Surgery SPOTS

1.Crohns dis
Ulcerative colitis
Skip lesions
Continuous
Cobbled appearance
Lead pipe appearance
Deep ulcers
Small supf ulcers
Longitudinal, tortuous ulcers
Pseudopolyps and rough mucosa
Haustra preserved
Haustra destroyed
Shortening less noticible
Bowel shortened
Local stenosis
Large bowel and rectum involved
Small bowel involved with colon in 50%
Sometimes mild distal ileitis
Rectum spared in 50%
N, small bowel not involved
Microscopic characteristics
Infl penetrates through bowel wall
Infl confined to mucosa and submucosa
Crypt abscess rare
Crypt abscess is common
Granuloma is common
Granulomas is rare
Complications
Crohns
UC
Abscesses
Ca of colon
Fistulae
Toxic megacolon
Bowel obstruction
Perforation of colon
Ca of colon
Haemorrhage
Ca of small bowel
stenosis
Toxic megacolon
stenosis
Systemic Cx of both:
Skin and mucosal lesions pyoderma gangrenosum + aphthous stomatitis
Uveitis
Arthritis and ankylosing spondylitis
Pericholangitis, sclerosing cholangitis, gallstones
Indications for surgery
Crohns
UC
Perforation = abscess/ fistula
Perforation
Obstruction that does not respond to Rx
Obstruction
Uncontrollable bleeding
Uncontrollable bleeding
=acute lesion resection of macroscopic
involved part
= chronic lesion fibrotic stricturoplasty
No response to conservative Rx
Toxic megacolon
Ca severe dysplasia
Children with FtT
Total colectomy remove colon and rectal mucosectomy

Ileostomy or ileal pouch with anal anastomoses

Pain in acute cholecystitis

Visceral pain dull, non specific, poorly localised arises in R hypochondrium

Infl worsens pain spreads to rest of abd, back and shoulder
Somatic peritoneal pain sharp localised, specific in R hypochondrium =
perforation!!!
Murphys sig pressure applied to R hypochondrium patient gasps with pain
Acute pancreatitis
Chronic pancreatitis
Severe abd pain, radiates to back
Attacks of severe abd pain/20% asymptomatic
days to months
Rapid pulse, shocked
Malnourished, emaciated
Guarding
Dependened on analgesics
Doughlike consistency
Impairment of exocrine fnc DM, malabs,
steatorrhoea
Ileus no bowel sounds
Small % prod pseudocyst
Pseudocyst as cx
Pale fatty stools on H2O
Haemorrhagic Grey-Turner sign
Loss of appetite, LOW, insomnia
=costovertebral angle
Cullen sign periumbilical
Perforated organ by PU
Acute cholecystitis
MI
Peptic ulcer dis
Irritable bowel sd
Ca
Gallstones
Acute intestinal obstruction
Mesenteric vascular occlusion
Renal colic
Dissecting aortic aneurysm
Ct dis with vasculitis
Pneumonia
ketoacidosis
Gallstone pancreatitis
older women, Hx of previous cholecystitis, no
previous attack
Imparcted stone in Ampulla of Vater -> bile
reflux into pancreatic duct -> extravasation of
enzymes
Gallstones in g.bladder and bile duct

Alcoholic pancreatitis
younger men, OH abuse, previous attacks
Increased protein content in pancreatic juice

Prot precipitate out and cause obstruction of

smaller pancreatic ducts

Acute pancreatitis
OH & gallstones = more than 80%
Hypertparathyroidism .: Ca 2+

Chronic pancreatitis
OH ->acute panc -> tissue destruction&
calcification
Obstruction of exocrine ducts:
1. Stenosis of sphincter of Oddi
2. Stenosis of pancreatic duct
3. Pancreas divisum
CF
Coelic fibrosis
Bile duct tumours
Nutritional AN

Hyperlipidaemia
Drugs: steroids, cyclosporine A, tetracyclines
Viral infections = mumps,Coxsackie B ascaris
Trauma
idiopathic
Oedematous interstitial pancreatitis
Chronic inflammation
Obstructions of ducts
Permanent destruction of tissue
Congestion
=>exocrine tissue destroyed first
Oedema
=> then endocrine
obstruction = complete recovery
Necrotising pancreatitis
>85% destroyed= insufficiency
Obstruction& Inflammation
Cx:
Enzyme release
Pseudocyst
Collagenase: c.t.
Stones and strictures
Lipase: neutral fat
Biliary strictures
Elastase: blood vessels =
duodenal stenosis
haemorrhage
pHT
Cx: secondary infection; recurrent:
Ca
calcification
Functions of Saliva
Digestion amylase, lingual lipase
Lubrication
Solvent
Oral hygiene
Excretion
Regulation of water balance
Tonus of LOS
tonus
tonus
Gastrin
Secretin fat digestion
glc
Progesterone pregnancy
Motilin
OH
H1 receptor
H2- receptor

PgF
Ach: muscarinic Rec
- Receptor
Substance P
Serotonin
Histology of salivary glands
Parotid
Largest
Surrounded by dense ct
capsule
Lymph & fat in septa
Tubule-alveolar gland
Uniform SEROUS

