pharm part 2 Flashcards
Name the antihelminthic therapy
Pyrantel pamoate
lvermectin
Diethylcarbamazine
Mebendazole (microtubule inhibitor}, Praziquantel (increased Ca2+ permeability, increased vacuolization)
What is the MOA of Chloroquine?
Blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia.
What are the clinical use of chloroquine?
Use in all marlarial species except falciparum
Due to resistance membrane pump that decrease intracellular concentration of drug.
What are the side effects of Chloroquine?
Retinopathy and pruritus
Important point of Malarial treatment.
- Treat P falciparum with artemether/lumefantrine or atovaquone/proguanil
- For life-threatening malaria, use quinidine in US (quinine elsewhere} or artesunate.
What are the medicine used to treat scabies and lice?
1) Permethrin
(inhibits Na+ channel deactivation —>neuronal membrane depolarization)
2) malathion
acetylcholinesterase inhibitor
3) lindane
blocks GABA channels ->neurotoxicity
Name the different medications used to anti protozal
Pyrimethamine (toxoplasmosis)
suramin and melarsoprol (Trypanosoma brucei)
nifurtimox (T cruzi)
sodium stibogluconate (leishmaniasis}.
Important point of ANTI-HIV
All ARTs are active against HIV-1 and HIV-2 with the exception of NNRTls
How NRTI help in treating in HIV?
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.
What are the different side effects of NRTIs?
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.
What are the different NRTIs?
Abacavir (ABC) Didanosine (ddl)
Emtricitabine (FTC) Lamivudine (3TC) Stavudine (d4T)
Tenofovir (TDF)
Zidovudine (ZDV, formerly AZT
What is the MOA NNRTls?
Bind to reverse transcriptase at site different from NRTis
Do not require phosphorylation to be active or compete with nucleotides.
What are the different side effects of NNRTIs?
Rash
Hepatotoxicity
Vivid dreams and CNS symptoms seen in efavirenz
Name the different NNRTIs
Delavirdine
Efavirenz
Nevirapine
What is the MOA of Protease inhibitors?
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.
What are the clinical side effects of of Protease inhibitors? “NAVIR”
hyperglycaemia
Gl intolerance (nausea, diarrhea)
lipodystrophy (Cushing-like syndrome). Nephropathy
hematuria, thrombocytopenia (indinavir).
Important point of Protease Inhibitors
Rifampin (potent CYP/UGT inducer) reduces protease inhibitor concentrations; use rifabutin instead.
What is the MOA of lntegrase inhibitors? “GRAVIR”
Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase.
What is the side effects of Integrase Inhibitors?
Increase creatinine kinase
Name the Anti HIV which are fusion inhibitor
Enfuvirtide
Maraviroc
What is the MOA of Enfuvirtide?
Binds gp41, inhibiting viral entry.
What is the MOA of Maraviroc?
Binds CCR-5 on surface ofT cells/monocytes, inhibiting interaction with gp120.
Name the NS5A inhibitors used for HCV and their MOA
HINT: LOV
Ledipasvir
Ombitasvir Velpatasvir
Inhibits NS5A, a viral phosphoprotein that plays a key role in RNA replication
Name the NS5B inhibitors used for HCV and their MOA
Sofosbuvir and Dasabuvir
Inhibits NS5B, an RNA-dependent RNA polymerase acting as a chain terminator
Prevents viral RNA replication
Name the NS3/4A inhibitors used for HCV and their MOA
Grazoprevir Simeprevir
Inhibits NS3/4A, a viral protease, preventing viral replication
What is the MOA of Ribavirin used for HCV?
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase
used as adjunct in cases refractory to newer medications.
What are the side effects of Ribavirin?
Hemolytic anemia
severe teratogen
What are the prophylactic medicine given in M avium–intracellulare?
Azithromycin, rifabutin
What is the MOA of Rifamycins (Rifampin, rifabutin, rifapentine)?
Inhibit DNA-dependent RNA polymerase.
What are the clinical indications of Rifamycins?
Mycobacterium tuberculosis
leprosy.
Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with H influenzae type b.
Important point of Rifamycins
It increases cytochrome P450 activity.
Tb Mutations reduce drug binding to RNA polymerase.
What is the MOA of isoniazid?
It decreases synthesis of mycolic acids.
