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Pharmacology- Test 2
| Question | Answer |
|---|---|
| What is epilepsy? | A group of disorders characterized by excessive excitability of neurons in the CNS which causes recurrent, spontaneous seizures |
| What is a seizure? | A sudden, stereotyped episode with a change in motor activity, sensation, behavior, or consciousness, a paroxysmal derangement of cerebral function, that is due to an abnormal electrical discharge in the brain. |
| What is a convulsion? | Refers to abnormal motor phenomena |
| What type of seizures produce immediate loss of consciousness? | Generalized Seizures |
| What is Lennox-Gastaut Syndrom(LGS)? | It is a severe form of epilepsy that usually develops during preschool |
| What non-drug therapy has the best success? | Neurosurgery |
| What one drug appears effective against almost all forms of epilepsy? | Valproic acid |
| What is a major risk when taking AEDs? | Suicidal thoughts & behaviors |
| What are the 2 groups of AEDs? | 1. Traditional AEDs 2. Newer AEDs |
| Which AED drugs are prescribed more widely? | Traditional AEDs |
| Which AEDs pose greater risk to the developing risk? | Traditional AEDs |
| Which drug has a small therapeutic index? | Phenytoin (Traditional AED) |
| Why is Carbamazepine (Traditional AED) unusual? | Its half life decreases as therapy progresses |
| What should be avoided when taking Carbamazepine? | Grapefruit juice |
| What drug is used to tx Migraines? | Valproic Acid |
| How are seizures initiated? | Seizures are initiated by discharge from a group of hyperexcitable neurons called a focus |
| Explain partial seizures. | Excitation undergoes limited spread from the focus to adjacent cortical areas |
| Explain generalized seizures. | Excitation spreads widely throughout both hempispheres of the brain |
| How do AEDs act? | Through 4 mechanisms: 1. Blockade of sodium channels 2. Blockade of calcium channels 3. Blockade of receptors for glutamate 4. Potentiation of GABA |
| What is glutamate? | An excitatory neurotransmitter |
| What is GABA? | An inhibitory neurotransmitter |
| What accounts for nearly half of all tx failures? | Nonadherence |
| Why must withdrawal from AEDs be done gradually? | An abrupt withdrawal can trigger SE |
| Phenytoin & Carbamazepine are active against: | Partial & tonic-clonic seizures |
| What drug causes gingival hyperplasia? | Phenytoin |
| Which drug out of the two is most often preferred? Why? Phenytoin or Carbamazepine | Carbamazepine b.c it is better tolerated |
| Which drug can cause potentially fatal liver injury especially in children under 2 years old? | Valproic Acid |
| Which drug can cause fatal pancreatitis? | Valproic Acid |
| Should women with major seizure disorders continue taking AEDs throughout pregnancy? | Yes |
| Explain how Phenytoin, Carbamazepine, Valproic Acid and Lamotrigine work? | They reversibly bind to sodium channels which prolongs channel inactivation |
| What are the signs of Phentoin toxicity? | Nystagmus, sedation, ataxia, diplopia & cognitive impairment |
| What are the side effects of Carbamzepine? | Leukopenia, anemia & thrombocytopenia |
| Antiepileptic drugs can exert their effect by increasing the effect of what? | Gamma-aminobutyric acid |
| Complex partial seizures differ from simple partial seizures in that they involve: | lack of response to the environment |
| What requires immediate nursing care for a patient taking phenytoin? | Nystagmus |
| What is an adverse reaction to Valproic acid that should be reported immediately? | Abdominal pain and lack of appetite |
| Levetiracetam (Keppra) can cause: | loss of muscle strength |
| What environmental factors trigger seizures? | Being asleep, transition between sleep and wakefulness (hypnogogia), tiredness & sleep deprivation, illness, constipation, menstruation, stress or anxiety and alcohol consumption |
| What daily life occurrences can trigger seizures? | Hyperventilation and flashing or flickering lights |
| What does Phenytoin produce which can cause potential drug interactions? | Produce a greater quantity of P450 enzymes |
| If a pt. is taking other drugs with Phenytoin what occurs? | The other drugs will be metabolized more quickly d/t the increased amount of P450 enzymes which will reduce their levels of concentration |
| What drugs cause interactions with Phenytoin | Cute Directors Entice Pretty Women C- Carbamazepine D- Digoxin E- Estrogens P- Phenobarbital W- Warfarin |
| What is the tonic phase of a seizure? | The stiffening phase |
| How is Phenytoin metabolized? | Hepatically |
| What drugs elevate carbamazepine levels? | Erythromycin & cimetidine |
| What are the multiple mechanisms of action with valproate (Depakote)? | 1. Increases GABA in the brain 2. Inhibits enzymes that inactivate GABA 3. Sodium channel inactivation 4.T-type Calcium channel inactivation |
| What are valproate (Depakote) pharmacokinetics? | 1. Well absorbed Orally 2. Excreted via urine 3. Plasma 1.2 life 15 hours |
| Valproic acid increases which drug's levels: | Phenobarbital |
| What does Valproate do to drugs that are highly bound to plasma proteins? | It displaces these drugs and causes them to be free in the body which can lead to toxicity (ex. phenytoin) |
| How does ethosuximide (Zarontin) work? | Inhibits T-type calcium channels in thalamic neurons |
| What are the pharmacokinetics for ethozuximide (Zarontin)? | 1. Well absorbed 2. Metabolized/excreted like Phenobarbital 3. 1.2 life 50 - 140 h |
| Is Warfarin a P450 inducer or inhibitor? | Inducer |
| What drugs can Warfarin not be given with? | The P450 inducers--> Phenobarbital, Phenytoin, Primidone and Carbamazepine |
| When taking a P450 inducer (Warfarin, Phenobarbital, Phenytoin, Primidone & Carbamazepine) what should you not give? | P450 inhibitors (Cimetidine & Grapefruit Juice) |
| When giving 2 P450 inducers what can happen to the pt? | The drugs levels in the pt. body may drop to sub-therapeutic levels which can put them at risk for strokes or seizures |
| What are the advantages to prescribe newer (adjunct) AED over traditional ones? | 1. Better tolerated 2. Lesser effects on fetus |
| Which newer (adjunct) AED is the only one that induces P450 enzymes? | Oxcarbazepine (Trilepal) |
| How does Lamotrigine (Lamictal) work? | 1. Blocks sodium channels not allowing the presynaptic release of glutamate 2. Also somewhat inhibits calcium channels |
| Where is Lamotrigine (Lamictal) metabolized? | Hepatically |
| What are the skin rashes the Lamotrigine (Lamictal) cause? | SJS Erythema Multiforme Toxic epidermal necrolysis |
| What new (adjunct) AED is not approved in the US? | Vigabatri(Sabril) |
| Which drug may induce absence myoclonic seizures? | Vigabatrin(Sabril) |
| Which drugs does Felbamate (Felbatol) increase their levels? | Phenytoin & Valproic Acid |
| What limits Felbamate (Felbatol) uses? | Its toxicity |
| What two AED are used to tx bipolar disorder? | Carbamazepine (Carbatrol) and Tiagabine (Gabitril) |
| Both Vigabatrin (Sabril) and Tiagabine (Gabitril) increase GABA action, explain how they do it. | 1. Vigabatrin (Sabril) inhibits GABA degradation 2. Tiagabine (Gabitril) inhibits GABA uptake |
| One of Tiagabine's (Gabitril) side effects is that it may: | induce seizures |
| What is Topiramate (Topamax) mechanism of actions? | 1. Potentiates GABA 2. Blocks sodium channels 3. Blocks calcium channels 4. Inhibits GluR action |
| What is Gabapentin? | An AED |
| How does Gabapentin work? | It inhibits calcium channels and increases GABA receptor action |
| How does Tiagabine an AED increase GABA action? | Inhibits GABA reuptake |
| How does Vigabatrin (Sabril) an AED increase GABA action? | Inhibits GABA degradation |
| How does Valproate an AED increase GABA action? | Inhibits GABA degradation |
| How does Gabapentin an AED increase GABA action? | Promotes GABA release |
| What drugs are indirect acting agonists for GABA? | Tiagabine, Vigabtrin (Sabril), Valproate, Gabapentin |
| What is the mechanism of action for the AED drugs Felbamate & Topiramate? | They block the actions of glutamate at AMPA & NMDA receptors |
| When does most SJS cases tend to occur? | Early spring and winter |
| What are the early signs and symptoms of SJS? | A nonspecific URI with fever, sore throat, chills, headache and malaise (from 1 -1 4 days), then the mucocutaneous lesions develop very abruptly |
| How long do SJS lesion outbreaks last? | 2 - 4 weeks |
| What is SJS mortality due to? | It is due to skin sloughing or necrosis |
| Which race gets SJS more frequently? | Caucasian |
| Which sex gets SJS more frequently? | Males |
| What age range usually gets this disease? | Individuals in their 20s-40s |
| What drug in SE Asia causes SJS? | Allopurino |
| What country described the earliest descriptions of tonic-clonic seizures? | Mesopotamia (Iraq) over 3000 years ago |
| What did Hippocrates think seizures were cause by? | From excessive phlegm/mucus or abnormal brain consistency |
| During the Middle ages, what did people think that caused seizures? | Divine beliefs |
| During the early 1900s what was considered a risk factor for epilepsy? | Excessive masturbation |
| Currently, many people believe that individuals with epilepsy are: | "abnormal" or "retarded" |
| Explain a simple partial seizure. | 1. With motor sings 2. With somatosensory or special-sensory symptoms 3. With autonomic symptoms or signs 4. With psychic symptoms |
| Explain a complex partial seizure. | 1. Simple partial seizures at onset, followed by impairment of consciousness 2. With impairment of consciousness at onset |
| Explain partial seizures evolving to secondarily generalized seizures. | 1. Simple partial seizures evolving to generalized seizures 2. Complex partial seizures evolving to generalized seizures 3. Simple partial seizures evolving to complex partial seizures evolving to generalized seizures |
| What are the 6 types of generalized seizures? | 1. Absence seizures 2. Myoclonic seizures 3. Clonic seizures 4. Tonic seizures 5. Tonic-clonic seizures 6. Atonic seizures |
| What are the 2 types of generalized absence seizures? | 1. Typical absence seizures 2. Atypical absence seizures |
| What is the best cellular marker of an epileptic event? | Paroxysmal Depolarizing Shift (PDS), which is a spike on the EEG |
| What does PDS represent? | A neuronal resting potential 10-15 times above a normal action potential |
