GI + Liver Flashcards
1
Q
Role of liver
A
Glucose and fat metabolism
Protein synthesis e.g. albumin, clotting factors
Detoxification and excretion
Defence against infection: bilirubin, ammonia, drugs and hormone
reticuloendothelial system
2
Q
Portal triad
A
Portal vein, hepatic A, bile duct
3
Q
Acute liver injury results
A
Liver failure, recovery
4
Q
Chronic liver injury results
A
Cirrhosis- scaring, can lead to liver failure
recovery
Liver failure (varices, hepatoma)
5
Q
Causes of liver cell death
A
necrosis (associated with neutrophils), or apoptosis
6
Q
Cirrhosis
A
Scarring of the liver, disturbs the portal triad
7
Q
Causes of acute liver injury
A
viral (A,B, EBV)
drug
alcohol
Vascular
Obstruction
Congestion
8
Q
Causes of chronic liver injury
A
alcohol
viral (B,C)
autoimmune
metabolic (iron, copper)
9
Q
Presentation of acute liver injury
A
malaise, nausea, anorexia, jaundice
rarer (more common in failure): confusion, bleeding, liver pain, hypoglycaemia
10
Q
Presentation of chronic liver injury
A
ascites, oedema, haematemesis (varices), malaise, anorexia, wasting easy bruising (clotting factors affected), itching, hepatomegaly, abnormal LFTs
rarer: jaundice (more related to acute), confusion
11
Q
Chronic liver injury- management
A
Lifestyle changes and supportive treatment
Consider liver transplant
11
Q
Acute liver injury- management
A
Identify and treat underlying cause
Monitor neurological status, blood tests
Consider liver transplant
12
Q
Serum ‘liver function tests’
A
No one global test
Serum bilirubin, albumin, prothrombin time: (give some index of liver function)
Serum liver enzymes: -cholestatic: alkaline phosphatase, gamma-GT
-hepatocellular: transaminases (AST, ALT)- don’t give index of liver function
13
Q
Jaundice
A
raised serum bilirubin
14
Q
Pre-hepatic jaundice
Unconjugated bilirubin problems
A
Gilberts, Haemolysis
15
Q
Hepatic jaundice
(conjugated bili) problems
A
Hepatitis: viral, drugs immune, alcohol
Ischaemia
Neoplasm
Congestion (CCF)
16
Q
Post-hepatic jaundice
(conjugated) problems
A
Gallstone: bile duct, Mirizzi
Stricture: malignant, ischaemic, inflammatory
17
Q
Prehepatic jaundice tests
A
Urine- normal
Stool- normal
Itching- no
Liver test- normal
18
Q
Cholestatic jaundice tests
A
Urine- dark
Stool- may be pale
Itching- maybe
Liver test- abnormal
19
Q
Jaundice history taking
A
Past history: biliary disease/intervention malignancy, heart failure blood products , autoimmune disease
Drug history (drugs/herbs started recently)
Social history- Alcohol, potential hepatitis contact (irregular sex, IVDU, exotic travel, certain foods)
Family Hx/ system review – rarely helpful
20
Q
Jaundice investigations
A
Liver enzymes: Very high AST/ALT suggests liver disease, some exceptions
Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultrasound
-no dilation means likely hepatic causes
Need further imaging: CT Magnetic resonance cholangioram MRCP Endoscopic retrograde cholangiogram ERCP
21
Q
Gallstone
A
Most form in gallbladder- smaller stone more of a risk, than large stone that remain gallbladder
Very common: 1/3 women over 60
70% Cholesterol, 30% pigment+/- calcium
22
Q
Gallstone risk factors
A
Risk factors: Female, fat, fertile (liver disease, ileal disease, TPN, clofibrate…)
23
Q
Gallstone symptoms
A
Most asymptomatic
Weight loss, jaundice, referred in right shoulder
24
Gallstones presentation- in gallbladder
Biliary pain- yes
Cholecystitis- yes
Obstructive Jaunice- maybe (mirizzi)
Cholangitis- no
Pancreatitis- no
25
Gallstones presentation- in bile duct
Biliary pain- yes
Cholecystitis- no
Obstructive Jaunice- no
Cholangitis- yes
Pancreatitis- yes
26
Gallstones: management- gallbladder
Laparoscopic cholecystectomy
Bile acid dissolution therapy (<1/3 success)
27
Gallstones: management- bile duct stones
ERCP with sphincterotomy and:
removal (basket or balloon)
crushing (mechanical, laser..)
stent placement Surgery (large stones)
28
Are the ducts always dilated on ultrasound as result of gallstones
Ducts not always dilated on ultrasound (esp with “stone” jaundice)
29
Isoniazid complications
Acute liver injury
30
DRUG-INDUCED LIVER INJURY (DILI)
1/10000 patients/yr
30% of Acute Hepatitis
>65% of Acute Liver Failure - 50% Paracetamol
- 15% idiosyncratic- not due to ODs
Commonest reason for drug withdrawal from formulary
31
Types of DILI
Hepatocellular- ALT >2 ULN, ALT/Alk Phos ≥ 5
Cholestatic- Alk Phos >2 ULN or ratio ≤ 2
Mixed- Ratio > 2 but < 5
direct toxicity and idiosyncratic DILI
32
DILI: DIAGNOSTIC APPROACH
what did you start recently- usually 1-12 weeks of starting, onset may be weeks after stopping
resolution: 90% within 3 months of stopping
5-10%: prolonged- high mortality rate
33
DILI: “Usual Suspects”
32-45% Antibiotics
15% CNS Drugs-
5% Immunosuppressants
5-17% Analgesics/ musculoskeletal (Diclofenac…)
10% Gastrointestinal Drugs (PPIs…)
10% Dietary Supplements
20% Multiple drugs
34
Examples of drugs that commonly cause DILI- Antibiotics
Augmentin, Flucloxacillin, Erythromycin, Septrin, TB drugs
35
Examples of drugs that commonly cause DILI- CNS
Chlorpromazine, Carbamazepine Valproate, Paroxetin
36
Drugs unlikely to cause DILI
Low dose Aspirin
NSAIDs other than Diclofenac
Beta Blockers
HRT
ACE Inhibitors
Thiazides
Calcium channel blockers
37
Paracetamol metabolism
Acetaminophen> Stable
Metabolite > Excretion
38
Paracetamol OD
High doses of paracetamol produces liver cell necrosis. The toxic metabolite binds irreversibly to to liver cell membranes
39
Management of paracetamol induced fulminant hepatic failure
N acetyl Cysteine (NAC)
Supportive to correct
-coagulation defects, fluid electrolyte and acid base balance, renal failure, hypoglycaemia, encephalopathy
40
Paracetamol-induced liver failure: severity indicators
Late presentation (NAC less effective >24 hr)
Acidosis (pH <7.3)
Prothrommbin time > 70 sec
Serum creatinine ≥ 300 µmol/l
Consider emergency liver transplant- otherwise 80% mortality
41
Ascites- causes
Chronic liver disease (most) +/- Portal vein thrombosis, Hepatoma, TB
Neoplasia (ovary, uterus, pancreas...)
