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PHARMA > PART 1 > Flashcards

PART 1 Flashcards

1
Q

DrHow to treated hyper phosphatemia due to CKD?

A

Sevelamer
Nonabsorbable phosphate binder that prevents phosphate absorption from the CI tract.

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2
Q

What is the mechanism of action of Cinacalcet?

A

Sensitizes Ca2+_sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ then leads decrease PTH

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3
Q

Name the condition in which Cinacalecet can be given?

A

2° hyperparathyroidism in CKD, hypercalcemia in 1° hyperparathyroidism (if parathyroidectomy fails) or in parathyroid carcinoma

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4
Q

How Demeclocycline treat SIADH?

A

ADH antagonist (member of tetracycline family)

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5
Q

What are the different side effects of SIADH?

A

Nephrogenic DI
photosensitivity
abnormalities of bone and teeth.

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6
Q

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

A

carcinoid syndrome
Acromegaly,
gastrinoma, glucagonoma,
esophageal varices.

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7
Q

What is the mechanism of action of lvabradine?

A

It prolongs slow depolarization (phase “IV”) by selectively inhibiting “funny” sodium channels.

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8
Q

In which condition Ivabradine given?

A

Chronic stable angina in patients who cannot take betablockers.
Chronic HFrEF.

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9
Q

What are the different effects of Ivabradine?

A

Luminous phenomena/visual brightness, hypertension
bradycardia.

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10
Q

Name the Anti-HTN given in pregnancy

A

Hydralazine, labetalol
methyldopa, nifedipine

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11
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.

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12
Q

What are the different Anti-HTN given in asthma?

A

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

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13
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.

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14
Q

Name the different CCB

A

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

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

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15
Q

What is the MOA of CCB?

A

It Block voltage-dependent L-type calcium channels of cardiac and smooth muscle -I muscle contractility.

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16
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.

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17
Q

What are the uses of Non-Dihydropyridines CCB?

A

Non-dihydropyridines: hypertension, angina
atrial fibrillation/Autter.

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18
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

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19
Q

What is the MOA of Hydralazine?

A

It increases cGMP—>smooth muscle relaxation
Vasodilates arterioles> veins; afterload reduction.

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20
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.

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21
Q

What are the different side effects of hydralazine?

A

Compensatory tachycardia (contraindicated in angina/CAD)
fluid retention
headache
angina
SLE-like syndrome.

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22
Q

When to use Neuromuscular blocking drugs?

A

It is use to paralyse muscle during surgery Or Mechanical ventilation

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23
Q

Which receptors are blocked by Neuromuscular blocking drugs?

A

Selective for Nm nicotinic receptors at neuromuscular junction but not autonomic Nn receptors.

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24
Q

Name the Depolarizing neuromuscular blocking drugs and what is the MOA of it?

A

Succinylcholine-strong ACh receptor agonist.

It produces sustained depolarization and prevents muscle contraction.

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25
Q

Important point of Depolarising neuromuscular blocking drugs

A

Reversal of blockade:

  • Phase I (prolonged depolarization)-no antidote available to reverse the action
    Block potentiated by cholinesterase inhibitors.
  • Phase II (repolarized but blocked
    ACh receptors are available, but desensitized)

may be reversed with cholinesterase inhibitors.

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26
Q

What are the side effects succinylcholine?

A

hypercalcemia
hyperkalemia
malignant hyperthermia.

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27
Q

What are the different Nondepolarizing neuromuscular blocking drugs?

A

Atracurium, cisatracurium
pancuronium, rocuronium
tubocurarine, vecuronium

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28
Q

How does Non-depolarise neuromuscular blocking drugs?

A

Competitive ACh antagonist

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29
Q

Important point of Non-depolarise Neuro muscular blocking drugs

A

Reversal of blockade-neostigmine (must be given with atropine or glycopyrrolate to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors

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30
Q

Name the different Spasmolytics, antispasmodics.

A

Baclofen
Cyclobenzaprine

Dantrolene
Tizanidine

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31
Q

What is the MOA of Baclofen?

A

GABA(B) receptor agonist in spinal cord.

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32
Q

What are the clinical used of Baclofen?

A

Muscle spasticity
dystonia
multiple sclerosis.

