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PHARMA > pharm part 2 > Flashcards

pharm part 2 Flashcards

1
Q

Name the antihelminthic therapy

A

Pyrantel pamoate
lvermectin
Diethylcarbamazine
Mebendazole (microtubule inhibitor}, Praziquantel (increased Ca2+ permeability, increased vacuolization)

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2
Q

What is the MOA of Chloroquine?

A

Blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia.

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3
Q

What are the clinical use of chloroquine?

A

Use in all marlarial species except falciparum
Due to resistance membrane pump that decrease intracellular concentration of drug.

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4
Q

What are the side effects of Chloroquine?

A

Retinopathy and pruritus

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5
Q

Important point of Malarial treatment.

A
  • Treat P falciparum with artemether/lumefantrine or atovaquone/proguanil
  • For life-threatening malaria, use quinidine in US (quinine elsewhere} or artesunate.
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6
Q

What are the medicine used to treat scabies and lice?

A

1) Permethrin
(inhibits Na+ channel deactivation —>neuronal membrane depolarization)

2) malathion
acetylcholinesterase inhibitor

3) lindane
blocks GABA channels ->neurotoxicity

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7
Q

Name the different medications used to anti protozal

A

Pyrimethamine (toxoplasmosis)
suramin and melarsoprol (Trypanosoma brucei)

nifurtimox (T cruzi)
sodium stibogluconate (leishmaniasis}.

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8
Q

Important point of ANTI-HIV

A

All ARTs are active against HIV-1 and HIV-2 with the exception of NNRTls

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9
Q

How NRTI help in treating in HIV?

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OHgroup).

Tenofovir is a nucleoTide; the others are nucleosides
All need to be phosphorylated to be active.

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10
Q

What are the different side effects of NRTIs?

A

Bone marrow suppression,
peripheral neuropathy
lactic acidosis (nucleosides)
anemia (ZDV)
pancreatitis (didanosine).

Abacavir contraindicated if patient has HLA-B*5701mutation due to increased risk of hypersensitivity.

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11
Q

What are the different NRTIs?

A

Abacavir (ABC) Didanosine (ddl)

Emtricitabine (FTC) Lamivudine (3TC) Stavudine (d4T)

Tenofovir (TDF)
Zidovudine (ZDV, formerly AZT

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12
Q

What is the MOA NNRTls?

A

Bind to reverse transcriptase at site different from NRTis
Do not require phosphorylation to be active or compete with nucleotides.

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13
Q

What are the different side effects of NNRTIs?

A

Rash
Hepatotoxicity
Vivid dreams and CNS symptoms seen in efavirenz

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14
Q

Name the different NNRTIs

A

Delavirdine
Efavirenz
Nevirapine

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15
Q

What is the MOA of Protease inhibitors?

A

Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts.

Thus, protease inhibitors prevent maturation of new viruses.

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16
Q

What are the clinical side effects of of Protease inhibitors? “NAVIR”

A

hyperglycaemia
Gl intolerance (nausea, diarrhea)

lipodystrophy (Cushing-like syndrome). Nephropathy

hematuria, thrombocytopenia (indinavir).

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17
Q

Important point of Protease Inhibitors

A

Rifampin (potent CYP/UGT inducer) reduces protease inhibitor concentrations; use rifabutin instead.

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18
Q

What is the MOA of lntegrase inhibitors? “GRAVIR”

A

Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase.

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19
Q

What is the side effects of Integrase Inhibitors?

A

Increase creatinine kinase

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20
Q

Name the Anti HIV which are fusion inhibitor

A

Enfuvirtide
Maraviroc

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21
Q

What is the MOA of Enfuvirtide?

A

Binds gp41, inhibiting viral entry.

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22
Q

What is the MOA of Maraviroc?

A

Binds CCR-5 on surface ofT cells/monocytes, inhibiting interaction with gp120.

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23
Q

Name the NS5A inhibitors used for HCV and their MOA
HINT: LOV

A

Ledipasvir
Ombitasvir Velpatasvir

Inhibits NS5A, a viral phosphoprotein that plays a key role in RNA replication

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24
Q

Name the NS5B inhibitors used for HCV and their MOA

A

Sofosbuvir and Dasabuvir
Inhibits NS5B, an RNA-dependent RNA polymerase acting as a chain terminator
Prevents viral RNA replication

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25
Q

Name the NS3/4A inhibitors used for HCV and their MOA

A

Grazoprevir Simeprevir
Inhibits NS3/4A, a viral protease, preventing viral replication

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26
Q

What is the MOA of Ribavirin used for HCV?