Pancreatitis, cardiac causes
42
Spider naevus
Vascular lesion characterized by anomalous dilatation of end vasculature found just beneath the skin surface- can be sign of cirrhosis, rheumatoid arthritis or hepatitis
43
Ascites- pathogenesis
Increased intrahepatic resistance + systemic vasodilation > secretion of Renin-angiotensin, Noradrenaline, Vasopressin + portal hypertension + low serum albumin
> fluid retention+ portal hypertension > ascites
44
Ascites- management
Fluid and salt restriction
Diuretics Spironolactone +/ Furosemide
Large-volume paracentesis + albumin
Trans-jugular intrahepatic portosystemic shunt (TIPS)
45
Alcohol liver disease and fat
Alcohol changes the way that hepatocytes metabolise and produce fat. Fat accumulation within hepatocytes is termed steatosis. It may be associated with acute liver injury, or as in the picture, chronic injury mediated by lymphocytes
46
Acute alcohol-related injury
causes hepatocyte ballooning and is mediated by neutrophils (acute alcoholic hepatitis)
47
Acute Decompensation
Fatty liver> alcohol hepatitis (90% of 1st episodes) or cirrhosis (more common later) +/ infection > acute decompensation
48
Alcoholic Liver Disease (ALD)
Main cause of liver death in UK
However, only 10-20% of heavy alcohol drinkers drinkers get serious ALD (unsure why)
Often not alcohol dependent
Poor outcome- 10 years survival 25%
49
Progression of Alcoholic Liver Disease (ALD)
Normal> Steatosis> Alcohol steatohepatitis/ fibrosis > Cirrhosis (or alcoholic hepatitis which can develop into cirrhosis) > Hepatocellular carcinoma
50
ALD management
Depends on type of liver disease
General- Stop drinking, Withdrawal symptoms treated with diazepam
51
Portal hypertension causes
cirrhosis, fibrosis, portal vein thrombosis
52
Portal hypertension- pathology
increased hepatic resistance, increased splanchnic blood flow
53
Portal hypertension complications
varices (oesophageal, gastric), splenomegaly
54
Liver transplantation for alcoholic liver disease?
Limited supply of liver, poor negative attitudes
However, post transplant survival similar to that for other liver diseases- did well
Drinking relapse –variable; recurrent ALD uncommon
55
Alcohol withdrawal treatment
Lorazepam
56
Causes of deterioration in chronic liver disease
Constipation
Drugs -sedatives, analgesics
NSAIDs, diuretics, ACE blockers
Gastrointestinal bleed
Infection (ascites, blood, skin, chest)
HYPO: natremia, kalaemia, glycaemia
Alcohol withdrawal (not typically)
Other (cardiac, intracranial)
57
Spontaneous bacterial peritonitis
Commonest serious infection in cirrhosis
based on neutrophils in ascitic fluid
Gram stain often neg; use blood culture bottles
After 1 episode:
-should have antibiotic prophylaxis
-consider liver transplantation
58
Renal failure in liver disease- causes
Drugs (diuretics, NSAIDS, ACEi, Aminoglycosides), Infection, GI bleeding, myoglobinuria, renal tract obstruction
59
Coma in patients with chronic liver disease
Hepatic encephalopathy (ammonia ...) infection, GI bleed, constipation, hypokalaemia, drug (sedatives, analgesics)
Hyponatraemia / hypoglycaemia
Intracranial event
60
Encephalopathy
disease in which the functioning of the brain is affected by some agent or condition
61
Bedside tests for encephalopathy
Serial 7’s
WORLD backwards
Animal counting in 1 minute
Draw 5 point star
Number connection test
62
Other consequences of liver dysfunction
Malnutrition, coagulopathy, endocrine changes, hypoglycaemia
63
Drug prescribing in liver disease- Analgesia
sensitive to opiates
NSAIDs cause renal failure
paracetamol safest
64
Drug prescribing in liver disease- Sedation
use short-acting benzodiazepines- with care!!
65
Drug prescribing in liver disease- diuretics
excess weight loss hyponatraemia
hyperkalaemia
renal failure
66
Drug prescribing in liver disease- Antihypertensives
Can often stop, avoid ACEi
67
Drug prescribing in liver disease-
Aminoglycosides
Avoid!!!
68
Consequences of liver disease
Malnutrition
Variceal bleeding
Encephalopathy
Ascites / oedema
Infections- antibiotics
69
Treatment of consequences of liver disease- Malnutrition
Naso-gastric feeding
70
Treatment of consequences of liver disease- Variceal bleeding
Endoscopic banding, propranolol, terlipressin
71
Treatment of consequences of liver disease- Encephalopathy
lactulos
72
Treatment of consequences of liver disease- Ascites / oedema
salt / fluid restriction
diuretics, paracentesis
73
Liver patient ‘gone off’- what to do
ABC, look at chart (vital signs, O2, BM(glucose), drug chart), look at patient (focus of infection and bleeding)
Tests- FBC, U&E, blood cultures, ascitic fluid, clotting, LFTs
74
Causes of chronic liver disease
Alcohol
Non Alcoholic Steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune cholangitis
Metabolic
Vascular - Budd-Chiari
75
Causes of chronic liver disease- immune
[autoimmune hepatitis, primary biliary cirrhosis, sclerosing
76
Causes of chronic liver disease- metabolic
haemochromatosis, Wilson’s, alpha-1 antitrypsin deficiency
77
Chronic liver- history taking
Past history: -alcohol problems, biliary surgery, autoimmune disease, blood products
Social history: alcohol, sexual
Drug history (all drugs!!)
Family history
78
Investigation of chronic liver disease
Viral serology
Immunology
Biochemistry
Radiological investigations
79
Investigation of chronic liver disease- Viral serology
Hepatitis B surface antigen, hepatitis C antibody
80
Investigation of chronic liver disease- Immunology
autoantibodies- AMA, ANA, ASMA,
coeliac antibodies
immunoglobulins
81
Investigation of chronic liver disease- biochem
iron/ copper studies
caeruloplasmin
24 hr urine copper
alpha1-antitrypsin level
lipids, glucose
82
Investigation of chronic liver disease- radiology
Ultrasound (USS) / CT / MRI
83
Normal flora
the community of microorganisms that live on another living organism without causing disease
84
Role of normal flora
produces antimicrobial substances which discourage infection by:
Inhibiting overgrowth of endogenous pathogens
Preventing colonisation by exogenous pathogens
85
Disruption to normal flora
Antibiotics can disrupt this balance increasing susceptibility to infections such as C.Difficile.
Peritonitis can occur as if normal barriers are breached
86
C.Difficile
Gram positive spore forming bacteria
Up to 5% of population have c.diff as normal flora
Many are asymptomatic but can become a problem if the normal gut flora is altered, most notably is due to broad spectrum antibiotics- rule of C's
87
Rule of C's
associated with a higher risk of C. difficile infection
clindamycin, ciprofloxacin (quinolones), co-amoxiclav (penicillins) and cephalosporins (particularly 2nd and 3rd generation)
88
C diff treatment
metronidazole or oral vancomycin.