Bacterial catalaseperoxidase (encoded by KatG) needed to convert INH to active metabolite.
What are the clinical side effects of Isoniazid?
Hepatotoxicity
cytochrome P-450 inhibition
drug-induced SLE
anion gap metabolic acidosis
vitamin B6 deficiency
seizures (in high doses, refractory to benzodiazepines)
How the resistance developed by TB against Isoniazid?
Mutations leading to underexpression of KatG.
What is the MOA of Ethambutol?
It decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.
What is the MOA of Stretopmycin?
Interferes with 30S component of ribosome.
What are the clinical side effects of Stretopmycin?
Tinnitus, vertigo
ataxia, nephrotoxicity.
What is the MOA of Fluoroquinolones?
It Inhibits prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV.
Important point of Fluoroquinolones
Bactericidal
Must not be taken with antacids.
Cipro inhibits CYP 450
What are the side effects of Fluoroquinolones?
GI upset
Superinfection
Skin rashes
Tendon rupture or tendonitis In elderly and patient take steroids
Prolong QT interval
What are the contraindications of Fluoroquinolones?
Contraindicated in pregnant women, nursing mothers, and children< 18 years old due to possible damage to cartilage.
What is the MOA of Daptomycin?
Lipopepticle that disrupts cell membranes of gram +ve cocci by creating transmembrane channels.
Important point of Daptomycin
It is not used for pneumonia (avidly binds to and is inactivated by surfactant).
What are the side effects of Daptomycin?
Myopathy, rhabdomyolysis.
What is the MOA of Metronidazole?
Forms toxic free radical metabolites in the bacterial cell that damage DNA.
Bactericidal, antiprotozoal.
What are the clinical side effects of Metronidazole?
Disulfiram-like reaction (severe Aushing, tachycardia, hypotension) with alcohol;
headache
metallic taste.
What are the MOA Of Sulfonamides and Dapsone?
Inhibit dihydropteroate synthase, thus inhibiting folate synthesis.
Bacteriostatic (bactericidal when combined with trimethoprim)
What are the clinical side effects of Sulfonamides?
Hypersensitivity reactions,
hemolysis if G6PD deficient.
nephrotoxicity (tubulointerstitial nephritis), photosensitivity,
Stevens-Johnson syndrome,
kernicterus in infants,
displace other drugs from albumin (eg, warfarin).
How bacteria develop resistance against Sulfonamides?
Altered enzyme (bacterial dihydropteroate synthase)
Decrease uptake
Increase PABA synthesis.
What are the clinical indications of Dapsone?
Leprosy (lepromatous and tuberculoid),
PCP prophylaxis, or treatment when used in combination with TMP.
What is the MOA of Trimethoprim?
Inhibits bacterial dihydrofolate reductase. Bacteriostatic.
What are the side effects of Trimethoprim?
Hyperkalemia (high doses), megaloblastic anemia, leukopenia, granulocytopenia, which may be avoided with coadministration of leucovorin (folinic acid).
What is the MOA of Aminoglycosides?
irreversible inhibition of initiation complex through binding of the 30S subunit.
Can cause misreading of mRNA.
Also block translocation.
Important Point of Aminoglycosides
Neomycin for bowel surgery.
Need oxygen for entering in cells so ineffective in anaerobes
What are the clinical side effects of Aminoglycosides?
Nephrotoxicity
neuromuscular blockade (absolute contraindication with myasthenia gravis)
ototoxicity (especially with loop diuretics), teratogenicity.
How resistance developed by bacteria against Aminoglycosides?
Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.
What is the MOA of Tetracyclines and Tigecycline?
bind to 30S and prevent attachment of aminoacyl-tRNA
Important Point of Tetracycline
Bacteriostatic
Limited CNS penetration.
Name the Tetracycline used in renal failure patient
Doxycycline is fecally eliminated and can be used in patients with renal failure
Why tetracycline shouldn’t be given with antacids, milk or iron containing preparation?
Divalent cations (Ca, Mg and Fe) inhibit drugs’ absorption in the gut.
What are the clinical side effects of Tetracycline?
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)
How resistance developed by bacteria against Tetracycline?
Decrease uptake or increase efflux out of bacterial cells by plasmid-encoded transport pumps.
What is the MOA of Chloramphenicol?
Blocks peptidyltransferase at 50S ribosomal subunit.
