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Pharmacology Flashcards

1
Q

what is the mechanism of Acetaminophen toxicity in the liver?

A

Specifically, acetaminophen is converted by CYP450 enzymes into NAPQI, which results in severe liver damage when accumulated in excess.

Acetaminophen is not a CYP inhibitor or inducer

sx: N/V, abdominal pain –> later on at higher doses, can cause hepaticc necrosis/juandice +/-encephalopathy, nephrotoxicity
antidote: NAC and activated charcoal

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2
Q

which diabetes drug can cause vitamin B12 deficiency if taken a long time

A

metformin (decreases absorption of)

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3
Q

Glucocorticoids MOA

A

steroid binding to intracellular glucocorticoid receptors followed by translocation to the nucleus where it inactivates NF-κB –>:

  • reduction in the transcription of proinflammatory mediators such as COX-2 , NOS, and inflammatory cytokines (IL-1 thru IL-6, IL-8, IL-10, IL-13, GM-CSF, TNF-α, Interferon-γ)
  • upregulation in the synthesis of annexin A1, which inhibits phospholipase A2 and neutrophil penetration through endothelium of blood vessels
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4
Q

Omalizumab MOA

A

Omalizumab binds mostly unbound serum IgE and blocks binding of IgE to the Fc portion of mast cells, preventing degranulation

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5
Q

T/F: M3 muscarine antagonists are not recommended in uncontrolled narrow-angle glaucoma.

A

true (tiotropium, atropine, scopalamine)

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6
Q

cocaine MOA

A

blocking reuptake of the neurotransmitters norepinephrine, dopamine, and serotonin.

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7
Q

What drugs are indicated for patient with acute gout attack

A

NSAID

Colchicine

corticosteroids/glucocorticoids (injection preferred)

^after NSAID failure

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8
Q

what drugs are indicated for preventative/chronic management of gout

A
  1. Xanthine oxidase inhibitors
    1. allupurinol, febuxostat
  2. probenecid

^reduce the urice acid level in the body

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9
Q

MOA of colchicine

A

microtubule inhibition by binding to tubulin –> white blood cell migration and phagocytosis is inhibited

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10
Q

colchicine adverse effects

A

GI:

N/V/D –> d/t loss of GI epithelium turnover which promotes BM

abdominal pain

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11
Q

what are the xanthine inhibitors

A
  1. allopurinol –> competitive inhibitor (mn: PURE competition)
  2. febuxostat –> non-competitive inhibitor
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12
Q

side effects of allopurinol

A

for this reason, many patients don’t tolerate it well. febuxostat is used as a second line of tx for patients who don’t tolerate allopurinol

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14
Q

MOA of allopurinol and febuxostat

A
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15
Q

Can we give patients aspirin for pain control of gout attack?

A

NO, not at normal dosages

it is dose dependent, see image

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16
Q

what co-administration needs to be given with the XO inhibitors

A

cochicine because the changing ration of uric acid in the blood due to the XO inhibitors can cause acute gout attacks which colchicine will supress

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19
Q

What DMARD is this based on the MOA shown

what’s its indication

A

leflunamide

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20
Q

what DMARD acts by inhibiting calcineurin?

what’s its indication

A

cyclosporin

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21
Q

probenecid side effects and administration precautions

A

Give with colchicine if acute setting

don’t use if renal problems

increased risk for developing uric acid kidney stones d/t increased secretion

Adverse Effects: GI irritation, rash, aplastic anemia; don’t give if pt has sulfa allergey

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22
Q

MOA of probenicid

whats its indication

A

blocks reabsorption of uric acid in proximal tubule –> increased excretion

indicated for gout

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24
Q

what is the indication for prescribing leflunamide

A

RA, if the patient fails Methotrexate

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26
Q

GAS (strep. pyogenes) virulence factors

A
  1. bacterial capsule is responsible for evasion of phagocytosis.
  2. protein F is required for adherence to the host cell
  3. Streptokinase lysis clots and helps invasion into tissues.
  4. C-5 peptidase lyses complement complexes evading the complement component of the immune system
  5. Streptococcal pyogenic exotoxin is responsible for generating fever and immunomodulation
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27
Q

indication and MOA of cyclophosphamide

A

indication: RA

MOA:

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28
Q

Staining features/virulence factors of Staphylococcus aureus

A
  1. gram positive
  2. beta hemolytic
  3. coagulase positive (differentiates s. aureus and s. epidermidis)
  4. catalase positive –> converts H2O2 to water and oxygen (differentiates it from strep)
  5. ferments mannitol
  6. contains alpha toxin and beta toxin

^pretty much all positives (mn: Aureas does All the Areas)

*** the other key thing that differentiates it from strep is that it is arranged in clusters rather than chains

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29
Q

what is the basic differentiating factor between staph aureus and strep pyogenes ( in terms of structure)

A
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30
Q

Food poisoning due to staphylococcal enterotoxin is characterized
by a short incubation period ___-___ hours

A

1-8 hours

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31
Q

True/False:

Coagulase-positive staphylococci are considered
pathogenic for humans

A

TRUE

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32
Q

treatment for penicillin G- resistant S. aureus

A

Penicillin G-resistant S. aureus strains from clinical
infections always produce penicillinase. They
constitute >95% of S. aureus isolates in communities in
the United States.

• They are often susceptible to β-lactamase-resistant
penicillins, cephalosporins, or vancomycin.
• Vancomycin-resistant strains are rare.

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34
Q
A

sulfa drug rxn

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35
Q

what are the 5 types of typhus infections and what was their causative agent

A
  1. Rocky Mountain spotted fever –> tickborne,
  2. scrub typhus, –> mite-borne
  3. rickettetsialpox, –> mite-borne
  4. endemic typhus, spread by a body louse
  5. murine endemic typhus spread by a flea.
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36
Q
A

Answer: DHFR and DHPS

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37
Q

what is the abx treatment for rickettsiae infection causing typhus?

A

tetracycline/docycycline

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39
Q

are are the two most likely late sequelae of streptococcal pyogenes infections

A
  1. rheumatic fever
  2. glomerular nephritis
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40
Q

Patient with anal itching presents. no other symptoms. microscopu of a the area shows this. What’s the diagnosis?

A

enterobius (pinworm) which is in the nematode family

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41
Q

which organism is most usually responsible for toxic shock syndrome

A

Staph

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42
Q

the ___________ lab test differentiates between staph aureus from non pathogenic staphylococci

A

Coagulase test

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49
Q

What drugs are indicated for patient with acute gout attack

A

NSAID

Colchicine

corticosteroids/glucocorticoids (injection preferred)

^after NSAID failure

How well did you know this?
1
Not at all
2
3
4
5
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50
Q

what drugs are indicated for preventative/chronic management of gout

A
  1. Xanthine oxidase inhibitors
    1. allupurinol, febuxostat
  2. probenecid

^reduce the urice acid level in the body

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51
Q

MOA of colchicine

A

microtubule inhibition by binding to tubulin –> white blood cell migration and phagocytosis is inhibited

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52
Q

colchicine adverse effects

A

GI:

N/V/D –> d/t loss of GI epithelium turnover which promotes BM

abdominal pain

How well did you know this?
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53
Q

what are the xanthine inhibitors

A
  1. allopurinol –> competitive inhibitor (mn: PURE competition)
  2. febuxostat –> non-competitive inhibitor
How well did you know this?
1
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54
Q

side effects of allopurinol

A

for this reason, many patients don’t tolerate it well. febuxostat is used as a second line of tx for patients who don’t tolerate allopurinol

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56
Q

MOA of allopurinol and febuxostat

A
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57
Q

Can we give patients aspirin for pain control of gout attack?

