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tara's pharm final review part one

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ENDOCRINE AXIS   HYPOTHALMOS TRIGGERS RELEASE OF TROPIC HORMONE (STIMULATING HORMONE) WHICH TRIGGERS TARGET ORGAN, TARGET ORGAN MAKES OWN HORMONE WHICH THEN TRIGGERS HYPOTHALMOS AND IT CONTINUES IN CIRCLE  
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INCREASE IN OWN HORMONE CAUSES   DECREASE IN STIMULATING HORMONE (NEGATIVE FEEDBACK)  
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(PD) ESTROGEN AND PROGESTERONE   NEGATIVE FEEDBACK ON FSH/LH RELEASE  
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INCREASE IN ESTROGEN AND PROGESTERONE EQUALS   DECREASE IN FSH/LH  
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FULL EFFICACY OF ORAL CONTRACEPTIVES   TAKES ONE MONTH  
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IF UTERUS HAS HEAVY SPOTTING   CAN USE OC WITH DECREASE PROGESTERONE COMPONENT  
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STILL NEED TO USE ALTERNATIVE PLAN FOR ONE MONTH WHEN   YOU CHANGE LEVELS OF HORMONE IN OC  
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OC IS ABOUT 85% EFFECTIVE WHEN   AROUND 2 WEEKS  
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(PK) ABSORPTION OF ANTIBIOTICS IS   DEPENDANT UPON GUT BACTERIA  
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ANTIBIOTICS   ALTERNATIVE CONTRACEPTION FOR ONE MONTH  
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METABOLISM OF ORAL CONTRACEPTIVES   SUBJECT TO ENZYME INDUCTION  
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SE/ADR'S OF OC CAN HAVE INCREASE OR DECREASE   ACNE AND WEIGHT  
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YAZ   CAN CAUSE K+ RETENTION  
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OC SE/ADR'S = ACHES   (A)BDOMINAL PAIN (GALL BLADDER DISEASE/ INTESTINAL INFARCTS), (C)HEST/CALF PAIN (DVT,PE,MI), (H)EADACHE (STROKE), (E)YE SIGHT (IF SUDDENLY CALL MD), (S)ELF EXAMS  
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CAN CHANGE SHAPE OF EYEBALL   ESTROGEN  
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EX QUESTIONS: ORAL CONTRACEPTIVES   NEGATIVE FEEDBACK, SUPPRESS FSH/LH  
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IF MISS MORE THEN 2 DAYS OF OC   USE BACK UP METHOD  
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OTHER DRUGS   CAN EFFECT EFFICACY OF OC  
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ACHES CAN BE SIGNS OF   THROMBOEMBULIS  
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CONTACT SIZES CAN BE AFFEECTED BY   ORAL CONTRACEPTIVES  
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REASON FOR CONDOM FAILURE   EXPRIATION DATES, IMPROPER STORAGE, IMPROPER SIZE, NO ROOM FOR EJACULATE, PUT WRONG SIDE OUT  
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TELLS YOU WHEN SOMETHING IS WRONG, BUT IT CAN PERSIST BEYOND BEING USEFUL   PAIN  
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2 TYPES OF PAIN   VISCERAL AND BONE/DENTAL  
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OPIATES FOR   VISCERAL  
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NSAIDS FOR   BONE/DENTAL  
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ACETAMINOPHEN FOR   VISCERAL AND BONE/DENTAL  
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BY THE #'S GOAL OF PAIN RELEIF IS   FULL PAIN RELIEF  
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AS LITTLE AS % REDUCTION MAY BE ALL THAT IS POSSIBLE WITH MEDS   30%  
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TEACH CLIENTS ABOUT   BEING REALISTIC WITH PAIN GOAL  
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PAIN DURING THE HEALING PROCESS, SNS INVOLVEMENT (INCREASE HR, BP), LITTLE PSYCHOLOGICAL COMPONENT   ACUTE PAIN  
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PAIN BEYOND THE HEALING PHASE, BLUNTED TO NON EXISTENT SNS RESPONSE, USUALLY SIGNFICANT PSYCHOLOGICAL COMPONENT   CHRONIC PAIN  
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GATE THEORY   REFLEXES NOT AWARE AT FIRST, HIGHER CORTICES (QUAL, QUANT), THALMUS IS FIRST AWARE OF PAIN(GENERIC)  
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NATURAL PAIN KILLERS IN CNS THAT WORK ON PERCEPTION OF PAIN,ARE PROTEINS AND CAN'T CROSS THE BLOOD BRAIN BARRIER   ENDORPHINS  
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MIMIC ENDORPHINS-MOST ARE STABLE IN STOMACH ACID AND CROSS THE BLOOD BRAIN BARRIER   OPIATES  
