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Pharmacology
Test questions
| Question | Answer |
|---|---|
| Explain "decreasing the afterload" | Drugs that dilate arteries or arterioles make it so that the Heart doesn't work so hard to pump after BP has been lowered |
| Explain "decreasing the preload" | Drugs that dilate veins decrease venous return to heart |
| 4 classes of drugs to treat CHF | 1. vasodilators 2. diuretics 3. cardiac glycosides 4. carbonic anydrase inhibitors |
| 3 classes of angina drugs | 1. nitrates - cause vasodilation 2. beta blockers 3. calcium channel blockers |
| which classes of drugs are used for exertional angina | beta blockers and nitrates |
| which class of drugs for vasospastic angina | calcium channel blockers |
| drug class: verapamil | calcium channel blocker |
| Describe the four classes of antiarrhythmia drugs | 1. interfere with Na ions/reduce excitability, so these drugs slow conduction velocity, prolong the refractory period adn decrease automaticity 2. beta-adrenergic blockers are used to counteract the increased sympathetic activity that accompanies heart di |
| what class is quinidine? | class 1 antiarrhythmic |
| what antiarrhythmic class is propranolol? | class 2 antiarrhythmic |
| what class is sotalol? | class three antiarrhythmic |
| what class is verapamil? | class 4 antiarrhythmic |
| formula for cardiac output | stroke volume x heart rate |
| formula for blood pressure | cardiac output x peripheral resistance |
| 5 classes to treat hypertension | 1. diuretics 2. adrenergic blockers 3. vasodilators 4. calcium channel blockers 5. ACE inhibitors |
| 3 types of adrenergic blockers | 1. alpha blockers 2. beta blockers 3. centrally acting |
| Which are more powerful: loop or thiazide diuretics | Loop (aka organic acid diuretics) |
| How do loop diuretics work? | inhibit transport of Na and Cl ions in loop of henle causing dramatic loss of these ions and water |
| How do loop diuretics relate to potassium? | They can cause hypokalemia. |
| Should you mix them with other diuretics? | Generally, no. |
| When are loop diuretics often used? (what dieases?) | Edema, CHF, renal disease |
| side effects of trazadone | priaprism, sedation, orhtostasis |
| why use atypical antipsychotics over regualar phenothiazines or non-phenothiazines | less EPS, works well in px with negative symptoms |
| SE clozapine | no eps, but aggranulocystitis |
| MOA atypical antipsychotics | MOA not well understood. likely differential binding to dopamine and seratonin receptors |
| side/adverse effects of narcotic analgesics | 1. mental confusion 2. GI: nausea/vomiting/constipation 3. tolerance/dependency 4. respiratory depression/arrest 5. urinary retention |
| does meperidine cause miosis or mydriasis? | mydirasis, all other narcotics cause miosis |
| MOA tylenol | inhibits prostaglandins in CNS not PNS, therefore you get antipyresis and analgesia but not antiimflammatory. (aka does not affect cycooxygenase in PNS) Does not affect platelet function |
| MOA Naproxen | inhibit COX enzymes therefore reduce prostaglandins (COX 1 is in all cells, COX 2 is released by active macrophages in response to tissue damage) |
| MOA amitriptylline | block reuptake of Norepinepherine and serotonin causing accumulation in synaptic cleft |
| MOA allopurinol | hypourecemic. inhibits xanthine oxidase so the body cant turn hypoxanthine into uric acid. The hypoxanthine is excreted in urine. no gout. |
| MOA sertraline | SSRI. blocks reuptake of seratonin |
| MOA nitrous oxide | TBD |
| MOA Naloxone | total narcotic antagonist. Attaches to opiod receptors and displaces opiate to rapidly reverse life threatening respiratory depression. |
| MOA amobarbital | Increase inhibitory effects of GABA, a neurotx that reduces excitability in cerebral cortex and especially in RAS. At high doeses they can cause general CNS depression similar to general anesthetics. |
| Stages of sleep | 1. somewhat aware but relaxed 2. become unaware and easily awakened 3/4. Slow wave sleep. Low-freq Delta waves 5. REM: rapid-eye movement, bursts of autonomic activity, dreaming. |
| Def of hypnotic vs sedative | hypnotic: to induce, maintain sleep sedative: to relax, reduce desire for physical activity |
| Can barbiturates be used for nausea/vomiting? | Yes, they're anticonvulsants. |
| Two main sites of action of barbiturates. | Cerebral Cortex and Reticular Formation |
| Two MOA of barbiturates | 1. reduce activity of RAS/cortex by promoting GABA 2. higher doses interfere with Na ion tx thru neuronal membranes |
| What is MOA of BZDs? | BZDs: Bind to part of GABA receptors to increase the amount of Chloride they allow into neuron, hyperpolarizing neurons more than just GABA acting alone. |
| Are BZDs lipid soluble? | Yes. |
| Do BZDs have active metabolites? | Some do. |
| Do BZDs cause induction? | No BZDs dont cause liver enzyme induction. |
| Do BZDs interfere with REM? | No. |
| How do BZDs affect Sleep stages? | Increase stage 2, Decrease Stage 4. |
| Can BZDs be used as sedatives? | Yes. |
| Neurotx involved in Parkinsons | Acetylcholine and dopamine |
| Cause of Parkinsons | Degradation of ACH and Dopamine receptors with then causes a decrease in release of dopamine in basal ganglia. Decrease of dopamine magnifies effects of ACH to stimulate muscles |
| Three signs of Parkinsons | 1. tremor at rest 2. bradykinesia 3. rigid stoop |
| How does ACH versus Dopamine affect muscle tone | ACH increases muscle tone, dopamine inhibits it |
| Stages of anesthesia | 1. Cortex inhibited 2. Excitement phase with complete depression of cortex and hypothalamus takes control 3. depression of hypothal. HR normalizes. desired stage 4. medullary paralysis, death 4. |
