LM Pancreas, GI

Pancreas and Gastrointestinal Tract Function Tests OBAMAS Mlm: Olav Assist. Prof. Pussadee Tobunluepop Faculty of Allied Health Sciences, Thammasat University



Outlines of Pancreas 1. Anatomy 2. Endocrine physiology 3. Exocrine physiology Exocrine secretions enzyme . Fluid secretions HCO; Control of exocrine pancreatic secretions 4. Pathology conditions Endocrine pancreatic disorders Inflammatory or necrotic pancreatic injury Destructive disorders 5. Pancreatic function tests

Anatomy of Pancreas enzionovnsasranooedoeoonand rained lascivious gnginnouoohboss pepsin / Endocrine n'onion'o arishm . ①- Exocrine stand LAoinarcdluaisem.lpuotcdlunisl;t.co

Anatomy of Pancreas Elongated , flattened pyramid shape Types of secretory cells: 1. 1% Islets of Langerhans: endocrine horImones 2. 98% Acinar cells, duct cells: exocrine secretions , bicarbonate baby duct cell bywon em Acinar cell .

Endocrine Physiology pa - cement's bathrooms modulator PB cell Moinuddinwww.op parcel, p f- cell

Pancreatic Endocrine Hormones bgfvoivwnmdobnoasiownmahsba.es Proinsvlin → Insulin inactive active gives mounts enzyme Usfs PP hormone

Exocrine Physiology 98 Yo Vos cell Awww ' ow o 611809 en2 . I 79 * groaning duodenal parton common bile duct to pancreatic duct nowon § duodenum

Pancreatic Exocrine Secretions Wateenzry-mecnl' reeadsaooro,h colorless!ooo y 1010689 not pancreatic juice ) * juice cell Wain pancreatic granulreansnis(i fceull nvocs tAioni naarl unemits) 1. Acinar cells: contain zymogen . 1th.1atMcoonsttaiinnacetnivzyemfoersm: mof ebomnutzuynimomn; leugsedm(ipnarcotiveenfozrmymes) 1.2 Some active enzymes Vigna active 2. Duct cells: secrete 2.1 Fluid Unis HCO - , 2.2 Electrolytes: Cations (Na+, K+, Ca2+ , Mg2+) especially bicarbonate ⑧

Digestive Enzymes 1. Inactive enzymes enzyme n' grantsoonassinsto go active wa : inactive 1.1 Proteases: trypsinogen, chymotrypsinogen proelastase, procarboxypeptidase 1.2 Inactive phosphatase A 2. Active enzymes 2.1 Nucleases: ribonuclease, deoxyribonuclease 2.2 Cholesterol esterase q 2.3 Amylase, lipase bWas 2 sides

Digestive Enzymes domination qmrrjawctoivieouoowroaaootivteiueem.rindnsooneanno8rmnosuesog.si functional unitogshcinarcdl I gents em . Tourists' oiosqnnosojwbycckorvag.us nerve

Controls of Pancreatic Exocrine Secretions an = moons: ginhimand Notgood enzyme man . no: Bashi win mounds HCOj . gives niggers enzyme

Pathology Condition I. Endocrine pancrae.waeatnhiocivosdoiogirsoooriorders: grbfgoin97monbdogUMIJVOSMNO.chDM,GUIUAN insulinoma, glucagonoma, somatostatinoma, Ppoma, gastrinoma, VIPoma II. Inflammatory or necrotic pancreatic injury: acute pancreatitis, chronic pancreatitis Nuo'owEnidUboWVW6w III. Destructive disorders: Iain'owbW% cystic fibrosis, pancreatic insufficiency

I. Endocrine Pancreatic Disorders 1. Diabetes Mellitus (DM) BUTUMW Major endocrine disorder www.alwna.in endocrine - cell of Islet cell destruction (DM type I) - Ketoacidosis bra n p - cell groinomg signalgents insulinId In' = DM I 2. Insulinoma insulin boo : btw - Tumor of pancreas islets - Overproduction of insulin cause hypoglycemia - Plasma glucose <40 mg/dL - s: admin malaria on nd ' - Elevated C-peptide demos c- peptide in

