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Terms in this set (283)
Clinical pharmacology encompasses
an understanding of how drugs work and their appropriate use in humans
What the body does to the drug. Includes processes of Absorption, Distribution, Localization on tissues, Biotransformation and Excretion.
Absorption Distribution Metabolism Excretion
Learning pharmacokinetics is of great practical importance in the choice and administration of a particular drug for a particular patient, e.g.
one with impaired renal function
What the drug does-its effects to the body, or an organ system. The term encompasses both MOE (mechanism of action) and END POINT (eg heart rate, blood pressure)
The actions of most drugs are mediated by
the binding and interaction of drug molecules with specific molecular substances located on the cell surface called RECEPTORS
The drug-receptor interaction leads to a molecular change in the receptor
which triggers a chain of events leading to a response
Receptors tend to be HIGHLY SPECIFIC
interacting with a limited number of structurally related molecules
Receptor interactions are like a LOCK and KEY eg
Ligand or G Protein mechanisms. AGONIST-RECEPTOR, AGONIST-RECEPTOR INTERACTION
DRUGS that activate a receptor response
DRUGS that block a receptor response
Actions on enzymes
Enzymes are biological catalysts. They speed up the chemical reactions and are not changed themselves.
Drugs that ALTER enzyme activity alter
PROCESSES catalyzed by the enzymes
Examples of drugs that alter enzyme activity
Cholinesterase inhibitors, Monoamine oxidase inhibitors
DRUGS THAT CHANGE CELL MEMBRANE PERMEABILITY
Blocks SODIUM channels
Blocks CALCIUM channels
Blocks POTASSIUM channels
OPENS POTASSIUM channels
COMBINING DRUGS WITH OTHER CHEMICALS
Examples of combination with other chemicals
Antacids, antiseptic effects of alcohol, phenol, Chelation of heavy metals
(medicine) the process of removing a heavy metal from the bloodstream by means of a chelate as in treating lead or mercury poisoning.
CHANGING PHYSICAL PROPERTIES
Mannitol, Changes osmotic balance across membranes, causes urine production (osmosis diuresis)
An osmotic diuretic is a type of diuretic that inhibits reabsorption of water and Na. They are pharmacologically inert substances.
Enter biochemical reactions in place of normal SUBSTRATE "Competitors".
Anti-metabolites result in
biologically inactive product
Examples of anti-metabolites
Some anti-neoplastics, Some anti-infectives
The magnitude of the effect following a drug-receptor interaction usually depends on the DOSE of the drug given.
Basically the AMOUNT of drug NECESSARY
to achieve a certain effect
More potent drug is the one that
requires LOWER dose to cause the SAME effect.
General rule from Gen Chem:
Like dissolves Like
Quickest route of absorption is
more water soluble
Lipophillics are are CONVERTED to
polar or water soluble ...so they can be excreted
Cytochrone P450 SUPERFAMILY (CYP) in liver
is a large and diverse group of enzymes that catalyze the oxidation of organic substances.
DOSE RESPONSE RELATIONSHIPS
Loading dose and Maintenance dose
Bolus of drug given initially to rapidly reach therapeutic levels.
Lower dose of drug given continuously or at regular intervals to maintain therapeutic levels
FACTORS ALTERING DRUG RESPONSES
Pediatric or geriatric, Immature or DECREASED HEPATIC, RENAL function
Big patients 'SPREAD' drug over a larger volume
Differences in sizes, Differences in fat/water distribution
Higher proportion of water
Lower plasma protein levels
There is more available drug, because protein is not binding to it.....think that is right!
Chronic disease states - decreased plasma protein binding - slower metabolism - slower excretion - dietary deficiencies - use of multiple medications - lack of compliance (forgetting to take meds etc)
...the study of mechanisms and factors associated with ADME..which is what the body does to the drug
ADMINISTRATION - ABSORPTION & DISTRIBUTION - ELIMINATION
Administered through CSF
Knowledge of drug pharmacokinetics
knowledge of ADME clarifies the relationships between dose, dose frequency, intensity of pharmacological effects, disease and adverse events
Orally administered drugs must be absorbed from the GUT (usually the upper small bowel, where the surface area is the greatest)
Not all of orally administered dose may enter the systemic circulation because of insufficient absorption, or because of metabolism in the gut wall or liver before the drug enters the systemic circulation
HEPATIC FIRST PASS METABOLISM
Affects orally administered drugs
Metabolism of drug by liver BEFORE drug
reaches systemic circulation
Drug absorbed into portal circulation MUST pass
through liver to reach systemic circulation
First Pass M. may reduce
availability of the drug
CAN YOU PASS THE FIRST PASS?
