PHARMACO LECTURE DRUGS/OTHER RANDOM DRUGS MENTIONNED

NAME WHAT IT IS/DOES WHEN TO USE + other things WHICH

LECTURE
Salbutamol Short acting B2 agonist
(bronchodil, clear mucus,
decrease capi leak)

Acute,
Exercise
Asthma
Salmeterol
Formeterol

Long acting B2 agonist
(bronchodil, clear mucus,
decrease capi leak)
Nightime,
Moderate severe asthma
Asthma
Budesonide
Flunisolide
Short acting corticosteroids
(less side effecs)
Asthma
-Better Fev1
-Potentiate b2 ago response
Asthma
Betamethasone
Dexamethasone
Long acting corticosteroids Asthma
-Better Fev1
-Potentiate b2 ago response
-More use nightime??
Asthma
Montelukast

Leukotriene antagonist
(LTD4 antago)

(Also zileuton (5lipooxigenase
block) and zafilurkast (cyst Lt
recept block)-less useful)

-ASA asthma
-(cold air, exercise)
-Decrease use of steroids
Asthma
Theophylline Methylxanthine
(bronchodilates, decrease mast
cell degranulation, increase
diaphragm cntility)
In severe/hospital cases
In nocturnal asthma not responding
to long action cortices

DANGEROUS, SMALL TI
Asthma
Sodium cromoglycate +
necrodomil
Inhib mast cell degranulation -Cold air asthma
-Exercise asthma
-Doesnt decrease use of corticos
Asthma
Ipratropium Blocks mAch receptors -Beta blockers asthma
(cant use beta ago because less
affinity)
-Severe asthma+copd
Asthma
Gefinitib/ erlotinib Anti-tyro kinase Lung carcinomas with EGFR
mutations
Pulmo/pleur
al/mediast
neos
Critozinib I dont know Lung adenocarcinoma with ALK
mutation
Pulmo/pleur
al/mediast
neos
Neostigmine Ach Esterase inhibitors
(increases Ach)
General uses:
-Glaucoma
-Myasth gravis
-Paroxysmal supraventricular
tachycardia
-Alzheimer
-Paralytic ileus
-terminating the effects of NMJ-
blocking drugs used in anaesthesia.
PNS
pharmacolog
y
Pralidoxime Ach esterase REACTIVATOR

(IV. Works on skel muscles but
not cns?)
Used in combination with atropine
to treat intoxication with
organophosphorus (ach esterase
inhibitors)
PNS
pharmacolog
y
Atropine Muscarinic antagonist
(to all M subtypes)
Blocks resp secretions
Blocks GI motility
Tx of AV block (increases HR and
contractility)
Pupil dilation (opht exam)
Antidote to organophosphorus
PNS
pharmacolog
y
Phygostigmine Ach Esterase inhibitors
(increases Ach)
Tx of atropine poisoning PNS
pharmacolog
y
Scopolamine Muscarinic agonist Transdermal use in motion sickness
Drops for eye dilatation
Peptic ulcer
PNS
pharmacolog
y
Isoproterenol Adrenoreceptor agonist for B1
and B2
Cardiac stimulation
Vasodilation
PNS
pharmacolog
y
Phenylephedrine Adrenoreceptor agonist for a1 (a
bit of a2 too)
Increase periph arterial resistance,
decreases venous capacitance

Decongestionant (local
vasoconstriction)

