Gastroenterology Review

Gastroenterology History
 Dyspepsia & Heartburn
 Dysphagia & Odynophagia
 Nausea and vomiting
 Abdoinal pain
 Abdominal swelling
 Appetite/weight gain
 Diarrhoea
 Constipation
 Bleeding
 Jaundice
 Pruritus
 Dyspepsia
&
Peptic Ulcer Disease
 DYSPEPSIA (INDIGESTION )
UPPER ABDOMINAL SYMPTOMS
*EPIGASTRIC PAIN .
*BLOATING.
*FULLNESS.
* BELCHING.
*HEARTBURN .
*NAUSIA & VOMITING
*EARLY SATIETY.
 Dyspepsia
 Common problem in the community - affects up to 40%
of individuals in 1 year
 Up to 60% of patients do not have an identifiable organic
cause - “functional”
 Nevertheless can be the presenting symptom of a number
of serious conditions
 May be the only symptom of malignancy
 Has Eesophageal, Stomach and Duodenal pathologies
 May indicate underlying gallstone disease
 Warrants OGD in patients over 55 or with alarming
symptoms & signs
 Etiology of DYSPEPSIA
1-NON-ULCER (Functional) DYSPEPSIA (50 % ).
{Dyspepsia of at least 3 Months duration for which no biochemical or
structural abnormality is found to explain the patients symptoms }.
2- PEPTIC ULCER DISEASE (20 % ).
3-REFLUX ESOPHAGITIS (15 – 20 % ).
4-N.E.R.D,Motility disorders
5 -Pancreatico-Biliary Disorders.
6- Medications :NSAIDs ,Antibiotics ,Theophyllins , Irons.
7-Dietary factors :Caffeine , Alcohol.
8- Metabolic & Endocrine : D.M , Hyperthyroidism ,
9-H .pylori.

10 –GASTRIC MALIGNANCY Is found in 1 – 2 % of patients with

dyspepsia, Age > 55 years + Alarm symptoms.
 SYMPTOM PATTERNS IN DYSPEPSIA
Ulcer-type symptoms Epigastric pain Relief with food or Antacid
Pain worse at night

Reflux symptoms Acid regurgitation

Heartburn
U.G.I. Flatulence
Retrosternal pain

Dysmotility symptoms Anorexia /Early satiety

Postprandial bloating
Nausea & or Vomiting
 Dyspepsia

Functional Non-GI Causes

Dyspepsia (cardiac disease,
muscular pain, etc.)

Structural Dyspepsia
(GERD, PUD, Pancreatic
disease, Gallstones, etc.)
 (Alarm Symptoms & Signs)
Indicators for investigation
 Vomiting (persistent)
 Bleeding/anaemia
 Abdominal mass/unexplained weight loss
 Dysphagia (progressive)
 (Age > 55)
Hiatal Hernia and Gastroesophageal Reflux
GERD
 Gastroesophageal reflux (GERD)
 GER is the reflux of chyme from the stomach to the
esophagus
 If GER causes inflammation of the esophagus, it is called
reflux esophagitis
 A normal functioning lower esophageal sphincter
maintains a zone of high pressure to prevent chyme reflux
 Conditions that increase abdominal pressure can contribute
to GER
 More common in people with hiatus hernia
 Manifestations
 Heartburn, regurgitation of chyme, and upper abdominal pain
within 1 hour of eating
Characteristics of Heartburn
 Epidemiology
 ~25% of the adult population experience
symptoms at least monthly
 5% experience daily symptoms.
 Incidence increases with age
 “Alarm Symptoms”
 Urgent referral for endoscopy for patients of any
age with dyspepsia when presenting with any of:
 Chronic gastrointestinal bleeding
 Progressive unintentional weight loss
 Progressive difficulty swallowing
 Persistent vomiting
 Iron deficiency anaemia
 Epigastric mass
 Choking (acid causing coughing, shortness of breath , or
hoarsness)
 Chest pain
 Longstanding symptoms requiring continuous treatment
 Diagnosis
 Therapeutic trial (3 months)
 Endoscopy
 Alarm sx
 To note mucosal changes

