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T9 MF3 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are 4 possible antibiotics that can be for a UTI before a culture has been gotten?

What are some other gerneral antibiotics that can be used to treat a UTI?

A
  1. Amoxicillin
  2. Septra
  3. Nitrofurantoin
  4. Fosfomycin

Nitrofurantoin, trimethoprim/sulfamethoxazole

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2
Q

What antibiotics are given for a complicated UTI?

A
  1. Ciprofloxacin (oral or IV) - ambulatory patients
  2. Ceftriaxone 3rd beneration (IV) - hospitalized patients
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3
Q

What antibiotic is given in the case of prostatitis and UTI?

A

A high concentration antibiotic such as ciprofloxacin, over the course of 6 weeks.

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4
Q

What is methenamine?

A

A crystallinec ompound producing formaldehyde in the low acidity condition of the bladder.

Used to help fight UTIs

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5
Q

What is phenazopyridine? What is a risk associated with it?

A

A local analgesic given in those with UTI to alleviate pain, irritation, discomfort, and urgency

(Not usually recommended –> risk of methemoglobinemia)

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6
Q

Fill out the following chart:

A
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7
Q

Fill in the following chart concerning diuretics:

A
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8
Q
  1. What are cephalosporins
  2. How do they work?
  3. What 4 groups of organisms are resistant to them?
  4. What are common (+1%) side effects?
  5. What are infrequent (0.1-1%) side effects?
A
  1. A class of antibiotics composed of a dihydrothiazine ring and a beta-lactam ring.
  2. Beta-lactam inhibits synthesis of peptidoglycan so that the bacterial cell wall cannot form.
  3. Listeria, Atypicals (ex. mycoplasma, chlamydia), MRSA, enterococci
  4. Diarrhea, nausea, rash, electrolyte disturbances, pain, inflammation at injection
  5. Vomiting, headache, dizziness, oral/vaginal candidiasis, pseudomembranous colitis, superinfection, eosinophilia, nephrotoxicity, neutropenia, thrombocytopenia, fever
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9
Q

What are bactericidal drugs? Give 4 examples

What are bacteriostatic drugs? Give 3 examples

A

Bactericidal = kill target organism (ex. aminoglycosides, cephalosporins, penicillins, quinolones)

Bacterostatic = inhibit or delay bacterial growth (ex. tetracycline, sulfonamides, macrolides)

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10
Q

What is a “generation” in regards to antibiotics?

A

A new form of the drug with greater spectrum of clinical use and ability to fight infection.

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11
Q

What is the difference between first, second, third, and fourth generation cephalosporins

A

1st = narrow spectrum

2nd = greater gram negative coverage but less gram positive coverage

3rd = greater gram negative coverage but less gram positive coverage

4th = greater gram negative coverage and gram positive coverage; use zwitterions; true broad-spectrum

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12
Q

What are the 6 things that loop diuretics decrease reabsorption of at the loop of Henle? How? (2 mechanisms)

A

Decreased reabsorption of Na+, Cl-, K+, Ca++, Mg++, and water

  1. Competitive binding for chloride binding site on Na+/K+/2Cl-, decreasing Na+, K+, Cl-, and water reabsorption (and thus Mg++ and Ca++ paracellular transport)
  2. Increased K+ secretion in DCT

-

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13
Q

What diuretic would you use in someone with kidney damage?

A

Loop diuretic

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14
Q

What drug class should be used to treat hypertension in the following conditions

A
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15
Q

Fill in the following chart for blood pressure medications:

A
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16
Q

Why is taking an NSAID bad in the context of renal artery stenosis?

A

NSAIDs reduce prostaglandin synthesis, which is normally released by the macula densa leading to vasodilation of the afferent arteriole.

Taking away this vasodilatory signal makes the problem worse.

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17
Q

Should ACE inhibitors be used in the context of renal artery stenosis?

A

Yes but carefully! It is good to reverse the hypertension but may lead to kidney failure due to suppression of GFR

Definitely not if it is a bilateral renal artery stenosis

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18
Q

What is the mechanism of action of thiazide diuretics and the subsequent outcome?

What are medical situations in which it is used? (2)

A

Thiazides act to inhibit the Na+/Cl- transporter (NCCT) on the apical side of the early DCT cells.

