dr. ferenc szalay professor emeritus
TRANSCRIPT
ÁLTALÁNOS ORVOSTUDOMÁNYI KARI. sz. Belgyógyászati Klinika
Dr. Ferenc SZALAY professor emeritus
Semmelweis University
Clinic for Internal Medicine and Oncology
Differential diagnosis in
gastroenterology
Lecture for English course medical students 2020.04.22.
Not own figures have been imported
from open databases via internet,
from public guidelines of international
societies.
DECLARATION
GI bleeding
Upper GI (UGIB) - Lower GI - Obscure
Altered bowel movement – Diarrhea, Constipation
Jaundice –
Liver diseases
Biliary diseases: Stone, PBC,PSC, Tumors
Abdominal pain – GI related and non GI related
Pancreatic diseases
Pancreatitis – acute and chronic
P. tumor
IBD: Ulcerative colitis (UC) - Crohn D (CD).
IBS – irritable bowel syndrome
Topics to be discussed
Good history taking
= half diagnosis
Don’t forget
Importance of physical investigation
Upper GI tract bleeding (proximal to the ligament of Treitz)
Hematemesis bright red blood
coffee grounds
Melaena black, terry stool, >100ml, >12 h
Lower GI bleeding (distal to the ligament of Treitz)
Melaena
Hematochezia bright red or maroon colored
Obscure bleedingSymptomst of iron deficiency
Combination
GI BLEEDING
Václav (Wenzel)Treitz
1819 – 1872
Ligament of Treitzsuspensory muscle
Superior mesenteric vein Superior mesenteric artery
The problem with GI bleeding
Mortality – up to 10-14% (US, UK)
despite modern diagnostic and threapeutic technics
Male:female= 2:1
Asymptomatic – mild – severe
Can be life threatening emergency situation
MASSIVE GI BLEEDING
Clinically significant bleeding
Most critical the first 48-72 hours
P > 100/min
systolic RR < 100 Hgmm
postural RR > 20 Hgmm
> 2U transfusion demand /24 h
Ulcer disease
Esophagitis
Esophagogastric Varices
Vascular lesions
Neoplasms
Diverticula
Hemorrhoids
Fissures
IBD
Infectious colitis
GI BLEEDING etiology
UGIB
LGIB
Obscure GIB
Tools for diagnosis
Clinical symptoms – iron deficiency
Endoscopy – upper, lower
push enteroscopy
Izotope scintigraphy
Angiography
Capsula endoscopy
CT Angiography
MRI?
Surgical exploration
5-10% of GIB
Angiography for GI bleeding
Main goals:
1.Confirm the diagnosis of bleeding
2.Localize the bleeding site
3.Provide transcatheter therapy as needed
Very specific (100% for both UGIB and LGIB)
Very sensitive (90% for UGIB, 86% for LGIB)
Successful if bleeding is greater than 0.5 mL/min
Angiographic
signs of bleeding
Extravasation of contrast into the
lumen of bowel
Patients must be bleeding
quite briskly
Indirect signs of bleeding
Extravasation outside of the
vessels
Pseudoaneurism
AV fistula
Hyperemia
Neovascularity
The goals of management of GI bleeding
in order of priority
1. Correct hypovolemia
(hemodynamic resuscitation)
2. Arrest hemorrhage by the least
invasive means
3.Prevent recurrent hemorrhage
ABDOMINAL PAIN
GI Tract related
Not GI related
>1018 medical
conditions
can cause abdominal pain
Which in the given case?
ABDOMINAL PAIN.
Interviewing / physical invest.
8questions
ABDOMINAL PAIN. Interviewing/physical invest.
Localization where?
Time when? duration? frequency?
Oneset suddenly? gradually?
Intensity how severe?
Character aching? burning? gnawing? colicky?
Radiation no or yes? travel anywhere?
Aggravating or meals? antacids? alcohol? defecation?
alleviating circumstances medications(aspirin)? body position?
urination? menstruation?
Associated symptoms fever? chills?
Sudden acute
Recurrent chronic
ONSET OF ABDOMINAL PAIN
BEDSIDE DIAGNOSTIC TESTS FOR ABDOMINAL PAIN
General appearance
Is there shock?