It is possible to avoid FPM by giving
drugs by other routes
SUBLINGUAL may occasionally be appropriate for NITRATES
Alternatively, the ORAL dose
can be increased appropriately
METHODS OF ABSORPTION
Diffusion through a lipid (cell membrane) - Diffusion through aqueous channel - With a carrier
For drugs to move through the body, they must move through cell membranes (lipid bilayers)
The simplest situation is a drug given intravenously that is distributed throughout the body via the blood stream
Following IV injection...
the drug passes through the lungs and heart, and then to dependent organs
Phase 1 and Phase 2 of Metabolism
Phase 1, medicine is changed to a more polar form, Phase 2, uses CONJUGATION in LIVER, then it becomes REALLY water soluble.
Consider Codeine and Cytochrome P450
Codeine is CONTRAINDICATED in renal disease...seem to be confused here!..something about CYP increasing..ah well..check this one later!
Organs and tissues with the greatest blood supply (eg brain, kidneys) are exposed to a greater amount of drug than those with a low blood supply
As a 'rule of thumb', the more lipophilic the drug, the more of it enters lipid-rich tissues; the less lipophilic the drug, the more remains in the plasma
The period during which a drug is distributed through body tissues
is termed the DISTRIBUTION PHASE
Metabolism converts lipophilic water INSOLUBLE NONPOLAR drugs into polar and water soluble products that can be easily excreted by the body
essentially - a DETOXIFYING process
Drugs are eliminated from the body by various processes, of which the most important are renal, biliary and (for volatile compounds such as anesthetics) respiratory. KIDNEY - LIVER - LUNGS
more on PHASE I and Phase II
Before elimination can occur, lipid-soluble drugs must be converted into more water-soluble compounds by processes known as PHASE I and PHASE II ENZYMATIC METABOLISM
The MOST important drug-metabolizing ENZYMES are
THREE FAMILIES of the cytochrome P450 SUPERFAMILY of HAEM Protein Enzyme Isoforms (CYP1A2, CYP2D6, and CYP3A4). These enzymes are responsible for the metabolism of a wide variety of drugs.
These enzymes are responsible for the metabolism of
a wide variety of drugs
BIOCHEM REVIEW: OIL RIG
Oxygen is LOSS of an electron, Reduction is GAIN of an electron
Phase one metabolism Biochem
DRUG + O2 + NADPH (and then, via CYP450) to DRUG (now polar), + H2O + NADP+
There are other NON-P450 Phase I rxns - eg
Alcohol dehydrogenase which breaks down alcohol and forms ACETYL ALDEHYDE - which then is broken down into ACETATE
Understanding CYP 34A
3 is the family (GRANDMOTHER) of drugs, A is the subfamily (MOTHER), 4 is the isoenzyme (DAUGHTER)
Isozymes (also known as isoenzymes or more generally as Multiple forms of enzymes) are enzymes that differ in amino acid sequence but catalyze the same chemical reaction. These enzymes usually display different kinetic parameters (e.g. different KM values), or different regulatory properties. The existence of isozymes permits the fine-tuning of metabolism to meet the particular needs of a given tissue or developmental stage (for example lactate dehydrogenase (LDH).
In phase 2 metabolism, instead of using OXIDASES, the body uses...
TRANSFERASES - transferring small polar molecules onto a drug - so O2 is not required as in phase 1
eg of polar molecules attached in phase 2 metabolism
Glucuonate, glutathionr, sulfate, ecetate..the product is called a CONJUGATE
Biochem of conjugation
Drug (+ acetyl co A using an enzyme called N-acetyl transferase)
metabolizes > 50% of available drugs
CYP 2D6 is famous for
Phase 1 and phase 2 cont...
In phase 1, reactive groups are introduced into the drug molecule by OXIDATION, REDUCTION, or HYDROLYSIS to a more polar form.
IN phase 2, these groups undergo CONJUGATION, usually in the liver with
GLUCURONIDE or Sulphate
In phase 2, a polar group is CONJUGATED to the drug
to SUBSTANTIALLY increase polarity of the drug.
ELIMINATION in LIVER DISEASE
Drug-metabolizing are present in many body tissues, including plasma, but are MOST ACTIVE in the LIVER.