-Can be used in acute hypotensive
emergency

-Pupil dilatation
PNS
pharmacolog
y
Clonidine Adrenoreceptor agonist
For a2 (a bit a1 too)
Local vasoconstriction action, but
acts on centers in brain so ultimately
has anti-HTA effects
PNS
pharmacolog
y
Amphetamines Adrenoreceptor agonist for a and
B receptors
PNS
pharmacolog
y
Pseudoephedrine Adrenoreceptor agonist for a and
B receptors
Has indirect action of NE release
from synapse
Nasal decongestion
(local vasoconstriction)
PNS
pharmacolog
y
Epinephrine Adrenoreceptor agonist for all a
and B receptors
Will stimulate the heart (cntility and
rate).
Vasoconstriction and
dilatation at same time.
-Can be used in surgery for local
vasoconstriction
-Used in anaphylaxis
PNS
pharmacolog
y
Norepinephrine Adrenoreceptor agonist for all
(a1, a2, B1) except B2.
Cardiac stimulation (hr, cntility) and
vasoconstriction
-Can be used in acute hypotensive
emergency
-Can be used in shock + MI
PNS
pharmacolog
y
Prasozin a1 antagonist
and mixed venous-arteriolar
vasodilator
-Anti-HTA (more in erect than
supine position)
-Also used in heart failure
-Syncope can occur w/ 1
st
doses
-Benign prostatic hyperplasia
(increases tone of smooth muscles in
bladder neck)
PNS
pharmacolog
y AND
Anti HTA,
vasodilators
Propranolol B1 and B2 antagonist Anti-HTA because:
1) B1 effect on heart
(decrease CO so decrease BP)
2) CNS action
3) Decreases renin release

Anti Angina because:
1) Decrease HR/CO
2)Decreases BP
3) Decrease cntility
=Decrease o2 demand.
Arrhythmia
Migraines
PNS
pharmacolog
y
Oxoprenolol Beta inverse agonist Blocks baseline activity of beta
receptors
PNS
pharmacolog
y
MAO inhibitors Increase cathecolamines Effect= increase thyramine
(precursor for cathecos I think) and
so increase BP
PNS
pharmacolog
y
L-Dopa Dopaminergic agonist -Used in Parkinson but side effects
b/c dopa is precursor to
catecholamines (will increase BP,
give nausea)
PNS
pharmacolog
y
Benzothiadiazines

1)Hydrochlorothiazide
(12h. HTA and heart
failure)

2) Indapamide
(used for HTA because
effect on arteriolar
smooth muscles more
than diuretic)

3)Metolazone (thiazide
like)
Thiazides-

Act in early distal tubule (On Na
and Cl transport)
-Better to use in HTA vs loop.
-Paradoxical use in Db insipidus
-HypercalciURIA (not emia).

Consequence:
increase Na delivery to distal Na/K
exchanger, you excrete more K:
hypokalemia.

Side effects =
1) fluid and e- imbalance (decrease
na, k, cl) metabo alkalosis, hypovol.
2) HyperSn rxns.
3) Metabo(hyperuricemia,
hyperglycemia, hypercalcemia)
Diuretics
Furosemide

*Broader dose response
curve and causes fewer
GI side effect than
ethacrynic acid. So its
more used.
Loop diuretic
(sulphonamide)
-Inhibits Na and Cl reabs in the
TAL

Side effects:
-Max doses can cause 1/3 body
fluids loss + hypotens
-Fluid and e- imbalance
-Ototoxicity (high doses in renal
failure)
-Hyperuricemia, hyperglycemia
-Hypersn rxns
-Effective diuretics even if decreased
GFR, hypoNa or acid base
imbalances.
-Shift of intrarenal blood flow from
juxtamedullary to cortical nephrons.
-Relaxes capacitance vessels (can
decrease cardiac preload so
decrease pulmo edema)
-Give w/ saline to get rid of
hypercalcemia.
Diuretics
Ethacrynic acid Loop diuretic

-Inhibits Na and Cl reabs in the
TAL
Same as furosemide Diuretics
Aldosterone
antagonists:

Spironolactone

Triamterene

Amiloride
K sparing diuretics

Spirono: comp antago of Na
reabsorption mediated by
aldosterone in CD

Triamterene: inhib of Na-(H,K)
exchange but indep of
aldosterone
To prevent or correct hypoK caused
by other diuretics
-Spiro: hepatic failure
Side effects:
All 3 have hyperkalemia and GI
upset. Spironolactone can also give
gynecomastia.
Diuretics
Mannitol, glucose,
sucrose
Osmotic diuretics
(urea and glucose must exceed
Tm values to be effective.
Mannitol and sucrose are just not
reabsorbed).
-Used in cerebral edema
Side effect: all osmotic diuretic can
increase plasma osmotic pressure
and cause plasma vol expansion.
-Can exaggerate heart failure
-HypoK, hypoNa if no diuresis,
HyperNa is inadequate h2o
replacement after diuresis.
Diuretics
Acetazolamide Acidifying diuretics

Acts on PT Inhib carbo
anhydrase= less H+ made. Less
H+ out = less Na in. More nahco3
out and more Cl in.
-Not used as diuretic alone
-Used in glaucoma and Urine
alkalinisation
-Used in altitude sickness
-Used in salicylates intoxication
because alkalinizes urine and help
excrete them.