3. Glucagonoma Glucagon 9 - Tumor of pancreas - Hyperglycemia simmeringon 9 minusnon - Weight loss - Plasma glucagon >200 pg/mL (<200) w :b Esdras Head ovogoivo' Wright Soma to Stant in 9 www.gmsgedgenz . 4. SomatostatinoWmouldaa- - Tumor of pancreas (head) - Older adult , common in women - Elevated somatostatin

5. Ppoma Pancreatic polypeptide - Tumors producing pancreatic polypeptide - Often with obstructive jaundice - Elevated PP levels ) )Gastrin 't\"\" 6. Gastrinoma, VIPoma - Tumors producting gastrin and VIP - Excess gastrin: Zollinger-Ellison syndwrwowm.oem.oonmi - Excess VIP: WDHA syI ndrome sinew : n'Ostrow , word , (watery diarrhea, hypokalemia, achlohydria)

II. Inflammatory (Necrotic Pancreatic Injury) 1. Acute pancreatitisAndOWENGuingonaw * Severe, knife-likedenpteadOiUnTa,ssignnatuionsa,sneataasha,v, 0o768m026iting * Pathogenesis: rain msn.tn Obstruction of pancreatic duct briamsoamnndoioooas or ampulla of Vater wahoos pancreatic duct or - ya Reflux of bile, pancreatic juice into pancreas Kishi em - n' grainsTall sink into soon banishing defog Acinar cell . banns Enugu Resulting in acinar cell injury Released of amylase, lipase and proteasebanh em n'functorsnorth . from damag-ed acinar cell and ductules

Pathogenesis of Acute Pancreatitis

* Causes of acute pancreatitis Gallstones Cholestasis amazon. ihmamsqaoiw olwgsn.hnAlcohol Hypersecretion of gastric and pancreatic secretion Generate protein plugs in pancreatic ductules Leading to pancreatic obstruction Alcndiojgsmoussem . rinihibnnmseioeucellohinsy rid :giooyowa:NNhtwiowy brinmooaarigs - Infection Baldo - Tumor towns - Medication conning nddgrsdgso! - Genetic - High triglyceride level (>1,000 mg/dL): chylomicrons obstruct capillaries>>ischemia r.ru triglyceride 9

* Labororatory diagnosis MSM 8 - Very high triglycerides (>1,000 mg/dL) Lapidaries bad Mrsa Amylase ng sinew z - aan's - Amylase > 3-4 X of URL AmylaseHnd : do Und ( Masao p - ) P-amylase (kinetic method) Tauri educing S - amylase Taco - (inhibit S-amylase with wheat germ, lectin) - - Lipase > 3-4 X of URL

ogvqudgsrbadigoeyrinsoun.i2.ChronicPancreatitis brianlifestyle Most common cause: chronic alcohol abuse F n Extensive destruction of gland Pancreatic tissue replaced with scar (fibrotic) tissue

III. Destructive Disorders 1. Cystic fibrosis (CF) so'sand animadversion - Autosomal recessive (infants, children) - Mutations in Cl- transporter gene non www.i-owoslsila' - endId Ioi em. Very glow - Viscous, low volume pancreatic secretions - Reduced pancreatic flow pancreatic duct obstruction, atrophy win obstruction

2. Pancreatic insufficiency (EPI) - Reduction or loss of pancreaticmoeunxtsoecmri. n00ehmfWuOWncbadtion - Weight loss and cachexia - Symptoms appear after 85% of acinar loss - Causes: * CF in children * Chronic pancreatitis in adult