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33
Q

Important point of Cyclobenzaprine

A

Acts within CNS mainly at the brain stem
It may cause anticholinergic side effects and sedation

It helps to relieve muscle spasticity

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34
Q

What is the MOA of Tizanidine?

A

Alpha 2 agonist and acts centrally

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35
Q

What are the clinical use of Tizanidine?

A

Muscle spasticity
multiple sclerosis

ALS
cerebral palsy

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36
Q

Name the Anti-Epileptic which increases GABA (A) action

A

Benzodiazepines
Phenobarbital
Topiramate
Valproic acid
Vigabatrin

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37
Q

What are the Anti-Epileptic which block Sodium channel?

A

Carbamazepine
Phenytoin
fosphenytoin
Topiramate
lamotrigine
Valproic acid

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38
Q

Name the Anti-epileptic which block Voltage gated calcium channel

A

Ethosuximide
Gabapentin
Levetiracetam

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39
Q

Name the Anti-epileptic for First line for recurrent seizure prophylaxis

A

Phenytoin
Fosphenytoin

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40
Q

What are the different side effects of Carbamazepine?

A

Diplopia
ataxia
dyscrasias (agranulocytosis, aplastic anemia)

liver toxicity
Teratogenic cleft· lip/palate, spina bifida)
induction of cytochrome P-450
SIADH, SJS

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41
Q

What are the side effects of Ethosuximide?

A

Fatigue
GI distress
Headache
Itching and Urticaria
SJS

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42
Q

What are the clinical side effects of lamotrigine?

A

SJS
Hemophagocytic lymphohistiocytosis

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43
Q

What are the clinical side effects of Levetiracetam?

A

Neuropsychiatric symptoms
Fatigue
Headache
Drowsiness

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44
Q

What are the clinical side effects of Phenobarbital?

A

Induction of cytochrome P450
Cardio respiratory depression

Sedation and tolerance dependence

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45
Q

What are the clinical side effects of phenytoin and fosphenytoin?

A

Syndrome like SJS, DRESS, SLE like syndrome
P450 induction
Hirsutism

Enlarged Gums
Nystagmus
Yellow brown skin

Osteopenia
Inhibited folate absorption
Neuropathy

Diplopia, sedation and ataxia

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46
Q

What are the clinical side effects of Topiramate?

A

Kidney STONE
Speech difficulties

Sedation and Slow Cognition
Weight loss
Glaucoma

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47
Q

What are the side effects of Valproic acid?

A

Pancreatitis
GI distress

Hepatotoxicity
Neural tube defects

Tremor
WEIGHT GAIN

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48
Q

What are the side effects of Vigabatrin?

A

PERMANENT vision loss

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49
Q

What are the different Barbiturates?

A

Phenobarbital, pentobarbital
thiopental, secobarbital.

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50
Q

What is the MOA of Barbiturates?

A

Facilitates GABA A action by increase duration of CL channel opening, thus Decrease neuron firing
(barbidurates increased duration).

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51
Q

Name the Benzodiazepine which can used in liver disease
Remember LOT

A

Lorazepam, Oxazepam, and Temazepam can be used for those with liver disease who drink a LOT due to minimal first-pass metabolism.

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52
Q

What is the MOA of benzodiazepine?

A

Facilitates GABA A action by increase FREQUENCY of CL channel opening, thus Decrease neuron firing

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53
Q

Name the Non Benzodiazepines which can use hypnotics

A

Zolpidem, Zaleplon, esZopiclone

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54
Q

Important point

A

Both Benzodiazepines and NON benzodiazepines action reversed by flumazenil

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55
Q

Name the medicine which block OREXIN (hypocretin) receptor

A

Suvorexant

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56
Q

What are the clinical conditions in which Suvorexant is contraindicated?

A

narcolepsy
combination with strong CYP3A4 inhibitors. Not recommended in patients with liver disease.

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57
Q

What is the MOA of Ramelteon?

A

Melatonin receptor agonist; binds MT1 and MT2 in suprachiasmatic nucleus.
Used in insomnia

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58
Q

What are the different MOA of Triptans?

A

prevent vasoactive peptide release
It induces vasoconstriction

It inhibits trigeminal nerve activation
Serotonin receptor agonist

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59
Q

What are the different side effects of Triptans?

