Term
|
Definition
- Called high ceiling diuretics: the more you give, the more effect you’re going to get, never reaching a plateau.
- They’re sulfonamide derivatives, with the exception of ethacrynic acid (because of allergies) |
|
|
Term
|
Definition
- They’re secreted into the proximal tubule by PSOASS, they go into the ascending loop of Henle and block Na/2Cl/K co-transport. - They act by relaxing smooth muscle, which is the main reason why BP decreases.
- They act as broncho and vaso dilators
- They decrease activity of carbonic anhydrase
- GFR and RPF are unaffected, giving the kidney a protective effect.
- Used primarily Intravenously to lower BP in cases of glaucoma, pulmonary edema or acute renal failure.
- Oral use of loop diuretics is mainly used in the event of emergency to decrease the BP
- Careful with titinus |
|
|
Term
| - Furosemide, torsemide, bumetanide. |
|
Definition
loop diuretics
bring down BP |
|
|
Term
|
Definition
- Urine volume
- uric acid
- Renal O2 consumption, this is a protective effect as well as GFR and RPF being unaffected.
- Glucose
- TG |
|
|
Term
|
Definition
-CSF production
- K+, be careful with hypokalemia and arrhythmias
- Mg, careful with hypomagnesemia
- Ca drops
- Cl, this causes acid to go down as well, leading to alkalosis.
-HDL |
|
|
Term
|
Definition
- Low ceiling diuretics: you give a dose, you get the effects very quickly. Giving more won’t give you the additional benefit.
- like the loop diuretics, they’re also sulfonamide derivatives. With the exception of ethacrynic acid. So guess what else happens? Yes the carbonic anhydrase is affected as well. |
|
|
Term
| - Chlorothiazide, hydrochlorothiazide, chlorthalidone, indapamide. |
|
Definition
|
|
Term
|
Definition
- They’re secreted into the proximal tubule by PSOASS, go to the early distal tubule and inhibit Na/Cl co transport. - Cheap meds that decrease BP, cardiac insufficiency
- They’re not used intravenously or in acute renal failure
- Only used orally, careful with K loss, so combine with K sparing drugs like aldosterone antagonists since aldosterone promotes Na reabsorption and K loss. Also you can use cycloamidine derivatives. |
|
|
Term
| what increases in thiazides? |
|
Definition
- Uric acid
- Urine volume
- Ca in plasma
- Glucose
- TG |
|
|
Term
| what decreases with thazides? |
|
Definition
- For diabetes insipidus, the urine volume goes down
- GFR and RPF so there is NO kidney protective effect here
- K, careful for arrhythmias (combine with K sparing drugs)
- Mg
- Ca in urine
- Cl, careful for alkalosis, plasma acid goes down as well
- HDL |
|
|
Term
|
Definition
aldosterone antagonist that keeps K in body
only orally and half-life of 2 hrs. DO NOT give with ANY OTHER K SPARING DIURETIC OR K SUPPLEMENTS OR ACE INHIBITORS.
steroidal side effects |
|
|
Term
|
Definition
aldosterone antagonist that keeps K in body
only iv and half life of 17 hrs. DO NOT give with ANY OTHER K SPARING DIURETIC OR K SUPPLEMENTS OR ACE INHIBITORS.
steroidal side effects |
|
|
Term
|
Definition
Cycloamidine derivatives
- Na channel blocker and Na/H exchange which keeps K in body
is metabolized by the liver |
|
|
Term
|
Definition
Cycloamidine derivatives
- Na channel blocker and Na/H exchange which keeps K in body
Ca increases so don’t use in people with hypercalcemia. Has a long half life |
|
|
Term
|
Definition
Carboanhydrase inhibitors
Alkaloid urine. is considered a diuretic but used much more for mountain sickness. It lowers your pH so that respiration remains intact since one hyperventilates at high altitudes. Can also be used for chronic glaucoma treatment and also sequential nephron blockade.
secreted in early proximal tubule |
|
|
Term
|
Definition
Xanthine derivatives
- They’re adenosine receptor blockers which dilates the efferent arteriole. Increasing the filtration rate and urine volume. |
|
|
Term
|
Definition
Xanthine derivatives
- They’re adenosine receptor blockers which dilates the efferent arteriole. Increasing the filtration rate and urine volume. |
|
|
Term
|
Definition
- They work by inhibiting the conversion of angiotensin I to angiotensin II. Decreasing the BP.
