ROSIGLIATAZONE EVALUATED FOR CARDIOVSCULAR OUTCOMES IN ORAL AGENT COMBINATION THERAPY FOR TYPE 2 DIABETES (RECORD): & MULTICENTRE, RANDOMISED, OPEN -LABEL TRIAL. PHILIP D HOME DM, STUART J POCOCK PHD. AND COLLEAGUES. ROSIGLITAZONE IS AN INSULIN SENSITISER USED IN COMBINATION WITH MEFORMIN, A SULFONYLUREA, OR BOTH, FOR LOWERING BLOOD GLUCOSE IN PEOPLE WITH TYPE 2 DIABETES. WE ASSESSED CARDIOVASCULAR OUTCOMES AFTER ADDITION OF ROSIGLITAZONE TO EITHER METFORMIN OR SULFONYLUREA COMPARED WITH THE COMBINATION OF THE OVER S-7 YEARS OF FOLLOW UP. WE ALSO ASSESSED COMPARATIVE SAFETY METHODS. IN A MULTICENTRE, OPEN-LABEL TRIAL, 4447 PATIENTS WITH TYPE 2 DIABETES ON METFORMIN OR SULFONYLUREA MONOTHERAPY WITH MEAN HAEMOGLOBIN ALC (HB A1C) OF 7-9% WERE RANDOMLY ASSIGNED TO ADDITION OF ROSIGLITAZONE (N=2220) OR TO A COMBINATION OF METFORMIN AND SULFONYLUREA (ACTIVE CONTROL GROUP, N=2227). ‘THE PRIMARY ENDPOINT WAS CARDIOVASCULAR HOSPITALISATION OR CARDIOVASCULAR DEATH, WITH A HAZARD RATIO (HR) NON INFERIORITY MARGIN OF 1.20. ANALYSIS WAS BY INTENTION TO TREAT. THIS STUDY IS REGISTERED WITH GOVERNMENT CLINICAL TRIALS NUMBER NCTO0379769. FINDINGS. 321 PEOPLE IN THE ROSIGLITAZONE GROUP AND 323 IN THE ACTIVE CONTROL GROUP EXPERIENCED THE PRIMARY OUTCOME DURING A MEAN 5-5 YEAR FOLLOW UP, MEETING THE CRITERION ON NON-INFERIORITY (HR 0.93, 95% CL 0.85-1.16), HR WAS 0-84 (0-59) FOR CARDOVASCULAR DEATH, 1-14 (0.80 - 1.63) FOR MYOCARDIAL INFARCTION, AND 0.72 (0.49-1.06) FOR STROKE. HEART FAILURE CAUSING ADMISSION TO HOSPITAL OR DEATH OCCURRED IN 61 PEOPLE IN THE ROSIGLITAZONE GROUP AND 29 IN THE ACTIVE CONTROL GROUP (HR2.10, 1.35 ~ 3.27, RISK DIFFERENCE PER 1000 PERSON-YEARS 2.6, 1.1-4.1). UPPER AND DISTAL LOWER, LIMB FRACTURE RATES WERE INCREASED MAINLY IN WOMEN RANDOMLY ASSIGNED TO RSIGLITAZONE. MEAN HBALC WAS LOWER IN THE ROSIGLITAZONE GROUP THAN IN THE CONTROL GROUP AT 5 YEARS. INTERPRETATION. ADDITION ROSIGLITAZONE TO GLUCOSE LOWERING THERAPY IN PEOPLE WITH TYPE 2 DIABETES IS CONFIRMED TO INCREASE THE RISK OF HEART FAILURE AND OF SOME FRACTURES, MAINLY IN WOMEN. ALTHOUGH THE DATA ARE INCONCLUSIVE ABOUT ANY POSSIBLE EFFECT ON MYOCARDIAL INFARCTION, ROSIGLITAZONE DOES NOT INCREASE THE RISK OF OVERALL CARDIVASCULAR MORBIDITY OR MORTALITY COMPARED WITH STANDARD GLUCOSE -LOWERING DRUGS.WHAT WAS THE MAIN PURPOSE OF THE STUDY? ake afr ‘TO TREAT PATIENTS WITH TYPE 2 DIABETES. To DETERMINE THE INCIDENCE OF HOSPITALIZATION IN PATIENTS TAKING ROSIGLITAZONE, ‘To DISCOVER THE EFFECTS THAT ROSIGLITAZONE HAS ON HEART FAILURE IN PATIENTS WITH TYPE 2 UMBETES, TO GET GOVERNMENT APPROVAL FOR ROSIGLITAZONE, LOWER DISULINE IN PEOPLE WITH TYPE 2 DIABETES LOWER 81000 GLUCOSE IN PEOPLE WITH TYPE 2 DIABETES INCREASE BLOOD GLUCOSE IN PECPLE WITH TYPE 2 DIABETES. [DIMINISH ISULINE IN PEOPLE WITH TYPE 1 OTAEETES. PARTICIPANTS WERE GIVEN SULFONYLUREA. PARTICIPANTS WERE GIVEN ROSISLITAZONE. PARTICIPANTS HAD NEARLY SIMILAR LEVELS OF HBAIC. PARTICIPANTS WERE ALL FROM THE SAME CENTRE. WHAT DOBS THE AUTHOR CONCLUDE REGARDING THE SAFETY OF ROSIGUTAZONE IN GLUCOSE-LOWERING ‘THERAPY FOR PATIENTS WITH TYPE-2 DIABETES? ona ‘THE PERCENTAGE OF PATIENTS RESULTING IN HEART FAILURE WAS VERY HIGH FOR BOTH GROUPS, ROSIGLITAZONE, IN GENERAL CAUSES HEART FAILURE ROSIGUTAZONE 15 GENERALLY SAFE, BUT NOT FOR WOMEN, ROSIGLATAZONE SHOULD BE USED ONLY FOR MALE PATIENTS. ADDITION ROSIGUTAZONE TO GLUCOSE LOWERING THERAPY IN PEOPLE WITH TYPE 2 DIABETES 15 ‘CONFIRMED To: oor INCREASE THE RISK OF HEART FAILURE AND OF SOME FRACTURES, MAINLY IN MEN. INCREASE THE RISK OF HEART FAILURE AND OF SOME FRACTURES, MAINLY IN WOMEN. ‘THE DATA ARE CONCLUSIVE ABOUT ANY POSSIBLE EFFECT ON MYOCARDIAL INFARCTION, ROSIGLITAZONE INCREASES THE RISK OF OVERALL CARDIVASCULAR MORBIDITY.PIGMENTARY DISORDERS IN LATIN AMERICA FALABELLA, RAFAEL DERMATOLOGIC CLINICS - VOLUME 25, ISSUE 3 W. 8. SAUNDERS COMPANY JULY 2007 PITYRIASIS ALBA (PA) IS A COMMON DISORDER, ‘OBSERVED IN LATIN AMERICAN PATIENTS. LESIONS DISCLOSE HYPOPIGMENTATION, MAINLY OBSERVED (ON FACIAL AREAS AND SUNLIGHT EXPOSED SURFACE OF ARMS AND FOREARMS; THOSE ON THE TRUNK AND LOWER EXTREMITIES ARE LESS COMMON. AN ATOPIC DIATHESIS IS PRESENT IN MOST PATIENTS, AND THE CONDITION FREQUENTLY DEVELOPS IN CHILDREN AND YOUNG ADULTS. THE AVERAGE LESION BEGINS WITH A SLIGHTLY HYPOPIGMENTED MACULE THAT ENLARGES GRADUALLY FROM 1 CM TO 3 CM AND MAY COALESCE WITH NEIGHBORING MACULES, RESULTING IN LARGER HYPOPIGMENTED DEFECTS. A FINE DESQUAMATION AND DRYNESS OF SKIN ARE CHARACTERISTIC AND THE CLINICAL PICTURE USUALLY WORSENS DURING SUMMER OR DURING FREQUENT WATERSPORT ACTIVITIES. & FOLLICULAR VARIETY WITH MILD HYPERKERATOSIS AT THE HAIR FOLLICLE OSTIUM FREQUENTLY OCCURS. ON HISTOLOGIC EXAMINATION, EPIDERMAL AND FOLLICULAR SPONGIOSIS, FOCAL PARAKERATOSIS, SLIGHT ACANTHOSIS, AND MILD SUPERFICIAL PERIVASCULAR INFILTRATES ARE SEEN. IN A STUDY, ULTRASTRUCTURAL, EXAMINATION DISCLOSED SMALL AND REDUCED NUMBERS OF MELANOCYTES AND MELANOSOMES. ALTHOUGH PA IMPROVES SPONTANEOUSLY AFTER PUBERTY, LOW POTENCY CORTICOSTEROIDS, SUCH AS 1% HYDROCORTISONE OR 0.5% DESONIDE, FREQUENT EMOLLIENT APPLICATION, AND SUNLIGHT AVOIDANCE/PROTECTION ARE USEFUL TO CONTROL THIS DISORDER. SKIN CONTACT WITH DIVERSE CHEMICALS MAY INDUCE ACQUIRED HYPOPIGMENTATION, WHICH MAY OCCUR EITHER DURING PROFESSIONAL ACTIVITIES OR AS AN INCIDENTAL EVENT. AREAS OF CONTACT, SUCH AS HANDS AND. FEET, MAY BECOME AFFECTED WITH OR WITHOUT INITIAL DERMATITIS, AND THEREAFTER HYPOPIGMENTATION OCCURS. SOME OF THE INVOLVED CHEMICALS ARE CATECHOL AND BENZENE DERIVATIVES USED AS ANTISEPTICS AND CLEANSERS, PESTICIDES, AND EPOXY RESINS COMMONLY USED IN HOUSEHOLD WORK. MACULAR LESIONS SHOW DIFFERENT GRADES OF HYPOPIGMENTATION OR ‘TRUE DEPIGMENTATION INDISTINGUISHABLE FROM VITILIGO; A PREVIOUS HISTORY OF SUBSTANCE CONTACT AND DERMATITIS ARE IN FAVOR OF THE CHEMICAL NATURE OF DEPIGMENTATION . ON HISTOLOGIC EXAMINATION, JUST A FEW MELANOCYTES ARE PRESENT AND REDUCED OR ABSENT MELANIN IS OBSERVED. TREATMENT OF DEPIGMENTATION IS DIFFICULT, BECAUSE MOST OF THE TIME ACRAL AREAS ARE INVOLVED AND MELANOCYTES IN AFFECTED AREAS ARE SCARCE. IF VITILIGO-LIKE DEPIGMENTATION BECOMES REFRACTORY TO MEDICAL THERAPY, MELANOCYTE GRAFTING MAY BE AN, IMPORTANT THERAPEUTIC SOLUTION.PITYRIASIS ALBA IS A COMMON DISORDER FREQUENTLY OBSERVED IN: a(F] Rms anp LeGs B[E] FACE, ARMS AND FOREARMS c[F] TRUNK AND LOWER EXTREMITIES. [EF] Face, sams ano legs PREGUNTA 2 THE AVERAGE LESION BEGINS WITH A SLIGHTLY HYPOPIGMENTED SPOT THAT: a(F] Grows FROM 1 703 cM. B[E] REDUCES FROM 1TO3CM [Fi] ENLARGES To 5 CM. INDEPENDENTLY