Side effect: metabolic acidosis.
Diuretics
Bile acids sequestering
resins (cholestyramine)
Acts on bile acids.
-Increases LDL receptors in the
liver (more cholest uptake = less
in circulation)

-Reduces LDL by 10-30%



Used in hypercholesterolemia and
diarrhea (used mostly for this)

Side effect: unpleasant taste,
constipation, GI pbs, interferes w/
abs of many drugs.
Hyperlipide
mia drugs
Nicotinic acid (natural B
vitamin)
-Increases HDL,
-Decreases LDL
-Decreases triglycerides
Hypercholesterolemia and
hypertriglyceridemia

Side effects: flushing, gastric
irritation, hyperglycemia.
Hyperlipide
mia drugs
Fibrates -Decrease adipose tissue lipolysis
-Reduces triglycerides
-Increases HDL
Hypercholesterolemia and
hypertriglyceridemia.
Hyperlipide
mia drugs
HMG-CoA reductase
inhibitors = STATINS
-Elimin rate-lim step in
cholesterol synthesis
= Decreases LDL
-Increases LDL receptors
-Increase HDL a bit ???
-Lowers LDL up to 50%

Side effects: myositis, hepatitis
Hyperlipide
mia drugs
Ezetimibe Cholesterol absorption inhibition Hyperlipide
mia drugs
Arterial vasodilators

(In tx are usually
combined w/ B
-Decrease afterload (decreases TPR)
-Increases preload (lack of venous dilation)
-Increased CO (increase preload, decrease afterload, symp comp
mechanism increase HR and SV)
Anti
HTA+vasodil
ators
BLOCKERS and
DIURETICS to
compensate for other
effects)
-Decrease TPR will decrease BP: symp comp mechanism = increase HR,
SV and symp tone on arterioles and venules. Still overall BP decrease.
-Reflex cardiac stimul may precipitate angina or infarct!!*Use B block
-Renal effects: favors juxtamedull nephrons (more na retention), RAA
stimulation. NA and water retention: will antago the BP lowering effects.
Hydralazine Arteriolar vasodilator -Effective anti-HTA
-Short T1/2, long duration
Side effects:
-Salt and water retention
-lupus at high doses
Anti
HTA+vasodil
ators
Minoxidil Arteriolar vasodilator -Powerful and orally effective
Side effects:
-Salt and water retention
-Palpitations, cardioacceleration
-Hirsutism with prolonged therapy


Anti
HTA+vasodil
ators
Diazoxide Arteriolar vasodilator -Powerful thiazide (NON diuretic)
-Hypertensive emergencies
-Salt and water retention
-Palpitations and cardioacceleration
-Hirsutism and hyperglycemia
Anti
HTA+vasodil
ators
Venous vasodilators Decreases preload,
Decrease CO.
Anti HTA,
vasodilators
Nitrates and nitrites Prodrugs that liberate NO when
metabolized.
No stimulates guanylyl cyclase---
increases GMP---Causes vascular
smooth muscle relaxation

-1
st
pass effect if P.O. better on
skin and mucous membranes.

-Some last 30-60 mins, some 6
hours.

-Can give headaches, palpits,
flushing, syncope.
-Decreases preload (decreases LV
wall tension and o2 requirements)
-Decreases TPR+BP ( so there is also
symp reflex activity (increases HR,
SV, tone). Decreases afterload
(decreases LV wall tension and o2
reqs here too).
-Dilation of large epicardial
conductive vessels and collats
(enhances flow to ischemic areas)