| What are the therapeutic strategies for managing epilepsy? | 1. Decide whether to treat 2. Decide how long to treat for 3. Use monotherapy whenever possible 4. Use simple regimens 5. Encourage compliance 6. Choose the best drug for the pt. seizure type |
| What are the 3 types of glutamate receptors GluRs? | 1. AMPA 2. Kainate GluRs 3. NMDA GluRs |
| What does carbamazepine (Carbatrol) induce? | Hepatic enzymes |
| Why would oxcarbazepine (Trilepal) preferred over carbamazepine (Carbatrol)? | It is better tolerated and just as effective as carbamazepine (Carbatrol) |
| What does oxcarbazepine (Trilepal) induce? | P450 isoforms which metabolizes certain drugs (estrogens) which can make birth control pills less effective |
| What does oxcarbazepine (Trilepal) not induce? | P450 isoforms that metabolize AEDs which can reduce levels of the active part of oxcabazepine (Trilepal) - doses of this drug may need to be increased |
| What does oxcarbazepine (Trilepal) inhibit? | P450 isoforms that metabolize phenytoin which can result in phenytoin toxicity |
| Why are lower levels of carbamazepine seen with phenobarbital and phenytoin? | These drugs induce P450 enzymes which in turn metabolizes carbamazepine quicker |
| Phenobarbital is similar to which drug? | Phenytoin |
| Phenobarbital induces: | liver enzymes |
| What is a major concern when taking Phenobarbital? | Makes birth control and warfarin less effective |
| What does primidone (Mysoline) induce? Results? | liver enzymes which results in birth control pills being less effective |
| What drugs decrease the half-life of lamotrigine (Lamictal)? | Enzyme inducers (carbamazepine, phenytoin, phenobarbital) |
| What drugs increase the half-life of lamotrigine (Lamictal) | Enzyme inhibitors (valproate acid) |
| How can levels of Tiagabine (Gabitril) be reduced? | By drug-metabolizing drugs such as phenytoin, phenobarbital and carbamazepine |
| What is Gabapentin (Neurontin) mechanism of action? | Increased GABA release by presynaptic neurons |
| Does Gabapentin (Neurontin) have drug interactions? | No significant interactions and is well tolerated |
| Pregabalin (Lyrica) is a potent derivative of: | gabapentin |
| Pregabalin (Lyrica) mechanism of action: | 1. Not completely known, it binds to calcium channels. 2. Increases GABA levels by boosting GAD which converts glutamate into an inhibitory GABA neurotransmitter |
| Pregabalin (Lyrica) increases what drugs? | 1. Benzodiazepines 2. Barbituates 3. Other depressants |
| Baclofen (Kenstrom, Lioresal) is excreted primarily by: | kidneys |
| Gamma-hydroxybutyric acid (GHB) is used for: | narcolepsy, body building and date rape |
| Name a few SSRIs. | Fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil) |
| Name a few SNRIs. | Venlafaxine (Effexor), duloxetine (Cymbalta) |
| Are there drugs to treat every addiction? | No |
| What drugs have the strongest dependence liability? | 1. Narcotic analgesics - Morphine, Diamorphine 2. Psychomotor stimulants - Cocaine, Nicotine |
| What is alcohol abuse more damaging then? | May be more damaging than heroin, cocaine and prescription drug abuse |
| What type of abuse has the most effects on those who are closest to the patient? | Alcohol abuse |
| Where is alcohol absorbed? | Absorbed from the stomach, small intestine and colon |
| Where is alcohol distributed? | Distributed to all tissues (crosses the BBB & the placenta) |
| How much alcohol is metabolized per hour? | 10 -15 ml per hour = 1 drink per hour |
| What does ethanol convert into? | Acetaldehyde |
| How long does the conversion from ethanol to acetaldehyde take? | It takes place slowly (about 15 mL/hr) |
| If you drink more than one drink per hour, what happens? | The conversion from ethanol to acetaldehyde will not be complete from the first drink and the ethanol to accumulate |
| What are some agents that have been used in the treatment of withdrawal? | Beta-blockers (propranolol - Inderal), Clonidine (a-adrenergic agonist), Antipsychotics (Phenotiazines - chlorpromazine), Antiepileptics (Phenytoin - Dilantin) |
| What are the 4 categories for opiates and opioids? | 1. Natural alkaloids of opium (morphine & codeine) 2. Synthetic derivatives of morphine (heroin) 3. Synthetic agents structurally similar to morphine (oxycodone, methadone) 4. Opioid antagonsits (antidotes) used to counteract overdoses (naloxone) |
| What is the mechanism of action of opiates? | Unknown but it appears to interact with specific receptors interfering with pain impulses |
| Where does the main pharmacological action of opiates take place? | Cerebrum and medulla of CNS |
| Where else does opiates effect? | Effects smooth muscle, glandular secretions of the respiratory and gi tracts |
| What are opiates & opioids primarily used for? | Relief of pain but also induce states of euphoria (= high abuse potential) |
| What are the opioids direct effects on neurons? | 1. They reduce neurotransmitter release by closing calcium channels 2. They inhibit postysynaptic neurons by opening potassium channels |
| What is a non-benzodiazepine that treats insomnia? | Ezopiclone (Lunesta) |
| What are the cardinal symptoms of Parkinson's disease? | Resting tremor, muscle rigidity, postural instability, and slowed movement (bradykinesia) |
| What are the non-motor symptoms that PD patients experience? | Autonomic disturbances, depression, psychosis and dementia |
| What is the most effective drug for PD? Why? | Levodopa b.c it treats the motor symptoms |
| What is levodopa always given in combination with? | carbidopa |
| In PD, what is there an imbalance between? | There is an imbalance between dopamine and ACh in the striatum |
| What is the most adverse effect of Levodopa? | Dyskinesias |
| What drug has no therapeutic effect on its own? | Carbidopa |
| What may patients develop after taking Amantadine for one month? | They develop livedo reticularis--> mottled discoloration of the skin |
| What type of drugs are used to tx the motor symptoms of PD? | Drugs that directly or indirectly activate dopamine receptors or drugs that block cholinergic receptors |
| How does Levodopa relieve motor symptoms? | Levodopa undergoes conversion to dopamine in the nerve terminals |
| What is the enzyme the converts levodopa to dopamine? | Decarboxylase |
| In what 2 ways can diminished response to levodopa occur? | 1. Wearing Off 2. Abrupt loss of effectiveness ("on - off" phenomenon) |
| What are the main adverse effects of levodopa? | Nancy Declined Harry Politely N- Nausea D- Dyskinesias H- Hypotension P- Psychosis |
| How to first- generation antipsychotics work? | They block dopamine receptors in the striatum |
| Which antipsychotic drugs (1st or 2nd) generation can negate the effects from the drug levodopa? | First-generation antipsychotics |
| What combination of drugs can lead to a hypertensive crisis? | Levodopa with a nonselective MAO inhibitor |
| Why does high-protein meals reduce therapeutic effects of L-dopa? | Amino acids compete with levodopa for absorption from the intestine and for transport across the blood-brain barrier |
| How does carbidopa enhance the effects of levodopa? | It prevents decarboxylation of leveodopa in the intestine & peripheral tissues |
| What oral nonergot dopamine agonist is a first-line drug to tx motor symptoms? | Pramipexole |
| How does Pramipexole and other dopamine agonists relieve motor symptoms associated with Parkinson's Disease? | They cause direct activation of dopamine receptors in the striatum |
| Why is a COMT inhibitor combined with levodopa? | It enhances levodopa's effects |
| What COMT inhibitors are availavle? | Entacapone & Tolcapone |
| How does COMT inhibitors work? | The drug inhibits metabolism of levodopa by COMT in the intestine and peripheral tissues which makes levodopa more available in the brain |
| How does Selegiline and Rasagiline enhance responses to levodopa? | It inhibits MAO-B which prevents dopamine breakdown |
| How do Anticholinergic drugs relieve symptoms of PD? | They block cholinergic receptors in the striatum |
| Levodopa promotes: | Dopamine synthesis |
| What are the two groups of dopamine agonists? | Ergot & nonergot |
| What are the nonergot derivatives? | PAR P- Pramipexole A- Apomorphine R- Ropinirole |
| What are nonergot derivatives highly selective for? | Dopamine receptors |
| What are the ergot derivatives? | Bromocriptine and Cabergoline |
| Which of the dopamine agonists group cause fewer side effects? Why? | The nonergot derivatives because of their selectivity |
| Which drug can cause sleep attacks? | Pramipexole |
| What drugs have been used the longest with PD patients? | Anticholinergic drugs |
| When pramipexole is combined with levodopa, patients are most likely to experience what symptoms? | Dyskinesias such as head bobbing and orthostatic hypotension |
| Does excessive dopamine inhibit muscle movement? | Yes |
| What is ballismus? | Violent movement of the limbs |
| What drug inhibits the conversion of levodopa to dopamine in the intestines and in tissue outside the CNS? | Carbidopa |
| Besides the cardinal signs of PD, what are other signs of this disease? | Small, cramped handwriting Stiff facial expression Shuffling walk Muffled speech Depression |
| When does PD usually develop? | Age 65 or greater |
| Levodopa (L-Dopa) has been available since: | 1960s |
| What is the most effective drug for PD? | Levodopa (L-Dopa) |
| What is Levodopa's (L-Dopa) mechanism of action? | Promotes synthesis of dopamine in the striatum |
| How does Levodopa (L-dopa) cross the BBB? | Transporter |
| How is Levodopa given? absorbed? | Given- Orally Absorbed- SI |
| Since Levodopa (L-dopa) is absorbed in the SI, what does it interfere with? | Diet |
| How is Leveodopa (L-dopa) broken down? | Decarboxylases & COMT (small portion) |
| What are the first line drugs for PD? | Dopamine agonists (Nonergot & ergot) |
| What are the advantages of ergot & nonergot drugs? | 1. There action isn't dependent on enzymatic conversion 2. They aren't potentially converted to toxic metabolites 3. They don't compete with dietary metabolites for GI absorption & BBB transport 4. They are less likely to induce dyskinesias |
| Are dopamine agonists less effective than levodopa? | Yes! |
| What PD drugs are highly selective for dopamine receptors? | Nonergots (Pramipexole (Mirapex), Apomorphine (Apokn), Ropinirole (Requip) |
| Does ergot or nonergot have fewer medication side effects? | Nonergots |
| How long does it take for the nonergot, Pramipexole (Mirapex) to become effective? | It can take weeks to develop |
| How long does it take for the nonergot, Pramipexole (Mirapex) to reach its peak plasma concentration? | 1 -2 hours |