A

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase
used as adjunct in cases refractory to newer medications.

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27
Q

What are the side effects of Ribavirin?

A

Hemolytic anemia
severe teratogen

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28
Q

What are the prophylactic medicine given in M avium–intracellulare?

A

Azithromycin, rifabutin

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29
Q

What is the MOA of Rifamycins (Rifampin, rifabutin, rifapentine)?

A

Inhibit DNA-dependent RNA polymerase.

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30
Q

What are the clinical indications of Rifamycins?

A

Mycobacterium tuberculosis
leprosy.

Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with H influenzae type b.

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31
Q

Important point of Rifamycins

A

It increases cytochrome P450 activity.
Tb Mutations reduce drug binding to RNA polymerase.

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32
Q

What is the MOA of isoniazid?

A

It decreases synthesis of mycolic acids.
Bacterial catalaseperoxidase (encoded by KatG) needed to convert INH to active metabolite.

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33
Q

What are the clinical side effects of Isoniazid?

A

Hepatotoxicity
cytochrome P-450 inhibition
drug-induced SLE

anion gap metabolic acidosis
vitamin B6 deficiency

seizures (in high doses, refractory to benzodiazepines)

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34
Q

How the resistance developed by TB against Isoniazid?

A

Mutations leading to underexpression of KatG.

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35
Q

What is the MOA of Ethambutol?

A

It decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.

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36
Q

What is the MOA of Stretopmycin?

A

Interferes with 30S component of ribosome.

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37
Q

What are the clinical side effects of Stretopmycin?

A

Tinnitus, vertigo
ataxia, nephrotoxicity.

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38
Q

What is the MOA of Fluoroquinolones?

A

It Inhibits prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV.

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39
Q

Important point of Fluoroquinolones

A

Bactericidal
Must not be taken with antacids.
Cipro inhibits CYP 450

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40
Q

What are the side effects of Fluoroquinolones?

A

GI upset
Superinfection
Skin rashes

Tendon rupture or tendonitis In elderly and patient take steroids
Prolong QT interval

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41
Q

What are the contraindications of Fluoroquinolones?

A

Contraindicated in pregnant women, nursing mothers, and children< 18 years old due to possible damage to cartilage.

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42
Q

What is the MOA of Daptomycin?

A

Lipopepticle that disrupts cell membranes of gram +ve cocci by creating transmembrane channels.

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43
Q

Important point of Daptomycin

A

It is not used for pneumonia (avidly binds to and is inactivated by surfactant).

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44
Q

What are the side effects of Daptomycin?

A

Myopathy, rhabdomyolysis.

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45
Q

What is the MOA of Metronidazole?

A

Forms toxic free radical metabolites in the bacterial cell that damage DNA.

Bactericidal, antiprotozoal.

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46
Q

What are the clinical side effects of Metronidazole?

A

Disulfiram-like reaction (severe Aushing, tachycardia, hypotension) with alcohol;
headache
metallic taste.

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47
Q

What are the MOA Of Sulfonamides and Dapsone?

A

Inhibit dihydropteroate synthase, thus inhibiting folate synthesis.
Bacteriostatic (bactericidal when combined with trimethoprim)

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48
Q

What are the clinical side effects of Sulfonamides?

A

Hypersensitivity reactions,
hemolysis if G6PD deficient.

nephrotoxicity (tubulointerstitial nephritis), photosensitivity,

Stevens-Johnson syndrome,
kernicterus in infants,
displace other drugs from albumin (eg, warfarin).

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49
Q

How bacteria develop resistance against Sulfonamides?

A

Altered enzyme (bacterial dihydropteroate synthase)
Decrease uptake
Increase PABA synthesis.

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50
Q

What are the clinical indications of Dapsone?

A

Leprosy (lepromatous and tuberculoid),

PCP prophylaxis, or treatment when used in combination with TMP.

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51
Q

What is the MOA of Trimethoprim?

A

Inhibits bacterial dihydrofolate reductase. Bacteriostatic.

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52
Q

What are the side effects of Trimethoprim?

A

Hyperkalemia (high doses), megaloblastic anemia, leukopenia, granulocytopenia, which may be avoided with coadministration of leucovorin (folinic acid).

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53
Q

What is the MOA of Aminoglycosides?

A

irreversible inhibition of initiation complex through binding of the 30S subunit.

Can cause misreading of mRNA.
Also block translocation.