Palpate the abdomen gently
Exemine for hernia
Listen to the bowel sounds
Rectal digital investigation
ACUTE ABDOMEN
Severe
Persistent
Sudden onset
Surgical intervention to treat (non surgical!)
Frequently associated with
nausea, vomiting, abd. distension,
fever, shock
CAUSES of ACUTE ABDOMEN
Trauma – blunt, perforating
Inflammation – appendicitis, cholecystitis, pancreatitis, pelvic,
Mechanical – small or large intestine, hernias,
Vascular – occlusive, aneurisma rupture
Perforation – any of above can end here
Tumor - intraabdominal bleeding
Non surgical causes
Surgical acute abdomen
When to operate?
Before sunset
or
Before sunrise
Non Surgical Causes
• Myocardial infarction (MI), Acute pericarditis
• PN, pulmonary infarction
• GE reflux, hepatitis
• Diabetic ketoacidosis (DKA )
• Acute Adrenal Insufficiency
• Acute Porphyria
• Rectus muscle hematoma
• Pyelonephritis, Acute salpingitis
• Sickle cell crisis
Clinical Diagnosis
ORIGIN OF ABDOMINAL PAIN
GI organs – OE, stomach, bowel, bile system, liver, pancreas
Kidney – urinary tract
Gynecological and obstetrics
Prostate
Blood vessels – artery, vein
Metabolic crisis (diabetes, porphyria, hypadrenia, C1 inhibitor def.)
Skin – herpes zooster
Hernia
Abdominal wall – muscle, shingle
Connective tissue
Poisoning – black widow spider bite, narcotic withdrawal
Functional and psychiatric causes- IBS
Referred pain – heart, lung, spine
ALTERED
BOWEL MOVEMENT
DIARRHEA
CONSTIPATION
DIARRHEA
DEFINITION OF DIARRHEA
Increase in stool water (loose or watery)
Increase in stool weight (>200g/day)
Increase in stool frequency
May be associated with
urgency
perianal dyscomfort
fecal incontinence
>2x /day liquid stool throughout 3 days
Absorbed
8800
9000
Into
200
CLASSIFICATION OF DIARRHEA
AcuteInfectious
Non infectious
Chronic
Funtional
Organic
ACUTE DIARRHEA
Infectiousbacterialviralparasiticmycotic
Non infectioustoxicantibioticsallergyGI bledingothers
Combined e.g. traveller’disease
CLASSIFICATION OF DIARRHEA
Osmotic
Secretory
Inflammatory
Decreased absorptive surface
Motility disorder
Combination of mechanisms – e.g.
OSMOTIC DIARRHEA
Mechanism Example Characteristics
Nonabsorbable molecules Lactase deficiency Watery stool, no blood or
in the gut lumen pus, improves with
fasting
Generalized Stool may contain fat
malabsorption globules or meet fibers
Mg2+ containing
laxatives
Lactulose
Excess of absorbable Sugar Watery diarrhea
molecules Must (Grape juice)
Watery diarrhea
SECRETORY DIARRHEA
Mechanism Example Characteristics
Increased secretion and/or
Decreased absorption of
Na+ or Cl-
Cholera
E coli heat-labile toxin
Bile salt enteropathy
Fatty acid-induced
Diarrhea
Zollinger-Ellison sy.
VIP-secreting tumor
Carcinoid
Large volume, watery
No blood or pus
No solute gap
Little or no response to
fasting
„rice water cholera stool”
1961
Seventh Cholera Pandemic (1961-)new strain of V. cholerae--El Tor strain;
first observed among Indonesian emigres to Egypt in 1905;
emerges as pandemic in 1961
INFLAMMATORY DIARRHEA
Mechanism Example Characteristics
Destruction of mucosa
Impaired absorption
Outpouring of blood,
mucus
Ulcerative colitis
Crohn disease
Shigellosis
Clostridium difficile
Amebiasis
Calcici virus
Rota v.
Norwalk v.
