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Pharmacology > First Pass Miss Exam 2 > Flashcards

First Pass Miss Exam 2 Flashcards

1
Q

Why is furosemide good for hypercalcemia? What drug should be used for hypocalcemia?

A

Blockage of NKCC prevents K+ from making lumen most positive charged, inhibiting calcium reabsorption.

For hypocalcemia, blocking NCC via HCTZ will facilitate reabsorption of calcium

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2
Q

Why is furosemide good in acute renal failure and hyperkalemia?

A

Increases renal blood flow and hence urine flow, which can flush out K+ (via principle cells) as well as intratubular casts

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3
Q

What is amiloride used for?

A

Prevention of diuretic induced hypokalemic acidosis
-> also prevents entry of lithium into principal cells (blocks ENaC), limiting aquaporin-2 interference in nephrogenic diabetes inspidus

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4
Q

What is spironolactone used for and why?

A
  1. severe CHF -> aldosterone mediates myocardial fibrosis, and spironolactone antagonizes this effect of cardiac remodelling
  2. Primary and secondary aldosteronism
  3. Hypertension with loop / thiazide diuretics to reduce K+ loss
  4. hepatic cirrhosis -> reduces edema
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5
Q

What are the two PCSK9 inhibitors and who uses them? How do they work?

A
  1. Alirocumab
  2. Evolucumab

= EVIL-LAIR

Used as a second line to statins when LDL remains high or statin side effects are high, but very expensive.

Increases the expression of LDL-R on liver by monoclonally binding PCSK9

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6
Q

What drug commonly increases plasma levels of statins and what can be taken instead?

A

Gemfibrizol, a fibrate to lower triglycerides

Can take fenofibrate instead

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7
Q

What are the statins metabolized via CYP3A4 and what drugs can make this a problem?

A

Simvastatin, lovastatin, and atorvastatin

Macrolides, azole antifungals, and HIV protease inhibitors may decrease their metabolize and increase risk of myopathy / rhabdomyolysis

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8
Q

What is the high vs low total cholesterol range?

A

Low / desirable: <200 mg/dL
High: >240 mg/dL

LDL: <100, high>160

HDL: <40, high >60

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9
Q

What is the mechanism of action of niacin?

A

Binds to and activates GPCR in adipose tissue, decreasing release of free fatty acids from stored triglycerides, reducing need for VLDL packaging by liver, and reduction in LDL.

HDL is increased by improved stability of Apoprotein A1

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10
Q

What is the effect of AT2 on the kidney?

A

Directly stimulates Na/H exchanger in proximal tubule, enhances aldosterone secretion, and increased GFR while decreasing RBF by constricting the efferent arteriole

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11
Q

What is the effect of AT2 on cardiac / vascular remodelling?

A

Stimulates the migration, proliferation, and hypertrophy of vascular smooth muscle cells, as well as hypertrophy of cardiac myocytes. Promotes myocardial fibrosis through aldosterone.

Also increases preload (volume expansion) and afterload (greater peripheral resistance)

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12
Q

Why are ACE inhibitors important in chronic heart failure? What effect does this have on cardiac output and stroke volume?

A

Reduce preload and afterload, thus slowing the progress of ventricular dilation

This actually increases cardiac output and stroke volume in CHF

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13
Q

Give two important side effects of ACE inhibitors?

A
  1. Persistant dry cough
  2. Hyperkalemia (due to decreased aldosterone secretion) -> especially a problem in renal failure or if patient is on another K+ sparing diuretic -> raised banana dacquiri
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14
Q

When are ACE inhibitors contraindicated?

A

Pregnant patients -> teratogenic

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15
Q

Give two angiotensin receptor (AT1) blockers: ARBs?

A
  1. Losartan

2. Valsartan

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16
Q

What is the neprilysin inhibitor and how does this work? Who is it used in?