- All of them have a long half life and are prodrugs (exception captopril and lisinopril, active) |
|
|
Term
|
Definition
| - ACE metabolizes bradykinin. ACE-I’s cause the accumulation of bradykinin. Bradykinin helps decrease the BP since it activates endothelium dependent NO synthase, which vasodilates. However, bradykinin promotes pro inflammatory cytokines, which increase vascular permeability, causing irritation of respiratory tract. |
|
|
Term
|
Definition
| the only ACE-I that contains S. gives off a metallic taste. Can cause allergic reactions. It is an active drug. Half life of 2 hrs. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| curious drop in risk of MI and stroke in diabetic patients. In non diabetic patients it decreased the chance of becoming diabetic and also showed a decrease in the risk of developing overt nephropathy. |
|
|
Term
|
Definition
- The end in -sartan
- they block the angiotensin II receptor. There are 4. It mainly affect AT1
- they’re all active drugs, only candesartan and olmesartan are prodrugs. |
|
|
Term
| Side effects of ACE and ARB’s |
|
Definition
- Persistent dry cough (however, less common with ARB’s)
- Angioedema (less common with ARB’s) Check for history of angioedema.
- Hyperkalemia due to decrease in aldosterone.
- Unilateral renal artery stenosis: a decrease in renal perfusion in the kidney. This can result in renal failure. Becauise it is unilateral the other kidney tries to compensate. You need to give small doses of the drug and watch the creatinine levels.
- DO NOT USE WHILE IN PREGNANCY |
|
|
Term
|
Definition
only direct renin inhibitor, used to decrease BP.
- Beta blockers (especially beta1) also inhibit the release of renin from the kidney |
|
|
Term
|
Definition
|
|
Term
|
Definition
- They’re adenosine 1 receptor blockers and unselective PDE inhibitors.
- At low concentrations they block adenosine receptors (make the HR go up, Bronchoconstriction does not occur since there are no enough receptors for this to occur) at moderate concentration, xanthines unselectively block PDE’s (increasing cAMP and cGMP relaxing smooth muscle and contracting striated muscle)and at highest concentration they release catecholamine’s.
, the effect on the smooth and striated muscle is not so pleasurable for the patient, also the increase in catecholamines causes an increase in HR, bronchodilaton, etc. |
|
|
Term
|
Definition
Xanthine derivatives
- They’re adenosine receptor blockers which dilates the efferent arteriole. Increasing the filtration rate and urine volume.
if given intravenously, they terminate the asthma attack. Given orally, they act as controllers.
1A2 metabolized. Potent inducers are smoking and BBQ so the drugs will wear off real quickly. Other inducers are omeprazole (PPI) barbiturates (lousy sleep inducers) carbamazepine (Na channel blocker used for seizures) phenytoin (Na and Ca blockers for seizures) Rifampin (makes you “orange”)
- Inhibition by cimetidine (H2 blocker) fluvoxamine (SSRI) Quinolones and macrolids. Very unpredictable.
- Side effects: if you take above 35 ug/ml they change from first to zero order kinetics, which means it becomes dose dependent. Tachyarrhythmia, nausea and vomiting, tremor, seizures, rhabdomyolysis. |
|
|
Term
|
Definition
: if given intravenously, they terminate the asthma attack. Given orally, they act as controllers.
1A2 metabolized. Potent inducers are smoking and BBQ so the drugs will wear off real quickly. Other inducers are omeprazole (PPI) barbiturates (lousy sleep inducers) carbamazepine (Na channel blocker used for seizures) phenytoin (Na and Ca blockers for seizures) Rifampin (makes you “orange”)
- Inhibition by cimetidine (H2 blocker) fluvoxamine (SSRI) Quinolones and macrolids. Very unpredictable.