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OPIATE CLASS: NATURAL DERIVATIVES   MORPHINE(GOLD STANDARD), CODIENE (POOR PAIN KILLER)  
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OPIATES HAVE SYNERGY WITH   ACETAMINOPHEN (ANALGESIA)  
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SEMI-SYNTHETICS   WEAKEST TO STRONGEST HYDROCODONE (LORTAB), OXYCODONE (PERCOCOET), HYDROMORPHONE (DILAUDID)  
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DON'T COMBINE WITH ACETAMINOPHEN   HYDROMORPHONE (DILAUDID)  
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STRONGEST SEMI-SYNTHETICS   OXYMORPHONE  
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EX QUESTION 4 CLIENTS-SAME DOSE, ROUTE WHO IS IN WORSE PAIN   ONE ON OXYMORPHONE  
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MOST SEVERE SE/ADR'S FOR OXYMORPHONE   RESP DEPRESSION  
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FULL SYNTHETICS   MEPERIDINE/DEMEROL FANTANYL/DURAGESIC  
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FENTANYL/DURAGESIC LAST   72 HOURS  
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GENERAL PHARMACEUTICS IF BRAND ENDS IN "CET"   OPIATE AND ACETAMINOPHEN  
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IF IT ENDS IN "COTIN"   SUSTAINED RELEASE (DON'T CRUSH)  
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PATCH DISPOSAL   FOLD AND FLUSH  
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PATCH   CLIP HAIR, AVAOID ALCOHOL/HEAT  
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(PK) ABSORPTION OF OPIATES   PO  
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(PK) METABOLISM OF OPIATES   SUBJECT TO ENZYME INDUCTION AND INHIBITION  
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OPIATES PO ROUTE ARE ALL SUBJECT TO   1ST PASS EFFECT  
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EXCRETION OF OPIATES   METABOLITES; RENALLY EXCRETED (CAN SEE IN PEE TEST)  
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EX QUESTION4 CLIENTS WHY IS ROUTE IMPORTANT PO VS IV FOR OPIATES   FIRST PASS EFFECT  
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science and engineering of dosage forms   pharmaceutics  
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what the body does to the drug (in vs out)   pharmacokinetics  
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what the drug does to the body   pharmacodynamics  
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too much drug   toxicology  
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function of the dose not the substance   toxicity  
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pharmaceutics Po routes   immediate release- short onset, short duration (acute) OR sustained release- short or long onset, long duration (maintence)  
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ex of sustained   XL,SR,CR end in "contin" =NEVER CRUSH  
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NEVER DO THIS TO PATCHES   CUT IN HALF  
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4 PHASES OF PHARMACOKINETICS   ABSORPTION, DISTRIBUTION, METABOLISM, EXCRETION  
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ABSORPTION AND DISTRIBUTION   RESPONSIBLE FOR DRUG GOING INTO THE BODY  
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METABOLISM AND EXCRETION   RESPONSIBLE FOR DRUG GOING OUT OF BODY  
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PRIMARY ORGAN FOR METABOLISM   LIVER  
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PRIMARY ORGAN FOR EXCRETION   KIDNEYS  
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(PK) ABSORPTION   PROCESS OF DRUG ENTERING THE BLOOD STREAM IV ROUTE BYPASSES THIS (QUICK AND PRECISE)  
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IN GENERAL; INCREASED BLOOD FLOW AT THE SITE OF ABSORPTION WILL   INCREASE ABSORPTION  
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DISTRIBUTION   DRUGS DO NOT DISTRIBUTE TO ALL TISSUES EQUALLY, ALL DRUGS ARE SOMEWHAT AMPHOTERIC(HYDRO/LIPID)  
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METABOLISM   ENZYMATIC, DEACTIVATES DRUGS AND OR ALTERS THEM AND MAKES THEM MORE HYDROPHILIC(WATER SOLUBLE=EASIER TO EXCRETE IN URINE)  
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DRUG "B" PREVENTS THE METABOLISM(DRUG OUT) OF DRUG 'A' WHICH LEADS TO DRUG ACCUMULATION AND POSSIBLE TOXICITY   ENZYME INHIBITION EX;TAGAMENT  
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DUE TO ENZYME INHIBITION   ASK 3 QUESTIONS-PRESCRIBED MEDS, OTC, AND HERBAL MEDS?  