A

Sacubitril
-> think of it inserting a cube into the neprilysin rather than a stick

Inhibits neprilysin, which is responsible for cleavage of natriuretic peptides which have good effects.

Used in combination with valsartan for treatment of heart failure

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17
Q

How do beta blockers reduce oxygen consumption by the heart?

A

They reduce the heart rate, allowing for increased filling time and stroke volume

Furthermore, they reduce the inotropy of the heart, resulting in less forceful contractions

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18
Q

What are the dihydropyridines of significance?

A
  1. Nefedipine - avoid in MI due to reflex tachycardia
  2. Amlodipine - longer halflife, no reflex tachycardia
    -> reduces mortality in LV dysfunction
    think the ‘dipin’ station for ice cream in sketchy
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19
Q

What are the non-dihydropyridine calcium channel blockers?

A
  1. Verapamil - Also has alpha 1 antagonist activity -> hypotension. It should not be used in heart failure but decreases digoxin’s clearance.
  2. Diltiazem

-> very vanilla and delicious dark chocolate ice cream

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20
Q

What is the mechanism of action of the non-dihydropyridine VGCC blockers?

A

They bind to the L type Calcium channel, but are cardioselective and will bind to both the open and inactivated form.

They reduce inward calcium current and delay channel closing, reducing the chronotropy and inotropy of the heart. -> contraindicated in AV block or with beta blockers due to excessive bradycardia

There is only minor blockage of L-type calcium channel on arteries

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21
Q

What are non-dihydropyridines used to treat and why?

A

Angina -> reduce cardiac work by reduction of inotropism

Supraventricular tachycardias -> delayed AV node conduction

Antiarrhythmia in general -> DO NOT USE IN HEART FAILURE DUE TO DECREASED INOTROPY

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22
Q

What drugs decrease cardiac remodeling?

A

Beta blockers (especially carvediol), ACE inhibitors / ARBs (through lack of aldosterone), spironolactone

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23
Q

What is the I-funny channel blocker and how does it work?

A

Ivabradine -> main use is reduction in tachycardia in people already on beta blockers

Blocks the channel in pacemaker cells, especially the SA node which is activated by hyperpolarization, and leads the pacemaker cells to spontaneously depolarize and allow calcium inside

If channel is a nonspecific channel (lets Na+ and K+ flow)

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24
Q

What is the mechanism of action of dihydropyridines?

A

They bind the L type Calcium channel in its open state, slowing calcium entry when it’s open, but not delaying its closure.

Dihydropyridines are vasoselective (rather than cardioselective), and prevent vascular smooth muscle contraction -> do not affect preload due to only arterial action

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25
Q

What is the mechanism of hydralizine and why is it not commonly given anymore? When is it given?

A

Mechanism unknown, relaxes arteriolar smooth muscle to reduce preload.

Not commonly given due to lupus-like syndrome.

Now given to patients who cannot handle standard therapy for heart failure (ACE + beta blocker + loop diuretic) in combination with a nitrate to reduce both preload and afterload

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26
Q

What is the mechanism of action of minoxidil? How does this relate to its contraindication?

A

Activates ATP-modulated potassium channel in smooth muscle, causing hyperpolarization and arteriolar relaxation

Contraindicated in patients with LV hypertrophy and diastolic dysfunction, as increased preload may lead to heart failure + pulmonary hypertension

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27
Q

What is the mechanism of action of sodium nitroprusside? What does it do to heart rate?

A

Generates nitric oxide, causing both venous and arterial relaxation, and a subsequent decrease in preload and afterload

Actually causes increase in heart rate (reflex)

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28
Q

What is nitroprusside used for?

A

Treatment of hypertensive emergencies such as acute aortic dissection (along with beta-blocker to reduce heart rate) or cardiogenic shock due to massive MI or rupture of papillary muscle

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29
Q

What is the mechanism of action of minoxidil? How does this relate to its contraindication?