What are the side effects of Chloramphenicol?
Anemia (dose dependent)
aplastic anemia (dose independent)
gray baby syndrome (in premature infants because they lack liver UDP-glucuronosyltransferase).
How resistance developed by bacteria against chloramphenicol?
Plasmid-encoded acetyltransferase inactivates the drug.
What is the MOA of Clindamycin?
Blocks peptide transfer (translocation) at 50S ribosomal subunit.
What is the MOA of Linezolid?
Inhibits protein synthesis by binding to 50S subunit and preventing formation of the initiation complex.
What are the clinical side effects of Linezolid?
Myelosuppression (especially thrombocytopenia)
peripheral neuropathy
serotonin syndrome (due to partial MAO inhibition).
How resistance developed by bacteria against Linezolid?
Point mutation of ribosomal RNA
What is the MOA of Macrolides?
Inhibit protein synthesis by blocking translocation.
It bind to the 23S rRNA of the 50S ribosomal subunit.
Important Point of Macrolides
Increases serum concentration of theophylline, oral anticoagulants.
Clarithromycin and erythromycin inhibit cytochrome P-450.
What are the clinical side effects of Marcolides?
Gastrointestinal Motility issues,
Arrhythmia caused by prolonged QT interval
acute Cholestatic hepatitis
Rash
eOsinophilia
How resistance developed by bacteria against Marcolides?
Methylation of 23S rRNA-binding site prevents binding of drug
What is the MOA of Colistin (polymyxin E), polymyxin B?
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
What are the side effects of Colistin (polymyxin E), polymyxin B?
Nephrotoxicity
neurotoxicity (eg, slurred speech, weakness, paresthesias)
respiratory failure.
Name the different Carbapenems
Hint: DIME
Doripenem
lmipenem
Meropenem
Ertapenem
How Carbapenems work?
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.
What are the clinical side effects of Carbapenems?
GI distress
rash
CNS toxicity (seizures) at high plasma levels.
What is the MOA of Monobactams ( Aztreonam )?
Prevents peptidoglycan cross-linking by binding to penicillinbinding protein 3.
Synergistic with aminoglycosides
No cross-allergenicity with penicillins.
Important point of Monobactams
For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.
What is the MOA of Vancomycin?
Inhibits cell wall peptidoglycan formation by binding (D-Ala-D-Ala) portion of cell wall precursors
Not susceptible to B-lactamases.
What are the clinical side effects of of Vancomycin?
NOTR
Nephrotoxicity, Ototoxicity, Thrombophlebitis,
red man syndrome
DRESS syndrome
How bacteria develop resistance against vancomycin?
Occurs in bacteria (eg, Enterococcus) via amino acid modification of D-Ala-D-Ala to D-Ala-D-Lac.
How Pencillin G and V work?
Bind penicillin-binding proteins (transpeptidases) and Block transpeptidase cross-linking of peptidoglycan in cell wall
What are the different side effects of Pencillin G and V?
Hypersensitivity reactions
direct Coombs ⊕ hemolytic anemia,
Drug-induced interstitial nephritis.
How bacteria developed resistance against Pencillin G and V?
β-lactamase in bacteria cleaves the β-lactam ring of Medication.
Mutations in PBPs.
Name the different Penicillinase-sensitive penicillins
Amoxicillin, ampicillin; aminopenicillins.
What are the different side effects of Penicillinase-sensitive penicillins?
Hypersensitivity reactions
rash
pseudomembranous colitis.
How bacteria developed Resistance against Penicillinase-sensitive penicillins?
Penicillinase (a type of β-lactamase) cleaves β-lactam ring.
Name the different penicillinase-resistant penicillins and how they work?
Hint; DON
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
What are the different side effects of penicillinase-resistant penicillins?
Hypersensitivity reactions
interstitial nephritis
How bacteria developed Resistance against Penicillinase-resistant penicillins?
MRSA has altered penicillin-binding protein target site.
Important Point of Piperacillin
Antipseudomonal penicillin.
What is the MOA of Cephalosporins?
β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.
Important point of Cephalosporins
Organisms typically not covered by 1st–4th generation
Listeria
Atypicals (Chlamydia, Mycoplasma)
MRSA
Enterococci
What are the different side effects of Cephalosporins?