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DRUG "B" INCREASES THE NUMBER OF ENZYMES THAT METABOLIZE DRUG 'A' WHICH COULD LEAD TO DECREASED THERAPEUTIC EFFECT   ENZYME INDUCTION-ASK SAME 3 QUESTIONS  
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INCREASE IN ENZYMES EQUALS   INCREASE IN RATE OUT  
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DECREASE IN ENZYMES EQUALS   DECREASE IN RATE OUT  
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(PK) EXCRETION   PRIMARY ORGAN-KIDNEY, SOME DRUGS BYPASS METABOLISM AND GO STRAIGHT TO EXCRETION  
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INCREASE IN BUN/CREAT   DECREASE IN RENAL FUNCTION  
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PHARMOCOKINETICS   THERAPEUTIC RANGE/WINDOW SUBJECT TO INHIBITORS=TOXICIITY AND INDUCERS=NO BENEFIT  
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PHARMACOKINETICS   FIRST PASS EFFECT-EXPLAINS WHY PO DOSES ARE HIGHER THEN IV, IM, DERMAL PATCH DOSES  
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PHARMOCODYNAMICS   AGONISTS, ANTAGONISTS  
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AGONISTS   PORMOTES BIOCHEMICAL PROCESSES  
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ANTAGONISTS   INHIBIT/PREVENT BIOCHEMICAL PROCESSES  
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SIDE EFFECT   AGONIST OR ANTAGONIST BINDING TO RECEPTORS CAUSING ADDITIONAL SIGNS AND SYMPTOMS, USUALLY UNDESIRABLE AND SOMETIMES DESIRABLE  
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SE VS ALLERGY   ALLERGY INVOLVES ACTIVATION OF IMMUNE SYSTEM EX;RAHSES, HIVES, ANAPHYLAXIS  
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PHARMACODYNAMICS   THERAPEUTIC INDEX  
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THERAPEUTIC INDEX   DIFFERENCE BETWEEN THERAPEUTIC AND TOXIC DOSES  
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ED50   EFFECTIVE DOSE FOR 50% OF POPULATION  
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TD50   TOXIC DOSE FOR 50% OF POPULATION  
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DIFFERENCE BETWEEN ED50 AND TD50   THERAPEUTIC INDEX  
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EX OF WIDE THERAPEUTIC INDEX   PENICILLIN  
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EX OF NARROW THERAPEUTIC INDEX   DIGOXIN, INSULIN, DILANTIN  
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NARROW THERAPEUTIC INDEX   EASY TO OVERDOSE ON- SPEND MORE TIME ASSESSING FOR TOXICITY  
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PHARMACOKINETICS WITH PHARMACODYNAMICS HALF LIFE   AMOUNT OF TIME IT TAKES FOR A DRUG CP(CONCENTRATION OF PLASMA) TO DECREASE BY 50%  
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EACH DRUG HAS ITS OWN   HALF LIFE  
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RENAL/HEPATIC DYSFUNCTION   LENGTHENS HALF LIFE  
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HALF LIFE 2 HOURS   MULTIPLY BY 5=10 HOURS IS THE AMOUNT OF TIME BEFORE IT WILL BE OUT OF BODY  
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ADENOSINE   HIGH DOSE STOPS HEART AND HALF LIFE=10-15 SECONDS  
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AMIODERONE   CAN HAVE A HALF LIFE OF 35 DAYS(CRAZY)  