In refractory cases sometimes faecal transplant- aims to restore the normal flora
89
Diarrhoea causes
Infective, inflammatory, loss of absorptive area, pancreatic disease, drugs, colon cancer, systemic disease, IBS, gastrectomy
90
Infective causes of diarrhoea
Campylobacter, salmonella, HIV, bacterial, amoebic dysentery, cholera
91
Diarrhoea- history
Onset/duration
Characteristics of stool
Food/drink
Travel
Immunocompromised
Unwell contacts
Hobbies + fresh water
Animal contact
Medications
92
Diarrhoea characteristics
floating: fat content ?malabsorption/ Coeliac
blood or mucus: ?inflammatory/ invasive infection ?cancer
Watery small bowel infection
93
Food and drink diarrhoea
Dodgy take-aways – food poisoning (eating food contaminated with microorganisms or toxins)
Meat/BBQs: campylobacter
Rice: bacillus cereus
Poultry: salmonella
Shellfish: norovirus, v.parahaemolyticus
94
Watery diarrhoea
non-inflammatory, proximal small bowel, bacterial, viral (rotavirus, norovirus) and parasitic causes
95
Water diarrhoea- bacterial causes
E coli
Clostridium perfringens – cooked meats
Bacillus cereus – reheated rice (vomiting +++)
Staph. aureus enterotoxin has a direct effect on vomiting centre in brain! <6hr exposure
96
Water diarrhoea- parasitic causes
Giardia – offensive diarrhoea, chronic, bloating, flatulence, nurseries/old age facilities
Cryptosporidium – swimming pools
97
Blood, mucoid diarrhoea
Inflammatory, colon, bacterial and parasitic causes
98
Blood, mucoid diarrhoea- bacterial causes
Shigella 🡪 shiga toxin, causes gross injury to bowel surface; MSM at risk
Salmonella – poultry, eggs and dairy
E coli
Vibrio parahaemolyticus – shellfish
C.Diff – antibiotics
Campylobacter – meats, BBQ
99
Blood, mucoid diarrhoea- parasitic causes
Entamoeba histolytica- travel, MSM
100
Most common GI infections in the UK
Mainly viral, ie rotavirus, norovirus
101
Diarrhoea definition
3 or more unformed stool per day plus one of the following:
Abdo pain
Cramps
Nausea
Vomiting
Dysenty
102
Traveller’s diarrhoea
occurs within 10 days of arrival from a foreign country, most commonly Enterotoxigenic E. coli, be aware of cholera
103
E.coli
Most strains are harmless
Some serotypes are pathogenic
104
Types of E coli
ETEC: EnteroToxigenic
EHEC: EnteroHaemorrhagic
EIEC: EnteroInvasive
EPEC: EnteroPathogenic
EAEC: EnteroAggregative
DAEC: Diffusely Adherent
105
E coli ETEC
leading bacterial cause of diarrhoea in children in developing world and most common cause of travellers diarrhoea
380000 deaths- mostly children in developing world
106
E colic EHEC
Shiga-like toxin – intensive inflammatory response
Can cause Haemolytic uraemic syndrome
107
Haemolytic uraemic syndrome
Bloody diarrhoea, abdo pain, no fever
Haemolysis
Renal failure
108
E. coli EIEC
Enteroinvasive, dysentery like illness, similar to shigella
109
Cholera
Contaminated food/water
Cholera toxin
Profuse watery “rice water” diarrhoea upto 20L a day
Vomiting
Rapid dehydration
110
Cholera treatment
Doxycycline and fluids
111
Immunosuppressed- more at risk to
Bacterial- Cryptosporidium, Mycobacteria, Microsporidia
Viral- CMV, HSV
Overall risk increased
112
Diarrhoea- lab tests
Stool tests- Microscopy, Culture
Ova, cysts and parasites, Toxin detection
Blood tests- Blood culture, Inflammatory markers (FBC/CRP)
113
Diarrhoea Red flags
Dehydration
Electrolyte imbalance
Renal failure
Immunocompromise
Severe abdominal pain
Cancer risk factors
Over 50, Chronic diarrhoea, Weight loss, Blood in stool, FH cancer, change in bowel symptoms
114
Diarrhoea- Key management principles
Fluids, electrolytes
Antiemetics if long time? (effective against vomiting and nausea)
Infection control
Do public health need to be connected, PPE when treating patient, deep cleaning
115
Are antibiotics a treatment for bacterial diarrhoea
No, unless they are immunocompromised
116
RUQ pain infections
Biliary sepsis aka ascending cholangitis
Liver abscess
Pneumonia
117
Lower abdominal pain infections
PID- pelvic inflammatory disease
118
Peptic Ulcer Disease
Helicobacter pylori- commonest cause of ulcer
Lives within mucus layer overlying the gastric mucosa
119
Peptic Ulcer Disease- treatment
CAP = Clarithromycin, Amoxicillin, PPI eg omeprazole
120
Acute Cholecystitis
Gallbladder inflammation, cystic duct obstruction by gall stones
RUQ or epigastric pain, fever and leucocytosis
121
Acute Cholecystitis- treatment
Diagnosis: By ultrasound
Treatment: IV fluids, analgesia and antibiotics
Surgery: Cholecystectomy
122
Ascending Cholangitis
Obstruction of the CBD
fever, abdominal pain, and jaundice (Charcot's triad)
High mortality
123
Ascending Cholangitis- management
Prompt admission and IV antibiotics
ERCP- endoscopic retrograde cholangiopancreatography
Cholecystectomy
124
Liver abscess causes
Bacterial : faecal flora eg E.coli, Klebsiella spp etc
Amoebic: Entamoeba histolytica
Hydatid: Echinococcus granulosus (dog tapeworm)
125
Peritonitis causes
Medical – SBP (spontaneous bacterial peritonitis), PID (pelvic inflammatory disease), dialysis related, TB
Surgical – perforation of GIT
126
Enteric fever
aka typhoid
Mortality 20% 🡪 < 1% with antibiotics!