| Is the nonergot drug, Pramipexole (Mirapex) widely distrubited? | Yes, it accumulates in RBC |
| Explain how the nonergot drug, Pramipexole is eliminated. | It is eliminated unchanged in the urine |
| What two drugs are used for infertility? | Bromociptine (Parlodel) & Cabergoline (Dostinex) --> Ergot drugs |
| What are the other less likely side effects with an administration of a dopamine agonist? | Confusion, Hallucinations or psychosis, sleepiness, drowsiness or sedation (may interfere with driving) |
| What drugs are primarily reserved for younger patients? | Dopamine agonists |
| What are relatively new drugs that slow down the breakdown of L-dopa in the intestines & periphery? | COMT Inhibitors-Tolcapone (Tasmar) & Entacapone (Comtan) |
| Carbidopa inhibits: | decarboxylases |
| What happens by inhibiting COMT? | It decrease levodopa metabolites that may be competing with levodopa for BBB transporters |
| What increases levodopa's half life by 50 - 75%? | COMT Inhibitors- Tolcapone (Tasmar) & Entacapone (Comtan) |
| When should COMT inhibitors be used? | Only in combination with levodopa |
| How are COMT inhibitors bound to plasma protein? | Highly bound |
| What is Tolcapone (Tasmar) indicated for? | It's indicate for patients whose symptoms can't be controlled by any other drug |
| When patients are taking Tolcapone (Tasmar) which must be monitored? | Their liver function |
| Selegiline (Deprenyl, Eldepryl) inactivates: | dopamine in the striatum |
| At high does Selegiline inhibits: | MAO-A & MAO-B (non-selective) |
| With Selegiline (Deprenyl, Eldepryl) there is no risk of: | a hypertnesive crisis |
| What did early studies of selegiline (Deprenyl, Eldepryl) suggest? | That it may delay the progression of PD |
| Why is selegiline (Deprenyl, Eldepryl) used in combination with levodopa? | It blocks the degradation of dopamine generated by levodopa |
| Selegiline doesn't inhibit: | peripheral metabolism of catecholamines |
| Selegiline's effectiveness declines in: | 12 to 24 months |
| If selegiline is given at high doses what is the hypertnesive crisis driven by? | Tyramine in the diet |
| Drug-Drug interactions with selegiline | 1. Intensifies levodopa responses (and side effects) 2. Causes dangerous effects if combined with meperidine (Demerol) --> a pain medication 3. It can be fatal when combine with fluoxetine (Prozac) |
| What is a mild PD drug? | Amantadine (Symmetrel) |
| What is a drug that is a weak antagonist of NDMA receptor? | Amantadine (Symmetrel) |
| What is Amantadine's (Symmetrel) mechanism of action? | Increases dopamine by inducing dopamine exocytosis and inhibiting its reuptake |
| What dose should be reduced with renal impairment? | Amantadine (Symmetrel) |
| How should Amantadine (Symmetrel) be taken? | 1. Alone 2. With levodopa or a dopamine agonist |
| What is Amantadine (Symmetrel) usually given for? | Used as an antiviral drug |
| Anticholinergic drugs can be taken: | alone or in combination with levodopa |
| What drugs are rarely used in elderly patients or with those that have cognitive problems b.c they increase confusion? | Anticholinergic effects- Trihexphenidyl (Artane), Benztropine (Cogentin), Biperiden (Akineton) |
| What are the new treatments for PD? | 1. Fetal cell transplantation 2. Gene transfer and delivery (GDNF/viral vectors) 3. Grafts 4. Stem cells 5. Coenzyme Q10 6. Deep Brain stimulation |
| What is Glial cell-derived neurotrophic factor (GDNF)? | It's a small protein that promotes the survival of many types of neurons |
| What is coenzyme q10? | It's a key component of the respiratory chain. It has the ability to transfer electrons (an antioxidant) |
| What is DBS (deep brain stimulation) approved for? | It is approved for advanced PD |
| What does DBS help with? | It may recover the pt. movement control and be able to live a normal life |
| What is a side effect of DBS? | Speech dysfluency or stuttering |
| What are other names for antianxiety agents? | Anxiolytics or tranquilizers(older term) |
| What are sedative-hypnotic drugs? | Drugs that depress the CNS function |
| What are the 3 major groups of sedative-hypnotics? | 1. Barbiturates 2. Benzodiazepines 3. Benzodiazepine-like drugs |
| What drugs are the first choice for anxiety and insomnia? | Benzodiazepines |
| All beneficial effects of benzodiazepines and most adverse effects result from: | depressant actions in the CNS |
| What are the adverse side effects of Benzodiazepines when administered intravenouslyy? | Profound hypotension, respiratory arrest and cardiac arrest |
| How do benzodiazepines work? | They enhance the actions of GABA |
| How are certain benzodiazepines selected for patients? | Since all of these drugs have essentially equivalent actions, they are selected based on their time course |
| What are benzodiazepines used for? | Anxiety, insomnia and seizure disorders |
| What side effect can triazolam (Halcion) cause? | Anterograde amnesia |
| Even though benzodiazepines are safe when used alone when can they become extremely hazardous? | When they are used in combination with other depressants |
| What is flumazenil (Romazicon) and when is it used? | Flumazenil is an antagonist which reserves the sedative effects of benzodiazepines |
| What are the benzodiazepine-like drugs? | Zolpidem, zaleplon & eszopiclone |
| How does ramelteon (Rozerem) work? | They activate receptors for melatonin |
| What are the three classes of barbituates? | 1. Ultrashort-acting agents 2. Short-to-intermediate acting agents 3. Long-acting agents |
| What are drugs that promote sleep? | Hypnotics |
| Why are benzodiazepines preferred to barbiturates? | They are safer, have low abuse potential, cause less tolerance and dependence and don't induce drug-metabolizing enzymes |
| What should you do to minimize withdrawal symptoms from benzodiazepines? | They should be discontinued gradually over a couple of weeks |
| What are the prinicipal adverse effects of benzodiazpines? | Daytime sedation and anterograde amnesia |
| What is the oldest sedative-hypnotic agents? | Ethanol |
| What sedatives were made in the 50s, 60s? | 50s- barbiturates 60s- benzodiazepines |
| What are sedatives? | They are drugs that decrease neural activity, moderate excitement and calm the person taking the drug |
| What are anxiolytics? | They are drugs intended to reduce anxiety or tension at doses which don't cause sedation or sleep |
| What are hypnotics? | They are drugs that produce drowsiness and facilitate the onset and maintenance of sleep |
| What are the symptoms of insomnia? | Difficulty falling asleep, awakening frequently during the night, waking up too early, inability to fall back to sleep or awakening feeling unrefreshed |
| What can happen if insomnia is left untreated? | It can affect a person's emotional, mental & physical health |
| What are the mechanisms of actions for benzodiazepines? | They increase responses to GABA |
| How long does it take before the onset of benzodiazepines? | The effects are immediate |
| What are the categories of benzodiazepines? | 1. Ultra-Short Acting 2. Short Acting 3. Intermediate Acting 4. Long Lasting |
| Are benzodiazepines lipid-soluble? | Yes, they cross the BBB easily |
| With whom do benzodiazepines persist longer with? | They persist longer in high fat-to-lean body mass |
| Do many people abuse benzodiazepines? | Yes |
| What is flumazenil (Romazicon)? | A benzodiazepine (receptor) antagonist, it is used to treat benzodiazepine overdose |
| What are benzodiazepines effects & uses? | Sedation & sleep, anxiety & aggression, muscle spasm relaxants, anticonvulsant effects, amnesia |
| What is the principal side effects on benzodiazepines? | Psychotic slowing |
| How long is flurazepam (Dalmane) effective for? | Up to 4 weeks |
| When does the peak hypnotic effect of flurazepam (Dalmane) reached? | 2-3 nights of use b.c of its long metabolite half life (47 - 100 hours) |
| When does the peak effect of temazepam (Restoril) occur? | 2-3 hours after an oral dose |
| What drug is recommended for short-term use (7-10 days)? | Temazepam (Restoril) |
| When is triazolam (Halcion) used? | Used intermittently for less than 2 - 4 weeks |
| What are the drugs of first choice for insomnia? | Zolpidem (Ambien) & ezopiclone (Lunesta) |
| What type of onset does Zolpidem (Ambien) have? | Rapid onset |
| How many Americans suffer from either chronic or occasional insomnia? | 100 million |
| How much was the US prescription sedative-hypnotic market worth in 2005? | 2.8 billion |
| What do benzodiazepines increase responses to? | GABA |
| What benzodiazepines are metabolized outside the liver? | OTL O- Oxazepam T- Temazepam L- Lorazepam |
| What type of benzodiazepines are used to manage insomnia? Medication names? | Shorter-acting & intermediate-acting Estazolam (Prosom) Flurazepam (Dalmane) Triazolam (Halcion) |
| What kind of action is Temazepam (Restoril)? | Intermediate - acting |
| What is the recommended usage for Temazepam (Restoril)? | Short-term use (7-10 days) |
| What type of action does Triazolam (Halcion) have? Peak? | Short-acting Peak - 1 -2 hours |
| What is effective as benzodiazepines but safer (sedatives)? | Zolpidem (Ambien) & Ezopiclone (Lunesta) |
| Which benzodiazepine for treating anxiety are short acting and an exception to the general rule? | Lorazepam (Ativan) |
| What is the peak action of Lorazepam (Ativan)? | 2 - 4 hours |
| Does lorazepam (Ativan) produce active metabolites? | No |
| How is lorazepam (Ativan) absorbed? | Rapidly |
| How is loazepam (Ativan) given? | IM, PO, IV |
| What is a potent 5HT1A agonist? | Buspirone |
| What is an anti-anxiety agent that isn’t chemically or pharmacologically related to benzodiazepines, barbiturates or other sedative/anxiolytic drugs? | Buspirone |
| How long does it take for the effect of Buspirone (BuSpar) to begin? | Several Days |
| Is there a risk of dependence when taking Buspirone (BuSpar)? | No |
| Which drug doesn’t intensify the effects of benzodiazepines or alcohol? | Buspirone (BuSpar) |
| What are SSRIs and SNRIs inhibitors of? | Serotonin Reuptake |
| What happens when serotonin is not reuptake? | It intensifies transmission at serotogenic synapses |
| When a patient is on SNRIs and SSRIs, how long does it take for blockage to occur? Therapeutic effects? | Blockage occurs quickly; therapeutic effect is slow to develop |
| How are SNRIs and SSRIs absorbed? | Well absorbed |
| What % of the SSRIs & SNRIs is bound to plasma proteins? | >90% |