PgE
Ach: nicotine rec
- Receptor
VIP
GIP
Submandibular

Sublingual

Dense ct capsule

NO ct capsule

Compound tubule-alveolar
Compound tubule-alveolar
MIXED:
MIXED:
20% - mucinous = serous
80% - mucinous = serous
demilumes
demilumes
80% - serous
20% - serous
Difference btw squamous cell ca and adenoma
Squamous cell Ca
Adenocarcinoma
Most common
Common in Western society
Middle or thoracic oes
Distal end of oes gastric Ca which affects
oes
Painless, progressive
Complication of GORD
dysphagia, LOW
Different growth patterns
Intestinal Metaplasia
Detected late
Detected early on followup of Barrets/PU
Spread:
Transmural
Contiguity
Lymphatics
haematogenous
DD
Infectious mononucleasis
HIV acute sero conversion
CMV
HHV6
Toxoplasmosis
Enteroviruses Cox. A, EV71
VZV
-Hand, foot & mouth dis
Herpetic gingivostomatitis
- Herpangia
Aphthous stomatitis
Portal- systemic anastomosis
location
portal
systemic
Clin pic pHT
Gastro-oes
L gastric V
Azygous V
Oes varices
anorectal
Sup rectal V cnt as
Inf & middle rectal V
Haemorrhoides

Para-umbilical
Bare area of liver

IMV
Para-umbilical V of
ant abd wall
Hep V cnt as portal V

into IVC
Supf epigastric V
Diaphragmatic V &
azygous V cnt as IVC

Caput medusa
Subphrenic abscess

Anastomoses btw foregut& midgut

Sup pancreaticoduodenal A with inf pancreaticoduodenal A (coelic+SM)
Anastomoses btw midgut& hindgut
Marginal A of Drummond btw middle colic A with L colic A
Surface anatomy of inguinal canal
1. Channel like passage through inf portion of ant abd wall
2. 4cm long from deep to supf inguinal ring
3. Runs obliquely, parallel to inguinal lig
4. Runs one fb above the medial half of inguinal lig
Hesselbachs triangle
Medial: lat borderof rectus sheath
Lateral: inf epigastric A
Inferior: inguinal lig
Contents of inguinal canal
Male
Ilio-inguinal nerve
Spermatic cord
Starts at deep inguinal ring and ends in testis
Ext spermatic fascia
Cremasteric fascia
Internal spermatic fascia
Female
Ilio-inguinal nerve
Round lig of uterus
Direct Hernia
Through abd wall through Hesselbachs
triangle
Medial to inf epigastric vessels
Prolapses through medial part of canal
through supf inguinal ring

Indirect Hernia
Transverses through deep inguinal ring ->
spermatic cord -> scrotum
Lat to inf epigastric vessels
Descends the whole length of inguinal canal

Round
Oval
Older people
Younger ppl
Less Cx
More Cx
Splits transverse fascia
Patent processus vaginalis
Extends anteriorly
Extends medially
Cx of inguinal hernias
Incarceration: inducible, obstruction
Strangulation: blood supply of incarcerated hernia is compromised ->ischaemia ->
bowel necrosis
Sliding hernia: hernia contents forms part of the hernia sac
Acute scrotum: strangulated indirect inguinal hernia (in scrotum)
Syptoms of haemorrhoids
Painless rectal bleeding bright red
Piles = prolapse
Constipation
Pruritis ani
Mucous drainage
Abdominal wall defects
1. Omphacele
2. Gastroschisis
Circular abd wall defect with umbilicus as
Slit like abd wall defect to R of umbilicus
centre
Contents is covered by translucent avascular
Bowel not covered by membrane =
membr ( peritoneum+amnion)
completely unprotected
Sac contains small, large bowel, stomach,
Sac usually conatin only bowel
liver
Other assc malformations
No other malformations except for
- vertebra
Bowel atresia
- ano-rectal
-cardiac
- trachea-oesophageal
- renal/radius
- limb
VACTERL
3. Familial polyposis
Autosomal dominant congenital
1000s of tubular adenomas in colon and rectum
Rectum is always affected
Clinical = rectal bleeding
Pre-malignant

Remove rectal mucosa and anastomose pouch of small bowel to anus

Clinical presentation of appendicitis
1. Sudden onset of epigastric/peri-umbilical pain
2. n + v
3. after few hours: shifting of pain to R iliac fossa, localised
4. direct and rebound tenderness
5. localised pain on cough, guarding
6. low grade fever + leukocytosis
7. Ro si gs sig = pai i R ilia fossa resulting from palpating the L iliac fossa
8. Psoas sign adductor pain
DD on appendicitis
Acute gastroienteritis
Ruptured corpus luteum/ ovarian cyst
Mittelschmerz
Urinary tract infection
Mesenteric adenitis
Renal colic

Perinesl team dissects out anus and removes

Continence is preserved
specimen from below
3. Hartmann procedure
- in old/weak pt
- Ca is excised, but distal rectum is closed and an end sigmoid colostomy is created
4. Adjuvant irradiation
- pre- and post operatively to reduce local recurrence
5. Chemotherapy
- 5FU regimens
- for Dukes B+C
Anatomical structures responsible for continence
Internal and external anal sphincter
Puborectal sphincter part of elevator ani muscle
Mucosa of anus

Clinical presentation of rectal Ca

Ulcer with rolled edges
-blood and mucus in stools
- tenesmus
- feeling that rectum is not completely empty after defaecation
- LOW

Histology of anus
1. Anal canal divided by pectinate line
Sup : columnar epithelium
Inf : squamous epithelium
2. Anal canal fold = anal columns
3. Epithelium changes to skin at orifice
4. Submucosa is rich in bloodvessel
5. No crypts of LieberKuehn

Dx of rectal Cancer
Same as colon Ca +
- digital rectal examination
- sigmoidoscopy, rectosigmoidoscopy
- US, XR, CT, metastases
NO BARIUM MEAL!!!

