors (ie Imatinib) |
|
|
How do the goiters of Hashimoto's, Subacute (DeQuervain), Riedel's thyroidistis? What are Hashimoto patients at an increased risk of? How else can Subacute (DeQuervain's) present? |
Hashimoto's - PainLESS goiter, ↑ risk of B-cell lymphoma of the thyroid Subacute - PainFUL goiter, may also present as hyperthyroidism early on in disease Riedel's - Rock hard painLESS goiter in a young patient (if pt is old consider anaplastic thyroid cancer) |
|
|
A patient with hyperthyroid symptoms and a goiter is scanned with a radionucleotide scan and found to have a diffusly "cold" thyroid with no nodules. What are the 3 possible causes for this |
Thyroiditis 1) Viral 2) Subacute (DeQuervain) Thyroidistis 3) Postpartum Thyroiditis |
|
|
What is the algorithm for management of a thyroid nodule? |
1) Check TSH 2a) If TSH is low → Radioactive Iodine Scan 2b) If TSH is high → Thyroid US 3) If a nodule is found on US or Iodine scan shows a "cold" nodule → FNA |
|
|
What is the most common type of thyroid cancer? How is it spread? How is Follicular thyroid cancer spread? What thyroid cancer has the worse prognosis and is associated with a rock hard thyroid in an elderly patient? What is the best chemo for thyroid cancer? |
Papillary = MC type, spread lymphatically Follicular = spreads hematogenously Anaplastic Levothyroxine = best chemo! |
|
|
What are the indications for a surgical parathyroidectomy in a patient with primary hyperparathyroidism? |
1) Symptoms of ↑ Ca²+ (Moans, Groans, stones, psych undertones) 2) Ca²+ > 1.0 above the upper normal limit 3) ↓ Cr Clearance 4) ↓ Bone Mineral Density 5) Age < 50 |
|
|
What is the medical management of primary hyperparathyroidism? |
- Cinacalcet - ↑ Ca²+ sensitivity of PTHr to suppress PTH secretion - Avoid TZDs (↑ Ca²+) and Lithium (↑ PTH) - Hydrate! - Hypercalcemia causes polyuria which can quickly dehydrate pateitn |
|
|
What is Albright's Hereditary Osteodystrophy? How does it effect Ca2+, PTH, Phosphorus, and Vit. D levels? What other features are characteristic? |
AHO (aka "Pseudohypoparathryoidism")= defective PTH receptor causing end-organs to be insensitive to PTH ↑ PTH, ↓ Ca2+, ↑ Phos, Normal Vit D Pts are short w/ shortened 4th metacarpal, developmental delay, and obese |
|
|
What PTH, Ca2+, Phosphate, and Vit. D levels can be expected with the following diseases? - 1° Hyperparathyroidism - Vit D deficiency (Rickets, Osteomalacia) - 2° Hyperparathyroidism - Hypoparathyroidism |
1° Hyperparathryoidism - ↑PTH, ↑Ca2+, ↓Phos, Normal Vit D Vit D Def - ↓Vit D, ↓-to normal Ca2+, ↑PTH, ↓Phos 2° Hyperparathyroidism (ie Renal Failure) - ↓Ca2+, ↑Phos, ↑PTH, ↓Active Vit D (1,25) Hypoparathyroidism - ↓PTH, ↓Ca2+, ↑Phos, ↓Active Vit D (1,25) |
|
|
What is the diagnostic workup for acromegaly? |
1) Serum Insulin-like Growth Factor-1 (IGF-1)
2) If ↑ IGF-1, then confirm with Oral Glucose Suppression Test (GH should ↓ w/ oral glucose, if GH remains high, then Acromegaly 3) Pituitary MRI - to evaluate mass |
|
|
What is treatment options for Acromegaly? |
- Transphenoidal Resection - If unressectable → Ocretotide - If Octreotide uneffective → Cabergoline (Dopa agonist) - If Cabergoline uneffective → Pegvisomant (GH receptor antagonist) |
|
|
What are the symptoms of a Basilar Artery stroke? |
- CN defects due to pons involvement - Altered mental status/coma due to RAS involvement - Contralateral body weakness and sensory defects - Vertigo & Nausea - Dysarthria |
|
|
What is the Cushing Syndrome diagnostic algorithm? |
1) Overnight Low-Dose Dex Suppression test - ↓ Cortisol → Exogenous steroid use 2) 24 hr Free Urinary Cortisol to confirm 3) High-Dose Dex Suppression test - ↓ Cortisol → Pituitary Adenoma → MRI 4) ACTH Level - - ↑ ACTH = Ectopic ACTH from tumor - ↓ ACTH = Adrenal Tumor → CT of abd. 5) If indeterminate → CRH level |
|
|
How do 1° Hyperaldosteronism (Conn Syndrome) 2° Hyperaldosteronism differ Non-aldosterone mineralcorticoid differ? |
1° Hyperaldosteronism - due to an adrenal adenoma or bilateral hyperplasia. ↑ Aldo, ↓ Renin, ↑ Aldo/Renin 2° Hyperaldosteronism - due to Renal A. stenosis, L. CHF, Nephrotic synd, cirrhosis. ↑ Aldo, ↑ Renin, ↓ Aldo/Renin Non-Aldo Mineralcorticoid (Cushing, Licorish) ↓ Aldo, ↓ Renin ↓ Aldo/Renin |