2-3% become carriers
127
Enteric fever symptoms
Generalised / R lower quadrant pain
High fever
“Relative bradycardia”
Headache and myalgia
Rose spots
Constipation/green diarrhoea
128
Enteric fever- management
Diagnosis- blood culture
Antibiotic, ?emergency surgery for complications
129
Enteric fever- complications
GI bleed
Perforation / peritonitis
Myocarditis
Abscesses
130
Hepatitis
Inflammation of the liver
131
Hepatitis differential diagnosis
viral (A, B, C, CMV, EBV)
drug-induced
autoimmune
alcoholic
132
Autoimmune hepatitis (AIH)
Progressive inflammatory liver condition, mostly effects females (75%), pathogenesis not fully understood
type 1- Anti nuclear (ANA), anti-smooth muscle, (ASMA)
Type 2- anti- liver/ kidney microsomal
133
Autoimmune hepatitis (AIH) clinical features
40% present with acute hepatitis
30% have cirrhosis at presentation
Patients may be asymptomatic or present with fatigue, and abnormalities in liver bichem or present with liver disease on examination
134
Autoimmune hepatitis (AIH) investigations
Liver biochem- ALT high, IgG raised
Liver biopsy- AIH requires liver biopsy for diagnosis and evaluate disease progression
135
Autoimmune hepatitis (AIH) treatment
prednisolone +/- azathioprine
136
Cirrhosis
Liver architecture is diffusely abnormal and interferes with liver blood flow and function, leads to portal hypertension and liver failure
137
Primary Biliary Cirrhosis (PBC)
Progressive disease- progressive destruction of interlobular bile ducts
Pathogenesis unknown
Mostly woman effected (90%)
138
Primary Biliary Cirrhosis/Cholangitis (PBC) clinical features
Mainly itching +/ fatigue, can be asymptomatic with lab abnormalities
other presentations include- dry eyes, joint pain, variceal bleeding and liver failure
139
Primary Biliary Cirrhosis/Cholangitis (PBC) investigations
Serum IgM- high
Liver biochem- often high serum alkaline is the only liver abnormality
Liver biopsy- required for diagnosis, characteristic portal tract infiltrate
140
Primary Biliary Cirrhosis/Cholangitis (PBC) management
Ursodeoxycholic acid- improves bilirubin and ALT levels, should be given in early phase, no benefit in advanced disease
Liver transplant
treatment of cholestatic itch- cholestyramine, Rifampicin, opioid antagonist
treatment of fatigue- disabling, trials for Modafinil (narcolepsy drug)
141
Ductopenia
destruction of the bile duct branch as a result of serve immune damage
142
Primary Sclerosing Cholangitis (PSC)
chronic cholestatic liver disease characterised by fibrosing inflammatory destruction of intra/ extrahepatic bile ducts
50% have IBS
10% develop into cholangiocarcinoma (bile duct cancer)
143
Primary Sclerosing Cholangitis (PSC) clinical features
With IBS- often asymptomatic and picked up by screening with high serum ALP
Symptoms include itching, pain ± rigors, jaundice
144
Primary Sclerosing Cholangitis (PSC) investigations
Magnetic Resonance Cholangiopancreatography (MRCP)- biliary changes- irregularity of calibre of both intra and extrahepatic ducts
145
Primary Sclerosing Cholangitis (PSC) management
Liver transplant- only proven treatment
Ursodeoxycholic Acid: unclear benefits
146
Haemochromatosis
Inherited disease (mostly autosomal recessive)characterised by excess iron deposition in various organs, leading to eventual fibrosis and functional organ failure
147
Haemochromatosis pathology
total iron content is v high (20-40g) vs normal person (3-4g). Iron content is particularly increased in the liver and pancreas (50-100x higher), but still higher in other organs
148
Haemochromatosis investigation
Serum iron/ ferritin elevated
Liver biochem often normal
genetic testing
149
Haemochromatosis management
Venesection- prolongs life and may reverse tissue damage- many initially to reduce iron to normal level, then a few a year
Screening- first degree relative need screened
150
Alpha1-antitrypsin deficiency
Results in inability to export alpha1-antitrypsin from liver. Neonatal jaundice, chronic liver disease in adults
Can lead -to liver disease (protein retention in liver)
-emphysema (protein deficiency in blood)
no medical treatment
151
Hepatocellular carcinoma
Primary liver tumour
Adenocarcinoma formed of cells resembling normal hepatocyte
Most occur in patients with cirrhosis
152
Hepatocellular carcinoma risk factors
Risk: highest for hepatitis B,C, haemochromatosis
lower: cirrhosis from alcoholic, autoimmune disease
Males >Females
153
Hepatocellular carcinoma presentation
May presents with decompensation of liver disease, weight loss ascites, or abdominal pain
154
Hepatocellular carcinoma treatment
Limited- Transplantation, resection or local ablative therapies
Sorafenib recently shown to prolong life
155
Non-alcoholic liver disease (NAFLD)
Includes Non-alcoholic fatty liver (NAFL) and Non-alcoholic steatohepatitis (NASH)
Commonest cause of chronic liver disease
156
Non-alcoholic fatty liver (NAFL)
Too much fat around liver
commonest cause of mildly elevated LFTs
157
Non-alcoholic steatohepatitis (NASH)
Fat around liver with inflammation, fibrosis
Important cause of cirrhosis(10-30% of patients develop cirrhosis)
158
NAFLD risk factors
Obesity (70%), DM (35-75%), hyperlipidaemia (20-80%)
159
NAFLD presentation
Usually asymptomatic, liver ache in 10%
160
How to distinguish between NAFL and NASH
Liver biopsy- inflammation present in NASH
161
NAFL treatment
Still no effective drug treatments
Weight loss works- the more the better
162
Hepatic vein occlusion
prevents blood from flowing out of the liver and back to the heart
Congestion causes acute or chronic liver injury
163
Hepatic vein occlusion causes
Thrombosis (Budd-Chiari syndrome)- may be underline thrombotic disorder
Membrane obstruction
Veno-occlusive disease (irradiation, antineoplastic drugs
164
Hepatic vein occlusion presentation
abnormal liver test, ascites, acute liver failure
165
Hepatic vein occlusion treatment
Anticoagulation
Transjugular intrahepatic portosystemic shunt
Liver transplantation
166
Causes of chronic liver disease
Alcohol
Non alcoholic steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune- autoimmune hepatitis, primary biliary cirrhosis, sclerosing cholangitis
Metabolic-haemochromatosis, Wilsons, 1 antitrypsin deficiency…
Vascular- Budd-Chiari
167
Chronic liver disease- history taking
Past history: alcohol problems, biliary surgery, autoimmune disease, blood products
Social history: alcohol, sexual
Drug history (all drugs!!)
Family history
168
upper GI bleeding
a very common medical emergency, 10% mortality risk
169
Melena
Blood in stool, black and tary
170
Haematemesis
Fresh blood in vomit
171
Coffee ground vomiting
Old blood in vomit
172
Common cause of upper GI bleeding
Peptic ulcer (most common), oesophageal varices
173
Glasgow-Blatchford score
stratifies upper GI bleeding patients, uses BP, blood urea, haemoglobin levels, tachycardia, melaena, syncope, hepatic disease, cardiac failure
174
Variceal bleed- suspect history
liver disease or alcohol excess
175
Variceal bleed treatment
Antibiotics and Terlipressin (vasopressin agonist) reduce mortality.
Endoscopy within 12 hours
176
Non-variceal bleed- suspect history
peptic ulcers, using certain medications; NSAIDs, anticoagulation or antiplatelets
177
Non-variceal bleed
treatment
Consider proton pump inhibitors.