Drug metabolism may therefore be IMPAIRED
in pts with LIVER DISEASE
Hepatic disease may increase
may cause liver damage
If creatinine is not good in a pt, eg older pts, chose
ACE INHIBITORS can be dangerous for
African Americans...causing swelling if lips, and occlusion of the airway
Steven Johnson Syndrome
Stevens-Johnson syndrome is a rare, serious disorder in which your skin and mucous membranes react severely to a medication or infection. Often, Stevens-Johnson syndrome begins with flu-like symptoms, followed by a painful red or purplish rash that spreads and blisters, eventually causing the top layer of your skin to die and shed.
Mucomyst brand of acetylcysteine is for inhalation (mucolytic agent) or oral administration (acetaminophen antidote), and available as sterile, unpreserved solutions (not for injection). The solutions contain 20% (Mucomyst-20) or 10% (Mucomyst-10) acetylcysteine, with edetate disodium in purified water.
How does it work?
N-acetyl cysteine treats acetaminophen (Tylenol) poisoning by binding the poisonous forms of acetaminophen that are formed in the liver. It is also an antioxidant, so it may play a role in preventing cancer.
check for carbon monoxide in blood..normal levels 1-3% of total hemoglobin.
Iron-containing oxygen transport metalloprotein
Hematocrit is a blood test that measures the percentage of the volume of whole blood that is made up of red blood cells. This measurement depends on the number of red blood cells and the size of red blood cells.
Midazolam has been associated with respiratory depression and respiratory arrest, especially when used for sedation in noncritical care settings. Use only in settings that can provide for continuous monitoring of respiratory and cardiac function .
ELIMINATION in RENAL DISEASE
Drug excretion is often reduced in pts with renal impairment; this is particularly important for drugs that are excreted UNCHANGED or have ACTIVE METABOLITES
An example is CODEINE; this is metabolized to form MORPHINE
which is further metabolized to to a 6-GLUCURONIDE compound.
Accumulation of this compound can occur in renal failure;
leading to excess sedation and respiratory depression.
Effects of other drugs
The activity of drug-metabolizing enzymes in the liver may be increased (induced) or reduced (inhibited) by external factors.
Cabamazepine, Phenobarbitone, Phenytoin, Rifampicin, Chronic ethanol consumption, Smoking, Barbecued meat, St. John's Wort
Cimetidine, Ciprofloxacin, Co-trimoxazole, Erythromycin, Ketoconazole, Grapefruit juice
Drug elimination can also be MEASURED in terms of CLEARANCE (in a manner analogous to creatinine clearance) by the volume of plasma cleared of drug per unit of time.
Creatinine is a breakdown product of creatine phosphate in muscle, and is usually produced at a fairly constant rate by the body. Wikipedia
Why is creatinine tested?
The test is done to see how well your kidneys work. Creatinine is removed from the body entirely by the kidneys. If kidney function is abnormal, creatinine levels will increase in the blood (because less creatinine is released through your urine). Creatinine levels also vary according to a person's size and muscle mass.
Normal levels of creatinine are
A normal result is 0.7 to 1.3 mg/dL for men and 0.6 to 1.1 mg/dL for women.
Females usually have a lower creatinine than males, because they usually have less muscle mass.
Half-life (t1/2) (elimination)
is a simpler means of understanding and using these elimination paramaters, and of facilitating patient care
Half life expresses information in terms of t1/2. THis is defined as the time taken for the plasma concentration of a drug
to DECREASE to 50% of the original value
This is clinically important because
it enables determination of : DOSING FREQUENCY, the time elapsed before a steady-state plasma concentration is reached following repeat dosing, whether use of a loading dose is appropriate
Quantitatively, most important route for parent drug metabolites, active secretion into urine
Important for a number of drugs, active secretion into bile
Sweat, tears, reproductive fluids, mild, lung, Minor contributor, passive diffusion
Several drug-metabolizing enzymes are subject to genetic variation in activity, and this can lead to large differences in in the rate of drug clearance from the plasma, unexpected prolongation of t1/2 and increased adverse effects.
Pharmacogenetic variations are relatively common
and may vary significantly between races
'Slow metabolizers' are more likely to develop adverse effects
such as peripheral neuropathy with isonizid
Peripheral neuropathy, a result of nerve damage, often causes numbness and pain in your hands and feet. People typically describe the pain of peripheral neuropathy as tingling or burning, while they may compare the loss of sensation to the feeling of wearing a thin stocking or glove.
Isoniazid is used alone or with other drugs to treat tuberculosis (TB) and to prevent it in people who have had contact with tuberculosis bacteria. It eliminates only active (growing) bacteria. Since the bacteria may exist in a resting (nongrowing) state for long periods, therapy with isoniazid (and other antituberculosis drugs) must be continued for a long time (usually 6 to 12 months).