A

NO, not at normal dosages

it is dose dependent, see image

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58
Q

what co-administration needs to be given with the XO inhibitors

A

cochicine because the changing ration of uric acid in the blood due to the XO inhibitors can cause acute gout attacks which colchicine will supress

How well did you know this?
1
Not at all
2
3
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5
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61
Q

What DMARD is this based on the MOA shown

what’s its indication

A

leflunamide

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62
Q

what are the best NSAIDs for gout?

A

sulindac, naproxen, indomethacin

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63
Q

what DMARD acts by inhibiting calcineurin?

what’s its indication

A

cyclosporin

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64
Q

probenecid side effects and administration precautions

A

Give with colchicine if acute setting

don’t use if renal problems

increased risk for developing uric acid kidney stones d/t increased secretion

Adverse Effects: GI irritation, rash, aplastic anemia; don’t give if pt has sulfa allergey

How well did you know this?
1
Not at all
2
3
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5
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65
Q

MOA of probenicid

whats its indication

A

blocks reabsorption of uric acid in proximal tubule –> increased excretion

indicated for gout

How well did you know this?
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3
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5
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67
Q

what is the indication for prescribing leflunamide

A

RA, if the patient fails Methotrexate

How well did you know this?
1
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2
3
4
5
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69
Q

GAS (strep. pyogenes) virulence factors

A
  1. bacterial capsule is responsible for evasion of phagocytosis.
  2. protein F is required for adherence to the host cell
  3. Streptokinase lysis clots and helps invasion into tissues.
  4. C-5 peptidase lyses complement complexes evading the complement component of the immune system
  5. Streptococcal pyogenic exotoxin is responsible for generating fever and immunomodulation
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70
Q

indication and MOA of cyclophosphamide

A

indication: RA

MOA:

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71
Q

Staining features/virulence factors of Staphylococcus aureus

A
  1. gram positive
  2. beta hemolytic
  3. coagulase positive (differentiates s. aureus and s. epidermidis)
  4. catalase positive –> converts H2O2 to water and oxygen (differentiates it from strep)
  5. ferments mannitol
  6. contains alpha toxin and beta toxin

^pretty much all positives (mn: Aureas does All the Areas)

*** the other key thing that differentiates it from strep is that it is arranged in clusters rather than chains

How well did you know this?
1
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2
3
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72
Q

what is the basic differentiating factor between staph aureus and strep pyogenes ( in terms of structure)

A
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73
Q

Food poisoning due to staphylococcal enterotoxin is characterized
by a short incubation period ___-___ hours

A

1-8 hours

How well did you know this?
1
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3
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5
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74
Q

True/False:

Coagulase-positive staphylococci are considered
pathogenic for humans

A

TRUE

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75
Q

treatment for penicillin G- resistant S. aureus

A

Penicillin G-resistant S. aureus strains from clinical
infections always produce penicillinase. They
constitute >95% of S. aureus isolates in communities in
the United States.

• They are often susceptible to β-lactamase-resistant
penicillins, cephalosporins, or vancomycin.
• Vancomycin-resistant strains are rare.

How well did you know this?
1
Not at all
2
3
4
5
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77
Q

what are the 5 types of typhus infections and what was their causative agent

A
  1. Rocky Mountain spotted fever –> tickborne,
  2. scrub typhus, –> mite-borne
  3. rickettetsialpox, –> mite-borne
  4. endemic typhus, spread by a body louse
  5. murine endemic typhus spread by a flea.
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78
Q
A

Answer: DHFR and DHPS

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79
Q

what is the abx treatment for rickettsiae infection causing typhus?

A

tetracycline/docycycline

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81
Q

are are the two most likely late sequelae of streptococcal pyogenes infections

A
  1. rheumatic fever
  2. glomerular nephritis
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82
Q

Patient with anal itching presents. no other symptoms. microscopu of a the area shows this. What’s the diagnosis?

A

enterobius (pinworm) which is in the nematode family

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83
Q

which organism is most usually responsible for toxic shock syndrome

A

Staph

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84
Q

the ___________ lab test differentiates between staph aureus from non pathogenic staphylococci

A

Coagulase test

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86
Q

what rare but strange MSK side effect can occur with taking fluoroquinalones

A

achilles tendon tear/rupture or swelling

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88
Q

what is an MAO

A

Monoamine oxidase

MAOI = drug that inhibites monoamine oxidase

*assoc with serotonin syndrome

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91
Q

T/F: metronidazole only works on anaerobes

A

TRUE

esp c diff, b frag, H pylori

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92
Q

what drug to use to treat necrotizing fascitis

A

clindamycin (with penicillin G)

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93
Q

ketoconazole

A

an antigunal medication

MOA: blocks ergosterol synthesis by inhibiting 17,20 lyase

AE: decrease in testosterone (p/w gynecomastia in men)

off label use: Cushing’s syndrome (b/c it also blocks upstream enzymes req. for cortisol synth.)

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94
Q

what are pediculocides

A

drugs that kill pediculus humanus (lice) of the head (capitis) and body (corporis)

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96
Q

what is ascaris

A

giant intestinal roundworm

causes intestinal pain, constipation (high pitched bowel sounds)

tx: mebendazole

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97
Q

mebendazole - what is it used to treat?

A

intestinal nematodes and tapeworms

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98
Q

what drugs are used to treat tapeworms

A

niclosamid, praziquantel, albendazole (or mebendazole)

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99
Q

praziquantel treats _______and _________

A

tapeworms (cestodes) and flukes (trematodes)

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100
Q

how does niclosamide work?

A

transport chain uncoupler

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101
Q

how does ivermectin work?

A

Glu Cl- channel agonistm

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102
Q

ivermectin treats

A

threadworm, dog heartowrm, wuchereria (elephantiasis), lice

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103
Q

limitation of treatment of lice with benzyl alcohol?

A

it only kills adult lice

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104
Q

what is “rid” OTC shampoo?

A

contain pyrethrins (from chrysanthemom flower), which kill lice via Na+ channel blockers

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105
Q

which drugs kill lice eggs and adults?

