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     Ahmed’s appetitePart A

    It almost noon when Ahmed, 50-year old retired construction engineer, closed his privateofce which he started a ew years ater his retirement and went home.

    !h, I’m so tired" #oney, have you $nished lunch yet%& said Ahmed while smo'ing hiscigarette or what seemed the $th time. (es, it’s ready"& said )ona, Ahmed*s wie.

    +o, how is your stomach pain% Is it etter%& as'ed )ona. It comes and goes, ut I eelless nauseated today.& answered Ahmed, while eating his second ite.

    +hortly ater starting his lunch, Ahmed stands to wash his hands. ust as usual, you havenot $nished your plate" Are you sure you did not eat at wor', ecause I spent time in the'itchen ma'ing this meal and now youre arely eating"& said )ona. #e loo'ed over ather Im sorry, I eel somewhat ull and a little o discomort ...& #e stepped out to thealcony to have a smo'e.

     /he net day, Ahmed wo'e up early on the wee'end to ta'e some iuproen or hisnagging 'nee pain. )ona’s voice came I am sorry aout yesterday1 I’ll coo' your avoritemeals or dinner tonight.& Ahmed replied, #oney, I 'now that you didn’t mean it.&

    Ahmed’s pain increased in the ollowing months, he 'ept s'ipping meals and eltnauseated more oten. It reached to a point where )ona ecame worried aout hisweight, seeing that he has lost aout 'g. Ahmed I am really worried1 I thin' you shouldgo to the hospital& said )ona, ut Ahmed reused and thought it was unnecessary.

     /wo wee's later, Ahmed panic'ed when he noticed that his stool was lac' and with)ona constantly demanding that he visit the doctor, Ahmed $nally relented and oo'ed

    an appointment.2uring the doctor’s visit, Ahmed was very anious ut once the doctor smiled at him, herelaed. I can’t eat very well1 my stomach pain is very annoying especially ater meals. Ieel nauseated very oten and my appetite is noneistent"& said Ahmed. I am not my sel anymore&.

    2on’t worry Ahmed, we are going to $gure it out. ust rela.& said 2r. 3ada. 3ow I needyou to answer some 4uestions, is that !%&

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    Questions

    6- (ou are a general practitioner in a primary health care clinic and Ahmed has came toyou complaining o the previously mentioned symptoms. /a'e a thorough history o hispresenting complaint, including his past medical, amily, and social history. 7(ear 89:; -

    < minutes

    a. Introduction=o Introduce yoursel > name?role, @on$rm patient I2, ain consent,

    Bnsure the patient is comortale.. # o presenting complaint=

    o +o what’s rought you in today%&o CCAADDEF and I@B 7where, when, aggravating and alleviating

    actors, associated symptoms, E elies; and 7Ideas, @oncerns,Bpectations; !r +!@GA/B&

    c. Past medical history=

    o astrointestinal disease > IF2?IF+?malignancy?BG2o +urgical history > e.g. appendectomy?colectomy?c-sectiono  /ravel #.

    d. 2rug and allergy history=o Haatives, Proton pump inhiitors, #8 receptor antagonists, +odium

    alginate?calcium caronate e.g. aviscon.o Gecreational drug use, I drugs.o 3+AI2+, +teroids, Fisphosphonates, contraceptives%o Any allergies%

    e. Jamily historyo astrointestinal disease > malignancy?IF2?BG2o #ereditary owel conditions > #3P@@?JAPo !ther signi$cant medical conditions

    . +ocial history=o +mo'ing, Alcohol, +eual history.o !ccupationo #ousing, lives with who%

    g. 2iet #=o Hac' o $er > constipation?luten > celiac disease?Jatty oods.

    h. +ystematic review=o @ardiovascular > @hest pain?Palpitations?2yspnea?