Endoscopy within 24 hours, longer than variceal
178
What has a bigger impact on patient survival for upper Gi bleeds, initial management or endoscopy
Initial assessment and management is more important than endoscopy in most cases
179
Difference in endoscopy treatment for variceal vs non variceal bleeding
Variceal- elastic band around bleed
Non-variceal- clipping bleed
180
Intraluminal intestinal obstruction
* tumour
– carcinoma
– lymphoma
* diaphragm disease
* meconium ileus
* gallstone ileus
181
Tumours obstructing GI lumen
Can form in wall and grow inwards/outwards, growth inwards leads to obstruction of gut
182
Diaphragm disease
NSAIDs damage GI wall, mainly small bowel, fibrous 'diaphragm' scarring occludes the bowel lumen
183
Diaphragm disease- difficult to diagnosis
Normally small bowel, can not use endoscopy or colonoscopy, need to use swallowable camera
184
Gallstone ileus
mechanical intestinal obstruction due to impaction of one or more gallstones within the gastrointestinal tract
185
intramural obstruction
of GI tract
* inflammatory
– Crohn’s disease
– diverticulitis
* tumours
* neural
– Hirschsprung’s disease
186
Crohn's disease obstruction
Characteristic 'cobblestone' appearance
187
Diverticular disease
Infection in the tiny pouches in the colon. The pouches are called diverticula
Typically occurs in sigmoid colon
Can be asymptomatic, may need removal of sigmoid colon
188
Diverticular disease- pathophysiology
Holes in muscularis (for blood vessels), points of weakness, lots pressure in colon, force mucosa into points of weakness, mucosa out pouches through muscularis, called diverticula
189
Perpetrating Diverticulitis
Diverticulitis, breach of diverticula, contents spill into peritoneum, can lead to peritonitis
190
intramural tumours
tumours grow outwards, compress bowel wall, leading to occulsion
191
Hirschsprung's disease
Congenital, due to missing nerve cells of muscle in colon
Part of bowel doesn't move, causes obstruction
192
extraluminal obstruction of intestinal wall
* adhesions
* volvulus
* tumour
– peritoneal deposits
193
adhesions of intestine
Usually result of previous surgery, causes bands fibrous tissue between different parts of intestine
Can cause kink inn bowel
194
volvulus- intestine obstruction
Sigmoid colon twists on itself, causing obstruction
195
peritoneal tumour
Tumour growing in peritoneum compresses intestine, causing obstruction, problem in palliative care
196
Small Bowel Obstruction (SBO)
Mechanical blockage of the small
intestine
197
Small Bowel Obstruction (SBO)- expanded definition
a form of Intestinal failure (IF) is the inability of the gut to absorb
necessary water, macronutrients (carbohydrate, protein, and fat),
micronutrients, and electrolytes sufficient to sustain life and requiring
intravenous supplementation or replacement
198
Small bowel obstruction (SBO) Aetiology
Compression- Adhesions (typically have episodes), hernia, tumour
Luminal- growth, foreign, stricture
Lack of peristalsis- Drugs (commonly opioids), electrolytes, neurological, serve Ileus/ postop
199
Small bowel obstruction (SBO) symptoms
Colicky pain, absolute constipation (not passing of wind or stool), distension, vomiting
200
Small bowel obstruction patient history
History of preventing compliant- onset, previous episodes (chronic suggests cancer)?
Previous surgery (suggests adhesions)
Medication (opioids= lack of peristalsis, or drugs that alter electrolytes)
Family history- cancer
Social history- functional status for surgery evaluation
201
Small bowel obstruction (SBO)- clinical examination
Distended, tympanic, tender, hernias, bowel sounds (tinkling or absent), scars, PR
202
Small bowel obstruction (SBO)- consequences
Perforation, nutrition, GI vitality (necrosis), Gut barrier/ translocation (bugs in bloodstream, leading to sepsis), fluid losses
203
Small bowel obstruction (SBO)- investigation
CT scan, blood test (FBC, U+E, lactate- increases with poorly perfused gut, c-reactive protein)
204
Small bowel obstruction (SBO)- treatment for all patients
Decompression- nasogastric tube
Fluid replacement/ maintenance, electrolyte replacement, Nutrition (>5 without intake may
need parenteral feed)
Surgery- remove bit obstructed, remove adhesion
205
Barrett’s oesophagus
AKA CELLO- columnar lined lower oesophagus
Metaplasia due to presence of stomach acid in oesophagus destroying the squamous epithelium, leading to stem cells rising up from stomach producing glandular epithelium which is protected by mucin
206
Metaplasia
change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type
207
Barret's oesophagus complications
Increase risk of oesophageal adenocarcinoma
208
Oesophageal
squamous cancer- risk factor
Smoking, high alcohol intake, not result of Barret's oesophagus
209
Oesophageal symptoms that require urgent endoscopy
Acid reflux, pain, difficulty swallowing
210
Gastric cancer global spread
Eastern Asia and eastern Europe high, linked to poor air quality, smoked and pickled food
211
Helicobacter pylori and gastric cancer
Not always a cause, but can cause epithelium change in stomach to intestinal metaplasia, can lead to dysplasia and then carcinoma
212
linitus plastica
Thicken wall, whole stomach infected by cancer
213
Gastric cancer prognosis
Low survival rate (10-20% after 5 year), due to non-specific presentation
214
Why is small intestine cancer uncommon
Fluidity and relative sterility of small bowel contents, and rapid transit time and of the relative sterility of the small bowel itself have been suggested as possible factors
215
Colorectal cancer- risk factors
Most cancers arise from adenomas (dysplastic epithelium, most don't turn into cancer), familial adenomatous polyposis (1% of colorectal cancer), hereditary nonpolyposis
colorectal cancer
216
Familial adenomatous polyposis
Born in normal colons, in teenage years form thousands of polyps in cancer, due to inherited genetic mutation
217
hereditary nonpolyposis colorectal cancer
(HNPCC)
a genetic disease of autosomal dominant inheritance. It is caused by a mutation in one of four genes of the DNA mismatch repair system
218
hereditary nonpolyposis colorectal cancer
(HNPCC)- reasons for identifing
risk of further cancers in index patient and
relatives
* possible implications for therapy
– tolerance of 5-FU etc.