A

malathion

spinosad

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107
Q

what toxicities/AEs are associated with Quinidine (class 1A antiarrhythmic)

A
  1. cinchonism: a syndrome of tinnitus, headache and dizziness
  2. thrombocytopenia
  3. QT prolongation (torsades, syncope)
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108
Q

what toxicities/AEs are associated with procainamide (class 1A antiarrhythmic)

A
  1. (chronic use) drug-induced lupus (sx arthralgia, arthritis, pleuritis, pericarditis, parenchymal pulmonary disease)
  2. QT prolongation (torsades, syncope)
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109
Q

what toxicities/AEs are associated with disopyramide

A
  1. acute heart failure (cannot be used in patients with impaired systolic function.)
  2. anticholinergic side effect sx: dry eyes, dry mouth, urinary retention
  3. QT prolongation (torsades, syncope)
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110
Q

what toxicities/AEs are associated with lidocaine

A

neurological side effects: tremor, convulsions (seizure), paresthesias

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111
Q

which drugs are high risk for causing DILE

A

There are four main drugs that are known for causing drug-induced lupus:

  • hydralazine
  • isonazid (INH)
  • procainamide
  • phenytoin/penicillamine
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112
Q

What are the class 1A antiarrhythmics

A

Quinidine (prom queen)
Procainamide (prom king)
disopyramide (disappear)

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113
Q

tx of choice for Wolff parkinson-white syndrome

A

procainamide

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114
Q

avoid class 1A antiarrhythmics (Quinidine (prom queen)
Procainamide (prom king)
disopyramide (disappear)) if a patient has _________

A 
heart failure (b/c negative inotropy can lead to heart failure) 
ESPECIALLY disopyramide
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115
Q

the class IB antiarrhythmics are

A

mexiletine (mexican flag)
lidocaine (lied to me)

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116
Q

which class of antiarrhythmics is best for heart damaged by ischemia?

A

class 1B (mexiletine and lidocaine)

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117
Q

what toxicities/AEs are associated with mexilitine

A

N/V

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118
Q

what are the class 1C antiarrhythmics

A

flecainide (flakes)
propafenone (purple phone)

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119
Q

indications for using class 1C antiarrhythmic drugs?

A

Ventricular tachycardia
other arrhythmias that are refractory to other tx (b/c it is most likely to cause an arrhythmia)

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120
Q

what toxicities/AEs are associated with propafenone?

A

metallic taste (fenny taste)

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121
Q

Beta-1 receptors are predominantly found in

A

the heart, the kidney, and fat cells.

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122
Q

when are beta blockers contraindicated?

A
  • when pt taking Ca2+ channel blockers (risk of AV block)
  • pheochromocytoma
  • cocaine toxicity

-bradycardia (non physiologic)

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123
Q

what is an off-label use for propanalol

A

Propranolol has the best CNS penetration among all beta blockers and is thus used as an anxiolytic (reduces sympathetic sx of anxiety)

another use is as a local anesthetic

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124
Q

which of the Class II (K blockers) antiarrhythmics is indicated for life threatening V Tach

A

amiodarone

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125
Q

what toxicities/AEs are associated with dronedarone?

A

GI disturbances (mn: you get motion sickness flying on a drone)

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126
Q

what toxicities/AEs are associated with class IV antiarrhythmics (verapamil and diltiazem)

A

hyperprolactinemia, flushing, bradycardia, constipation
more serious: heart block and SA node depression*
therefore, contraindicated in pts with bradycardia and heart failure

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127
Q

dangerous drug interaction with class IV antiarrhythmics (verapamil and diltiazem)

A

don’t give with beta blockers –> decreases conduction velocity

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128
Q

what toxicities/AEs are associated with adenosine (Misc antiarrhythmic)

A

flushing, bronchoconstriction, dyspnea, chest pain, hypotension

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129
Q

Digoxin MOA

A

mimics effect of vagal nerve innervation:

  1. decreases AV node firing (via inhibiting the sodium/potassium-ATPase in cardiac myocytes. This inhibition increases the intracellular sodium content –> The increase in intracellular Na+ decreases the activity of the Na+/Ca2+ exchanger, which results in an increase in the intracellular Ca2+ concentration –> increase in cardiac contractility)

BUT, it’s a positive inotrope (increased contractility, so that the heart can pump more blood with fewer contractions)

*obviously these effects are complimentary, but it can seem counterintuitive because positive inotropy is also an effect of the sympathetic nervous system via beta 1 rec activation

ind/for HFrEF (adjunct) and A-fib

does not provide mortality benefit

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130
Q

what toxicities/AEs are associated with digoxin

A

+N/V/D + confusion, tachyarrhythmias (+/- AV block), and visual changes (particularly “Halo-ing” and yellowing appearance of visual objects (“xanthopsia”)), hyperkalemia (a/w pooer prognosis) and hyponatremia (d/t direct inh. of na/k pump)

Digoxin is renally cleared and has a narrow therapeutic window, so toxicity frequently results from alterations in kidney function.

antidote: magnesium, digoxin specific immune fabs

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131
Q

which class IV antiarrhythmic can be used to treat HTN

A

diltiazem

132
Q

what side effects are common to all Class IV antiarrhythmics (Ca channel blockers)

A

constipation, hyperprolactinemia, heart block, bradycardia

133
Q

what are the calcium channel blockers

A

Dihydropyridines (selective for Ca2+ channels on vascular smooth muscle so they treat HTN)
Amlodipine
Nicardipine
Nifedipine

Non-dihydropyridines (selective for heart tissue so they treat arrhythmias)
verapamil
diltiazem

134
Q

what are the indications for Ca channel blockers (by type)

A

dihydropyridines (-dipine): HTN (main indication), angina, Raynaud’s phenomenon, cerebral vasospasms after subarachnoid hemorrhage
non-dihydropyridines (verapamil and diltiazem): tachyarrhythmias, angina, HTN (diltiazem only)

135
Q

what side effects are common to all dihydropyridines (-dipine)

A

reflex tachycardia, vasodilation, gingival hyperplasia

136
Q

what are the sx of alcohol withdrawal

A

anxiety, tremors, diaphoresis, and possibly seizures

137
Q

what is Lactulose and what is it indicated for

A

a synthetic disaccharide laxative → decreases absorption of ammonia in the bowel: lactulose is converted to lactic acid by intestinal flora → acidification in the gut leads to conversion of ammonia (NH3) to ammonium (NH4+) → ammonium is excreted in the feces → decreased blood ammonia concentration

used for hepatic encaphlopathy

138
Q

1st line tx for status epilepticus

A

IV benzodiazapines

MOA: enhance effects of GABA at GABA-A rec –> increased Cl influx –> no AP

139
Q

prophylaxis for recurrence of status epilepticus

A

phenytoin

MOA: blocks presynaptic voltage gated Na channels

Black box warning: Hypotension and cardiac arrhythmias with rapid infusion

n/b it’s a P450 inducer

140
Q

a pt develops elevated serum creatinine or even acute renal failure following initiation of ACE inhibitor for HTN. What’s the pathogenesis of this?

A

ACE inhibitors lower angiotensin II levels, causing systemic vasodilation and reduced blood pressure. However, they also cause efferent arteriolar dilation and lower intraglomerular pressure, preventing the kidney from maintaining GFR in the setting of reduced renal perfusion. Many patients experience up to a 30% increase in serum creatinine within 2-5 days of starting ACE inhibitors. Patients with bilateral RAS (who are heavily dependent on angiotensin II to maintain GFR) can experience a precipitous fall in GFR and develop acute renal failure.

n/b: This affect does not occur in the affarent arterioles because there are sufficient local vasodilators (PGs and NO) to counteract the effects of ang II

141
Q

a pt develops hyperkalemia following initiation of ACE inhibitor for HTN. What’s the pathogenesis of this?

