Pharmacology Flashcards
ACEI is the 1st line drug for DM & HTN, explain how it works. (2)
When should you not prescribe ACEI? (3) What should be prescribed for pregnant women with HTN? (4)
Why sometime ARB is used instead of ACEI? (2)
High ACE = High A2 & Low bradykinin
ACEI (-pril) reverse this.
Less A2 for v.c. & ALDO action (NA in K out) & ADH stimulation
» Hypotension, RF, Low NA, High K, Acidosis
More bradykinin for bronchoconstriction & v.d. with increased permeability
» Dry cough, angioedema
Contraindication:
1. Pregnancy
2. Sulfur Allergy
3. Angioedema
For pregnant women with HTN, give HMLN
Hydralazine
Methyldopa
labetalol
Nifedipine
ARB (-sartan):
ARB is an AT1 blocker
ACE is not affected, so still Low bradykinin.
bradykinin related Dry cough & angioedema will not occur.
What are the 3 types of IHA? How to diagnose it? (2)
- AIHA (IgM[Anti-I/P], IgG[SLE])
- DIIHA (Penicillin, Methyldopa, Quinidine)
- AlloAb
Penicillin: BPO mimic RBC Ag, trigger IgG against it
Methyldopa: Change Rh shape, trigger IgG against it
Quinidine ([S]BPC): Quinidine binds IgM, C’»_space; MAC on RBC
Labs of hemolytic anaemia (Hb Low, MCV[RETIC] & LDH & DB High), DAT+
briefly describe sympathetic & parasympathetic drugs, in terms of the neurotransmitter involved & the receptors of those neurotransmitters. (2)
Based on the physiology, name 4 anticholinergic for symptoms related to heart, lung, GI & Bladder respectively. (4)
Name 2 direct muscarinic agonist for glands & Bladder, and 2 indirect muscarinic agonist for muscle weakness & Alzheimer’s disease. (4)
neurotransmitter: NE vs ACh
receptor: alpha & beta vs N & M
M receptor:
M1,4,5 at CNS
M2 at heart
M3 at Urinary / GI tract, Glands, Eye, Lung
anticholinergic:
Atropine for bradycardia
Ipratropium for Asthma/COPD
Dicyclomine for IBS
Oxybutynin for overactive bladder
direct M agonist:
Pilocarpine for Sjogren’s syndrome & CF diagnosis
Bethanechol for urinary retention
indirect M agonist (anticholinesterase):
Pyridostigmine for myasthenia gravis (Anti-Ach R)
Donepezil for Alzheimer’s disease
Diuretics? (5)
How to know which drug is prescribed based on K, HCO3, CA, pH? (4)
Why we use some diuretic to treat SALI toxicity historically? (1)
- Loop (-ide)
- Thiazide
- K-sparing (spironolactone)
- Carbonic anhydrase I
-H2CO3»_space; HCO3 (reabsorb) & H+ (excrete, CL follows, NA reabsorb) - Mannitol
High K = K-sparing
Low HCO3 = Carbonic anhydrase I
High CA = Thiazide ; Low CA = Loop
High pH = Thiazide & Loop (ALDO compensation)
Low pH = K-sparing (ALDO) & Carbonic anhydrase I (»Type2 RTA)
SALI is an acid, alkaline urine favors its excretion, Carbonic anhydrase I acidify blood & alkalized urine.
For sympathetic drugs, describe the receptors involved & outline the classification. (4)
State the use of phenylephrine, midodrine, methyldopa. (3)
What is the difference between dobutamine & albuterol? (1) Name an analyte that should be monitored when albuterol / beta-blockers is prescribed. (1) How about digoxin? (1)
Why Theophylline can be used to treat asthma? (1)
When is E & NE indicated? When should E instead of NE be used? (2)
Alpha 1 (Gq»_space; Ca2+)
1. stimulate v.c. & sphincter contraction
2. inhibit renin release
Alpha 2
1. Anti-sympathetic
2. inhibit insulin release
3. stimulate PLT aggregation
Beta 1 (Gs»_space; cAMP)
1. Increase HR & SV
2. stimulate v.d. of coronary artery
3. increase renin release
4. inhibit PLT aggregation
Beta 2
1. bronchodilation (2 lungs)
2. Tocolysis (uteral muscle relaxation)
3. smooth muscle cell K uptake (hypokalemia)
phenylephrine is alpha 1 agonist for nasal congestion
midodrine is alpha 1 agonist for hypotension
methyldopa is alpha 2 agonist for hypertension
dobutamine & albuterol are both beta agonist, but dobutamine acts on beta 1 (heart, CHF) & albuterol acts on beta 2 (lung, Asthma)
beta 2 agonist like albuterol causes HypoK, beta blockers causes HyperK. Digoxin causes HyperK
Theophylline is a PDE I. The accumulation of cAMP mimics beta 2 agonist in causing bronchodilation.