p[F] chances cour PREGUNTAB TO CONTROL THIS DISORDER IT Is USEFULTO: @] USE ANON FREQUENT EMOLLIENT APPLICATION ] KEEP AWAY FROM THE SUN, a B [©] USE HIGH POTENCY CORTICOSTEROIDS c B ©] Lc THE PROTECTION OF THE SUN HYPOPIGMENTATION OCCURS WHEN: a (F] SKIV HAS CONTACT WITH DIVERSE CHEMICALS B[E] WE HAVE INCIDENTAL ACTIVITIES c[F] we take comTisone. p/P] weuse sun erorecTion. PREGUNTA LO PITYRIASIS ALBA IS DANGEROUS BECAUSE: @] PATIENTS BECOME INTOLERANT TO LIGHT. ©] SOME OF THE TREATMENTS ARE TOXIC. a 5 c[F] PRE-CANCEROUS LESTONS CAN FORM p [E] dsuceTe surceay 1S SOMETIMES REQUIRED.UPPER RESPIRATORY TRACT INFECTIONS IN CHILDREN ZORC, JOSEPH J. CLINICAL PEDIATRIC EMERGENCY MEDICINE EL SERVIER DOI.10.1016.CPEM.209.03.008 MARCH 2009. UPPER RESPIRATORY TRACT INFECTIONS (INCLUDING OTITIS MEDIA) ARE THE MOST COMMON ILLNESSES AFFECTING CHILDREN. ON AVERAGE, CHILDREN EXPERIENCE AROUND SIX TO EIGHT UPPER RESPIRATORY TRACT INFECTIONS (URTIS) EACH YEAR. ALTHOUGH THESE INFECTIONS USUALLY ARE MILD AND SELF LIMITING, THEY OCCASIONALLY LEAD TO COMPLICATIONS THAT CAN BE LIFE THREATENING. MOST URTIS CAN BE PLACED WITHIN THREE MAIN CATEGORIES OF INFECTION: RHINOSINUSITIS, PHARYNGITIS, AND OTITIS MEDIA. WITHIN EACH CATEGORY OF ILLNESS THERE IS A RANGE OF RELATED CONDITIONS THAT MAY HAVE SIMILAR OR OVERLAPPING CLINICAL PRESENTATIONS. SOME JUDGMENT IS REQUIRED IN DETERMINING WHICH PART OF THE RESPIRATORY MUCOSA IS MOST AFFECTED. IN THIS ARTICLE, THE TERM "RHINOSINUSITIS" IS USED TO DESCRIBE ILLNESSES WITH PREDOMINANTLY NASAL SYMPTOMS (INCLUDING THE COMMON COLD, NASOPHARYNGITIS, AND SINUSITIS). THE TERM "PHARYNGITIS" IS USED ‘TO DESCRIBE ILLNESSES WHEN SORE THROAT IS MOST PROMINENT (INCLUDING TONSILLITIS). THE TERM “OTITIS MEDIA" IS USED TO DESCRIBE ILLNESSES WITH PREDOMINANTLY MIDDLE EAR SYMPTOMS. (INCLUDING ACUTE OTITIS MEDIA [AON], OTITIS MEDIA WITH EFFUSION [OME], AND CHRONIC ‘SUPPURATIVE OTITIS MEDIA [CSOM]). CHILDREN WHO HAVE COUGH AS THE PREDOMINANT SYMPTOM ARE CONSIDERED TO HAVE BRONCHITIS (A LOWER RESPIRATORY TRACT INFECTION). TO MAKE MATTERS MORE COMPLICATED, ALL AREAS OF THE RESPIRATORY MUCOSA MAY BE AFFECTED, SIMULTANEOUSLY OR AT DIFFERENT TIMES, DURING ONE ILLNESS. THE CAUSE OF THESE RESPIRATORY MUCOSAL INFECTIONS MOST COMMONLY IS VIRAL BUT CAN BE BACTERIAL AND MANY INFECTIONS INVOLVE BOTH VIRUSES AND BACTERIA. IN DEVELOPED COUNTRIES, 80TH VIRAL AND BACTERIAL INFECTIONS ARE LIKELY TO BE SELF LIMITED. PERSISTENT DISEASE IS MOST LIKELY TO INDICATE & BACTERIAL INFECTION.\WOHY ARE UPPER RESPIRATORY TRACTINFECTIONS 0 DIFFICULT TO DIAGNOSEIN CHILORENT THEY GET MANY OF THEM. a THE SYMPTOMS OF DIFFERENT URTIS OWEALAP. ‘THERE ARE DIFFERENT KINDS OF URTIS. AAG \WIRAL AND BACTERIAL INFECTIONS BUST. AN EXAMBLE OF & LOWER RESPIRATORY INFECTION IS: ARIA i (CAUSE OF THE ILLNESS IN RESPIRATORY INFECTIONS 15 BEST DETERMINED SY THE PRESENCE OF 8 VIRAL INFECTION. PRESENCE OF @ BACTERIAL INFECTION, Coe ABA AFFECTED BART OF THE RESPIRATORY MUCOSA. MAIN AREA AFFECTED IN INFECTIONS TEAMED OTITIS MEDIA" IS THE: AAA OME, AM, ANDSCOM ALL BELONG TO THE FAMILY OF THE INFECTION CALLED: Sn wm AAG ‘OTITIS MECIA,FREQUENCY OF GERD SYMPTOMS IN ELDERLY PATIENTS WHO COME TO A FAMILY MEDICINE CLINIC. OBJECTIVES: TO ASCERTAIN THE PREVALENCE OF GASTROESOPHAGEAL REFLUX DISEASE (GERD) IN ELDERLY PEOPLE ATTENDING TO FAMILY MEDICINE CLINICS. MATERIAL AND METHODS: THE STUDY WAS CONDUCTED BY USING A PROSPECTIVE DESIGN IN WHICH PARTICIPANTS WERE RANDOMLY SELECTED FROM A FAMILY MEDICINE CLINIC LOCATED IN MEXICO CITY. THE STUDY WAS RUN FROM AUGUST TO. SEPTEMBER 2003, AND INCLUDED PATIENTS AGED SIXTY YEARS OR OLDER, REGARDLESS OF GENDER. THEY SHOULD NOT HAVE COGNITIVE DAMAGE, WHICH WAS ASCERTAINED BY THE FOLSTEIN MINI MENTAL STATE EXAMINATION. THOSE PATIENTS THAT DID NOT ACCEPT TO PARTICIPATE AND THOSE HAVING INCOMPLETE OR ILLEGIBLE MEDICAL RECORDS WERE EXCLUDED. THE SOCIO-DEMOGRAPHIC (CHARACTERISTICS TEST AND CARLSSON-DENT TEST WERE APPLIED. THE INFORMATION ABOUT DIAGNOSIS, DRUGS PRESCRIPTIONS, AND PHARMACOLOGICAL AND NO PHARMACOLOGICAL GASTROESOPHAGEAL PROTECTION WAS OBTAINED FROM THE MEDICAL CHARTS AND PRESCRIPTIONS. RESULTS: 400 ELDERLY PATIENTS WERE EVALUATED BY USING THE CARLSSON-DENT TEST. GERD PREVALENCE WAS 25% (IC 95 % 21-29) THE AVERAGE AGE OF PATIENTS WITH AND WITHOUT GERD WAS 68 + 7 YEARS AND 70 + 7 YEARS RESPECTIVELY (P = .002). WOMEN SUFFERED GERD MORE FREQUENTLY THAN MEN (P = 0.001). GERD DIAGNOSIS WAS NOT FOUND IN ANY OF THE REVIEWED MEDICAL CHARTS. ANTACIDS, HISTAMINE- 2 RECEPTOR ANTAGONISTS (H2 AS) AND WERE PRESCRIBED IN 39% (IC 95 % 34-44) OF PATIENTS WITH GERD AND IN 18% (IC 95 % 15-21) WITHOUT GERD. CONCLUSIONS: ELDERLY PATIENTS ATTENDING TO PRIMARY CARE FACILITIES OFTEN HAVE GERD. SYMPTOMS, BUT THEY ARE NOT PROPERLY DIAGNOSED OR FOLLOWED UP. THE CARLSSON-DENT QUESTIONNAIRE IS AN ALTERNATIVE TO IDENTIFY GERD PATIENTS.ABOUT THE DESIGN OF THE STUDY: i oo wp RESEARCHERS USE & PROSPECTIVE DESIGN, PARTICIPANTS WERE FAMILY MEDICINE SPECIALIST FROM MEXICO CITY SELECTED ATRANOOM. Za] PARTICIPANTS ARE SELECTED ATRANOOM FROM A FAMILY MEDICINE CLINIC FROM AN ELOGRLY FEMALE E] Loeay PATIENTS WERE INCLUDED WITHOUT CONSIDERING GENDER. TWAS ORIGINALLY PLANNED TO € CONE IN THREE MONTHS. {INCLUSION OF PATIENT CRITERIA WAS: CERTAINLY NOTTO BAVE ANY BRAIN DAMAGE. ‘TO HAVE COGNITIVE COMPETENCE PROVEN BY THE FOLSTEIN MINI MENTAL STATE EXAMINATION. NOT TO ACCEFTTO PRATICIFATE IN THE STUDY. AAA ‘THERE WERE INCOMPLETE ILLEGISLEMECICAL RECORDS. REEEARCMERE OBTAIN THE INFORMATION ABOUT SIAGNOSIE, ORUGE PREECRIFTIONE, AND MARMACDLOGICAL AND ND PHARMACOLOGICAL GASTROESOPHAGEML PROTECTION FROM, cae > AA A SOCIO-DSMOGHAPHIC CHARACTENISTICS TEST. A CARLESON-OENT TEST. GLNIC DATABASES. AIM OF THESTUOV GLVEAS A REEULT: E] cero mrevavence was 250. AVERAGE AGE OF PATIENTS WITH AND WITHOUT GERD WAS 68 + 7 YEARS AND 704 7 YEARS RESPECTIVELY. ] WOMEN SurFERED GID MORE FREQUENTLY THANMEN. ©] anaciog, Maas AND WERE PRESCHIGED IN-Z% OF PATIENTS WITHGERD. MAIN CONCLUSION OF THE STUDY WAS: PATIENTS WITHOUT GERD STILL RECEIVED TREATMENT. PARTICIPANTS OFTEN HAD GERD SYMPTOMS. PATIENTS IDENTIFIED WITH GERD SYMPTOMS WERE DLAGNOSED AND FOLLOWED UP CORRECTLY. ALA ‘THE CARL SSON-DENT QUESTIONNAIRE WAS THE BEST ALTERNATIVE 70 IDENTIFY GERD PATIENTS.NEW THINKING ON HOW TO PROTECT THE HEART BY JANE E. BRODY SURGERY MAY NOT BE THE SEST WAY TO AVOID A HEART ATTACK OR SUDDEN CARDIAC DEATH, THE NEXT STEP 1S FINDING OUT WHAT CAN WORK AS WELL OR BETTER TO PROTECT YOUR HEART. MANY MEASURES ARE PROBABLY FAMILIAR: NOT SMOKING, CONTROLLING CHOLESTEROL AND