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54
Q

Important Point of Aminoglycosides

A

Neomycin for bowel surgery.
Need oxygen for entering in cells so ineffective in anaerobes

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55
Q

What are the clinical side effects of Aminoglycosides?

A

Nephrotoxicity
neuromuscular blockade (absolute contraindication with myasthenia gravis)

ototoxicity (especially with loop diuretics), teratogenicity.

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56
Q

How resistance developed by bacteria against Aminoglycosides?

A

Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

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57
Q

What is the MOA of Tetracyclines and Tigecycline?

A

bind to 30S and prevent attachment of aminoacyl-tRNA

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58
Q

Important Point of Tetracycline

A

Bacteriostatic
Limited CNS penetration.

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59
Q

Name the Tetracycline used in renal failure patient

A

Doxycycline is fecally eliminated and can be used in patients with renal failure

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60
Q

Why tetracycline shouldn’t be given with antacids, milk or iron containing preparation?

A

Divalent cations (Ca, Mg and Fe) inhibit drugs’ absorption in the gut.

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61
Q

What are the clinical side effects of Tetracycline?

A

GI distress
discoloration of teeth and inhibition of bone growth in children

photosensitivity.
Teratocylines are teratogenic; generally avoided in pregnancy and in children (except doxycycline)

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62
Q

How resistance developed by bacteria against Tetracycline?

A

Decrease uptake or increase efflux out of bacterial cells by plasmid-encoded transport pumps.

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63
Q

What is the MOA of Chloramphenicol?

A

Blocks peptidyltransferase at 50S ribosomal subunit.

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64
Q

What are the side effects of Chloramphenicol?

A

Anemia (dose dependent)
aplastic anemia (dose independent)

gray baby syndrome (in premature infants because they lack liver UDP-glucuronosyltransferase).

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65
Q

How resistance developed by bacteria against chloramphenicol?

A

Plasmid-encoded acetyltransferase inactivates the drug.

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66
Q

What is the MOA of Clindamycin?

A

Blocks peptide transfer (translocation) at 50S ribosomal subunit.

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67
Q

What is the MOA of Linezolid?

A

Inhibits protein synthesis by binding to 50S subunit and preventing formation of the initiation complex.

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68
Q

What are the clinical side effects of Linezolid?

A

Myelosuppression (especially thrombocytopenia)
peripheral neuropathy
serotonin syndrome (due to partial MAO inhibition).

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69
Q

How resistance developed by bacteria against Linezolid?

A

Point mutation of ribosomal RNA

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70
Q

What is the MOA of Macrolides?

A

Inhibit protein synthesis by blocking translocation.
It bind to the 23S rRNA of the 50S ribosomal subunit.

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71
Q

Important Point of Macrolides

A

Increases serum concentration of theophylline, oral anticoagulants.
Clarithromycin and erythromycin inhibit cytochrome P-450.

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72
Q

What are the clinical side effects of Marcolides?

A

Gastrointestinal Motility issues,
Arrhythmia caused by prolonged QT interval

acute Cholestatic hepatitis
Rash
eOsinophilia

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73
Q

How resistance developed by bacteria against Marcolides?

A

Methylation of 23S rRNA-binding site prevents binding of drug

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74
Q

What is the MOA of Colistin (polymyxin E), polymyxin B?

A

Cation polypeptides that bind to phospholipids on cell membrane of gram ⊝ bacteria.

Disrupt cell membrane integrity result leakage of cellular components lead to cell death

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75
Q

What are the side effects of Colistin (polymyxin E), polymyxin B?

A

Nephrotoxicity
neurotoxicity (eg, slurred speech, weakness, paresthesias)
respiratory failure.

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76
Q

Name the different Carbapenems
Hint: DIME

A

Doripenem
lmipenem

Meropenem
Ertapenem

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77
Q

How Carbapenems work?

A

lmipenem is a broad-spectrum, B-lactamase resistant carbapenem.

Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.

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78
Q

What are the clinical side effects of Carbapenems?

A

GI distress
rash
CNS toxicity (seizures) at high plasma levels.

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79
Q

What is the MOA of Monobactams ( Aztreonam )?

A

Prevents peptidoglycan cross-linking by binding to penicillinbinding protein 3.

Synergistic with aminoglycosides
No cross-allergenicity with penicillins.

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80
Q

Important point of Monobactams

A

For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

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81
Q

What is the MOA of Vancomycin?