    +yncope?!rthopnea?Peripheral edemao Gespiratory > 2yspnea?@ough?+putum?CheeKe?#emoptysis?@hest

    paino I > Appetite?3ausea?omiting?Indigestion?2ysphagia?Ceight

    loss?Adominal pain? Fowel haito Lrinary > olume o urine

    passed?Jre4uency?2ysuria?Lrgency?Incontinence

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    o @3+ > ision?#eadache?)otor or sensory disturance?Hoss oconsciousness? @onusion

    o )usculos'eletal > Fone and Moint pain?)uscular paino 2ermatology > Gashes?+'in rea's?Llcers

     

    8- Ater ta'ing the history rom )r. Ahmed you have made a diNerential diagnosis list.Chat are the possile diNerential diagnoses or )r. Ahmeds symptoms% 7year :; 760minutes;

    • astric cancer.

    • Acute ulcers 7occur at times o severe physiological stress > e.g. severeurns?head inMury;.

    BG2. 7astro esophageal reOu disease;

    • 2rug-induced dyspepsia.

    • @rohns disease.

    • ollinger-Bllison syndrome 7i H. pylori is negative, or has een eradicatedand ulceration is reractory?recurrent;.

    • Irritale owel syndrome.

    • #epatitis.

    • @hronic pancreatitis.

    • allstones.

    • 2iverticular disease.

    • Adominal aortic aneurysm.

    • @oronary heart disease.

    :- Ater listing your diNerentials you had to perorm physical eamination to ruleout some conditions and reach a diagnosis. Perorm a physical eamination on)r. Ahmed and ma'e sure to ta'e consent and ensure his privacy andcon$dentiality. 2on’t orget to ta'e the vital signs 7year:; 760 minutes;

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    As with other systems, positioning o the patient and ade4uate eposure o their adomen is critical when eamining the adomen. Chen you come topalpate the adomen, it is essential that the patient e lying Oat with legsstraight and arms y their side. +upporting the patient’s head with a pillowwill ma'e them more comortale. It is important to eamine the adomen

    rom the right side o the patient, even when the eaminer is let-handed"It is virtually impossile to accurately palpate the liver and spleen rom thelet side.

     /he routine or eamining the adomen consists o the same componentsused in the eamination o the chest and other systems.

    o I3+PB@/I!3

    o PAHPA/I!3

    o PBG@L++I!3

    o AL+@LH/A/I!3

    INSPECTION:o )a'e sure that your suMect is suitaly positioned 7i.e. lying Oat;,

    then eamine as ollows=o A3( +@AG+ 7note type and position;

    o +/GIAB 7stretch mar's;

    o 2I+/B3+I!3

    o @!3/!LG+

    o L)FIHI@L+

    o BI3+

    o PLH+A/I!3+o I+IFHB PBGI+/AH+I+

    o PAI3 !3 @!L#I3

    o PAI3 !3 +/GAI#/ HB GAI+I3

    PALPATION:o +tart y identiying the regions which the adomen is divides.o 2iNerent organs and intra-adominal structures can

    characteristically e palpated in each o these regions. Feorecommencing palpation, the suMect should e= relaed, Carm and

    don’t orget to as' the patient to point to any area that is tender.

    o Lsually the routine palpation moves in an orderly ashion througheach o the regions or 4uadrants. #owever, i the patient identi$esan area o tenderness it is est to start ACA( rom that point and$nish with the tender region.

    o When palpating look for:- Areas o guarding?rigidity

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    - @ross tenderness- Geound tenderness- Palpale masses

    PERCUSSION:

    o Percussion is used to= 2e$ne the sites o maMor organs 7liver, spleen, 'idneys and

    ladder; 2etect the presence o ascites 7Ouid in the peritoneal cavity; >

    i.e. Qshifting ullness’

    AUSCULTATION:o Lsing your stethoscope, listen to your suMects adomen and

    identiy the ollowing= F!CBH +!L32+= 3ormal adominal sounds are sot, gurgling,

    intermittent and their re4uency varies depending on when thelast meal have een eaten. Houd, high pitch sound, with

    tin'ling 4uality indicates ostructed owel. @omplete asenceo owel sound or R min indicates paralytic ileus.

    +I/B !J A!G/I@ A32 GB3AH FGLI/+= Genal ruits heard aoveumilicus S8-8.5cm to right or let o midline using thediaphragm o the stethoscope. /he presence o ruits mayindicate narrowing o these arteries that would re4uire urtherinvestigation.