BLOOD PRESSURE, EXERCISING REGULARLY AND. STAYING AT A HEALTHY WEIGHT. BUT SOME NEWER SUGGESTIONS MAY SURPRISE YOU. IT IS NOT THAT THE OLD ADVICE, LIKE EATING A LOW-FAT DIET OR EXERCISING VIGOROUSLY, WAS BAD ADVICE; IT WAS BASED ON THE BEST AVAILABLE EVIDENCE OF THE TIME AND CAN STILL BE VERY HELPFUL. THE WELL-ESTABLISHED RISK FACTORS FOR HEART DISEASE REMAIN INTACT: HIGH CHOLESTEROL, HIGH BLOOD PRESSURE, SMOKING, DIABETES, ABDOMINAL OBESITY AND SEDENTARY LIVING. BUT BEHIND ‘THEM A RELATIVELY NEW FACTOR HAS EMERGED THAT MAY BE EVEN MORE IMPORTANT AS A CAUSE OF HEART ATTACKS THAN, SAY, HIGH BLOOD LEVELS OF ARTERY-DAMAGING CHOLESTEROL. THAT FACTOR, IS C-REACTIVE PROTEIN, OR CRP, A BLOOD-BORNE MARKER OF INFLAMMATION THAT, ALONG WITH COAGULATION FACTORS, 1S NOW INCREASINGLY RECOGNIZED AS THE DRIVING FORCE BEHIND CLOTS ‘THAT BLOCK BLOOD FLOW TO THE HEART. EVEN IN PEOPLE WITH NORMAL CHOLESTEROL, IF CRP IS ELEVATED, THE RISK OF HEART ATTACK IS TOO. DIET REVISITED THE NEW DIETARY ADVICE IS ACTUALLY BASED ON A RATHER OLD FINDING THAT PREDATES THE MANTRA TO EAT A LOW-FAT DIET. IN ‘THE SEVEN COUNTRIES STUDY STARTED IN 1958 FOUND THAT HEART DISEASE WAS RARE IN THE MEDITERRANEAN AND ASIAN REGIONS WHERE VEGETABLES, GRAINS, FRUITS, BEANS AND FISH WERE ‘THE DIETARY MAINSTAYS. BUT IN COUNTRIES LIKE FINLAND AND THE UNITED STATES WHERE PLATES WERE TYPICALLY FILLED WITH RED MEAT, CHEESE AND OTHER FOODS RICH IN SATURATED FATS, HEART DISEASE AND CARDIAC DEATHS WERE EPIDEMIC. THE FINDING RESULTED IN THE WELL-KNOWN ADVICE ‘TO REDUCE DIETARY FAT AND ESPECIALLY SATURATED FATS (THOSE THAT ARE FIRM AT ROOM TEMPERATURE), AND TO REPLACE THESE HARMFUL FATS WITH UNSATURATED ONES LIKE VEGETABLE OILS. WHAT WAS MISSED AT THE TIME AND HAS NOW BECOME INCREASINGLY APPARENT 1S THAT THE HEART-HEALTHY MEDITERRANEAN DIET IS NOT REALLY LOW IN FAT, BUT ITS MAIN SOURCES OF FAT — ‘OLIVE OIL AND OILY FISH AS WELL AS NUTS, SEEDS AND CERTAIN VEGETABLES — HELP TO PREVENT HEART DISEASE BY IMPROVING CHOLESTEROL RATIOS AND REDUCING INFLAMMATION.ACCORDING 70 THE ARTICLE, THE BEST WAWTO AVOID A HEART ATTACK IS: EATING A LOW FAT DUET AND EXERCISING VIGOROUSLY. RAVING A SURGERY. on me ARIA ACCORDING 70 THE ARTICLE, THE SEST DIET TO FOLLOW IS: ALOW-FAT DIET SATURATED FATS AED MEAT ANO CHEESE AGA ono» A MEDITERRANEAN DUET, i | i 8 LW CARBORVORATES: UNEATURATED FATS, on wp ro fe] acomeat ano cesese [e eI DRINKING RED WINEIS GIO FOR YOU BECAUSE: IT MAKES YOU RELA HAS ANTIOXIDANT PROPERTIES. IT PREVENTS THE FORMATION OF CHOLESTEROL ono» ALIAS IVS EASY TO OIGEST FROM THE ARTICUS WE-CAN CONCLUDE THAT: a[E] i werouow a Low-FaT CIE AND SxSaCISE VIGOROUSLY WEWILL AVOID HAVING A HEART ATTACK GOING TO THE PERIODONTIST, EXERCISING IS MINUTES A DAY, RELAXING, AND FOLLOWING A MEDITERRANEAN O1ST WE WILL AVOID MAWING A MEART ATTACHE TAKING VACATION, SYSRCISING VIGOROUSLY AND FOLLOWING A MEDITERRANEAN DIET WE WILL AVOID HAVING A BEART ATTACK PRACTICING THE RELAXATION RESPONSE ONCE OR TWICE A DAY BY BREATHING DEEPLY AND ARYTHMICALLY IN A QUIET PLACE WILL AVOID HAVING A HEART ATTACK. aMATERNAL MORBIDITY, MORTALITY, AND RISK ASSESSMENT MATERNAL MORTALITY IS THE TIP OF THE MATERNAL MORBIDITY ICEBERG; SEVERAL OBSTETRIC, ANESTHETIC, AND SOCIAL CHALLENGES IMPACT MORBIDITY AND MORTALITY IN WOMEN, MATERNAL MORTALITY IS THE YARDSTICK TO MEASURE WHEN HEALTH CARE PERSONNEL FAIL TO RECOGNIZE RISKS, LACK INTERDISCIPLINARY COMMUNICATION, OR PROVIDE SUBSTANDARD CARE, THUS RESULTING IN COMPLICATIONS DURING PREGNANCY, LABOR, OR DELIVERY. PREGNANCY-RELATED DEATH IS DEFINED BY THE INTERNATIONAL CLASSIFICATION OF DISEASES, LOTH REVISION (ICD-10) AS THE DEATH OF A WOMAN WHILE PREGNANT OR WITHIN 42 DAYS. OF TERMINATION OF PREGNANCY, DESPITE THE CAUSE OF DEATH. ALTHOUGH THE RISK FOR DEATH FROM COMPLICATIONS OF PREGNANCY DECREASED DRAMATICALLY DURING THE 20TH CENTURY IN THE UNITED. STATES, THE CENTERS FOR DISEASE CONTROL AND PREVENTION (CDC) REPORTS A FAIRLY STATIC MATERNAL MORTALITY RATIO (MMR), OF APPROXIMATELY 7.5 MATERNAL DEATHS PER 100,000 LIVE BIRTHS. IN THE YEAR 2000, A COLLABORATIVE EFFORT INVOLVING WORLD HEALTH ORGANIZATION (WHO), UNTTED NATIONS CHILDREN'S FUND (UNICEF), AND UNITED NATIONS POPULATION FUND (UNFPA) ESTIMATED 660 MATERNAL DEATHS, THUS AVERAGING 11 MATERNAL DEATHS PER 100,000 LIVE BIRTHS, PLACING THE MMR ABOVE THE STATISTICS REPORTED BY THE CDC. THESE SURVEYS ON MATERNAL MORTALITY SURVEILLANCES ARE LIMITED IN SCOPE BECAUSE THE INFORMATION IS OBTAINED FROM. DEATH CERTIFICATES, AND VARIOUS STATES OR ACADEMIC INSTITUTIONS COULD BE UNDERREPORTING. ACCURATE STATISTICS ARE LACKING, THUS RESULTING IN ONLY A SNAPSHOT OF THE ACTUAL MATERNAL MORBIDITY AND MORTALITY. THE RECENT WHO ESTIMATE IN THE UNITED STATES SHOW THAT MATERNAL MORTALITY IS APPROXIMATELY 17 IN 100,000 PREGNANCIES. THIS ESTIMATE 1S SIGNIFICANTLY HIGHER THAN THE GOAL SET BY THE U.S. DEPARTMENT OF HEALTH AND HUMAN, SERVICES IN HEALTHY PEOPLE 2010, WHICH SETS THE TARGET FOR MATERNAL MORTALITY AT LESS ‘THAN 3.3 IN 100,000 LIVE BIRTHS. SOME REGIONAL REPORTS DOCUMENT RATIOS AS HIGH AS 22.8 PER 100,000 LIVE BIRTHS, WHICH IS AN UNACCEPTABLY HIGH RATE. IN UNITED STATES, THE MOST COMMON CAUSES OF MATERNAL DEATHS, ALTHOUGH THEY VARY AMONG STATES, INCLUDE THROMBOEMBOLISM; AMNIOTIC FLUID EMBOLISM; HEMORRHAGE; COMPLICATIONS OF HYPERTENSION, INCLUDING PREECLAMPSIA AND ECLAMPSIA; AND INFECTION. PULMONARY DISEASE, ANESTHESIA-RELATED DEATHS, AND CARDIOMYOPATHY ARE ALSO SIGNIFICANT CONTRIBUTORS TO MATERNAL MORBIDITY AND MORTALITY.FOR MATERNAL MORTALITY A RISK FACTOR COULD BE: ‘EXCESIVEINTERCUE CIAUNARY COMMUNICATION BY MEALTH CARE FEREONNEL, FAILURE TO RECOGNIZE RISKS BY HEALTH CARE PERSONNEL. EULTH CARE FERSOWNE, PROVIDE STANDARD CARE, one ABA ALL ABOWE ARE RISK FACTORS. MAIN REABON WHY THE MATERNAL MORTALITY SURVEILLANCES ARE LIMITED IN SCOPE WOULD BE BECAUSE THE INFORMATION IS OBTAINED OF DEATH CERTIFICATES. A SITUATION OF UNDERREFORTING. BECAUSE VARIOUS STATES OR ACADEMIC INSTITUTIONS COULD 8€ OVERREFORTING. API on ee ‘THE MATERNAL MORTALITY SURVEILLANCES ARE ACCURATE. ACCORDING TO THE FINDINGS FROM THE STUDY CONDUCTED SY WHO, UNICEF ANDTHE UNFPA WHATIS THE a[E] PREGNANCY RELATE DEATH IS THE DEATH OF A PREGNANT WOMAN. Za) PREGMANCY REALTEO OEATH IS THE DELTH OF A WOMAN WITHIN 42 DANE OF TERMINATION PREGUANCY, DEERITE THE CAUEEOF DEATH, Fa] THE RISC OF Dene FROM COMPLICATIONS OF AREGRNCY DECREASED ORAMATICANLY OURING THE 2TH (CENTURY IN THE UNITED STATES, o[S] tema statismics anzasovemecne stamsmics. a MATERNAL MORTALITY 1S APPROXIMATELY 17 IN 19,000 PREGNANCIES. ‘THE RESULTS HAVE NOT EEN WHAT THEY