GU Flashcards

1
Q

What is Leuprolide? What does it do? How do I remember?

A

GnRH**. Agonist if **pulsatile** => Fertile. Antagonist if **continuous** => fight prostate cancer. **Leude behavior like a pro is disgusting; I lide it gets my genitals going.

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2
Q

What is Methyltestosterone? What are the side effects?

What is Danazol? What is it for? What are the side effects? How do I remember this?

A

Pre-testosterone => Testosterone. Small balls and premature closure of epiphyseal plates (teratogen).

Partial testosterone agonist. Used to treat Endometriosis** and **Hereditary Angioedema. Masculinization, weight gain, and edema. Danzo is a genocidal guy with partially good intentions to rid those blood eyes (angioedema) and endometriosis.

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3
Q

What are estrogen drugs used for? What are the key risks whenever giving estrogen?

What is a SERM?

How does Clomiphene work? What is it used for? What are the side effects? How do I remember this shit?

How does Raloxifene work? What is it used for? How do I remember this shit?

How do Progestins work for birth control?

A

Hormone replacement therapy, rarely used birth control, and androgen-dependent prostate cancers. Increased risk of endometrial cancer/clotting.

Selective Estrogen-Receptor modulators.

blocks feedback inhibition => GnRH => LH/FSH => ovulation**. #1 treatment for an/oligoovulation. Multiple simultaneous pregnancies, visual disturbances, ovarian enlargement, and hot flashes. A _Clo_ne of **mi** **phenedishly sexy penis blocks all inhibition in women => super women.

Selective agonis on bone** => **treat osteoporosis**. **Roxanne** is a **fene** to dance(no OP) like that, it talks to my **boner

Thickening of cervical mucus/inhibit endometrial proliferation (less menstruation and prevents implantation)

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4
Q

What is Finasteride? What does it treat?

How do I remember this shit?

What is Flutamide? What is it used in?

What are the secondary testosterone inhibitors? What are they used for? What can they also cause?

A

5α-reductase inhibitor => inhibits DHT => treat BPH/baldness.

I _Fin_ished growing and my _as_ to ride is huge, I don’t need DHT too.

Competitive inhibitor of testosterone. Prostate cancer

I Flu** **ta** **mide prostate cancer clinic.

Ketoconazole (Inhibits Desmolase) and Spironolactone (Inhibits steroid binding). Polycystic ovarian syndrome. Gynecomastia and Amenorrhea

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5
Q

What is Tamoxifen? What is it primarily used for? How do I remember this shit?

What are the Aromatase inhibitors? What does Aromatase inhibitors inhibit? How do I remember them?

What are the Abortion drugs? What are they? How do I remember this shit?

A
  • *Tam_my took _tox**ic chemo for her ER-positive breast cancer and now takes Tamoxifen** to **fend off new breast cancer.
  • *Ana** took a strole and was stopped by her Exe mustang’s Aroma. Making her lose some of her feminist views.

Mifepristone (Anti-Progesterone) and Misoprostol (PGE1). Mi** w_ife’s **prist**_ene _**tone**_d vagina _**Miso** clos_e **to keeping if she aborted.

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6
Q

What are Ritodrine/Terbutaline? When do you use them?

A

β2 agonists to prevent premature contractions. (It is Rito for fetuses to drine peacefully as we try to keep them away from terbulant lines like “Fuck you bitch”)

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7
Q

What is Tamsulosin?

A

α1-antagonist used for BPH as it is specific to α1A,D(Prostate) not α1B (vascular). Tam**my _**su** **l**_ucky t**o** not have the **sin** of BPH. Even though it is like **A** she **Don’t have a prostate

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8
Q

What are the basic types of diuretics?

A

Osmotic diuretics, Carbonic Anhydrase inhibitors, Loop diuretics, Thiazide diuretics, K-sparing diuretics, and ACE inhibitors

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9
Q

What is the osmotic diuretic? What is its MOA? What is it best for?

A

Mannitol. Forces to piss a lot. Pulmonary edema (especially in anuria)

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10
Q

What is the main Carbonic Anhydrase inhibitor? How does it work? What are the side effects of it?

A

Acetazolamide. Keeps Bicarbonate from turning into CO2 so it is trapped in the lumen. Alkalizes urine, Acidifies blood**(useful for altitude sickness), neuropathy, **NH3 toxicity, and is sulfa drug

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11
Q

What are the Loop diuretics? What do they inhibit? What do they lose? What are they used for? What are their side effects?

A

Furosemide(Sulfa) and Ethacrynic acid(not-sulfa). Na/K/2Cl symporter. Ca/K/Na/Cl. Edematous states, HTN, and hypercalcemia. Ototoxicity, Nephritis, and Gout

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12
Q

What is the main Thiazide diuretic? What does it prevent? What does it lose? What is it used for? What are its side effects?

A

NaCl reabsorption in DCT. Na/K/Cl. calciuria(spares Ca**), HTN, and **nephrogenic diabetes insipidus. Hyperglycemia/Lipidemia/Uricemia/Calcemia and is a Sulfa drug

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13
Q

What are the K-sparing diuretics? What do they block?

A

Spironolactone (antiandrogen**/I Spy Ron Lactating, O_K_**?), Triamterene, Amiloride, Eplerenone. Aldosterone(Spironolactone does it directly)

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14
Q

What are the ACE inhibitors? What is ACE? What does this cause? What are the side effects?

What are they good for?

How do I remember this shit?

A

Captopril**, Enala_pril, Lisinopril_. Angiotensin-converting enzyme => blocks Angiotensin II and prevents inactivation of bradykinin (kallikrein activates => cough) => high rennin release(reflex), diuresis, and prevents unfavorable heart remodeling. Cough, Angioedema (blood swelling/similar to hives but deeper), Proteinuria, Taste changes, hypOtension, Pregnancy problems(fetal renal damage), Rash, Increased rennin, Lower angiotensin II(CAPTOPRIL**), hyperkalemia, and significantly decreases GFR

HF, Diabetic nephropathy, HTN, LV dysfunction after MI

ACE fighter pilots love the -pril of flying *Cough* K? But I prefer to inhibit those sensations and stay relaxed without children

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15
Q

What are the Angiotensin II Receptor Blockers (ARBs)? What do they do?

A

The -sartans. Similar to ACE inhibitors but NO kallikrein = NO cough.

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16
Q

Describe in detail the following hormones; Renin, Angiotensin II, Anti-diuretic hormone, and Aldosterone

A
  • Renin = Produced by Juxtaglomerular cells due to; Low renal blood pressure(what it actually detects), Low [plasma Na] in the DCT(through paracrine transmitters), and β1 stimulation. => Angiotensin I(pre-active state that can still be inhibited by bradykinin/ACE inhibitors)
  • Angiotensin II; Stimulates Na/H antiport(on PCT)/Aldosterone/ADH/smooth muscles on arterioles(especially efferent, Increasing BP/GFR)/Hypothalamus(thirst). Also, limits reflex Bradycardia (due to increased BP)
  • Anti-diuretic hormone(ADH/Vasopressin); Stimulates aquaporine insertion in principle cells(CD), vasoconstriction at high doses (increase BP), allows urea reabsorption (absorbing a lot of water and concentrating urine), and many CNS effects (not completely understood)
  • Aldosterone; Increases Na channels and Na/K ATPase insertion in principal cells. Excretes K and H+ => Water absorption and slight alkalosis