A

Coronary vasospasm (contraindicated in patients with CAD or vasospastic angina)

mild paresthesia
serotonin syndrome

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60
Q

How to classify dopamine agonist?

A

Ergot: bromocriptine
Non-ergot: pramipexole, ropinirole

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61
Q

What are different side effects Non-ergot Dopamine agonist?

A

nausea, impulse control disorder (eg, gambling)
postural hypotension, hallucinations
confusion, sleepiness, edema.

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62
Q

What is the MOA of Amantadine?

A

It increases dopamine availability by increase dopamine release and decrease dopamine reuptake

It is mainly used to reduce levodopa induced dyskinesias

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63
Q

What are the different side effects of Amantadine?

A

peripheral edema
livedo reticularis
ataxia

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64
Q

Name the anti Parkinson medicine Which increase L-dopa availablity in CNS

A

1) carbidopa: blocks peripheral conversion of l-DOPA to dopamine by inhibiting DOPA decarboxylase.

2) Entacapone and tolcapone prevent peripheral l-DOPA degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT

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65
Q

What are the Anti-Parkinson medicine which prevent dopamine breakdown in CNS?

A

1) Selegiline, rasagiline
2) Tolcapone

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66
Q

What is the MOA of Tolcapone?

A

crosses BBB and blocks conversion of dopamine to 3-methoxytyramine (3-MT) in the brain by inhibiting central COMT.

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67
Q

What is the MOA of rasagiline and Selegiline?

A

Block conversion of dopamine into DOPAC by selectively inhibiting MAO-B, which is more commonly found in the Brain than in the periphery

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68
Q

Important point:

A

Always decrease the availablity of Cholinergic as its presence worsen the symptoms of Parkinson

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69
Q

What is the MOA of Riluzole?

A

It decreases neuron Glutamate Excitotoxicity

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70
Q

What is the MOA of Tetrabenazine?

A

Inhibit vesicular monoamine transporter (VMAT) by decreasing dopamine vesicle packaging and release

Used in Huntington chorea and Tardaive dyskinesia

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71
Q

What is the MOA of Memantine?

A

NMDA receptor antagonist
It helps prevent excitotoxicity (mediated by Ca2+)

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72
Q

What is the MOA of Tramadol?

A

A very weak opioid agonist which also inhibits the reuptake of norepi and serotonin
Given in chronic pain

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73
Q

What are the side effects of tramadol?

A

Decrease seizure threshold
Serotonin syndrome

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74
Q

Name the Mixed agonist and antagonist opioid analgesics

A

Pentazocine
Butorphanol

75
Q

What is the MOA of Pentazocine?

A

K- opioid receptor agonist
U- opioid receptor weak antagonist Or partial agonist
Given in Analgesics for moderate to severe pain

76
Q

What is the MOA of Butorphanol?

A

K- opioid receptor agonist
U- opioid receptor partial agonist

Used in Severe pain like labour or migraine

77
Q

Important point of Butorphanol

A

Not easily reversed with naloxone

78
Q

What is the MOA of Opioid Analgesics?

A

Decrease synaptic transmission by close presynaptic Ca2+ channels, open postsynaptic Potassium channels

Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.

79
Q

Name the Opioid Antagnoist

A

Antagonist: naloxone, naltrexone, methylnaltrexone.

80
Q

Important point of Opioid medicine

A

All leads to miosis except meperidine

Toxicity treated with naloxone (opioid receptor antagonist) and relapse prevention with naltrexone once detoxified.

81
Q

Name the antifungal meds which inhibit cell wall synthesis
*Hint = fungin

A

Anidulafungin, caspofungin, micafungin.
All are Echinocandins

82
Q

What are the clinical use of and side effects Echinocandins?

A

Invasive aspergillosis
Candida

S.E = GI upset, flushing (by histamine release)

83
Q

How Amphotericin B and nystitin work?

A

*Hint = Cell membrane

They Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes.

84
Q

What are the clinical uses of Amphotericin B?

A

Serious, systemic mycoses

Cryptococcus (amphotericin B with/without Aucytosine for cryptococcal meningitis)

Blastomyces, Coccidioides, Histoplasma, Candida, Mucor.

lntrathecally for fungal meningitis.
Supplement K+ and Mg2+ because of altered renal tubule permeabilit

85
Q

What are the side effects of Amphotericin B?