A

Activates ATP-modulated potassium channel in smooth muscle, causing hyperpolarization and arteriolar relaxation -> increased preload, decreased afterload

Contraindicated in patients with LV hypertrophy and diastolic dysfunction, as increased preload may lead to heart failure + pulmonary hypertension
-> give with a loop diuretic and beta blocker

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30
Q

Why are beta-blockers always given with direct arterial vasodilators?

A

Otherwise, will cause reflex tachycardia and increase in renin secretion (beta1-antagonism will counter this)
-> minoxidil, sodium nitroprusside, hydralazine

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31
Q

What is ultralente insulin?

A

Very slow absorption - also suspended with zinc (like Lente insulin)

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32
Q

What two insulins are very rapidly acting and what is their mechanism?

A

Lispro insulin and aspart insulin

They are insulin with mutations introduced so insulin does not associate into its hexameric form

“Girls And Lads, Rest Now, Don’t Go”
Glulisine Aspart Lispro, Regular NPH, Detimir Glargine

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33
Q

What are the symptoms of a hypoglycemic state and what can induce it?

A

Sweating, tremor, blurred vision, and mental confusion

Exercise and stress can also precipitate this (exercise increases glucose uptake by cells)

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34
Q

What are the cutoff’s for diabetes and typical treatment goal of HbA1c?

A

> 6.5% = diabetes

Goal: Reduce to <7%

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35
Q

What are the adverse reactions of sulfonylureas?

A
  1. Induction of severe hypoglycemia
  2. Stimulation of appetite (due to hypoglycemia) -> weight gain
  3. High failure rate as disease progresses (beta cell failure)
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36
Q

What are the adverse effects of metformin use and who is it contraindicated in?

A

GI disturbances -> dose-related, especially at start of therapy - think of the girl puking at the guy professing his love

Lactic acidosis (from decreased usage of lactate in gluconeogenesis)

  • > avoid in renal disease, liver disease, or alcoholics
  • > think of the broken kidney plate with spilled milk on it
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37
Q

What are the thiazolidinediones (TZDs) also called? What drugs are in this class?

A

Glitazones

Includes:

  1. Rosiglitazone
  2. Pioglitazone

Think girl with glitter - Roses are red -> rosiglitazone
Pioglitazone just think of that dude eating too much pie to get fat

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38
Q

What are the meglitinides?

A

Repaglinide
Nateglinide

Think of my boy Nate Representing! And the gliding goose for glinides!

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39
Q

What are the adverse effects of glitazones? How does this relate to their usage

A

This keeps them from being used alot, only used as second line in combination:

  1. Hepatotoxicity
  2. Congestive heart failure from 3. Edema - > think of the dude eating pie / donuts with baggy pants and the crushed heart
  3. Weight gain -> significant -> that dude was fat
  4. Heart attack
  5. Bone loss -> bone breaking chairleg
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40
Q

What are the three sulfonylureas primarily being used today?

A
  1. Glimepiride
  2. Glipizide
  3. Glyburide

Think of the two ducks “riding” mother goose, and a smaller goose making a “z” in the ice for glipiZide

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41
Q

What drug is a GLP-1 homolog isolated from Gila monster?

A

Exenatide - resistant to DPP-4 protease
Liraglutide - other homolog with resistance to DPP-4 due to one amino acid change

Think of the -tide detergent used to wash the four clothes

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42
Q

What are the actions of exenatide and liraglutide?

A

Induces insulin release, depresses glucagon release -> good for post-prandial surge

Also: Blunts appetite by delaying gastric emptying

  • > associated with significant weight loss!
  • > liraglutide even approved for obesity
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43
Q

What are exenatide / liraglutide given with? Adverse effect?

A

Approved for combination use with sulfonylureas and metformin, may cause nausea

Also may induce hypoglycemia if given in combination with sulfonylureas

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44
Q

What drug is a DPP-4 inhibitor, and what is its primary benefit over the GLP-1 homologs? What is its main side effect?