EXPECTED. ale e[E] mavenwan MORTALITYIS AT LESS 3.31N 100, 000LIVE BIRTHS. cE off MATERNAL MORTALITY IS 22.8 PER 190,000 LIVE BIRTHS. ABOUT THE CAUSES OF MATERNAL DEATHS WHICH WOULOBE CONSIDERED A CONTRIBUTOR FROM THE AMSIOTIC FLUID EMBOLISM. PREECLAMPSIA AND ECLAMPSIA, anor aL] (4)VACCINE TAKES AIM AT HYPERTENSION ORLANDO, FLA: SOME PATIENTS WITH HYPERTENSION HAVE INADEQUATE CONTROL OF BLOOD PRESSURE BECAUSE THEY ARE NOT CONSISTENTLY ADHERENT IN TAKING THEIR MEDICATIONS. BUT HELP MAY BE ON THE WAY IN THE FORM OF A VACCINE THAT LOWERS BLOOD PRESSURE BY CONTROLLING ANGIOSTENSIN Il, SUGGEST FINDINGS FROM A SMALL SAFETY STUDY PRESENTED AT THE SCIENTIFIC SESSIONS OF THE AMERICAN HEART ASSOCIATION IN NOVEMBER. ‘THE STUDY OF 72 PATIENTS WITH MILD-TO-MODERATE HYPERTENSION, PRESENTED BY JURG NUSSBERGER, MD, PROFESSOR OF MEDICINE AT THE UNIVERSITY HOSPITAL OF THE CANTON OF VAUD, LAUSANNE, SWITZERLAND, FOUND THAT AT 14 WEEKS, THOSE INJECTED WITH CYTOO6-ANGQB (AT 0,4, AND 12 WEEKS) HAD A DAYTIME SYSTOLIC BLOOD PRESSURE THAT WAS 5.6 MM HG LOWER AND A. DIASTOLIC BLOOD PRESSURE 2.8 MM HG LOWER THAN THOSE OF PATIENTS WHO RECEIVED PLACEBO. (CYT00S-ANGQS, WHICH IS UNDER DEVELOPMENT BY CYTOS BIOTECHNOLOGY AG (ZURICH, SWITZERLAND), IS A VIRUS-SHAPED NONINFECTIOUS PARTICLE THAT IS CHEMICALLY COUPLED WITH ANGIOTENSIN IL, AND OCTAPEPTIDE VASOCONSTRICTOR. SUCH COUPLING INDUCES THE BODY TO PRODUCE ANTIBODIES AGAINST THIS SMALL MOLECULE TOP MINIMIZE ITS EFFECTS ON CONSTRICTING BLOOD VESSELS. NUSSBERGER SAID HE IS NOT CONCERNED THAT THE VACCINE MIGHT CAUSE HYPOTENSION BECAUSE ANTIBODY TITERS STARTED TO DECREASE SHORTLY AFTER THE BOOSTER OF TWELVE WEEKS INDUCED PEAK ANTIBODY LEVELS. HE ALSO SAID THE LIKELIHOOD OF VACCINE- INDUCED ANTIBODIES CROSS-REACTING WITH OTHER PROTEINS WAS MINIMAL BECAUSE THE SMALL SIZE OF THE TARGET MOLECULE LIMITS THE NUMBER OF EPITOPES THAT COULD BE AFFECTED. NUSSBERGER SPECULATED THAT IF THE CYTOOS-ANGQS VACCINE IS ULTIMATELY APPROVED, PATIENTS WOULD BE ABLE TO AVOID THE NEED FOR MEDICATION BUT WOULD REQUIRE & BOOSTER SHOT 2 OR 3 TIMES A YEAR. HE SAID THE NEXT STEP IN STUDYING THE VACCINE WILL BE TO CONDUCT ANOTHER, SMALL TRIAL TO DETERMINE THE APPROPRIATE DOSING TO CREATE THE LARGEST ANTIBODY RESPONSE AND GREATEST REDUCTIONS IN BLOOD PRESSURE. MORRIS J. BROWN, MD, PROFESSOR OF CLINICAL PHARMACOLOGY AT THE UNIVERSITY OF CAMBRIDGE IN ENGLAND AND PAST PRESIDENT OF THE BRITISH HYPERTENSION SOCIETY, SAID THE FINDINGS OF THE STUDY (WHICH WAS FUNDED BY CYTOS) ARE “INTRIGUING" BUT OFFERED A CAVEAT. "I AM A LITTLE WARY OF TOP-LINE RESULTS FROM BOITECHS, ESPECIALLY SECONDARY EFFICACY VARIABLES IN A PRIMARY SAFETY STUDY,” HE SAID. BROWN HAS. ALSO HAD A HAND IN ATTEMPTS TO CREATE A HYPERTENSION VACCINE, PMD3117, UNDER DEVELOPMENT BY PROTHERICS PLC IN RUNCORN, ENGLAND (BROWN Mj ET AL. CLIN SCL.ABQUT PATIENTS THAT OON"T TAKE THEIR TREATMENT REGULARY: ono» AAA THIS SATIENTS HAVE AN ADEQUATE CONTROL OF BLOOD ARESEURE, ‘THEY ARE CONSISTENTLY ADHERENT IN TAKING THEIR MEDICATIONS. THEY MUST HAVE & RESULAA DIET CONTROL. THEY HAVE AN INADEQUATE CONTROL OF BLOOD PRESSURE ASQUT THE WORKING MECHANISM OF THE VACCINE: ono ARAL 17S WORKING MECHANISM 15 BY CONTROLLING THE ANGIOTENSIN 1. 17S WORKING MECHANISM 15 2Y CONTROLLING THE ANGIOTENSIN 11 17'S WORKING MECHANISM IS BY CONSTRICTING L000 VESSE:S. ITINQUDEE ANTISODIEE CROSS-REACTION WITH OTHER PROTEINS. \WeITH RESPECT TO THE CYTDOS-ANGNS WACCINE, CONSIDERATION MAVE SEEN MADE THAT: one» AAA THE VACCINE MAY PRODUCE MVFERTENEION, {THE VACCINE OES NOT INOUCE ANTIBODIES CAOSS-AEACTION WITH PROTEINS. ‘THE VACCINE MAY CAUSE HYPOTENSION. THE VACCINE MIGHT CAUSE IMOTENCY, \WORATIS THE REASON OF THE REOUCED NUMBER OF AFFECTED ERITOPES 7 ARIAB ono y BECAUSE OF THE SMALL SIZE OF THEERITOPES. GECAUSE OF THE SMALL SIZE OF THE TARGET MOLECULE. [BECAUSE ANTIBODY TITERE STARTED TO DECREASE, THE MUMBER OF EPITOPES WAS NEVER AFFECTED. WORAT SHALL SE DONE TO OETERMINE THE LARGEST ANTISO DW RESPONSE AND GREATEST REDUCTIONS IN BLOOD AAA one» ASMALL THIAL TO OETERMINE THE AIGHT DOSING HAD TO SE CONDUCTED. BOOSTER SHOTZOR TIMES A YEAR. ANGIOTENSIN IE AND OCTAFEFTIOE VASOCONSTRICTOR INDUCE THE BODY TD PRODUCE ANTIBODIES. ANGIOTENSIN II WOULD ALONE REGULATE THE BLOOD PRESSURE.WILLIAM THOMAS GREEN MORTON ON OCTOBER 16, 1846, DEMONSTRATED THAT ETHER COULD INDUCE INSENSIBILITY TO THE SURGEON'S KNIFE, A JAW TUMOR WAS REMOVED FROM GILBERT ABBOT BY JOHN COLLINS WARREN AT THE MASSACHUSETTS GENERAL HOSPITAL IN FRONT OF AN AUDIENCE OF MEDICAL PROFESSIONALS. THE NEWS OF THIS PUBLIC DEMONSTRATION TRAVELED QUICKLY, GIVEN THE NATURE (OF COMMUNICATION IN THE 1840S. ON DECEMBER 16, 1845, THE INFORMATION IN THE FORM OF A LETTER ARRIVED IN LONDON. ON DECEMBER 19, THE FIRST ETHER ANESTHETIC WAS GIVEN IN THE UNITED KINGDOM FOR THE REMOVAL OF A TOOTH. ON DECEMBER 21, THE FAMOUS SURGEON ROBERT LISTON AMPUTATED THE LEG OF A BUTLER, AND UTTERED THE FAMOUS WORDS, “THIS YANKEE DODGE BEATS MESMERISM HOLLOW” JAMES YOUNG SIMPSON, THE PROFESSOR OF MIDWIFERY IN EDINBURGH, SCOTLAND, WAS AMONG THE FIRST TO USE ETHER FOR THE RELIEF OF LABOR PAIN. ON JANUARY 19, 1847, HE USED ETHER TO AMELIORATE THE PAIN OF LABOR. THIS FIRST CASE, THAT OF A YOUNG WOMAN WITH RICKETS AND A SEVERELY DEFORMED PELVIS, WAS AT GRAVE RISK OF DYING AND THERE WAS NO HOPE FOR A LIVE BIRTH. BY USING ETHER, THE MOTHER SURVIVED THE COMPLICATED DELIVERY PAIN-FREE. THAT SAME JANUARY DAY, SIMPSON WAS APPOINTED THE QUEEN'S PHYSICIAN IN SCOTLAND. SIMPSON CONTINUED TO PROVIDE ANESTHESIA IN CHILDBIRTH FOR BOTH COMPLICATED AND NORMAL DELIVERIES; HOWEVER, HE RAPIDLY BECAME DISSATISFIED WITH ETHER AND SOUGHT A MORE PLEASANT, RAPID-ACTING ANESTHETIC. AT THE SUGGESTION OF DAVID WALDIE, HE EXPERIMENTED WITH CHLOROFORM, WHICH HAD FIRST BEEN PREPARED IN 1831. ON THE EVENING OF NOVEMBER 4, 1847, SIMPSON AND HIS FRIENDS INHALED IT AFTER DINNER AT A PARTY IN SIMPSON'S HOME. THEY PROMPTLY FELL UNCONSCIOUS AND, WHEN THEY AWOKE UNDER THE TABLE AND CLEARLY OFF THEIR DINING ROOM CHAIRS, WERE DELIGHTED WITH THEIR SUCCESS. WITHIN 2 WEEKS, SIMPSON SUBMITTED. HIS FIRST ACCOUNT OF CHLOROFORM'S USE TO THE LANCET.IN THE NINETEENTH CENTURY, THE RELIEF OF OBSTETRIC PAIN HAD SIGNIFICANT SOCIAL AND RELIGIOUS CONSEQUENCES, WHICH MADE ANESTHESIA DURING CHILDBIRTH A CONTENTIOUS SUBJECT. THE BATTLE CENTERED ON WHETHER, RELIEVING LABOR PAIN WAS CONTRARY TO GOD'S WILL. THE PAIN ASSOCIATED WITH CHILDBIRTH WAS. BELIEVED TO BE A DEVINE PUNISHMENT FOR ORIGINAL SIN. SHORTLY AFTER GIVING HIS FIRST OBSTETRIC ANESTHETICS, SIMPSON PUBLISHED A PAMPHLET ENTITLED ANSWERS TO THE