Types of anal Ca
Squamous Ca of mucosa in the anal canal above the pectinate line
Squamous Ca of cutaneous epithelium
Malignant melanoma of epi above pectinate line

Managment of rectal Cancer

1. Abdomino-perineal resection
Removal of rectum and anus
Permanent sigmoid colostomy
2 teams operate simultaneously

2. Anterior resection
Abd approach
Excision of sigmoid colon and part of rectum
with tumour and free border of 5cm
Descending colon is sutured to rectum

Management of anal Ca
Chemotherapy Nigro chemoregulation regimen: 5FU+ mitomycin for 6weeks
Irradiation for 6 weeks
Resection:
0-4 cm from anus abd.perineal resection
4-8 cm from anus depending
8-12 cm from anus anterior resection

LN palpable block dissection

Haemorrhoids Blood supply
Venous drainage
Internal haemorrhoidal plexus sup haemorrhoidal V
Portal system
- situated above mucocutaneous jnc, covered by mucosa
- varices internal haemorrhoids
External haemorrhoidal plexus -> systemic venous system
- situated below mucocutaneous jnc
- covered by skin
- Varices external varices
Cx of Haemorrhoides
Thrombosed haemorrhoids with inflammation
Prolapsed
Bleeding
Congestion
Necrosis and submucosal haemorrhage
Strangulation
Secondary infection
Management of colon Ca AdenoCa
1. R ascending colon:
R hemicolerectomy
Lymphatics adjacent to ieocolic vessels
Iliotransverse colonic anastomosis
2. L descending colon:
L hemicolrectomy
Incl splenic flexure
Ascending colon is anastomosedto descending colon
3. Transverse colon:
Resection of transverse colon
Incl hepatic and splenic flx
Ascending colon is anastomosed to descending colon
4. Sigmoid colon:
Resection of sigmoid colon and part of descending colon
Remove IMAand branches to eliminate lymphatic drainage
Mobilze splenic flx

Anastomose decs colon to anus

Dukes criteria = colorectal Ca
1. Dukes A: confined to mucosa 5 yr survival 90%
2. Dukes B1: infil through m.mucosa, but confined to bowel wall 80%
Dukes B2: infil through serosa 60%
3. Dukes C1: fewer than 4 LN involved 40%
Dukes C2: more than 4 LN involved 20%
4. Dukes D: distal metastases 5%
Causes of Appendicitis
Acute because of obstruction:
Faecoliths
Food residues
Lymphoid hyperplasia
Carcinoid tumour
TB, typhoid, yersinia, actinomycosis
Cx of acute appendicitis
Perforation -> peritonitis -> subphrenic abscess
Abscess
Fistula
Mucocele
Blood spread
septicaemia
- liver abscess
- suppurative pyelophlebitis
Diverticulosis
In sigmoid colon
Muscle wall thickened, lumen narrowed
Wall of diverticulum contains no muscle only mucosa close to blood vessel
Me kels di erti ulu : full thi k ess us le all
Causes
Low fibre diet
abd pressure

Complications
Diverticularis
Pericolic abscess

- Stenosis, circumferencal filling defect, destroyed

mucosal pattern
XR, CT for staging, metastases

Fistulae
Perforation
Haemorrhage

Causes of lower GIT bleeding

Infl bowel disease
Diverticular dis
Piles and fissures
Polyps
Metastatic dis
Colon Ca L
Kaposi sarcoma
Premalignant colonic conditions
Familial polyposis
Gardners sd
UC
Crohns
Neoplastic polyps adenomas - tubular, tubulovillus, villus
Clinical presentation of Ca of colon
R ascending colon
Wide lumen, thin elastic wall, liquid contents
Fungating growth pattern
- fatigue, weakness underlying anaemia
hypochromic
Occult blood +
Pain in RHchondrium

L descending colon
Smaller lumen, semisolid faeces
Tumour infiltrates circumferentially ->
stenosis
Fatigue
Change of bowel habits
Constipation/ diarrhoea
Blood in stool
Vague/colicky pain due tu obstruction

Dx of colonic Ca:
Faecal occult blood
CEA carcino embryoinic Ag
Sigmoidscopy and colonoscopy
Barium enema: R
- filling defect = polypoid
- destroyed mucosal pattern
L
- apple core appearance

Motility of large intestine

1. Mixing
1. Large circular constrictions
2. Combined with longitudinal strips = haustra
To expose all faecal materials to surface -> absorption of fluid -> semifluid ->
semisolid
2. Propulsive
1. slow haustral contractions NB in caecum and ascending colon
2. mass movement:
NB in transverse and sigmaoid colon
Constrictive ring at area of distension
Then rapidly 20 cm distal to constriction loose haustration contract as a unit ->
forcing faeces down colon; when in rectum, desire to defaecate
3. Retroperistalsis
1. from transverse colon to caecum -> time in prox of colon for abs
Control of peristalsis
Gastrocolic reflex to empty bowel as soon as stomach is full
Duodenocolic reflex
Extrinsic nerve supply
Complications of Constipation
Children
Abd pain
encopresis
Enuresis
Anal prolapsed and fissure
FtT

1.

2.