- Side effects: if you take above 35 ug/ml they change from first to zero order kinetics, which means it becomes dose dependent. Tachyarrhythmia, nausea and vomiting, tremor, seizures, rhabdomyolysis. |
|
|
Term
| - Amrinone, milrinone, enoximone, vesnarinone |
|
Definition
2) PDEIII selective inhibitors
- They affect the heart, most have an ending in –rinone
- They are positive inotropes and vasodilators= inodilators. The BP and O2 consumption remains unchanged |
|
|
Term
| - Cilomilast and roflumilast |
|
Definition
PDE4 selective inhibitors
- They are marketed for respiratory problems/inflammation like asthma and COPD but are disappointing in this area |
|
|
Term
|
Definition
PDE5 selective inhibitors
affects PD6 which affects vision. |
|
|
Term
|
Definition
PDE5 selective inhibitors
longer duration, affects PDE11 which hurts back |
|
|
Term
| good things about statins |
|
Definition
cadiovascular: promostes release on NO synthase, making endothelium stronger, decrease Rho/Ras less proliferation, decrease adherence of monocytes to endothelium, MMP decreases, collagen goes up,
Osteoporosis: lack of farnesy, less ruffled border, less osteoclasts
prevents strokes, MI, cardiac arrhythmias, reduces inflammation, risk of osteoporosis, colon cancer, depression and anxiety, Alzheimer’s and MS. |
|
|
Term
Loving
Someone
Profoundly
Adds
Frustrating
Rage |
|
Definition
L-natural, lipophillic, prodrug, 3A4
S- natural, lipophillic, produg, 3A4
P- natural,hydrophilic,active,not metabolized, 50% bound
A- synthetic,lipophillic, active,3A4, long HL
F- synthetic, lipophillic,active, 2C9
R- synthetic,hydrophillic, active, 2C9/2C19, long HL |
|
|
Term
|
Definition
| azole antifungals, cimetidine, ciprofloxacin, erythromycin, grapefruit juice, cyclosporin. |
|
|
Term
|
Definition
1) Hepatotoxicity: most risk from 3-12 months. Its dose related, and elevates transaminases.
2) Myotoxicity: myalgia (muscle aches and weakness) myopathy (myalgia and high creatinine) rhabdomyolysis (myopathy and myoglobinea and myoglobinuria) essentially muscle cells rupture and go through kidney giving urine a weird color. Careful with K, it leaks as well so cardiac arrhythmia.
- NO PREGGIES |
|
|
Term
|
Definition
a sublingual spray for acute angina attack.
NO donor
It drops the BP as well. It has a short half life. Used as a patch for continuous supply. |
|
|
Term
|
Definition
used in cyanide poisoning
hemoglobin + Nitrite = methehemoglobin
CN + methehemoglobin = cyanomethehemoglobin
thiosulfate + cyanomethemoglobin= hemoglobin, thiocyanane and sulfite |
|
|
Term
|
Definition
| makes hemoglobin back from methemoglobin |
|
|
Term
- Isosorbide mononitrate:
- Isosorbide dinitrate: |
|
Definition
|
|
Term
|
Definition
| NO donor and K channel opener. Doesn’t mess with the heart because it’s extremely selective for the K channels in vasculature. Careful with the side effects, headaches and mouth ulcers!! |
|
|
Term
|
Definition
angina drugs drugs that have nothing to do with NO release
: it reduces O2 consumption be decreasing available Ca in myocardial cells |
|
|
Term
|
Definition
angina drugs drugs that have nothing to do with NO release
makes myocardial cell use more glucose and use up less O2 |
|
|
Term
|
Definition
| slows down the heart by only acting on the pacemaker of the heart. |
|
|
Term
| contraindications of NO donors |
|
Definition
PDE5 inhibitors: remember these are to enlarge vasculature in penis. Giving NO donors and PDE5 inhibitors will drop the BP way too much.
alpha 1 blockers: ending in – zosin or –sulosin. Not too bad but both drugs drop BP. |
|
|
Term
|
Definition
- Cholinergic antagonist in muscarinic receptor
- Used as mydriasis inducer. Bad thing is that it takes forever to wear off.
- Atropine takes away the inhibition on the heart by the parasympathetic NS. It also increases the likelihood that a beta agonist will be able to act.
- Atropine blocks brochosecretions, it’s useful when you want to intubate.
- Atropine is also used as antidote for organophosphate poisioning. |
|
|
Term
|
Definition
| Think mad hatter, red beet, dry as bone, blind as a bat, hot as a hare and micropsia. |
|
|
Term
|
Definition
| : it’s just like atropine but it doesn’t cross the BBB. Synthetic quaternary amine with no central effects. Available as oral and iv. If you ever have an over production parasympathetic activity in the periphery, you have increased GI or bradycardia. Much weaker than atropine. |
|
|
Term
|
Definition
Inhaled antimuscarinics
- Good for COPD /asthma. Since they inhibit the parasympathetic NS which causes bronchoconstriction and increased brochosecretions |
|
|
Term
|
Definition
selective M3 blocker.