| What are the principal side effects of SNRIs and SSRIs? | Sexual dysfunction, weight gain, withdrawal syndrome |
| What should SSRIs never be used with? | MAOIs |
| Name some SSRIs. | Fluoxetine (Prozac), Sertraline (Zoloft), Paroextine (Paxil) |
| Name some SNRIs. | Venlafaxine (Effexor) & Duloxetine (Cymbalta) |
| When are SNRIs and SSRIs contrainindicated? | 1. Patients are on MAOIs 2. There is liver or kidney disease 3. There are seizures or epilepsy 4. There is bleeding or a blood clotting disorder 5. There is glaucoma 6. There is bipolar disorder 7. There is drug abuse or suicidal thoughts |
| What is Methaqualone? | It was developed in Indian (1950s) as an anti-malarial drug |
| What is the key component of a Quaalude? | Methaqualone |
| During the 70s, what were Quaaludes used for? | Sleeping pills |
| In the 1970s, what were Quaaludes used for? | Users would “lude out” by combing the drug with alcohol to achieve a drunken, sleepy high |
| What can happen if an individual overdoses on Methaqualones? | Respiratory arrest, delirium, kidney or liver damage, coma & death |
| What is Methaqualones mechanism of action? | B-adrenergic receptor antagonists |
| What is Methaqualone similar to? | A hypnotic-sedative similar to barbiturates |
| What is a very addictive CNS depressant? | Methaqualone |
| In 1965, what was methaqualone first introduced for? | Anxiety & Sleep disorders |
| What drug had an erroneous reputation as an aphrodisiac? | Methaqualones |
| What is today’s use in the US for Methaqualones? | Minimally |
| What do counterfeited Quaaludes sole on the street contain? | Sedatives other than methaqualone |
| What it the most effective tx for drug dependence when there are no drugs available? | Cognitive – behavioral interventions |
| What is cognitive – behavioral therapy? | Combines behavioral therapy, family education, individual counseling, drug testing and encourage for nondrug-related activities |
| When is a woman an alcoholic? | 7 drinks/wk. or more than 3 drinks/occasion |
| When is a man an alcoholic? | 14 drinks/wk. or more than 4 drinks/occasion |
| When is an elder person an alcoholic? | Older than 65 years having more than 7 drinks/week or 3 drinks/occasion |
| What are the pharmacological effects of alcohol? | Depressed CNS, Increases GABA – mediated inhibition, Increases inhibition of calcium channels, Increases inhibition of NMDA – receptor function, intellectual and motor activity drops, Increase salvia & gastric secretions, Diuresis, Brain & liver damage |
| What is the pharmacokinetics of alcohol? | Hepatic metabolism, 50 % of Asians have an inactive aldehyde dehydrogenase (Disulfiram – effect) → makes them get drunk easily |
| Alcohol Abuse & the Liver | Causes fatty liver, alcoholic hepatitis, hepatic cirrhosis |
| What is a fatty liver? | Accumulation of lipids in hepatocytes, slightly enlarged liver |
| What is alcoholic hepatitis? | Hepatomegaly, inflammation, jaundice and pain |
| What is hepatic cirrhosis? | Loss of liver structure and function, portal hypertension and internal bleeding |
| Alcohol Abuse & the GI tract | Toxicity to the epithelium, ulcers and etiologic reason of acute & chronic pancreatitis |
| Alcohol Abuse & Myotoxicity | Causes wasting and degeneration of muscle and cardiomyopathy |
| What is cardiomyopathy? | Arrhythmias, degeneration of myocardium, CHF |
| Alcohol Abuse & the Blood | Causes anemias, depression of leukocyte migration to inflamed areas |
| Alcohol Abuse & Endocrine Effects | Causes diuresis, tocolytic activity, lower circulation testosterone in chronic male alcoholics, lower estradiol & progesterone in female alcoholics, transient hyperglycemia |
| What is a tocolytic activity? | It inhibits uterine contractions |
| Alcohol Abuse & Teratogenic effects | Causes fetal alcohol syndrome |
| What is alcohol abuse more damaging then? | Heroin, cocaine and prescription drug abuse |
| Where is alcohol absorbed? | Stomach, SI & colon |
| Where is alcohol distributed? | All tissues (crosses the BBB & the placenta) |
| Naltrexone (ReVia, Depade) | An opioid receptor antagonist. A synthetic congener of the opioid agonist oxymorphone (Numorphan). Naltrexone is also related to the potent opioid antagonist, naloxone (n-allylnoroxymorphone) (Narcan). |
| What is naltrexone's mechanism of action? | It blunts craving of pleasure derived from drinking alcohol |
| What are the side effects of naltrexone? | Nausea, headache, constipation, dizziness, nervousness, insomnia, drowsiness, anxiety |
| What type of drug when used in combination with disulfiram causes hepatotoxicity? | Naltrexone |
| What class of drug treats alcohol withdrawal best? | Benzodiazepines--> Lorazepam (Ativan) & oxazepam (Serax) |
| Why is lorazepam and oxazepam preferred to use on patients with liver disease for alcohol withdrawal? | Because the 1.2 lives of other benzodiazepines can be prolonged significanlty |
| What is death due to Cocaine usually do to? | Cocaine induces hyperthermia which causes death |
| What is another name of Amphetamine? | Non-catechol sympathetic amine |
| What are the side effects of Amphetamine? | 1. Addiction 2. Insomnia, irritability, dizziness 3. CV effects (palpitations, hypertension) 4. GI effects (vomit, abdominal cramps, diarrhea) |
| What drug's main contraindication is for hypertension? | Amphetamine |
| Adderall | An amphetamine which is a psychostimulant composed of racemic mixture of amphetamines which is used for ADHD & narcolepsy |
| What drug is used as a study drug at many colleges? | Adderall |
| What is Adderall reported to do? | Help focus energy and concentration to a much higher level than normal --> allows the user to focus and stay awake |
| What are the contraindications for Adderall? | MAOIs, SSRIs, SNRIs, TCAs, bupropion |
| What are the other names for Ephedrine? | Ephedra, Ma Huang |
| What is Ephedrine's mechanism of action? | Directly stimulates adrenoceptors & indirectly stimulate the release of NE (a mixed-acting adrenergic agonist) |
| What drug remains unchanged in urine? | Ephedrine |
| How does compulsive use of nicotine occur? | Tolerance + physical + psychological dependence |
| What drug causes addiction? | Nicotine |
| What type of withdrawal does nicotine have? | Physical withdrawal syndrome |
| What is the treatment of nicotine addiction? | Combination of counseling and drugs |
| What are the 2 classes of drugs that helps with nicotine addiction? | 1. Direct acting drugs: Nicotine agonists (Nicotine Replacement Therapy-NRT), Nicotine partial-agonists (Varenicline) 2. Drugs acting through non-nicotinic mechanisms (Bupropion) |
| Give examples of NRT. | 1. Nicotine polacrilex chewing gum (Nicorette); lozenges (Commit) 2. Nicotine transdermal patches (Nicodrem CQ, Nicotrol) 3. Nicotine inhaler (Nicotrol inhaler): Nicotine nasal spray (Nicotrol NS) |
| What is Varenicline (Chantix, Champix)? | It reduces cravings for and decreases the pleasurable effects of smoking |
| What is Bupropion (Zyban) (Wellbutrin)? | Atypical antidepressant that reduces cravings and nicotine withdrawal effects |
| What are the pharmacological effects of Cannabis (THC)? | 1. Acts on the CNS 2. Induces a feeling of relaxation and well being (similar to ETOH) 3. Induces sharp sensory awareness 4. Diminishes short-term memory 5. Diminished motor coordination 6. Catalepsy (stunned) |
| What does Cannabis increase? | Appetite, bronchodilation, analgesia, tachycardia, vasodilation (blood-shot eyes) |
| What are the pharmacokinetics of cannabis? | 1. Effects take about 1 hour to develop 2. Highly lipophilic 3. Stays in fat tissues for several days then leaves |
| When does physical dependence occur with Cannabis? | Occurs only in high doses |
| What should Cannabis be not classified as? | Addictive |
| What kind of syndrome can Cannabis cause? | Withdrawal syndrome |
| What drugs are rapidly becoming drugs of abuse worldwide? | Prescription drugs |
| What are the 3 classes of drugs that are misused/abused worldwide? | 1. Opioids (prescribed for pain) 2. Anxiolytics (prescribed for anxiety and sleep disorders) 3. Stimulants (prescribed for narcolepsy, ADD & obesity) |
| Does crushing, chewing or dissolving tablets destroy the controlled-drug release feature of tablets? | No |
| What happens if a drug contains niacin and is crushed? Snorted? | Niacin gives an unpleasant taste and GI discomfort, if it's snorted the powder irritates nasal passages |
| Why do individuals with eating disorders use laxatives? | Purging |
| Why are laxatives not effective? | Most of the calories are absorbed by the SI and using laxatives for weight loss isn't effective |
| What are the mechanisms of action of laxatives? | Acts by irritating the lining of the intestines or by directly stimulating peristalsis |
| What does prolonged use of laxatives do to a body? | The bowels become unresponsive and constipation occurs |
| What are the diet pills that were abused? | Fenfluramine + Phentermine cocktail (Fen Phen) |
| What is the mechanism of action of Fenfluramine (Pondimin)? | Inhibits serotonin reuptake (an SSRi) leading to CNS effects including a feeling of satiety. |
| History of Fen Phen | 1. 1992 doctors began prescribing a fenfluramine + phentermine (Fastin) cocktail as an 'off-label' drug (not approved by the FDA) 2. 1997- Fen Phen caused pulmonary htn and heart-valve disease due to excess serotonin --> withdrawn from the marke |
| Phentermin (Fastin) | Appetite suppressant of the amphetamine class |
| Anabolic (Androgenic) Steroids | Used to increase protein anabolism, muscle mass (with exercise), appetite & sexual drive |
| What are the side effects of anabolic (androgenic) steroids? | 1. No clear or demonstrable effects in adult males 2. Dramatic effects on young females (masculinization) 3. Genitalia of infants are affected when mothers use androgens 4. Females may have spotting due to progestin activity of testosterone analogs |
| Volatile Substance Abuse (VSA) | Inhalation of volatile substances which occurs mainly among adolescents and consists of glue sniffing and solvent sniffing |
| What are the most abusive volatile substances?1 | 1. Contact adhesives (toluene) 2. Gasoline 3. Halogenated solvents 4. Volatile hydrocarbons 5. Aerosol propellants 6. Halocarbons (found in fire extinguishers) |
| What is VSA dose-dependence similar to? | Hypnotic sedatives |
| What does small doses of VSA lead to? | Euphoria and other behavior similar to those caused by ethanol |
| What does high doses of VSA lead to? | Convulsions, coma and death |