Pancreatic Function Tests MSM 828 1. Lundh test UN Ohioanwound bind birds agro o: gamin from riddled nanometer - Indirect method to stimulate pancreatic secretions - Liquid meal: 5% protein, 6% fat, 15% CHO, 74% non-nutrient fiber - Duodenal aspirate taken in 10-20 min intervals over 2 hr period for lipase or trypsin activity - Non-specificity ① ② mountain's brain pining Wo , bwdoog2. Secretin/CCK test Massoud:oivhm.fawoana.br hm , secret in lock bowl - After 6 hr or overnight fast, stimulation of pancreatic secretion with intravenously administered of secretin followed or not by CCK administration I- Collection of duodenal aspirate for 30, 60 or 80 min - Test for pH, secretory rate, enzyme activities, bicarbonate

3. Fecal fat analysis - Failure to digest and/or absorb fats is 0s,t8e87adot.gogr/rVhgfeqa - Screening test sudan III staining, fecal fat droplets stain yellow-orange to red with dye now Sudan test guarantorwho go ow : 4. Sweat Electrolyte Med 96M$ O (IWM Obtain ) - Na+, Cl- concentration in sweat for diagnosis of CF - 2-5 folds increase in CF children ( 60 mmol/L)

5. Serum enzymes 5.1 Serum amylase - - Acute pancreatitis amylase 9 2-3 24- Increased wiotphiniionnwho 2 hr,.388 .pagoenyaaklbiinnos bleaht. Arm, yclalsee aPirganantacrooen by kWi'mdonntehsybbaonrondaturboento.uhnr9n8 to3 S- nEUormal within 3-5 days - Urine amylase more sensitivei. Massa Idaho: bosons's Shonda obiton indicator - Ratio of amylase clearance/creatinine clearance: Urias x serum ore × too % Amylase clearance/creatinine urine UA/SA x SC/UC x 100serum amylase Acute pancreatits:08- % (normal value < 3.1%)

* Other causes of increased amylase: - Salivary gland disease (no lipase) S- amylase 9 - Fallopian tubes n'Onishi (no lipase) - Renal failure: decrease clearance of amylase - Macroamylasemia = amylase bound to Ig: Amylase TUTU riv - - Urine amylase I main Amylase Talla' - Serum amylase = gist amylase I bboibnon 8 amylase 9

5.2 Serum lipase isnen2s4itivhityr,Anddid' notlipcalseeafraairgnrcouend - Incqrsejwafsweo.gwg itah-8ino 4-8 hr,n ion.i Apmeyalakse . by kidneyofWOOheon and return to normal within= oepigwnsrbbflofonmwno.ie MET 8 baton 58 . 18-814 0day7s ¥ - Persist longer than amylase, half-life: lipase > amylase - Increase lipase level: - acute pancreatitis - fractures of bones Sensitivity 9 - Amylase - fat embolism specificity 9 . lipase piano ④ ow

Case study } Acute pancreatitis BUN 24 mg/dl 7 - 24 Acute pancreatitis Creatinine 1.20 mg/dl M: 0.60 - 1.20 AST 98 U/L 5 - 40 Hrh: Amylase Taz ALT 43 U/L 5 - 40 ALP 153 U/L 30 - 157 0000W boats Hoi Amylase 113 U/L 10 - 110 Lipase 720 U/L 31 - 186 lipase noesEmma Ign dominion 9 Isnt on 1 bins Vv Amylase Bibi

Outlines of GI tract 1. Anatomy of GI tract 2. Digestion eioeu 3. Absorption grow 4. Gut hormones him . 5. Pathological conditionTssn 6. Gastrointestinal functioMnsmtSMest

Anatomy of GI Tract - Muscular tube with epithelial cells - Digestive, absorptive organ ai out ofnow - Elaborate hormonal and neural regulatory network - Major components are : * Enzymes (break down maecioreuofomriagoallaencilules) * Water * Electrolytes 7m

