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Gast Rouw
Gast Rouw
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❖ CHPS → due to hypertrophy of the pyloric muscularis mucosae, narrowing is
exacerbated by local inflammation & edema
❖ Annular pancreas:
• Normal development: ventral pancreatic bud developed at 5 th week of
gestation, at 7th week it rotate behind the 2nd part duodenum to fuse with
the dorsal bud at the 8th week.
• Abnormal migration of the ventral bud → annular pancreas, due to
adherence of the bud to the duodenum or dorsal bud before rotation
• Clinical picture : asymptomatic, pancreatitis (due to pancreatic duct
obstruction), duodenal obstruction
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❖ Clinical picture of pancreatic divisium? Most of patients, it is clinically silent,
may predispose to recurrent pancreatitis, there are two main duct
systems that drain different portion of the pancreas
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GIT ANATOMY
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❖ If the liver continue to bleed after Pringle’s maneuver → IVC or hepatic veins
are the sources of bleeding
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❖ Surgical landmark for the appendix: the tinea coli begin as continuous layer of
longitudinal muscle that surround the rectum just below the serosa, at the
recto-sigmoid junction it condensed to be 3 distinct longitudinal bands
souuround the colon that converge at the root of appendix. (has the same
function as the outer layer of muscularis externa)
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❖ Horizontal transection of the rectus abdominus carry the risk of?
Superior & inferior epigastric arteries supply the rectus abdominus, inferior
artery pass posterior to the rectus abdominus at the level of the arcuate line →
injury lead to significant hematoma due to loss of the the supporting posterior
rectus sheath.
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❖ Common iliac artery branches (before passing inguinal ligament) :
• Inferior epigastric artery (pass medially, superiorly)
• Deep circumflex iliac artery (pass laterally)
❖ Renal vessels:
o Right renal : shorter, vein runs in front of artery, right gonadal vein
drain directly into IVC
o Left renal : longer, vein run between aorta & SMA causing its
compression “Nutcracker effect” → ↑↑ pressure in left renal vein (left
testicular vein drain in the renal vein) → Varicocele ; this why
varciocele occur more on the left
❖ What is the origin of the left gonadal artery?
- Abdominal aorta not left renal artery ☺
❖ IVC is formed by union in common iliac veins at level of L4-5; it enters the
thorax at level of T8 (VOA – 8/10/12)
❖ Where are the watershed areas of GUT: splenic flexure (between superior
mesenteric artery & IMA) & recto-sigmoid junction (sigmoid artery &
sup. Rectal artery)
❖ Ligament of treitze
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❖ Which branches supplied by splenic artery will be most affected by splenic
artery occlusion. Short gastric arteries as they have very poor anastomosis,
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unlike left gastro-epiploic artery which is has strong anastomosis.
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❖ Gastric varices:
o Portal hypertension cause ↑↑ pressure in the left gastric vein → both
gastric & esophageal varices.
o Superior mesenteric vein → cause varices in the lower stomach
o Splenic vein thrombosis (due to chronic pancreatitis, tumors, pancreatic
cancer) → ↑↑ pressure in short gastric veins → fundal varices only with
normal esophagus, rest of the stomach.
❖ Splenic Vein Thrombosis – affects short gastric veins draining antrum of the
stomach, producing gastric (fundal) varices only
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❖ Lymphatic drainage of the rectum : either internal iliac or inferior
mesenteric
→ Either in bowel wall (epicolic), around arterial arcades (paracolic), around
mesenteric vessels (intermediate)
→ 1 site of nodal metastasis are the sentinel lymph nodes first 1-4 nodes
st
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❖ Anastomosis between IMS & SMA :
• SMA & IMA are the main blood supply of the small & large intestine.
• Many anastomosis connect them.
a) Marginal artery of Drummond (principal)
b) Arc of Riolan (mesenteric meandering artery)
• So IMA is not always reconnected during aneurysmal repair
• N.B. IIA & EIA make anastomosis with other arteries to supply the
rectum, abdominal wall
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❖ Alkaline phosphatase → present in liver, bone, placenta, intestine, kidney,
leukocytes, and neoplasm. Threefold elevation in ALP = liver disease.