- Used for urinary incontinence since they mediate detrusor contractility mainly
- M3 receptors can induce GI contraction, saliva production and iris sphincter function. So blocking them would do the opposite, constipation and dry mouth. |
|
|
Term
|
Definition
less M3 selective than darifenacin but works just as well
- Used for urinary incontinence since they mediate detrusor contractility mainly
- M3 receptors can induce GI contraction, saliva production and iris sphincter function. So blocking them would do the opposite, constipation and dry mouth. |
|
|
Term
|
Definition
| it has an anticholinergic effect but mainly marketed as antihistamine. It enters the brain and is a potent sedative. |
|
|
Term
|
Definition
| anticholinergic, but primarily NMDA receptor antagonist useful for pain |
|
|
Term
|
Definition
| anticholinergic drug used in Parkinson’s. Since dopamine is too low we try to decrease Acetylcholine. |
|
|
Term
|
Definition
| : anticholinergic given to improve movement. A tertiary amine. |
|
|
Term
|
Definition
| anticholinergic drug for Parkinson’s . |
|
|
Term
|
Definition
| : little muscarine but lots of muscimol. A GABA agonist, which causes sedation and delirium. Crosses BBB. |
|
|
Term
|
Definition
| a non selective M3 agonist. A topical treatment for glaucoma, it probably increases aqueous outflow by dilating the veins. Remember that M3 induces GI movement and saliva production. |
|
|
Term
|
Definition
| a selective M3 agonist. Increases the secretion of glands (juicy). Treats sjogren's syndrome (chronic dry eye). Produces saliva. |
|
|
Term
|
Definition
| not selective for any of the muscarinic receptors, but works just as well. Treatment for urinary incontinence |
|
|
Term
|
Definition
Alzheimer’s treatment
Inhibits cholinesterase in the CNS. It also inhibits butylcholinesterase in the periphery.
. It has significant side effects: like nausea and vomiting the worst one though is liver damage, since it also blocks the cholinesterase in periphery, it elevates liver enzymes. |
|
|
Term
|
Definition
it has greater selectivity for cholinesterase in the CNS than the butylcholinesterase in the periphery
So the main advantage is the lack of hepatotoxicity. Also it has super long half life, which makes it a one a day drug! Should be the first option in treating Alzheimer’s. |
|
|
Term
|
Definition
Alzheimer’s treatment
blocks both cholinesterase and butylcholinesterase. Available as a patch as well. |
|
|
Term
|
Definition
isoquinoline tubocurarine, an NDMR that blocks nicotinic ionotropic channels
south america |
|
|
Term
|
Definition
blocks nicotinic receptors
NMDR that's an amino steriod
Africa |
|
|
Term
|
Definition
Potent NDMR reversal, binds to AchE
. No CNS penetration (can’t use for Alzheimer’s ). Longer acting. Side effects: bronchosecretions and bradycardia. Mostly excreted renally. |
|
|
Term
|
Definition
| binds weakly to AchE. Low half life, No CNS penetration (can’t use for Alzheimer’s. fewer muscarinic side effects than neostigmine. To control dropping HR due to sympathetic overstimulation |
|
|
Term
|
Definition
Used as an immunosuppressant for myasthenia gravis at low doses but the mechanism is fuzzy. It is also used as cancer treatment by inhibiting DHFR and decreasing RNA and DNA synthesis.
It’s metabolized by the same enzymes that metabolize penicillin and like drugs, so toxic build up happens since the excretion is impaired. |
|
|
Term
|
Definition
Immunosuppresant drug for myasthenia gravis
A calcireurin inhibitor which turns out to inhibit Interleukins. |
|
|
Term
|
Definition
Immunosuppresant drug for myasthenia gravis
A calcireurin inhibitor which turns out to inhibit Interleukins. |
|
|
Term
|
Definition
| inhibits AchE in periphery. Mild. No CNS penetration, Potent, long lasting. In addition to Myasthenia Gravis treatment, it was also given to troops before war so in case of OP the AchE enzyme was already occupied. |
|
|
Term
|
Definition
| reactivates inhibited cholinesterase. Good for organophosphate poisoning |
|
|
Term
| central anticholinergic syndrome |
|
Definition
- overdose of atropine like drugs
- symptoms: mad as a hatter, hot as a hare, red as a beat, dry as bone, blind as bat and micropsia.