A

ACE inhibitors decrease ang II –> ang II not available to stimulate secretion of aldosterone from adrenal gland –> decreased aldosterone –> decreased expression of Na/K ATPase –> decreased Na reabsorption and K secretion in the distal and collecting tubules

*to remember the direction that Na and K are flowing, remember that in the Na/K ATPase, K is entering the cell, and Na is leaving the cell. The side of the cell where the blood vessel runs, is by default “outside” as in the rest of the body, rather than the side with the lumen (in the kidneys).

142
Q

what drugs are a/w acute tubular necrosis?

A

aminoglycosides, vancomycin, antiretrovirals, foscarnet, cisplatin, ethylene glycol

other things (not drugs): lead, radiocontrast agents, myoglobinuria from rhabdomyolysis, and hemoglobinuria

143
Q

statin MOA

A

inhibition of the rate limiting step in cholesterol synthesis (HMG-CoA reductase)

144
Q

in utero lithium exposure (tx for bipolar disorder) can cause what defect

A

Ebstein’s anomaly in infants. Ebstein’s anomaly is characterized by apical displacement of the tricuspid valve leaflets, decreased volume of the right ventricle, and atrialization of the right ventricle.

​​​​​​​

145
Q

how does cabergoline affect pituitary adenoma?

A

​​​​​​​Prolactin levels typically fall significantly within the first 2-3 weeks of therapy with a corresponding improvement in hypogonadal symptoms. Although decreased tumor size may not be visible on imaging for several weeks, mass-effect symptoms (eg, visual field defects) usually start to improve much sooner, often within the first several days of treatment with eventual normalization in many cases.

146
Q

What are the non-sedating antihistamines and how do they work?

A
  1. cetirizine (mn: setirizine is second generation)
  2. Loratadine
  3. fexofenadine
  4. desloratadine

called 2nd generation antihistamines, they are non sedating because they are are hydrophilic and have poor penetration of the blood-brain barrier (BBB).

147
Q

what is the MOA of orListat (weight loss drug)

A

inhibits resorption of fats in the du-O-denum by c-O-valently binding lipases

mn: starts with an O for duodenum and covalent binding, has an L for loss of weight

148
Q

What does a benzodiazapine overdose look like and what is the antidote?

A

The presence of sedation with normal vital signs and an unremarkable physical examination is most consistent with benzodiazepine overdose.

Flumazenil functions as a competitive antagonist at the benzodiazepine binding site and may be used as an antidote to reverse benzodiazepine sedation related to overdose or procedural sedation.

**by contrast, and opioid overdose would present with resporatory depression (At least)

149
Q

antidote to anticholinergic toxicity?

A

physostigmine (acetylcholinesterase inhibitor)

150
Q

antidote to antipsychotic medication overdose

A

diphenhydramine

151
Q

anatidote to serotonin syndrome

A

cyproheptadine

152
Q

antidote to cocaine overdose

A

benzodiazapines (bind to GABA-a receptor, enhancing transmission)

153
Q

antidote to cholinergic crisis

A

atropine then pralidoxime

Atropine binds to and inhibit muscarinic acetylcholine receptors,

154
Q

how is metformin metabolized

A

renally

155
Q

Management of gastroesophageal reflux disease includes lifestyle and dietary modifications (eg, weight loss, tobacco avoidance) and medications such as

A

proton pump inhibitors (PPIs) (eg, pantoprazole, omeprazole) or histamine 2 receptor antagonists (eg, famotidine). PPIs irreversibly inhibit the H+/K+ ATPase on parietal cells, which decreases gastric acid secretion.

156
Q

what are the kidney acting drugs and where do they act?

A

COLT PAw Mn for the diuretics in order of where they operate

  1. Carbonic anhydride inhibitors: pct
  2. Osmotic diuretics: pct (eg mannitol) ..indicated for acute high ICP
  3. Loop diuretics : ascending limb of loop of Henley . E.g furosemide.. prevents sodium potassium chloride reuptake
  4. Thiazide diuretics: dct (acting on na/cl cotransporters) ..best for HTN and elderly e.g. Chlorothiazide. Chlorthalidone. Hydrochlorothiazide
  5. Potassium sparing diuretics: cd
    1. Aldosterone receptor blockers (a type of k sparing): CD e.g. Spironolactone
    2. ENaC channel inhibitors → decrease sodium reabsorption: amiloride, triamterene
157
Q

mech. of extrapyramidal sx in haloperidol toxicity

A

​​​​​​​Blockade of central dopamine D2 receptors in the brain leads to the extrapyramidal symptoms

PSEUDOPARKINSONISM · AKATHISIA · DYSTONIC REACTIONS · TARDIVE DYSKINESIA.

158
Q

​​​​​​​organophosphate toxicity p/w

A

can cause bronchorrhea/bronchospasm and bradycardia, clinical features are dominated by other findings of cholinergic excess (eg, salivation/drooling, lacrimation, diaphoresis); pupils are also usually constricted.

159
Q

heparin acts on which anticoagulation protein

A

antithrombin III. binds to/increases activity of it

160
Q

Hirudin

Lepirudin

Bivalirudin

Desirudin

Argatroban

dabigatran

what are these drugs?

A

direct thrombin inhibitors

indications: HIT (alternative to heparin), coronary syndromes, AFIB

161
Q

warfarin MOA

A

Vit K antagonist via epoxide reductase inhibition

162
Q

which medications interfere with folate metabolism and are therefore a/w neural tube defects

A

Valproic acid

Phenytoin

TMP

Sulfonamides

methotrexate

163
Q

what are the drug induced causes of restrictive lung disease

A

mn: BB AMMo

  1. Bleomycin
  2. Busulfan
  3. AMiodarone
  4. MethOtrexate
164
Q

what are the aromatase inhibitors

A

aromatase converts testosterone to estradiol

they are anastrazole, letrozole, exemestane

165
Q

tx for hepatic encephalopathy

A

lactulose (ist line) : lactulose (gets converted to lactic acid –> acidifcation of gut causing conversion of ammonia into excretable form)

rifaximin (add on drug): oral abx that decreases ammonia producing intestinal bacteria

166
Q

what is atropine used for

A

It’s a muscarinic antagonist, so it’s used to

  1. reverse excessive muscarinic activation (e.g. antidote for organophosphate poisoning)
  2. bradycardic arrest
  3. to dilate the pupil (but on the flipside can cause acute closed angle glaucoma in older adults)
167
Q

cocaine moa

A

Cocaine is an indirect sympathomimetic that acts to inhibit the reuptake of as norepinephrine, dopamine, and serotonin from the neuronal synapse

168
Q

PCP Moa

A

Phencyclidine (PCP) acts as an N-methyl-D-aspartate receptor antagonist.

169
Q

Nitroprusside

what is it?

what is it used for?

A

a vasodilator used to treat cardiogenic shock and would worsen the blood pressure in distributive shock

It is metabolized into nitric oxide (NO), which is a potent vasodilator in the smooth muscle of the vasculature that acts by increasing cyclic guanosine monophosphate (cGMP

AE: metabolite of nitroprusside, thiocyanate, can build up and cause toxicity, which presents as nausea and vomiting.

170
Q

what is the pressor of choice in pts with septic shock with acidosis.

A

vasopressin (ADH) works well in acidic environments

171
Q

Etanercept

what is it

what is it for?