| Diuretics (aka water pills) | 1. Increase sodium and water excretion by the kidney through inhibition of renal sodium transport --> treats edema and hypertension |
| What type of drug is one of the most commonly used drugs? | Diuretics |
| Functions of the kidney | 1. Fluid volume and solute homeostasis 2. Excretion of metabolic wastes, drugs and other foreign compounds 3. Endocrine 4. Regulation of BP |
| What does the endocrine system produce? | 1. Erythropoietin 2. Active Vitamin D 3. Vasoactive mediators (renin) |
| What does the fluid homeostasis consist of? | 1. Water 2. Electrolytes (Na, K, Cl, Ca, Mg, phosphate, sulfate) 3. Acid-base balance |
| Formation of Urine | Urine is formed by filtration in the glomerulus (cortex), modified by the nephron (cortex & medulla), and then drains --> collecting duct --> renal pelvis --> ureter --> bladder |
| What is the weight and size of each kidney? | Weight: 150 g Size: 11 cm long x 6 cm wide x 3 cm thick |
| 1 kidney | Only need one for survival, this one kidney compensates by increasing functional activities |
| Can the kidney repair itself to some extent? | Yes, but it can't form new nephrons |
| Nephron | 1. Functional unit of the kidney 2. ~ 1 million nephrons/kidney 3. Two components: Vascular & Tubular |
| What is the first step in urine formation? | Glomerular Filtration |
| Glomerulus | Acts as a colander - permits water and ions through, but not RBS or proteins (or drugs bound to proteins) |
| Layers of Glomerulus | 1. Capillary endothelium 2. Basement membrane 3. Podocytes |
| Why does 20% of the plasma fluid filter in the nephron? | Capillary hydrostatic |
| What type of excretion is used when the main mechanism of drugs is urinary excretion? | Tubular Secretion |
| What type of excretion is important for the excretion of H+ and K+? | Tubular Secretion |
| What is the normal glomerular filtration rate (GFR)? | 125 mL/min. |
| What happens when an individual has renal disease? | GFR decreases which causes less fluid and solutes to be filtered = decreased excretion of water and solutes |
| Calculation of GFR | Measurements of serum creatinine levels (an increase in serum creatinine = decrease in GFR) |
| How much water is filtered per day? Excreted? | Filtered- 180 L Excreted- 1.5 L |
| What happens to the unexcreted water and solutes? | They are returned to the circulation by tubular reabsorption |
| What does the proximal tubule reabsorb? | 1. Sodium (65% of filtered sodium) 2. Water, osmotically driven by sodium reabsorption (65% of filtered water) 3. Chloride, potassium, bicarbonate, calcium, magnesium, phosphate, sulfate 4. All filtered organic solutes (glucose & a.a.) |
| What does the proximal tubule secrete? | 1. Protons (acidifies urine) 2. Organic acids and bases (drug excretion) |
| What does the early distal convoluted tubules do? | Reabsorbs sodium on NaCl cotransporter |
| What does the collecting duct & late distal convoluted tubule (aka distal nephron) do? | 1. Site of final urine modification 2. Reabsorbs sodium (controlled by aldosterone) 3. Secretes potassium 4. Secretes protons (can reduce urine pH to 4.5-5) 5. Reabsorbs water relative to ADH to form an ADH concentrate or dilute (no ADH) urine |
| What happens in the absence of ADH? | The collecting duct is impermeable to water |
| What does ADH deficiency result in? | Diseases such as diabetes insipidus --> characterized by excretion of large volumes of dilute urine |
| What is 60% of our body weight? | Total body water |
| Intracellular fluids (inside cells) | 28 L |
| Extracellular fluid (outside of cells) | 14 L 1. Interstitial fluid- 11 L (fluid surrounding cells) 2. Plasma - 3 L - fluid component of blood |
| Edema | Accumulation of excess fluid in the interstitial compartment --> becomes apparent with ~ 3 L increase in volume |
| What maintains and enhances edema? | Renal sodium and water retention (not good) |
| Renin | Released by the kidney, cleaves angiotension I from angiotensinogen made by the liver |
| How does the body monitor fluid volume? | Pressure |
| What does a drop in pressure activate? | Regulatory mechanisms (ex. renin-angiotensin-aldosterone system to conserve sodium and water) |
| Mechanism of Action: Diuretics | Doesn't directly affect water transport --> indirectly inhibits sodium reabsorption at various sites along the nephron, resulting in more water & sodium excretion |
| Diuresis | Increased output of urine |
| Natriuresis | Increased output of sodium |
| When 1% of fluid/solute reabsorption is blocked what happens? | Urine output increases by 1.8 L = 4 pound weight loss |
| Diseases that cause edematous states | 1. CHF 2. Hepatic cirrhosis with ascites 3. Renal disease |
| Secondary uses of diuretics | 1. Prevent renal failure by maintaining urine flow 2. Kidney stones 3. Acute treatment of hypercalcemia 4. Glaucoma 5. Altitude sickness 6. Diabetes insipidus |
| Diuretic classes of drugs (-1) | 1. Carbonic anhydrase inhibitors 2. Loop diuretics 3. Thiazide diuretics 4. Potassium-sparing diuretics--> Aldosterone antagonists & Sodium channel blockers 5. Osmotic |
| Besides osmotic diuretics, how do the first 4 classes work? | Prevent passive water reabsorption by inhibiting sodium reabsorption by the kidney |
| Diuretics - Adverse Effects | 1. Hypovolemia (leads to HTN) 2. Loss/gain of electrolytes 3. Acid-base imbalance |
| When are adverse effects seen from a a diuretic drug? | 2 weeks after taking it |
| What can happen when a diuretic blocks sodium reabsorption at one nephron site? | 1. Interfere with other renal functions linked to it 2. Alter transport activity at other nephron sites |
| With the exception of spironolactone, where do all diuretics act? | Within the tubular lumen (side of cells facing the urine) |
| With the exception of mannitol, how do diuretics gain luminal entry? | By tubular secretion in the proximal tubule |
| What are the other common uses of carbonic anhydrase inhibitors (other than diuresis)? | 1. Metabolic alkalosis, particularly with fluid load 2. Induce urinary alkalinization 3. Glaucoma 4. Acute mountain sickness (altitude) |
| What carbonic anhydrase inhibitors are used for glaucome? | dorzolamide, brinzolamide, topical CAIs --> reduce intraocular pressure |
| Pharmacokinetics of Carbonic Anhydrase Inhibitors | 1. Near complete oral absorption 2. Diuresis within 30 minutes, maximal at 2 hours, persists for 12 hours after a single dose 3. Renal route of excretion |
| What are the most efficacious diuretics? | Loop (High-Ceiling) Diuretics |
| What are the 2 derivatives of Loop Diuretics? | 1. Sulfonamide Derivatives 2. Phenoxyacetic Acid Derivatices |
| What are the medicines in the sulfonamide derivatives class of Loop Diuretics? | 1. Furosemide (Lasix)- most frequently prescribed 2. Torsemide (Demadex) 3. Bumetanide (Bumex) |
| What is the medication that is in the sulfonamide derivative class of Loop Diuretics? | Ehtacrynic Acid (Edecrin) |
| What are loop diuretics drug interactions? | 1. Ototoxicity (caution aminoglcosides) 2. Digoxin toxicity- hypokalemia 3. Lithium toxicity d/t decrease excretion 4. NSAIDs blunt diuretic effect |
| What are thiazides drug interactions? | 1. Digoxin toxicity- hypokalemia 2. Lithium toxicity- decreased excretion 3. NSAIDs- decrease diuretic effect |
| How are K-Sparing diuretics used? | In combination with loop or thiazide diuretics |
| Hyperkalemia and K-Sparing Diuretics | 1. Is d/t decreased potassium excretion 2. Avoid K+ supplements 3. Don't use in combo with spironolactone 4. Caution when used with ACE inhibitors, angiotension blockers, or direct renin inhibitors |
| What is another name for kidney stones? | Triamterine |
| What is Spironolactone (Aldactone) mechanism of action? | 1. Receptor antagonist of aldosterone 2. Aldosterone increases synthesis of Na+ channels in collecting duct 3. Spironolactone competes with aldosterone for binding to mineralocorticoid receptors, which prevents production of Na+ channels |
| Why does Spironolactone (Aldactone) have a slow onset of action? | Need to get rid of sodium channels already formed which takes 1 - 2 days |
| Hyperkalemia & Spironolactone (Aldactone) | 1. Avoid K+ supplements 2. Don't use in combination with triamterine or amiloride 3. Caution when used with ACE inhibitors, angiotension receptor blockers or direct renin inhibitors |
| What is spironolactone (Aldactone) used in combination with? | Loop or thiazide diuretics to increase diuresis |
| Where do K+ diuretics affect the nephron? | Collecting duct |
| What type of diuretic causes a mild increase in Na+ excretion, a decrease in K+ and increased urinary output? | K+-Sparing Diuretics |
| What type of diuretics cause an increase in K+ excretion? | Thiazide & Loop Diuretics |
| How do you treat hypokalemia d/t loop or thiazide diuretics? | 1. Reduce dietary NaCl intake (decrease collecting duct Na+ reabsorption --> decrease K+ secretion) 2. Increase dietary K+ intake (bananas, OJ) 3. K+ Supplements 4. Add K+-sparing diuretics |
| Increased excretion of what two ions lead to hypokalemia and metabolic alkalosis? | K+ and H+ |
| Where do thiazide diuretics effect the nephron? | Distal Convoluted Tubule |
| What is the most commonly prescribed class of diuretics? | Thiazide |
| What drug class has a milder diuresis compared to loop diuretics? Why? | Thiazide diuretics b.c the nephron site reabsorbs less sodium (10% filtered load) |
| What drug class of diuretics is less effective than loop diuretics? Why? | Loop diuretics for patients with renal insufficiency b.c patients with renal insufficiency have low GFR= most of the fluid is reabsorbed by the time it reaches the distal convoluted tubule |
| What is the first line therapy for mild-to-moderate hypertension? | Thiazide diuretics |
| What drug is used in combination with loop diuretics for sever resistant edema? | Thiazide Diuretics |
| What do all thiazide diuretics have? | An unsubstituted sulfonamide group |
| What is recurrent kidney stone formation due to? | Excessive calcium excretion |
| What do thiazides increase? | Distal tubular calcium reabsorption |
| What are the adverse effects of thiazides similar to with the exception of not having ototoxicity and hypocalcemia? | Loop Diuretics |
| What types of electrolyte imbalances can thiazides/loop diuretics cause? | 1. Hyponatremia 2. Hypochloremia 3. Hypomagnesemia 4. Hypokalemia 5. Hypocalcemia (loop only) |
| How much reabsorption does the thick ascending limp of the loop of Henle do? | 20% of filtered sodium |