 Esophageal biopsies

 Motilitiy studies
 Low LES pressures are associated with reflux
 pH monitoring ( GOLD STANDARD )
 The most precise measure for the presence of acid in
the esophageal lumen (24 hour monitoring)
 GERD Complications
 Benign stricture
 Perforation
 Haematemesis
 Barrett’s oesophagus
>3cm columnar epithelium in lower 1/3 of oesophagus
Must be confirmed by biopsy
Risk of adenocarcinoma (20% for low grade dysplasia, 50% for
high grade displasia
Monitor with OGD, PPI, ? Oesophagectomy for high grade
dysplasia in young fit adults
 GERD Management
 Advice – weight loss, stop smoking, stop alcohol, avoid
stooping
 Medical – exclude CA if >55, control acid secretion
(PPI/H2antagonist), protect oesophagus (alginates),
prokinetics (metoclopramide)
 Surgical – Nissen fundoplication
 Failed medical management
 Complications
 Long term dependance on medical therapy
 Peptic Ulcer Disease
 A break in the epithelium of the oesophagus,
stomach or duodenum
 5 – 10% of the general population will have PUD in
their lifetime, 50% will recur
 Due to Imbalance between protective and aggressive
factors
 Investigations – FBC, FOB, OGD, Urease breath
test
 0001% mortality rate
 Gastric Mucosa & Secretions

The Defensive Forces The Aggressive Forces

Bicarbonate Helicobacter pylori
Mucus layer HCl acid
Pepsins
Mucosal blood flow
NSAIDs
Prostaglandins
Bile acids
Growth factors
Ischemia and hypoxia.
Smoking and alcohol
Peptic Ulcer
 Etiology
 H.Pylori
 Almost all patients with H. pylori have antral gastritis
 Eradication of H. pylori eliminates gastritis
 Nearly all patients with DU have H. pylori gastritis
 80% of patients with GU have H. pylori gastritis

 Drugs
 NSAIDS
 Corticosteroids
No effect of spicy foods
 Hyperacidity
 Zollinger – Ellison Syndrome

 Cigarette smoking
 Rapid gastric emptying
Helicobacter pylori

80% 95% DU
GU
 H pylori and disease
Half of worlds population infected
100 % damage to gastric structure

Many infected indiviudals no (silent) disease

17 % Peptic Ulcer (90 – 95 % duodenal ulcer patients has Hp)

(70 – 85 % gastric ulcer patients has Hp)

2% Gastric carcinoma (85 % of patients has Hp)

X% Nonulcer dyspepsia (50 % non ulcer dyspepsia patients)

MALT lymphoma
Coronary Artery Disease
 NSAIDs:
 Prevalence of Endoscopic NSAID-Induced Ulceration
Mean Range

 Gastric Ulcer 15 % 10 to 30%

 Duodenal Ulcer 5% 4 to 10 %

 Clinically Significant Ulcers 2% 1 to 4%

 Risk Factor Analysis
 Family History:
For both DU and GU, FH pattern appears distinct: 1st-degree relatives of DU
patients have a 3x increase in DU; in contrast, relatives of patients with GU have
a 3x increase in the GU.
 Smoking:
Evidence supports an association between smoking and PUD in H.
pylori infected subjects, but it does not increase the recurrence of
peptic ulcers after successful eradication of H. pylori.
 Dietary fat: No association
 Coffee: No association
 High stress / Type A: In a case-control study: quantifying the # of
stressful life events and distress scores did not differentiate patients
with DU from age-matched controls.
 Clinical Presentation
 Recurrent Epigastric Pain (The most common symptom)
 Burning
 Hunger Pain ( Occurs 1-3 hours after meals )
 Relieved by food  DU
 Precipitated by food  GU
 Relieved by antacids
 Radiate to back (consider penetration)
 Pain may be absent or less characteristic in one-third of patients especially
in elderly patients on NSAIDs
 Duodenal Ulcer and Type II Gastric
Ulcer (Prepyloric and Antral)
 Male
 Hunger pain, relieved by food, periodicity
 Back pain if ulcer is penetrating
 Posterior erosion – haematemesis
 Anterior erosion – peritonitis
 Pyloric stenosis – gastric outflow obstruction
 Type I Gastric Ulcer (Proximal)