A

Sitagliptin (Januvia) -> think of someone sitting down washing those clothes that have been cliptin’ to the clotheslines

Can be taken orally, does not show GI disturbances.

However, no associated weight loss :/

Side effect: Acute pancreatitis

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45
Q

What are the SGLT2 inhibitors?

A

Dapagliflozin
Canagliflozin

Drugs ending in -gliflozin -> think of the guy flossing in the corner of the classroom and he “CAN look pretty DAPper”

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46
Q

What is the mechanism of action of the TZDs and what drug are they similar to?

A

Similar to metformin, in that they reduce insulin resistance without posing hypoglycemia risk

Mechanism: activate PPARy receptor, expressed in white adipocytes which is a nuclear transcription factor. This suppresses the release of resistin from white adipocytes

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47
Q

What are the clinical uses / benefits of SGLT2 inhibitors?

A

Taken orally, modest HbA1c reduction in combination with metformin.

Also reduces CVD outcomes and may promote weight loss due to excretion of glucose

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48
Q

What are the two thyroid replacement therapies and which one is typically used?

A
  1. Levothyroxine - T4
  2. Liothyronine sodium - T3

T4 is used because it is cheaper and has a long half-life for easy treatment.

T3 is only used to treat acute symptoms

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49
Q

What class of drugs reduce thyroid hormone synthesis? What are they?

A

Thioureylenes
2 main agents:
1. Methimazole
2. Propylthiouracil

50
Q

What is the major adverse reaction of thioureylenes in general, and specifically propylthiouracil?

A

Thioureylenes -> can cause hypothyroidism over time if dose is not adjusted properly

Propylthiouracil -> HEPATOTOXICITY -> common cause of liver transplant. Give methimazole instead generally

Propylthiouracil good in acute thyroid attack (along with beta blockers and iodine) due to inhibition of peripheral deiodinase

51
Q

How can iodide lead to short-term treatment of hyperthyroidism? When is it practically used?

A

Relatively rapid inhibition of thyroid hormone release

  • > reduces the vascularity to the thyroid gland
  • > Only transient effects, not good in the long-term

Practically used prior to thyroidectomy for reducing size / vascularity of the thyroid gland

52
Q

What are the symptoms of thyrotoxicosis?

A

This is caused by hyperthyroidism / Graves disease:

  1. Exophthalmus
  2. Goiter
  3. Warm, flushed, and moist skin
  4. Tachycardia
  5. Muscle tremor
  6. Anxiety, insomnia, paranoia
  7. Osteoporosis - increased bone turnover in longstanding disease
53
Q

What is the mechanism of action of nitrates which is beneficial?

A

Increase in NO causes vasorelaxation, primarily affecting veins but secondarily arteries and arterials.

Decreased venous capacitance leads to a reduction in preload, which is beneficial for failing hearts with lots of pulmonary congestion / dilation

Decreased arterial tone leads to reduction in afterload as well, reducing cardiac work

54
Q

Why does high preload tend to occlude coronary vessels?

A

Leads to high end-diastolic pressure in failing hearts, and shortens the length of diastole, allowing for less time for oxygen delivery to myocardium (which occurs during diastole)

This explains why nitrates allow for greater oxygen availability / reduce oxygen consumption

55
Q

Why are nitrates especially good in unstable angina?

A

Nitrates also decrease platelet aggregation, decreasing the chances of forming thrombi

56
Q

What is sildenafil used to treat in the cardiovascular world?

A

Pulmonary hypertension due to pulmonary fibrosis. Causes relaxation of pulmonary artery (PDE5 is found here), which reduces the right-sided afterload

57
Q

What are the untoward effects and metabolism of sildenafil?

A

Flushing, visual disturbances, and headache

Priapus (erection >4 hours) is rare

Can cause MI if used with nitrates due to extreme hypotension

Metabolized via CYP3A4

58
Q

What does digoxin do to action potential duration in the heart?

