3894247
| Question | Answer |
| WHAT ARE AUTACOIDS? | LOCAL HORMONES THAT ARE RELEASED FROM PARTICULAR CELL DAMAGE |
| WHAT IS UNIQUE ABOUT THE RELEASE AND BREAKDOWN OF AUTACOIDS? | THEY ARE RELEASED AND BROKEN DOWN RAPIDLY |
| WHERE ARE AUTACOIDS RELEASED? | USUALLY LOCALLY, SOMETIMES SYSTEMICALLY |
| WHAT ARE EICOSANOIDS? | PROSTAGLANDINS AND LEUKOTRIENES |
| WHERE IS LINOLEIC ACID LOCATED? | BOUND TO THE CELL MEMBRANE |
| WHAT HAPPENS WHEN THE CELL MEMBRANE IS DAMAGED? | LINOLEIC ACID RELEASES/ACTIVATES PLA2 WHICH RELEASES ARACHINDONIC ACID |
| ARACHIDONIC ACID IS OXIDIZED BY ... BECOMING ... | OXIDIZED BY LIPOXYGENASE, BECOMING 5-HPETE |
| 5-HPETE IS FURTHER OXIDIZED BY ... BECOMING... | OXIDIZED BY DEHYDRASE, BECOMING LTA4 |
| WHAT IS LTA4? | AN INTERMEDIATE FOR: LTB4, LTC4, LTD4, LTE4 |
| WHAT IS THE FOUNDATIONAL VOCABULARY FOR LTA4? | LEUKO-LEUKOCYTES TRI-3 CONJUGATE II-BONDS 4- 4 II-BONDS TOTAL |
| LTA4 IS CONJUGATED BY.. AND BECOMES... | GLUTATHIONE S-TRANSFERASE, AND BECOMES LTC4 |
| WHAT EXACTLY DOES GLUTATHIONE S-TRANSFERASE DO TO LTA4? | ADDS CYSTINE, GLYCINE, AND GLUTAMIC ACID |
| LTC4 IS PROCESSED BY ... AND BECOMES... WHAT IS REMOVED? | PROCESSED BY: GGTP BECOMES: LTD4 GLUTAMIC ACID IS REMOVED |
| LTD4 IS PROCESSED BY ... AND BECOMES... WHAT IS REMOVED? | PROCESSED BY: DIPEPTIDASE BECOMES: LTE4 GLYCINE IS REMOVED |
| WHAT IS UNIQUE ABOUT LTE4? | IT IS THE MOST STABLE LT+ STRUCTURE ONLY CYSTINE REMAINS |
| WHAT DO ALL THREE (LTC4, LTD4, LTE4) DO? | CONTRACT SMOOTH MUSCLE IN BROCHOTUBULES VASOCONSTRICTION VIA GPCR LT1 AND LT2 RECEPTORS DECREASE CORONARY BLOOD FLOW |
| IF LTA4 IS NOT CONJUGATED WITH GLUTATHIONE S-TRANSFERASE, WHAT ELSE CAN HAPPEN? | LTA4 CAN BE HYDROLYZED VIA HYDROLASE *AN EPOXIDE IS REMOVED |
| WHAT IS THE PRODUCT OF LTA4 HYDROLIZATION? | LTB4 |
| WHAT DOES LTB4 DO? | RECRUITS NEUTROPHILS TO DAMAGE SITES *THE MAIN PURPOSE OF LTB4 |
| WHAT RECEPTORS DOES LTB4 ACT UPON? | BLT1 AND BLT2 RECEPTORS |
| IF ARACHIDONIC ACID IS NOT LIPOXYGENATED, WHAT OTHER PATHWAY IS INITIATED? | COX I AND COX II (CYCLOXYGENASE) MAKES A PENTANE RING THAT HAS OXYGENS |
| WHAT ARE SOME DIFFERENCES BETWEEN COX I AND COX II? | COX I: EVERYWHERE, PLATELETS ONLY USE COX I COX II: INDUCEABLE! WHEN WANT TO INHIBIT PAIN OR INFLAMMATION THAT'S PGI2 LINKED |