Hypersensitivity reactions
autoimmune hemolytic anemia
disulfiram-like reaction
vitamin K deficiency
Low rate of crossreactivity even in penicillin-allergic patients
nephrotoxicity of aminoglycosides.
How bacteria developed resistance against cephalosporins?
Inactivated by cephalosporinases (a type of β-lactamase).
Structural change in penicillinbinding proteins (transpeptidases).
Name the different B-lactamase inhibitors Clavulanic acid
Avibactam
Sulbactam
Tazobactam
amoxicillin-clavulanate, ceftazidime-avibactam, ampicillin-sulbactam, piperacillin-tazobactam
Name the Indirect Cholinomimetic agonist (Inhibits ACHe)
Donepezil
Edrophonium
galantamin
Neostigmine
Pyridostigmine
Physostigmine
rivastigmine
What are the clinical indications of Neostigmine?
Postoperative and neurogenic ileus and urinary retention
myasthenia gravis
Reversal of neuromuscular junction blockade (postoperative).
Name the Indirect Cholinomimetic agonist (Inhibits ACHe) which used in anticholinergic Toxicity
Physostigmine
Important Point
Jimson weed (Datura) gardener’s pupil (mydriasis)
Name the Muscarinic antagonists used for Motion sickness and COPD, asthma
Scopolamine For Motion Sickness
Ipratropium, tiotropium for COPD, asthma
Name the Muscarinic antagonist used in Urge Incontinence
Solifenacin, Oxybutynin
Flavoxate, Tolterodine
Name the Muscarinic antagonist used for irritable bowel syndrome
Hyoscyamine, dicyclomine
Name the Muscarinic antagonist used to reduce airway secretion preoperatively and reduce oral drooling as well as PUD
Glycopyrrolate
Name the Muscarinic antagonist used in Parkinson and acute dystonia
Benztropine
trihexyphenidyl
Name the SSRI and how they work?
Fluoxetine, fluvoxamine, paroxetine, sertraline, escitalopram, citalopram.
Inhibit 5-HT reuptake.
What are the clinical condition in which SSRI given?
Depression, generalized anxiety disorder
panic disorder
OCD, bulimia, binge-eating disorder
social anxiety disorder, PTSD
premature ejaculation, premenstrual dysphoric disorder
What are the side effects of SSRI?
Serotonin syndrome
GI distress
SIADH
sexual dysfunction (anorgasmia, erectile dysfunction, libido)
mania precipitation if underlying bipolar disorder.
What is the MOA of SNRI and Name the different SNRI?
Venlafaxine, desvenlafaxine, duloxetine, levomilnacipran, milnacipran.
Inhibit 5-HT and NE reuptake.
What are the different side effects of SNRI?
Depression
generalized anxiety disorder
diabetic neuropathy
social anxiety disorder
panic disorder
PTSD, OCD
What are the side effects of SNRI?
Raise BP
stimulant effects
sedation
sexual dysfunction
nausea.
How TCA work?
TCAs inhibit 5-HT and NE reuptake.
Alpha blocker and Anticholinergic also
What are the clinical indication of TCA?
MDD
peripheral neuropathy
chronic neuropathic pain
migraine prophylaxis
OCD (clomipramine)
nocturnal enuresis (imipramine).
How Monoamine oxidase inhibitors work and name the different MOA inhibitor
Nonselective MAO inhibition dopamine)—->levels of amine neurotransmitters (norepinephrine, 5-HT, dopamine).
What is the MOA of Vilazodone and Vortioxetine?
Inhibits 5-HT reuptake
Used for MDD
What are the clinical side effects of Vilazodone and Vortioxetine?
serotonin syndrome
headache, diarrhea, nausea, anticholinergic effects.
sexual dysfunction, sleep disturbances, anticholinergic effects.
How Trazodone work and what are the clinical indication of it?
Primarily blocks 5-HT2 , α1-adrenergic, and H1 receptors; also weakly inhibits 5-HT reuptake
insomnia and Depression.
What are the clinical side effects of Trazodone?
sedation, nausea, priapism, postural hypotension.
What is the MOA of Mirtazapine?
α2-antagonist ( release of NE and 5-HT)
potent 5-HT2 and 5-HT3 receptor antagonist, and H1 antagonist.