A

Fever with chills
Hypotension
Arrhythmia

Nephrotoxicity
Anemia
IV phlebitis

86
Q

What are the clinical use of Nystatin?

A

oral candidiasis (thrush)
topical for diaper rash or vaginal candidiasis.

87
Q

How Terbinafine work?

A

Inhibits the fungal enzyme squalene epoxidase result no squalene epoxide production

88
Q

What is the clinical use of terbinafine?

A

Dermatophytoses (especially onychomycosis-fungal infection of finger or toe nails).

89
Q

What are the side effects of Terbinafine?

A

GI upset, headaches
hepatotoxicity
taste disturbance

90
Q

What is the MOA of Azoles?

A

Inhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol.

91
Q

What are the clinical use of Azoles?

A

Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types.

ltraconazole may be used for Blastomyces, Coccidioides, Histoplasma, Sporothrix schenckii. Clotrimazole and miconazole for topical fungal infections.

Voriconazole for Aspergillus and some Candida.
lsavuconazole for serious Aspergillus and Mucor infections.

92
Q

What are the side effects of Azoles?

A

Testosterone synthesis inhibition (gynecomastia, especially with ketoconazole)

liver dysfunction (inhibits cytochrome P-450).

93
Q

What is the MOA of flucytosine?

A

Inhibits DNA and RNA biosynthesis by conversion to 5-Auorouracil by cytosine deaminase.

94
Q

What is the clinical use of Flucytosine?

A

Systemic fungal infections (especially meningitis caused by Cryptococcus) in combination with amphotericin B.

95
Q

What is the Side effect of flucytosine?

A

Bone marrow suppression

96
Q

What is the MOA of Griseofulvin?

A

Interferes with microtubule function; disrupts mitosis.
Deposits in keratin-containing tissues (eg, nails}.

97
Q

What are the clinical use of Griseofulvin?

A

Oral treatment of superficial infections;

inhibits growth of dermatophytes (tinea, ringworm).

98
Q

What are the clinical side effects of Griseofulvin?

A

Teratogenic, carcinogenic, confusion, headache
disulfiram-like reaction
cytochrome P-450 and warfarin metabolism

99
Q

What are the MOA of Oseltamivir and zanamivir?

A

Inhibit influenza neuraminidase -> release of progeny virus.

100
Q

What is the MOA of Baloxavir?

A

Inhibits the “cap snatching” (transfer of the 5′ cap from cell mRNA onto viral mRNA) endonuclease activity of the influenza virus RNA polymerase result decrease viral replication.

101
Q

What is the MOA of Remedesivir?

A

The active metabolite inhibits viral RNA-dependent RNA polymerase and evades proofreading by viral exoribonuclease (ExoN) result decrease viral RNA production.

102
Q

What are the MOA of Acyclovir, famciclovir, valacyclovir?

A

Preferentially inhibit viral DNA polymerase by chain termination.
These drugs need thymidine kinase for their activation so doesn’t work against CMV

103
Q

What are the different side effects Acyclovir, famciclovir, valacyclovir?

A

Obstructive crystalline nephropathy and acute kidney injury if not adequately hydrated.

104
Q

What is the MOA of Ganciclovir?

A

It inhibits viral DNA polymerase but need viral viral kinase for activation (as this drug is monophosphate) which CMV has.

105
Q

What are different side effects of Ganciclovir?

A

Myelosuppression
Renal Toxicity

106
Q

What is the MOA of Foscarnet?

A

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor.

Binds to pyrophosphate-binding site of enzyme and this drug doesn’t need enzyme for its activation.

107
Q

What is the clinical indication of foscarnet?

A

CMV retinitis in immunocompromised patients when ganciclovir fails
acyclovir-resistant HSV.

108
Q

What are the different side effects of Foscarnet?

A

Nephrotoxicity, multiple electrolyte abnormalities can lead to seizures.

109
Q

What is the MOA of Cidofovir?

A

inhibits viral DNA polymerase.
Does not require phosphorylation by viral kinase.

110
Q

What are the clinical indication of Cidofovir?