Moderate elevated ALP → GGT
❖ Superficial inguinal lymph nodes drain all skin below the umbilicus except
testis (para-aortic) & posterior calves, glans penis (deep inguinal LNs)
❖ Femoral triangle:
• Femoral artery → mid-inguinal point (midway between pubic tubercle,
ASIS)
• Femoral vein cannulation → ~ 1 cm below the inguinal ligament, ~ 1 cm
medial to femoral artery pulsation
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❖ Groin hernia :
a) Direct & indirect hernia occur above the inguinal ligament, while the
femoral hernia occur below it
b) Femoral hernia is more common in ́♀ & tend to occur on the right side.
Direct hernia Indirect hernia
Protrusion through triangle Failure of obliteration of
of Hasselbach. process vaginalis
Less prone to incarcerate More common, more on Rt.
side
Less prone to descend to Better felt by tip of finger
scrotum
Best felt with pulp of finger
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❖ Causes of direct inguinal hernia:
• As the floor of HAsselbach’s triangle is formed of tranversalis fascia …
breaking down of this fascia either by chronic wall injury or CT abnormality
→ protrusion & direct inguinal hernia
❖ Testicular descent :
- occur slowly from week 8 – full term, palpable testes at inguinal canal
mostly descend spontaneously at age of 6 months
- The deep inguinal ring is an opening in the fascia transversalis lateral to the
inferior epigastric vessels and superior to the mid-inguinal point (midway
between the ASIS and the pubic tubercle).
- The superficial inguinal ring is an opening in the external oblique muscle
aponeurosis and lies above and medial to the pubic tubercle.
- The conjoint tendon is the common tendon of the transverses abdominis
and internal oblique muscles. It forms part of the posterior wall of the
inguinal canal.
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GIT PHYSIOLOGY
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❖ Cholecystokinin → responsible for secretion of enzymes from acinar cells
While secretin responsible for secretion of fluid rich in HCO3 & poor in Cl to
neutralize the acidity from stomach (with no effect on enzymes production)
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❖ Gastric acid secretion :
• Histamine → H2 receptors ∷ ↑↑ cAMP
• Ach → M3 ∷ ↑↑ IP3
• Gastrin → CCB receptors ∷ ↑↑ IP3
→ ↑↑ Histamine though ECL cells
❖ Neutralization of the gastric acidity:
1) Brunner glands in the duodenum: most numerous at the pylorus, may be
found in ampulla of Vater, the ducts of these glands extend through the
muscularis mucosa and termiate in the crypt of Lieberkuhn
2) Pancreatic ductules: produce watery secretions containing ↑↑ concentration
of bicarbonate ions, emptied in the duodenum
❖ gastric acid secretion:
• there are 3 phases of gastric acid secretion.
1) Cephalic phase: stimulated by smell & taste of food, mediated by vagal
stimulation
2) Gastric phase: stimulated by chemical irritation of the stomach,
mediated by gastrin & histamine (from ECL cells)
3) Intestinal phase: very minor role in gastric acid secretion. Ileum & colon
produce peptide YY → inhibit ECL cells → ↓↓ gastric acid production.