|
|
What labs would you expect with primary adrenal insufficiency (addison's disease)? |
↓ Na+ and ↑ K+ due to low aldosterone
Eosinophilia (CANADA-P) ↓ Cortisol ↑ ACTH |
|
|
How do the following types of Congenital Adrenal Hyperplasia (CAH) present? - 11β-Hydroxlase Deficiency - 21α-Hydroxlase Deficiency - 17α-Hydroxlase Deficiency |
11β-Hydroxlase - HTN (Aldo is ↓, but precursor DOC is ↑ and acts as a mineralcorticoid), Virualization in girls 21α-Hydroxlase - Hypotension, Virualization in girls. ↑ 17-OH-pregesterone 17α-Hydroxlase - HTN, ambiguous genitalia in boys due to low androgens |
|
|
What are the typical cancers seen in each of the MEN syndromes? |
MEN1 - Parathryoid, Pituitary, Pancreas MEN2A - Parathyroid, Pheo, Medullary thyroid MEN2B - Pheo, Medullary thyroid, Mucosal neuromas (*also Marfanoid habitus!) |
|
|
What opportunistic infections can be seen at the following CD4 counts in HIV? What is the treatment for each? CD4 < 200 CD4 < 100 CD4 < 50 |
CD4 < 200 = PCP → SMX/TMP, Candidiasis → Fluconazole, TB → RIPE CD4 < 100 = Toxoplasmosis → Pyrimethamine + Sulfadiazine + Leucovorin CD4 < 50 = MAC → Macrolides, Cryptococcus meningitis → Ampho B + Flucytosine, CMV → Gancyclovir. |
|
|
What is the next step of action if a health care worker is accidentally exposed to HIV? |
Test patient and health-care worker immediately and follow-up in 6 wks and 6 mths. Start ART = Tenofivir + Emtricitabine + Raltegravir for 4 wks |
|
|
What is the accepted treatment plan for HIV patients? |
Start HAART as soon as infection is confirmed. HAART = 2 NRTI's + 1 of the following: NNRTI, PI, or Integrase Inhibitors |
|
|
What class of HIV drugs work by inhibiting reverse transcriptase to prevent the production of DNA and have the shared SE of Lactic Acidosis + Lipodystrophy? What are the 3 main agents used and their specific SE? |
**NRTI's** - Abacavir - life-threatening hypersensitivity - Zidovudine (used in pregnancy and given to babies of HIV+ mothers) - BM suppresion - Tenofivir - Kidney injury, Osteoporosis |
|
|
What class of HIV drugs work by inhibiting reverse transcriptase to prevent the production of DNA and have the shared SE of a rash? What is the main agent in this class and its specific SE? |
**NNRTI's** - Efavirenz - teratogenic, Neuropsych. Symp (nightmares + depression) |
|
|
What class of HIV drugs work by interfering with viral replication and have the shared SE of Metabolic Derangements and GI toxicity? What are the 2 main agents in this class and their specific SE? |
**Protease Inhibitors** - Atanzanavir - hyperbilirubinemia
- Ritonavir - inhibits Cyt. P450 |
|
|
What class of HIV drugs works by blocking the integration of the viral genome into the host genome? |
Integrase Inhibitors (end in -gravir) |
|
|
What specific HIV drug works by blocking CCR5 coreceptor binding to prevent virus entry into the cell? |
Maraviroc |
|
|
What are the difference between type 2 and type 3 hypersensitivity reactions? |
Type 2 - Antibodies against cellular antigens (ie host cells) leading to NK, complement, and macrophage activation Type 3 - Antibodies against soluble antigens causing formation of immune complexes that activate complement |
|
|
What are the time-frames and mechanisms of the 3 types of transplant rejections? |
Hyperacute - occurs in 1st 24 hrs. Due to Anti-donor Ab's due to poor organ matching. Irrev. Acute - occurs in 6 days - 1 yr. Due to Anti-donor T cell proliferation, reversible w/ immunosuppressive drugs Chronic - occurs > 1yr. Multiple causes. Immunosuppressive drugs delay course |
|
|
Immunosuppresive drug that is metabolized by xanthine oxidase and thus should never be paired with Allopurinol! |
Azathioprine |
|
|
Immunosuppressive drug that causes nephrotoxcity when given systemically. |
Tacrolimus |
|
|
Immunosuppressive drug that causes severe leukopenia. |
Muromonab |
|
|
Immunosuppressive drug that causes thrombocytopenia and hyperlipidemia. |
Rapamycin |
|
|
Immunosuppressive drug that causes Leukopenia and lymphoma and is used to treat SLE nephritis and Graft-vs-Host Disease. |
Mycophenolate |
|
|
Immunosuppressive drug that causes visual disturbances and is often used to treat SLE and RA. |
Hydroxycholorquine |