| With the inhibition of Na, K and Cl cotransporters in loop diuretics what does it indirectly prevent? | Reabsorption of calcium and magnesium |
| What drug class can help promote diuresis when GFR is low? | Loop Diuretics |
| What disease is loop diuretics used for in the rapid fluid mobilization? | Pulmonary edema due to CHF |
| Loop diuretics treat edema associated with: | Hepatic, cardiac or renal disease (when unresponsive to other diuretics) |
| Loop diuretics treat hypertension related to: | Renal disease |
| How do loop diuretics treat anion overdose? | It inhibits reabsorption of Br-, F- |
| Why do loop diuretics cause hypotension? | Due to volume depletion and venodilation |
| IV furosemide | 1. Loop Diuretic 2. Treat pulmonary edema rapidly 3. Diuresis: 5 minutes 4. Duration: 2 hours |
| What do carbonic anhydrase inhibitors affect? | The proximal tubule in the nephron |
| Why do carbonic anyhydrase inhibitors cause metabolic acidosis? | CBecause of urinary loss of bicarbonate (limits use t0 2 - 3 days) |
| What do carbonic anyhydrase inhibitors cause kidney stones? | Calcium salts insoluble in alkaline urine |
| What serves as a supplemental elimination mechanism which allows more to be excreted than filtered? | Tubular Secretion |
| What is particularly important for drugs that bind to plasma proteins and aren't filtered into the urine by glomerulus? | Tubular Secretion |
| Tubular Reabsorption | Selective movement from urine back to blood |
| Where does ADH cause insertion of water channels (aquaporins)? | Collecting duct cells --> allows water to be reabsorbed, driven by high osmolality of the medullary interstitial fluid |
| What do diuretics compromise? | Normal operation of the kidney to promote excretion of water |
| How do osmotic diuretics differ from other diuretics? | 1. Mechanism of action 2. Indication for use |
| How do osmotic diuretics help prohylatically with renal failure? | Increase urine flow to help prevent kidney shutdown when GFR is very low |
| How do you minimize adverse effects of diuretics? | Time doses to allow drug-free periods between periods of diuresis = kidney to readjust ECF |
| How do you prevent nocturia for patients on diuretics? | Encourage patients to take diuretics in the morning |
| What are inadequate responses to diuretic therapy? | 1. Noncompliance with diuretic use and salt restriction 2. Decreased or delayed absorption of diuretic 3. Decrease renal blood flow or GFR - increased diuretic dose to increase delivery 4. Add another diuretic 5. Drug-drug interactions |
| What is Beta blockers mechanisms of action? | Unclear, but they may: - Protect from excessive sympathetic stimulation - Protect against dysrhythmias |
| What drug class can high doses be harmful to the patient? | Beta blockers |
| What are the newer ACE inhibitors? | Benazpril, Fosinopril, Lisinopril, Moexipril, Perindopril, Quinapril, Ramipril (Altace), Trandolapril |
| How is a p wave produced? | Atrial depolarization |
| How is a QRS segment produced? | Depolarization in the ventricles |
| How is a T wave produced? | Re-polarization of the ventricles |
| What are the common causes of HR? | 1. Abnormally high cholesterol levels (hyperlipidemia) 2. Smoking 3. Hypertension 4. Diabetes 5. Obesity/Starvation |
| Does hf mean heart attack? | No |
| What is heart failure? | The heart is unable to pump sufficient blood to meet needs |
| What is heart failure characterized by? | 1. Inadequate tissue perfusion (fatigue, shortness of breath) 2. Signs of volume overload (venous distention, fluid retention) |
| What are the major cause of heart failure? | - Chronic hypertension - Myocardial infarction - Valve disease - Coronary artery disease - Aging of myocardium |
| Explain the cardiac remodeling of heart failure. | - Ventricles grow larger and spherical - Increase wall thickness (hypertrophy) |
| What does the decline in CO result in with CHF? | - Further cardiac and arterial distribution - Increased sympathetic tone (d/t baroreceptor reflex) - Water retention and increased blood volume - All the above contribute to further loss of cardiac function |
| What drugs should be avoided with CHF? | - Antidysrhythmic agents - Calcium channel blockers (CCBs) - NSAIDS |
| Why shouldn't NSAIDs be used with CHF patients? | - Decrease the effects of diuretics - Increase peripheral resistance - Increase rate of CHF |
| What is the device therapy used for CHF patients? | - Implanted cardioverted-defibrillators (ICDs) - Cardiac resynchronization therapy (CRT) - Implantable hemodynamic monitors - Left ventricular assist devices (LVADs) |
| Should people with CHF exercise? | Yes |
| What types of drugs are included with Renin-Angiotensin-Aldosterone System (RAAS) Blockers? | 1. Ace Inhibitors 2. Angiotensin II Receptor Blockers (ARBS) 3. Aldosterone Antagonists 4. Direct Renin Inhibitors (DRIs)- new class of drug, drug: Aliskiren (Tekturna) |
| What other agents are used for CHF? | 1. Direct Vasodilators 2. Inotropic Agents |
| Name some direct vasodilator medications. | - Hydralazine, mioxidil - Organic Nitrates- Nitroglycerin |
| Name some Inotropic Agents. | 1. Cardiac (Digitalis) Glycosides- Digoxin 2. Sympathomimetics- Dobutamine 3. Phosphodiesterase Inhibitors- Amrinone 4. Milrinone |
| What is the ACE inhibitors, ACE stand for? | Angiotension-Converting Enzyme Inhibitors |
| What are ACE inhibitors mechanism of action? | 1. Block production of angiotension II 2. Block breakdown of bradykinin (bradykinin accumulates) 3. Dilate arterioles and veins 4. Reduce blood volume (via kidney action) --> approved for HTN 5. Reverse pathologic changes in heart and vessels |
| How do ACE inhibitors reverse pathologic changes in heart and vessels? | Via angiotensin II and aldosterone |
| What are all ACE Inhibitors therapeutic effects? | - Inhibition of ACE - Inhibition of kinase II (ACE's name when substrate is bradykinin) |
| What are the pharmacokinetics of captopril (Capoten)? | - Rapidly absorbed after oral administration - Rapid elimination with 1.2 life = 2 hours - Secreted unchanged in urine - Multiple therapeutic uses: CHF, HTN, MI |
| What do all ACE Inhibitors interact with? | Diuretics, antihypertensive agents, lithium, drugs that increase potassium |
| Where is Enalapril converted? And to what? | Enalapril (pro-drug) is converted to the liver to Enalaprilat (active form) |
| What are the pharmacokinetics of Enalapril (Vasotec) & Enalaprilat? | - Rapidly absorbed after oral administration - Slow eliminiation - 1.2 life = 11 hours |
| Rampiril (Altace) | An ACE inhibitor that is used prophylatically for MI, stroke and death in high risk CV patients |
| What ACE inhibitor has multiple uses? | Captopril (Capoten) |
| With the exception for lisinorpil, where are all of the new ACE inhibitors converted? | All of the new ACE inhibitors are pro-drugs that are converted in the SI and liver to an active form |
| What is the 1.2 life and administration of the new ACE inhibitors? | - Orally administered (some with food) - Prolonged 1.2 lives |
| What drug class has similar effects as ACE inhibitors? | Angiotensin Receptor Blockers (ARBs) |
| What drug class has less cardiac remodeling effects than that of ACE inhibitors (kinins)? | Angiotensin Receptor Blockers (ARBs) |
| What class of drugs are reserved for patients that can't tolerate the side effects of ACE inhibitors? | Angiotensin Receptor Blockers (ARBs) |
| What do ARBs not cause that ACE inhibitors case? | Hyperkalemia, cough, angioedema |
| Where do ARBs cause angiotension II receptor blockage? | Direct action in blood vessels, adrenals and all other tissues |
| What do ARBs cause? | Prominent dilation of arterioles (lesser effect in veins) |
| What drug is used for stroke prophylaxis? | Losartan (Cozaar)-- an ARB |
| What are ARBs primarily used for? Secondary use? | Primary- CHF Secondary- HTN |
| Why are ARBs used to tx HTN? | They are used in stead of ACE inhibitors to protect kidneys from damage d/t type 2 diabetic neuropathy |
| What are the pharmacokinetics of ARBs? | Adminstered- Oraly Half life- 2 h |
| Why do ARBs not cause cough and angioedema as compared to ACE inhibitors? | It doesn't inhibit kinase II = drop in bradykinin |
| What is Telmisartan? | RAAS ---> ARB |
| What suppresses the release of aldosterone? | ARBs |
| What type of drugs can cause vasodilation? | ACE inhibitors, ARBs, calcium channel blockers (CCBs), sympatholitics and direct vasodilators |
| Where do vasodilator drugs act on? | - Arterioles - Veins - Arterioles & Veins |
| What are the effects of drugs that are vasodilators of arterioles? | - Decrease cardiac "afterload" = increased CO & tissue perfusion |
| What is cardiac "afterload"? | The force against which the heart must work to pump blood |
| What do drugs that dilate veins do? | - Reduce blood force = reducing of ventricular filling which decrease "preload" |
| What is cardiac "preload"? | The degree of stretching of ventricles prior to contraction |
| Why are vasodilator drug selectivity a major determinant of therapeutic and side effects? | Because of the hemodynamic responses to the arterioles and veins |
| What are the therapeutic effects of Isosorbide Dinitrate (Isordil)? | - Used in combo with hydralazine - Selective dilation of veins - |
| What does Isosorbide Dinitrate (Isordil) have a similar mechanism of action as? | Nitroglycerin (nitroprusside) |
| What type of drugs can cause vasodilation? | ACE inhibitors, ARBs, calcium channel blockers (CCBs), sympatholitics and direct vasodilators |
| Where do vasodilator drugs act on? | - Arterioles - Veins - Arterioles & Veins |
| What are the effects of drugs that are vasodilators of arterioles? | - Decrease cardiac "afterload" = increased CO & tissue perfusion |
| What is cardiac "afterload"? | The force against which the heart must work to pump blood |
| What do drugs that dilate veins do? | - Reduce blood force = reducing of ventricular filling which decrease "preload" |
| What is cardiac "preload"? | The degree of stretching of ventricles prior to contraction |
| Why are vasodilator drug selectivity a major determinant of therapeutic and side effects? | Because of the hemodynamic responses to the arterioles and veins |
| What are the therapeutic effects of Isosorbide Dinitrate (Isordil)? | - Used in combo with hydralazine - Selective dilation of veins - |
| What does Isosorbide Dinitrate (Isordil) have a similar mechanism of action as? | Nitroglycerin (nitroprusside) |
| How is isosorbide dinitrate (isordil) administered? | Orally |