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GERD   COMPROMISED LES IN THE PRESENCE OF ACID, TX BY DECREASE ACIDITY OF STOMACH, DON'T OVER EAT, AVOID ALCOHOL, PEPPERMINT, SPICEY FOODS,HIGH FAT MEALS, CAN OCCUR AROUND THE CLOCK SO NEEDS TO BE MANAGED AROUND THE CLOCK  
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ACETYLCHOLINE ANTAGONIST-PROMOTES ACID RELEASE   ANTICHOLINERGICS  
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ALL CAUSE DRY MOUTH, DRY EYES, URINARY RETENTION, CONSTIPATION, AND IF THEY CROSS INTO THE CNS THERE IS A RISK FOR DELIRIUM   ANTICHOLINERGICS (SHORT HALF LIFE)  
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H2-ANTAGONIST (TIDINE) EX CIMETIDINE (TAGAMENT)   BLOCKS HISTAMINE AT THE H2 RECEPTOR, ONLY DOSED 2-3 TIMES PER DAY SO BETTER THEN ANTICHOLINERGIC AND CHEAP  
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STRONG ENZYME INHIBITOR   TAGAMENT-SO IMPORTANT TO ASK WHAT THEY ARE TAKING B/C IT CAN AFFECT OTHER DRUGS METABOLISM  
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ONLY DOSED 1-2 TIMES PER DAY, A IITTLE EXPENSIVE, BUT THE HAVE NO BROAD PHARMACOKINETIC INTERAACTIONS (METABOLISM)   PROTON PUMP INHIBITORS (PRAZOLE) EX OMEPRAZOLE (PRILOSEC)- ONLY AVAIL GENERICALLY  
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ANTACIDS (ACUTE)   FORM OF METAL ION BOUND TO A BASE, A BASE IS WHAT NEUTRALIZES THE ACID, THE METAL IS WHAT CAUSES THE SE/ADR'S  
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SODIUM BICARB   DUE TO THE NA, IT IS GOING TO CAUSE INCREASED WATER LOAD, SO BAD FOR CARDIOVASCULAR ISSUES  
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CALCIUM CARBONATE- TUMS   CAN HAVE ACID REBOUND WITH OVERUSE  
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ANTACIDS   AVOID NA BICARB WITH CARDIO VASCULAR ISSUES  
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MOM   PULLS WATER INTO BOWEL, WHICH CAUSES DIARRHEA  
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ALUMINUM   CAUSES CONSTIPATION  
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MOM AND ALUMINUM TOGETHER   MAALOX=STOOL SOFTNER  
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CLIENT C/O HEART BURN FOLLOWED BY CONSTIPATION   USE MAALOX  
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BULK LAXATIVES (FIBER)-SAFEST ONE   METAMUCIL-CITRACEL  
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DON'T TAKE WITH MEDS AND MAKE SURE PT IS HYDRATED   BULK LAXATIVES  
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STIMULANT LAXATIVE   SYSTEMICALLY ABSORBED AND END UP IN BREAST MILK  
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OSMOTIC LAXATIVES   MAG CITRATE- IT CLEANS YOU OUT, MOST LIKELY ABUSED BY DIETERS  
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LUBRICANT LAXATIVES   MINERAL OIL=FOOD FOR BACTERIA IN LUNGS, IF YOU ASPIRATE, CAN LEAD TO BRONCHITIS THEN COPD THEN DEATH  
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FLAMMABLE, DISCONTINUE PROIR TO SURGERY (24HOURS)-CAN CATCH ON FIRE   LACTULOSE  
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FOR TX OF IRON DEFIENCY ANEMIA, REPLACEMENT THERAPY(AGONIST), PHARMACOKINETICALLY-REQUIRES A ACIDIC ENVIRONMENT TO BE ABSORBED, SO POSSIBLE ISSUES WITH MEDS THAT TX ACID   IRON SALTS  
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IRON SALTS   GIVE +/- 1 HOUR FROM ANTACIDS, BECAUSE H2 ANTAGONIST AND PROTON PUMP INHIBITORS ARE AROUND THE CLOCK-GIVE WITH VIT C (ACIDIC)  