A

It shortens it -> probably due to increased potassium conductance due to higher levels of Ca+2 in cytoplasm

59
Q

Why might the early side effects of digoxin toxicity progress to way worse ones?

A

Early side effects = GI distress.

Vomiting can cause hypokalemia (due to compensatory K+ excretion for H+ absorption)

Hypokalemia increases cardiac pacemaker rate, action potential duration, and is arrhythmogenic, predisposing to DADs of digoxin

60
Q

What are the primary indications for dopamine?

A
  1. Short-term managment of congestive heart failure associated with renal dysfunction (increases blood flow to mesentery and kidneys via D1 receptors)
  2. Cardiogenic / septic shock at high doses
61
Q

What is the mechanism of action of adenosine in anti-arrhythmia? Use?

A

Binds P1 purinergic receptors that open G-protein regulated potassium channels, inhibiting SA node, atrial and AV nodal conduction

-> immediate termination of supraventricular tachycardia (half-life of 6 seconds)

62
Q

What is the mechanism of action of ranolazine and what condition is it used in?

A

Inhibits the late sodium current which tends to be very large in ischemic tissues (this is a constant leak during depolarization). This channel normally increases intracellular sodium, facilitating increased calcium and a reduction in diastole length. Ranolazine thus decreases calcium and oxygen demands on the heart (useful in angina, but contraindicated in heart failure). It also inactivates the Ikr channel and can lead to prolonged QT interval.

63
Q

When is amiodarone used?

A

In atrial tachycardia as an oral med, can also treat recurrent ventricular tachycardias and fibrillation

64
Q

What are the non-cardiac side effects of amiodarone?

A

Pneumonitis leading to pulmonary fibrosis

Hyper or hypothyroidism (it is an analog of thyroxin)

CNS symptoms

Also has many CYP3A4 and digoxin interactions

65
Q

What is procainamide used for, and what are its untoward effects?

A

Drug of second choice for ventricular / atrial arrhythmias

Untoward effects -> possible torsades de pointe and can result in lupus-like disease in long-term use (like hydralazine)

66
Q

What is one beta-blocker which can be used against ventricular tachycardia?

A

Sotalol (has Class 3 properties with K+ channel blocking effect)

Typically beta-blockers and calcium channel blockers can only be used against supraventricular arrhythmias

67
Q

What are the metabolic actions of estrogen? How does this influence cardiovascular risk?

A
  1. Salt / water retention at higher doses -> can increase blood pressure / cause edema
  2. Decreases in LDL and increases in HDL
  3. Increases several clotting factors

Overall, consensus is increased CV disease risk

68
Q

What is estrogen usually given with and why?

A

A progesterone -> prevents endometrial hyperplasia and increased risk of endometrial cancer associated with monotherapy

69
Q

Who is estrogen therapy contraindicated in?

A

People with estrogen-dependent neoplasms (uterine and breast cancer)

Estrogen treatment during pregnancy (especially first trimester) -> can cause feminization of males

70
Q

What are the synthetic estrogens for clinical use?

A
  1. Diethylstilbestrol - it’s “still the best” way to keep from being pregnant!
  2. Ethinyl estradiol

Much longer lasting with less first pass metabolism

71
Q

What is progesterone secreted in response to?

A

Synthesized and secreted in response to the LH which induces ovulation, and is maintained by hCG of implanted trophoblast

72
Q

Other than in combination with estrogens for oral contraception / HRT, what are the monotherapy uses of progestins?

A
  1. Dysfunctional uterine bleeding
  2. Severe endometriosis
  3. Metastatic endometrial carcinoma
73
Q

What are the four main synthetic progestins?

A
  1. Medroxyprogesterone
  2. Norethindrone
  3. Norgesterel
  4. Ethynodiol (conjugated to ethynyl group at C17)
    MENN are phony
74
Q

What are two important estrogen receptor competitive antagonists?