Adults
Haemorrhoids
Spastic colon
Diverticular disease
Colon Ca

Approach to GIB in children

Clinical
Severity vital signs, HCT, ongoing losses
Acute onset or chronic blood loss: Fe deficiency
Stigmata of dis: FtT, purpura, liver and spleen
Management
Resuscitation as required -> Ringers lactate

Stop bleeding
- mostly spontaneous
- Vit K
- blood component therapy
- emergency endoscopic approach

3.

ID site of haemorrhage
Hx
Character of blood
- haematemesis = fresh/ coffee ground
- haematochezia = fresh with stool/ mucous/ jelly dark
- melaena = tarry black
- upper gut endoscopy
- lower gut contrast studies/ isotope scan/ endoscopy
4. ID and manage aetiology
5. follow up for recurrence

Diarrhoea
Osmotic
Disappears with fasting
Disappears with ingestion of offensive
substance
Electrolyte abs is not impaired low
[electrolyte] in stool and water
Cause:
Ingestion of poorly abs elements
= MgSO4, MgPO4, mannitol, sorbitol
= lactose intolerance
Excessive water is drawn into lumen

Secretory
Does not disappear with fasting
Not
Electrolyte abs impaired
Cause:
Infection - cholera
Enterotoxins
Peptides fromendocrine tumours VIP,
calcitonin
- Net secretion of Cl- or HCO3
- inhibition of net Na+ abs
-stimulated sectretion by epi cells

Mixed = Rota virus

Abdominal Pain
1. Organic, dysfnc, psychogenic
2. Recurrent abd pain = RAP 3> episodes in last 3months/ 1 episode/ month for last 3
years.
Organic abd pain
Dysfnc abd pain
< 5yr, >14yr
9yr 5-14yr
Pain located away from umbilicus,
Peri-umbilical pain, gradual onset,
specific& localised
constant, vague

Pain radiates to the back, shoulder or

Pain does not radiate/ minimally
elsewhere
Nocturnal pain that wakes child up
Pain does not wake child up
Pain aggrevated/ relieved by eating
Pain unrelated to meals, activity, foods
Vomiting, LOW, anorexia, change in stool
Pallor, tiredness
pattern
Abd mass/ organ enlargement
Soft, non-distended abd
- occult/ fresh bleeding
More common in girls
- urine AN
- AN blood count
- anal skin tags
Assc with fever, rash, jaundice,
listlessness
Family Hx: PU, CF, lactose intolerance
Hirschsprungs dis = congenital intestinal aganglionosis
1. Pathology:
No ganglion cells in neuronal plexi of bowel wall
No wave of relaxation which precedes peristalsic contraction
2. Clinical:
Neonates: delay in passage of meconium, stooling
Older children: FtT, chronic constipation, abd distension -> megacolon
Rectal exam: explosive decompression
3. Complications:
Perforation of caecum -pressure in colon
Fulminating enterocolitis
4. Diagnosis: XR, Barium meal, another XR after 24h, rectal biopsy -> no ganglion
cells
5. Rx: colostomy at 6 months
Neonatal bowel obstruction
Intestinal obstruction: vomiting, distension, constipation
Duodenal, jejuno-ileal atresia
Meconium ileus -> CF
Intestinal malrotation = volvulos
Hirschsprung dis
later in life
Hypertrophic PS 3-6 weeks of age, projectile, non-bilious vomiting
Intussusceptions 5-9 months; Roat virus = lead point
Adhesion
Strangulated inguinal/ umbilical hernia

Causes of small bowel obstruction

Extrinsic
Adhesions
Hernias strangulated
Tumour
Intussusceptions
Volvulus
Intrinsic
Croh s dis
Radiation stricture
Ischaemic stricture
Tumour
Intraluminal
Food bolus obstruction
Gallstone ileus
Trichobezoar
Symptoms of dyspepsia
1. Abd pain/ discomfort
2. Early satiety
3. Bloatedness
4. Nausea
5. Distension
Organic pain
Pathology; ID cause for symptoms, symptoms
disappear with Rx
Localised abd pain
Nocturnal pain
Assc with maels
Non-recurrent
Causes:
- PUD
- gastric Ca
- symptomatic gallstones
- pancreatitis/ Ca
DM gastroparesis
Mesenteric ischaemia
Complication of PUD
Haemorrhage
Perforation

GOO
Penetration into surrounding organs with fistula formation
Malignant transformation rare
Pathogenesis and pathology of H.pylori (GN bacillus)
Pathogenesis:
Lives beneath mucous layer, where pH almost neutral
Buffers acidity by prod of urease -> produces NH4+ from urea
Raises pH around H.pylori
Release of cytotoxins -> local inflammation -> chronic gastritis
Pathology:
Stimulates acis production by parietal cells
Reduces mucosal resistence to acid and pepsin
In 1%; pangastritis -> gastric atrophy and hypochloridia -> proliferation of H.pylori
-> mutagenic nitritis -> predisposition to Ca
Diagnosis:
Endoscopy with biopsy
Barium meal
Urea breath test for H.pylori

Functional dyspepsia
No structural/ biochemical AN
Vague pain in central abd
No nocturnal pain
Not assc with meals
Recurrent episodes
Causes:
IBS
Motility disorders

Causes of abd distension in children

1. Fluid
2. Gaseous distension
3. Faeces retention
4. Tumours
5. Inflammatory masses (peritoneal LN, abscesses)
6. Organ enlargement incl bladder
Causes of ascites in children
1. Lymphatic obstruction: TB, congenital, neoplastic
2. intarvascular hydrostatic pressure: pHT
3. intarvascular oncotic pressure: hypoalb
4. Inflammation and permeability : peritonitis
5. Na+ and H2O retention by kidneys
Clinical features of gastric ulcer
Epigastric pain
N+v
Reflux