 Less male predominance (still more common

in males)
 Older age group (>50)
 Epigastric pain worse on eating
 Weight loss
 Nausea and vomiting
 Gastritis and chronic anaemia
 Peptic Ulcer Disease
 Duodenal Ulcers  Gastric Ulcers
 20 to 50 years old  > 50 years old
 High stress occupations  Work at jobs requiring
 Genetic predisposition physical activity
 Pain when stomach is empty  Pain after eating or
 Pain at night
when stomach is full
 Frequency = 4 times more
 Usually no pain at night
common than gastric ulcers
 Usually associated with
hyperacidity
 H. Pylori Diagnosis
 Serology– 90% sensitive, 95% specific – not good for
following treatment
 Biopsy– 98% sensitive – 98% specific
 Urea breath test– 95% specific, 98% specific – can be
used to document eradication
 Stool antigen test – 90% sensitive, 95% specific –
can be used to confirm eradication
 Natural History
 20 – 50% heal untreated
 80% heal in 4 weeks of treatment
 75% recur in 6 – 12 months
 More recur in patients with
H. pylori, smokers, NSAID users
 Milk and tobacco slow healing
 Management of Peptic Ulceration
 Medical : Eradication therapy for H pylori ( Tripple Therapy
)
 Surgical – Elective treatment for ulcers no longer
performed, therapeutic OGD/laparotomy for acute
complications
 Strategies in Ulcer therapy

Pre-Hp
Reduce acid
Long-term therapy!!
Take antacids
Surgery
Post-Hp
Find cause
Eliminate cause
Control symptoms in the meantime
H. Pylori Treatment
 Recurrence Rate/year in
Healed PUD

H.P(without Eradication) Anti-Ulcer Therapy H.P Eradication

G.U 59 % 25 % 4%

D.U 67 % 25 % 6%
 Dysphagia
 Difficulty Swallowing
 Types
 Mechanical obstructions ( Tumours / Stricture )
 Neuromuscular ( Stroke , Myasthenia Gravis )
 Motility & Functional obstructions ( Achalasis & DES )
 Common causes
 Young adults –Reflux strictures, Achalasia
 Older adults –Malignancy, Reflux strictures
 Investigations
 CBC
 Gastroduedenoscopy vs. Barium Swallow
 CXR
 Carcinoma of the Oesophagus
 Common (90% are malignant )
 Presents with dysphagia, weight loss, anaemia,
anorexia
 Associated with male sex, alcohol, esophagitis,
achalasia, smoking
 8% of Barrett’s develop into adenocarcinomas
 90% are squamous , 10% adenocarcinoma
 Diagnosed on Ba swallow/OGD
 5 year survival rate : 5 15 %
 Esophageal carcinoma
 Squamous cell carcinoma
 More prevalent worldwide
 Risk factors: long-standing
esophagitis, achalasia,
smoking, alcohol, diet (low
vitamins and zinc), genetics
 50% in middle 1/3
 Adenocarcinoma
 More common in USA
 Occurs on top of
Barrett esophagus
 More in distal 1/3
 Achalasia: Clinical Pearls
 Majority present between 20 to 40 years
 Solid and liquid dysphagia common >90%
 Regurgitation, weight loss, chest pain 40-60%
 Barium Study: Accuracy ~95%
 Endoscopy
 Decreased Sensitivity (retained food)
 Necessary to r/o pseudoachalasia
 More rapid onset of symptoms
 Late onset (age >60)
 Difficult to pass scope through EGJ
 Manometry
 Gold Standard
 ↑LES tone, ↓LES relaxation, aperistalsis distal 2/3 esophagus
 Achalasia: Clinical Pearls, cont.
 Treatment
 Medical (don’t usually work)
 Nitrates
 CCB

 Botulinum toxin
 Pneumatic Dilation
 Surgical Myotomy
 Heller's Myotomy. Open or laparoscopic
 Diffuse Esophageal Spasm (DES)
 Related Disorders of Esophageal Hypermotility
 Barium Study
 Corkscrew pattern
 Manometry
 >20% simultaneous nonperistaltic contractions (>30mmHg)
 Potential Therapeutic options (most ineffective)
 Medical (TCAs, Nitrates, CCBs)
 Dilation
 Botox Injection
 ODYNOPHAGIA
 Painful Swallowing
 CAUSES OF ODYNOPHAGIA

1- Drug Induced Esophagitis:

2-Infectious Esophagitis : Candidia /HSV /CMV.
3- Corrosive Esophagitis .
4- Severe Reflux Esophagitis
Drugs-Induced Esophagitis

Drug-Induced Esophagitis
•ASA/NSAIDS
•Doxycycline
•FeSO4
•Alendronate
•potassium
 Gastrointestinal Dysfunction
 Nausea
 A subjective experience that is associated with a number of conditions
 The common symptoms of vomiting are hypersalivation and tachycardia
 Anorexia
 A lack of a desire to eat despite physiologic stimuli that would normally
produce hunger
 Retching
 Nonproductive vomiting

 Vomiting ( Neuromuscular reflex )

 The forceful emptying of the stomach and intestinal contents through the
mouth
 Several types of stimuli initiate the vomiting reflex
 Projectile vomiting
 Projectile vomiting is spontaneous vomiting that does not follow nausea
or retching
 Causes of Nausea and Vomiting

 Peptic ulcer disease

 Gastric outlet obstruction
 Intestinal obstruction
 Acute gastritis
 Acute cholecystitis
 Acute pancreatitis
 Acute hepatitis
 HICCUPS (HICCOUGHS ) CAUSES
*Gastric Distention.
*Sudden temperature changes.
*C.N.S . Pathology.
*Metabolic : Uraemia /D.M / Hypocapnia /Electolytes
imbalance /Toxic drugs &Alcohol.
*Vagus &Phrenic nerve irritation.
*Surgical :Anaesthesia &postoperative.
*Psychogenic &Emotional stress.
 Constipation
 Constipation is defined as infrequent or
difficult defecation
 Pathophysiology
 Neurogenic disorders, functional or mechanical
conditions, low-residue diet, sedentary lifestyle,
excessive use of antacids, changes in bowel habits
*Medications *Metabolic abnormalities
opioids Spinal cord compression
calcium-channel blockers *Dehydration
anticholinergic
*Autonomic dysfunction
*Decreased motility
*Malignanc
Ileus
*Mechanical obstruction
 DIARRHEA
 It is a Symptom or a Sign NOT a Disease
 AS A SYMPTOM
 Frequency of bowel action A
Combination
 Looseness of stools
of these
 Increase in stool volume

 AS A SIGN
 Stools weight more than 240 gm/24 hours
 Abdominal Pain
 Is a symptom of a number of gastrointestinal disorders
 Gastrointestinal bleeding
 Upper gastrointestinal bleeding
 Esophagus, stomach, or duodenum
 Lower gastrointestinal bleeding
 Below the ligament of Treitz, or bleeding from the
jejunum, ileum, colon, or rectum
 Hematemesis
 Hematochezia
 Melena
 Occult bleeding ? Malignancy
 Upper Gastrointestinal Bleeding

Acute (> 90% of cases)