What are side effects of Mirtazapine?
sedation
Increase appetite, weight gain
Dry mouth
Name the medicine used for smoking cessation
Bupropion (Inhibits NE and DA reuptake)
Varenicline (Nicotinic ACh receptor partial agonist)
How does Omalizumab work?
It binds mostly unbound serum IgE and blocks binding to FcεR
What are the different Antileukotrienes?
1) Montelukast, zafirlukast—block leukotriene receptors
2) Zileuton—5-lipoxygenase inhibitor
What are the clinical indications of Montelukast, zafirlukast?
aspirin induced and exercise-induced asthma.
Which test should be send before giving Zileuton?
Hepatotoxic
What is the MOA of Tiotropium and ipratropium?
Competitively block muscarinic receptors, preventing bronchoconstriction.
What are the different inhaled glucocorticoids?
Fluticasone budesonide used in chronic asthma
How do inhaled glucocorticoids work?
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
How does Minoxidil work?
Direct arteriolar vasodilator.
Name the different Anti laxatives (BOSEL)
Bulk-forming laxatives
(Methylcellulose, psyllium)
Osmotic laxatives
(Lactulose, magnesium citrate, magnesium hydroxide, polyethylene glycol)
Stimulant laxatives
(Bisacodyl, senna)
Emollient laxatives
(Docusate)
Lubiprostone
How does Emollient laxatives work?
Surfactants that decrease stool surface tension, promoting water entry into stool
What is the MOA of Orilstat?
.
Inhibits gastric and pancreatic lipase which decrease breakdown and absorption of dietary fats
It is taken withfat-containing meals
Important point of Octreotide
Increased risk of cholelithiasis due to CCK inhibition.
What is the MOA of Misoprostol?
PGE1 analog.
It is involved in production and secretion of gastric mucous barrier, decrease acid production.
What are the clinical use of Misoprostol?
Prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production).
Also used off-label for induction of labor (ripens cervix).
What are the different side effects of Misoprostol?
Diarrhea.
Contraindicated in patients of childbearing potential (abortifacient).
What are the different side effects of Aluminum hydroxide?
Constipation
Hypophosphatemia,
Osteodystrophy,
Proximal muscle weakness
Seizures
What are the different side effects of Calcium carbonate?
Hypercalcemia (milk-alkali syndrome)
rebound acid
What are the different side effects of Magnesium hydroxide?
Diarrhea
hyporeflexia
hypotension
cardiac arrest
What are the different side effects of PPI?
.
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)
What are the different side effects of Cimetidine?
Inhibit CYP 450
Anti androgenic
cross blood-brain barrier (confusion, dizziness, headaches) and placenta
Cimetidine decreases renal excretion of creatinine.
What are anti-HTN avoided in Asthma?
Avoid nonselective Beta-blockers to prevent B2-receptor-induced bronchoconstriction.
Avoid ACE inhibitors to prevent confusion between drug or asthma-related cough.
What are the different Anti-HTN given in asthma?
.
ARBs
Ca2+ channel blockers
thiazide diuretics,
cardioselective beta-blockers
Important point
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.
Name the different CCB
Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine (dihydropyridines, act on vascular smooth muscle)
diltiazem, verapamil (non-dihydropyridines, act on heart).
Name the different CCB
Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine (dihydropyridines, act on vascular smooth muscle)
diltiazem, verapamil (non-dihydropyridines, act on heart).
What are the different uses of dihydropyridines CCB?
Dihydropyridines (except nimodipine): hypertension, angina (including vasospastic type), Raynaud phenomenon.
Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).
Nicardipine, clevidipine: hypertensive urgency or emergency.
What are the side effects of different CCB?
*
Gingival hyperplasia
*Dihydropyridine
peripheral edema, Aushing, dizziness
*Non-dihydropyridine
cardiac depression, AV block, hyperprolactinemia (verapamil), constipation.
What are the clinical indications of hydralazine?
*
Severe hypertension (particularly acute), *HF (with organic nitrate).
Frequently coadministered with a b-blocker to prevent reAex tachycardia.
Name the medicine used in HTN emergency
labetalol, clevidipine
Fenoldopam, nicardipine
Nitroprusside.
How does Nitroprusside work and what is the main side effects?
Short acting vasodilator (arteries = veins)—> cGMP via direct release of NO
It Can cause cyanide toxicity (releases cyanide).