Anorexia and LOW

Perforation = haematemesis + melena

Management of GU
1. H.pylori eradication
PPI + clarithromycin+ amoxicillin/metranidazole
PPI+ bismuth+ tetracycline+ metranidazole
2. Medical treatment
Antacids Al, Mg, Ca salts
H2 Receptor blockers Cimetidine, Ranitidine
PPI Omeprazole
Mucosal protective agents
Sucralfate
Misoprostol PG analogue
Colloidal bismuth compound
3. Lifestyle changes
stop smoking, avoid NSAIDS, no/moderate OH
4. Surgical Rx
Gastrectomy = Billroth 1 anastomoses
Vagotomy
= truncal + drainage
= truncal and antrectomy
= highly selective vagotomy
Approach on to obstructive jaundice
LFT:
conjugated BR
ALP
N serum alb
GGT
ALT, AST
Radiological investigations
ERCP
US
PTC
MRCP
CT

Impila poisoning
Callipses laureola in herbal medicine
Hypoglc
Renal damage
Centrilobular necrosis of liver
Sudden vomiting, diarrhoea, convulsions, coma
No jaundice, acidotic, floppy
Biochemical evidencve of liver failure

High mortality and residual morbidity

Infant with persistent jaundice
Neonatal hepatitis
Pig stools = yellow
AST/ALT
GGT/AST ratio <2
Serology might be +
Scan no obstruction
Refer in due course
Cultures might be +
Traet accordingly
Causes of HCC:
Hep B/C
Liver cirrhosis
Aflatoxin = Aspergillus

Reye sd
Preceding viral inf treated with salicylates
Progressive anicteric hepatic encelopathy
and microvascular fatty infiltration of
viscera
No jaundice, mtb acidosis, hypoglc
Biochemical:
AST, ALT
NH3
Prolonged PT
alb serum
acute phase reactants
Leucocytosis
High mortality and morbidity in
SURVIVORS
Biliary obstruction
White stools
AST/ALT/GGT
Serology might be Cultures Scan obstruction
Explanatory laparotomy/ intraop
cholangiogram
GGT/AST >2
Early surgery if possible

Factors that influence intestinal flora

pH stomach antacids, PPI pH
antibiotics disturb commensals -> superinfection
pyloric stenosis - bacteria in mouth
diarrhoea - bacteria
stasis - bacteria
diet high meat bacteroids
IM - candida

Liver tumours
Benign
Haemangioma cavernous/most common
Adenoma
Biliary Harmatoma
Focal nodular hyperplasia

- HBsAb IM
If markers are positive repeat serology after 6 months
HBsAg still + - chronic carrier
HBeAg still + - supercarrier highly infective
2. HBV DNA PCR
Qualitative
Quantative, viral load

Malignant
HCC = hepatoma 85%
Cholangiosarcoma
Angiosarcoma
Hepatoblastoma
Fibrolamellar hepatoma

Clinical presentation of pHT

1. Haemorrhage
2. Jaundice
3. Hepatosplenomegaly
4. Ascites
5. Caput medusa
6. Encelopathy
7. Signs of liver dis clubbed fingers, spider naevi, palmar erythema
Complications of pHT
1. Oes varices/ GIB
2. Hypersplenism
3. Ascites - lymph formation on surf of liver and intestines
4. Renal failure - alb
5. Hepatic encephalopathy

Diagnosis of HCV
1. Serology of blood
Anti HCV = exposure
2. HCV RNA PCR
Qualitative
Quantative, viral load
3. RIBA radio immunoblot assay
Detects viruses itself
4. Genotyping
Prognostic and therapeutic value
Generall Lab request
HAV: anti-HAV IgM
HBV:
1. HBsAG
2. HBcAb/ anti-HBc
3. HBsAb/ antiHBs
- HCV: anti-HCV
HBV infection
Past HBV infection
HAV anti-HAV IgM HAV anti-HAV IgM HBV 1. HBsAg +
HBV 1. HBsAg 2. anti-HBc +
2. anti-HBc +
3. antiHBs 3. antiHBs +
HCV anti-HCV HCV anti-HCV

Clinical presentation of liver cirrhosis

Anorexia, LOW, malaise
pHT
liver disease
Complications of liver cirrhosis
liver failure
pHT
HCC
Diagnosis of Hep B
1. Serology on blood
Antigens:
-HBsAG = active infection
-HBeAg = greater infectivity
Antibodies:

- HBcAb IgM
- HBcAb
- HBeAb

Complication of gallstones
Cholecystitis
Gallstones ileus
Stones of bile duct -> obstructive jaundice
Cholangitis
Benign bile duct stenosis

HBV vaccinated
HAV anti-HAV IgM HBV 1. HBsAg 2. anti-HBc 3. antiHBs +
HCV anti-HCV