A

Inhibits cell wall peptidoglycan formation by binding (D-Ala-D-Ala) portion of cell wall precursors
Not susceptible to B-lactamases.

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82
Q

What are the clinical side effects of of Vancomycin?
NOTR

A

Nephrotoxicity, Ototoxicity, Thrombophlebitis,
red man syndrome
DRESS syndrome

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83
Q

How bacteria develop resistance against vancomycin?

A

Occurs in bacteria (eg, Enterococcus) via amino acid modification of D-Ala-D-Ala to D-Ala-D-Lac.

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84
Q

How Pencillin G and V work?

A

Bind penicillin-binding proteins (transpeptidases) and Block transpeptidase cross-linking of peptidoglycan in cell wall

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85
Q

What are the different side effects of Pencillin G and V?

A

Hypersensitivity reactions
direct Coombs ⊕ hemolytic anemia,
Drug-induced interstitial nephritis.

86
Q

How bacteria developed resistance against Pencillin G and V?

A

β-lactamase in bacteria cleaves the β-lactam ring of Medication.
Mutations in PBPs.

87
Q

Name the different Penicillinase-sensitive penicillins

A

Amoxicillin, ampicillin; aminopenicillins.

88
Q

What are the different side effects of Penicillinase-sensitive penicillins?

A

Hypersensitivity reactions
rash
pseudomembranous colitis.

89
Q

How bacteria developed Resistance against Penicillinase-sensitive penicillins?

A

Penicillinase (a type of β-lactamase) cleaves β-lactam ring.

90
Q

Name the different penicillinase-resistant penicillins and how they work?
Hint; DON

A

Dicloxacillin, nafcillin, oxacillin.

MOA same as Pencillin G and V
penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring

91
Q

What are the different side effects of penicillinase-resistant penicillins?

A

Hypersensitivity reactions
interstitial nephritis

92
Q

How bacteria developed Resistance against Penicillinase-resistant penicillins?

A

MRSA has altered penicillin-binding protein target site.

93
Q

Important Point of Piperacillin

A

Antipseudomonal penicillin.

94
Q

What is the MOA of Cephalosporins?

A

β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.

95
Q

Important point of Cephalosporins

A

Organisms typically not covered by 1st–4th generation
Listeria
Atypicals (Chlamydia, Mycoplasma)
MRSA
Enterococci

96
Q

What are the different side effects of Cephalosporins?

A

Hypersensitivity reactions
autoimmune hemolytic anemia

disulfiram-like reaction

vitamin K deficiency

Low rate of crossreactivity even in penicillin-allergic patients
nephrotoxicity of aminoglycosides.

97
Q

How bacteria developed resistance against cephalosporins?

A

Inactivated by cephalosporinases (a type of β-lactamase).
Structural change in penicillinbinding proteins (transpeptidases).

98
Q

Name the different B-lactamase inhibitors Clavulanic acid

A

Avibactam
Sulbactam
Tazobactam

amoxicillin-clavulanate, ceftazidime-avibactam, ampicillin-sulbactam, piperacillin-tazobactam

99
Q

Name the Indirect Cholinomimetic agonist (Inhibits ACHe)

A

Donepezil
Edrophonium
galantamin
Neostigmine

Pyridostigmine
Physostigmine
rivastigmine

100
Q

What are the clinical indications of Neostigmine?

A

Postoperative and neurogenic ileus and urinary retention
myasthenia gravis
Reversal of neuromuscular junction blockade (postoperative).

101
Q

Name the Indirect Cholinomimetic agonist (Inhibits ACHe) which used in anticholinergic Toxicity

A

Physostigmine

102
Q

Important Point

A

Jimson weed (Datura) gardener’s pupil (mydriasis)

103
Q

Name the Muscarinic antagonists used for Motion sickness and COPD, asthma

A

Scopolamine For Motion Sickness

Ipratropium, tiotropium for COPD, asthma

104
Q

Name the Muscarinic antagonist used in Urge Incontinence

A

Solifenacin, Oxybutynin
Flavoxate, Tolterodine

105
Q

Name the Muscarinic antagonist used for irritable bowel syndrome

A

Hyoscyamine, dicyclomine

106
Q

Name the Muscarinic antagonist used to reduce airway secretion preoperatively and reduce oral drooling as well as PUD

A

Glycopyrrolate

107
Q

Name the Muscarinic antagonist used in Parkinson and acute dystonia

A

Benztropine
trihexyphenidyl

108
Q

Name the SSRI and how they work?

A

Fluoxetine, fluvoxamine, paroxetine, sertraline, escitalopram, citalopram.