– do not recognise DNA damage
– apoptosis not activated
219
macroscopic features
of colorectal cancer
38% of colorectal cancer (anus, rectum and rectosigmoid junction) can be felt on digital rectal examination
220
What is the most common colorectal tumour
adenocarcinoma
221
Treatment for colorectal cancer at each progression
Adenoma- endoscopic resection
Colorectal adenocarcinoma- surgical resection
Metastatic colorectal adenocarcinoma- chemo, palliative care
222
Hepatitis
inflammation of the liver
(acute< 6 months, chronic persists beyond 6 months)
223
Acute hepatitis- symptoms
None or non-specific, e.g. malaise, lethargy, myalgia
Gastrointestinal upset, abdominal pain
Jaundice + pale stools / dark urine
224
Acute hepatitis- clinical signs
Tender hepatomegaly ± jaundice
± signs of fulminant hepatitis (acute liver failure), e.g. bleeding, ascites, encephalopathy
Blood tests- Raised transaminases (ALT/AST >> GGT/ALP) ± raised bilirubin
225
Causes of acute hepatitis- infectious viral
Hepatitis A, B ± D, C & E
Human herpes viruses, e.g. HSV, VZV, CMV, EBV
Other viruses
226
Causes of acute hepatitis- infectious non- viral
Spirochaetes, e.g. leptospirosis, syphilis
Mycobacteria, e.g. M. tuberculosis
Bacteria, e.g. bartonella
Parasites, e.g. toxoplasma
227
Causes of acute hepatitis- non-infection
Drugs
Alcohol
Other toxins / poisoning
Non-alcoholic fatty liver disease
Pregnancy
Autoimmune hepatitis
Hereditary metabolic causes
228
Chronic hepatitis symptoms
Can be asymptomatic or have non-specific symptoms only
229
chronic hepatitis- clinical signs
Clubbing, palmar erythema, Dupuytren’s contracture, spider naevi, etc
Transaminases (ALT/AST) can be normal
230
chronic hepatitis- clinical signs compensated
liver function maintained
231
chronic hepatitis- clinical signs decompensated
coagulopathy (↑PT, INR); jaundice (↑bilirubin); low albumin; ascites (± bacterial peritonitis); encephalopathy
232
chronic hepatitis- complications
hepatocellular carcinoma (HCC); portal hypertension (varices, bleeding)
233
chronic hepatitis- causes, infection
Hepatitis B ± D, C (& E)
234
chronic hepatitis- causes, non- infection
Drugs
Alcohol
Other toxins / poisoning
Non-alcoholic fatty liver disease
Autoimmune hepatitis
Hereditary metabolic causes
235
Most common form of viral hepatitis
chronic hepatitis B ≈ 257 million
then, chronic hepatitis C ≈ 71 million
236
Hepatitis A (HAV)
Contaminated food & water
Linkage to access to safe drinking water & socioeconomic indicators
HICs- travel, MSM (men sex with men), IV drug use
237
Hepatitis A: Clinical
Short incubation period (15-50 days), acute
Symptomatic
Rarely acute liver failure
100% immunity after infection
238
Hepatitis A: symptoms
Symptomatic- Pre-icteric phase: constitutional symptoms + abdominal pain
Icteric phase (few days to 1 week after pre-icteric phase)
239
Hepatitis A: serological response
anti- HAV IgM initially, anti-HAV IgG provide immunity
240
Hepatitis A: Management
Supportive
Monitor liver function
Primary prevention- vaccines
241
Liver function measures
INR, albumin, bilirubin
242
hepatitis E
4 genotypes- affect different parts of world
G1+2- similar to HAV, transmission through food and water
G3+4- undercooked meat
243
Hepatitis E: Clinical
>95% cases asymptomatic
Usually self-limiting acute hepatitis
Extra-hepatic manifestations (neurological)
244
Chronic Hepatitis E
Risk of chronic infection (GT3/4 only) in immunosuppressed patients
e.g. transplant recipients, HIV patients
rapid progression to cirrhosis
245
Hepatitis E: serological response
anti-HEV IgM initially, partial immunity from anti-HEV IgG
246
Hepatitis E: Management
Acute- supportive, monitor for acute-on-chronic liver failure
Chronic- Reverse immunosuppression (if possible)
If HEV RNA persists, treat with ribavirin ≥ 3 mths
247
Hepatitis E: Prevention
Avoid eating undercooked meats (especially if immunocompromised)
Screening of blood donors
Vaccines in development
248
hepatitis B
Blood-borne virus
Transmission via blood and body fluids
249
Hepatitis B natural history adults !!!!!
Acute HBV infection
Symptomatic- Spontaneous resolution (rick of re-activation with immunosuppression
Chronic HBV infection- asymptomatic Cirrhosis> Hepatocellular carcinoma or Decompensated cirrhosis
250
Hepatitis B natural history (neonates and infants)
251
Hepatitis B: serological response
!!!
anti-HB core IgG- exposure to HBV infection
Hepatitis B surface antigen- Current HBV infection
252
Acute Hepatitis B: presentation & management
Incubation period: 30 to 180 days (mean 75 days)
Supportive management
Monitor liver function (INR, albumin, bilirubin, etc.)
Rarely fulminant hepatitic failure: 0.1 to 0.5%
Oral nucleos(t)ide analogue (tenofovir, entecavir)
Liaise with hepatology / liver transplant centre
Management of close contacts (HBV vaccine if non-immune ± HBIG )
253
254
Hepatitis B: clearance in acute phase
255
256
Hepatitis B: failure to clear / chronic infection
257
Chronic hepatitis B: who to treat?
!!!!!
e-antigen (eAg)- high viral load
e-antibody (eAb)- high immune response
Treat people in immune reactive and immune escape stage
258
Chronic hepatitis B- treatment- pegylated interferon-α 2a
Immunomodulatory
stimulates immune response
Weekly subcutaneous injection
48 week long treatment course
Offers best chance of treatment-free control
Side effects & need for monitoring
259
pegylated interferon-α 2a side effects
260
Chronic hepatitis B- treatment- oral nucleos(t)ide analogues
Inhibit viral replication
HBV DNA polymerase
One tablet once a day
High barrier to resistance
Minimal side effects
Renal monitoring (TDF)
May be required lifelong
261
Hepatitis B: Prevention
Antenatal screening (HBsAg testing) of pregnant mothers
Screening ± immunisation of sexual and household contacts
Childhood immunisation
Universal screening of blood products
262
Hepatitis D
Defective RNA virus
Requires Hep B antigen presence to replicate
Blood-borne virus
Transmission via blood and body fluids
263
Hepatitis B + D coinfection
Infected by hep B + D together, increased risk of fulminant hepatitis in acute infection
264
Hepatitis B + D superinfetion
Infected by hep B, then hep D, acute on chronic hepatitis
accelerated progression to liver fibrosis
265
Hepatitis B + D coinfection natural history
266
Hepatitis D test
Hepatitis D antibody: if positive, test HDV RNA
267
Hepatitis D treat
pegylated inteferon-α 48 weeks (2020: Myrcludex B)
268
Hepatitis C
Blood-borne virus
Transmission via blood and body fluids- IV drug use, blood products
269
Hepatitis C natural history (immunocompetent adults)
!!!