| Does digoxin (Lanoxin) prolong life? | No |
| How does digoxin (Lanoxin) increase myocardial contractility? | Inhibits Na+/K+ ATPase leading to Ca++ accumulation thus augmenting power of muscle ctx |
| What is the result of using Digoxin which increases CO to the body? | - Sympathetic tone declines - Urine production increase - Renin release declines |
| What are the pharmacokinetics of digoxin (Lanoxin)? | Administered- Oral (variable/partial) 1.2 life- 1.5 days Eliminated- Renally |
| What drug acts as an inodilator (increased contractility and vasodilation)? | Milrinone (Primacor) |
| What are the therapeutic effects of milirone (Primacor)? | Used to improve cardiac contractility and performance |
| Inodilator | A drug with positive inotropic and vasodilator effects |
| How is amrinone and milrinone (Primacor) given? | IV infusion |
| How long is the indication of milrinone? | Indicated for short term use only |
| What is the sinoatrial (SA) node considered? | The heart pacemaker |
| What causes dysrhythmias? | - Disturbed impulse formation or automaticity - Disturbed impulse conduction |
| What are the 2 main types of dysrhythmias? | - Supraventricular dysrhythmias - Ventricular dysrhythmias |
| How do you treatment dysrhythmias? | Tx has 2 phases: 1. Termination of dysrhythmia- electrical countershock, drugs or both 2. Long term suppression with drugs |
| How is a ventricular tachycardia stopped? | Cardioversion shock |
| How are most VT episodes terminated? | Painlessly with antitachycardia pacing |
| What drug classes are used for dysrhythmias? | 1. Na+ Channel Blockers 2. B-Blockers 3. K+ Channel Blockers 4. Ca ++ Channel Blockers |
| How is asthma triggered? | - Allergens - Unknown (60%) |
| What are the symptoms of asthma? | - Bronchoconstriction - Airway inflammation - Bronchia hyperactivity |
| What happens during an asthma attack? | The smooth muscles constrict and air flow is decreased and also it can be decreased by mucus and inflammation |
| What drives inflammation? | Inflammation d/t the release of histamines |
| What mediates reflex bronchoconstriction? | Vagus nerve |
| What are the immediate effects of mediators? | Bronchoconstriction |
| What is a gradual effect of mediators? | Inflammation (activation and infiltration of inflammatory cells) |
| What do granules attract? | Other inflammatory mediators (domino effect) |
| What are the pharmcotherapeutics of asthma drugs? | 1. Bronchodilators 2. Anti-inflammatory drugs |
| WHat do bronchodilators do? | Causes smooth muscles to relax |
| What are the bronchohodilators? | 1. B-adrenergic agonists (B2) 2. Methylxanthines- caffeine 3. Anticholinergics- block ACE effects |
| What are the anti-flammatory agents? | 1. Corticosteroids 2. Cromolyn & related agents (block the mast cell from exploding) 3. Leukotriene modifiers |
| What are the advantages of asthma inhalation drugs? | 1. Drugs go to the body directly 2. Minimal systemic effects (corticosteroids cause generalized effect) 3. Rapid acting |
| What are the devices used for inhaled asthma therapies? | - Metered Dose Inhalers (MDI) - Dry Powder Inhalers - Nebulizers |
| Beta 2 Adrenergic Agonists | Inhaled-short-acting - Albuterol (Proventil, Ventolin) - Bitolterol ( Tornalate) - Terbutaline (Brethaire) Inhaled-long-acting - Salmeterol (Serevent) - Formoterol (Foradil) Oral - Albuterol (Proventil, Ventolin) - Terbutaline (Brethine) |
| Methylxanthines | Can't inhale, has to be taken orally - Theobromin - Theophylline - Caffeine |
| Anticholinergics | Blocks the vagus nerve & stops muscles from contracting, inhaled - Ipratropium - Tiotropium |
| Anti-inflammatory drugs | Corticosteroids Inhaled - Bechlomethasone dipropionate (Beclovent, Vandercil) - Budesonide ( Pulmicort Turbohlaer) - Flunisolide (Aerobid) - Flucicasone Propionate (Flovent) Oral ( only used when necessary) - Prednisone - Prednisolone |
| What are the drugs that are used prophyllatically with asthma patients? | - Cromolyn & Nedocromil - Cromolyn inhaled (Intal) - Nedocromil inhaled (Tilade) |
| Anti-inflammatory drugs--> Leukotriene Modifiers | - Zafirlukast, oral (Accolate) - Zileuton, oral (Zyflo) - Montelukast, oral (Singulair) |
| What is the mechanism of action for B2-adrenergic agonists? | Act via stimulation of adenyl cylase --> Results in increase in cAMP |
| How do B2-adrenergic help with? | - Bronchodilation - Increase in mucociliary transport |
| What is the most effective bronchodilator agents? | B2-adrenergic agonists |
| What type of drugs are related (similar pharmacological actions) to xanthine? | Methylxanthines |
| When asthmatic patients lie down what happens? | Causes bronchoconstriction |
| What are Methylxanthines cortical action? | - Decreased drowsiness - Decreased fatigue - Restlessness - Arousal - Anxiety - Insomnia |
| What are the Methylxanthine's medullary response (respiratory center)? | - Increased respiratory drive - Increased sensitivity of medullary respiratory receptors to CO2 |
| What are the Methylxanthine's smooth muscle response? | - Bronchodilation |
| What are Methylxanthines MOA? | - Inhibit Phosphodiesterase (Results in increase in cAMP and cGMP) - Increase in cAMP causes activation of PKA --> bronchodilation, decrease in inflammatory cell activity |
| What is the PKA? | Blocks the enzyme that breaks it down |
| What are the proposed MOA of Theophylline? | - Phosphodiesterase inhibition (non-selective) - Adenosine receptor antagonism - Stimulation of catecholamine (epinephrine) release |
| What is epinephrine? | B2-agonist |
| What are the asthma anticholinergic agents? | - Ipratropium bromine (Atrovent) --> only occasionally used - Act to block vagal impulses which cause bronchoconstriction - Used via inhalation --> MDI, Nebulizer solution |
| What are the most effective anti-asthma drugs available? | Corticosteroids |
| How are corticosteroids administered? | Inhaled (usually), but also can be oral or IV |
| What are corticosteroids help with? | Airway caliber and bronchial reactivity |
| Inhaled corticosteroids | - Used according to schedule, helps prevents fires - Topical - Minimal side effects if any systemic effects |
| How do glucocorticoids reduce symptoms of asthma? | Suppressing inflammation |
| By suppressing inflammation, what do glucocorticosteroids reduce? | Bronchial hyperreactivity |
| What asthma drugs are reserved for patients with sever asthma? Why? | - Potential for toxicity and can't be controlled unless asthma can't be controlled by other meds |
| What are the most inhaled corticosteroids? | - Beclomethasone (Vanceril) - Budesonide (Pulmicort) - Flunisolide (Aerobid) |
| Beclomethasone (Vanceril) | Prodrug, metabolized to beclomethasone mono-propionate |
| Budesonide (Pulmicort) | - Most widely used agent in the world - Nebulized form available |
| What is the most potent inhaled corticosteroid? | Fluticasone (AeroBid) |
| What makes glucocorticoids invalubale? | Increase the # of bronchial B2 receptors and their responsiveness to B2 agonists |
| What is less effective than inhaled corticosteroids? | Cromolyn & Nedocromil |
| What does cromolyn & nedocromil (Tilade) function as? | - Mast cell degranulation inhibitors, which prevents histamine and other mediators release - Inhibits eosinophils, macrophages and other inflammatory cells |
| What drug is useful to prevent exercise-induced asthma? | Cromolyn & Nedocromil |
| How is cromolyn & nedocromil absorbed the best? | Inhaled |
| Leukotrienes | Chemical factors released by cells that cause inflammation, bringing about bronchoconstriction, eosinophil infiltration, mucus production and airway edema |
| What are the most important Leukotriene modifiers? | LTD4 receptor antagonists - Zafirlukast (Accolate) - Montelukast (Singulair) |
| Anti-IgE monoclonal antibodies | Omalizumab (Xolair) |
| Omalizumab (Xolair) | An antibody that blocks the trigger on mast cells (used preventively) - Very expensive |
| COPD | - Collective term for emphysema, bronchitis - Impairment of airflow that isn't fully reversible - Congenital: D/t alpha1- antitrypsin deficiency |
| COPD Drugs | Long-acting B2-agonists and tiotropium |
| Hemostasis | The process by which we keep blood fluid balanced (between clotting and unclotting) |
| Coagulation | Fibrin clot |
| Fibrinolysis | Clots are broken down |
| What are the 3 phases of hemostasis? | 1. Primary hemostasis 2. Coagulation 3. Fibrinolysis |
| What does clotting require? | - Intact vessels/supporting tissues - Requires platelet plug/scaffold - Requires generation of fibrin polymer |
| Anticoagulant Drugs | Reduce the formation of fibrin |
| What are the indications for anticoagulation? | 1. Prophylactically 2. Therapeutic |
| What is a Vitamin K antagonists? | Warfarin, Coumadin |
| Warfarin Pharmacokinetics | - Absorbed: Orally - Metabolized: Liver - Half-life: 1.5 - 2 days - Onset: 2 - 3 days |
| What is monitored for patients on Warfarin? | INR |
| What is the INR norm? | 2 - 3 |
| What are the risks for taking Warfain? | - Bleeding - Paradoxical thrombosis "coumadin skin necrosis" |
| Warfarin Risks & Bleeding | - Fetal malformations (teratogenic) - Fetal hemorrhage - Gross malformations - CNS defects - Optic atrophy- women of child bearing age MUST be informed and use appropriate birth control |
| Warfarin Risks & Paradoxical Thrombosis | Is only in the presence of Protein C or Protein S deficieny |
| What are drugs that increase the effect of Warfarin? | - Aspirin, salicylates (decrease albumin binding) - Sulfonamides (decrease metabolism) - Acetominophen - Amioddarone - Azoles (antifungal) - Cimetidine - Some cephalosporines |
| What are drugs that increase Warfarin? | - Carbamazepine (increase metabolism) - Phenobarbitol - Pheytoin - Rifampin - OCPs (increase clotting factor synthesis) - Vitamin K - Cholestyrine - Colestipol |
| Heparins | Glycosoaminoglycan polymers of various sizes |
| Where are heparins derived from? | Pig intestine and cow lung tissue |
| What are the heparins anticoagulant activity mediated by? | - Increasing the affinity of anti-thrombin-III for thrombin - Direct inhibition of F.Xa |
| What is unfractioned heparin? | Anticoagulant activity mediated by increasing affinity of AT-III heparin |
| Low Molecular Weight Heparin | - Anticoagulant activity mediated by its anti-Xa activity - 1.2 life inversely proportional to the mean molecular weight |
| Selective Factor Xa Inhibitors | - Synthetic anticoagulants that bind to anti-thrombin, thereby causing it to rapidly inactivate activated factor X (factor Xa), decreasing the formation of thrombin from prothrombin - Fondaparinux was the first class of this class of agents |