So used in:
-Angina pectoris
-Preservation of myocardium after
infarction
-Control hypotension
-Heart failure.
Anti HTA,
vasodilators
Nitroprusside Mixed arteriolar-venular dilators
(there is also prasozin in this
categorie)
-Used IV for hypertensive
emergencies
-Metabolized to SNC(?)-can
accumulate and cause toxicity if
renal failure
Anti HTA,
vasodilators
CALCIUM CHANNEL
BLOCKERS
-more vascu effect=
Nifedipine
-Intermediate=
diltiazem
-More electrophysiol
effects= Verapamil
-Impair E-C coupling in cardiac
and vascular SM
-Dilate coronaries and periph
arterioles
-Decrease cardiac contractility
Use in:
-Coronary heart disease
-Hypertension
-Vasospastic disorder
-Supraventricular
tachydysrhythmias

Side effects: hypoTA, conduction
Anti HTA,
vasodilators

defects, ankle swelling, flushing,
headaches.
ACE INHIBITORS
(ends in PRIL).
Ex: captopril, enalapril
-No AngII, no bradykinin
degradation
-Lowers TPR and BP
Used in
-Hypertension
-Heart failure
-Diabetic kidney disease
Side effects:
-Hypotension, angioedema, cough
(bradykinins), taste disturbance.
Anti HTA,
vasodilators
ANG II BLOCKERS
(startans ending)
-Block AT1 receptor subtype,
effects are similar to ACE
inhibitors (but no cough)
-Hypertension, heart failure and
diabetic kidney disease used too.
Anti HTA,
vasodilators
Quinidine Class Ia antiarrhythmic
-Na blocking
-K blocking
-Decreases V in N and diseased
tissues
-Decreases ventricular
automaticity
-Increase APD
-Decreases number of premature
complexes
-Prevents re-entry
-Suppresses atrial re-entry

Fast channel blocking effects:
-Less extrasystole
-Slows ventricular tachycardia
-Can suppress DAD arrhythmia (INa
suppr)

Adverse effect: long QRS, LONG QT
(especially in Ia), pro-arrhythmia
Anti-
arrhythmics


Lidocaine Class Ib antiarrhythmic
-Blocks Na only
-Decreases V in diseases tissue
-Decreases APD
-Decrease ventricular
automaticity
Fast channel blocking effects:
-Less extrasystole
-Slows ventricular tachycardia
-Can suppress DAD arrhythmia (INa
suppr)

Adverse effect: LONG QT, pro-
arrhythmia (Not as much as Ia and
Ic)
Anti-
arrhythmics

Flecainide Class Ic antiarrhythmic
-Blocks Na and a bit of K
-Decreases V really well
-Decreases ventricular
automacity
-Increases ADP
-Unbinds slowly
Fast channel blocking effects:
-Less extrasystole
-Slows ventricular tachycardia
-Can suppress DAD arrhythmia (INa
suppr)
-Suppresses atrial re-entry

Adverse effect: Long QRS, LONG QT,
pro-arrhythmia

Anti-
arrhythmics

Class III drugs
-Amiodarone
-Sotalol
-Bretylium
-Dofetilide
Class III anti-arrhythmics
-Blocks K, increases APD
-Also have anti-symp effects
(except dofetilide)= blocks slow
tissue re-entry

*Amiodarone has class I (Na), II
(Ca), III (K) actions = most
effective drug
Blocking re-entry

Adverse effects:
Long QT (=more EADS, ventricular
arrhythmia risk)
Sinus bradi, AV block risk
Hypotension
Anti-
arrhythmics

I skipped all the
anticoagulant drugs

Imatinib Block the action of the fusion
protein BCR-ABL
For chronic myeloid leukemia
-Needs to be taken all life long
because not curative
Clinical
hemato
Beta 2 agonist:
-Ritodrine
-Terbutaline
-Salbutamol


(not that much used)
Alpha receptor in the uterus are
excitatory and beta are
inhibitory, so blocking them
blocks contractions Mediated
by cAMP
To prevent pre term delivery

*Lots of side effects-
-Will cause vasodilation too, so
hypotension, this will cause
compensatory increase in HR, SV,
BP. Can even cause arrhythmia. Can
cause pulmonary edema.
-Will cause increase glycemia
-Shits in serum K (correts itself with
time)
-Fetal tachycardia
Drug for
growth and
labour and
post partum
Synthetic oxytocin -To induce labour
-Post delivery (along w/
ergonovine) to prevent post partum
bleeding
-For oxytocin challenge test to
assess urteroplacental insufficiency