- Diarrhea, Urination, Miosis, Bronchorrhea, Bronchospasm, Emesis, Lacrimation, Laxation, Salivation |
|
|
Term
|
Definition
| Powerful anticholinesterase effect. Penetrates the BBB. Used in the trials of Nigeria. |
|
|
Term
|
Definition
Non selective alpha receptor blocker
the treatment of phaeochromocytoma: a tumor that releases epinephrine and norepinephrine, leading to extremely elevated BP since the vessels are constricted.
- Contraindication: the problem is that since you’re blocking the alpha receptors you’re forcing the catelcholamines to go to the beta receptors, leading to massive vasoconstriction. For this, you give Mg in order to relax smooth muscle. |
|
|
Term
|
Definition
| : treats benign prostatic hyperplasia. Alpha 1 selective, but not uroselective. Careful with orthostatic hypotension. |
|
|
Term
|
Definition
| treats benign prostatic hyperplasia. selective alpha 1 blocker, not uroselective. Careful with orthostatic hypotension. |
|
|
Term
|
Definition
| treats benign prostatic hyperplasia. More alpha 1A selective than the last two, but not entirely. |
|
|
Term
|
Definition
| treats benign prostatic hyperplasia. a selective alpha 1A blocker, more than the others.Not especially better |
|
|
Term
|
Definition
| most alpha 1A blocker so far. It has no effect on vasculature so don’t worry about orthostatic hypotension. Interferes with sexual function. |
|
|
Term
|
Definition
exclusively an alpha 2 receptor agonist.
- These are presynaptic receptors that control neurotransmitter release.
Category B drug, a safe drug. Pregnancy safe. Competitive inhibitor of DOPA decarboxylase, reducing the synthesis of epinephrine and norepinephrine. Instead, it gets converted into alpha-methy-norepinephrine, which is an exclusive agonist of pre synaptic alpha2 receptors in the CNS. Shuts down sympathetic NS making it clonidine like. |
|
|
Term
|
Definition
- These are presynaptic receptors that control neurotransmitter release.
used to lower BP, but not easy to work with especially intravenously since it also like alpha1 receptors. This is an issue, because before it gets to the alpha2 receptors in the brain, it interacts with alpha1 receptors in the periphery vasoconstricting vessels, making the BP go up. Now it is marketed more as a sedative and analgesic. Good because no respiratory depression. |
|
|
Term
|
Definition
| - These are presynaptic receptors that control neurotransmitter release. selective agonist for the imidazoline1 receptor, decreases sympathetic activity, decreases BP. |
|
|
Term
| Adverse drug reactions of Centrally acting alpha2 imidazoline1 receptor agonists |
|
Definition
| because the parasympathetic NS is enhanced, sedation, dry mouth, bradycardia, orthostatic hypotension, impotence, fluid retention and edema (so give a diuretic along preferable a thiazide) and oddly enough constipation, nausea and gastric upset. |
|
|
Term
|
Definition
| an alpha1 agonist, vasoconstrictor. Available as an OTC medicine. |
|
|
Term
|
Definition
| an alpha1 agonist, vasoconstrictor. Available as an OTC medicine. |
|
|
Term
|
Definition
| an alpha1 agonist, vasoconstrictor. Available as an OTC medicine. Unusual name because it’s old. |
|
|
Term
| - Epinephrine and norepinephrine |
|
Definition
the most potent endogenous alpha1 receptor agonsits
are not selective for alpha vs beta but if given the choice, epinephrine will go to beta and norepinephrine will go to alpha. |
|
|
Term
|
Definition
- Useful for asthma (by relaxing smooth muscle), uterus relaxation (delaying delivery—remember Mg as an alternative) and hyperkalemia (gets K into the cell—first line would be insulin/dextrose)
- An additional side effect that is beneficial is the decrease of release of histamine and leukotrienes so it has a mild anti-inflammatory effect. |
|
|
Term
|
Definition
Short acting beta2 agonist
Reliever drug for asthma
They have a little affinity for beta1 as well (1:4) the side effects are going to be increased HR. this actually goes hand in hand with beta2 agonists. A bronchodilator, but because of this, you get tachycardia. Metabolized. Renally secreted. Racemic mixture, R is the good guy. |
|
|
Term
|
Definition
| the isolated R enantiomer of albuterol. Beta2 affinity off the roof. Good thing since tachycardia is less. More metabolized tho. |
|
|
Term
|
Definition
beta 2 agonist treatment for asthma
slow onset and long acting, cannot be used as a reliever because the effects take too long to kick in. |
|
|
Term
|
Definition
beta 2 agonist treatment for asthma
rapid onset and long acting, can be used as a reliever drug due to STAT onset and a controller drug due to long acting. |
|
|
Term
|
Definition
synthetic catecholamine. Racemic that is pseudo beta1 selective.