RELIGIOUS OBJECTIONS ADVANCED AGAINST THE EMPLOYMENT OF ANESTHETIC AGENTS IN MIDWIFERY AND SURGERY AND OBSTETRICS, WHICH ARGUED AGAINST THESE RELIGIOUS PROHIBITIONS.WILLIAM THOMAS GREEN MORTON USED THES ON A PATIENT'SO THERE WOULD BE NO SENSIGILITY IN THE OPERATION. ETHER ON A PATIENT TO REDUCE THE SEVEIBILITY DURING THE OPERATION (ETHES TO OISINFECT THE KNIFE IN THE OPERATION ANO OTHER OPERATING EQUIPMENT ARAL ono» ETHER INSTEAD OF AN ANESTHETIC. CURING A PATIENT WHO MAD RIOXETS AEDUCING THE LASOA PAIN OF A WOMEN WHEN GIVING BIRTH WITH 4 DEFORMED PELVIS: e e ©] meoucine Tee sain oF suncERY [A] savinc THe News0an ROM OYEING IN CALDSIATH ono py USING ETHER FOR CHILESIRTH 70 ONLY USE CHLOROFORM FOR CHILDEIATH a ©] To CONTINUE USING ETHER AND CHLOROFORM FOR CHILDBIRTH e A PROVIDE ANESTHESIA DN CHILDBIRTH FOR, 207TH COMPLICATED AND NORMAL CELIVERIES: ITIS EVIDENT THAT THIS NEW PRACTICE OF USING ANESTHESIA IN CHILOGIATH HAD SOCIAL AND RELIGIOUS SIMPSON WAS IN FAVOR OF AELIGIOUS BELIEFS IN CHILDBIRTH PRACTICE [SIMPSON WAS IM FAVOR OF SOCIAL SELIEFS ABOUT CHILDBIRTH PRACTICE SIMPSON WAS AGAINST RELIGIOUS BELIEFS IN CHILOGIATH PRACTICE APIA ones SIMPSON WAS AGAINST THESE RELIGIOUS PROMISITIONS: ‘THE PAIN ASSOCIATED WITH CHILOSINTH WAT BELIEVED TO BE CAUSED AS, (CONSEQUENCE OF DEFORMED PELVIS, A DEVINE PUNISHMENT FOR ORIGINAL SIN, BECAUSE OF LUCK OF ANESTHETICS. one > AAA 71-YEAR-OLD MALE PRESENTED WITH A 2-WEEK HISTORY OF A HARD, PAINFUL, NONPULSATILE MASS: IN HIS LEFT UPPER ARM. EXAMINATION REVEALED A CRAGGY, MOBILE MASS OF IRREGULAR BORDERS IN ‘THE LEFT ARM MEASURING 6 x 4 CM. ULTRASONOGRAPHY OF THE LEFT ARM DEMONSTRATED A DEEP OVOID HYPERECHOIC MASS LOCATED IN THE LONG AXIS OF THE LEFT TRICEPS MUSCLE. MRI SHOWED INTERMEDIATE SIGNAL MASS IN THE TRICEPS MUSCULATURE ON T1-WEIGHTED IMAGES WITH FAT SATURATION. THIS LESION WAS CONFINED TO THE EXTENSOR COMPARTMENT OF THE ARM. A. PRESUMPTIVE DIAGNOSIS OF SOFT TISSUE SARCOMA WAS CONSIDERED. AN INCISIONAL BIOPSY REPORTED METASTATIC SQUAMOUS CELL CARCINOMA WITH A POSSIBLE LUNG PRIMARY, FURTHER SUPPORTED DLE TO A POSITIVE CK7 AND NEGATIVE CK20 STAIN ON IMMUNOHISTOCHEMISTRY. CT SCAN OF THE CHEST REVEALED A LEFT UPPER LOBE LESION MEASURING 4 x 2 CM, FIBER-OPTIC BRONCHOSCOPY AND BIOPSY CONFIRMED THE DIAGNOSIS OF STAGE IV SQUAMOUS CELL LUNG CARCINOMA. HE UNDERWENT PALLIATIVE RADIOTHERAPY TO THE MASS IN THE ARM. THIS PROVIDED GOOD RELIEF FROM PAIN AND SWELLING WITHIN 2 WEEKS OF COMPLETING TREATMENT. SYSTEMIC ‘THERAPY WAS NOT OFFERED ON THE BASIS OF POOR AND DETERIORATING PERFORMANCE STATUS. UNFORTUNATELY, THE PATIENT DIED WITHIN 10 WEEKS OF PRESENTATION. INTRAMUSCULAR METASTASES IN CANCER PATIENTS ARE RARE. THIS IN ITSELF IS QUITE PECULIAR BECAUSE MUSCULAR MASS ACCOUNTS FOR APPROXIMATELY 50% OF TOTAL BODY WEIGHT. IT IS THOUGHT THAT MUSCULAR CONTRACTILE ACTIONS, LOCAL PH ENVIRONMENT, AND ACCUMULATION OF LACTIC ACID AND OTHER, METABOLITES CONTRIBUTE TO THE RARE OCCURRENCE OF THIS PHENOMENON. THE TRUE INCIDENCE OF MUSCULAR METASTASIS REMAINS UNKNOWN, BUT AN AUTOPSY SERIES SUGGESTS THAT ITS INCIDENCE COULD BE AS LOW AS 0.8%. LUNG CARCINOMA SEEMS TO SE THE UNDERLYING PRIMARY CANCER IN MOST OF THESE CASES. MANY OTHER TUMORS, SUCH AS KIDNEY, STOMACH, PANCREAS, THYROID GLAND, BREAST, OVARY, PROSTATE, AND BLADDER CANCERS HAVE BEEN SPORADICALLY DESCRIBED IN ASSOCIATION WITH INTRAMUSCULAR SECONDARIES. HOWEVER, PRIMARY PRESENTATION OF AN INTRAMUSCULAR METASTASIS, SUCH AS DEMONSTRATED BY OUR PATIENT, REMAINS AN EXCEPTIONALLY UNUSUAL OCCURRENCE. THE MOST FREQUENT PRESENTATION OF MUSCULAR METASTASIS IS PAIN WITH OR WITHOUT SWELLING. DIAGNOSIS OF THIS CONDITION, EVEN WITH RADIOLOGIC IMAGING IS OFTEN TRICKY BECAUSE IT CAN BE CONFUSED WITH AN ABSCESS OR SOFT TISSUE TUMORS, HIGHLIGHTING ‘THE VALUE OF HISTOLOGIC DIAGNOSIS. TREATMENT IN THE FORM OF RADIOTHERAPY, CHEMOTHERAPY, (OR EVEN METASTASECTOMY OFTEN PROVIDES PALLIATION ONLY. MOST PATIENTS DIE IN LESS THAN A. YEAR FROM DIAGNOSIS.(BASED ON THE CLINICAL ANDTHE DIVERSE IMAGING STUDI"S FINDINGS WHICH OF THE FOLLOWING WAS THE FRESUMTIVE DIAGNOSIS OF THE ATTENDING MEDICAL TEAM: A DES? OVOID MASS LOCATED IN THELETT TRICEPS MUSCLE CONSIDERED A PROBABLE e[E] amass oF cat SATURATION OSSERVED.ONMAL ON TLWEIGHTED IMAGES. 4 PRESUMSTIVE OIAGNOSIS OF SOFTTISEUE SARCOMA LOCATED IN THELEFT TRICEPS MUECLE, ©] A CUAGNDEIE OF METASTATIC EQUAMOUS CELL CARCINOMA, VWITH A POSSISLE PRIMARY OF THELUNG. ‘THE PATIENT WAS SUBMITTED TO PALLIATIVE CARE ANO NOT SYSTEMIC THELAPY BASED ON WHAT AERSON? 8(F] 4 s0srmve cer ana NEGATIVE C20 STAIN ON IMMUNDMIETOCMEMISTRY IS OF POOR PROGNOSIS. THE DIAGNOSIS OF STAGEIV SQUAMOUS CELL LUNG CARCINOMA WAS NOT CONFIRMED ON FISER-OFTIC c[E] Honey UNceaWenr PALLIATIVE RADIOTHERAPY BECAUSE OF COST-EEMERIT REASONS, BASED ON A POOR ANG OETERIOAMTING PERFORMANCE STATUS SYSTEMIC THERAPY WAS OEFERRED FOR (QUALITY OF LIFE PALLIATIVE THERAPY. THE MUBCULAR MASS ACCOUNTS FDR APPROXIMATELY 50% OF TOTAL SODW WEIGHT. MUSCULAR CONTRACTILE ACTIONS. LOCAL PH ENVIRONMENT. ACCUMULATION OF LACTIC ACID AND OTHER METABOLITES. ‘WIGS 18 THE PRIMARY UNDERLYING CANCER IN MOST CASES OF INTRAMUSCULAR METASTASES? LUNG CARCINOMA, KIDNEY AND BLADDER CANCER. ‘STOMACH AND PANCREATIC CARCINOMA. on o> API BREAST AND OVARIAN CANCER, PRESENTATION OF THE AFFECTED SITE WITH PRIM, WITH OR WITHOUT SWELLING. FEVER AND SEFEIS. a 82] tRomsosis oF ts anrecten ScReMTTy. ie USUALLY INOOLEVT ANO ONLY FOUND AT AUTOREY.MIGRAINE IS CONSIDERED TO BE AN EPISODIC CONDITION WITH NO LONG-TERM CONSEQUENCES. HOWEVER, RECENT STUDIES SUGGEST THAT MIGRAINE ATTACKS MAY BE ASSOCIATED WITH PATHOLOGIC CHANGES IN THE BRAIN, PARTICULARLY IN THE CEREBELLUM. THE OBJECTIVE OF THE PRESENT STUDY WAS TO DETERMINE WHETHER INDIVIDUALS NOT REPORTING HEADACHE COMPARED. WITH INDIVIDUALS REPORTING MIGRAINE SYMPTOMS, PARTICULARLY AURA, IN MIDLIFE ARE AT INCREASED RISK OF LATE-LIFE INFARCT-LIKE LESIONS FOUND ON MAGNETIC RESONANCE IMAGING (MRI) WITHOUT CONSIDERATION OF CLINICAL SYMPTOMS. A POPULATION-BASED STUDY OF MEN AND WOMEN IN REYKJAVIK, ICELAND (COHORT BORN 1907-1935; N= 4689; 57% WOMEN) WERE FOLLOWED UP SINCE 1967, EXAMINED, AND INTERVIEWED ABOUT MIGRAINE SYMPTOMS IN MIDLIFE (MEAN AGE, S1 YEARS: RANGE, 33-65 YEARS). BETWEEN 2002 AND 2006, MORE THAN 26 YEARS LATER, BRAIN MRIS WERE PERFORMED. PARTICIPANTS REPORTING HEADACHES ONCE OR MORE PER MONTH WERE ASKED ABOUT MIGRAINE SYMPTOMS INCLUDING NAUSEA, UNILATERAL LOCATION, PHOTOPHOBIA, VISUAL DISTURBANCE, AND NUMBNESS. THESE INDIVIDUALS WITH HEADACHE WERE CLASSIFIED AS HAVING MIGRAINE WITHOUT AURA, MIGRAINE WITH AURA, OR