1. Digestion * Digestion begins in mouth and is completed in proximal portion of small intestine eioeubbdg BUNK ma

Digestive Action of Mouth Ingestioneioeoo ofvefrosionedwsMtWimulates production of saliva 3 pairs of saliva glands: saliva including salivary amylase and lingual lipase n'onslaught 3 of Saliva: viscid, watehrim-bwaatesrendum, mbinugc--inS--caomnylatsaeining secretions acting as lubricant Chewing increase surface areabendedd thtNNN.Wed to enhance action of digestive enzymes

Digestive Action of Stomach cellfwnr.IM:01970 1. Mucous cells: secrete mucus to protect surface from acid and enzymes 2. Surface epithelial cells: secrete mucus 3. Parietal cells: produce HCl and intrinsic factor 4. Chief cells: produce p=epsinogen which converted into pepsin - at pH 3 pepsinogen #'pepsin 5. G cells: produce ghamst, rin (*1, 2 found in entire stomach *3, 4 found in body of stomach *5 found in antrum)

Digestive Action of small intestine - As chyme enter, several GI hormones are released - Hormones enter portal blood system and act on: *Various regions of GI tract *Stimulating contraction of gall bladder (releasing bile salts) *Pancreatic secretion of bicarbonate (to neutralize gastric acid) and release of pancreatic proenzymes Oj;hm nosoju mounts . en z n'in Win HC . , med ON07 Uld

HCl Dimaria neo Vagus nerve Wnt gas Pepsinogen → Pepsin 18809 protein from chief cell Gastrin ns.rjw parietal cell hired a Hd pH 3 Antral cell Hats Gastrin Nudo wants Hcoj on buffer Hd i nd: Missmounts - HCG

2. Absorption 1. Carbohydrate absorption gabardinehogdy - Disaccharides are split into monosacEcn harides by disaccharidase (lactase, sucrase, maltase) located on microvilli !Mono sac growth now 818on now Active - Monosaccharides are absorbed by specific transport active transport mechanism 2. Protein absorption qn absorb Gugu amino acid Taco special transport - Dipeptides are absorbed more rapidly than amino acids by special transport mechanisms - Specific absorptive mechanisms for various types of amino acid located in mucosal surface

3. Fat absorption Baobabs MobbWitherow protein - FA and monoglycerides diffuse into intestinal epithelial cells and interact with binding protein \\- Long-chain (16-18 C) FA→arFewiwreaepsott3e-4r8ifibetwd to form triglycerides and bound to apoB-48 to form chylomicron transpon'rowtensdD' toohh lymphatic and released into lymphatic system, 508117 thoracic duct before entry into bloodstream blood - Medium-chain (8-10 C) FA rapidly enter portal blood stream and bind to albuminliving' inoaiaartvnv Alb - Vitamins D, E, A and K are absorbed with lipids - 4. Water and Sodium Absorption win now Na \" Gagarin woo active - Water is transported by bulk flow with Na+ absWorOpWtOion I- Na+ is absorbed by active transport mechanism with absorption of amino acids, bicarbonate and glucose

5. Calcium Absorption gatameoimrnougsrros Vit D - Primarily under influence of vitamin D - Regulated by calcium binding protein in mucosa 6. Iron Absorption Jadakiss Fe\" Fabrivlog U Fest - Absorbable form is ferrous state (Fe2+) - Enter and transported to mucosa cells, released into plasma after oxidation to ferric state (Fe3+), and attached to transferrin for delivery to iron storage cells in BM 7. Formation of Stool qno.gr n'NFU ooh andonewww.n-800oneimsqgqor: - Water, K+, and bicarbonate are actively absorbed and return to circulation - Progressive dehydration and action of bacteria on residual of food substances lead to formation of feces

Gut Hormones 2 families of gut hormones: - Gastrin family: gastrin, cholecystokinin (CCK), motilin, enkephalin - Secretin family: secretin , vasoactive intestinal polypeptide (VIP), glucagon, gastric inhibitory polypeptide (GIP), bombesin