net effect is beta1 agonism which increases the inotropy of the heart and makes it beat faster. Surgeons like to use it to increase the heart rate. |
|
|
Term
|
Definition
| an endogenous catecholamine. Its effect is dependent on the dose. At a renal dose (low dose) it’s a dilator of the renal vasculature. Increases perfusion of kidneys in states where this might be impaired, like in surgery. At a middle dose it’s cardiac and has a beta1 agonist effect, the inotrope of the heart increases as well as HR. At a high dose it has an alpha1 effect, which vasoconstricts, increasing the afterload and BP and O2 consumption making the heart work harder. |
|
|
Term
|
Definition
| equivalent to renal dose dopamine. |
|
|
Term
|
Definition
synthetic catecholamine with vasodilating effects like beta2.
- Increases cAMP so it increases heart inotropy |
|
|
Term
|
Definition
| synthetic catecholamine. A non-selective beta agonist (beta1 and beta2) beta1 induces the positive inotropic effect with HR and pumping increasing. Beta 2 induces vasodilation which reduces the afterload. The increase in O2 consumption is moderate. Acts quick. You can call inodilator. |
|
|
Term
|
Definition
| antiarrhythmic drug that is non selective, fat soluble so it goes into the brain. Na blocker (class I and II) No ISA (the more blocker you give, the more blocking affects you get).1A and 2D6 metabolism. |
|
|
Term
|
Definition
| antiarrhythmic drug that is beta1 selective, so it has no effect on vasculature, just on heart. No ISA either. Fat soluble. 2D6 metabolism. |
|
|
Term
|
Definition
| beta1 selective, no ISA, water soluble. Renal excretion. |
|
|
Term
| - Water soluble beta1 agonists |
|
Definition
| PANS; Pindolol, Atenolol, Nadolol, Sotalol. |
|
|
Term
| - Adverse drug reactions of beta blockers |
|
Definition
| careful with asthmatic/COPD people! Since beta blockers restrict ability of bronchodilation. Not the main drug to lower BP or HR in these patients. Negative effect on metabolic profile (increase TG and LDL and glucose and dreams if its fat soluble) |
|
|
Term
|
Definition
| if you overdose on the drug it’s not too much of a big deal ,initially u get the beta blockage but the more u give turns out to be an agonist effect. Also does not have a negative effect on the metabolic profile. |
|
|
Term
| - To treat a beta blocker overdose: |
|
Definition
| : low BP due lack of heart pumping. Treat with insulin or glucagon, good inotrophes that do not rely on beta receptors. |
|
|
Term
|
Definition
| beta1 receptor blocker that is quickly degraded by plasma esterases (like remifentanil, procaine, cocaine) so it’s the only ultra-short acting beta blocker. |
|
|
Term
|
Definition
| mixed non cardioselective alpha/beta blcokers. Reduces afterload, less vasoconstrictive. |
|
|
Term
|
Definition
| mixed non cardioselective alpha/beta blcokers. Reduces afterload, less vasoconstrictive. |
|
|
Term
|
Definition
| cardio selective beta1 blocker with NO effects. 2D6 |
|
|
Term
|
Definition
| most potent anesthetic GABA agonist, most lipophilic, anesthetic. Almost 20% metabolized! Risk of malignant hyperthermia (treatment: dantrolene) |
|
|
Term
|
Definition
inhaled GABA agonist anesthetic
2% metabolized, risk of seizures. |
|
|
Term
|
Definition
inhaled GABA agonist anesthetic
practically no metabolism. |
|
|
Term
|
Definition
inhaled GABA agonist anesthetic
much more rapid onset and offset, but weaker. 4% metabolized risk of kidney damage. |
|
|
Term
|
Definition
inhaled GABA agonist anesthetic
no metabolism. Ultra rapid |
|
|
Term
|
Definition
| NMDA antagonist anesthetic (similar to ketamine).Inhibits B12 dependent enzymes. Lack of myelin. Least potent. |
|
|
Term
|
Definition
- the only DMR perfect for intubation (curare like)
- binds to the nicotinic recept keeping Na channels open for a bit
- initially most of it is degraded by AchE in the periphery
- only 5% make it to the junction, takes minutes for AchE to degrade it |
|
|
Term
|
Definition
a test for measuring the level of neuromuscular blockade. Four consecutive stimuli are delivered along the path of a nerve (ulnar), and the response of the muscle is measured in order to evaluate stimuli that are blocked versus those that are delivered. Four equal muscle contractions will result if there is no neuromuscular blockade, but, if nondepolarizing blockade is present, there will be a loss of twitch height and number, which will indicate the degree of blockade. This test is commonly used in intensive care units.