NONMIGRAINE HEADACHE. A COMPREHENSIVE CARDIOVASCULAR RISK ASSESSMENT WAS PERFORMED AT SOTH EXAMINATIONS. THE PRESENCE OF INFARCT-LIKE LESIONS (TOTAL) AND SPECIFICALLY LOCATED IN THE CORTICAL, SUBCORTICAL, AND CEREBELLAR REGIONS WERE THE MAIN OUTCOME MEASURE. INFARCT-LIKE LESIONS WERE PRESENT IN 39.3% OF MEN AND 24.6% OF WOMEN. AFTER ADIUSTING FOR AGE, SEX, AND FOLLOW-UP TIME, COMPARED WITH THOSE NOT REPORTING HEADACHES ONCE OR MORE PER MONTH (N= 3243), THOSE WITH MIDLIFE MIGRAINE WITH AURA (N= 361) HAD AN INCREASED RISK OF LATE-LIFE INFARCT-LIKE LESIONS (ADJUSTED ODDS RATIO [OR], 1.4; 95% CONFIDENCE INTERVAL [CI], 1.1-1.8) THAT SPECIFICALLY REFLECTED AN ASSOCIATION WITH CEREBELLAR LESIONS IN WOMEN (PREVALENCE OF INFARCTS 23.0% FOR WOMEN WITH MIGRAINE WITH AURA VS 14.5% FOR WOMEN NOT REPORTING HEADACHES; ADJUSTED OR, 1.9; 95% Cl, 1.4-2.6 VS A 19.3% PREVALENCE OF INFARCTS FOR MEN WITH MIGRAINE WITH AURA VS 21.3% FOR MEN NOT REPORTING HEADACHES; ADJUSTED OR, 1.0; 95% Cl, 0.6 ~1.8; P<.04 FOR INTERACTION BY SEX). MIGRAINE WITHOUT AURA AND NONMIGRAINE HEADACHE WERE NOT ASSOCIATED WITH AN INCREASED RISK. MIGRAINE WITH AURA IN MIDLIFE WAS ASSOCIATED WITH LATE- LIFE PREVALENCE OF CEREBELLAR INFARCT-LIKE LESIONS ON MRI. THIS ASSOCIATION WAS STATISTICALLY SIGNIFICANT ONLY FOR WOMEN.AECEVT STUDIES SUGGEST THAT MIGRAINE ATTACKS MAY SE ASSOCIATED WITH PATHOLOGIC CHANGES IN THERATY, WHICH LOCALIZATION IN PARTICULAR 15 CONSIDERED? THE CEREBELLUM. THE WHITE MATER. THE RYPOCAMPUS. One» THEFRONTAL LOBE. WITH MIDLIFE MIGRAINE WITH AURA HAD AY ODOS RATIO“ OF I~ OF LATEUFE INFARCT-UME LESIONS, THIS WAS MORE SPECIFICALLY OBSERVED IN WMICM GROUST (CEREBELLAR LESIONS IN WOMEN. (CEREBELLAR LESIONS IN MEN. CORTICAL LESIONS IN WOMEN, Ono 4) SUBCORTICAL LESIONS IN MEN, TRE MAIN OUTCOME MEASURES OF THE STUDY WERE THE PRESENCE OF INFARCT-IME LESIONS [SPECIFICALLY LOCATED IN WHICH REGIONS? (CORTICAL, CEIESELLAA AND MEDULLA CELONGATA REGIONS. CORTICAL, SUBCORTICAL, ANO CERESELLUR REGIONS. (CEREBELLAR, SUBCORTICAL AND WHITE MATTER REGIONS. ono 4] PERIVENTRICULAR, MYROCAMAUE AND OCCIPITAL REGIONS. \WEDCH OF THE FOLLOWING TYPES OF BEADACHES WERE NOT ASSOCIATED WITH AN INCREASED RISK OF INFARCT-LIME LESIONS AT FOLLOW -UET POST-TRAUMATIC READACHE HEADACHE AND MIGRAINE WITH AURA, MIGRAINE WITHOUT AURA AND NON-MIGRAINE MERDACHE, Ones SINUSITIS AND MIGRAINEHOMBRE DE 20 ANOS, ES ATENDIDO EN EL SERVICIO DE CONSULTA EXTERNA, POR PRESENTAR DIFICULTAD RESPIRATORIA POSTERIOR A ESFUERZO FISICO. ANTECEDENTES: RINITIS ALERGICA DURANTE LA INFANCIA. EXPLORACION FISICA: SE AUSCULTAN SIBILANCIAS RESPIRATORIAS. LA REACCION DE HIPERSENSIBILIDAD PRESENTE EN ESTE PACIENTE ES LA TIPO: ql Al Bl a B 0 c m D> wt LA INMUNOGLOBULINA QUE PARTICIPA EN ESTE PADECIMIENTO ES: coe FAIBIE zoom» HOMBRE DE 9 ANOS, ES ATENDIDO EN CONSULTA POR TOS, DISNEA AL HACER EJERCICIO, CONSTIPACION Y PRURITO NASAL SIN PREDOMINIO DE HORARIO DE TRES ANOS DE EVOLUCION. ANTECEDENTES: HA SIDO HOSPITALIZADO EN DOS OCASIONES REQUIRIENDO USO DE NEBULIZADOR, NO TIENE ANTECEDENTES FAMILIARES SIMILARES. EXPLORACION FISICA: MUCOSA NASAL HIPEREMICA CON HIPERTROFIA DE CORNETES, AMIGDALITIS HIPERTROFICA CON IMPORTANTE DIFICULTAD PARA HABLAR. NO SE ESCUCHAN SIBILANCIAS EN TORAX. PARA CORROBORAR EL DIAGNOSTICO SE DEBE SOLICITAR: CULTIVO DE EXUDADO FARINGEO. DETERMINACION DE EOSINGFILOS EN MOCO NASAL. BIOMETRIA HEMATICA COMPLETA. BIA A B c D PRUEBAS CUTANEAS CON ALERGENOS. LO MAS PROBABLE ES QUE LA CAUSA DE ESTE PADECIMIENTO ES: ACAROS Y CASPA DE LOS ANIMALES. ESTREPTOCOCO B HEMOLITICO. INFECCIONES VIRALES. HONGOS. soe> qb) FlOF essesHOMBRE DE 68 AiOS. ATENDIDO EN CONSULTA POR PRESENTAR UN CUADRO DE DISNEA DE MODERADOS ESFUERZOS, SINCOPE DE ESFUERZO EN TRES OCASIONES DURANTE LOS ULTIMOS 2 MESES, DOLOR PRECORDIAL LEVE OCASIONAL ACOMPAMADO DE MAREOS. ANTECEDENTES DE ESTREfIIMIENTO QUE SE MANEJA CON SENOSIDOS. EXPLORACION FISICA: PULSOS DEBILES, RECULARES CON UNA FC DE 64 LPM, TA 110/70 MMHG. LA AUSCULTACION MUESTRA UN SOPLO SISTOLICO CON FOCO MAS ACENTUADO EN EL SEGUNDO ESPACIO INTERCOSTAL DEL LADO DERECHO, IRRADIADO AL CUELLO. LA TELE DE TORAX MUESTRA UNA CARDIOMEGALIA I1/IV. CONSIDERANDO EL DIAGNOSTICO MAS. PROBABLE EN ESTE PACIENTE EL ELECTROCARDIOGRAMA DEBE MOSTRAR: ALE] crccumenro 0¢ cavioaves DERECHAS. [F] ALTERACTONES COMPATIELES CON HIPERTROFIA VENTRICULAR 12QUIEROA. [FP] FIBRILactén AURICULAR. IE] sLoqueo av avanzaco. EL SIGUIENTE PASO PARA CONFIRMAR EL DIAGNOSTICO ES: [F] prueea ve esruenzo. ©] PRUEBA DE INCLINACION. ECOCARDIOGRAMA. soap e] caTeTERISMO CARDIACO. LA ETIOLOGIA MAS PROBABLE EN ESTE PACIENTE ES DE ORIGEN: Aa[E] Fanmacotésico. B METABOLICO. cl] avrommune, |r] vesenerarivo.MUJER DE 90 AflOS ES ATENDIDA EN CONSULTA PORQUE TUVO UN DESMAYO HACE 8 DIAS. ANTECEDENTE: 15 GESTAS. EXPLORACION FISICA: TA 150/60 MM HG, FC 40 LPM, PULSOS AMPLIOS E IRREGULARES. APEX EN EL QUINTO ESPACIO INTERCOSTAL EN LA LINEA MEDIOCLAVICULAR. RUIDOS CARDIACOS ARRITMICOS, ‘SOPLO SISTOLICO EXPULSIVO AORTICO II/VI. CAMPOS PULMONARES LIMPIOS. VARICES EN MIEMBROS INFERIORES. ELECTROCARDIOGRAMA: AUSENCIA DE ONDA P CON COMPLEIOS QRS IRREGULARES, FRECUENCIA VENTRICULAR MEDIA DE 40 LEM. EN ESTA PACIENTE EL DIAGNOSTICO ETIOLOGICO MAS PROBABLE ES: A[P] ESCLEROSIS AGRTICA. B FIBRILACION AURICULAR LENTA. [FJ INSUFICIENCIA VENOSA. |e] sincore. AL PACIENTE SE LE SOLICITA UN MONITOREO ELECTROCARDIOGRAFICO DE 24 HORAS (HOLTER), EL CUAL REPORTA PREDOMINANCIA DE RITMOS LENTOS < 40 POR MINUTO Y EL TRATAMIENTO DE PRIMERA ELECCION PARA ESTA PACIENTE ES: ©] ADMINISTRA ANTITROMBOTICOS. ADMINISTRAR BLOQUEADORES ALFA-1. (©) ADMINISTRAR CALCTOANTAGONISTAS ooe> COLOCAR MARCAPASO DEFINITIVO.MUJER DE 18 ANOS, ATENDIDA EN CONSULTA POR CANSANCTO AL JUGAR VOLEY BALL EN SU COLEGIO. ANTECEDENTES: BRONQUITIS DE REPETICION EN EDAD ESCOLAR. PRODUCTO DE SEGUNDA GESTA, PARTO EUTOCICO A TERMINO, APGAR 9. E.F.: EUPNEICA, AFEBRIL, TA 138/74, FC 80 LPM, FR 1SRPM. R.C.R. CON SOPLO CONTINUO PARAESTERNAL SUBCLAVICULAR IZQUIERDO. CAMPOS PULMONARES VENTILADOS, PULSOS ARTERIALES CON AMPLITUD AUMENTADA. EN EL ELECTROCARDIOGRAMA Y LA RX DE TORAX DE ESTA PACIENTE ES MUY PROBABLE QUE SE ENCUENTREN DATOS DE: SOBRECARGA DE CAVIDADES IZQUIERDAS. SOBRECARGA DE AURICULA DERECHA, SOBRECARGA DE VENTRICULO DERECHO. com> 31 Al SOBRECARGA DE LAS CUATRO CAVIDADES. EL TRATAMIENTO DE ELECCION EN ESTA PACIENTE ES: INTERVENCIONISMO CARDIOLOGICO. CIRUGIA CARDIACA URGENTE. MANEJO MEDICO INICIAL. Cd AAA CIRUGIA CARDIACA ELECTIVA.HOMBRE DE 53 ANOS PREVIAMENTE SANO, PRESENTA FIEBRE NO CUANTIFICADA DE TRES SEMANAS DE EVOLUCION ACOMPAIANDOSE DE ESCALOFRIOS