270
Hepatitis C testing
HCV antibody
If +ive, HCV RNA (to see if infection is active)
If +ive, HCV genotype (to determine type of HCV)
271
Hepatitis C treatment- Directly-acting antiviral (DAA) therapy
Combination of antivirals
Drugs have different effects on different genotypes (need to know genotype)
272
Hepatitis C: Prevention
No vaccine
Previous infection does not confer immunity
Blood screening
Cure of 'transmitters", ie programs to reduce IV drug use
273
Coeliac disease
Autoimmune entropy caused by ingestion of gluten
1/4 are genetically predisposed to disease
274
Coeliac disease management
Gluten free diet- strict and lifelong
Dietitian review
Bone density score
Prescription of GF foods
Immunisation
275
Coeliac disease symptoms
severe diarrhoea, excessive wind and/or constipation.
persistent or unexplained gastrointestinal symptoms.
iron, vitamin B12 or folic acid deficiency.
anaemia.
tiredness
276
Coeliac disease associated diseases
Addison’s Disease
Arthritis
Autoimmune Hepatitis
Hashimoto’s Thyroiditis
Idiopathic Dilated Cardiomyopathy
IgA Nephropathy (Berger’s Disease)
Multiple Sclerosis (MS)
Sjogren’s Syndrome
Type 1 Diabetes Mellitus
277
Mucosal Ischemia
Ischemia of blood vessels that supply mucosal layer of stomach, leads to reduce mucin layer and can lead to an ulcer
Common with people with in haemodynamic shock
278
Mucosal Ischemia - treatment
Reverse the mucosal ischemia- cell revert back to normal
PPIs/ H2 blockers to remove acid
279
Causes of gastric ulceration
NSAIDs, Helicobacter pylori (H. pylori), mucosal ischemia, bile reflux, alcohol (high percentage spirits)
280
Helicobacter pylori (H. pylori)
Live in mucin layer in stomach, can lead to acute inflammation, long term helicobacter can cause intestinal metaplasia
281
Causes of malabsorption
Insufficient intake, defective intraluminal digestion, insufficient absorptive areas, lack of digestive enzymes, defective epithelial transport, lymphatic obstruction
282
Causes of malabsorption- Defective intraluminal digestion
Pancreatic insufficiency (CF, pancreatitis), Defective bile secretion (lack of fat solubility- biliary obstruction, ileal resection), Bacterial overgrowth
283
Causes of malabsorption- Insufficient absorptive areas
Coeliacs disease, Crohn's disease, extensive parasitic infection (giardia lamblia), small intestinal resection or bypass
284
Causes of malabsorption- lack of digestive enzymes
disaccharidase deficiency (lactose intolerance- disaccharide broken down in small intestine, causes large release of CO2 and sugars causes diarrhoea), bacterial overgrowth
285
Causes of malabsorption- defective epithelial transport,
Abetalipoproteinemia, primary bile acid malabsorption (mutations in bile acid transporter protein)
286
Gallstones types
Cholesterol, pigment stones (bile acid, phosphate, Mg) + mixed stones
287
Commonest type of gallstones
Cholesterol stones
288
Biliary anatomy
Liver produces bile
Gallbladder stores bile
Responds to CCK
Biliary system drains into D2 (Ampulla of Vater)
289
Gallstones- 5 Fs
fat, female, forty, fertile, fair (skin/ hair)
290
Gallstones pathology
Biliary colic, jaundice, pancreatitis, cholecystitis (stone in stone bladder), choledocholithiasis (stones in bile duct), Cholangitis, Gallstone ileus, Mirizzi syndrome (stone in impacted in Hartman pouch)
291
Biliary colic signs + symptoms
Post prandial colicky pain (worse with fats, RUQ), nausea/ vomiting,
292
cholecystitis signs and symptoms
Constant pain, fever, rigours, tender as inflamed gallbladder contacting peritoneum
293
choledocholithiasis signs and symptoms
jaundice
294
Cholangitis signs and symptoms
Fever >39, jaundice
295
Gallstones investigations
Ultrasounds (USS), FBC, LFTs (alkaline phosphates, ALT, bilirubin, albumin), Clotting factors, amylase (pancreatic damage), MRCP (MRI of bile system)
296
Mirizzi syndrome
297
Gallstone Ileus
a mechanical intestinal obstruction due to impaction of one or more gallstones within the gastrointestinal tract
298
Gallstones treatment
Antibiotics, analgesia- NSAIDs with PPI cover, ECRP (to remove stone from bile duct), cholecystectomy, bile duct exploration/ reconstruction (surgical removal of stone)
299
Pancreatitis- I GET SMASHED
Idiopathic, Gallstones, Ethanol, Trauma. Steroid use, Mumps, Autoimmune, Scorpion stings, Hypercalcemia + hypertriglyceridemia, ECRP, Drugs
300
Most common cause of pancreatitis in England
Gallstones
301
Pancreatitis- signs and symptoms
Abdominal pain that radiates to the back, Nauseas/ vomiting, Low BP, high HR/ RR, low SATS, high temp
302
Pancreatitis complications
Auto digestion, SIRS
303
Pancreatitis complications- Auto digestion
Haemorrhage, pseudoaneurysm, portal thrombosis, necrosis, infected necrosis, pseudocyst
304
Pancreatitis complications- SIRS*****
ARDS,
305
Pancreatitis- severity score
Modified Early Warning Score (MEWS), good history, response to resuscitation
306
Modified Early Warning Score (MEWS)
HR, BP, RR, core body temp, mental status and urine output
307
Pancreatitis treatment
Supportive (fluids, nutrition, antibiotics, critical care), ECRP (to remove stones from bile duct), Cyst drainage, treat pancreatic failure for both exocrine (replace enzymes) and endocrine (diabetic) function
308
Chronic pancreatitis
Flares of pancreatitis with or without trigger, pain, malnutrition, pancreatic duct strictures, may need drainage procedure or total pancreatectomy
309
Chronic idiopathic inflammatory bowel disease (CIIBD)
Crohn's disease, Ulcerative colitis
310
Crohn's disease
Transmural, non continuous inflammation that can occur anywhere in the GI tract
311
Characteristic Crohn's disease appearance
Scarring causes 'cobblestone' appearance
312
Main complications of Crohn's disease
Mainly affects bowel, malabsorption, obstruction, perforation, fistula formation, neoplasia
313
Ulcerative colitis
Only affects mucosa, starts at the rectum and is continuous inflammation, working up the bowel
314
Ulcerative colitis complications
Affects many different parts of the body, Colon, joints, eyes, skin, liver
315
CIIBD- aetiology
Currently unknown
316
Function of Peritoneum- In health
Visceral lubrication
Fluid & particulate absorption
317
Function of Peritoneum- In disease
Pain perception.
Inflammatory and immune responses
Fibrinolytic activity
318
Which is more sensitive to pain (from pressure, temp and laceration) visceral or parietal peritoneum?
Parietal peritoneum
319
Peritonitis
Inflammation of Peritoneum
320
Peritonitis : Classification- onset
Acute : Sudden Onset. Eg Bacterial
Chronic : Gradual Onset . Eg TB
321
Peritonitis : Classification- Source of origin
Primary : No documented Source
Secondary : Bowel Perforation, Appendicitis
322
Peritonitis : Aetiology
Bacterial, gastrointestinal and non-gastrointestinal
Chemical, e.g. bile, barium
Traumatic, e.g. operative handling
Ischaemia, e.g. strangulated bowel, vascular occlusion
Miscellaneous, e.g. familial Mediterranean fever
323
Paths to Peritoneal Infection
Gastrointestinal perforation
Transmural translocation (no perforation)
Exogenous contamination
Female genital tract infection, e.g. pelvic inflammatory disease
Haematogenous spread (rare), e.g. septicaemia
324
Paths to Peritoneal Infection- Transmural translocation
Pancreatitis, ischaemic bowel, primary bacterial peritonitis
325
Paths to Peritoneal Infection- Gastrointestinal perforation
Perforated ulcer, appendix, diverticulum
326
Paths to Peritoneal Infection- Exogenous contamination
drains, open surgery, trauma, peritoneal dialysis
327
Clinical feat. of localised peritonitis
Pain
Nausea and vomiting
Fever
Tachycardia
Localised guarding
Rebound tenderness
Shoulder tip pain ( subphrenic)
Tender rectal and / or vaginal examination (pelvic peritonitis).