- A depolarizing muscle relaxant will decrease the amplitude.
- A non depolarizing muscle relaxant will fade |
|
|
Term
|
Definition
| abduction, perpendicular to palm, radial and medial nerves |
|
|
Term
|
Definition
| adduction, perpendicular to palm, ulnar nerve, what you check in relaxometer (TOF) |
|
|
Term
|
Definition
| flexion, in plane of palm, ulnar and median nerves |
|
|
Term
|
Definition
| opposition, median nerve, if this is gone, you compensate with adduction |
|
|
Term
|
Definition
| extension, plane of palm, radial nerve |
|
|
Term
| - Adverse effects of DMR's |
|
Definition
o fasciculation’s result in myalgia for young females.
o Increased pressure everywhere.
o Since SUX mimic Ach it will result in bradycardia and bronchospasm. Give glycopyrrolate, a peripheral muscarinic receptor blocker.
o Hyperkalemia (think fasciculation make contents squeeze out) . m
o Masseter muscle spasm-> malignant hyperthermia. Another drug that may cause this is halothane. Muscle contraction makes heat and CO2, hyperventilate the patient. Give dantrolene. |
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Term
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Definition
| that thins the blood by inhibiting platelet aggregation. Most of it is also broken down by AChE before going to the liver (20%) and metabolized to active drug that binds to P2RY12 receptor inhibiting platelet aggregation. If the esterases are missing, more goes to the liver, more blood thinning. |
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Term
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Definition
| thins the blood by inhibiting platelet aggregation. Most of it is also broken down by AChE before going to the liver (20%) and metabolized to active drug that binds to P2RY12 receptor inhibiting platelet aggregation. If the esterases are missing, more goes to the liver, more blood thinning. |
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Term
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Definition
| measures the level of esterases in the blood by the level of inhibiton. If it inhibits a lot, then there are a lot of esterases. Not performed in everyone because it’s rare to have low esterase activity |
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Term
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Definition
- They block the opening of Na channel, so there is no depolarization at all. No fasciculation.
- NDMR’s come in two flavors (isoquinolines – curium from south America) or (aminosteroids – curonium from Africa) |
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Term
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Definition
- Isoquinolines
- Metabolized by esters, shortest duration of action from all NDMR’s (SUX is still shortest overall). |
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Term
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Definition
- Isoquinoline
Hoffmann degradation, careful with Laudanosine accumulation. intermediate duration |
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Term
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Definition
- Isoquinoline
Hoffmann degradation, careful with Laudanosine accumulation. intermediate duration. |
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Term
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Definition
- Isoquinoline
Not metabolized, only kidney. Longest duration. |
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Term
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Definition
aminosteriod
Most vagolytic, both kindey and liver, long acting. |
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Term
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Definition
aminosteroid
both kidney and liver, longest acting. |
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Term
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Definition
| both kidney and liver, intermediate acting. |
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Term
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Definition
| only kidney. Intermediate acting. |
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Term
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Definition
• Monitor iv line, EKG, oxymetry and BP
• Wash out nitrogen from lungs. 10 minutes on oxygen mask.
• Sedate: thiopental or diazepam.
• Analgesic: fentanyl or related compound (if not, HR goes up)
• Ventilate with bag since now you have a barbiturate and opioid.