    R- (ou had $nished eamining )r. Ahmed and ruled out some diNerentials. (ouhave re4uested some la investigations. Ater getting the results you havemade a certain diagnosis which is Tpeptic ulcer. Chat do you 'now aout pepticulcers% 7year 89:; 7-U minutes;.

    2e$nition= It is a condition o painul sores or ulcers in the super$cial epithelialcells penetrating down to the muscularis mucosa in the stomach or duodenum .

    @auses=

    - inection y #elicoacter pylori 7#. pylori;

    Jre4uent use o nonsteroidal anti-inOammatory drugs 73+AI2s;7 3+AI2s can

    cause damage to the gastroduodenal mucosa via several mechanisms=impairment o the arrier properties o the mucosa, suppression o gastricprostaglandin synthesis, reduction o gastric mucosal lood Oow and intererencewith the repair o super$cial inMury, impairing the restitution process, intereringwith hemostasis and inactivating several growth actors that are important in

    mucosal deense and repair.;

    - smo'ing

    http://www.webmd.com/arthritis/features/pain-relief-how-nsaids-workhttp://www.webmd.com/arthritis/features/pain-relief-how-nsaids-work

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    - Bcessive drin'ing o alcohol- radiation therapy- Bcess acid production rom stomach cancer

    - what are the signs and symptoms o peptic ulcer disease 7 not necessary allpresent in the case; %

    • Furning sensation or pain in the area etween the chest and umilicus 7epigastria;

    • dull pain in the stomach

    • Hoss o appetite.

    • loating

    • urping or acid reOu

    • #earturn 7urning sensation in the chest.

    !ther signs and symptoms

    Hess oten, ut ulcers may cause severe signs or symptoms such as=

    • omiting o lood V which may appear red or lac'

    • 2ar' lood in stools or stools that are lac' or tarry

    • Bpigastric tenderness.

    • 3ausea or vomiting

    • Lneplained weight loss

    • Appetite changes

    5- Ater you have made your diagnosis, you received a call rom your consultantand he was very high tempered he is the type that wants everything to eperect he wont allow any mista'es. he as'ed you to come y his ofceand as'ed you the ollowing 4uestions=7 year :; 7 65-80 minutes;

    - what is the pathophysiology o peptic ulcer disease%

    Llcers may occur with hypersecretion o hydrochloric acid and pepsin, causing

    imalance etween gastric luminal actors and degradation in the deensiveunction o the gastric mucosal arrier, when acid and pepsin invade a wea'enedarea o the mucosal arrier, histamine is released. #istamine will stimulateparietal cells to secrete more acid. Cith the continuation o this vicious cycle,erosion occurs to orm the ulcer.

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    - #e showed you the ollowing picture and as'ed you to rieOy descrie theanatomy o the stomach and duodenum=

    • Present in left h!po"onriu#, and

    epigastriu# 7pain elt here;.• R parts= undus, ody, antrum and pylorus.

    • 8 opening= cardiac and pyloric ori$ces.

    • Caria" ori$ce have only ph!siologi"al 

    sphin"ter. #owever, the p!lori" ori$ce have

    $oth anatomical and physiological sphincter.• 8 curvatures= greater and lesser curvatures.

    • 8 +uraces= Anterior and posterior +uraces.

    Foundaries=

    • Anteriorl!= liver, diaphragm and anterior

    adominal wall.• Posteriorl! 7stomach ed;= transverse colon, transverse mesocolon, pancreas E

    splenic artery, spleen, let 'idney and suprarenal gland let part o diaphragm

    and the lesser sac.• Flood supply= right and let gastric arteries supply the lesser curvature.

    Gight and let gastroepipolic arteries supply the

    greater curvature.+hort gastric artery which is derived rom splenic artery supply the undus.

    • enous drainage into the portal circulation.

    • Hymphatic drainage= let and right gastric node, let and right

    gastroepipolic node and short gastric node. Bventually, all lymphatic rom

    the stomach reach celiac node.

    2uodenum parts+uperior2escendingIneriorAscending

    H6

    2uodenal ulcercommon site  .

    H6-H:

    Around thehead o thepancreas.

    )aMor duodenalpapilla >ampulla

    H:

    @ross theinerior venacava and aorta.

    Posterior tosuperior

    mesentericartery.