Lidocaine viscous, a local anesthetic, is used to treat the pain of a sore or irritated mouth and throat often associated with cancer chemotherapy and certain medical procedures. Lidocaine viscous is not normally used for sore throats due to cold, flu, or infections such as strep throat.
Parasympathetic erection or ejaculation?
Responses to ANS STIMULI
Effector organ - SNS Response - PNS Response
SNS - raise rate contractility & conduction velocity, PNS lower rate contactility & conductio velocity
SNS - raise conduction velocity, PNS lower conduction velocity
SNS - Raise contractility & conduction velocity, PNS - none
SNS - Relaxation of bronchial muscle, PNS - Contraction of muscle DON'T CONFUUUUSE THESE!!!!!!!!!
SNS - Constriction, PNS - none
SNS - LOWERS motility and tone & contraction of sphincters, PNS RAISES motility and tone & relaxation of sphincters
Skin pilomotor muscles (arrector muscles) cold-stress
SNS - Piloerection, PNS - none
Sweat glands & Spleen capsule
SNS - Secretion & contraction, PNS - none
Radial muscle of iris
SNS - Contraction = mydriasis (dilation of pupil), PNS - none HEY this is DILATION>>>not constrilction!!!
Sphincter muscle of IRIS
SNS - none, PNS - CONTRACTION = Miosis (constriction of pupil)
Ciliary muscle uscle /ˈsɪli.ɛəri/ is a ring of striated smooth muscle in the eye's middle layer (vascular layer) that controls accommodation for viewing objects at varying distances and regulates the flow of aqueous humour into Schlemm's canal. It changes the shape of the lens within the eye, not the size of the pupil which is carried out by the sphincter pupillae muscle
SNS - Relaxation for far vision (to run from the bear), PNS - contraction for near vision (to focus on the beer)
SNS - inhibition of secretion, PNS - Secretion
SNS - none, PNS - Secretion (crying while drinking beer watching a movie...but eyes dry up to run from a bear)
SNS - none, PNS Secretion
SNS - Inhibition of secretion, PNS - Secretion
SNS - Thick secretions (so you don't choke on your spit when you run), PNS - thin secretion (for kissing!)
The most important FEEDBACK LOOP from a pharmacology perspective
Baroreceptor reflex is located
in the CAROTID SINUS and AORTIC ARCH
B reflex actions
If BP falls...
baroreceptors cause VASOCONSTRICTION and ELEVATION of cardiac output
if BP rises
baroreceptors cause VASODILATION and REDUCTION of cardiac output
In most organisms regulated by the ANS, the PNS provides the DOMINANT TONE
Autonomic tone is the
The effect of the autonomic nervous system on the heart rate..
SEVEN PROCESSES in NEUROTRANSMITTER ACTION
Neurotransmitter molecules are synthesized from PRECURSERS under the influence of ENZYMES
Neurotransmitter molecules are stored in VESICLES
Neurotransmitter molecules that leak from their vesicles are DESTROYED by enzymes
ACTION POTENTIALS cause vesicles to FUSE with the presynaptic membrane and RELEASE their neurotransmitter into the SYNAPSE.
Released neurotransmitter molecules BIND with AUTORECEPTORS and INHIBIT subsequent neurotransmitter release
Released neurotransmitter molecules BIND to POSTSYNAPTIC RECEPTORS
Released neurotransmitter molecules are DEACTIVATED either by REUPTAKE or ENZYMATIC DEGRADATION
Solubility of a solute in oil/solubility in water
The higher ie greater solubility in oil more easily moves
The lower more difficult to move across membrane ie polar substances, ions, large etc
sum of atomic weights
pH at which 50% of the drug is ionized
Barbituate; Use = Ca+ channel blocker; (sedation, anesthesia); ADEs = Drowsiness
barbiturate that is a white odorless slightly bitter powder (trade name Seconal) used as a sodium salt for sedation and to treat convulsions
barbiturate that is a hygroscopic powder (trade name Pentothal) that is a strong barbiturate that acts rapidly
solid drugs or chemicals that absorb moisture from air
The movement of substances into or out of cells without the expenditure of energy or the involvement of transport proteins in the cell membrane. Also called simple diffusion.
place where drug has its effect, site of action, site of drug/receptor interaction
what are ionized drugs?
polar = water-soluble
what are non-ionized drugs?
less polar = more lipid-soluble
Think of structure of acid as having a
It has a carboxyl: COOH / COO-
Think of a base as having an
amino: NH3+ / NH2
What is pKa for acids and bases?
acid dissociation constant, the pH at which 50% of the molecules are ionized
pKa example of a weak acid
aspirin (pKa 3.5)
pKa example of weak base
morphine (pKa 8.0)
A useful concept about drugs
They tend to exist in the ionized form when exposed to their "pH-opposite" chemical environment.