*Safe except for uterine
hyperstimulation that could lead to
fetal distress. Could also give water
intoxication if admin in large doses
with electrolyte-free solution.
Drug for
growth and
labour and
post partum
Inhibitors of
prostanglandin
synthesis
Delay onset or prolong spontaneous
labour
Drug for
growth and
labour and
post partum
Magnesium sulfate Unknown mechanism of action,
prob competes w/ calcium

-Need IV 4-8mEq/L
Prevent seizure asso w/ pre
eclampsia

Can also inhibit uterine contractions

*Side effects: transient
hypotension+flushing with bolus
dose
*Over 12-15 mEq, can give resp
depression and cardiac conduction
defect, but this isnt the therapeutic
range
Drug for
growth and
labour and
post partum
Prostaglandins E2 and
F2a


-Its the best drug to induce labour
in early months of pregnancy
(therapeutic abortions)
-Induction of labour at term too
-Helps with cervical ripening (local
E2 application)

*Side effects are GI: nausea,
vomiting, diarrhea.
Drug for
growth and
labour and
post partum
L thyroxine (T4) Thyroid hormone replacement T3 is given only for quick response Thyroid
L triiodothyronine (T3)
Liotrix (4:1 T4:T3)
1,6/kg or 100-150 mg / day
Elderly: start w/ 12-25 mg/day an
increase by 25 mg/day in 2-4
weeks.

Functions test 6 months later

Propythiouracil and
methimazole
Anti thyroid hormones

Drugs that inhib peroxidase
catalyzed step in thyroid
hormone synthesis

PTU inhibits conversion of T4 to
T3 in periphery and is more
bound to plasma prots than MMI
Used to counter hyperthyroidism

* Side effects: skin rash,
agranulocytosis

PTU: 100-200 mg BID or TID
MMI: 5-20 mg BID, decrease to DIE
when pt is euthyroid.

Early effects in 1-2 weeks, euthyroid
in 6-8 weeks.

When given for graves disease also
give a beta-blocker to control sx of
hyperthyroidism.



Tx for 12-24 months
Thyroid
Iodide Inhibits T3 T4 release
Decrease gland vascularity, size
Use preop before thyroid surgery

Effects starts in 24 h, peaks 10-15
day. Decrease with time

*Avoid in pregnancy, can cause fetal
goiter
Thyroid
Radioactive Iodine 131-I (t1/2 of 8 days) ---
antithyroid tx

and 123-I (T1/2 of 13 hours)---
For thyroid scans
To cause thyroid destruction by
radiation thyroiditis (leads to
fibrosis and atrophy)---used in
graves disease

4-6 months to be effective, may
need more than 1 tx. Could also lead
to hypothyroidms eventually.
Otherwise its safe.

There will be a release of t4, t3 from
thyroid in 10-14 days, so in older
patient they need to add a b blocker
(and thionamide??) to ctrl sx caused
by that.
Thyroid
Clomiphene citrate Infertility drug
-Inhibits the negative feedback of
estradiol on pituitary and
hypothalamus
How to use it:
-Give progestin 5 days, induce a
withdrawal bleed then use
clomiphene citrate:
1.Increase amount of drug will
preferentially increase FSH
2.Increase duration of giving drug
Infertility and
contraception
increases LH
3. Add hCg-Substitute for LH

Lh and Fsh will rise a bit, then we
stop the drug, they go down a bit
but surge back up. Means we
synchronized the hormones well.

Could be used in MALE infertility
too (off label used, tried by
physician sometimes)
Bromocriptine Anti-prl For prl secreting pituitary tumours Infertility and
contraception

Pituitary
adrenal axis
HCG Mimics LH Can help tx infertility in women and
in men
Infertility and
contraception
Gossypol Male contraceptive -Induces shedding of sperm from
seminiferous tubules
-Suppresses sperm production
-Reversibility depends on length of
exposure
-Irreversible in some men
-Hypokalemic effect

Side effect: muscle weakness

Trials: two deaths of heart condition
because hypokalemia.

Infertility and
contraception
Sildenafil When sexual stimulation cuases
local relase of NO, inhibition of
PDE5 by sildenafil causes
increased levels of cGMP in the
corpus cavernosum, resulting in
SM releaxion and inflow of blood
to corpus cavernosum.