A
  1. Tamoxifen
  2. Clomiphene

Imagine an ox climbing a fence to block an estrogen receptor

-> remember the trans forms are going against the receptor, just like trans- people go against the norm

75
Q

What are clomiphene and tamoxifen used for?

A

Clomiphene - infertility, blocks hypothalamic feedback and upregulates FSH / LH

Tamoxifen - estrogen-sensitive tumors in pre and post menopausal women

76
Q

What is leuprolide and what is it used for?

A

GnRH analog - prolonged stimulation of GnRH receptor will desensitize and inhibit release of FSH and LH (needs to be pulsatile)

Used as an anti-estrogen, anti-androgen, and in the treatment of uterine fibroids as well as endometriosis

77
Q

What are the three aromatase inhibitors (and hence antiestrogens), and which are irreversible / reversible?

A

Irreversible: Exemestane (gonna X out that stain of aromatase)

Reversible: Letrozole, Anastrozole

  • > reversibly bind the heme of aromatase CYP
  • > Anastronaut lets the heme go
78
Q

What are aromatase inhibitors used for in pre-menopausal women?

A

Induction of ovulation in infertility -> drop in E2 levels will cause negative feedback removal in these infertile women, causing LH to spike, triggering ovulation

79
Q

Who are androgens contraindicated for in why?

A
  1. Children -> virilization and disturbances in growth and bone development
  2. Pregnant women -> maculinization of female fetus can result
80
Q

What are the four primary androgen drugs?

A
  1. Testosterone salts
  2. Oxandrolone
  3. Methyltestosterone
  4. Fluoxymesterone

FOTM - flavor of the month

81
Q

What is Danazol and what is it used for?

A

An ethinyl derivative of testosterone -> used in treatment of endometrosis by inhibiting FSH / LH

82
Q

What drug is an antiandrogen by blocking 5alpha-reductase?

A

Finasteride

  • gonna have an “ass to ride” because you look like a girl
83
Q

What is the mechanism of action of cyproterone acetate and what is it used for?

A

“cyproterone” -> gonna lock up these sex offenders in a crypt

Competitive antagonist of dihydrotestorone -> used for inhibition of libido of male sex offenders and severe hirsutism

Inhibits many virilization effects

84
Q

What drugs are used in combination with leuprolide for the treatment of prostate cancer and what is their mechanism of action?

A

Flutamide or bicalutamide (less hepatotoxic)

  • > nonsteroidal competitive antagonist of androgen receptor
  • > play the flute or bicalute, am i right
85
Q

What is the mechanism of action of abiraterone acetate and what is it used for?

A

Inhibits testosterone synthesis by inhibiting CYP17A1 (17alpha hydroxylase), an enzyme needed to make androgens from progestins

Think of how abir castrated wesley and stopped androgen synthesis

Used for treatment of castration-resistant prostate cancer

86
Q

What is the mechanism of action of spironolactone? What is it used for?

A

Competitive antagonist for androgen receptor (as well as aldosterone receptor)
-> used for treatment of female hirsutism (like cyproterone acetate)

87
Q

What causes endometriosis and what are two primary drugs used for its treatment?

A

Excess estrogen levels, especially in reproductive years. Same treatment as for uterine fibroids

Can be treated with GnRH analogs:
Leuprolide
Nafarelin

It is nefarious for stopping GnRH

88
Q

What is the newest and hippest drug for the treatment of both endometriosis and uterine fibroids? How does it work? Why might it be preferable to Leuprolide or Nafarelin?

A

Cetrorelix acetate: GnRH antagonist

Preferable because there is no initial increase in symptoms (those drugs take a while to desensitize GnRH receptors)

89
Q

What is the oxytocin antagonist and what is it used for?

A

Atosiban
-> suppression of pre-term labor

Gotta BAN that baby

90
Q

What are the treatments for Paroxysmal Nocturnal Hemoglobinuria?