A

Etanercept inhibits tumor-necrosis factor (TNF) activity by competitively binding to TNF and preventing it from interacting with cell surface receptors. It is an anti-inflammatory agent used for the treatment of rheumatoid arthritis, psoriasis, and psoriatic arthritis.

172
Q

Benzodiazepines moa

A

Benzodiazepines act by binding to the benzodiazepine binding site of GABA a receptors, which allosterically modulates the binding of GABA, resulting in an increased frequency of chloride ion channel opening

173
Q

which lipid lowering agent is most effective at reducing cardiovascular events

A

statins

HMG CoA reductase inhibitor

174
Q

indications for Niacin (Vit B3) over fibrates or statins?

A

Niacin (vitamin B3) given in pharmacologic doses is the most effective agent for raising HDL levels, but does not reduce the risk of cardiovascular events and is associated with adverse effects (eg, flushing, hyperglycemia). It is primarily used for patients who have failed other lipid-lowering drugs.

Fibrates activate peroxisomal proliferator-activated receptor alpha, a transcription factor that increases lipoprotein lipase activity. Fibrates decrease triglyceride levels and raise HDL levels. However, fibrates are inferior to statins for reducing cardiovascular events and are primarily used to prevent pancreatitis in patients with very high triglyceride levels.

175
Q

hydroxyurea MOA

A

inhibits ribonucleotide reductase and therefore inhibits cell division during S phase

Ind/for

  • acute and chronic myelogenous leukemia
  • primary myelofibrosis
  • sickle cell dz (first line)

AE: megaloblastic anemia

176
Q

what is the antidote to metoprolol toxicity (pt on metoprolol with syncopal episode)

A

glucagon because it activates beta receptors

177
Q

The treatment of choice for pulmonary sarcoidosis is________

A

oral glucocorticoid therapy.

178
Q

what ligands signal via JAK-STAT pathway (non rec. tyrosine kinase) (mn: JAcK the PIGGl_ET_)

A

Prolactin, Interleukins and IFN, GH, G-CSF, EPO, TPO

179
Q

which ligands (other than the adrenergic ones) signal via the Gq –> PLC —> PKC pathway? (mn: Q magazine –> Tough, Angsty Guys take Oxy and get Gas

A

TRH, Ang II, GnRH, oxytocin, gastrin

180
Q

T/F: desmopressin (ADH analog) and vasopressin act at the same receptor

A

FALSE

Unlike vasopressin (natural ADH), desmopressin has a negligible impact on the V1 receptor (Ie it’s selective for the kidney with V2 rec) and does not use the PLC pathway to exert its effect.

181
Q

MOA for dihydropyridine vs non-dihydropyridines

A

Nondihydropyridine CCBs exert their primary action by blocking the L-type calcium channels, thereby decreasing phase 0 depolarization and conduction velocity in the sinoatrial and AV nodes.

182
Q

tx for giardia

A

metronidazole

183
Q

indications for octreotide

A

A synthetic drug that mimics the action of somatostatin and is used in treating acromegaly, carcinoid tumors, vasoactive intestinal peptide tumors, pancreatitis, and gastrointestinal bleeding

184
Q

TMP-SMX MOA

A

Both of these antibiotics inhibit the folate synthesis pathway. In the folate synthesis pathway, pteridine and para-aminobenzoic acid are incorporated into folic acid. Also inhibition of dihydrofolate reductase

They block these steps

ind/for: (mn)

  • Toxoplasmosis prophylaxis
  • m
  • Pneumocystis jirovecii pneumonia
  • Shigella
  • Salmonella
  • m
  • urinary tract(traX) infections

AE: megaloblastic anemia, agranulocytosis, leukopenia

185
Q

what comprises the “triple therapy” indicated for H. Pylori

A
  1. PPIs
  2. Clarithromycin
  3. amoxicillin/metronidazole
186
Q

what differentiates DILE from SLE

A

DILE can manifest with various features that are also seen in idiopathic SLE (e.g., fever, arthritis, malar rash, serositis) but typically does not affect the CNS or kidneys, unlike SLE.

187
Q

“Assuming the drug follows first-order kinetics, approximately how long will it take for drug Y to reach steady state?”

how do you solve this

A
  1. first, you need the principle that in First-order kinetics, a drug infused at a constant rate takes 4–5 half-lives to reach steady state
  2. then you need to calculate the half-life (image)
  3. then multiply the half life value times 4

If you’re given the half life, then just multiply that times 4-5

188
Q

what is the equation for Filtration fraction

A

FF=GFR/RPF

RPF=RBF(1-HCT)

189
Q

trastuzumab, panitumumab, erlotinib, pan and imatinib are what types of targeted immunotherapy drugs and what are their indications

A

they all target tyrosine kinase receptor

Trastuzumab is ind/for HER2+ breast and gastric cancer

panitumumab ind/for metastatic colorectal cancer,

Imatinib is ind/for CML and kit-positive gastrointestinal stromal tumors

erlotinib is HER1/EGFR inhibitor ind/for non–small cell lung cancer and pancreatic cancer. (Not all non–small cell lung cancers respond to erlotinib. If the tumor has a K-Ras mutation or EML4-ALK translocation, another drug should be used.)

190
Q

what type of targeted immunotherapy drug is bortezomib and what’s it’s indication

A

inhibits a proteasome that degrades IκB (IκB downreguates NF-kB entry into cell) –> inhibit degredation of inhibitor of NF-kB = more inhibition of NF-kB

ind/for multiple myeloma and mantle cell lymphoma

191
Q

what type of targeted immunotherapy drug is rituximab and what’s it’s indication

A

acts on CD20 recs on B cells, making them more susceptible to attack by the immune system

ind/for non-hodgkins lymphoma, CLL, ITP, TTP, AIHA, RA, MS

192
Q

what type of targeted immunotherapy drug is bevacizumab and what’s it’s indication

A

VEGF inhibitor (inhibits blood supply to cancer cells)

ind/fo non–small cell lung cancer; glioblastoma; and cancers of the colon, cervix, ovaries, and breast. It is also used to treat noncancerous disorders such as diabetic retinopathy and macular degeneration.

193
Q

erlotinib AE

A

adverse effects include diarrhea, an acne-like rash, anorexia, and fatigue. The degree of rash often correlates with drug efficacy. Rarer, but more serious, adverse effects are interstitial lung disease and hepatic failure.

194
Q

imatinib AE

A

Adverse effects include GI distress, edema, and hepatotoxicity.

195
Q

panitumumab AE

A

Adverse effects include rash and dermatologic toxicity, severe infusion reactions, pulmonary fibrosis, and electrolyte abnormalities.

196
Q

trastuzumab AE

A

Like most monoclonal antibodies, trastuzumab can lead to fever, chills, nausea, dyspnea, and rashes. The biggest concern in terms of toxicity is congestive heart failure.

197
Q

What adverse effects are expected to be see (in common) during targeted therapy with crizotinib, erlotinib, panitumumab, and trastuzumab ?

A

What adverse effects are expected to be see during targeted crizotinib, erlotinib, panitumumab, and trastuzumab therapy?

198
Q

Adverse effects of rituximab

A

Adverse effects of rituximab are fewer than those associated with many other chemotherapeutic agents. The most common are weakness, nausea, diarrhea, edema, and increased infections.