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❖ Trypsinogen is activated in the duodenum by its brush border enzyme
enteropeptidase → deficiency cause protein & fat malabsorption→
diarrhea, Failure to thrive, edema
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❖ Pancreatic fluid is isotonic, contain same amount of Na, K as ECF. Due to
action of secretin → ↑↑ HCO3 & ↑↑ pancreatic juice flow SO in High flow
→ ↑↑ HCO3, Low flow → ↑↑ Cl ( → )الطبيعيchloride & HCO3 are exchanged
at the apical surface of pancreas, so ↑↑ HCO3 lead to ↓↓ Cl and vice versa
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❖ notice some characters of vitamin B12 absorption
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GIT PATHOLOGY
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❖ Suppurative parotitis : note that post-surgical or post-intubation due to lack
of salivation an dry mouse, may be complicated by infection
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❖ Cause of reflux in scleroderma ➔ esophageal dysmotility (not uncoordinated
motility) due to atrophy & fibrous replacement of the muscle → LES become
atonic & dilated
Barrett esophagus
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❖ Risk factors of esophageal cancer:
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o Areas of keratinization “keratin pearls” (arrows)
o Inter-cellular bridges (picture)
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❖ Pathogenesis of pernicious anemia :
❖ Stress related mucosal injury → multiple, small circular lesion ranging from
erosion to full thickness ulcers. Due to local ischemia
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❖ Gastric adenomcarcinoma :
• Intestinal type: resemble colon carcinoma, consists of columnar &
cuboidal epithelium grow as polipoidal mass inside the lumen of the
stomach
• Signet ring type: doesn’t form any glands; with cells contain abundant
mucin droplets (signet ring cells), tend to infiltrate the stomach wall due to
loss of E-cadherin → Linitis plastica.
• Most important factor that control survival is degree of wall infiltration &
regional lymph nodes
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❖ Zollinger Elison syndrome :
o Ulcers beyond duodenal bulb suggest ZES
o Normally, secretin inhibit the gastrin release & ↑ pancreatic release → ↑↑
gastri after secretin = ZES (gastrinoma)
❖ Clinical picture of ZES:
• Peptic ulcer refractory to therapy, diarrhea≫≫ as gastric acid damage
intestinal epithelium and inactivate pancreatic enzymes
• Investigations must directed toward exclusion of MEN 1 as Most ZES are
sporadic, 20 – 30% of them are associated with MEN1 syndrome
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❖ Malabsortion :
• Although it is classicaly cause steatorrhea, it may cause anorexia, weight
loss,fatigue …etc.
• Because fat have the most complex pathway fro absorption, it is the
earliest & ost severly affected in generalized malabsorption →
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testing for fat malabsorption is the most sensitive strategy for screening.
• Qualitative assay of stool by sudan III stain is important
❖ Celiac disease:
• L/M: villous atrophy, crypt hyperplasia, intra-epithelial lymphocytic
infiltration
• Age of onset 6 – 24 month.
• Malabsorption occur due to atrophy of villi → ↓↓ area for absorption
especially in duodenum & proximal jujenum
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❖ Small intestinal bacterial overgrowth (SIBO):
• Enteric bacteria cause :
1) ↑↑ production of vitamin K, folate
2) Inhibit proliferation of pathogenic bacteria
3) Digest unabsorbed sugars
• SIBO → ↑↑ vitamin K & folate level, although it cause malabsorption of fat
soluble vitamins (DEKA)
❖ Lactose intolerance :
o Prevelant in Asia & Africa population
o Other causes :
1) Primary lactase defieicny : Normal histological appearance
a. Hereditary : rare AR disease
b. Acquired due to lactose non persistence (↓↓ lactase
producton by md childhood) common in Asians 90%,
Africans and Hispanic
2) Acquired inflammation → bacterial overgrowth, infectious
enteritis, Crohn’s disease
❖ Whipple disease:
• Caused by gram positive actinomycete → proliferate only within
macrophages with no inflammatory response
• Show PAS +ve granules, diastase resistant granules (consist of lysosomes
& partially digested bacteria)
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❖ Enteric oxaluria (Crohn’s disease)
• Normally, intestinal oxalate bind to calcium to form insoluble Ca + oxalate
that excreted in feces.