    H:-H8

    2uodenoMeMunalOeure.

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      %loo suppl!:- Lpper part o duodenum y superior pancreaticoduodenal Artery. Its

    vein drainage to portal vein.- Hower part o the duodenum y inerior pancreaticoduodenal artery. Its

    vein drainage to superior mesenteric vein which also drains into the

    portal vein.  L!#phati" rainage:Lpper part= pancreaticoduodenal nodes WX gastroduodenal nodes WX

    celiac nodesHower part= pancreaticoduodenal nodesWX superior mesenteric nodes

    - he as'ed you also on how acid is secreted%

     /he stomach parietal cells secrete #E and @l- y the action o two separate

    pumps. #E

     is secreted to the lumen y mean o #E

      E

     A/Pase active transporterpump, the #E secreted is coming rom rea'ing down o #8! into !#- and #E. /he !#- comines @!8 -either rom cellular metaolism or plasma- to orm #@!:.@l-  is secreted y secondary active transport. 2riven y the #@!:- concentrationgradient #@!:- is transmitted into the plasma while @l- get into the parietal celland then to gastric lumen.

    - /he consultant pinpointed on the mechanism o reerred pain o peptic ulcerand as'ed you to eplain the mechanism= 

     /he nerves which supply pylorus and $rst part o duodenum relay on the samesegments y which the nerves that ss4 *upply s'in o epigastria thus when painis produced in pylorus or duodenum the aNerent will travel to spinal cord

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    segments and rom there the eNerent will travel to the epigastria so pain issensed there.

    Y- Huc'ily you have answered all o the consultants 4uestions correctly and was

    allowed to e dismissed rom his ofce. #e also gave you the permission to starttreating the patient. 7 year 89:; 765-80 minutes;.

    what are your $rst line options o treatment=

    6-reduce stress

    8- 4uit smo'ing

    :- lose weight

    R- avoid eating heavy greasy meals

    5- avoid eating eore sleeping 

    - ut since )r. Ahmed is already has a leeding stool, you should evaluate hishemodynamic status and start treating him immediately. list the availale drugs, andwhat will e the $rst line=

    • Treat#ent: A& antise"retor! agents:

    '& () re"eptor antagonist: revesile competitive inhiition o #8 receptors.ery eNective in inhiiting nocturnal acid secretion. Inhiit histamine, gastrin9 Ach 7less than PPI;.

    Promotes healing o duodenal ulcers. 2rugs end with >tidine.@imetidine may interere with hepatic metaolism. Genal ecretion.

    )& *Proton&pu#p inhi$itor: loc' acid secretion y irreversily inactivating #? A/Pase pump at the parietal cell surace. Cea'ly asic, activated in canaliculio parietal cells. )ost eNective treatment. 2rugs end with >praKole. 3otadministred with other acid suppressors. Btremely sae, inhiits @(PR50.PantropraKole 9 reepraKole have no signi$cant interactions.

    +& Others: antimuscarinics 7signi$cant +B;, astrin antagonist 7loweNectiveness; 9 somatostatin analogues 7re4uire parenteral administration;

    %&C!toprote"ti,e agents - #u"osal strengtheners:'& Su"ralfate: adheres to ulcer 9 acts as a arrier. +timulates mucosal

    protective mechanisms. Antacids 9 meals shouldn’t e ta'en within:0 min oadministration. AB= constipation 9 inhiits asorption o some drugs.

    )& P. analogues: B 9 I Ps generally protective, inhiit acid secretion 9increase mucus 9 lood Oow. /isoprostol: PB analogue, used in patientsusing 3+AI2s w?high ris' o ulcer. ABs pain sensitiKation, uterine contraction7@I in pregnancy;, diarrhea, headacheZetc.

    +& %is#uth Chelate: not 6st line, used in comination. Jorms precipitate whichinds to ulcer orming a arrier1 enhance P synthesis, stimulate mucus 9icaronate secretion. Also has moderate direct antimicroial activity against

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    #.pylori. +Bs inc. lac' stool 9 tongue, damage to 'idney 9 @3+ 7ismuthtoicity;. 2on’t ta'e w?meals, antacids or other meds.