What is the MOA of Fenoldopam?
Dopamine D1 receptor agonist—>coronary, peripheral, renal, and splanchnic vasodilation result in decrease BP and increase natriuresis.
Also used postoperatively as an antihypertensive
What is the MOA of nitrates?
Vasodilate by increased NO in vascular smooth muscle which result in increased cGMP and smooth muscle relaxation
Dilate veins»_space; arteries
Decrease preload.
What are the clinical indications of nitrates?
Angina
ACS
Pulmonary edema
What are the conditions in which nitrates cannot be used?
Contraindicated in right ventricular infarction, hypertrophic cardiomyopathy, and with concurrent PDE-5 inhibitor use.
What are the different side effects of Nitrates?
Reflex tachycardia (treat with β-blockers), methemoglobinemia
hypotension
flushing
headache
“Monday disease”
Important point
Pindolol and acebutolol are partial β-agonists that should be used with caution in angina
What is the MOA of Ranolazine?
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.
What are the different side effects of Ranolazine?
Constipation
Dizziness
Headache
How does Sacubitril work?
It is a neprilysin inhibitor which Prevents degradation of bradykinin, natriuretic peptides, angiotensin II, and substance P
Resulted in vasodilation and decrease ECF volume.
Name the clinical condition in which Sacubitril used
It Used in combination with valsartan (an ARB) to treat HFrEF.
What are the different side effects of Sacubitril?
Hypotension
hyperkalemia
cough, dizziness
contraindicated with ACE inhibitors due to angioedema (both drugs bradykinin).
What are the different bile acid resins and what is the mechanism of action of it?
It prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more
Cholestyramine, colestipol, colesevelam
How does Ezetimibe help in improving lipid profile?
It prevents cholesterol absorption at small intestine brush border.
What is the moa of Fibrates?
Activate PPAR-α–>upregulate LPL which increasedTAG clearance
Activate PPAR-α—->induce HDL synthesis
What are the different side effects of fibrates?
Myopathy ( risk with statins)
cholesterol gallstones (via inhibition of cholesterol 7α-hydroxylase)
How does NACIN help in improving lipid profile?
It inhibits lipolysis (hormone-sensitive lipase) in adipose tissue
It reduces hepatic VLDL synthesis
What are the different side effects of NACIN?
Flushed face (prostaglandin mediated; decrease by NSAIDs or longterm use) Hyperglycemia
Hyperuricemia
What is the MOA of PCSK9 inhibitors?
Alirocumab, evolocumab
Inactivation of LDL-receptor degradation which result removal of LDL from bloodstream
What are the different side effects of PCSK9 inhibitors?
Myalgias
delirium
dementia
other neurocognitive effects
What are the different clinical condition which required digoxin?
HF (contractility)
atrial fibrillation (conduction at AV node and depression of SA node)
Name the condition which increased toxicity of digoxin
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).
What are the different side effects of digoxin?
Cholinergic effects (nausea, vomiting, diarrhea), blurry yellow vision
arrhythmias
AV block
Hyperkalemia
What are the different Class 1A antiarrhythmic?
Quinidine
procainamide
disopyramide
Name the Class 1B Antiarrhythmic
Lidocaine
phenytoin
mexiletine.
What are the different Class 1C Antiarrhythmic?
Flecainide
propafenone
Name the clinical condition in which Class 1a Antiarrhythmic used
Both atrial and ventricular arrhythmias, especially reentrant
ectopic SVT and VT.
Name the clinical condition in which Class 1b antiarrhythmic used
Acute ventricular arrhythmias (especially postMI)
digitalis-induced arrhythmias.
1B is Best post-MI.
What are the clinical condition in which Class 1c Antiarrhythmic used
SVTs, including atrial fibrillation
Only as a last resort in refractory VT.
What are the different side effects of Class 1A antiarrhythmic?
Cinchonism (headache, tinnitus with quinidine)
Reversible SLE-like syndrome (procainamide)
HF (disopyramide)
thrombocytopenia
torsades de pointes due to QT interval.
What are the different side effects of Class 1B antiarrhythmic?
CNS stimulation/depression
cardiovascular depression
What are the different side effects of Class 1C Antiarrhythmic?