Small frequent stools
With blood and pus
Fever
Clostridium difficile
Pseudomembranous colitis
Increasing incidence of
Clostridium diff. infection
Causes:
Use and Overuse of antibiotics
Widespread and continous use PPIs
DECREASED ABSORPTIVE SURFACE DIARRHEA
Mechanism Example Characteristics
Impaired resorption of
electrolytes
Bowel resection
Enteric fistula
Bariatric surgery
Celiac disease
Variable
Celiac disease
Villous atrophy,
T Lymphocytes
Glutene sensitive
enteropathy
Primate oesophagus as substrate
Celiac disease: Endomysial/transglutaminase antibodies
Antigen: IgA to tissue
transglutaminase
located in the
muscularis mucosa
Up to 100% of the
patients with coeliac
disease (gluten
sensitivity) were positive
for endomysial antibodies.
In patients with IgA
deficiency, assessment of
IgG transglutaminase
and endomysial
antibodies is
reccomended.
IgA deficient endomysial antibodiesAntigen: IgG to tissue transglutaminase
Staining of
network of
fibres around
smooth
muscle cells
in the
muscularis
mucosa.
MOTILITY DISORDER DIARRHEA
Mechanism Example Characteristics
Increased motility with
decreased time for
absorption of electrolytes
and/or nutrients
Decreased motility with
bacterial owergrowth
Hyperthyreoidism
Irritable bowel syndrome
Scleroderma
Diabetic diarrhea
Variable
Malabsorption
STEATORRHEAL CAUSES
Mechanism Example Characteristics
Inraluminal maldigestion
Mucosal malabsorption
Postmucosal obstruction
Pacreatic exocrine
insufficiency
Cholestatic liver diseases
Bacterial overgrowth
Whipple’s diseases
Celiac disease
Lymphangiectasia
Tumor
Trauma
Greasy, foul smelling stool
Difficult-to-flash diarrhea
Weight loss
Irregular fold pattern
and thickened walls
Whipple’s disease
Whipple’s disease
Tropheryma whippelii
Ubiquitous actinomyces
Macrophage dysfuntion
is prerequisite of the
disease
Unusual trilaminal
cell wall
Fluorescent in situ
detection of rRNA
Easy to diagnose and
treat – if you think of it
Tropherhyma
whippelii
bacilli
within the
macrophages
Encephalopathy
(occasionally)
Lymphadenopathy
(same morphology
as gut)
Malabsorption
and diarrhea
Arthritis
(often)
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Whipple’s disease
DIARRHEA CAUSING DRUGS
Gastrointestinal drugsMg-containing drugsMisoprostolOlsalazine
Lipid decreasing drugsClofibrate,GemfibrozilLovastatinProbucol, Orlistat
Cardiac/AntihypertensiveDigitalisQuinidineProcainamideHydralazineBeta-blokkolókACE-gátlókDiuretikumok
Neuropsychiatric drugsLithiumFluoxetine (Prozac)Alprazolam (Xanax)Valproic acidEthosuximideL-Dopa
AntibioticsAmpicillinCephalosporinsErythromycinClindamycin
Oncology drugs
OthersTheophyllineThyroid hormonesColchicineNSAID
LAXATIVES
CONSTIPATION
Constipationcomon problem
M<F
Recent onset Constipation
or
Chronic constipation
CHRONIC CONSTIPATION
< 2x / week (> 12 month) infrequent defecation
or 2 of the below
• < 3x / week
• Straining with defecation (> 25%)
• Hard stools (> 25%)
• Sense of incomplete
fecal evacuation (> 25%)
(Rome criteria)
CHRONIC CONSITPATION GENERALLY RESULTS FROM:
Inadequate fluid intake
Inadequate fiber intake
Disordered colonic transit
Anorectal dysfunction
SECONDARY COUSES OF CHRONIC CONSTIPATION
Neurological diseases
Periferal Central
Megacolon congenitum Multiple sclerosis
Chagas-disease Spinal cord injury
Diabetes mellitus Parkinson-disease
Autonomic neuropathy Stroke
Intestinal pseudo-obstruction
Non neurological abnormalities
Anatomical obstructionDiverticulosisTumorStricture
Psychiatric diseasesDepressionDietary factors
Scleroderma
Endocrinological diseases
Hypothyreosis
Hyper/hypocalcemia
Pregnancy
Porphyria
Panhypopituitarism
Myotonic dystrophy
SECONDARY COUSES OF CHRONIC CONSTIPATION
CAUSES OF CONSTIPATION
Dietary factors – inadequate fluids, low-fiber foods
Physical inactivity – prolonged bed rest, inadequate exercise
Pregnancy
Advanced age
Drugs – long list
Metabolic abnormalities – hypokalemia, hyperglycemia, uremia,
porphyria, amyloidosis
Endocrine – hypothyroidism, hypercalcemia, glucagonoma,
pheochromocytoma
Lower bowel abnormalitiesColon, Rectum, Anus
Anorectal and pelvic floor diseases
Neurological – innervation disorders
Psychogenic disorders
Enema (chronic use)
Home remedies and OTC medications
Dietary fiber (bulk-forming laxatives)
Lubricant laxatives – mineral oil or emulsion
Emollient laxatives
Hyperosmolar laxatives –sorbitol, polyethylene glycol
Saline laxative – magnesium sulphate, Mg-citrate
Stimulant laxatives – cascara, senna, bisacodyl (Dulcolax),
prunes
Enemas
Suppositories – glicerin
Combination products
Treatment: TREAT THE UNDERLINING CAUSE!