199
Q

bevacizumab AE

A

Adverse effects include hypertension, fatigue, nausea, headache, arthralgia, and nosebleeds.

200
Q

what kind of targeted immunotherapy is denosumab and what’s its indication

A

a monoclonal antibody against RANK-L, which, in turn, is an activator of NF-κB.

201
Q

Loop diuretics AE

(furosemide, torsemide, bumetanide)

A
  1. sensorineural hearing loss, tinnitus, vertigo
  2. hypokalemia, hypocalcemia

mn: I will be FUROus if you don’t keep me in the loop

“You bet (bu-met anide)”

and “Torso before thighs”

202
Q

thiazide diuretic AE

A

hyponatremia, hypomagnesemia, hypercalcemia

203
Q

what are the ototoxic drugs

A

aminoglycosides, salicylates, cisplatin, loop diuretics

204
Q

ACE inhibitor AE

A

Side effects include Cough, Angioedema, Teratogenesis (neonatal renal failure), elevated Creatinine, (decreased GFR), Hyperkalemia (from reduced aldosterone) and Hypotension

mn: Captopril’s CATCHH

*use caution in pts with bilateral renal artery stnosis

205
Q

In the kidney, angiotensin II preferentially constricts the efferent arteriole, which increases glomerular filtration. Blockade of this response is accomplished by what drug classes

A

by ACE inhibitors (eg, ramipril) or angiotensin II receptor blockers (eg, losartan, valsartan) causes the filtration pressure to fall, leading to a reduced GFR

206
Q

argatroban, bivalirudin, and dabigatran are all what type of drugs

A

Direct thrombin (IIa) inhibitors

207
Q

hemophilia A 1st line treatment

A

Factor 8 replacement

208
Q

Ticagrelor MOA and indication

A

Ticagrelor binds the adenosine diphosphate (ADP) P2Y12 receptor on platelets, blocks ADP-mediated activation of the glycoprotein IIb/IIIa receptor complex –> prevents platelet aggregation by blocking.

ind/for: acute coronary syndrome and in patients undergoing percutaneous coronary intervention.

209
Q

Microangiopathic hemolytic anemia is an AE of what drugs

A

cancer chemotherapy drugs (eg, cisplatin, cyclophosphamide).

210
Q

what is DRESS syndrome

A

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a type 4 HSR that typically occurs 2-8 weeks after exposure to high-risk drugs

mn: I spilled ALL the CARBs with that Phenny, LAMe Sulfur smell (on my dress) –> allopurinol, carbamazipine, phenytoin, lamotrigine, Sulfonamide abx (TMP-SMX)

+dapsone, minocycline, vancomycin

sx: high fever with generalized, high surface area rash + end organ damage, generalized lymphadenopathy (+eosinophilia on CBC)

211
Q

what sleep aid drug can be given to elderly

A

Ramelteon, a melatonin agonist, has a lower side-effect burden than other sedative-hypnotic agents and is effective in reducing time to sleep onset in the elderly.

Benzodiazepines, antihistamines, and sedating antidepressants should be avoided in the treatment of insomnia in elderly patients due to their adverse effects.

212
Q

which antidepressant can cause priapism

A

trazadone

213
Q

tx for pinworms

A

albendazole, mebendazole, pyrantal pamoate

214
Q

doxorubicin toxicity

A

DILATED cardiomyopathy

215
Q

methotrexate AE

A

hepatitis, pulmonary fibrosis, bone marrow suppression

216
Q

what drugs are valsartan and losartan

A

Ang 2 rec blockers

mn: -artan = A R Ten-uate (ang 2 rec attenuation)

(block ang II rec type 1)

effects: decrease vasoconstricion and secretion of aldosterone

AE: angioedema, hyperkalemia, decreased GFR, hypotension, teratogen

217
Q

what is aliskiren

A

direct renin inhibitor –> decreased conversion of angiotensinogen to angiotensin I –> less vasoconstriction and decreased secretion of aldosterone

mn aLESkiREN: LESS RENin with aliskiren.

218
Q

AE of ACE inhibitors

A

(ACE inhibitor)

mn: CAPTOPRIL:

  • Cough, Angioedema,
  • Pemphigus vulgaris,
  • Teratogenicity,
  • hypOtension,
  • high Potassium,
  • Renal failure,
  • Increased creatinine,
  • Low GFR.
219
Q

what drugs are captopril and lisinopril

A

ACE inhibitors

220
Q

what drug is indapamide

A

thiazide diuretic

along with chlorthalidone and hydrochlorothiazide

MOA

221
Q

what drug is succinylcholine?

A

depolarizing neuromuscular blocking drug (The only one)

MOA: agonist at nicotinic (type m) rec agonist –> prolonged depolarization/inability to contract the muscle

Ind/for: surgery or mechanical ventilation

222
Q

what drug is used before general anesthesia to decrease salivary and bronchial secretions (helps maintain airway patency) and prevent myocardial depression (minimizes risk of hypotension)

A

atropine, a muscarinic acetylcholine rec antagonist

223
Q

In myasthenia gravis

patients are VERY sensitive to __________ and VERY insensitive to ____________

^both NMJ blockers

A

VERY sensitive vecuronium and

insenstitive to succinylcholine, respectively

because in MG, there’s antibodies against the AcH receptors, which causes downregulation of the number of these receptors

224
Q

antidote to heparin overdose

A

protamine sulfate

225
Q

which thyroid drug has 2 MOAs

A

Propylthyiouracil

  1. blocks peripheral conversion of T4 to T3
  2. inhibits thyroid peroxidase (does iodine organification and coupling of iodotyrosines)

by contrast, methimazole only does the latter.

n.b Beta blockers are also able to block T4 –> T3 conversion

226
Q

MOA of choelstyramine

A

bile acid sequestrant

227
Q

dronedarone, amiodarone, sotolol, ibutilide, dofetilide

^these belong to what drug class

A

class III antiarrhythmics: K+ channel blockers

*but dronedarone and amiodarone share the same MOA as all the other classes

228
Q

AE of amiodarone

A
229
Q

what drugs are Spironolactone, Triamterene, Eplerenone, and Amiloride

A

K-sparing diuretics

the ones ending in -one are aldosterone rec blockers (in late DCT and CD)

triamterene and amiloride are ENaC blockers

mn: To remember that Spironolactone, Triamterene, Eplerenone, and Amiloride are K+-sparing, think of STEAK!

230
Q

what kind of drug is amlodipine and what are the other drugs in its class

A

dihydropyridine CCBs (ind/for htn b/c they act at L type Ca channels on vascular smooth muscle AND ind/for arrhythmia beause they also act at those same channels, decreasing phase 0 depolarization and conduction velocity in the sinoatrial and AV nodes.)

mn: -di-p-ine (di (hydro)- p (yrid) - ine

the others are:

Nicardipine
Nifedipine

231
Q

what drug is bicalutamide

A

it goes with flutamide (anti-androgen)

MOA: competitive inh. at androgen receptor

ind/for coadministration with GnRH to avoid temporary overstimulation of androgen rec prior to downregulation of the receptors

mn: don’t BICker over a FLUTe

232
Q

what drug is abiraterone

A

17α-hydroxylase/17,20-lyase inhibitor

233
Q

metformin MOA and AE

A

inhibiting mitochondrial glycerol-3-phosphate dehydrogenase, which reduces availability of gluconeogenesis substrates (eg, glycerol, lactate)

.Metformin also upregulates AMP-activated protein kinase, which inhibits lipogenesis and subsequently lowers circulating lipid levels.