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SE/ADR'S OF IRON SALTS   N/V-THEY CAN TAKE WITH FOOD IF ISSUE, CONSTIPATION-CAN USE BULK LAXATIVE BUT DON'T GIVE AT THE SAME TIME, IRON GIVES YOU BLACK STOOLS NOT TARRY(GI BLEED)  
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CHILDHOOD DEATH FROM OVERDOSE, SO KEEP OUT OF REACH OF CHILDREN   IRON  
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non producers of insulin so must get it from an outside source(tend to be younger)   type 1 diabetic  
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normal insulin is released by pancreas and has 2 phases   1st one:basal- 1 unit of insulin per hour from pancreas 2nd one; post prandial(meal)- 5 units of insulin in an hour after a meal from pancreas  
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post prandial mimick   regular insulin  
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basal mimick   lantus (long acting insulin)  
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(PK) ABSORPTION OF INSULIN   FOR REGULAR INSULIN EASILY PASS THROUGH MEMBRANE AND THAT GIVES IT SHORT ONSET AND SHORT DURATION (BOLUS)  
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HAS AN ACID PH, BUT AT THAT ACID PH IT FORMS LONG CHAINS, SO IT DOESN'T EASILY FIT THROUGH THE MEMBRANE, BUT W/ BUFFERS, THERE IS A REGULAR/STEADY BREAKUP, SO ONCE IT IS BROKEN, IT CAN EASILY PASS THROUGH, BUT B/C IT PEAKS SLOWLY-LONGER PEAK AND DURATION   LANTUS (LONG ACTING)  
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CAN'T MIX WITH ANY OTHER INSULINS   LANTUS(CLOUDY)  
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DON'T FOR SQ INSULIN INJECTIONS   DON'T HAVE EXCESS HEAT, RUB SITE, FLEX MUSCLES  
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EXERCISE WILL CHANGE   INSULIN NEEDS-CONSULT MD FIRST-CARRY GLUCOSE SOURCE WITH THEM  
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ALCOHOL CONSUMPTION SHOULD BE AVOIDED WITH DIABETICS B/C   IT MESSES UP THEIR GLUCOSE CONTROL (FLUSH OF BLOOD THROUGH SKIN)  
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CARE OF SQ INSULIN   ROTATE SITE(SAME TYPE) EX ARM TO ARM  
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MORE LIFE DANGEROUS   HYPOGLYCEMIA S/S- FIGHT OR FLIGHT(^HR, ALTERED BREATHING, DIAPHORETIC)  
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FAMILY INVOLVED WITH INSULIN TX B/C   MAY CONFUSE S/S OF HYPOGLYCEMIA WITH INTOXICATION  
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HYPERGLYCEMIA- SICK DAYS   IF THEY FEEL FLU LIKE S/S AND EXCESS THIRST-CALL MD HAVE SOME WIGGLE ROOM W/ HYPERGLYCEMIA  
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STORAGE AND HANDLING-INSULIN   NO EXCESS HEAT, NO CARS,NO FREEZE/FROST, BEST PLACE IN FRIDGE DOOR, KEEP SUPPLIES TOGETHER,  
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INSULIN FRESH FROM FRIDGE WILL   STING, ROLL TO WARM-IF YOU SHAKE IT WILL ALTER DOSE  
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NEED TO KNOW FOR INSULIN   MEDIC ALERT BRACLET, PARENTS SHOULD ALSO READ PT INFO  
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INFECTIOUS DISEASE- GRAM POSITIVE   STAPH AND STREP (MRSA)  
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GRAM NEGATIVE   E.COLI, PSEUDOMONOS, AUROGENOSA  