Inhibit 5-HT reuptake.

109
Q

What are the clinical condition in which SSRI given?

A

Depression, generalized anxiety disorder
panic disorder
OCD, bulimia, binge-eating disorder

social anxiety disorder, PTSD
premature ejaculation, premenstrual dysphoric disorder

110
Q

What are the side effects of SSRI?

A

Serotonin syndrome
GI distress
SIADH
sexual dysfunction (anorgasmia, erectile dysfunction, libido)
mania precipitation if underlying bipolar disorder.

111
Q

What is the MOA of SNRI and Name the different SNRI?

A

Venlafaxine, desvenlafaxine, duloxetine, levomilnacipran, milnacipran.

Inhibit 5-HT and NE reuptake.

112
Q

What are the different side effects of SNRI?

A

Depression
generalized anxiety disorder
diabetic neuropathy

social anxiety disorder
panic disorder
PTSD, OCD

113
Q

What are the side effects of SNRI?

A

Raise BP
stimulant effects
sedation
sexual dysfunction
nausea.

114
Q

How TCA work?

A

TCAs inhibit 5-HT and NE reuptake.
Alpha blocker and Anticholinergic also

115
Q

What are the clinical indication of TCA?

A

MDD
peripheral neuropathy
chronic neuropathic pain

migraine prophylaxis
OCD (clomipramine)
nocturnal enuresis (imipramine).

116
Q

How Monoamine oxidase inhibitors work and name the different MOA inhibitor

A

Nonselective MAO inhibition dopamine)—->levels of amine neurotransmitters (norepinephrine, 5-HT, dopamine).

117
Q

What is the MOA of Vilazodone and Vortioxetine?

A

Inhibits 5-HT reuptake
Used for MDD

118
Q

What are the clinical side effects of Vilazodone and Vortioxetine?

A

serotonin syndrome
headache, diarrhea, nausea, anticholinergic effects.
sexual dysfunction, sleep disturbances, anticholinergic effects.

119
Q

How Trazodone work and what are the clinical indication of it?

A

Primarily blocks 5-HT2 , α1-adrenergic, and H1 receptors; also weakly inhibits 5-HT reuptake

insomnia and Depression.

120
Q

What are the clinical side effects of Trazodone?

A

sedation, nausea, priapism, postural hypotension.

121
Q

What is the MOA of Mirtazapine?

A

α2-antagonist ( release of NE and 5-HT)
potent 5-HT2 and 5-HT3 receptor antagonist, and H1 antagonist.

122
Q

What are side effects of Mirtazapine?

A

sedation
Increase appetite, weight gain
Dry mouth

123
Q

Name the medicine used for smoking cessation

A

Bupropion (Inhibits NE and DA reuptake)
Varenicline (Nicotinic ACh receptor partial agonist)

124
Q

How does Omalizumab work?

A

It binds mostly unbound serum IgE and blocks binding to FcεR

125
Q

What are the different Antileukotrienes?

A

1) Montelukast, zafirlukast—block leukotriene receptors
2) Zileuton—5-lipoxygenase inhibitor

126
Q

What are the clinical indications of Montelukast, zafirlukast?

A

aspirin induced and exercise-induced asthma.

127
Q

Which test should be send before giving Zileuton?

A

Hepatotoxic

128
Q

What is the MOA of Tiotropium and ipratropium?

A

Competitively block muscarinic receptors, preventing bronchoconstriction.

129
Q

What are the different inhaled glucocorticoids?

A

Fluticasone budesonide used in chronic asthma

130
Q

How do inhaled glucocorticoids work?

A

It inhibits the synthesis of virtually all cytokines and Inactivate NF-κB, the transcription factor that induces production of TNF-α and other inflammatory agents

131
Q

How does Minoxidil work?

A

Direct arteriolar vasodilator.

132
Q

Name the different Anti laxatives (BOSEL)

A

Bulk-forming laxatives
(Methylcellulose, psyllium)

Osmotic laxatives
(Lactulose, magnesium citrate, magnesium hydroxide, polyethylene glycol)

Stimulant laxatives
(Bisacodyl, senna)

Emollient laxatives
(Docusate)

Lubiprostone

133
Q

How does Emollient laxatives work?

A

Surfactants that decrease stool surface tension, promoting water entry into stool

134
Q

What is the MOA of Orilstat?
.