| kappa receptors | mediate pentazocine-like analgesia, meaning only mild Resp depression |
| mu | mediate morphine-like analgesia, euphoria and respiratory depression, Best for pain control. |
| sigma | dysphoria, hallucinations, respiratory and vasomotor stimulation |
| Do narcotics act on CNS and PNS | no. CNS only. |
| Narcotic effects GI: Renal: | GI: two effects- increases smooth muscle tone and causes contactions/spasms (aka diarrhea) or inhibit parasymp stimulation of GI by blocking relase of ACh (aka constipation) |
| define bradykinin- what should we know about them? | peptide that causes blood vessels to dilate. ACE inhibitors increase amount of bradykinin |
| define prostaglandins | (lipids) hormones that mediate the inflammatory response. G2 and H2 stimulate peripheral pain receptors and construct vessels. They are metabolized to substances that produce erythema, edema and pain. |
| define histamines | biogenic amine released by mast cells upon tissue injury; functions as a neurotx and guides leukocytes to site of injury. |
| Cox-1 versus cox-2 | cox-1 is in all cells and effects platelet aggregation (clotting) and synthesis of stomach mucus, cox 2 is released by mast cells upon injury to produce prostaglandins from arachandonic acid. |
| MOA of anti inflammatory drugs | block cox-1 and cox-2 pathways. nonselective drugs (aspirin, ketoprofen and indomethacin) block both. Selective cox-2 inhibitors (celecoxib, refecoxib, veldecoxib) are selecitve for cox-2 and avoid stomach irritation associated with blocking cox 1. |
| ASA MOA? what does this mean? | . |
| NSAID/salicylate Adverse Effects | Large doses can cause salicylism-tinnitus, HA, nausea, hyperentilation due to CNS stimulation. Toxicity from depression of medulla control of respiration. So body cant remove CO2 leading to respiratory acidosis then metabolic acidosis. decrease in BP. De |
| Define gout | Inflammatory disease. Deposition of uric acid crystals in joint fluid and soft tissue. Uric acid is formed from metablism of nucleic acids but humans cant use uric acid so kidneys excrete it. So people overproduce it or cant excrete it. When uric acid acc |
| define xanthine oxidase | enzyme that makes uric acid from hypoxanthine. |
| MOA hypourecemics | drugs that inhibit xanthine oxidase (allopurinol). Hypoxanthine is excreted in urine. |
| compare absence seizures to simple partial seizures to complex partial seizure | absence seizures are classified as general seizures and involve brief episodes of blank staring or rapid blinking 10 seconds to 2 minutes (aka petit mal). simple partial is a single defective motor-sensory pathway usually affecting a single muscle group o |
| generalized seizure | aberrant electrical activity in both hemispheres. Classified as tonic-clonic, myoclonic or absence |
| tonic clonic | full body motor convulsions aka grand mal. tonic refers to sustained muscle contractions. clonic refers to convulsive spasms in which rigidity and relaxation alternate in rapid succession. tonic clonics usually last 1 to 2 minutes. |
| status epilepticus | series of grand mals with no cessation. major medical emergency. diazepam! |
| MOA of TCAs | tricyclics block reuptake of NE and serotonin |
| MOA if SSRIs | block reuptake of serotonin |
| MOA MAOIs | block reuptake of Dopamine, Serotonin, NE |
| MOA Venlafaxine | Down N Sad. Blocks reuptake of Dopamine, serotonin, NE |
| Buproprion | Blocks dopamine |
| Diagnosing depression requires what symptoms? | One of the following: 1. depressed most of day or diminshed interest or pleasure in nearly all of life activities Four of the following: 1. Significant wt loss or gain 2. Insomnia or hypersomnia 3. Fatigue or loss of energy 4. Feelings of worthles |
| What's the time element associated with diagnosing depression? | The symptoms must occur within same 2-week period. Must exhibit change from previous function. Diagnosis only made when symptoms cant be attributed to other drugs, recent bereavement. |
| Def of Anxiety | uncomfortable feeling of vague fear or apprehension accompanied by physical sensations. |
| Symptoms of anxiety | Mental: worry, fear, difficulty concentrating Physical: SOB, tachycardia, trembling, pacing, sweating |
| Types of anxiety | Situational: short therm 2-3 weeks General disorder: requires 3 out of the following 6 symptoms - restlessness, fatigue, irritability, muscle tension, difficulty concentrating, disturbed sleep. Must occur for longer than 6 months. Unrealistic worry about |
| What is panic disorder? | acute, very short episodes, fear of losing control |
| MOA of anxiety | actication of sympathetic and limbic systems that control and regulate emotions and behaviors. prolonged activation leads to neurosis. |
| define psychosis | impaired mental function interferes with ability to meet ordinary demands of life. symptoms similar to depression. |
| negative symptoms of psychosis | alogia, avolition, anhedonia, affective blunting, attention impairment |
| MOA phenothiazines | blocks EVERYTHING: dopamine, also serotonin, epi, NE, |
| MOA atypical antipsychotics | not fully understood, differential binding to dopamine/serotonin. work well in px with negative symptoms. little to no EPS |
| what are effects of blocking D1 versus D2 | block D1, you get partial antipsychotic effects but can cause EPS block D2, full antipsychotic effects no EPS |
| MOA antiemetics | block dopamine AND serotonin receptors in CTZ of medulla. Also some histamine antagonists can reduce emesis and control N/V |
| What does stimulation of D2 cause? | N/V |
| MOA cardiac glycosides |
Created by:
manka