Gallstone pancreatitis
Ca of gallbladder
5 most NB causes of jaundice
1. OH
2. Drugs
3. Gallstones
4. Viral infection
5. Cancer
Imaging of bile duct
1. Ultrasound
Shows dilated bileducts obstructive jaundice
Gallstones in ducts or gallbladder
Mass in head of pancreas
2. ERCP
Dye injected in bile and pancreatic duct
Shows filling defects in dilated ducts gallstones in ducts
Narrowing of bile/pancreatic duct proximal dilatation Ca of head of pancreas
1. US
2. ERCP
3. CT
4. MRCP
5. PTC
6. Operative cholangiography
7. Post-op cholangiography
8. AXR
9. Radio-nuclide imaging
Risk of cholesterol stones
Forty +
Female
Fertile
Fat
Fair
Family history
Functions of liver
1. Nutrient and Vit mtb

synthesis of:

aa, plasma proteins

Glucose, glycogen
Fatty acids
Bile acids
Urea
2. Storage glycogen, fat, Vit ADB12, Cu, Fe
3. Blood reservoir 350ml
4. Filter bacteria, RBC
5. Detoxification and degradation
By conjugation, oxidation, methylation
Body waste, hormones, drugs
6. Bile secretion excretory and secretary fnc
Bilesalts
Bile pigments(BR)
Hepatic N and AN fnc
Normal
Abnormal
Synthesis and secretion of circulation
1. Albumin
1. Oedema
2. Coagulation factors I, II, VII, IX,
2. Coagulopathy - prothrombin time
X& - antitrypsin
Intermediate mtb of nutrients
1. Glucose
1. Hypoglycaemia
2. FA& cholesterol
2. s-cholesterol
3. Amino acids
3. branched aa, oromatic aa
Biotransformation of lipophilic compounds
1. Protein urea
1. Hepatic encelopathy
2. Drugs
2. sensitivity to Rx
3. Unknown factors
3. Hyperdynamic circulation
Salt retention
Ascites
Cerebral oedema
Bile formation
Pruritis, jaundice
Brain centers involved in vomiting
CTZ
Vomiting center
Outside bbb
Inside bbb
Neurotransmitter = dopamine, serotonin
Neurotransmitter =acetylcholine
Anti-emetics = dopamine antagonist =
Anti-emetics = muscarinic antagonist and
metocloperamide
antihistamines cyclizine (Valoid), meclizine
Anti-emetic drugs
1. 5-HT3- receptors antagonists

= serotonin => granisetron, ondanosetron, tropisetron

Chemotherapy induced vomiting
Peripheral and central receptors
Can prevent vomiting up to 24hr
2. Metoclopramide
Dopamine antagonist = CTZ
Used in radiatin sickness, post-op, drug-induced/ mtb nausea
Extrapyramidial SE akathasia, dystonic, dyskinesia, Parkinson-like symptoms, children:
convulsions, neuromuscular
3. Anti- histamines
Vomiting centre
Teratogenic
Motion-sickness
Cyclizine Valoid 4-6hrs
Meclyzine 12-24hr, more sedating
Functions of following enzymes
gastrin
CCK
HCl
Released from duodenum
when chime is released
IF
pancreatic enzymes
released
pancreatic secretion
Contraction of gallbladder&
relaxation of Oddi
intestinal secretion
emptyning of stomach

Secretin
Stimulates ducts and
epithelium in pancreas
NaHCO3- in duodenum
- neutralizes chime
- optimal pH for enzymes
Emptying of
stomach

insulin secretion
Hypertrophy of gastric mucosa
perfusion of gastric walls
Contraction of GOS, small intestine
Relaxation of sphincter of Oddi

Bilesecretion
1. Hepatocytes flows peripherally
[bile acids], [cholesterol] + organic substances
2. Ducts adds watery solution of Na+ and HCO3- = bilecanaiculi -> terminal bileduct->
hepatic duct-> common bile duct
nd
2 secretion stimulated by secretin, bile as much as 100%

DD on acute cholecystitis
3. Pancreatitis
4. Perforated PU
5. Renal calculus
6. Acute appendicitis
7. Liver infections
8. Coronary thrombosis
Complications of a sliding hh
1. Stenosis
2. Inflammatory reflux
3. Chronic bleeding ->Fe deficiency anaemia
4. Barretts oes
5. Schatzki ring
Clinical picture of lesion of the facial nerve
Paralysis of facial muscle =
1. Cant show teeth
2. Drooling
3. Cant blow out cheeks
4. Blinking, eye closure
5. Cant raise eyebrows
6. Pucking of lips
Management of Ca of tongue
anterior 2/3
9. T +T : & irradiatio if ell differe tiated
free order
10. T3: irradiation + N1, N2; elective resection of LN, block dissection, N3 irradiation
Posterior 1/3
11. Late, anaplastic
12. Irradiation
13. LN block dissection
14. Poor Px
Oral lesions in AIDS pt:
15. Oral hairy leukoplakia EBV
16. HHV8
17. Severe herpes labialis

18. CMV oesophagitis

19. Candida
Contents of saliva
99.5% - water
0.5% - electrolytes
Proteins
Glucose
Digestive enzymes
Lysozymes
NPNs
Mech of salivary secretion
Acinar level
1. Active secretion of Cl into lumen (Na/K pump)
2. Cl in lumen draws cations from plams into lumen
3. Osmotic gradient primary secretions = plasma
Control of secretion
1. Neuronal autonomic
2. Humoral changes in composition
Phases
1. Cephalic: smell, taste, sight, thought
2. Oral: mechano, chemoreceptors in mouth
3. Gastric: by substance which irritate/stimulate gastric mucosa
Common causes of dysphagia
1. Obstruction by foreign body
2. Ca
3. Reflux oesophagitis
4. Achalasia
5. Stenosis
6. Pharyngeal diverticulum Zenkers
Dx:
7. Endoscopy with biopsy
8. XR
9. Barium meal
10. pH studies
11. pressure studies