 NSAIDs
 Peptic ulcer disease
 Erosive gastritis
 Ruptured esophagogastric varices
 Mallory-Weiss tear
 Erosive esophagitis
 Upper GI Bleeds
 Young – PUD, congenital lesions, varices
 Old – Tumours, PUD, angiodysplasia
 Investigations –CBC, Fluid balance, LFTs,
clotting, OGD, angiography, cross match
 Minor bleeds – observe, monitor, arrange OGD
 Major bleeds – resuscitate, urgent OGD (PPI
given afterwards only), treat the cause
 Oesophageal Bleeds
 Reflux – small volumes, bright red, Hx
 CA – scanty debris, rusty, other symptoms
 Varices – sudden onset, painless, large
volumes, darker, portal HT *treat with
pressors*
 Mallory-Weiss – bright red, history of
vomiting
 Stomach Bleeds
 Gastritis – small volumes, bright, follows
NSAIDS/alcohol/stress
 Ulcer – larger size, painless, herald smaller
bleeds, ? coffee grounds
 CA – rare, small bleeds, suggestive history
 Congenital lesions – spontaneous in young,
otherwise well, moderate bleeds
 Duodenal Bleeds
 Ulcer – history, usually melaena present, risk
factors, coffee grounds
 Aorto-enteric fistula – rare (except in post-op
AAA patients), fatal
 Rectal bleeding - Questions
 Duration of symptoms – yrs, months
 Previous episodes or treatment
 Is the blood:
 mixed in with stool
 separate – found on toilet paper/splashes in toilet bowl
 Fresh or altered blood - ? Lower vs upper GI bleed
Main differentials :
 Haemorrhoids (piles)
 Colonic carcinoma
 Diverticular disease / bleeding ulcer
 Anal fissure
 Anal carcinoma (rare)
 Lower Gastrointestinal Bleeding
Acute (> 90% of cases)
 Diverticulosis
 Ischemic colitis
 Angiodysplasia
 Colonic polyps
 Carcinoma
 Hemorrhoids
 Radiation colitis
Gastrointestinal Bleeding
 Gastric Carcinoma
 Clinical features of all upper GI presentations with post-
prandial fullness
 Male/Female 2:1,
 Predisposing factors – diet (fish, pickled vegetables),
atrophic gastritis, pernicious anaemia, previous gastric
surgery, polyps, blood group A
 Investigations –CBC, LFT, OGD, Ba Meal, CT scan
 5 year survival rate : 5%
Common sites of metastasis include peritoneum, spleen,
pancreas, transverse colon
 Treatment of Gastric CA
 Most are not resectable
 Poor response to combination chemotherapy
 Palliative surgery – gastrectomy,
gastrojejunostomy
 If resectable usually total gastrectomy and
oesophagojejunostomy with node clearance
Esophagoscopy
 Indications and Contraindications
 Indications include:
 Dysphagia
 Reflux
 Hematemesis
 Atypical chest pain
 Many other conditions
 Contraindications:
 To assess reflux symptoms that respond to medical
management
 A uncomplicated sliding hiatal hernia
 Complications
 The minor ones:
 Lacerations of the lips or tongue
 Dislodgment or fracture of teeth and possible aspiration
 Major complication
 Esophageal perforation
 Cervical esophagus (40%)
 Mid esophagus (25%)
 Distal esophagus (35%)
 Morbidity and mortality from perforation is directly related
to the time interval between the occurrence of injury,
diagnosis and repair
 Malabsorption
 Mostly medical causes
 Giardiasis ( Watery Diarrhoea )
 Coeliac disease – clasically diarrhoea,
steatorrhoea and weight loss, although often
vague symptoms
 Whipples disease – fat malabsorption secondary
to infection, presents with steatorrhoea,
arthralgia and malaise
 Radiation and ischaemic enteropathy
 Surgical Causes
 Crohn’s disease
 Short bowel syndrome - <50cm functioning terminal
ileum, global malabsorption
 B12 deficiency after terminal ileum resection
 Iron deficiency after gastrectomy
 Blind loop bacterial overgrowth – exclusion of a loop of
ileum (Crohn’s, post surgery, fistula) with bacterial
growth digesting nutrients
 Diagnosis of Infectious Diarrhea
 History
 Work
 Travel
 Eating
 Ill contacts
 Recent antibiotics
 HIV or immunocompromised
 Stool C&S, O&P (x1), fecal blood and leukocytes if no
improvement in 48 hours or severe disease with bloody stools,
fever, dehydration : Consider sigmoidoscopy
Liver Diseases
&
Dentistry
 Liver : Normal physiology
 Secretion of bile for fat absorption
 Short term sugar storage (glycogen)
 Aged RBC breakdown and excretion of
bilirubin
 Synthesis of coagulation factors
 Synthesis of albumin
 Drug metabolism
 ESLD: (Regardless of Cause)
 Loss of Synthetic function:
 Vit K dependant coagulation factors (II, VII, IX, X)
 Hypoalbuminemia (edema)

 Portal hypertension
 Esophageal, umbilical, hemorroidal varices
 Ascites (abdominal fluid build-up)
 Splenomegaly (thrombocytopenia)

 Loss of de-toxification function: ammonia

Encephalopathy
 ESLD: (Regardless of Cause)
 Bone marrow toxicity: anemia, leukopenia and
thrombocytopenia
 Endocrine disturbances: testicular atrophy and
gynecomastia
 Esophagitis / gastritis

 Elevated Liver enzymes: AST / ALT

 ESLD: (Regardless of Cause)
 Elevated bilirubin: causing Jaundice

 Elevated INR: causing bleeding

 Decreased albumin: causing edema and ascites

 Altered drug metabolism: unpredictable

Drug effect can be Up or Down

 CHRONIC LIVER DISEASE
(Any cause)