Increased Ca++ reabsorption and decreased Na+ and water reabsorption

  1. Hypertension
  2. Edema from heart failure or liver failure
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19
Q

What are contra-indications for taking a thiazide diuretic? (7)

What are some possible adverse effects?

A
  1. Hypotension
  2. Allergy to sulphur-containing medications
  3. Gout
  4. Renal failure
  5. Lithium therapy
  6. Hypokalemia
  7. Diabetes

Adverse = low K+/Na+/Mg+ in blood, high glucose/lipids/urea in blood, low Ca++ in urine

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20
Q

What are 2 classes of potassium sparking diuretics? How do they work? What are 2 examples of each?

A
  1. Mineralocorticoid receptor antagonist –> blocks aldosterone’s effects on principal cells –> inhibition of Na+/water reabsorption and K+ secretion

Ex. Spironolactone, eplerenone

  1. Sodium channel blockers –> directly inhibit Na+ entry into cells –> indirectly inhibit water entry into cells and K+ secretion into lumen

Ex. Amiloride, Triamterene

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21
Q

What medication leads to serum creatinine being overestimated and urine creatinine being underestimated?

A

Septra. It competes with creatinine for secretion at the PCT

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22
Q

Where does furosemide act? What does it do?

How does furosemide get to its place of action?

A

Furosemide acts on NKCC2 in the thick ascending limb of the LOH

Furosemide is bound to plasma proteins and is not really filtered. It enters the tubule via the organic anion channel in the PCT

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23
Q

What are 9 classes of oral anti-glycemics?

A
  1. Thiazolidinediones (glitazones)
  2. Sulfonylureas
  3. Meglitinides (glinides)
  4. SGLT2 inhibitors (gliflozins)
  5. Glucagon-like peptide-1 receptor agonist
  6. Dipeptidyl peptidase-4 inhibitor
  7. Biguanides
  8. Dopamine agonist
  9. Alpha glucosinase inhibitors
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24
Q

Fill in the following chart regarding details of oral anti-glycemics:

A
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25
Q

Thiazolidinediones (TZD)

  1. What is the mechanism of action?
  2. What are the main effects? (6)
  3. What are some side effects? (3)
A

Activation of PPARs –> bind to DNA with retinoid X receptor –> altered transcription –> fewer fatty acids in circulation –> more dependent on glucose for energy

Effects:

  1. Modified adipocyte differentiation
  2. Increased storage of fatty acids in adipocytes
  3. Increased adiponectin levels
  4. Increased leptin levels
  5. Decreased insulin resistance
  6. Decreased inflammatory molecules

Side effects = water retention, increased risk of UTI, reduced BMD

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26
Q

Sulfonylureas:

  1. What is the mechanism of action?
  2. What are the main effects? (4)
  3. What are some side effects? (5)
A

Bind to ATP-K+ channel on pancreatic beta cells –> closure of channels –> retention of K+ inside cells –> depolarization of cells –> opening Ca++ channels –> Ca++ rushes in –> increased exocytosis of insulin from cells

Effects:

  1. Increased insulin secretion
  2. Decreased hepatic glucose production
  3. Decreased lipolysis
  4. Decreased liver clearance of insulin

Side effects = hypoglycemia, GI upset, headache, hypersensitivity, risk of CV death

27
Q

Meglitinides

  1. What is the mechanism of action?
  2. What are some side effects? (2)
A

Same as sulfonylureas but weaker effects.

Side effects = hypoglycemia, increased risk of cancer

28
Q

SGLT-2 Inhibitors

  1. What is the mechanism of action?
  2. What are some side effects? (4)
A

Bind to SGLT-2 transorter on apical side of PCT cells –> decreased Na+ output and decreased glucose re-absorption.

Side effects = ketoacidosis, increased risk of UTI, increased risk of candidal vulvovaginitis, hypoglycemia

29
Q

GLP-1 Agonists

  1. What is the mechanism of action?
  2. What are the main effects? (4)
  3. What are some side effects? (1)
A

Activate glucagon-like peptide receptors –> stimulation of greater insulin release and glucagon release based on levels of glucose consumed

Effects

  1. Increased insulin secretion
  2. Increased number of beta cells in pancreas
  3. Delayed gastric emptying –> spreading out glucose absorption over time
  4. Decreased overall food intake