E & NE: adjunct to local anesthetic, shock
E only: asthma, as E also acts on beta 2
Patient faint after taking nitrates for , name 1 possible reason. (1)
He is taking sildenafil (PDE5 I), which causes vasodilation & exacerbate hypotension caused by nitrates.
Based on neuron physiology, explain why metyrosine is used in pheochromocytoma, Reserpine is used in hypertension, amphetamine is illegal, TCA & MAOI & Cocaine works in depression. How SSRI differ from TCA? (1)
metyrosine inhibit enzyme converting tyrosine to dopa.
Reserpine inhibit VMAT, NE is metabolized by MAO before release
amphetamine stimuate release of neurotransmitter, including NE & Dopamine, causing euphoria & subsequent reliance.
TCA & Cocaine are reuptake inhibitor.
SSRI inhibit serotonin reuptake only, while TCA is serotonin + NE, MAOI is serotonin + NE + Dopamine.
What is the difference between phentolamine & phenoxybenzamine, prazocin & tamsulocin? (1)
Why don’t you give beta blockers first for pheochromocytoma & asthma patient? (1)
Name an antidote of beta blockers. (1)
Both are alpha antagonist for pheochromocytoma, but phenoxybenzamine effect is irriversible
Both are alpha 1 antagonist for BPH, but tamsulocin has no effect on HTN.
NE excess in pheochromocytoma acts on alpha & beta R. All NE goes to alpha if beta blocker is used, causing serious hypertension. beta 2 is for bronchodilation, so beta blocker is a bad idea for patient with asthma
Glucagon, it raises cAMP (like beta agonist & PDE I)
What is the common property of the drugs requiring TDM? (1)
Name 4 drugs. (4)
They have low therapeutic index.
Phenytoin, Digoxin, theophylline, Warfarin (by INR)
What is Cephalosporin? (1)
Give the drug names of the 5 generations of Cephalosporin. (5)
Cephalosporin is an antibiotic acts by cell wall destruction (Gram+)
1st: Cefazolin, Cefalexin (Skin)
2nd: others (Abdominal [anaerobic])
3rd: Ceftriaxone, Cefotaxime (Lung)
4th: Cefepime (Serious infection / FUO, Pseudomonas)
5th: Ceftaroline (MRSA)
What are the 10 classes of antibiotics? (10)
Antibiotic Can Terminate Protein Synthesis For Microbial Cells Like Germs.
Aminoglycoside: 30s ribosome, (-), sepsis, -mycin
Cephalosporin: beta-lactam, Cef-
Tetracycline: 30s ribosome, STI, -cycline
Penicillin: beta-lactam, Skin, -cillin
Sulfonamide: inhibit folate synthesis, UTI, Sulfa-
Fluoroquinolone: inhibit DNA replication (topoisomerase), -floxacin
Macrolide: 50s ribosome, (+), Lung, -thromycin
Carbapenem: beta-lactam, UTI, -penem
Lincosamide: 50s ribosome, (+), Lung, Clindamycin
Glycopeptide: beta-lactam, (+), Vancomycin
MALT = Protein
Dopamine and dobutamine are both sympathomimetic for CHF, what are the 2 key differences between them?
- Dopamine increases BP
- Dopamine increases kidney perfusion
Can Antiarrhythmic Drugs treat arrhythmia with slow heat rate? (1)
No.
All Antiarrhythmic Drugs try to resume cardiac rhythm by slowing down heart rate, so they have no use if the arrhythmia itself is caused by bradycardia
Explain how Antipsychotics drugs affect mesolimbic, mesocortical, nigrostriatal, & tuberoinfundibular pathway in the brain. (4)
Why 2nd generation antipsychotics lower the risk of EPS? (1)
Give 4 symptoms of EPS. (4)
What is NMS? (1) Name a condition that require monitoring by CBC. (1)
Antipsychotics drugs decreases dopamine release in brain, treating schizophrenia
mesolimbic: low dopamine lowers hallucination
mesocortical: low dopamine worsen lost of emotion
nigrostriatal: low dopamine causes EPS
tuberoinfundibular: low dopamine causes high prolactin (risperidone)
2nd generation antipsychotics has 5HT2a inhibition, such that dopamine stimulation is greater than therapeutic but lower than toxic level that can lead to EPS.
EPS
1. dystonia (anti-cholinergic)
2. parkinsonism (anti-cholinergic)
3. akathesia (beta-blocker)
4. tardive dyskinesia
Neuroleptic malignant syndrome (NMS) is a severe form of EPS that progresses to rhabdomyolysis
agranulocytosis by clozapine
What is lithium used for ? (1)
bipolar disorder (cycles of mania & depression)