PORTAL HYPERTENSION HEPATOCELLULAR FAILURE HCC

*P.S.E. *JAUNDICE.
*VARICES. *COAGULOPATHY.
*ASCITES.
*S.B.P
*H.R.S
Etiology of Chronic Liver Diseases & Cirrhosis
 Alcoholic liver disease
 Viral hepatitis
 Parasites (schistosomiasis)
 Autoimmune Liver Diseases( Biliary disease )
 Primary hemochromatosis
 Cryptogenic cirrhosis
 Wilson’s, 1AT def
 Hepatic-Venous outflow obstruction
 Toxicant and drugs
 Metabolic abnormality
 NASH
 Malnutrition
 Clinical Manifestation

 Onset: Slowly Progressive

Majority: 3~5 years or 10 years
Minority: 3~6 months

 Stages: Compensated
Decompensated
 Compensated Stage
 Fatigue
 Loss of appetite

 Anorexia

 Abdominal discomfort

 Abdominal pain

 Hepatomegaly (slightly or moderately)

 Splenomegaly
 Decompensated Stage

 Deterioration of Liver Function

 Feature of Portal Hypertention

 Complications of Cirrhosis
 Portal Hypertension
 Synthetic Dysfunction
 Coagulopathy

 Encephalopathy

 Immunodeficiency
 Malnutrition
 HCC

79
 Xanthelasma
 Scleral icterus
 Jaundice
 Fetor hepaticus
 Parotid hypertrophy
 Spider angioma
 Gynecomastia
 Ms wasting
 Bleeding tendency (bruising)
 Anemia
 Palmar erythema
 Dupuytern’s cont
 Astrexis
 Ankle edema
Jaundice
 Jaundice

 Jaundice is a yellowish discoloration of the sclera, skin,

mucus membranes, and body fluids caused by the
deposition of bile pigments
 It is usually caused by either an increased production or
decreased excretion of bilirubin from the body
 Jaundice can be classified into:
 Prehepatic jaundice (increased production)

 Hepatic jaundice (decreased excretion)

 Post-hepatic jaundice (decreased excretion)

 Pre-Hepatic
 Haemolytic anaemia – hereditary
spherocytosis, sickle cell, thalassaemia,
Gilbert’s syndrome
 High levels of unconjugated bilirubin, normal
LFTs, raised reticulocytes
 Investigate further with blood film and
autoantibody screen
 Hepatic
 Hepatic injury – viral hepatitis, sclerosis,
cirrhosis, poisons, drugs
 Bilirubin tends to be conjugated, (jaundice
occurs out of failure to excrete, not conjugate)
 Abnormal LFTs (raised ALT/AST)
 Investigate further with viral titres, USS, liver
biopsy
 Post-Hepatic
Wall Lumen Outside Lumen

•Raised conjugated bilirubin (absorbed from biliary tree)

•Decreased urinary urobilinogen (bilirubin does not
make it to the small bowel)
•Obstructed LFTs (raised ALP and GGT)
•Further investigation with USS, and then ERCP/CT as
appropriate
 Jaundice
Pre-Hepatic/ Unconjugated hyperbilirubinaemia
 ↑Production: Haemolysis
 ↓Uptake
 ↓Conjugation – Gilbert’s, Crigler-
Hepatic /Mixed Najjar

ALT/AST

 Hepatocellular damage +/-

cholestasis:
 Viruses: Hep A,B,C…CMV,
EBV
 Alcoholic Hepatitis,
Cirrhosis, metastases
 Drugs – Paracetamol od, TB,
Valproate, MAOI
 Obstruction of CBD:
 Gallstones, Ca Head Panc, LN
 Drugs: Abx
 Biliary cirrhosis, atresia, cholangitis
 Mirrizi’s Syndrome

Post Hepatic/ Conjugated hyperbilirubinaemia ALP

Jaundice
REVIEW CLASSIFICATION OF
JAUNDICE
PRE-HEPATIC
heamolysis
INTRA-HEPATIC
hepatitis, cirrhosis, congenital
hyperbiliruniaemia
POST-HEPATIC
gallstones, tumours, strictures,
biliary atresia