A

Inhibits gastric and pancreatic lipase which decrease breakdown and absorption of dietary fats
It is taken withfat-containing meals

135
Q

Important point of Octreotide

A

Increased risk of cholelithiasis due to CCK inhibition.

136
Q

What is the MOA of Misoprostol?

A

PGE1 analog.
It is involved in production and secretion of gastric mucous barrier, decrease acid production.

137
Q

What are the clinical use of Misoprostol?

A

Prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production).

Also used off-label for induction of labor (ripens cervix).

138
Q

What are the different side effects of Misoprostol?

A

Diarrhea.
Contraindicated in patients of childbearing potential (abortifacient).

139
Q

What are the different side effects of Aluminum hydroxide?

A

Constipation
Hypophosphatemia,
Osteodystrophy,
Proximal muscle weakness
Seizures

140
Q

What are the different side effects of Calcium carbonate?

A

Hypercalcemia (milk-alkali syndrome)
rebound acid

141
Q

What are the different side effects of Magnesium hydroxide?

A

Diarrhea
hyporeflexia
hypotension
cardiac arrest

142
Q

What are the different side effects of PPI?
.

A

Increased risk of C difficile infection
Pneumonia
acute interstitial nephritis
Vitamin B12 malabsorption
Decrease serum Mg2+/Ca2+ absorption (potentially leading to increased fracture risk in older adults)

143
Q

What are the different side effects of Cimetidine?

A

Inhibit CYP 450
Anti androgenic
cross blood-brain barrier (confusion, dizziness, headaches) and placenta
Cimetidine decreases renal excretion of creatinine.

144
Q

What are anti-HTN avoided in Asthma?

A

Avoid nonselective Beta-blockers to prevent B2-receptor-induced bronchoconstriction.
Avoid ACE inhibitors to prevent confusion between drug or asthma-related cough.

145
Q

What are the different Anti-HTN given in asthma?
.

A

ARBs
Ca2+ channel blockers
thiazide diuretics,
cardioselective beta-blockers

146
Q

Important point

A

Beta blockers must be used cautiously in decompensated CHF and are contraindicated in cardiogenic shock
In HF, ARBs may be combined with the neprilysin inhibitor sacubitril.

147
Q

Name the different CCB
Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine (dihydropyridines, act on vascular smooth muscle)

diltiazem, verapamil (non-dihydropyridines, act on heart).

A
148
Q

Name the different CCB

A

Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine (dihydropyridines, act on vascular smooth muscle)

diltiazem, verapamil (non-dihydropyridines, act on heart).

149
Q

What are the different uses of dihydropyridines CCB?

A

Dihydropyridines (except nimodipine): hypertension, angina (including vasospastic type), Raynaud phenomenon.

Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).

Nicardipine, clevidipine: hypertensive urgency or emergency.

150
Q

What are the side effects of different CCB?
*

A

Gingival hyperplasia
*Dihydropyridine
peripheral edema, Aushing, dizziness

*Non-dihydropyridine
cardiac depression, AV block, hyperprolactinemia (verapamil), constipation.

151
Q

What are the clinical indications of hydralazine?
*

A

Severe hypertension (particularly acute), *HF (with organic nitrate).

Frequently coadministered with a b-blocker to prevent reAex tachycardia.

152
Q

Name the medicine used in HTN emergency

A

labetalol, clevidipine
Fenoldopam, nicardipine
Nitroprusside.

153
Q

How does Nitroprusside work and what is the main side effects?

A

Short acting vasodilator (arteries = veins)—> cGMP via direct release of NO

It Can cause cyanide toxicity (releases cyanide).

154
Q

What is the MOA of Fenoldopam?

A

Dopamine D1 receptor agonist—>coronary, peripheral, renal, and splanchnic vasodilation result in decrease BP and increase natriuresis.

Also used postoperatively as an antihypertensive

155
Q

What is the MOA of nitrates?

A

Vasodilate by increased NO in vascular smooth muscle which result in increased cGMP and smooth muscle relaxation

Dilate veins&raquo_space; arteries
Decrease preload.

156
Q

What are the clinical indications of nitrates?

A

Angina
ACS
Pulmonary edema

157
Q

What are the conditions in which nitrates cannot be used?

A

Contraindicated in right ventricular infarction, hypertrophic cardiomyopathy, and with concurrent PDE-5 inhibitor use.

158
Q

What are the different side effects of Nitrates?

A

Reflex tachycardia (treat with β-blockers), methemoglobinemia
hypotension
flushing
headache
“Monday disease”

159
Q

Important point

A

Pindolol and acebutolol are partial β-agonists that should be used with caution in angina

160
Q

What is the MOA of Ranolazine?

