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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%