Unconjugated bilirubin
Conjugated bilirubin (water soluble)
 Causes of Hepatomegaly
Regular generalized enlargement without jaundice

Regular generalized enlargement with jaundice

Irregular generalized enlargement without jaundice

Irregular generalized enlargement with jaundice

Localized swellings
Manifestation of ESLD
 Manifestation of ESLD

 Spider telangiectasias  Splenomegaly

 Palmar erythema  Ascites
 Nail changes
 Caput medusae
 Dupuytren's contracture
 Fetor hepaticus
 Jaundice
 Gynecomastia
 Asterixis
 Testicular atrophy

 Hepatomegaly
 Symptoms of Advanced Cirrhosis
 Fatique, weakness
 Nausea, vomiting and loss of
appetite
 Weight loss, muscle wasting
 Jaundice, dark urine
 Unusual bruising
 Spider naevi, caput Medusae
 Bloody, black stools or
unusually light-colored stools
 Vomiting of blood
 Abdominal swelling
 Swollen feet or legs
 Red palms
 Gynecomastia
 Loss of sex drive
 Menstrual changes in
women
 Generalized itching
 Sleep disturbances,
confusion,desorientation,
tremor, ataxia, asterixis
 Visible signs
of advanced liver cirrhosis

Gynecomastia

Ascites

Caput Medusae

Umbilical hernia
 Complications of ESLD
 Malnutrition  Pulmonary Hypertension
 Encephalopathy {Hepatopulmonary
 Coagulopathy syndrome}
 Portal Hypertension  Hepatorenal Syndrome
 Variceal Hemorrhage {HRS}
 Spontaneous Bacterial
Peritonitis {SBP}
 Hyponatremia
Signs of ESLD
Caput Medusae
Spider Angiomas
Esophageal Varices
 Laboratory Findings
 Aminotransferases -  Globulins
AST & ALT  Serum sodium
 Alkaline phosphatase  Hematologic abnormalities
 Gamma-glutamyl - Anemia
transpeptidase (GGT) -Thrombocytopenia
-Leukopenia
 Bilirubin -Neutropenia
 Albumin -Coagulation defects
(PT & INR)
 Pancreatitis
 Caused by gallstones and/or alcohol
 Enzymatic spillage, inflammation, oedema and
necrosis of the pancreas
 Presents with moderate upper abdominal pain radiating
to back, nausea, vomiting, pyrexia, tachycardia,
paralytic ileus and occasionally retroperitoneal
bleeding (Grey Turner’s and Cullen’s signs)
 Confirm diagnosis with amylase >1000 (lab
dependent)
 ABG, CXR, ECG – these patients are often very sick
 Complications
 Acutely – abscess, sepsis, necrosis, ATN,
haemorrhage, pseudocyst formation
 Chronic pancreatitis
- CBD obstruction, diabetes, fibrosis,
inflammation, steatorrhoea
- Surgical management (drainage of dilated
ducts) appropriate in a small minority
 Treatment of Pancreatitis
 IV fluids, analgesia, anti-emetic
 Monitor observations, renal and respiratory
function
 Analgesia
 Evidence for ERCP if proven CBD stone
 Highly conservative
 Pancreatic Neoplasms
 Adenocarcinoma affecting any part of the pancreas
 Endocrine tumours cause a variety of syndromes from secreted
peptides
 M>F, more common after age 50
 Predisposed to by smoking, diabetes, chronic pancreatitis
 Symptoms and presentation dependent on site
- Tail (15%) malignant ascites, anaemia, metastases (peritoneal,
liver)
- Body (25%) back pain, anorexia, weight loss, steatorrhoea,
diabetes
- Head (55%) painless progressive jaundice
- Periampullary (5%) as above, occasionally with duodenal
obstruction causing vomiting
 Investigations and Prognosis
 USS – biliary tree, occasionally visible mass
 CT scan +/- biopsy or ERCP +/- biopsy
 90% of patients are dead within 12 months of
diagnosis
 Tissue type important (better prognosis for non-
pancreatic peri-ampullary tumour)
 Management
Palliation
 Coeliac nerve ablation (body tumours)
 Enzyme supplements, insulin
 Relieve jaundice by ERCP
 Surgery
Curative
 Rarely appropriate
 Requires early presentation
 Whipple’s pancreatico-duodenectomy