| WHAT IS THE PRODUCT ONCE ARACHIDONIC ACID IS CYCLOOXYGENATED? | PGG2 |
| PGG2 IS OXYGENATED BY ... BECOMING... | OXYGENATED BY: PEROXIDASE BECOMING: PGH2 |
| WHAT IS PGH2? | AN INTERMEDIATE FOR TXA2, PGI2, PGE2, PGF2ALPHA, PGD2 |
| WHAT DOES THE 3RD LETTER MEAN IN REGARDS TO THE PG COMPOUNDS? | AN INDICATOR FOR WHICH RECEPTOR IT WILL ACT UPON: PGE2: EP1 AND EP2 PGD2: DP1 ETC ALSO INDICATED THAT THERE IS A PENTANE RING |
| WHAT IS UNIQUE ABOUT TXA2? | NOT SPECIFICALLY A PROSTAGLANDIN, BUT IT IS A PRODUCT OF ARACHIDONIC ACID + CYCLOOXYGENASE PATHWAY |
| WHAT DOES PGE2 DO? | MANY ROLES! RELAX OR CONTRACT SMOOTH MUSCLES (UTERINE/INTEST) (CONCENTRATION AND RECEPTOR DEPENDENT) ACTIVATE(LOW CONCENT) /INHIBIT (HIGH CONCENT) PLATELET AGGREGATION |
| WHAT DOES PGF2ALPHA DO? | ALWAYS ALWAYS ALWAYS CONTRACTION F = FORCE = CONTRACTION CONTRACTION OF UTERINE, VASCULAR, INTEST, BRONCHO (SMOOTH MUSCLES) |
| WHAT DOES PGD2 DO? | CONTRACTION: INHIBIT PLATELET AGGREGATION |
| WHAT DOES PGI2 (PROSTACYCLIN) DO? | INHIBITS PLATELET AGGREGATION I = INHIBIT VASODILATION *DEPENDS ON CONCENTRATION |
| IN SUMMARY, IF PHOSPHOLIPIDS DON'T USE THE LOX PATHWAY, WHAT IS THE OTHER? | PHOSPHOLIPIDS --> ARACH ACID --> COX (I + II) --> PROSTAGLANDINS, THROMBOXANES, PROSTACYCLIN |
| IN SUMMARY, IF PHOSPHOLIPIDS DON'T USE THE COX PATHWAY, WHAT IS THE OTHER? | PHOSPHOLIPIDS --> ARACH ACID --> 5-LOX --> LEUKOTRIENES (LTB4, LTC4, LTD4, LTE4) |
| IN THE CELL MEMBRANE, WHAT RECEPTORS ARE RESPONSIBLE FOR RELAXATION? WHAT AUTACOIDS ARE RESPONSIBLE? | IP: PGI2 EP2, EP4: PGE2 DP1: PGD2 |
| WHAT IS UNIQUE ABOUT PGE2 IN REGARDS TO RECEPTORS? | PGE2 ACTIVATES EP RECEPTORS 1 THROUGH 4 |
| IN THE CELL MEMBRANE, WHAT RECEPTORS ARE RESPONSIBLE FOR CONTRACTION? WHAT AUTACOIDS ARE RESPONSIBLE? | TP: TXA2 FP: PGF2ALPHA EP: PGE2 |
| IN THE CELL MEMBRANE, WHAT RECEPTOR IS RESPONSIBLE FOR INHIBITION? WHAT AUTACOID IS RESPONSIBLE? | EP3: PGE2 |
| WHAT DRUG PRODUCTS INHIBIT CYCLOOXYGENASE? | NSAIDS |
| WHAT DRUG INHIBITS PGI2 THEREBY ANTAGONIZING IP RECEPTORS? | EPOPROSTENOL USES G2 PATHWAY CAUSES RELAXATION AND INHIBITS PLATELET AGGREGATION |
| WHAT DRUGS INHIBIT PGF2ALPHA THEREBY ANTAGONIZING FP RECEPTORS? | CARBOPROST, LATANOPROST CAUSES CONTRACTION |