A

It Inhibits the late phase of inward sodium current thereby reducing diastolic wall tension and oxygen consumption.

Does not affect heart rate or blood pressure.

161
Q

What are the different side effects of Ranolazine?

A

Constipation
Dizziness
Headache

162
Q

How does Sacubitril work?

A

It is a neprilysin inhibitor which Prevents degradation of bradykinin, natriuretic peptides, angiotensin II, and substance P
Resulted in vasodilation and decrease ECF volume.

163
Q

Name the clinical condition in which Sacubitril used

A

It Used in combination with valsartan (an ARB) to treat HFrEF.

164
Q

What are the different side effects of Sacubitril?

A

Hypotension
hyperkalemia
cough, dizziness

contraindicated with ACE inhibitors due to angioedema (both drugs bradykinin).

165
Q

What are the different bile acid resins and what is the mechanism of action of it?

A

It prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more

Cholestyramine, colestipol, colesevelam

166
Q

How does Ezetimibe help in improving lipid profile?

A

It prevents cholesterol absorption at small intestine brush border.

167
Q

What is the moa of Fibrates?

A

Activate PPAR-α–>upregulate LPL which increasedTAG clearance

Activate PPAR-α—->induce HDL synthesis

168
Q

What are the different side effects of fibrates?

A

Myopathy ( risk with statins)
cholesterol gallstones (via inhibition of cholesterol 7α-hydroxylase)

169
Q

How does NACIN help in improving lipid profile?

A

It inhibits lipolysis (hormone-sensitive lipase) in adipose tissue
It reduces hepatic VLDL synthesis

170
Q

What are the different side effects of NACIN?

A

Flushed face (prostaglandin mediated; decrease by NSAIDs or longterm use) Hyperglycemia
Hyperuricemia

171
Q

What is the MOA of PCSK9 inhibitors?

A

Alirocumab, evolocumab

Inactivation of LDL-receptor degradation which result removal of LDL from bloodstream

172
Q

What are the different side effects of PCSK9 inhibitors?

A

Myalgias
delirium
dementia
other neurocognitive effects

173
Q

What are the different clinical condition which required digoxin?

A

HF (contractility)
atrial fibrillation (conduction at AV node and depression of SA node)

174
Q

Name the condition which increased toxicity of digoxin

A

renal failure (decrease excretion)

hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+-ATPase)

drugs that displace digoxin from tissue-binding sites, and decrease clearance (eg, verapamil, amiodarone, quinidine).

175
Q

What are the different side effects of digoxin?

A

Cholinergic effects (nausea, vomiting, diarrhea), blurry yellow vision
arrhythmias
AV block
Hyperkalemia

176
Q

What are the different Class 1A antiarrhythmic?

A

Quinidine
procainamide
disopyramide

177
Q

Name the Class 1B Antiarrhythmic

A

Lidocaine
phenytoin
mexiletine.

178
Q

What are the different Class 1C Antiarrhythmic?

A

Flecainide
propafenone

179
Q

Name the clinical condition in which Class 1a Antiarrhythmic used

A

Both atrial and ventricular arrhythmias, especially reentrant

ectopic SVT and VT.

180
Q

Name the clinical condition in which Class 1b antiarrhythmic used

A

Acute ventricular arrhythmias (especially postMI)
digitalis-induced arrhythmias.
1B is Best post-MI.

181
Q

What are the clinical condition in which Class 1c Antiarrhythmic used

A

SVTs, including atrial fibrillation
Only as a last resort in refractory VT.

182
Q

What are the different side effects of Class 1A antiarrhythmic?

A

Cinchonism (headache, tinnitus with quinidine)

Reversible SLE-like syndrome (procainamide)

HF (disopyramide)

thrombocytopenia
torsades de pointes due to QT interval.

183
Q

What are the different side effects of Class 1B antiarrhythmic?

A

CNS stimulation/depression
cardiovascular depression

184
Q

What are the different side effects of Class 1C Antiarrhythmic?

A

Proarrhythmic, especially post-MI (contraindicated)

IC is Contraindicated in structural and ischemic heart disease

185
Q

important point of Beta blockers

A

Propranolol can exacerbate vasospasm in vasospastic angina.
Treat β-blocker overdose with saline, atropine, glucagon.

186
Q

What are the different Class 3 antiarrhythmic?