Jaundice / Icterus
Liver related – hepatitis, toxic, DILI, Gilbert sy
Biliary obstruction – stone, tumor, stricture
Prehepatic, hemolytic jaundice
corpuscular, extra-corpuscular
Classification of jaundice
Liver diseases
Acute – chronic Focal - diffuse
Classification according to the etiology
Hepatitis –
Viral – HAV, HBV, HCV, HEV, EBV, CM
Autoimmune (AIH), PBC, PSC
Bacterial - Leptospirosis, Syphilis, Brucellosis
Protozoal – Malaria, Tripanosomiasis, Amebiasis
Toxic –
Death cup (Amanita) poisoning
Alcohol – ethanol, methanol
Industrial toxins
Drug induced (DILI)
Paracetamol, NSAID, antimicrobal Ds, Statins, Psychiatric
Circulatory, vascular
Shock, Budd-Chiary, portal vein thrombosis
Focal diseases
Hemangiomas, Cysts, Adenomas, FNH, Tumors: HCC, Metastases
Biliary diseases
Gall stone disease
Cholecystolithiasis
Stone in common bile duct
Mirizzi syndrome
Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Prevalence: 10-100/1.000.000 (in relatives > 100x)
95% female (30-60 év)
Chronic, intrahepatic cholestasis
Progressive disease
Autoimmun mechanism
Itching is common symptome
Duration variable, 20-30 y
PRIMARY BILIARY CHOLANGITIS (PBC)
DIAGNOSIS
4 pillars
Clinical picture – fatigue, itching, xanthomas
Lab signs of cholestasis - ALP, GGT, Se.bi
Autoantibodies – AMA M2, ANA Sp100, gp210
Exclusion of extrahep.obstr. – US, MRI, ERCP
HISTOLOGY and NATURAL HISTORY
4 stages
I. Small-medium bile duct injury, inflammation
II. Periportal inflammation and bile duct proliferation
III. Granulomas and scarring
IV.Cirrhosis
Primary sclerosing cholangitis (PSC)
Progressive disease
biliary cirrhosis
portal hypertonia
liver failure
Average survival 12 years
Cholangiocarcinoma common (3-10-36%)
intrahepatic 15%, hílar 65% distal 20%
DIAGNOSIS
Chemical laboratory
ALP, GGT, Se. Bilirubin
Autoantibodies – pANCA (85%)
Imaging - US, cholangio MR, ERCP
Histology
TREATMENT
Endoscopic dilatation of dominant stenosis
Antibiotics in case of bacterial cholangitis
Fat soluble A, D, E, K vitamins
LIVER TRANSPLANTATION
Diseases of pancreas
Pancreatitis
Acute
Chronic
Pancreas tumor
ACUTE PANCREATITISESSENTIALS OF DIAGNOSIS
Abrupt onset of deep epigastric pain, often with radiation
to the back.
History of previous episodes, often related to alcohol
intake.
Nausea, vomiting, sweating, weakness.
Abdominal tenderness and distention and fever.
Leukocytosis, elevated serum amylase, elevated serum
lipase, creatinin, LDH, AST(GOT), glucose. Hbg↓, Ca↓
Imaging
• US
• radiographs of the abdomen – gallstones
– sentinel loop (segment of air-filled small intestine)
– colon cutoff sign (gas-filled segment of transverse colon abruptly ending at the area of pancreatic inflammation)
• CT scan - gold standard!