• Check for light on laryngoscope.
• Give SUX, watch for fasciculations
• Insert laryngoscope, watch for inverted V
• Auscultate for position and use devices to make sure you’re in the right place.
• Connect ventilator, 21% oxygen, 60% N2O and 1% isoflurane.
• SUX goes away, add another muscle relaxant, add another analgesic and re-sedate.
• After surgery, antagonize any residual muscle relaxant, so use neostigmine, to control dropping BP due to parasympathetic activity, give atropine or glycopyrrolate. |
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Term
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Definition
• Short pathway, occurs in trauma.
• Think warfarin
• Test using INR
• Vitamin K dependent
• Oral anticoagulants (warfarin) inhibit vitamin K reductase which replenishes vitamin K
• The pathways that are dependent of vitamin K are 2, 7, 9, and 10 in the colagulating cascade. Protein C and S are vitamin K dependent on the anti-coagulating cascade. |
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Term
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Definition
Only orally
Stops all vitamin K dependent factors (2, 7, 9, 10 in pro and protein C and S in anti)
Onset of action is delayed since you first have to deplete the current vitamin K. if you need anticoagulation STAT -heparin-
Monitor by INR, available for home use. Extremely important since warfarin effects are unpredictable
2C9 metabolized which differs by ethnic groups, making it unpredictable
Inhibits vitamin K reductase which difference between enzymes, making it more unpredictable
Can be affected by other drugs that are 2C9 metabolized
Also by drugs that inhibit 2C9: decreasing its metabolism and enhancing the effects |
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Term
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Definition
necrosis. It is thought because protein S and C are blocked first there is an accumulation on thrombin, since 2,7,9, and 10 are still working. In this case you’d give heparin which is immediate.
Also, risk of osteoporosis, purple toe syndrome and a NO NO in pregnancy |
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Term
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Definition
| vitamin K (delayed effect) and FFP (fresh frozen plasma supplies coagulation factors) |
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Term
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Definition
• Longer pathway, occurs in chronic states.
• think heparin
• Test using the PTT
• Used intravenously |
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Term
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Definition
Immediate acting
Long polysaccharide: activates AT III which inhibits factor X. main mode of action. But it also affects factor II. You monitor with PTT. Antagonize with protamine (an anticoagulant that binds with heparin)
Long polysaccharide: activates only AT III which inhibits factor X. Cannot be monitored with PTT, instead factor X. Cannot be antagonized. Longer half life, pricey.
It’s OK in pregnancy |
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Term
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Definition
| Heparin induced thrombocytopenia, osteoporosis |
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Term
| Heparin induced thrombocytopenia |
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Definition
| caused by the formation of abnormal antibodies that activate platelets, making thrombin. |
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Term
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Definition
| iv use, direct thrombin inhibitor. Treatment for HIT (heparin induced thrombocytopenia) |
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Term
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Definition
| iv use, direct thrombin inhibitor. Treatment for HIT (heparin induced thrombocytopenia) |
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Term
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Definition
| iv use, direct thrombin inhibitor. Treatment for HIT (heparin induced thrombocytopenia) |
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Term
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Definition
| iv use. Reversibly binds to thrombin. |
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Term
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Definition
| oral administered thrombin inhibitor. |
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Term
| - Apixaban and rivaroxaban |
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Definition
| orally administered factor X inhibitors |
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Term
| - Glanzmann’s thrombasthenia |
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Definition
| defective IIa/IIIb receptors |
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Term
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Definition
| reduces the ability of platelets to stick. Platelet COX is sensitive to aspirin at low doses. At higher doses endothelium is affected. Binds irreversibly to platelet COX |
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Term
| - Prasugrel and clopidogrel |
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Definition
| : bind to P2Y12 and ADP receptors. Inhibiting platelet aggregation, Use when ASA contraindicated. |
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Term
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Definition
| GP IIa/IIIb inhibitors. Inactivating aggregation |
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Term
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Definition
| Commonly used substance . Adenosine reuptake inhibitor since adenosine is one of the substance that reduces that stickiness of platelets. |
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Term
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Definition
| cheap. Activates all plasminogens, not selective to clots. |
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Term
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Definition
| activates only plasminogen bound to clot |
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Term
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Definition
| antidote for too much plasminogen activation |
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