A

CMV retinitis in immunocompromised patients;
Acyclovir-resistant HSV

111
Q

What is the side effects of Cidofovir?

A

Nephrotoxicity (coadminister cidofovir with probenecid and IV saline to decrease toxicity).

112
Q

Important point of Cholinomimetic (agonist) agents

A

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients.

113
Q

Name the Cholinomimetic (agonist) agents (P-MCB)

A

Pilocarpine
Methacholine

Carbachol
Bethanechol

114
Q

What are the clinical indications of Pilocarpine?

A

Given in open angle glaucoma as it contracts ciliary muscle of eye

Given in close angle glaucoma as it stimulates pupillary sphincter

Resistant to ACHe and also cross BBB
Potent stimulator of sweat, tears, and saliva (used in Sjögren syndrome).

115
Q

What is the clinical indication of Methacholine?

A

Stimulates muscarinic receptors in airway when inhaled so used in asthma diagnosis.

116
Q

What is the clinical indication of CARBACHOL?

A

Constricts pupil and relieves intraocular pressure in open-angle glaucoma.

117
Q

What is the clinical indication of Bethanechol?

A

Activates bladder smooth muscle by acting on muscarinic receptors so used in urine retention

resistant to AChE
no nicotinic activity.

118
Q

What is MOA of Dextromethorphan?

A

It is Antitussive which antagonizes NMDA glutamate receptors

119
Q

How to avoid toxicity of Dextromethorphan?

A

If used excessively can produce opioid effects
Naloxone can be given for overdose

120
Q

What syndrome could occur due to Dextromethorphan?

A

Serotonin syndrome if the medicine combine with other serotonergic agents.

121
Q

What are the different first generation H1 antihistamine?

A

Diphenhydramine
dimenhydrinate

chlorpheniramine
doxylamine.

122
Q

What are the clinical uses of H1 antihistamine?

A

Allergy
motion sickness

vomiting in pregnancy
sleep aid.

123
Q

What are the different side effects of H1 antihistamine?

A

Sedation
antimuscarinic
anti-α-adrenergic

124
Q

What are the different 2nd generation H1 antihistamine?

A

Loratadine
fexofenadine

desloratadine
cetirizine.

125
Q

What is the Moa of Pseudoephedrine, phenylephrine?

A

Activation of α-adrenergic receptors in nasal mucosa—->local vasoconstriction

126
Q

What are the clinical uses of Pseudoephedrine, phenylephrine?

A

Reduce hyperemia
edema (used as nasal decongestants)
open obstructed eustachian tubes.

127
Q

What are the various side effects of Pseudoephedrine, phenylephrine?

A

Hypertension
Rebound congestion (rhinitis medicamentosa) if used more than 4–6 days

Associated with tachyphylaxis
Can also cause CNS stimulation/anxiety (pseudoephedrine).

128
Q

Name the medicines used in pulmonary hypertension

A

Endothelin receptor antagonists—> bosentan

PDE-5 inhibitors—>sildenafil

Prostacyclin analogs —>epoprostenol, iloprost.

129
Q

How does Prostacyclin work?

A

PGI2 (prostacyclin) with direct vasodilatory effects on pulmonary and systemic arterial vascular beds.
Inhibits platelet aggregation.

130
Q

What is single most side effects of Bosentan?

A

Hepatotoxicity so monitor LFT

131
Q

Name the drugs work against IL-5 or It’s receptor (Anti IL-5 monoclonal antibody)

A

Mepolizumab, reslizumab—against IL-5

Benralizumab—against IL-5 receptor α.

132
Q

How does Anti IL-5 monoclonal antibody work?

A

It Prevents eosinophil differentiation, maturation, activation, and survival mediated by IL-5 stimulation.

133
Q

How does Roflumilast work?

A

It inhibits PDE4 result bronchodilation
Used in COPD to reduce exacerbations

134
Q

How does Methylxanthines (Theophylline) work?

A

It dilates bronchus by inhibiting PDE

135
Q

Name the beta blockers which decrease aqueous humour synthesis

A

Timolol
betaxolol
carteolol

136
Q

How diuretics help in treating glaucoma?