A

Amiodarone, Ibutilide
Dofetilide, Sotalol

187
Q

What is the MOA of αα-glucosidase inhibitors ?

A

Inhibit intestinal brush-border α-glucosidases result delayed carbohydrate hydrolysis and glucose absorption and decrease postprandial hyperglycemia.

188
Q

What are the different side effects of αα-glucosidase inhibitors?.

A

GI upset, bloating
Not recommended in renal insufficiency

189
Q

How does Amylin analogs (Pramlintide) work?

A

Decrease glucagon release
Decrease gastric emptying

190
Q

What is the side effects of Amylin analogs (Pramlintide)?

A

Hypoglycemia, nausea
Satiety (often desired

191
Q

How does DPP-4 inhibitors works?

A

Inhibit DPP-4 enzyme that deactivates GLP-1 result decrease glucagon release
Decrease gastric emptying
Increase glucose-dependent insulin release.

192
Q

How does DPP-4 inhibitors work?

A

Respiratory and urinary infections, weight neutral
satiety (often desired).

193
Q

What are the DM medicine which Decrease glucose absorption?

A

α-glucosidase inhibitors
—> Acarbose, miglitol

194
Q

How does Sodium-glucose co-transporter 2 inhibitors work?

A

Block reabsorption of glucose in proximal convoluted tubule.

195
Q

What are the different side effects of Sodium-glucose co-transporter 2 inhibitors?

A

Glucosuria (UTIs, vulvovaginal candidiasis)
Dehydration (orthostatic hypotension)

weight loss.
Use with caution in renal insufficiency ( efficacy with GFR).

196
Q

How does Thiazolidinediones work?

A

Activate PPAR-γ (a nuclear receptor)—> increased insulin sensitivity and levels of adiponectin—> regulation of glucose metabolism and fatty acid storage.

197
Q

What are the different side effects of Thiazolidinediones?

A

Weight gain, edema, HF
Risk of fractures
Delayed onset of action (several weeks)

Rosiglitazone: risk of MI, cardiovascular death.

198
Q

Name the DM which Increase glucose-induced insulin secretion

A

GLP-1 analogs
—>Exenatide, liraglutide, semaglutide

DPP-4 inhibitors
—>Linagliptin, saxagliptin, sitagliptin

199
Q

How GLP1 analogs work?

A

Decrease glucagon release
Decrease gastric emptying
glucose-dependent insulin release.

200
Q

What are different side effects of GLP1 ANALOG?

A

Nausea, vomiting, pancreatitis. Weight loss (often desired).
Increased satiety (often desired)

201
Q

What are the side effects of Sulfonylureas and Meglitinides?

A

Disulfiram-like reaction with first-generation sulfonylureas only (rarely used)

Hypoglycemia ( risk in renal insufficiency)

Weight gain

202
Q

Name the DM medicine which increased insulin sensitivity

A

Biguanides (Metformin)
Thiazolidinediones (Pioglitazone, rosiglitazone)

203
Q

How Metformin works?

A

Inhibit mitochondrial glycerol-3-phosphate dehydrogenase (mGPD)—-> Inhibition of hepatic gluconeogenesis and the action of glucagon.

Increased glycolysis, peripheral glucose uptake (increased insulin sensitivity).

204
Q

What are different side effects of metformin?

A

GI upset
Lactic acidosis (use with caution in renal insufficiency)
Vitamin B12 deficiency
Weight loss (often desired).

205
Q

Name the different types of Insulin

A

Rapid acting
–>Lispro, Aspart, Glulisine

Short acting
–>regular

Intermediate acting
–>NPH

Long acting
–>detemir, glargine

206
Q

Name the DM medicine which increased insulin secretion

A

Sulfonylureas (1st gen)
–>Chlorpropamide, tolbutamide

Sulfonylureas (2nd gen)
–> Glipizide, glyburide

Meglitinides
–>Nateglinide, repaglinide

207
Q

How do Sulfonylureas and Meglitinides work?

A

Close K+ channels in pancreatic B cell membrane—> cell depolarizes—> insulin release via increased Ca2+ influx.

208
Q

How Demeclocycline treat SIADH?

A

ADH antagonist (member of tetracycline family)

209
Q

What are the different side effects of SIADH?

A

Nephrogenic DI
photosensitivity
abnormalities of bone and teeth.

210
Q

What are the different indications of Somatostatin (octreotide)?
C-AGE

A

carcinoid syndrome
Acromegaly,
gastrinoma, glucagonoma,
esophageal varices.

PHARMA (2 decks)

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