ACUTE PANCREATITIS –IMAGING
Gallstones: 45%
Alcohol: 35%
Other 10%
Medications
Hypercalcemia
Hypertriglyceridemia
Obstructive
Post-ERCP
Hereditary
Trauma
Viral Vascular/ischemic
Postcardiac bypass
Idiopathic: 10%
Causes of Acute Pancreatitis (% of Cases)
Gallstones
45%
Vascular causes and vasculitisischemic-hypoperfusion states after cardiac surgery
Connective tissue disorders and
thrombotic thrombocytopenic purpura (TTP)
Cancer of the pancreas
Hypercalcemia
Periampullary diverticulum
Pancreas divisum
Hereditary pancreatitis
Cystic fibrosis
Renal failure
Uncommon causes
Infections
mumps, coxsackievirus,
cytomegalovirus, echovirus, herpes V.
bacteria: tbc, leptospirosis
parasites ascaris, clonorchis
Scorpion toxin
Autoimmune
e.g., Sjögren's syndrome
Rare causes
Gallstones
Common bile
duct
Biliary pancreatitis
CHRONIC PANCREATITIS
CHRONIC PANCREATITIS – ETIOLOGY
Alcohol 70%
Pancreatic duct obstruction
Tumor
Trauma
Pancreas divisum
Fibrosis
Cystic fibrosis
Hyperlipidemia
Herediter pancreatitis
Tropical pancreatitis
Hyperparathyreoidism
Chronic pancreatitis other 10%
PANCREATIC CANCERIncreasing incidence - 10/100000
Poor prognosis (worst GI tumor) – 5 y survival <5 %
Male > Female
Age related incidence (65-80 y)
Etiology smoking
exogene factors
hyperinsulinemia (Type II DM)
genetic predisposition
Histology 90% ductal
Localization head (70%), body (20%), tail (10%)Diagnosis
Treatment
Obstructive jaundice
Abdominal pain
Loss of body weight
Jaundice
Steatorrhoea
Leading symptoms of P.cancer
INFLAMMATORY BOWEL DISEASES (IBD)
Ulcerative colitis (UC)
Crohn disease (CD)
Localized to colon
Ulcers of mucous membrane
Pseudopolyps
Prone to malignancy
PSC common
Terminal ileum and/or any part of GI tract
Segmental
Transmural - granulomatous
Fistulas, stenosis
No increase in rate of PSC
Differential diagnosis of ULCERATIVE COLITIS
Crohn’s disease
Infectious colitis - detected on stool culture
Shigella –dysenteria
Entamoeba histolytica – protozoon parasyte caused inflammation
Pseudomembranous colitis – Clostridium difficile associated colitis
Ischemic colitis - inadequate blood supply, typically affects the elderly
Radiation colitis - in patients with previous pelvic radiotherapy
Chemical colitis
Malignancy – cancer may present as acute flare of colitis or vice versa
It is important to rule out when the colitis is refractory to the treatment
Differential diagnosis of CROHN DISEASE
Ulcerative colitis –
Intestinal tuberculosis
NSAID enteropathy
Bechet’s disease
Celiac disease
Irritable bowel syndrome
IRRITABLE BOWEL SYNDROME (IBD)
The Rome IV criteria
Recurrent abdominal pain
- on everage, at least 1 day/week in the last 3 months
Associated with two or more of the following criteria:
- Related to defecation
- Association with a change in frequency of stool
- Associated with a change in form (appearance) of stool
IBS Classification
Diarrhea predominant (IBS-D)
Constipation predominant (IBS-C)
Alternating stool pattern (IBS-A)
Postinfectious (IBS-PI)
Differential diagnosis of IBS
Colon cancer
IBD
Thyroid disorders – hyperthyreodism or hypothyroidism
Giardiasis
Carcinoid sy.
Microscopic colitis
Bacterial overgrowth (SIBO)
Eosinophilic gastroenteritis
Celiac disease
Non-celiac gluten sensitivity
Lactose intolarence
Bile acid malabsorption
Dyssynergic defecation
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