• In CD ➔ diseased terminal ileum → ↓↓ bile acid absorption → ↓↓ fat
absorption → fat in the intestine bind to the free calcium to be
excreted in the stool, leave the oxalate frre without calcium → absorped
→ oxlalate stones
❖ Toxic megacolon :
• UC ≫ CD, C. difficile, other inflammatory colitis
• Transmural inflammation → release cytokines & inflammatory mediators
→ colonic SM paralysis ➔ rapid distension, thinning wall, perforation
• Diagnosis need X-ray ➔ colon dilatation, multiple air-fluid level, free air
• Barium enema and colonoscopy are contraindicated
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❖ Gross picture of Crohn’s disease:
• Although rectum is usually spared, perianal diseases are very common
• Bowel wall thickening (due to transmural inflammation)
• Cobble stone appearance (serpeginous depressed ulcerations with normal
healthy mucosea in between)
• Creeping fat (mesenteric fat become wrapped around the colon)
❖ Short bowel syndrome: massive small bowel resection & Crohn disease → ↓↓
in absorptive surface area → postprandial voluminous diarrhea
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❖ Pathogenesis of acute appendicitis:
• Luminal obstruction is the first inciting event (either by fecolith, lymphoid
hyperplasia…. Etc.) → retained mucus & distension of the appendix →
halting the venous circulation & resultant hypoxia to the wall → bacterial
invasion ☺
❖ Appendicitis:
• Visceral pain → luminal distension, stretching of smooth muscle; refered
by T10
• Somatic pain → due to irritation of parietal peritoneum
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❖ Pathogenesis of Hirsch-sprung disease :
o Migration of neural crest cells begins at 8th week (proximal colon), migrate
along vagal nerve fibers completed by 12 th week (rectum)
o Cl/P : bowel is filled, rectum is empty, tone f anal sphincter is increased
o Sigmoid colon affected in 75% of cases, but rectum and anus always
involved
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❖ Meckel’s diverticulum:
• Clinical picture of Meckel’s diverticulum → gastric mucosa (being the
commonest) → hematochazia & melena, pancreatic mucosa (2 nd most
common)
• When vitalline ducts obliterate? Week 7
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❖ Malrotation and midgut volvulus :
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• The gut herniate through the umbilicus at week 6, re-enter the abdominal
cavity after 270o counter-clockwise rotation. At week 8 – 10 week. The gut
is normally fixed to the wall by wide based mesentery
• In mal-rotation, the caecum is present at RUQ instead of RLQ with
persistant of Ladd’s band (pass from the caecum and right colon to
retroperitoneum encircle 2nd part duodenum)
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❖ Complications follow the gastro-jujenostomy operation: iron deficiency
anemia will occur as iron is absorbed mainly in duodenum & proximal
jujenum, also malabsorption of Vitamin D, B12, Calcium
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❖ Colonic polyps:
Tubulo-villous polyp
Serrated polyp
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• Signet ring carcinoma : signet ring means clear cytoplasm with
peripherally located nucleus
• Villous adenoma: long like villi extending from the surface, often large
& sessile.
Can cause watery mucus diarrhea, electrolyte imbalance.
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• Tubular polyps: small, pedunculated. Consists of dysplastic colon cells in
tubular architecture.
❖ Tubulo-villous adenoma:
Pic. 1 (villous) pic. 2 (tubular component)
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❖ Colon carcinoma :
o Right colon : IDA, nonspecific symptoms
o Left colon : IO, change in bowel habits (alternating constipation &
diarrhea is characteristic for IBS)
o Recto-sigmoid : hematochazia
o Rectum : tenesmus, small caliber stool
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❖ Mention the difference between cancer associated CRC & sporadic CRC in
terms of age of onset, origin, location, multifocality histoly & mutations
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❖ Mutation of APC gene of 5q → ↑↑ β-catenin → uncontrolled cell proliferation.
❖ Adenoma carcinoma sequence (other gene abnormalities):
• Inhibition of caspases → cysteine proteases that essential in apoptosis
• Increased activity of COX-2 enzyme → found in many forms of colon
cancer & inherited polyposis syndromes
This may be due to need for PGs → epithelial proliferation
Regular aspirin intake is associated with ↓↓ risk of colon cancer
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❖ Pathogenesis of ascites in cirrhosis :
• Mechanical compromise of the portal venous blood, ↑↑ vasoactive peptides
→ vasodilatation of splanchnic vessels & vasoconstriction of the systemic
vessels ➔ ↑↑ portal vein hydrostatic pressure
• vasoconstriction of systemic vessels → RAAS → Na & H2O retention →
more ascites
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▪ Due to estrogen effect on arteriolar dilatation.