A

Decrease aqueous humor synthesis via inhibition of carbonic anhydrase

137
Q

Important point of Beta block and diuretics (AZT) in treatment of aqueous humour synthesis

A

No pupillary or vision changes noted if BB prescribed

138
Q

How alpha agnoist help in treating glaucoma?

A

1) Decrease aqueous humor synthesis via vasoconstriction (epinephrine)

2) Decrease aqueous humor synthesis (apraclonidine, brimonidine)

3) Increasedoutflow of aqueous humor via uveoscleral pathway

139
Q

Name the alpha agnoist used in treatment of glaucoma

A

Epinephrine (α1 )
apraclonidine
brimonidine(α2

140
Q

What are the different side effects of glaucoma?

A

Mydriasis (α1 ); do not use in closed-angle glaucoma
Blurry vision,
Ocular hyperemia

foreign body sensation,
ocular allergic reactions
ocular pruritus

141
Q

How does Prostaglandins treat Glaucoma?

A

Increased outflow of aqueous humor via resistance of flow through uveoscleral pathway

142
Q

What are the side effects of glaucoma?

A

Darkens color of iris (browning)
eyelash growth

143
Q

How does Cholinomimetics (M3 ) work?

A

Increased outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

144
Q

What are the side effects of Cholinomimetics (M3 )?

A

Miosis (contraction of pupillary sphincter muscles)

And cyclospasm (contraction of ciliary muscle)

145
Q

Name the Cholinomimetic given in glaucoma

A

Direct: pilocarpine, carbachol

Indirect: physostigmine, echothiophate

146
Q

Important rules of Anesthesia:

A

Best anesthetic drug is CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.

Drugs with decrease solubility in blood = rapid induction and recovery times.
Drugs with increased solubility in lipids = increased potency.

147
Q

What are the different inhaled anesthetics? DHIMES

A

Desflurane
halothane
isoflurane
methoxyflurane
enflurane,
sevoflurane
N2O

148
Q

What are the different “EFFECTS” of inhaled anesthetics?

A

Myocardial depression
respiratory depression
postoperative nausea/vomiting

Increased cerebral blood flow and ICP
Decrease Cerebral metabolic demand

149
Q

What are the side effects of Inhaled anesthetics?

A

Hepatotoxicity (halothane)
nephrotoxicity (methoxyflurane)

proconvulsant (enflurane, epileptogenic), expansion of trapped gas in a body cavity (N2 O).

150
Q

How Malignant hyperthermia occur?

A

Mutations in ryanodine receptor (RYR1) cause increasedCa2+ release from sarcoplasmic reticulum.

151
Q

What are the different IV anesthetics?

A

Thiopental
Midazolam
Propofol
Ketamine

152
Q

Name the IV antiepileptic used in anesthesia induction

A

Thiopental
Midazolam
Propofol

153
Q

What are the IV anesthetics Facilitates GABA (A)?

A

Thiopental
Midazolam
Propofol

154
Q

What is the MOA of ketamine?

A

NMDA receptor antagonist

155
Q

What IV anesthetics used in ICU sedation?

A

Propofol

156
Q

Name the IV anesthetic lead to Dissociative anesthesia

A

Sympathomimetic
Ketamine

157
Q

What are the side effects of ketamine?

A

Increased cerebral blood flow
Emergence reaction possible with disorientation
hallucination
vivid dreams

158
Q

What are the side effects of Thiopental?

A

Decrease cerebral blood flow
High lipid solubility
Effect terminated by rapid redistribution into tissue, fat

159
Q

Name the different local anesthetics

A

Esters
procaine, tetracaine, benzocaine, chloroprocaine

Amides
lidocaine, mepivacaine, bupivacaine, ropivacaine, prilocaine

160
Q

How the sensitivity loss after using local anesthetics?

A

Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure.

161
Q

What are the different side effects of local anesthetics?

A

CNS excitation
severe cardiovascular toxicity (bupivacaine), hypertension, hypotension

arrhythmias (cocaine)
methemoglobinemia (benzocaine, prilocaine

162
Q

How vasoconstrictor (epinephrine) enhance action of local anesthetics?

A

vasoconstrictors (usually epinephrine) to enhance block duration of action by decrease systemic absorption.

163
Q

How does Mannitol work?