A
  1. Allogeneic bone marrow transplant - risky
  2. Eculizumab - antibody against C5, reduces need for blood transfusions and thrombosis risk
  • > its gonna cull ur wallet cuz its so expensive
  • > makes you susceptible to encapsulated bacterial infection
91
Q

What is fondaparinux used for?

A

Thromboprophylaxis of patients undergoing hip / knee surgery, or for PE / DVT prophylaxis

92
Q

What is the prototype direct thrombin inhibitor? How does it work?

A

Hirudin, other drugs with -rudin ending (no int’rudin)
Also -gator- from sketchy: argatroban

Irreversible inhibitor of thrombin which was isolated from leech saliva

93
Q

In what conditions is warfarin indicated?

A

Start therapy after acute DVT or pulmonary embolism

Prevent embolism in patients with acute MI, prosthetic heart valves, or atrial fibrillation

94
Q

What drugs increase the anticoagulant effect of Warfarin?

A
  1. Cephalosporins - kill bacteria in GI tract that make vitamin K, and directly inhibit the vitamin K epoxide reductase
  2. Aspirin
  3. Ginseng
  4. Ginkgo biloba
95
Q

What drugs decrease the anticoagulant effect of Warfarin?

A
  1. Barbituates
  2. Rifampin
  3. St. John’s wort
  4. Vitamin K -> the antidote of Warfarin overdose!!
96
Q

What are the risks of heparin toxicity?

A
  1. Major bleeding

2. Heparin-induced thrombocytopenia (HIT)

97
Q

What are the derivatives of t-PA now in use and why?

A

Alteplase, Reteplase, Tenecteplase (think of the playset)

-> longer half life than regular t-PA, so they have more convenient dosing

98
Q

What is the primary toxicity of t-PA and what might reverse this?

A

A whole body thrombolytic state which can cause bleeding.

Could be reversible via Aminocaproic acid (think of lady capping the paint) -> inhibitor of fibrinolysis by blocking the interaction between fibrin and plasmin. This might be a problem with problematic clots not being able to be busted by body.

99
Q

What are high and low molecular weight heparin indicated for?

A

Both: Venous thrombosis, pulmonary embolism, surgery, disseminated intravascular coagulation
HMWH: Acute MI
LMWH: Unstable angina

100
Q

Why is clopidogrel an attractive medication and what is it used for?

A

Has a better toxicity profile than aspirin (upper GI bleed, especially in combination with warfarin / clopidogrel), less frequent thrombocytopenia / leukopenia

Used with aspirin after angioplasty, also in patients with recent MI (guy playing guitar in the stands) or stroke (guy painting the wall), peripheral artery disease (pipe coming out of grill), or acute coronary syndrome (Angina anvil)

101
Q

What is the MoA of clopidogrel?

A

Antagonizes ADP receptors for platelet aggregation

think of the guy manning the “-grel” who blocks the ADP receptor with his hot dog bun

102
Q

What is the clinical use of cilostazol?

A

PDE3 inhibitor, direct vasodilator -> he lost his ball

Treatment of intermittent claudication from peripheral artery disease, especially calves.
-> contraindicated in CHF due to fluid retention (kind of like pio or rosaglitazone)

103
Q

What are the approved indications for growth hormone treatment?

A
  1. Pituitary dwarfism
  2. Genetic disorders of Noonan syndrome, Prader-Willi (paternally imprinted 15q11) - father willy and Turner syndrome - X cart wheel girl
  3. Idiopathic short stature - short kid
  4. Adult GH deficiency - due to pituitary adenoma / head trauma
  5. Muscle wasting in AIDs
104
Q

What is recombinant IGF-1 called? When is it used?

A

Mecasermin

  1. Laron syndrome
  2. When anti-GH antibodies are present
  3. Growth failures unresponsive to GH
105
Q

What are the manifestations of acromegaly?