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C&S TELLS YOU   WHAT THE BUG IS AND WHAT KILLS IT, BUT WE DON'T WAIT-START EMPIRIC THERAPY(BEST GUESS)  
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EMPIRICALLY GRAM NEGATIVE W/O C&S FOR   UTI  
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GRAM POSITIVE -MOST OF THE TIME IS   SKIN INFECTION EX;CELLULITIS  
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ONCE C&S IN-OFTEN CHG ABT-CALLED   STREAMLINE THERAPY-4 REASONS-LESS $, LESS TOXIC, LIMIT RESISTANCE, LIMIT SUPER INFECTION(ON TOP OF)  
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COMMON IN WOMEN POST ABT   YEAST  
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ABT NEED TO BE RESERVED FOR WHEN REALLY NEEDED DUE TO   RESISTANCE  
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TIMING FOR ABT   NEED CONSISTENT,SAME TIME EACH DAY-FIRST DOSE KILLS WIMPY ONES, SKIPPED DOSE LEAVES THE STRONGER ONES  
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NEED TO FINISH ABT B/C   IF YOU STOP-MORE RESILENT STRAINS CAN REGROW  
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IF MISS ABT(WITHIN 2 HOURS) TAKE IT   IF LONGER THEN 2 HOURS-WAIT TILL NEXT DOSE  
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BETA-LACTAMS-PENICILLINS OLDER   1ST PCN-NATURAL PCN-COVER GRAM+ > - ,ALTERED PCN INTO NEW CLASS-ANTISTAPHYLOCOCCAL PCN'S (COVER + > -) EX OXICILLIN  
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BETA-LACTAMS-PENICILLINS NEWER   AMINOPENICILLINS-COVER +/- EQUAL(EX; AMOXICILLIN, AMPICILLIN) AND ANTIPSEUDOMONAS-COVER GRAM - > + ( EX; PIPERCILLIN)  
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ENZYME THAT BREAKS UP PCN, SO IT DOESN'T WORK WELL   BETA-LACTAMASE  
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COMMONLY ADDED TO BROAD SPECTRUM ABT'S TO BLOCK ENZYME, THEREFORE WILL PREVENT PCN FROM GETTING BROKEN UP   BETA-LACTAMASE INHIBITORS EX; AMOXICILLIN W/ CLAVULANIC ACID=AUGMENTAN(BREATHES NEW LIFE INTO OLD ABTS  
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CLAVULANIC ACID OVERCOMES   ENZYME  
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ALL PCN'S WILL   SOFTEN STOOL(DIARRHEA)-DON'T DOUBLE UP  
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CEPHALOSPORINS (PD)   B-LACTAMS-CELL WALL LYSIS -NO INHIBITORS  
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CEPHALOSPORINS DIVIDED INTO GENERATIONS   1ST GENERATION-GRAM + > - 2ND GEN-GRAM + = - 3RD GEN-GRAM - > + (MIRRORS PROGRESSION OF PCN'S)  
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CLIENT WITH UTI   3RD GENERATION BEST  
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SLIENT SKIN INFECTION   1ST GENERATION BEST  
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CLIENT HAVING ABDOMINAL SX   PROPHAYLAXIS-SO WE USE 2ND GENERATION  
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(PK) CEPH/-CILLINS EXCRETION   ^BUN/CREAT= DECREASE RENAL FUNCTION, SO SINCE ABT ARE RENALLY EXCRETED IT WILL GIVE YOU A LONGER HALF LIFE AND IF THEY BUILD UP IN BODY-CAN BE TOXIC, SO IF RENAL IMPAIRED-MAINTAIN SAME DOSE BUT LONGER DOSE INTERVAL  
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HOLY CRAP THAT'S ENOUGH FOR NOW SEE PART TWO FOR THE OTHER HALF:)    
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