Y DIAFORESIS PROFUSA; REFIERE ADEMAS PERDIDA DE PESO DE 5 KG. NIALGIAS Y ARTRALGIAS. E.F.: MICROHEMORRAGIAS EN DEDOS Y PLANTAS DE AMBOS PIES. LA AUSCULTACION DEL TORAX MUESTRA UN SOPLO CORRESPONDIENTE A INSUFICIENCIA MITRAL IIV/VI. EL LABORATORIO REPORTA UNA HB DE 8.3 G/DL, LEUCOCITOS 12 500, VSG 60 MM/H (NORMAL HASTA 20) CREATININA 0.8 G/DL. EL AGENTE CAUSAL MAS PROBABLE EN ESTE CASO ES: [©] STREPTOCOCCUS VIRIDANS. B[C] STREPTOCOCCUS PNEUMONIAE. [©] CARDIOBACTERIUM HOMINIS. D[F] STAPHYLOCOCCUS COAGULASA NEGATIVO. EL TRATAMIENTO INICIAL PARA ESTE PACIENTE DEBE INCLUIR: [©] VANCOMICINA Y GENTAMICINA. [C] PENICILINA Y GENTAMICINA. [©] AMPICILINA Y SULBACTAM. [©] cuarrtromicina, PREGUNTAG9 EN EL CULTIVO DE SANGRE, CRECIO STREPTOCOCCUS BOVIS, EL ORIGEN MAS PROBABLE DE LA BACTERIA GASTROINTESTINAL. opontoLdeico. PIEL Y TEDOS BLANDOS. URINARIO.HOMBRE DE 33 ANOS, ADICTO A DROGAS INTRAVENOSAS, ES ATENDIDO EN CONSULTA POR CONVULSIONES GENERALIZADAS Y ESTADO CONFUSIONAL ACOMPANADO DE FIEBRE DE 4 SEMANAS DE EVOLUCIGN Y PERDIDA DE PESO NO CUANTIFICADA. A LA EXPLORACION FISICA: TA DE 90/60 MM HG, FC 110 LPM, TEMPERATURA 38 °C, FR 22 RESPIRACIONES POR MINUTO. EXAMENES DE LABORATORIO: HB DE 9.8 G/DL, LEUCOCITOS DE 16 300/MM3, PLAQUETAS 94,000/MM3. LA TELE DE TORAX MUESTRA INFILTRADOS EN PARCHE. SE ENVIAN HEMOCULTIVOS SERIADOS (3) QUE A LAS 24 HORAS SE REPORTAN POSITIVOS PARA CRECIMIENTO BACTERIANO POR LO QUE SE REALIZA UNA TINCION DE GRAM. EL HALLAZGO MAS PROBABLE EN LA TINCION DE LA MUESTRA ES: A[E] Cocos GRAM NEGATIVOS, B[F] Cocos GRAM FOSITIVOS. c[E] BACILOS GRAM NEGATIVOS. p [F] actos Gram Positivos. PREGUNTA7S EN ESTA PACIENTE, LA VALVULA MAS PROBABLEMENTE DANADA A(e] mrrrat. B[E] Adrtica. c[F) TRICUsPIDE. p[E] Puumonar. LA DURACION DEL TRATAMIENTO EN SEMANAS PARA ESTE PACIENTE ES: 4, coe AAG) 10.MUJER DE 72 ANOS ES ATENDIDA EN CONSULTA POR CUADRO DE DISNEA DE MODERADOS: ESFUERZOS, SINCOPE DE ESFUERZO EN TRES OCASIONES DURANTE LOS ULTIMOS 2 MESES. REFIERE DOLOR PRECORDIAL LEVE OCASIONAL, ACOMPANADO DE MAREOS. E.F.: PULSOS DEBILES, REGULARES CON FC DE 64 LPM, TA 100/70 MM HG. AUSCULTACION CON SOPLO SISTOLICO CON FOCO MAS ACENTUADO EN EL SEGUNDO ESPACIO INTERCOSTAL DEL LADO DERECHO IRRADIADO AL CUELLO. LA TELE DE TORAX MUESTRA UNA CARDIOMEGALIA II/IV. EL HALLAZGO MAS PROBABLE EN EL ECOCARDIOGRAMA DE ESTE PACIENTE ES: DILATACION DE LAS CAVIDADES IZQUIERDAS. INSUFICIENCIA PULMONAR SEVERA. Fi Fi [=] GRADIENTE TRANSVALVULAR PULMONAR INCREMENTADO. [7] HIPERTROFIA CONCENTRICA DEL VENTRICULO IZQUIERDO. coe LA VALVULA CARDIACA MAS PROBABLEMENTE AFECTADA ES: MITRAL. AORTICA. PULMONAR, coer AGI EIA TRICUSPIDEA. EL TRATAMIENTO DEFINITIVO DE ESTE PACIENTE ES: NITRATOS. DIURETICOS. \VALVULOPLASTIA. coap AAA REEMPLAZO QUIRURGICO CON PROTESIS.HOMBRE DE 56 ANOS, ES ATENDIDO EN LA CONSULTA POR PRESENTAR EN ANTEBRAZOS Y MANOS PRURITO, ERITEMA Y ESFACELACION CON EXACERBACION DESDE HACE TRES MESES. AGREGANDOSE EDEMA FACIAL, MACULAS EN CUELLO Y PARTE ALTA DE TORAX. ANTECEDENTE DE TRABAJAR EN FABRICA DE CEMENTOS DESDE HACE 20 ANOS. EXPLORACION FISICA: PLACA ERITEMATOSA CON HIPERQUERATOSIS EN MIEMBRO PELVICO DERECHO CON EDEMA Y HUELLAS DE RASCADO. EL DIAGNOSTICO MAS PROBABLE ES: DERMATITIS ATOPICA. DERMATITIS POR CONTACTO. PSORIASIS. soap API AID URTICARIA. PARA INTEGRAR EL DIAGNOSTICO LO MAS RECOMENDABLE ES REALIZAI ESTUDIO EPIDEMIOLOGICO. ESTUDIO DE CONTACTOS. ESTUDIO DE AGENTES CONTAMINANTES. soa > APIA ESTUDIO DE FACTORES DE RIESGO EN LA EMPRESA Y AMBIENTALES. NINO DE 8 ANOS ES ATENDIDO EN CONSULTA EXTERNA POR PRESENTAR ERUPCION EN CUELLO Y PLIEGUES ANTECUBITAL Y POPLITEO, ACOMPANADA DE PRURITO. ANTECEDENTE: FAMILIARES CON ASMA. EL HALLAZGO DE LABORATORIO QUE APOYA EL DIAGNOSTICO ES: BASOFILIA. LINFOCTTOSIS. EOSINOFILIA. NEUTROPENIA. ABIES ooo > TRATAMIENTO LOCAL DE PRIMERA ELECCION PARA ESTE PACIENTE ES: Fe TAZAROTENO. HIDROCORTISONA. PREDNISONA. coe IB AIG CLOTRIMAZOL.ADOLESCENTE DE 17 ANl0S CON LESIONES DERMATOLGGICAS EN CARA Y TRONCO. LAS LESIONES COINCIDEN CON EL CAMBIO DE CIUDAD ¥ DE DIETA POR MOTIVOS DE ESTUDIO. ADEMAS DEJAN CICATRIZ QUE PREOCUPA MUCHO AL PACIENTE. E.F.: COMEDONES EN DIFERENTES ESTADIOS DE EVOLUCION EN ESTE PACIENTE EL DIAGNOSTICO MAS PROBABLE ES: FOLICULITIS. ROSACEA. ACNE VULGAR. pvao> 3] 2] FB) MILIARIA. ENTRE LAS MEDIDAS PREVENTIVAS PARA ESTE PACIENTE SE RECOMIENDA: ANTIBIGTICO V.0. DE MANERA PERMANENTE. UTILIZAR JABON NEUTRO Y EMOLIENTES. EJERCICIO, DIETA BAIA EN GRASAS, JABGN NEUTRO. EVITAR EXPONERSE AL SOL. I = Fy = soap MUJER DE 48 AfJOS, ATENDIDA EN CONSULTA POR CEFALEA FRONTAL DE PREDOMINIO MATUTINO. ANTECEDENTES GINECOOBSTETRICOS: CICLOS MENSTRUALES IRREGULARES. E.F: ESTATURA 1.54 M, PESO 82 KG, TA 140/100, GLUCEMIA EN AYUNAS DE 125 MG/DL, TRIGLICERIDOS 240 MG/DL, HDL 37, COLESTEROL TOTAL 320 MG/DL. EL DIAGNOSTICO DE ESTA PACIENTE ES: OBESIDAD MORBIDA. SINDROME METABOLICO. HIPERTENSION ARTERIAL ESENCIAL. | SINDROME PREMENOPAUSICO. com> a LAS ALTERACIONES FISIOPATOLOGICAS EN ESTA PACIENTE SON: HIPERCOAGULABILIDAD E HIPERLIPIDEMIA. HIPERTENSION ARTERIAL ¥ DIABETES MELLITUS. RESISTENCIA A LA INSULINA E HIPERINSULINEMIA, com> AIAG DISLIPIDEMIA E HIPERTENSION ARTERIAL.FEMENINO DE 56 AfJOS, ACUDE A CONSULTA POR PRESENTAR DESDE 2 SEMANAS PREVIAS HIPOSTENIA, HIPODINAMIA, PERDIDA DE PESO, POILIFAGIA, POLIURIA. ANTECEDENTES: PADRE DIABETICO. EXPLORACION FISICA: OBESIDAD ABDOMINAL, PESO: 100 KG., TALLA 1.68 M. EXAMENES DE LABORATORIO: GLUCOSA DE 120 MG/DL, COLESTEROL 200 MG/DL, TRIGLICERIDOS DE 360 MG/DL, COLESTEROL-HDL 30. EL MECANISMO FISIOPATOLOGICO DESENCADENANTE ES: AUMENTO DE INTERLEUCINA-6. DISMINUCION DE SELECTINA. AUMENTO DE LA ADIPONECTINA. DISMINUCION DE LEPTINA. 