| WHAT DRUGS INHIBIT PGE2 THEREBY ANTAGONIZING EP1 AND EP2 RECEPTORS? | ALPROSTADIL, MISOPROSTOL, THEY ARE PGE1 DERIVATIVES (NOT SYNTHESIZED FROM ARACH ACID) DINOPROSTONE IMPORTANT FOR UTERINE CONTRACTIONS *ALL DRUGS CAN INHIBIT EP1 AND EP2 |
| WHAT ANTAGONISTIC DRUG INHIBITS 5-LOX, PREVENTING ARACH ACID FROM BECOMING LEUKOTRIENES? | ZILEUTON INHIBITS BRONCHOCONSTRICTION |
| WHAT ANTAGONISTIC DRUG INHIBITS CysLT1 AND CysLT2? | MONTELUKAST, ZAFIRLUKAST INHIBIT BRONCHOCONSTRICTION |
| WHAT DOES CysLT1 AND CysLT2 DO? | PROMOTE INFLAMMATION |
| WHAT IS A SIDE EFFECT OF HIGH CONCENTRATIONS OF PGE2 AND PGF2ALPHA? | DIARRHEA |
| WHAT DO THE LTs DO? | POTENT BRONCHOCONSTRICTORS, CAUSES ERYTHMA (REDNESS) AND WHEAL (SWELLING) |
| NSAIDS ARE KNOWN TO ... COX | INHIBIT |
| WHAT ARE PGE1 DRUGS? | ALPROSTADIL, MISOPROSTOL |
| WHAT ARE PGE2 DRUGS? | DINOPROSTONE |
| WHAT ARE PGF2-APHA DRUGS? | CARBOPROST LATANOPROST |
| WHAT ARE PGI2 DRUGS? | EPOPROSTENOL, ILOPROST, TREPROSTINIL |
| WHAT IS SUBSTANCE P? | A TYPE OF PEPTIDE CALLED TACHYKININ (RAPID KININ) A NEUROTRANSMITTER EVERYWHERE IN THE BODY: CNS, GUT, NEURONS, ETC |
| WHAT DOES SUBSTANCE P STIMULATE? | NK1 RECEPTOR |
| WHAT DOES SUBSTANCE P DO? | VASODILATOR, CAUSES NAUSEA, PAIN SENSATION |
| WHAT DO YOU TEST TO SEE IF PT HAS SEROTONIN SYNDROME? | LOOK AT THE 5-HYDROXYINDOLEACETIC ACID LEVELS IN URINE |
| 5-HT1 LOCATION | CNS, ENDOTHELIAL CELLS, PNS, GI |
| 5-HT1 RESPONSE | NEURONAL INHIBITION |
| 5-HT1 AGONISTS | SUMATRIPTAN (1D/1B) BUSPIRONE (1A) |
| 5-HT1 ANTAG | NONE |
| 5-HT1 SIGNAL TRANSDUCTION | Gi/Go, DROP IN cAMP |
| 5-HT2 LOCATION | CNS, SMOOTH MUSCLE, PLATELETS |
| 5-HT2 RESPONSE | VASOCONSTRICTION, PLATELET AGGREGATION |
| 5-HT2 AGONISTS | LYSERGIC ACID DIETHYL AMIDE (LSD) *IN CNS |
| 5-HT2 ANTAGONISTS | METHYLSERGIDE, KETANSERIN, RITANSERIN, CRYPROHEPTADINE LSD (PERIPH NS) |
| 5-HT2 SIGNAL TRANSDUCTION | Gq, PLC, DAG, IP |
| 5-HT3 LOCATION | SENSORY NERVES, GIT |
| 5-HT3 RESPONSE | PAIN, WHEAL, FLAIR, EMESIS |
| 5-HT3 AGONISTS | NONE |
| 5-HT3 ANTAGONISTS | ONDANSETRON, ETC |
| 5-HT3 SIGNAL TRANSDUCTION | LIGAND-ACTIVATED DEPOLARIZING ION CHANNEL **ONLY ONE NOT G-COUPLED |
| 5-HT4 LOCATION | CNS, GIT |
| 5-HT4 RESPONSE | PERISTALSIS |
| 5-HT4 AGONISTS | CISAPRIDE, TEGASEROD |
| 5-HT4 ANTAGONISTS | NONE |
| 5-HT4 SIGNAL TRANSDUCTION | Gs, INCREASE IN cAMP |
| WHERE IS 5-HT (SEROTONIN) FOUND? | ENTEROCHROMAFFIN CELLS OF GIT, NEURONS, PLATELETS |