Acids are increasingly ionized with...
increasing pH (basic environment) whereas
Bases are increasingly ionized with...
decreasing pH (acid environment)
Cromolyn sodium (2.0)
Intal / mast cell stabilizer (respiratory inhalant) / asthma & bronchospasm
commonly used diuretic (trade name Lasix) used to treat hypertension and edema
a sulfonamide (trade name Gantanol) used to treat infections (especially infections of the urinary tract)
a barbiturate used as a sedative and as an anticonvulsant (long-acting)
an anticonvulsant drug (trade name Dilantin) used to treat epilepsy and that is not a sedative
a diuretic (trade names Hygroton and Thalidone) used to control hypertension and conditions that cause edema : Effective in lowering blood pressure to prevent Heart Attack
Chlordiazepoxide is used to relieve anxiety and to control agitation caused by alcohol withdrawal.
Potassium Sparing Diuretic
a drug (trade name Tagamet) used to treat peptic ulcers by decreasing the secretion of stomach acid
an alkaloid narcotic drug extracted from opium
Antiviral compound sometimes used to treat influenza type A infections.
log (protonated) / (unprotonated) = pKa - pH
(Overdose sampling) Acid drugs concentrate in...
(Overdose sampling) Basic drugs concentrate in...
Diffusion of basic drugs into stomach results in...
almost complete ionization in that low pH environment
How can actions of amphetamine be prolonged in an overdose?
(weak base pKa 10) ingest bicarbonate to alkalinize the urine. This will increase the fraction of amphetamine in non-ionized form, which is readily reabsorbed across the luminal surface of the kidney nephron...
Why acidify urine in in amphetamine overdose?
To increase kidney clearance of amphetamine.
Def. of strong electrolytes.
Compound which is ionized at all body pH values. They are poorly lipid soluble.
Ex. of strong electrolytes (strong acid)
Glucuronic acid derivatives of drugs.
Ex. of strong electrolytes (strong base)
Quaternary ammonium compounds such as acetylcholine
Membrane transfer ways (3)
Passive diffusion, carrier mediated (active or passive), endocytosis
Carrier-mediated, does NOT require energy, substance CANNOT be against its concentration gradient.
Why is facilitated diffusion needed?
To transport endogenous compounds whose rate of movement across membranes by simple diffusion would be too darn slow.
Active transport occurrence:
neuronal membranes, choroid plexus, renal tubule cells, hepatocytes
a vascular plexus of the cerebral ventricles that regulate intraventricular pressure. Produces CSF
Renal tubule cells
synthesize glucose during fasting and add it to the blood, and they can catabolize many organic compounds. They act as a kind of counter-current exchange system to remove hydrogen ions from the body.
liver cells; produce bile, absorb and secrete nutrients like glucose, and secrete plasma proteins
Active transport major features
Carrier-mediated, selectivity, competitive inhibition by congeners, requires energy, saturable, moves AGAINST concentration gradient.
The process of a substance reducing the activity of an enzyme by entering the active site in place of the substrate whose structure it mimics.
any compound that shares the same functional group with another compound
Property of enzymes and receptors that causes the reaction rate to increase linearly as more active sites become occupied; this increase in reaction rate will continue until all the enzyme active sites become saturated with subsrate
process by which a cell takes material into the cell by infolding of the cell membrane. It invaginates, then forms an intracellular vesicle.
the process by which a substance is released from the cell through a vesicle that transports the substance to the cell surface and then fuses with the membrane to let the substance out
Tend to respond well to diuretics. Diuretics improve responsiveness to ACE inhibitors. Also respond well to Ca ++ channel blockers.
Often managed with ACE inhibitors or Ca ++ channel blockers.
Tend to respond well to diuretics. The elderly are especially sensitive to volume depletion. Ca ++ channel blockers or ACE inhibitors are also reasonable choices. On the other hand, β-blockers can precipitate heart failure.
β-blockers (without ISA) and rate-slowing Ca ++ channel blockers are good choices. Dihydropyridine Ca ++ channel blockers may cause reflex tachycardia because of their vasodilatory effects, which will worsen angina.