Anatomical factors preventing reflux:

1. intrinsic tonic constrictions
2. angle of His
3. crurae of diaphragm
4. intra-abd position of distal oes
5. mucosal rosettes
6. phreno-oesophageal ligament
7. pressure difference
Causes of heartburn in pregnancy is because of decreased tonus of LOS due to higher
progesterone levels
Management of GIB
Conservative:
a) NGT
b) IVI maintenance/ rescusce
c) Send blood sample for cross-matching
d) Suppression of gastric acid secretion Cimetidine
: - depends on indication and dx
Indications for in upper GIB
1. Relative
Pt over 50,
Bled to shock
Atherolsclerosis
Deep/chronic ulcer
2. Absolute
Persistent bleeding despite conservative management
Deep chronic ulcer with thrombus
3. Urgent
Massive haemorrhage
Stomach cannot be rinsed
Causes:
1 PU
2 gastritis
3 Mallory-Weiss tear
4 Oes varices

5 reflux oes.itis
6 Ca
Factors that increase bile production:
1. Parasympathetic
2. Secretin
3. CCK
4. Gastrin
5. Bile
Factors that decrease gastric emptying
Chyme in duodenum
volume
unprocessed food
Not isotonic
pH
Hormones
CCk
Secretin
GIP
Somatostatin
Position
Not standing
Factors that increase gastric emptying
Motilin
Insulin
Thyroxin
Gastrin
Defaecation reflex
Faeces move down the rectum via mass movement propulsions
Intrinsic reflex:
1. Distension of rectum, stimulation of myenteric plexus
2. Peristalsis in descending colon, sigmoid& rectum
3. Wave reaches anus
Relaxation of internal anal sphincter
Voluntary relaxation of external sphincter
4. Defaecation

Extrinsic reflex
1. Parasympathetic reflex intensify intrinsic reflex
2. Stimulus distension of rectum and internal sphincter
Lactation reflex
1. Suckling ->
2. Mechanoreceptors in nipple->
3. Hypothalamus ->

4.
5.
6.
7.
8.

Nervous pathway
Posterior pituitary
Oxytocin
Contraction of myoepithelial
Cells surrounding alveoli
Milk ejection

prolactin inhibitory hormone(dopamine)

anterior pituitary
Prolactin
milk secretion

Compare small intestine with colon

Gutters and spaces
1. R paracolic exit: sup and inf
2. L paracolic exit: inf
3. R infracolic no exit
4. L infracolic exit: inf
5. R&L subphrenic spaces
6. R&L subhepatic spaces
7. Bare area of liver
Abscess of appendix -> pus in hepatorenal space-> subdiaphragmatic abscess
R paaracolic gutter-> hepatorenal spaces-> R subphrenic space-> L subphrenic space
Borders of omental foramen
Anterior: free border of lesser omentum (cnt bile duct, hepatic A proper, L portal V)
Posterior: IVC
st
Inferior: 1 part of duodenum and hepatic A
Superior: caudate lobe of liver
Recesses of omental bursa
Superior, splenic, inferior

Lymph drainage of the breast

1. Apical/ infraclavicular nodes
2. Pectoral nodes/anterior
3. Subscapular nodes/posterior
4. Central axillary LN
5. Lateral nodes
6. Parasternal nodes
7. Deltopectoral nodes
Pain
Visceral pain
Poorly localised
Vague and persistent
Central abd fore-, mid-, hindgut area
Sympathetic nerves
Foregut epigastrium T5-T9
Midgut umbilical region T9-T11
Hindgut hypogastric region T11-T12
Colicky pain
Histology of small intestine and colon
Small intestine
Mucosa
1. Villi
2. Plicae circularis

Somatic pain
Well localised
Sharp and severe
Can be referred
Somatic afferent fibres

Layers of stomach
MUCOSA
Exacerbated by movement
Colon
4. No villi
5. Plicae semicircularis

Epithelium

1.
2.
3.
4.
5.
6.

Simple columnar
Abs cells 90%
Goblet cells
Enteroendocrine cells
Paneth cells
Crypts of Lieberkuehn

1.
2.
3.
4.
5.
6.

Lamina propria

1.
2.
3.

Lacteals
Plasma cells, EP, lymphocytes
Peyers pat hes

1.
2.

Simple columnar
Abs cells
Goblet cells
Enteroendocrine cells
No Paneth cells
Colonic glands stem cells at
base
NO lacteals
GALT/MALT

Muscularis
mucosa
SUBMUCOSA

1.
2.
1.
2.
1.
2.

inner cicular s.m.

Outer longitudinal s.m.
Loose c.t
Bru ers gla ds
Inner circular
outer longitudinal

1.
2.
1.
2.
1.
2.

inner cicular s.m.