Proarrhythmic, especially post-MI (contraindicated)
IC is Contraindicated in structural and ischemic heart disease
important point of Beta blockers
Propranolol can exacerbate vasospasm in vasospastic angina.
Treat β-blocker overdose with saline, atropine, glucagon.
What are the different Class 3 antiarrhythmic?
Amiodarone, Ibutilide
Dofetilide, Sotalol
What is the MOA of αα-glucosidase inhibitors ?
Inhibit intestinal brush-border α-glucosidases result delayed carbohydrate hydrolysis and glucose absorption and decrease postprandial hyperglycemia.
What are the different side effects of αα-glucosidase inhibitors?.
GI upset, bloating
Not recommended in renal insufficiency
How does Amylin analogs (Pramlintide) work?
Decrease glucagon release
Decrease gastric emptying
What is the side effects of Amylin analogs (Pramlintide)?
Hypoglycemia, nausea
Satiety (often desired
How does DPP-4 inhibitors works?
Inhibit DPP-4 enzyme that deactivates GLP-1 result decrease glucagon release
Decrease gastric emptying
Increase glucose-dependent insulin release.
How does DPP-4 inhibitors work?
Respiratory and urinary infections, weight neutral
satiety (often desired).
What are the DM medicine which Decrease glucose absorption?
α-glucosidase inhibitors
—> Acarbose, miglitol
How does Sodium-glucose co-transporter 2 inhibitors work?
Block reabsorption of glucose in proximal convoluted tubule.
What are the different side effects of Sodium-glucose co-transporter 2 inhibitors?
Glucosuria (UTIs, vulvovaginal candidiasis)
Dehydration (orthostatic hypotension)
weight loss.
Use with caution in renal insufficiency ( efficacy with GFR).
How does Thiazolidinediones work?
Activate PPAR-γ (a nuclear receptor)—> increased insulin sensitivity and levels of adiponectin—> regulation of glucose metabolism and fatty acid storage.
What are the different side effects of Thiazolidinediones?
Weight gain, edema, HF
Risk of fractures
Delayed onset of action (several weeks)
Rosiglitazone: risk of MI, cardiovascular death.
Name the DM which Increase glucose-induced insulin secretion
GLP-1 analogs
—>Exenatide, liraglutide, semaglutide
DPP-4 inhibitors
—>Linagliptin, saxagliptin, sitagliptin
How GLP1 analogs work?
Decrease glucagon release
Decrease gastric emptying
glucose-dependent insulin release.
What are different side effects of GLP1 ANALOG?
Nausea, vomiting, pancreatitis. Weight loss (often desired).
Increased satiety (often desired)
What are the side effects of Sulfonylureas and Meglitinides?
Disulfiram-like reaction with first-generation sulfonylureas only (rarely used)
Hypoglycemia ( risk in renal insufficiency)
Weight gain
Name the DM medicine which increased insulin sensitivity
Biguanides (Metformin)
Thiazolidinediones (Pioglitazone, rosiglitazone)
How Metformin works?
Inhibit mitochondrial glycerol-3-phosphate dehydrogenase (mGPD)—-> Inhibition of hepatic gluconeogenesis and the action of glucagon.
Increased glycolysis, peripheral glucose uptake (increased insulin sensitivity).
What are different side effects of metformin?
GI upset
Lactic acidosis (use with caution in renal insufficiency)
Vitamin B12 deficiency
Weight loss (often desired).
Name the different types of Insulin
Rapid acting
–>Lispro, Aspart, Glulisine
Short acting
–>regular
Intermediate acting
–>NPH
Long acting
–>detemir, glargine
Name the DM medicine which increased insulin secretion
Sulfonylureas (1st gen)
–>Chlorpropamide, tolbutamide
Sulfonylureas (2nd gen)
–> Glipizide, glyburide
Meglitinides
–>Nateglinide, repaglinide
How do Sulfonylureas and Meglitinides work?
Close K+ channels in pancreatic B cell membrane—> cell depolarizes—> insulin release via increased Ca2+ influx.
How Demeclocycline treat SIADH?
ADH antagonist (member of tetracycline family)
What are the different side effects of SIADH?
Nephrogenic DI
photosensitivity
abnormalities of bone and teeth.
What are the different indications of Somatostatin (octreotide)?
C-AGE
carcinoid syndrome
Acromegaly,
gastrinoma, glucagonoma,
esophageal varices.