Status post myocardial infarction
Good choices are β-blockers without ISA (sympathetic stimulation is unwanted post-MI) and ACE inhibitors or ARBs. Optimally, after myocardial infarction every patient will receive a β-blocker and an ACE inhibitor or ARB.
Good choices are ACE inhibitors, Ca ++ channel blockers, and α 2-agonists. β-blockers should be used with caution because they can mask hypoglycemia and increase the risk of developing type 2 diabetes mellitus.
Avoid diuretics because thiazides and loops can worsen uric acid control.
Bilateral renal artery stenosis
Avoid ACE inhibitors, ARBs, and renin inhibitors because these drugs can precipitate acute renal failure in this population.
Advanced renal insufficiency
Select a loop diuretic over a thiazide diuretic. Select other antihypertensives on the basis of which ones are not excreted renally.
Good choices are loop diuretics (which will also reduce edema and congestive symptoms), β-blockers, ACE inhibitors, ARBs, and aldosterone antagonists.
Do not use β-blockers in patients who are actively wheezing. β 1-selective agents are preferred in this population.
Rationale for Use of Drug Combinations in Angina
Nitrates and β-blockers
Nitrates decrease preload and cause venous pooling. β-Blockers prevent nitrate-induced reflex tachycardia.
Nitrates and Ca ++ channel blockers
Nitrates reduce preload. Dihydropyridines decrease afterload or rate-slowing Ca ++ channel blockers reduce heart rate.
Ca ++ channel blockers and β-blockers
β-Blockers prevent reflex tachycardia associated with dihydropyridine-induced blood pressure decrease.
Nitrates, Ca ++ channel blockers, and β-blockers
Dihydropyridines reduce afterload. Nitrates reduce preload. β-Blockers decrease heart rate and contractility to blunt nitrate-induced and dihydropyridine-induced reflex tachycardia.
Hypertension is defined as:
A systolic blood pressure >140 mm Hg
A diastolic blood pressure >90 mm Hg
HT Risk groups
Risk groups: older, African and Mexican Americans, postmenopausal women, obese
Chronic renal failure
Pheochromcytoma (catecholamine secreting tumor)
Oral contraceptive induced
Reduce systolic BP to <130
Reduce diastolic BP to <80 mm Hg
Prevention of long-term complications
Consequences of hypertension:
Use drug therapy if
BP elevated after implementation of lifestyle changes
Attempt is made to decrease drugs or dosages after
12 months of therapy
Antihypertensive Sites of Drug Action
Adrenergic nerve terminals
Cardiac beta receptors
Vascular alpha1 receptors
Vascular smooth muscle
Beta1 receptors on juxtaglomerular cells
Angiotensin II receptors
Aldosterone receptor blockers
Indirect Anti-Adrenergic Agents: Clonididine
Centrally-acting Alpha2 Agonists
Reduce NE release
Reduce impulses along the sympathetic nerves
Reduce activation of alpha and beta receptors in the periphery
Adrenergic Antagonists Beta Blockers effects are?
Reduced cardiac output
Reduced force of contraction
Reduced velocity of impulse conduction
Slow heart rate
Reduce myocardial workload & oxygen demands
USES: High BP, MOA: Beta 2 agonist, Lowers NE, Brainstem , Lowers HR, Myocardial cont. ADVERSE EFFECTS
USES: Prostate enlargement, Stop RAAS, Renal dilation. MOA: Beta 1 receptors on juxtaglomerular cells. Beta 1, 2 agonist. Lowers release of renin, and Angiotensin 2. ADVERSE:
USES: Hypertension, Angina, arrhythmia, MI, MOA: Beta blocker, ADVERSE: beta blocker
calcium blocker (trade name Procardia)
USES: Diuretic, lower BP MOA: Renal tubules, salt and water excretion, lower blood volume, ADVERSE: Hyperkalemia
USES: High BP, MOA: Relax VSM, ADVERSE
USES: Prostate enlargement, High BP, MOA:Vasular A1 receptor, Dilation of arterioles and veins, ADVERSE
USES: High BP, MOA: Adrenergic nerve terminals, ADVERSE:
USES: High BP, MOA: Sympathetic ganglia, dilation of arterioles and veins, (rarely used) ADVERSE
USES: Lower fat MOA: -statin ? ADVERSE
Co Enzyme Q10
USES: Inotropic agent, Flabby heart, MOA: Heart, natural supplement, ADVERSE
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