Outer longitudinal s.m.
C.t.
Large blood vessels
inner circular
outer longitudinal-> 3 taenia

MUSCULARIS
EXTERNA

coli-> Haustra
Duodenum = partly serosa/adventitia
Serosa
Rest = serosa
Omental appendices
Histology of the breast
Nipples:
i)
15-25 lactiferous ducts open
ii)
Open in lactiferous sinus
iii)
C.t. and s.m. around ducts
iv)
Glands of Montgomery in areola
Glandular tissue:
i)
Coopers liga e ts = .t septa hi h di ide i to lo es
ii)
20 glands = lobe-> subdivided lobules => compound tubule-alveolar glands
iii)
Alveoli lined by single layer of cuboidal epithelium - > RER -> protein production
iv)
Myoepithelial cells
SEROSA

Epithelium: simple columnar mucus cells

Lamina propria: loose ct, lymph follicles, gastric glands
Muscularis mucosae: circular and longitudinal
SUBMUCOSA
Loose ct
MUSCULARIS EXTERNA
Inner oblique, circular, longitudinal
SEROSA
Ct, mesothelial cells
Complications of oral infections
1. Spread
2. Cavernous sinus thrombosis
3. Septicaemia
4. Endocarditis
5. AW obstruction
6. Mediastinitis
Ludwigs angina
Streptococci, Staph, GN
Severe cellulitis
Submaxillary space-> sublingual and
submental space
Penetrating gunshot, trauma
Drainage, Pen, clindamycin

Peritonsillar abscess/ Quinsy

Group A HS and anO2
Acute infection
Btw tonsil and sup pharyngeal constrictor
muscle
Drainage, Pen, clindamycin

Cx of a retropharyngeal abscess
1. Haemorrhage
2. Rupture into AW with aspiration
3. Laryngeal spasm
4. Bronchial erosion
5. Jugular vein thrombosis
Palliative managemnent of oes Ca dysphagia
REPEATED DILATATION!!!
1. Stenting
2. Radiotherapy
3. Laser therapy
4. Photodynamic therapy
5. OH injection
6. Chemotherapy
Pathophysiology in oes Ca
1. Strictures
Dysphagia
Regurgitation - > aspiration
2. Malignant involvement of adjacent structures
Oes-tracheal fistula
Oes-bronchial fistula
Vocal chord paralysis
Pharyngeal swallowing
1. Soft palate contracts -> lifts and closes post nares
2. Elevation of hyoid, larynx -> close vocal chords
3. Tongue presses on soft palate -> close oral cavity
4. Longi muscle contraction of pharynx -> open pharynx
5. Relaxation of inf pharyngeal sphincter -> opens oes
6. Constriction of sup sphincter -> peristalsis -> forces food into oesophagus
7. Swallow
Vomiting mechanism
1. Deep inspiration
2. Closure of glottis
3. Elevation of soft palate

4.
5.
6.
7.

Abd muscle and diaphragm contraction

intra-abd pressure
Relaxation of LOS
Expulsion

Sliding hh
Stomach slides through hiatus
Gastro-oes jnc lies in chest cavity
Reflux
Covered by peritoneum
Causes of aphthous ulcers
HHV8
CMV
EBV
HPV
HSV1

Rolling hh
Stomach rolls up anteriorly through hiatus
Cardia remains in N position
No reflux

Functions of the spleen

1. Filtration of the blood
AN and aging blood cells
White cells and platelets coated with Ab
Denatured Hb Heinz bodies
Nuclear remnents Howell Jolly bodies
Fe granules Pappenheimer bodies
2. Immunological functions
Synthesis of IgG
Clearance of pathogens, opsonised erythrocytes
Production of complement
Surveillance of malignant cells
3. Haemopoeisis
In foetus
Mechanisms of splenomegaly
1. Congestion:
pHT
splenic vein thrombosis
2. immune hypertrophy
bacterial endocarditis, infectious mononucleosis

3.

4.

5.

6.

RBC destruction
Spherocytosis
Thallasaemia major
Neoplastic
Meatastatic Ca
Hairy cell leukaemia
Myeloproliferative
Myelofibrosis
Essential thrombocytopaenia, purpura
Miscellenous
Splenic cysts
Haemangioma
Abscess
Splenic infarct
Splenic A aneurysm

Management of breast Ca
OPERABLE
STAGE 1
Mass confined to breast
No nodes
No metastases
1. Modified radical mastectomy ( breast
tissue& axillary block dissection)
OR
Removal of mass with 2cm border,
complete dissection of axillary LN& irradiation
2. Adjuvant chemo
Staging via needle Bx, CXR, ALP
INOPERABLE
STAGE 3
Mass infiltrates skin/chest wall
LN >5cm &/ fixed
Advanced local disease
1. Neo-adjuvant chemo (irradiaton)
2.
3. Irradiation
Staging via Histology of lesion, oestrogen
receptors

STAGE 2
Mass confined to breast
Mobile nodes in axilla
No skin or chest wall infiltration
1. Modified radical mastectomy with
detachment of pec major for more
thorough axillary block dissection
2. Adjuvant chemo
Staging via CXR, ALP, radio-isotope liver scan,
bone scan

STAGE 4
Any local lesion
Any node involvement
Distal metastases
1. Palliative chemo
2. Hormonal treatment
3. Lo al lesio : / irradiatio

Common problems during lactation

1. Insufficient milk production
2. Cracked nipples
3. Engorgement
4. Mastitis
5. Breast abscesses
6. Breast
7. Relactation
CI for breastfeeding
1. Bilateral mastitis
2. Narcotic abuse and psychosis
3. Chemotherapy
4. Medication = lithium
5. Maternal disease: Varicella, HCV, syphilis, herpes lesion on nipple, HIV?
6. Neonatal disease: primary lactose intolerance, galactosaemia
Advantages of breastfeeding
1. Optimal nutrition
2. MP and antibodies
3. Lowers incidence of allergies
4. Lowers incidents of infant sudden death sd
5. Easily digested
6. Baby rarely overweight
7. Milk: hygienic, cheap, convenient
8. bonding btw mother and baby
9. Ovulation is suppressed = natural birth control