    0& Car$eno1olone: derived rom li4uorice root. Accelerate healing o gastriculcers 9 promotes the production o mucus. +igni$cant +Bs= mineralcorticoideNect 73a 9 #8! retention; [hypertension, al'alosis, 9 hypo'alemia.Precipitate to glaucoma 9 urinary retention.

    2& Anta"is: simplest, wea' ase to raise p# 9 inhiit ormation o pepsin. )osteNective against duodenal ulcers. Al@l:7constipation; or )g@l87diarrhea; oroth. /a'e antacids 8h eore o ater other drugs. +ome additives are addedwith antacids including=

    Alginatesoam layer over gastric contents to reduce reOu.Si#eti"onereduce ule ormation to prevent reOu.

    O1etha3aine+urace anaesthetic. Esince he is using 3+AI2s, #e should continue using PPIs or

    prostaglandin analogues, or replace 3+AI2s with @!\-8 inhiitors to avoid reoccurrence.

    I the patient’s # level is low start resuscitation.

    - (ou also ordered Lrea reath test, to investigate or helicoacterpylori inection, and it came ac' positive.  Chat is the treatment

    plan now%Fismuth, Amoicillin, clarithromycin, tetracycline, 9

    metronidaKole.

      /riple regime o PPI, )etrondiaKole, 9 amoicillin or clarithromycin is usedwith X]0^

    - why antiiotics are used in cominations%

    Natural 4%iologi"al5 Causes

    Sele"ti,e Pressure

    In the presence o an antimicroial, microes are either 'illed or, i they carryresistance genes, survive. /hese survivors will replicate, and their progeny will4uic'ly ecome the dominant type throughout the microial population.

    /utation

    )ost microes reproduce y dividing every ew hours, allowing them to evolverapidly and adapt 4uic'ly to new environmental conditions. 2uring replication,mutations arise and some o these mutations may help an individual microesurvive eposure to an antimicroial.

     

    .ene Transfer

    )icroes also may get genes rom each other, including genes that ma'ethe microe drug resistant.

    So"ietal Pressures

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     /he use o antimicroials, even when used appropriately, creates a selectivepressure or resistant organisms. #owever, there are additional societalpressures that act to accelerate the increase o antimicroial resistance.

    Inappropriate Use

    +election o resistant microorganisms is eacerated y inappropriate use oantimicroials. +ometimes healthcare providers will prescrie antimicroialsinappropriately, wishing to placate an insistent patient who has a viral inectionor an as-yet undiagnosed condition.

    Inae6uate 7iagnosti"s

    )ore oten, healthcare providers must use incomplete or imperect inormationto diagnose an inection and thus prescrie an antimicroial Must-in-case orprescrie a road-spectrum antimicroial when a speci$c antiiotic might eetter. /hese situations contriute to selective pressure and accelerate

    antimicroial resistance.

    (ospital Use

    @ritically ill patients are more susceptile to inections and, thus, oten re4uirethe aid o antimicroials. #owever, the heavier use o antimicroials in thesepatients can worsen the prolem y selecting or antimicroial-resistantmicroorganisms. /he etensive use o antimicroials and close contact amongsic' patients creates a ertile environment or the spread o antimicroial-resistant germs.

    Agri"ultural Use+cientists also elieve that the practice o adding antiiotics to agricultural eedpromotes drug resistance. )ore than hal o the antiiotics produced in theLnited +tates are used or agricultural purposes.6, 8 #owever, there is still muchdeate aout whether drug-resistant microes in animals pose a signi$cantpulic health urden.

    - #ow does #. pylori cause ulcers%

    #. pylori are adapted to live in the harsh, acidic environment o the stomach. /hese acteria can change the environment around them and reduce its acidityso they can survive. Chich allows them to penetrate the stomach lining andcause ulcers.

    - )r. Ahmed as'ed you aout the possile complications o peptic ulcer i itwas untreated, so you answered him y=

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    6-ostruction

    8- peroration 7posterior wall o the stomach WX perorate to pancreas WXerosion to splenic artery WX ac' pain and atal hemorrhage;

    :- atrophy gastritis

    R- gastric malignancy 

    - #e also as'ed you how come in normal conditions gastric acid dont causedamage to stomach lining%