▪ Correlate with the severity of liver diseases
▪ SHBG → produced from liver + uterus / testis
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❖ Pathogenesis of Reye’s syndrome :
• Hepatic dysfunction: with vomiting, hepatomegaly and all lab finding of
hepatitis but no jaundice, it show microvesicular steatosis (small fat
vacuoles in the cytoplasm)
• Encephalopathy: due to the hepatic dysfunction & hyperammonemia
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❖ Mechanism of hepatic encephalopathy: ↑↑↑ ammonia in the blood → altered
amino acid transport across BBB, ↓ neuro-transmitter metabolism ➔ ↑↑
GABA, ↓↓ glutamate
❖ Any liver disease, notice the relation & ratio between AST, ALT… it
may be the clue
❖ Hepatitis A virus:
o Outbreaks usually from contaminated water, food, steamed shellfish (USA)
o Clinical picture : children ➔ mostly silent or anicteric, adults ➔ severe
icteric , aversion to smoking
o Vaccine → given to high risk peoples, unvaccinated contact
❖ Hepatitis D virus :
o It resemble the Dane particle of HBV
o HDAg – replication defective as it must be coated by the external coat
HBsAg to penetrate hepatocyte either super/Co-infection
❖ Clinical picture of acute hepatitis B virus:
• Incubation period ~ 3months
• May develop serum sickness like syndrome + RUQ pain
• Extensively ↑↑ AST & ALT, mostly non-icteric hepatitis
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• +/- ↑↑ PT = poor prognosis
❖ Histo-pathology of acute viral hepatitis (all of them give the same picture)
• Panlobular lymphocytic infiltrates
• Ballooning hepatocytes
• Hepatocytic necrosis & apoptosis→ form rounded acidophilic bodies
called Councilman bodies or apoptotic bodies
• Kupffer cells → phagocyte hepatocellular debris → hypertrophy & laden
with lipofuscin pigment
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❖ Effect of rifaximin & uses :
• Action: ↓↓ bacterial RNA synthesis by binding with DNA dependant RNA
polymerase
• Non absorbable antibiotic that affect GUT flora
• Used with lactulose (↓↓ PH → ↑↑ conversion of ammonia to ammonium)
• Used in traveler’s diarrhea
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❖ Biliary atresia:
o The baby born normal, extra-hepatic biliary tree undergo destruction
either immune mediated or viral mediated.
o Clinical picture reveal firm hepatomegaly (due to inflammation), absent or
abnormal GB
o Clinical picture & lab is consistent with obstructive jaundice
o Biopsy ➔ IHBRs proliferation, portal tract edema & fibrosis
o Once diagnosed → Kazai operation if not death in 2 years due to biliary
cirrhosis
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❖ What is the cause of DUbin Johson syndrome : AR disorder due to mutation in
bilary transport protein called multi-drug resistance protein 2
❖ Dubin Johnson syndrome :
• Due to mutation in canalicuar membrane transport protein
• The liver appears black → impaired excretion of epinephrine
metabolite that accumulates in the hepatocyte within
lysosomes.
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❖ Copper metabolism ******:
o Copper is absorbed in stomach & duodenum → bind loosely with albumin to
reach liver
o In liver; copper + α2 globulin ➔ ceruloplasmin → secreted to the plasma
o Ceruloplasmin & un-absorbed copper → secreted into bile & excreted by
feces (primary route for copper excretion)
o Renal loses of copper represent 5 – 15% of daily excretion.
❖ Hemochromatosis :
o First clinical picture appear when total iron > 20 g
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o Clinical picture include atypical arthritis (psudogout), hypogonadism
o ♀ protected from early onset due to blood loss in menses, pregnancy
o Hisotloogical picture differentiate iron from lipofuscin by perussian blue
stain.