A

It increases serum osmolality by shift fluid from interstitium to intravascular space which result in increased urine volume and decrease intraocular as well as intracranial pressure

164
Q

What are the clinical uses of mannitol?

A

Drug overdose,
elevated intracranial/intraocular pressure.

165
Q

What are the side effects and contraindications of mannitol?

A

Dehydration
hypo- or hypernatremia
pulmonary edema
Contraindicated in anuria, HF.

166
Q

What are the clinical uses of Acetazolamide?

A

Glaucoma
Metabolic alkalosis

altitude sickness (by offsetting respiratory alkalosis)
idiopathic intracranial hypertension.

167
Q

What are the various side effects of Acetazolamide?

A

Proximal renal tubular acidosis (type 2 RTA), paresthesias
NH3 toxicity and sulfa allergy

hypokalemia
Promotes calcium phosphate stone formation (insoluble at high pH)

168
Q

Name the various Loop diuretics

A

Sulfonamide containing Furosemide, bumetanide and torsemide

Nonsulfonamide containing Ethacrynic acid (but more ototoxic)

169
Q

What are the various outcomes of loop diuretics?

A

Abolish hypertonicity of medulla, preventing concentration of urine.
Associated with increased PGE (vasodilatory effect on afferent arteriole)
Increased calcium excretion

170
Q

What are the clinical uses of Loop diuretics?

A

Edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema).
Hypertension, hypercalcemia

171
Q

What are the various side effects of loop diuretics?
H AND GOA

A

Hypokalemia, Hypomagnesemia

metabolic Alkalosis,
Nephritis (interstitial
Dehydration

Gout
Ototoxicity
Allergy (sulfa)

172
Q

Name the various thiazide diuretics

A

Hydrochlorothiazide
chlorthalidone
metolazone.

173
Q

What are the clinical uses of Thiazide?

A

Hypertension
HF
idiopathic hypercalciuria

Nephrogenic diabetes insipidus
osteoporosis

174
Q

What are the various side effects of Thiazide?

A

Hypokalemic metabolic alkalosis
Hyponatremia

hyperglycemia
hyperlipidemia

hyperuricemia
hypercalcemia
Sulfa allergy.

175
Q

Name the various Potassium-sparing diuretics
SEAT

A

Spironolactone
Eplerenone
Amiloride
Triamterene

176
Q

What are the different MOA of Potassium sparing diuretics?

A

Spironolactone and Eplerenone block aldosterone receptor in CCT
Triamterene and amiloride block Na+ channels at the same part of the tubule.

177
Q

What are the clinical uses of Potassium sparing diuretics?

A

Hyperaldosteronism
K+ depletion
HF
hepatic ascites (spironolactone)
nephrogenic DI (amiloride)
antiandrogen (spironolactone)

178
Q

What are the various side effects of Potassium sparing diuretics?

A

Hyperkalemia (can lead to arrhythmias)
Endocrine effects with spironolactone (eg, gynecomastia, antiandrogen effects)
metabolic acidosis

179
Q

How do Thiazide and Loop diuretics lead to alkalosis?

A

1) Volume contraction–> increased AT-II which enhancd Na+/H+ exchange in PCT result increased HCO3 reabsorption (“contraction alkalosis”)

2) k+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells

3) In low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule–> alkalosis and “paradoxical aciduria”

180
Q

What is the mechanism of action of Aliskiren?
.

A

Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I.

Relatively contraindicated in patients already taking ACE inhibitors or ARBs and contraindicated in pregnancy

181
Q

Name the medicine which causes serotonin syndrome

A

Psychiatric drugs:
MAO inhibitors, SSRIs, SNRIs, TCAs, vilazodone, vortioxetine, buspirone

Nonpsychiatric drugs:
tramadol, ondansetron, triptans, linezolid, MDMA, dextromethorphan, meperidine, St. John’s wort

182
Q

How to treat serotonin syndrome?

A

1) Benzodiazepines and supportive care
2) Cyproheptadine (5-HT2 receptor antagonist) if no improvement

183
Q

Name the medicine which causes dystonia

A

Typical antipsychotic
anticonvulsants (eg, carbamazepine) metoclopramide

184
Q

What are the medicine which treat dystonia?

A

Benztropine or diphenhydramine

PHARMA (2 decks)

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