| WHAT ARE THE EFFECTS OF 5-HT ON THE CARDIOVASC SYSTEM? | ACTIVATES CHEMORECEPS LWRS HEART RATE AND BP [BARORECPT REFLEX] (5-HT3) VASOCONSTRICT (5-HT2 RECEPT) ON VASC SM MUSCLE (EXCEPT IN BL VESSLS IN HRT AND SKELE MUSC, 5-HT2) CAUSES PLATELET AGGRE (5-HT2) |
| WHAT ARE THE EFFECTS OF 5-HT (SEROTONIN) ON GIT? | SIMULATES MOTILITY OF INTESTINE (5-HT1-4) HYPERSECRETION MAY OCCUR IN CARCINOID TUMORS (EXCESSIVE 5-HT IS RELEASED) |
| WHAT ARE THE EFFECTS OF 5-HT (SEROTONIN) ON PERIPH NERVOUS SYSTEM? | DEPOLARIZES SENSORY FIBERS, PAIN, INFLAMMATION (5-HT3) ACTIVATES CHEMORECEPTOR REFLEXES (5-HT3) |
| WHAT ARE THE EFFECTS OF 5-HT (SEROTONIN) ON CNS? | THERMOREGULATION (HYPERTHERM IF NO REGUL) BEHAVIROAL MODIFIC (5-HT2) *LSD VOMITING (5-HT3) |
| WHAT ARE THE 5-HT2 DRUGS? | METHYLSERGIDE, CYPROHEPTADINE, KETANSERIN |
| WHAT ARE THE 5-HT3 DRUGS? | ONDANSETRON (ANTAG) METOCLOPRAMIDE (ANTAG) *DOPAMINE ANTAG TOO |
| WHAT IS THE 5-HT4 DRUG? | TEGASEROD |
| WHAT ARE THE SYMPTOMS OF SEROTONIN SYNDROME? | IT IS: EXCESSIVE SEROTONIN SYMPTOMS: HYPERTHERMIA, MUSCLE RIGIDITY, HYPERREFLEXIA, RAPID CHANGES IN MENTAL FUNCTION, CHANGE IN VITAL SIGNS, HYPERACTIVE BOWEL SOUNDS, MYDRIASIS (DILATION), COMA |
| WHEN IS SEROTONIN SYNDROME MORE LIKELY TO OCCUR? | WHEN COMBINATION OF DRUGS AFFECTIN 5-HT ARE USED TOGETHER |
| WHAT IS BRADYKININ? | A NON-PEPTIDE THAT IS CONVERTED FROM A HIGH MW (KININOGEN) BY KALLIKREIN |
| WHAT IS ANOTHER KININ FOUND IN URINE? | KALLIDIN (LYSYLBRADYKININ) |
| WHAT IS THE TARGET OF ACE INHIBITORS? | PEPTIDYL DIPEPTIDASE (ANGIOTENSIN-CONVERTING ENZYME) |
| WHAT ARE THE TWO MOST POTENT VASOCONSTRICTORS IN THE RENIN-ANGIOTENSIN SYSTEM? | ANGIOTENSIN II AND III |
| WHAT DOES BRADYKININ DO? | A POTENT VASODILATOR-LIKE HISTAMINE INCREASES VASCULAR PERMEABILITY TO PRODUCE 'WHEAL AND FLARE' *NOT ANTAG BY HISTAMINES INDIRECTLY INCREASES CARDIAC OUTPUT AND HR |
| USES FOR BRADYKININ | POWERFUL ALGESIC AGENT (CAUSES PAIN) PROMOTES RLSE OF PGs IN KIDNEYS ASSOCIATED WITH ACUTE INFLMMATION, SHOCK AND ANAPHYLAXIS |
| WHAT DO ACE INHIBITORS DO IN REGARDS TO BRADYKININ? | INHIBIT DEGRADATION OF BRADYKININ THEREFORE, INCREASING BRADYKININ'S ACTIVITY *DECREASE BP, WHEEZING/COUGHING FROM INCREASE OF BK |
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