Peripheral conditionner

Used to maintain an erection

Side effects:
headache, flushing, (the 2 most
common) dyspepsia, nasal
congestion

Other similar drugs:
TADALAFIL:
LONG half life (17 hrs). PDE5 selective. Still
clinical activity 24 hrs after dosing. Cialis =
the week-ender

VARDENAFIL:
T 1/5 is like 45 minutes.
Infertility and
contraception
PGe1, Vasointestinal
peptide

Peripheral initiator

(See notes for the central
drugsless imp I think)
Injected in penis to start erection Infertility and
contraception
Finasterdide : 5 alpha
reductase inhibitors
(Proscar or propecia)

Alpha adrenergic
blockers
For BPH-helps urinates Infertility and
contraception
In prostate cancer:
-Estrogen (DES)-but
causes gynecomastia.
-GnRH agonists +
androgen receptors
antagonists (flutamide)
(cyproterone acetate)
-GnRH antagonists
now the most used--
5alpha-reductase
inhibitors (prophylaxis
maybe)


Skipped chemo drugs
lecture.

Insuline-General Diabetes type I or advanced type
II
Doses:
Type 1: 0,6-0,7 units/kg/day
Type 2: 0,2-1 units/kg/day
(varies because some ppl still have
endogenous production)

CZI insuline Regular/fast actin insulin Regular (or CZI) insuline should be
given 30 minutes before meals

Intermediate insulin
(NPH)
Intermediate insuline (NPH): should
be given 30 mins to 1h before meals

Sulfonylureas Leads to decrease efflux of K and
increase influx of calcium. Leads
to secretions of insuline.
-Direct stimulation of insulin
secretion from the pancreas
-Reduces glucagon secretion
-Increases tissues sensitivity to
insulin b/c more receptors
-Reduced hepatic insulin
extraction

Predictors of good response:
-Obesity
-Onset over 40 y.o
-Onset since less than 5 years
-Insulin req under 40 units/day
TYPE II Db w/o contraindications
With prolonged used of this drug, the
serum insulin concentration tends to return
to pretreatment levels w/o a concomitant
increase in serum glucose concentration

Side effects:
-Reduction in glucagon
-Closure of K channels
in extrapancreatic tissue
*Cant be given if sulfas allergies
*Be careful in certain patients
because metabolized by liver and
kidney.
*No for patients that are pregnant,
breastfeeding, not in stress.
*Can induce hypoglycemia

Diabetes and
stuff
Metformin Inhibit neoglucogenesis Type II db

Side effects:
-Most common side effect = GI
-Rare side effect: lactic acidosis
(makes it CI in pts with renal
insufficiency, severe hepatic or
cardiovascu disease)
Diabetes and
stuff
Thiazolidinedione Ppar-gamma agonists
Decreases insulin resistance in
muscle, fat and liver
Side effects: weight can and liver
toxicity.
Do not used them with pregnant
pts, liver disease, heart failure pts
Rosiglitazone:
Diabetes and
stuff


Got a warning two years ago for myocardial
insufficiency and poss of heart attack. Has
been lifted since, but
not much used anymore.

Meglitinide Insuline secretagogue
Mechanism is similar to
sulfonylureas
-Modulate beta cell secretion of
insuline via K regulation. But no
direct effect on insuline secretion
(which sulfo have)
Fast onset

Caution in liver and kidney
insufficiency
Diabetes and
stuff
Nateglinide Insulin secretagogue

Acts via closure of atp sensitive K
channels
Doesnt give hypoglycemia and is
safe in patients with low renal
function
Diabetes and
stuff
Exenatide GLP-1 drug GLP-1, insulin secretagogue, inhibits
glucagon secretion, delays gastric
emptying; sc formulation

Diabetes
Sitagliptin GLP-1 drug Inhib synth of glp1
DPP-4 inhibitor, oral formulation

Diabetes
Alpha glucosidase
inhibitors
(acarbose, miglitol)
Competitive antagonist of a-
glucosidase in the intestines

Delays digestion of carbs
Not much used anymore

Has lots of GI side effects

Cant be given in inflammatory
bowel disease and in hepatic
diseases
Diabetes