| Fondaparinux | - SQ - 100% bioavailability - Peak action at 2 hours - 1.2 life- 17 - 21 hours - Excreted thru the kidneys - Monitored by aPPT |
| Direct Thrombin Inhibitors | Agents that decrease the rate of clot formation by directly inhibiting the action of thrombin thru blockade of the active catalytic site of the thrombin molecule |
| What are the drugs that are direct thrombin inhibitors? | Lipirudin Argatroban Bivalirudin D |
| When fibrinolysis is initiated by the administration of drugs what is it called? | Thrombolysis |
| What are the 2 most important Thrombolysis drugs? | - Streptokinase 0 |
| What are sodium channel blockers? | - Antidysrhythmic drugs - Class 1 - MOA: Block sodium channels = decreased impulses in the atria ventricles and His-Purkinje system |
| Di-Ethyl Ether | A Hydrocarbon - Not Very Potent - Very Fat Soluble - Very Slow Induction and Emergence Times |
| Newer Inhalational Agents | - Halogenated - Increases Potency - Decreases Flammability |
| Stages of Anesthesia | Created by Guedel - 1930s -Described with Ether because it had a Slow Onset of Action Four Stages Described - Fast Acting Agents used Today do not Usually Allow us to see "Stages" |
| Stage 1 of Anesthesia | From Onset of Anesthetic Administration to Loss of Consciousness |
| Stage 2 of Anesthesia | From Loss of Consciousness to the Onset of Surgical Anesthesia |
| Stage 3 of Anesthesia | (4 Planes Described) Overall from Surgical Anesthesia to Loss of Respiration |
| Stage 4 of Anesthesia | From Loss of Respiration to Coma/Death "Anesthetic Overdose" |
| Thiopental | Intravenous Agent was Introduced into Clinical Practice in 1935 |
| Halothane | The First of the “New” Inhalational Anesthetics was Introduced in 1956. |
| Skeletal Muscle Relaxants | Introduced into Clinical Practice in 1959. Classification of the Types of Anesthesia |
| Types of Local Anesthetic | 1. Field Block 2. Intravenous Block (Bier Block) 3. Infiltration (Into the Wound) |
| Regional Anesthesia | 1. Spinal (Sub-Arachnoid Block - Lower Abdominal Surgery & Lower Extremity Surgery) 2. Epidural ( Labor, Delivery - Vaginal, C-Section) 3. Axillary Block - Wrist Block - Ankle Block |
| Amnesia | Absence of Memory |
| Analgesia | Absence of Pain |
| Anesthesia | Absence of All Sensation |
| Components of General Anesthesia | Amnesia, Analgesia, Anesthesia, Muscle Relaxation & Hemodynamic Stability |
| Amnesia Agents | - Benzodiazepines (Diazepam & Midazolam)- Sometimes Referred to as Sedatives or Tranquilizers - Can cause anterograde amnesia and little analgesia |
| Analgesiac Agents | Primarily Narcotics (Morphine, Fentanyl,Sufentanil, Remifentanil) - Intravenous NSAID(Ketorolac) |
| Anesthesiac Agents | - Induction Agents - Maintenance of Anesthesia |
| Induction Agents | Pentothal, Etomidate, Ketamine, Propofol, Narcotics, Benzodiazepines |
| Maintenance of Anesthesia | Inhalational Anesthetics, Narcotics,Benzodiazepines |
| Muscle Relaxating Agents | - Depolarizing(Succinylcholine) - Non-Depolarizing (Curate Type) |
| "Balanced" General Anesthesia | - Combinations of Drugs to Accomplish What is not Possible with a Single Agent. - Allows use of Lower Concentrations of Inhalational Anesthetics as well as Other Agents - Greater Safety |
| Inhalational Anesthetics | Halothane, Enflurane, Isoflurane, Desflurane, Sevoflurane, Nitrous Oxide <---these are the only drugs that are administered as gases |
| Potency | The “Strength” of a Drug ED50 |
| Inhalational Anesthetic Potency | Measured as Anesthetic Concentration in Alveolar Gas M.A.C. - Minimal Alveolar Concentration |
| MAC - Minimal Alveolar Concentration | MAC - the Minimum Anesthetic Concentration in the Alveolar Gas Which will Produce Immobility in 50% of Patients in Response to Surgical Stimulation (Skin Incision) |
| Lower MAC = | Higher Anesthetic Potency |
| Halothane | 0.75 as % in Air or Oxygen |
| Enflurane | 1.68 as % in Air or Oxygen |
| Isoflurane | 1.16 as % in Air or Oxygen |
| Desflurane | 5 to 6 as % in Air or Oxygen |
| Sevoflurane | 2.1 as % in Air or Oxygen |
| Nitrous Oxide | 105. as % in Air or Oxygen |
| Methoxyflurane | 0.16 as % in Air or Oxygen |
| Balanced Anesthesia | Multiple Drugs - Lower Concentrations Fewer Side Effects of Any Given Drug Greater Margin of Safety |
| Inhalational Anesthetic Elimination | Major Route of Elimination is the Lungs - Currently Used Inhalational agents are Metabolized to a Variable, but Small Extent |
| Metabolism of Inhalational Anesthetics | - Metabolism Does Not Affect the Time Course of Anesthesia - Toxicity of the Agent is Related to the Degree of Metabolism |
| Methoxyflurane Toxicity Risk | Diabetes Insipidus from Metabolism to Fluoride |
| Enflurane Toxicity Risk | Metabolism to Fluoride Possible Nephrotoxicity (Higher Fluoride Levels in Obese Patients) |
| Halothane Toxicity Risk | Hepatotoxicity - Exact Mechanism Unknown |
| What are the types of anesthesia? | 1. Local 2. Regional 3. General |
| What type of anesthesia is used for brief surgical procedures under one hour? | IV Bock |
| How does toxicity from local anesthesia occur? | Because it is injected intravascularly |
| What type of anesthesia can last a couple of days? | Epidural |
| What is 10 times more potent than morphine? 100 times? | Fentanyl, Sufentanil |
| What are non-depolarizing muscle relaxants? | - Mivacurium (Short-Acting) - Atracurium or Vecuronium (Medium-Duration) - Pancuronium (Long-Acting) - Pipercurium/Doxacurium (Very Long-Acting) |
| What is the differences between depolarizing and non-depolarizing muscle relaxants? | - Depolarizing: Muscle quivering - Non-depolarizing: Flaccid paralysis |
| Why can't you OD on tylenol w/codeine? | Because the tylenol will make you sick before you OD on the codeine |
| Malignant Hyperthermia | - Unique to general anesthesia - Triggered by Succhinlcholine & Halothane or an Inhalation agent |
| Hypermetabolic State | - Increased CO2 production - Increased O2 production - Metabolic acidosis, cyanosis, mottling of skin |
| Malignant Hyperthermia- Physiology | 1. Hypermetabolic state 2. Increased Sympathetic Activity 3. Muscle Damage 4. Hyperthermia |
| MH & Increased Sympathetic Activity | Tachycardia, HTN, Arrhythmias |
| MH & Muscle Damage | - Masseter Spasm, Generalized Rigidty, Hyperkalemia, Myoglobinemia, Myoglobinuria |
| Hyperthermia & MH | Is a late sign - Fever, Sweating |
| MH Tx | - Stop Offending Agents - Cooling Blankets, Solutions - Labs, Invasive Monitoring - Complete Surgery ASAP - Sodium Dantrolene, Sodium Bicarb |
| Neuromuscular Blocking Drugs | - Muscle Relaxants --> Drugs that cause paralysis - Support of Ctrl Ventilation |
| How do neuromuscular blocking drugs "muscle relaxants" work? | Interrupt nerve impulses at the neuromuscular junction |
| What drug causes unconsciousness but doesn't provide adequate analgesia? | Halothane (Fluothane) |
| Nitrous Oxide Advantages | - Excellent Analgesia - Nonflammable - Very rapid onset and recovery - Little or no toxicity - If used as an adjunctive med, it will allow the other drug to be decrease |
| What increases MAC values? | Hyperthermia |
| What drug assists in restoring and maintaining a normal sinus rhythm? | Quinidine ( Na+ Sodium Channel Blocker) |
| Altough Quinidine is classified as a Na+ channel blocker, what is quinidine also classified as? | K+ Channel Blocker- most antiarrhythmic agents have such multiple actions |
| What do sodium channel blockade result in? | Increased threshold and decrease automaticity |
| What does potassium channel blockade result in? | Delays repolarization |
| When is quindine used? | - Used to maintain normal sinus rhythm - Treats supraventricular & ventricular dysrhythmias |
| Quindine MOA | - Vagal inhibition (anti-muscarinic) and alpha-adrenergic receptor blocker |
| Quindine Side Effects | - Diarrhea & other GI symptoms - Cinchoism - Cardiotoxicity - Can double dig levels by displacing it from albumen |
| What is SL nitroglycerin used for? | Relieve symptoms of angina or as a prophylactic before demanding activities |
| What is nitroglycerin's MAO? | Vasodilation --> reduces myocardial preload and therefore decreases myocardial oxygen demand |
| What happens with the production of nitric oxide? | Activated guanylyl cyclase --> increased concentration of cyclic GMP which results in vasodilation by increasing the rate of light-chain myosin dephosphorylation |
| Nitroglycerin Side Effects | - Heading - Orthostatic hypotension - Reflex Tachycardia - Potentiated hypotensive drugs: B-Blockers, verapamil (Viagra) |
| What antianginal drug is extensively metabolized by P450 enzymes (inhibitors or inducers)? | Ranolazine (Ranexa) |
| Ranolazine (Ranexa) Side Effects | Prolongs QT intervals- indicated as a first-line drug |
| What can Ranolzaine be used in combo with? | - Beta-blockers - Nitrates - CCBs - ACE Inhibitors - ARBs - antiplatelet - lipid-lowering |
| What do the class of Ib Na+ blockers do? | - Accelerates repolarization - Little or no effect on ECG |
| What is lidocaine (Xylocaine) used for? | Ventricular dysrhythmias |
| Lidocaine's Pharmacokinetics | - Given IV b.c of its rapid hepatic elimination |
| Lidocaine's side effects | - Drowisness & confusion - Respiratory arrest and Convulsions (High doses) |
| What drugs are in the IC: Na+ Channel Blockers class? | - Flecainide (Tambocor) - Propagenone (Rhythmol) |
| What are the side effects of the IC: Na+ Channel Blockers? | - Potentially dangerous - Nausea, blurred vision, GI disturbances |
| What are the IC: Na+ Channel Blockers MOA? | - Supraventricular & ventricular dysrhythmias - Decrease in CO & contractility |
| B-blockers MAO | Adrenergic receptor blocking agents |
| Name some B-blockers | - olol |
| What beta-blocker also blockers K+ channels? | Sotalol |
| K+ Channel Blockers MAO | Delay repolarization of fast action potential, which prolongs the action potentials |
| K+ Channel Blockers Used | - Bretylium (VD) - Aminodarone (SV & VD) - Dofetilide (SV) - Ibutilide |
| What drug is only approved for life-threatening ventricular dysrhytmias? | Aminodarone (Cordarone) - K+ channel blocker |
| What drug has complex effects in the heart and crosses the placenta? | K+ Channel Blockers |
| What drug has an extremely long 1.2 life (25-110 days) and causes cardiotoxicity, lung damage and vision impairment? | Aminodarone (Cordarone) - K+ channel blocker |
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Itsme583