AE: B12 def (chronic administration), lactic acidosis (d/t increase lactate production as a result of inhibited gluconeogenesis), and diarrhea.

Contraindicated in pts with renal insufficiency b/c it is renally excreted

234
Q

Acute Angle closure gloucoma can be precipitated by what medications

A

topical and systemic medications that cause pupillary dilation, such as alpha-adrenergic agonists (eg, naphazoline) and drugs with strong anticholinergic effects (eg, tricyclic antidepressants, antihistamines). Acute blockage results in a rapid rise in intraocular pressure that typically causes severe eye pain, conjunctival injection, and corneal edema (haziness). If not corrected, the elevated pressure can damage the optic nerve and cause permanent vision impairment.

235
Q

what drugs are Terazosin, doxazosin, prazosin, and tamsulosin

A

selective alpha 1 adrenergic antagonists ind/for BPH and (last line) for HTN

236
Q

amphotericin B toxicity

A

The most dangerous adverse effect of amphotericin B is its nephrotoxicity; this is due to both a decrease in glomerular filtration rate and direct toxic effects on the tubular epithelium. Nephrotoxicity can lead to anemia (decreased erythropoietin production) and electrolyte abnormalities. Hypokalemia and (less often) hypomagnesemia are common due to an increase in the membrane permeability of the distal tubule. Hypokalemia can cause weakness and arrhythmias. ECG findings in hypokalemia include T wave flattening, ST-segment depression, prominent U waves, and premature atrial and ventricular contractions. Profound hypokalemia can cause ventricular tachycardia or fibrillation

237
Q

which lipid lowering drug can cause gallstones

A

fibrates

238
Q

which diuretic can cause senorineural hearing loss

A

furosemide

239
Q

indications fro Carbonic anhydrase inhibitors such as acetazolamide

A
  • narrow angle glaucoma,
  • pseudotumor cerebri /idiopathic Intracranial HTN
  • metabolic alkalosis or resp alkalosis as in altitude sickness
  • cystinuria (cysteine kidney stone prevention) –> alkalinzation of the filtrate/urine makes cystine more soluble
240
Q

aspirin should be avoided in yound children d/t risk of Reye syndrome EXCEPT for in what condition

A

Kawasaki disease (medium vessel vasculitis)

to avoid coronary artery aneurysm

Reye syndrome p/w: N/V/D, hepatomegaly, AMS and lethargy

241
Q

lithium AE and Toxicity

mn: L(hi)THIUM

A

Low (or High) Thyroid

Heart (Ebstein anomaly)

Insipidus – nephrogenic diabetes Insipidus (ADH resistance in the renal collecting ducts) snd CKD

Unwanted movements (tremor)

Thiazides, ACE inhibitors, NSAIDs, and other drugs affecting clearance are implicated in lithium toxicity.

manifestation of frank TOXICITY:

  1. N/V
  2. slurred speach
  3. seizures
  4. hyperreflexia
  5. ataxia

treat with hydration with isotonic sodium chloride

242
Q

dextromorphan MOA and AE

A

NMDA glutamate rec. antagonist

abuse potential –> antidote = naloxone

AE.: serotonin syndrome if used with other serotinergic drugs

243
Q

what drugs are cetirizine, loratadine, fexofenadine, and desloratadine

A

2nd gen antihistamine (don’t cross CNS, so less sedating)

244
Q

AE of acetazolamide (carbonic anhydrase inhibitor)

A

proximal renal tubular acidosis (type 2RTA)

paresthesias

NH3 toxicity

hypokalemia

calcium phosphate stones

245
Q

Mixed metabolic acidosis and respiratory alkalosis can be seen in __________toxicity, as the acidic metabolites trigger the brain to hyperventilate and eliminate excess acid in the form of CO2.

A

aspirin

246
Q

N-acetyltransferase polymorphism affects metabolism of which drugs

A

isoniazid, sulfasalazide, hydralazine

N-acetyltransferase polymorphism refers to the fact that there’s a natural variance in the expression of N-acetyltrasferease in the liver which is responsible for metabolizing these ^ drugs

247
Q

carbamazepine AE

A
  1. SJS and DRESS syndrome
  2. drug induced SIADH
  3. Aplastic anemia and agranulocytosis
  4. CYP induction
248
Q

what drugs can cause anticholinergic toxicity

A
  1. atropine, scopolamine (motion sickness med)
  2. antihistamines
  3. TCAs

sx with mn: red as a beet, dry as a bone, hot as a haire, blind as a bad, mad as a hatter, full as a flask

antidote: physostigmine (AChE inhibitor)

249
Q

acetaminophen MOA

A
250
Q

what acid base abnormality is found in salicylate poisoning

A

early poisoning sx: salicylates directly stiulate respiratory center, –> hyperventilation and respiratory alkalosis

late sx: salicylates disrupt Ox Phos –> body switches to anaerobic metabolism –> lactic acidosis

other sx unrelated to acid base abnormalities: N/V, headache, tinnitus, fever, AMS

antidote: activated charcoal and sodium bicarb (alkalization of urine promotes salicylate excretion)

251
Q

severe TCA overdose Tox symptoms

A

mn: 3 C’s for tri-Cy-Cli-Cs

  1. convulsions
  2. cardiotox (QT prolong, arythmias)
  3. coma or obtundedness

+hyperpyrexia (temp >106 F)

tx: charcoal and supportive care (+ECG monitoring) + sodium bicarb to prevent arrhythmias
n. b that these are the sx of severe overdose. anticholinergic sx can also occur at lower doses

252
Q

beta blockers toxicity

A

HEART

  1. bradycardia
  2. AV block
  3. acute heart failure

LUNGS

  1. dyspnea, bronchospasm

METABOLIC

  1. hypoglycemia + hypoglycemia unawareness
  2. dislipidemia

CNS (severe)

  1. sedation
  2. seizures
253
Q

neostigmine moa and indication

A

inhibit the degradation of acetylcholine (AChE inhibitor)

reversal agent for -curium agents (as used to induce paralysis during procedures)

254
Q

Which abx are a/w ototoxicity?

A

The macrolides and vancomycin

macrolides: every cop is an ass face

erythro-

clarithro-

azyithro-

fidazomicin

255
Q

main AE of Fluoroquinolones

A

diarrhea, rash, headache, dizziness

256
Q

dofetilide and ibutilide are what kind of drugs

A

class III antiaryhthmics (K+ channel blockers)

along with dronedarone, amiodarone, and sotolol, but these 2 are selective for K channels

257
Q

tx for Congenital Toxoplasmosis.

A

Pyrimethamine, Sulfadiazine, and Leucovorin

258
Q

Organisms Typically not covered by 1st–4th generation cephalosporins are

A

LAME: Listeria, Atypicals (Chlamydia,Mycoplasma), MRSA, and Enterococci.