A
  1. Generalized thickening of extremities with swelling of internal organs
  2. Expansion of skull at fontanelle
  3. Jaw protrusion
  4. Life threatening complications: Enlarged heart, HBP, T2DM, heart / kidney failure
106
Q

What are the somatostatin analogs used to treat excess GH? What are their side effects?

A

Octreotide
Lanreotide

Side effects include nausea, gallstones, and flatulence (+ steatorrhea - think of the girl on the yellow stool who looks like she’s gonna vom)

107
Q

What is the GH antagonist and when is it used?

A

Pegylated drug called “pegvisomant” - think of ants on the tire swing

Used if somatostatin agonists are ineffective at treating acromegaly

108
Q

What is the role of ADH in limiting blood loss during injury?

A
  1. Induces secretion of Factor 8 and von Willebrand factor from vascular endothelium -> promotes clotting

Think of vascular endothelial area with von Willebrand pool table and 8 ball on the table (V2-like receptor, remember the V2 receptor is Gs and moves AQP2 to basolateral membrane of principle cell)

  1. Vasoconstriction

Think of the guy at hole V1, via Gq receptor bending his golf club for vasoconstriction

109
Q

What can desmopressin be used for, other than central DI?

A

Nocturnal enuresis, and some coagulation disorders including von Willebrand disease and mild hemophilia A (factor 8 deficiency)

110
Q

What can cause SIADH?

A

Multitudinous causes, most affecting CNS or ectopic lung production: brain tumor, trauma, meningitis / encephalitis, or small cell carcinoma of lungs

111
Q

What are the adverse reactions of desmopressin?

A
  1. Vasoconstriction -> contraindicated in coronary artery disease
  2. Water intoxification - really bad in high blood pressure and heart failure
  3. Hyponatremia - due to overdilution of blood, manifests as headache and nausea before CNS effects. Avoid in renal failure
112
Q

What is the primary drug which is an endothelin inhibitor, its indication, and major untoward effect?

A

Bosentan, indicated for atrial pulmonary hypertension

-> think of boss man stan giving the “end of the line” slip for endothelin

Teratogenic and fatally hepatotoxic (think of the sweat spot on his shirt)

113
Q

What are two natriuretic peptide drugs?

A

Nesiritide - recombinant BNP - it’s necessary to turn the tide!
Ularitide - recombinant urodilatin

  • > used in acute heart failure, to increase diuresis via increased GFR, decreased RAA (decreases proximal sodium uptake), decreased ADH and directly dilate arterioles via cGMP
  • > natural release stimulated by processing increasing blood pressure / volume
  • > can cause acute renal failure tho
114
Q

What is the drug which can inhibit neprilysin and what is it given with?

A

Sacubitril, given with valsartan, an AT1 receptor antagonist

-> approved for heart failure

115
Q

What drug is approved in the US for treatment of veno-occlusive events and how does it work?

A

Hydroxyurea

-> increases production of fetal hemoglobin, interfering with polymerization of HbS

116
Q

What is the cause of most nutritional iron deficiency in the US?

A

Blood loss, especially in females due to menstruation.

Is also caused by increased requirements during pregnancy (6x as much iron needed per day in pregnancy)

117
Q

What is folate needed for?

A

Both purine and pyrimidine synthesis, as well as making methionine from homocysteine

118
Q

What will deficiency in either B12 or B9 cause?

A

Decreased synthesis of methionine and S-adenosylmethionine, leading to interference with numerous methylation “one-carbon metabolism reactions”

-> stores are directed away from nucleic acid synthesis, halting production of new cells

119
Q

How is folate absorbed?

A

In the early small intestine, typically in the MeFH4 form, via receptor-mediated endocytosis of reduced polyglutamates

120
Q

Who typically gets a folate deficiency?

A

Elderly patients, poor patients, and people with diets lacking vegetables, eggs, and meat.

Alcoholics + patients with liver disease are very susceptible due to diminished capacity for folate stores in liver

Pharmacology (54 decks)

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