▪ Hemosiderin contain ferrous → turn blue on stain
▪ Lipofuscin don’t contain ferrous → don’t turn blue
▪ Both appear brown deposits
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❖ Histological features of GVHD in liver :
• Similar to PBC: lymphocytic inflammation, destruction of IHBR, necrosis
of periportal tissues, granulomas & bile staining
• GVHD → commonly affect skin, liver, GIT
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❖ Cholesterol excretion is done by 2 different mechanisms :
1) Conversion into bile acids: cholesterol is changes to bile acids → bile salts
2) Free insoluble cholesterol:
• ↑↑ free cholesterol & ↓↓ bile salts ➔ precipitation of formation of
cholesterol stones
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❖ Characteristics & composition of pigment gall stones:
- Usually significant number, small speculated and friable
- High amount of calcium carbonate & phosphate → often radio-opaque on
x-ray
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❖ Biliary sludge:
• Gall bladder hypomoility → ↑↑ dehydration of the bile → precipitation &
accumulation of materials → sludge (GB mud)
• Cholecystokinin cause only partial & slow emptying of the GB
• Biliary sludge is a known precursor of cholesterol stones, cause biliary colic,
cholecystitis also.
❖ Gallstone ileus :
o Cause intermittent bowel obstruction, till it reach ileo-cecal valve →
cause complete SBO
o Pneumobilia is also exisit
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❖ Hereditary pancreatitis :
• Trypsin is secreted in inactive form, premature activation of trypsinogen =
acute panceatitis.
• Multiple mechanisms to avoid the premature inactivation
1) Production of serine peptidase inhibitor Kazal type 1 (SPINK 1)
act as trypsin inhibitor. Mutation of this protein cause rare hereditary
panceatitis
2) Trypsin can act as its own inhibitor → by cleaving active trypsin.
❖ Risk factors for pancreatic cancer: (+) smoking (the most important
environmental factor) , MEN syndrome , Peutz-Jeuher syndrome, Lynch
syndrome
❖ Acute pancreatitis:
• Premature (intra-cellular) activation of trypsin is due to acinar damage
either directly or due to impaired blood flow
• 80% of cases are due to stones, alcohol. 20% are other causes (+)
sulfasalazine, coxackie virus, M. pneumonie, structural abnormalities in the
pancreas
• Hypertriglyceridemia :
- ↑↑ TGs → ↑↑ FFA (normally bind to albumin)
- If TGs > 1000 → beyond binding capacity of albumin → FFA directly
injured the pancreatic acinar cells
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❖ Pancreatic pseudo-cyst:
o Unlike true cysts lined by epithelia cells, pseudo-cysts lined by granulation
tissue and fibrosis
o Mature psudocyst → after 4 – 6 weeks become fibrotic wall
o Mostly at lesser curvature
❖ Alcohol induce pancreas to secrete protein rich fluid that precipitate inside the
pancreatic ductules and plug the duct → calcify
Chronic alcoholic cause macrocytosis even in absence of anemia
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GIT PHARMACOLOGY
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❖ Adverse effects seen after discontinuation of PPI :
Long use of PPI → ↓↓ H secretion → ↑↑ gastrin roduction → ↑↑ parietal cell
hypertrophy. Sudden withdrawal of PPI lead to rebound gastric aci
hypersecretion & recurring of symptoms so PPI must be
tapered slowly
❖ Indications for use celecoxib: any patient need aspirin but have PUD or
bleeding tendency as celecoxib have potent anti-inflammatroy properties but
without these effects
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Misoprostol → used for NSAIDs induced peptic ulcer
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• Vestibular nausea: due to irritation if the cochlea & vestibule (e.g.
motion sickness, vertigo) → activation of H1 & M1 receptors in the inner
ear ➔ best treated with muscarinic antagonists, anti-histaminincs
• Centeral nausea: due to irritation of D2 receptors in CTZ (in area
postrema) e.g. in migraine ➔ best treated by anti-dopaminergic
drugs, ondansteron → if not effective, add NK 1 receptor antagonists
(prevent substance P) these drugs are used mainly in cancer induced
chemotherapy
• NeuroKinin 1 antagonist →Aprepitant, Fosaprepitant
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