7S zao> EL PASO INICIAL EN EL TRATAMIENTO DE ESTE PACIENTE ES: APLICACION DE INSULINA. ADMINISTRAR SECRETAGOGOS. DIETA Y EJERCICIO. caog> AGIA HIPOLIPEMIANTES.MUJER DE 25 ANOS CON ANTECEDENTE DE DIABETES TIPO 1, CURSA EL PRIMER TRIMESTRE DEL ENBARAZO. HA LLEVADO DE MANERA IRREGULAR SU CONTROL GLUCEMICO. SE PRESENTA ASINTOMATICA A LA CONSULTA DE CONTROL PRENATAL CON UROCULTIVO POSITIVO CON 100,000 UFC/ML PARA E. COLI, SIN PIURIA SIGNIFICATIVA. LA PACIENTE MUESTRA PREOCUPACION Y PREGUNTA. (UAL ES EL RIESGO QUE LA DIABETES Y EL TRATAMIENTO GENEREN A SU PRODUCTO. PARA ESTA PACIENTE, LA ASEVERACION MAS ADECUADA, ES 1 [E] ELLA Y SU PRODUCTO TIENEN MENOR RIESGO QUE LAS DIABETICAS GESTACIONALES. =] NO EXISTE MAYOR RIESGO EN TANTO SE MANTENGA LA GLICEMIA EN AYUNO POR DEBAJO DE 120 MG/DL. LA INSULINA NO ATRAVIESA LA BARRERA PLACENTARIA, POR LO QUE EL EMBARAZO SERA DE CURSO NORMAL. DE NO MANTENERSE CONTROL GLUCEMICO EL RIESGO DE MALFORMACIONES INCREMENTA HASTA DIEZ VECES. B PARA ESTA PACIENTE LA INTERPRETACION MAS ADECUADA DEL RESULTADO DEL UROCULTIVO ES: DEBE ATENDERSE AL RESULTADO Y PROPORCIONAR TRATAMIENTO ANTIBIOTICO. SOLO RECIBIRA TRATAMIENTO ANTIBIOTICO SI PRESENTARA SINTOMATOLOGIA. EL RESULTADO DE LABORATORIO ES PRODUCTO DE CONTANINACION DE LA MUESTRA. REQUIERE UN SEGUNDO CULTIVO CON TOMA DE MUESTRA. voce q] BIG) GlHOMBRE DE 56 ANOS, ATENDIDO EN CONSULTA POR AUMENTO DE VOLUMEN, DOLOR, CALOR LOCAL E HIPEREMIA DE RODILLA DERECHA DE 2 DIAS DE EVOLUCION. NIEGA TRAUMATISMO, REFIERE HISTORIA DE EPISODIOS DOLOROSOS SEMEJANTES, HACE UN ANO EN PRIMERA METATARSOFALANGICA DERECHA Y OTRO HACE 6 MESES EN TOBILLO IZQUIERDO. EXPLORACION FISICA: NODULOS SUBCUTANEOS: IRREGULARES EN CODOS Y SE CONFIRMA FLOGOSIS DE RODILLA DERECHA, EL DIAGNOSTICO DEFINITIVO ES MEDIANTE: RECOLECCION DE ORINA DE 24 HORAS. PERFIL BIOQUIMICO. ARTROCENTESIS Y BUSQUEDA DE CRISTALES. BIOPSIA DE NODULO. 5 = = Fy csoo> EL MECANISMO DE PRODUCCION MAS PROBABLE QUE LE OCURRE ES: HIPERSECRECION. HIPOEXCRECION. MEDICAMENTOS. soap 7] |B] BI INGESTA EXCESIVA DE CALCIO. MUJER DE 26 ANOS, ES ATENDIDA EN CONSULTA EXTERNA POR PRESENTAR DESDE HACE VARIAS. SEMANAS TEMBLOR FINO DISTAL, SENSACION DE ANGUSTIA, SUDORACION PALMAR, HA PERDIDO PESO EN LOS ULTIMOS MESES. SIN ANTECEDENTES DE IMPORTANCIA. EXPLORACION FISICA: TA 130/86 MM HG, PESO S4 KG., TALLA 160 CM., EXOFTALMOS, SUDORACION PALMAR, PIEL HUMEDA Y CALIENTE, FC 110 LPM, ABDOMEN CON RUIDOS PERISTALTICOS INCREMENTADOS. EN ESTE PACIENTE VA A ENCONTRAR UNA DISMINUCION DE: TSH. T4 LIBRE. T4 TOTAL, TBR. caa> IA Bl EL TRATAMIENTO DE PRIMERA ELECCION PARA ESTA PACIENTE ES: ©] Yop 131. =| yoouro. S = METIMAZOLE. caa> TIROIDECTOMIA.MUJER DE 45 ANOS, ACUDE A CONSULTA EXTERNA, POR PRESENTAR DESDE HACE 4-5 SEMANAS FATIGA FACIL, CONSTIPACION INTESTINAL E INTOLERANCIA AL FRIO, HA TENIDO INCREMENTO DE PESO DE APROXIMADAMENTE 6 KG. EN 3 MESES. EXPLORACION FISICA: TA DE 116/86 MM HG, PESO 74 KG., TALLA 162 CM., FC 56 LPM, PIEL SECA, RUIDOS CARDIACOS RITMICOS, ABDOMEN BLANDO, NO DOLOROSO, EDEMA MODERADO DE PIERNAS. EN ESTE PACIENTE SE VA ENCONTRAR UN AUMENTO DE: TSH. aL. T4 TOTAL. TR. com> BAB EL TRATAMIENTO DE PRIMERA ELECCION PARA ESTE PACIENTE ES: TRIVODOTIRONINA. LEVOTIROXINA. YODURO. come AIPIPIP METIMAZOLE.MUJER DE 77 ANOS, INGRESA A URGENCIAS POR DESHIDRATACION SEVERA, ASTENIA ADINAMIA, CON POLIURIA Y POLIDIPSIA, DOLOR DE MIEMEROS INFERIORES E HIPERTERMIA NO CUANTIFICADA. ANTECEDENTES: DIABETES MELLITUS, MAL CONTROLADA Y ABANDONO FAMILIAR. £.F.: PRESION ARTERIAL 150/105 , TEMP DE 38°C, MUCOSAS ORALES DESHIDRATADAS, TONO OCULAR DISMINUIDO, GIORDANO POSITIVO. LABORATORIO: GLUCOSA DE 540 MG/DL, UREA 80 MG/DL, CREATININA 3.2 MG/DL, SODIO 125 MEQ, POTASIO 6.7 MEQ. LEUCOCITOS 15 MIL MM3. EL TRATAMIENTO INMEDIATO PARA ESTE PACIENTE ES: INSULINA. HIDRATACION. Fi Fi 7) ANTIBIOTICOTERAPIA. Fi po o> DIALISIS. LA CAUSA MAS PROBABLE DE LA SINTOMATOLOGIA DEL PACIENTE ES: COMPLICACIONES TARDIAS DE LA DIABETES. PROCESO INFECCIOSO URINARIO. SUSPENSION DE TRATAMIENTO MEDICO. TRANSGRESION DIETETICA. soap ARIAJOMBRE DE 16 ANOS, LLEVADO POR SUS FAMILIARES Y ATENDIDO EN EL SERVICIO DE URGENCIAS, POR DETERIORO PROGRESIVO DEL ESTADO DEL ALERTA, DIFICULTAD PARA RESPIRAR, NAUSEA Y VOMITO; 2.Fl.: SOPOROSO, MUCOSAS ORALES SECAS, TAQUICARDICO CON TAQUIPNEA. LABORATORIC -EUCOCITOS 13,800/MM3, GLUCOSA 420 MG/DL, SODIO 118 MEQ/L, POTASIO 3.0 MEQ/L, UREA 80 AG/DL, CL 110 MEQ/L, PH 7.10, PCO2 18 MM HG, HCO3 10 MG/DL, DEFICIT DE BASE -18. EN ESTE PACIENTE SE VA ENCONTRAR UN AUMENTO DE: GLUCONEOGENESIS. GLUCOGENOLISIS. CAPTACION DE GLUCOSA POR MUSCLLO. vsam> CAPTACION DE GLUCOSA POR LA CELULA, LA ALTERACION METABOLICA EN ESTE PACIENTE ES: ©) actDosis LAcTICA. ACIDOSIS METABOLICA, ©) ACIDOSIS HIPERCLOREMICA. vsaa> ALCALOSIS RESPIRATORIA.HOMBRE DE 40 AflOS ATENDIDO EN CONSULTA POR PRESENTAR CANSANCIO Y PARESTESIAS EN MIEMBROS INFERIORES, A LO QUE SE AGREGA PERDIDA DE PESO NO CUANTIFICADA DESDE HACE APROX. 2 MESES. ANTECEDENTES: PADRE DIABETICO FALLECIG DE INFARTO DE MIOCARDIO; ES SEDENTARIO Y ACOSTUMBRA COMER ALIMENTOS RICOS EN GRASAS Y CARBOHIDRATOS. E.F-: TA 160/100 , FC 100 LPM, FR 26 POR MIN, TEMP 36.8 ©C, PESO 107 KG., TALLA 1.71 M., REGULAR ESTADO GENERAL, CARDIOPULMONAR Y ABDOMEN SIN DATOS. EXAMENES DE LABORATORIO: GLICEMIA 400 MG/DL, COLESTEROL TOTAL 260 MG/DL, TRIGLICERIDOS 358 MG/DL; GENERAL DE ORINA CETONURIA +, GLUCOSURIA +++. EL TRATAMIENTO INMEDIATO PARA ESTE PACIENTE ES LA ADMINISTRACION DE: (©) ansuuina, =) suuroniwureas. [| BIGUANIDAS. [= Tazounoineoronas. com> EL ESTUDIO DE LABORATORIO IDEAL PARA MONITOREAR A LARGO PLAZO EL TRATAMIENTO DE ESTE PACIENTE ES: [F) PRUEBA DE TOLERANCIA A LA GLUCOSA. [7 Gucema cantar, A 8 [© GLICEMIA EN avUNAS. « D[®) HEMOGLOBINA GLICOSILADA.MUJER DE 18 ANOS, ES ATENDIDA EN CONSULTA POR PRESENTAR PALPITACIONES Y EVACUACIONES DIARREICAS EN PERIODOS FRECUENTES. ANTECEDENTES: BOCIO EN RAMA MATERNA. E.F.: TA 160/90 , FC 120 LPM. PACIENTE IRRITABLE, ANSIOSA, CON SUDORACION EXCESIVA. APEX ENERGICO. RUIDOS: CARDIACOS INTENSOS. PERISTALSIS AUMENTADA, PULSOS ARTERIALES PERIFERICOS INTENSOS. EN ESTA PACIENTE SE VA A ENCONTRAR AUMENTO DE: HORMONA LIBERADORA DE TIROTROPINA. HORMONA ESTIMULANTE DE LA TIROIDES. ‘TRIYODOTIRONINA Y TIROXINA, cog> Fy Fi Fi Fi ANTICUERPOS ANTITIROIDEOS. ESTA PACIENTE DEBE SER TRATADA CON UN MEDICAMENTO QUE ACTUE A NIVEL DE: INHIBICION DE PEROXIDASA TIROIDEA. LIBERACION DE TSH. LIBERACION DE TIROTROPINA. ANTICUERPOS ANTITIROIDEOS. oom > a) lBHOMBRE DE 83 ANOS, ATENDIDO EN CONSULTA EXTERNA, PRESENTA DESDE HACE UNA SEMANA. ANOREXIA, NAUSEA, DISTENSION ABDOMINAL LEVE, DOLOR EPIGASTRICO DE MODERADA INTENSIDAD QUE DISMINUYE CON INGESTA DE ALIMENTOS, POSTERIORMENTE EVACUACIONES OBSCURAS Y VOMITO EN POZOS DE CAFE, HA PERDIDO APROXIMADAMENTE 6 KG. EN 2 MESES. ANTECEDENTES: TABAQUISMO IMPORTANTE, ABUSO FRECUENTE DE ALCOHOL. EXPLORACION FISICA: PALIDO, TA 130/86 MM HG, PESO 69 KG., TALLA 174 CM., ABDOMEN BLANDO, POCO DOLOROSO EN EPIGASTRIO, SIN DATOS DE IRRITACION PERITONEAL. EXAMENES DE LABORATORIO: HEMOGLOBINA DE 10.9 GR/DL, LEUCOCITOS 7200/MM3, PLAQUETAS 145,000/MM3, CREATININA 1.6 NG/ML, UREA 56 MG/DL. EL MECANISMO HOMEOSTATICO AFECTADO EN ESTE PACIENTE ES: COMPETENCIA DEL ESFINTER ESOFAGICO INFERIOR. INTEGRIDAD DE LA MUCOSA GASTRICA © DUODENAL. PRESION DEL SISTEMA PORTA. csoo> 5] G] BB) MOTILIDAD GASTRICA. EL DIAGNOSTICO DEFINITIVO SE ESTABLECE MEDIANTE: MANOMETRIA ESOFAGICA. TOMOGRAFIA COMPUTADA. SERIE ESOFAGOGASTRODUODENAL, PANENDOSCOPIA. csoo> 3] 2) BB)