SAQs Flashcards
5 mechanisms of microbial resistance
- Target site mod: PBP alteration on bacteria, dec affinity of drug for its target.
- Beta-lactamase enzyme: cleave B-lactam ring in penincillin, ceph, carbapenems
- Efflux pump: pump antibiotics before reaching target site (tetracycline)
- Transformation: Transfer of free DNA from dead bacteria w resistant gene & incorporate into its genome
- Transduction: transfer resistant DNA from virus to bacteria
- Conjugation: transfer genetic material btwn bacteria thru pills (E.coli)
MOA of insulin
Insulin binds to receptors on cell memb & activate glucose transporter (GLT-4) to translocate to of m. cell, liver cell, adipose tissue open the portal for transport of glucose from blood into cell. Therefore, decrease glucose in bloodstream. In:
m cell: use energy thru cellular resp -> ATP
adipose tissue: convert glucose -> fat for long term E
liver cell: glucose -> Glycogen.
Common AE of Insulin
Hypoglycemia (headache, dizziness, anxiety, tachy)
Hypotension
Lipodystrophy (fat accumulation on injection site)
List 3 diff btwn Sedatives and Hypnotics
- Sedative induce soothing, calm, reduce anxiety
Hypnotics induce sleep - Low dose of CNS Depressant -> sedation
High dose of CNS Depressant -> hypnotics - Sedatives have longer duration of action & extended period of time to manage anxiety.
Hypnotics have shorter duration of action to induce sleep & minimize hangover effect next day. - sedatives treat anxiety, hypnotics used for insomnia
5, sedatives act on limbic system & hypnotics act on midbrain & ascending RAS (reticular activating sys).
Antichlorgenic
-> examples
-> MOA
-> AE
Antichlogenic:
1) SAMA (Ipratropium)
↳ MOA: acts on M-3 receptors on lungs,
prevent acetylcholine binding, ↓ Ca2+
↓ bronchoconstriction
anti-inflammatory & Bronchodilation effect.
↳ AE: dry mouth, cough, bronchitis, GI, nausea
↳ CI: paenuts & soy
2) LAMA (Tiotropium)
↳ same MOA
↳ for COPD
↳ AE: dry mouth, cough, bronchitis, GI, nausea
↳ CI: paenuts & soy
Drug for acute relief of asthma:
> eg, duration & onset, MOA, AE
Beta blockers:
1) SABA (Salbutamol, Levabuterol)
↳ Onset & Duration: 4-6mins
↳ MOA: acts on B-2 receptors on lungs,
activate adenylate cyclase
↑ Cyclic AMP ↓ Ca2+
anti inflammatory & Bronchodilation effect.
↳ AE: Salbutamol (tremor, insomnia, UTI, headache, dizzy, vomit,,,)
Levabuterol (tachycardia, Hypotension, hypokalemia)
Drug for Noctural asthma
> drug class&Eg, Duration&onset, MOA, AE
LABA (Salmeterol, Formoterol)
↳ Onset: 10min Duration: 12hrs
↳ MOA: act on B-2 receptors, same mechanism as SABA but has Bronchodilation effect only, thus must be prescribed w an inhaled corticosteroids.
↳AE: headache, tremors, nasal congestion, dizziness, tachycardia, hypotension
Explain the relations of drug & Pregnancy in terms of Pharmacokinetics & Pharmacodynamics
Pharmacokinetics
↳ ↓ Absorption: ↓ Gastric emptying ↓ HCL,
vomiting -> ↓ absorption of oral drugs
↳ Distribution: ↑ blood volume & fat -> drugs are more dispersed & dec efficacy, ↓ plasma protein & albumin thus inc unbound free drugs
↳ Metabolism: ↓ CYP450 enzyme (CYP1A2&2C19)
drugs include-theophylline, clozapine, olanzapine
↳ Excretion: ↑ GFR ↑ Clearance of drug
(↑ clearance, ↑ dose)
Pharmacodynamics
↳ inc fetal sensitivity to tetratogen, mutagen, carcinogen
5 effects of drugs excretion on milk production
- Protein binding;
↑ protein bound drugs (ibuprofen) ↓ enter - Lipid solubility:
↑ lipid soluble drugs ↑ enter (opiods) - Molecular weight
↓ size, ↑ passage (eg, codeine)
↑ size , ↓ passage (eg, unfrationed Heparin) - Ionization
due to acidic environ, basic drugs ionized & get trapped, ↑ enter
(eg, codiene, barbiturates) - Maternal pharmacogenomics
some women sensitive to codiene -> CNS depression
Explain the DDI using the pharmacodynamics and pharmacokinetics concept w examples
pharmacodynamics:
1) direct interacton: 2 drugs act on same organ but have additive/antagonistic effect
↳ Warfarin + aspirin = inc bleeding risk
↳ CNS depressant = enhance drowsiness
↳ loop diuretics + thiazide diuretics = both promote diuretics but acts on diff locations (loop->loop of henle, thiazide->distal convoluted tubule) when used together= synergistic effect > inc diuresis -> hypokalemia & dehydration
2) Indirect interaction: one drug alter response of the other
↳ diuretics (dec K) -> inc toxic effect of digoxin & Amiodarone
↳ NSAIDs (inc Na&H2O -> dec effects of anti-hypertensives
pharmacokinetics:
A: metoclopramide inc gastric emptying
cholestyamine dec absorption
D: drug compete for plasma protein bounding to albumin, inc unbound drugs, inc risk AE
M: Induction of CYP enzyme ↑ met -> fail therapy
(carbamazepine, rif…, phenytoin, phenobarbitone)
Inhibition -> ↓met -> ↑ risk AE
(grapefruit juice, clari/erythromycin, cimetidine)
E: competition btwn drugs for excretory & efflux transporters (P-glycoprotein) in kidney.