259
Q

Patients with gonococcal urethritis who have coinfection with C trachomatis or uncertain C trachomatis status (as in this patient whose NAAT results are pending) require what abx regimen

A

a third-generation cephalosporin (eg, ceftriaxone) and a tetracycline (eg, doxycycline) to cover gonococcus and possible C trachomatis coinfection. Patients with gonococcal urethritis who have negative C trachomatis NAAT should be treated with third-generation cephalosporin (eg, ceftriaxone) alone

260
Q

drug of choice for slowing the progression of or preventing diabetic nephropathy

A

The main therapies used to prevent diabetic nephropathy are ACE inhibitors or AT receptor blockers (ARBs). These antihypertensive drugs act by reducing AT II levels, thus reducing intraglomerular pressure by preferentially dilating the efferent arteriole.

ACE inhibitors protect the kidney in early diabetic nephropathy by reducing the high glomerular pressures (hyperfiltration) seen in early stages of disease.

261
Q

milrinone MOA

A

By blocking PDE-3, milrinone increases the amount of cAMP available inside myocardial cells and the smooth muscle cells of the peripheral vasculature. In myocardial cells, increased cAMP leads to increased cardiac contractility. In vascular smooth muscle cells, increased cAMP leads to smooth muscle relaxation because the normal effect of cAMP is to reduce the activity of myosin light chain kinase. Therefore increased cAMP secondary to milrinone leads to decreased peripheral vascular resistance.

262
Q

which steroid drug has predominately mineralcorticoid (aldosterone) effect

A

fludrocortisone, which is why it’s used to treat primary adrenal insufficiency

263
Q

which abx is assoc with “red man” syndrome (RMS),

A

“red man” syndrome (RMS), a non-allergic drug reaction that occurs when vancomycin is infused too rapidly.

RMS arises due to the direct activation of mast cells by vancomycin, which results in the release of vasoactive mediators (eg, histamine).

264
Q

tx for Raynaud phenomenon

A

CCBs

265
Q

MOA of botulinum toxin

A

Botulinum toxin prevents vesicular fusion by cleaving a component of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor complex

266
Q

TCAs MOA

A

TCAs inhibit the reuptake of serotonin and norepinephrine (but their chief AE is d/t anticholinergic activity rather than serotonin syndrome) and block H1 receptors, α1-adrenergic receptors, and muscarinic receptors.

267
Q

what drug is amoxapine

A

TCA

along with:

Amitriptyline, nortriptyline,

imipramine, desipramine, clomipramine,

doxepin

268
Q

Diphenoxylate and loperamide are what kind of meds

A

both opiate-based medications designed to inhibit peristalsis in the gastrointestinal tract

269
Q

Treatments for hepatic encephalopathy

A

include lactulose (increases conversion of ammonia to ammonium) and rifaximin (decreases intraluminal ammonia production).

270
Q

tx for Wilson’s dz

A

ammonium tetrathiomolybdate: facilitates urinary excretion of copper

penicillamine: copper chelating agent

trientine: copper chelating agent

zinc: competes with copper for absorbtion in the gut via the same transporter

271
Q

management of esophageal varices

A

Acute management of variceal hemorrhage requires rapid lowering of portal pressure. Somatostatin and octreotide (a long-acting somatostatin analog) inhibit the release of hormones that induce splanchnic vasodilation, indirectly causing splanchnic vasoconstriction and reduced portal blood flow.

272
Q

what’s the MOA of canagliflozin and dapagliflozin

A

for this reason, check creatinine before rx

273
Q

what drugs are hydroxyzine, promethazine, chlorpheniramine, diphenhydramine ​​​​​​​

n.b. first-generation antihistamines are lipophilic and easily cross the blood-brain barrier, where they may cause significant sedation and cognitive dysfunction. First-generation antihistamines are considered potentially inappropriate medications for elderly patients, especially those with pre-existing cognitive or functional impairment.

A

first-generation antihistamines

274
Q

what drugs are loratadine, cetirizine

A

Newer-generation antihistamines

do not have the same degree of antimuscarinic, antiserotonergic, or anti-alpha adrenergic properties and their side effects are minimal. Moreover, second-generation antihistamines are less lipophilic, do not readily cross the blood-brain barrier, and are usually nonsedating.

275
Q

what drugs are canagliflozin, dapagliflozin and empaglioflozin

A

SGLT-2 inhibitors (PCT of kidney) –> increase glucose excretion by blocking the reabsorption cotransporter –> used for diabetes

a/w UTIs and yeast infections, polyuria, weight loss, dehydration,

contraindications: CKD, Urinary tract anomalies
mn: the sugar FLOZ (flows) out

276
Q

which antithyroid medication, methimazole or PTU, is preferred in the 1st trimester

A

Methimazole is preferred for most non pregnant patients due to the hepatotoxicity of PTU. However, methimazole has potential teratogenic effects, so PTU is preferred in the first trimester of pregnancy.

mn: P = primary/first , T=trimester, U= use

277
Q

what is the EXACT MOA of apixaban

A

Direct factor Xa inhibitors (eg, apixaban) are often used for stroke prevention in atrial fibrillation as they are administered orally and do not require monitoring of drug levels (unlike warfarin). This class of medications blocks the active site of factor Xa, which prevents it from converting prothrombin to thrombin. Direct factor Xa inhibitors are denoted by names that end in “Xa-ban.”

NOT conversion of X to Xa!!!

278
Q

what drugs are argatroban, bivalirudin, and dabigatran

A

direct thrombin inhibitors

279
Q

What drug to use to lower BP without worsening ECG abnormalities

A

dihydropyridine CCBs

Nifedipine, amlodipine, felodipine (because they predominately act on blood vessels, not the heart)

280
Q

dapsone MOA, AE, and indications

A

inhibits bacterial synthesis of dihydrofolic acid, via competition with para-aminobenzoate for the active site of dihydropteroate synthase, thereby inhibiting nucleic acid synthesis.

DRESS, hemolytic anemia, methemoglobinemia (contraindicated in G6PD deficiency)

ind/for dermatitis herpetiformis, leprosy, malaria, pneumocystitis jiroveci prophylaxis

281
Q

prophylactic tx to prevent pneumocystitis pneumonia (for immunocompromised)

A

TMP/SMX

Atovaquone and dapsone are alternative agents used to in patients with trimethoprim-sulfamethoxazole allergy.

282
Q

1st line tx for PTSD

A

SSRIs or SNRIs

283
Q

what class of drugs are exenatide, liraglutide

A

GLP-1 agonists (for diabetes control) –> increases insulin release

AE: pancreatitis, weight loss

284
Q

which drug class can cause transient bluish discoloration to vision

A

PDE-5 inhibitors (sildenafil, tadalafil, avanafil, verdenafil)

(b/c PDE5 inhibitors can also inhibit PDE6 in the retina, which is involved in color vision)

can also cause sudden monocular vision loss, affarent pupillary defect, and opticn disc edema (less common)

285
Q

what drugs are used as prophylaxis against catecholamine surge following adrenalectomy

A

phenoxybenzamine (alpha blocker) then beta blocker (but not beta blocker first)

286
Q

which drugs can cause interstitial lung disease

A

amiodarone, methotrexate, bleomycin

287
Q

which drugs can cause SIADH

A

most common drugs include

carbamazepine,

oxcarbazepine,

chlorpropamide,

cyclophosphamide,

selective serotonin reuptake inhibitors (SSRI)

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