Side effects = increased risk of pancreatitis/pancreatic cancer

30
Q

DPP-4 Inhibitors

  1. What is the mechanism of action?
  2. What are some side effects? (8)
A

Inhibit DPP-4 which normally inhibits GLP-1 –> GLP-1 free to act on beta cells and increase insulin secretion

Side effects = hypoglycemia, nasopharyngitis, headache, nausea, heart failure, skin reactions, rheumatoid arthriits, risk of pancreatitis/pancreatic cnacer

31
Q

Metformin:

  1. What is the mechanism of action?
  2. What are the main effects? (5)
  3. What are some side effects? (3)
A

Inhibition of hepatic gluconeogenic genes

  1. Decrease gluconeogensis by the liver
  2. Increased insulin sensitivty
  3. Enhanced peripheral glucose uptake
  4. Decreaserd insulin-induced suppression of fatty acid oxidation
  5. Decreased absorption of glucose from the GI tract

Side effects = GI irritation, lactic acidosis, decreased TSH (if you already have hypothyroidism)

32
Q

What are 4 drugs that inhibit the organic anion channels of the kidneys? What drugs can they affect because of this?

A
  1. Ibuprofen –> methotrexate
  2. Indomethacin –> zidovudine
  3. Salicylate –> methotrexate
  4. Probenecid –> ciprofloxacin, chlorothiazide, furosemide, cisplatin, penicillins, cephalosporins
33
Q

What are 4 drugs that inhibit the organic cation channels of the kidneys? What drugs can they affect because of this?

A
  1. Cimetidine –> amiloride, bisoprolol, metformin, quinidine, ranitidine
  2. Ranitidine –> procainamide, triamterene
  3. Triamterene –> cimetidine, ranitidine
  4. Trimethoprim –> digoxin, procainamide
34
Q

What are 4 drugs that inhibit p-glycoprotein pump of the kidneys?

What are 7 drugs that inhibit p-glycoprotein pump of the kidneys and USE it?

What are 5 drugs that use p-glycoprotein pump of the kidneys?

A

Inhibit = clarithromycin, local anaesthetics, progesterone, testosterone

Inhibit and use = amiodarone, atorvastatin, Ca++ channel blockers, erythromycin, fluoroquinolones, propanolol, hydrocortisone

Use = dexamethasone, estradiol, etoposide, morphine, vincristine

35
Q

Fill in the following chart for types of insulin

A
36
Q

What is the progression of insulin administratino over the course of diabetes:

A
  1. Long-acting insulin at 0.1 U/kg daily
  2. Titrate long-acting until morning sugar is normal
  3. If unable to get A1C at goal, add rapid at biggest mealtime
  4. If unable to get A1C at goal, add rapid at 2 mealtimes
  5. If unable to get A1C at goal, add rapid at 3 mealtimes (basal bolus)

(Give 70/30 2x a day if basal bolus is not wanted)

37
Q

What is hydrocortisone?

Give some indications for its use. (7)

What is its potency as compared to prednisolone and dexamethasone

A

Exogenous cortisol

  1. Addison’s disease
  2. Hypercalcemia
  3. Inflammatory conditions (ex. asthma, COPD, Lupus, IBD, thyroiditis)
  4. Hyper-active immune system
  5. Collagen disease
  6. Shock
  7. Transplantation

4x less potent than prednisolone; 40x less potent than dexamethasone

38
Q

What is florinef/fludrocortisone?

Give some indications for its use. (4)

What is its potency as compared to cortisol and aldosterone?

A

Synthetic mineralocorticoid with anti-inflammatory activity

  1. Addison’s disease
  2. CAH
  3. Orthostatic intolerance
  4. Postural orthostatic tachycardia syndrome

10x as potent as cortisol; 250-800x as potent as aldosterone

39
Q

What are 4 examples (technical and market names) of GnRH analogues?

A
  1. Histrelin - Vantas
  2. Leuprorelin - Lupron
  3. Triptorelin - Decapeptyl
  4. Goserelin - Zoladex
40
Q

What is testolactone?

A

An aromatase inhibitor

41
Q

What are two risk from taking systemic estrogen therapy?

A
  1. DVT
  2. Endometrial cancer
42
Q

What are 5 contraindications to taking estrogen in HRT?

A
  1. Undiagnosed vaginal bleeding
  2. Severe liver disease
  3. Pregnancy
  4. Venous thrombosis
  5. Personal history of breast cancer
43
Q

What are different ways to adminsister estrogen?