Probenecid inhibit transporters secreting Penincillin, ciprofloxin, ↓ excretion & ↑ plasma protein
What is the standard first-line treatment regimen for H. pylori infection?
Triple therapy, which includes:
- two antibiotics (such as amoxicillin 1g and clarithromycin 500mg) + proton pump inhibitor (PPI) like omeprazole. This regimen is usually prescribed for 10 to 14 days to effectively eradicate the bacteria.
- if allergic to penincillin: metronidazole 400mg (2/day)
Clinical Case Scenario:
A 62-year-old female with a history of hypertension and type 2 diabetes presents with recurrent abdominal pain, especially after meals. An upper endoscopy reveals chronic gastritis, and biopsies confirm the presence of Helicobacter pylori. The patient has a documented allergy to penicillin.
Question:
What alternative treatment regimen for H. pylori should be considered for this patient, given her penicillin allergy?
For this patient with a penicillin allergy, an appropriate alternative treatment regimen for H. pylori would be quadruple therapy, which includes:
Tetracycline (antibiotic).
Metronidazole (antibiotic).
Bismuth subsalicylate (protective agent).
Proton Pump Inhibitor (PPI), such as omeprazole (to reduce stomach acid).
Compare Benzodiazepines & Barbiturates in terms of eg, use, MOA, AE
eg) Benzodiazepines: diazepam, lorazepam, clonazola, temazolam, midazolam, diazepam
Barbiturates: Phenobarbital, Pentobarbital, Secobarbital, Thiopental, Primidone
Use) Benz: hypnotics, m. relaxant
Bar: Seizure, sedation, insomnia, IV anesthesia.
MOA) Benzodiazepines-act on alpha&gamma subunits of GABA, increasing frequency of opening Cl- channels, rapid influx, hyperpolarization, dec neural excitatory signaling. Relieve stress
Barbiturates act on alpha&beta subunits of GABA, increasing duration of opening Cl- channels
AE) Be: dizziness, ataxia, diplopia, ADR withdrawal
Bar: sleep walking, hallucinations, sedation, resp. depression, high risk overdose
Case: A 35-year-old woman comes to the clinic complaining of anxiety and difficulty sleeping. She has no significant medical history and is currently not taking any medications. The physician prescribes lorazepam.
Question 1: What is the primary use of lorazepam in this case? Drug class?
Question 2: What is a common side effect she should be aware of when taking lorazepam?
Answer: A common side effect is dizziness, which can increase the risk of falls.
1: Benzodiazepine, Lorazepam is used as an anxiolytic to relieve anxiety and as a hypnotic to aid sleep.
2: A common side effect is dizziness, which can increase the risk of falls (Ataxia).
Case: A 42-year-old male with generalized anxiety disorder (GAD) is prescribed diazepam for acute anxiety relief. He has a history of alcohol use disorder but has been sober for six months. After several weeks, he reports increased anxiety and difficulty sleeping despite taking the medication as prescribed.
Question 1: Given the patient’s history of alcohol use disorder, what concerns should the healthcare provider have regarding the potential for developing dependence on diazepam, and what alternative strategies could be considered for managing his GAD?
Question 2: If the patient develops withdrawal symptoms upon discontinuation of diazepam, what would be the recommended approach to manage his withdrawal safely?
1: The healthcare provider should be concerned about the risk of developing psychological and physical dependence on diazepam, especially since both alcohol and benzodiazepines act as central nervous system depressants. Alternative strategies could include cognitive-behavioral therapy (CBT), selective serotonin reuptake inhibitors (SSRIs) for long-term management of GAD, or non-benzodiazepine anxiolytics like buspirone.
2: The recommended approach would be to gradually taper the dosage of diazepam rather than abrupt discontinuation to minimize withdrawal symptoms. The tapering schedule should be individualized based on the patient’s response, and adjunctive medications (e.g., SSRIs or non-benzodiazepine anxiolytics) might be introduced to help manage anxiety during the taper.