Pathological Conditions 1. Malnutrition 8761678072178 2. Stomach pathologicFINaNlIS conditionshollow780767d 3. Malabsorption syndrogaminsaeids 4. Carcinoid syndrome 5. Large intestine diseases onlookers'

1. Malnutrition Causes : - Abnormal food intake GUIDING - Abnormal digestion edouard - Abnormal absorption gainsaid

2. Stomach Pathological Conditions 2.1 Ulcers (Peptic ulcers)bbWDfw not IN7 2 07 UW - Excess acid action Asn n'7978690: egadnot - Common in stomach, duodenum - Risk factors: genetic (blood groups O), infections (H. pyroli) 2.2 Cancer Jr: I 8g - Over half of gastric cancers: pylorus, antrum

2.3 Zollinger-Ellison syndrome - Extreme form of peptic ulcer - Caused by gastrin secreting tumor of pancreas (gastrinoma) or antral G-cell Gastrin in HCl 9 Stimulate hypersecretion of HCl qamr.si/vaw Interfere fat digestion in duodenum Steatorrhea -

2.4 Pernicious anem( iMaegaantodblavstiictaamneimnia ) malabsorption B12 -Autoimmune destruction of gastric mucosa particularly parietal cells (non- specific Ab) and intrinsic factor blocking Ab (specific Ab) Mn Vit 13126Wh: absorb INTO' - Vitamin B12 deficiency leads to damage to posterior columns of spinal cord and in megaloblastic anemia - Schilling test for vitamin B12 absorption

3. Malabsorption Syndromes 3.1 True malabsorgpatinisasnlid: icngannot absorb nutrients, results of impaired intestinal mucosa 3.2 Maldigestigoanbo:ronceanounUsnedd by pancreatic insufficiency, lead to fat malabsorption and streatorrhea 3.3 Celiac disease: inflammation of intestine and l=oss of villi and microvilli ma lactase sins uiioeo lactose Idfa' 3.4 Lactose intolerance: lack of lactase (historical not milk drinkers)

4. Carcinoid Syndrome Absorb again of - Vascular flushing, diarrhea 0,897 di IIbsin - High level of serotonin and kinins serotonin 9 - Screening procedure for 5-HIAA in u5-rHinI AAe 9 fulton dad (5-hydroxyindoleacetic acid, metabolite of serotonin)

5. Large Intestine Diseases 5.1 Diarrhea: Severe diarrhea: Na+, K+, bicarbonate, b water depletion loss - 1. Solute malabsorption (osmotic diarrhea) caused by poorly absorbed substances or intestinal malabsorption 2. Secretion of fluid into intestine (secretory diarrhea): secretion of ions stimulated by toxin, endotoxin 3. Motility disturbance: increase motility, decrease transit time, decrease absorptive efficiency 5.2 Cancer of coloNn:bBaanrtmdarn:ectum: screening test: occult blood and colonoscopy for high-risk patients

Gastrointestinal Function Test 1. Test of gastric acidity Msm pH - Measurement of pH - Anacidity (achlorhydria), pH >6 (normal pH <3) nssoqn.qiw.IR ants nor fasting 2. Gastric stimulation test of demos pH - Gastric fluid: appearance, pH, volume, mM of H+ from fasting patient to determine unstimulated acid and after stimulation with administered penta-gastrin to determine maximum secretory ability Id rinks

3. Fat absorption test: fat screening: staining with fat-specific stain and serum carotene 4. D-xylose absorption Test Aw D- xylose g n Gauna oog . jejunum - D-xylose is absorbed passively in small intestine, not present in blood, not metabolized and filtered by glomerulus, at least 50% is excreted in urine within 24 hr - Fasting patient, 25g D-xylose in 300-500 mL water (0.5g/kg body weight for children with max of 25g) - After administration, collection at 2 hr for blood and 5 hr period of urine - Low levels of urine, plasma: adsorptive defect in jejunum