A
  1. Trans-dermal
  2. Rings in the vagina
  3. Creams
  4. Oral
  5. Patches
  6. Vaginal suppositories
  7. Sprays
44
Q

What are 2 different schedules for taking estrogen as an HRT in treating menopause?

A
  1. Estrogen alone with annual endometrial biopsy
  2. Estrogen every day with progesterone taken for a week every 3-4 months
45
Q

How does mifepristone lead to abortion?

A

It is a progesterone receptor antagonist.

It makes the endometrium unsuitable for pregnancy causing the embryo to detach.

46
Q

How does methotrexate lead to abortion?

A

It is a dihydrofolate reducatse inhibitor.

It interferes with DNA synthesis which prevents placental villi from proliferating.

47
Q

What are some side effects, pros, and cons of medical abortion?

A

Side effects = abdominal pain/cramps, N/V, diarrhea, prolonged uterine bleeding, vaginal bleeding

Pros = effective and noninvasive, out-patient

Cons = experience of miscarriage, 3 visits (2 meds + F/U)

48
Q

What are common drugs/drug classes contraindicated in pregnancy?

A

Acetaminophen, alochol, aspirin, ACEI, ARBs, beta-blockers, cyclophosphamide, lithium, methotrexate, NSAIDs, opiates, penicallmines, quinolones, SSRIs, streptomycin, tamoxifen, valproic acid, warfarin

49
Q

Fill in the following chart concerning warfarin vs. heparin in pregnancy

A
50
Q

What are 3 types of exogenous prostaglandins?

A
  1. Dinoprostone
  2. Misoprostol
  3. Prostin
51
Q

What is mifepristone?

What is it used for?

A

A progesterone receptor antagonist

Used in cervical ripening and labour induction

Used in therapeutic abortion prior to 9 weeks

52
Q

What is a hygroscopic dilator? Give 3 examples.

A

A substance that relies on water absorption to swell, forcibly dilating the cervix

Laminaria, Dilapan, Lamicel

53
Q

What is an example of an oxogenous oxytocin?

A

Pitocin

54
Q
  1. When is general endotracheal anesthesia indicated during labour? (3)
  2. What are advantages (3)?
  3. What are disadvantages (3)?
  4. What are complications? (3)
A
  1. Emergency C/S, instrumental vaginal delivery, entrapment of head during breech
  2. Rapid, low incidence of hypotension, relaxes cervix and uterus
  3. Risk of aspiration, neonatal depression, postpartum hemorrhage
  4. Pneumonia/pneumonitis, matneral hypoxic cerbral injury, upper airway injury
55
Q
  1. What are 3 categories of systemic analgesics?
  2. What are advantages of using these during labour? (2)
  3. What are disadvantages of using these during labour? (4)
A
  1. Opioid agonists, partial opioid agonists, partial opioid antagonists
  2. Easily given, no adverse effect on labour progress
  3. Nausea/vomiting, respiratory depression, oversedation, may decrease FHR variability
56
Q

What are 3 kinds of regional blockades given in labour pain management?

A
  1. Spinal sensory nerve block
  2. Pudendal nerve block
  3. Caudal/saddle block
57
Q

What are 2 types of spinal regional blockades. Define each.

A
  1. Epidural analgesia = insertion at L2-3 or L3-4 in peridural fat; intermittent bolus injection or continuous infusion
  2. Spinal analgesia = insertion at L2-3 or L3-4 into subarachnoid space over 2-3 minutes
58
Q

What are the advantages, disadvantages, and contra-indications of epidural analgesia during labour?

A
59
Q

What are the advantages, disadvantages, and contra-indications of spinal analgesia during labour?

A
60
Q

Where is a pudendal nerve block given?

When is it best used?

A

Transvaginal infiltration of pudendal nerves bilaterally at the place where they exit the Alcock canal and circumnavigate the ischial spines

Best used during second stage of labour

61
Q

Where s a caudal block given?

A

The cauda equina through the sacral hiatus

62
Q
  1. What are 2 ways to administer local analgesia in labour?
  2. What are 3 types of local analgesia used in labour?
A
  1. Field block (nerve endings in vulva), paracervical (sensory nerves leaving uterus)
  2. Bupivacaine, lidocaine, chloroprocaine
63
Q

Give an example of an inhaled analgesic used during labour.

A

Entonox

T9 MF3 (6 decks)

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