328
Diffuse (generalised) peritonitis- Early
Abdominal pain (worse by moving or breathing)
Tenderness
Generalised guarding
Infrequent bowel sounds (paralytic ileus)
Fever
Tachycardia
329
Diffuse (generalised) peritonitis- Late
Generalised rigidity
Distension
Absent bowel sounds
Circulatory failure
Thready irregular pulse
(Hippocratic face)
Loss of consciousness
330
Peritonitis- Investigations
Urine dipstix for urinary tract infection.
ECG if diagnostic doubt (as to cause of abdominal pain) or cardiac history.
Bloods I U&Es I Full blood count (WCC)
Serum amylase (acute pancreatitis/ others like perf duodenal ulcer)
331
Medical management of peritonitis
Correction of Fluid Loss & Circulating Volume
Antibiotics
Urinary Catheterisation I Gastric Decompression
Analgesics
332
Surgical treatment of peritonitis
Remove or divert cause:
Repair of perforated viscus – peptic ulcer
Excision of perforated organ
With or without drainage
With or without restoring continuity
Peritoneal lavage
333
Ascites
Detectable collection of Fluid in the peritoneal cavity
Chronic accumulation of Fluid within the peritoneal cavity
334
Ascites- Classification
Stage 1 detectable only after careful examination / Ultrasound scan (Mild)
Stage 2 easily detectable but of relatively small volume.
Stage 3 obvious, not tense ascites. (moderate)
Stage 4 tense ascites. (Large)
335
Refractory ascites
not mobilised
or early recurrence (after therapeutic paracentesis) <4 weeks
Cannot be prevented by medical therapy
336
Diuretic resistant ascites
refractory to dietary sodium restriction and intensive diuretic treatment
337
Diuretic intractable ascites
ascites that is refractory to therapy due to the development of diuretic induced complications that preclude the use of an effective diuretic dosage
338
Ascites - Causes
Cirrhosis- 75%, main cause
Malignancy- 10%
Heart failure, TB, pancreatitis
339
Ascites malignancy causes
gynecologic neoplasms gastrointestinal malignancies
breast cancer
340
Ascites - Portal Hypertension
- Pathophysiology
A state of sodium water imbalance
Interplay of various neurohormonal agents – renin, aldosterone, sympathetic nervous system, nitric oxide
341
Ascites -Non Portal hypertension- Pathophysiology
Malignancy
Cardiac Failure
Nephrotic syndrome
342
Ascitis in Liver Cirrhosis - Pathophysiology
Portal Hypertension
Shunting of Blood into the systemic Circulation
Splanchnic Vasodilation (release of vasodilators NO)
Systemic Blood Pressure falls due to vasodilation
Renal Hypoperfusion
Activation of RAAS
Increased Na & H20 Retention by kidney
Increased Plasma Hydrostatic Pressure
Increased Transudation of fluid in Peritoneal Cavity
Ascites
343
Exudative Ascites
Occlusion / obstruction of lymphatic /venous drainage
Ascites Protein Concentration above 25 gm/l
344
Transudative Ascites
passage of fluid through a membrane – osmotic pressure, hydrostatic pressure
Protein concentration below 25 gm/l
345
Ascites- Exudate causes
Congestive cardiac failure
Constrictive pericarditis
Nephrotic syndrome
Myxoedma
Bud Chiari Syndrome – Hepatic venous thrombosis
Chylous ascites
346
Ascites- Transudate causes
Cirrhosis
Hypoproteinemic states
-Protein losing enteropathy
-Malnutrition
-Tuberculosis ( minority)
-Malignancy ( minority)
347
Ascites RF in history
Relating to liver disease- long term heavy alcohol consumption, infection (chronic viral hep, IV drug use, travel)
-Non-alcoholic steatohepatitis (Cirrhosis, DM type 2
Obesity, Hypercholesterolemia)
GI/ ovarian cancer
Cardiac
Renal- nephrotic syndrome
Malnutrition- selective protein deficiency
348
Ascites- Clinical Presentation - Symptoms
Abdominal distension
Clothes getting tighter
? Gaining wait
Nausea, Loss of appetite
Constipation
Cachexia- wasting ? weight loss
Pain / Discomfort
Present – malignant
Absent – non malignant
Associated symptoms of underlying cause
349
Ascites- Clinical Presentation - Signs
Abdominal distension
Fluid thrill
Jaundice and other stigmata of liver disease (If liver causse of disease)
350
Ascites- diagnosis- analysis of ascitic fluid
Naked eye assessment
Chemistry
-Proteins
-Amylase
Microscopy
-Cytology
-Organisms
Culture
351
Ascites- diagnosis- Naked eye assessment of ascitic fluid
Most ascitic fluid is transparent and tinged yellow
Pink/ blood tinged fluid implies trauma or malignancy
Cloudy fluid with a purulent consistency indicates infection
352
Ascites- diagnosis- radiology
X-Ray ( 500ml)
Ultra sound scan ( at least 20ml)
CT abdomen (< v small amt)
353
Ascites- diagnosis- Serum Ascites Albumin Gradient [SAAG]
Serum albumin - ascites albumin
Value 1.1 g/dl important cut off ( 97% accuracy)
>1.1 g/dl – Portal hypertension
<1.1 g/dl – non portal hypertensive cause
354
Ascites treatment
*Treatment of underlying cause
*Portal hypertension- salt and fluid restrictions, diuretics, albumen/ colloid replacement
*Paracentesis
*Shunts
-Portosystemic shunts (liver cirrhosis)
-Peritoneovenous shunt- for patients with medically intractable ascites
355
Ascites treatment- portal hypertension
Salt and Fluid restriction
Diuretics
Albumen / colloid replacement
356
Paracentesis
procedure performed in patients with ascites, during which a needle is inserted into the peritoneal cavity to obtain ascitic fluid
357
Crohn's disease treatment- general
No curative treatment
Aims to induce/maintain clinical remission
358
Crohn's disease treatment- Induce remisson
Glucocorticosteroids- 1st line
Early Anti-TNF agents- for patients with poor prognosis
Management of extra-intestinal symptoms
Consider antibiotics
359
Crohn's disease treatment- Maintain remission
Azathioprine, mercaptopurine + methotrexate- conventional maintenance therapies
Anti- TNF agents + novel biological therapies
360
Crohn's disease treatment- surgical management
Indication for surgery- failure of medical therapy, complications, presence of perianal sepsis
Strictureplasty- to widen strictures
Subtotal Colectomy + Ileorectal anastomosis- if CD involves all of Colon and minimally rectum
Panproctocolectomy with an end ileostomy- if CD involves all of colon and rectum
361
Crohn's disease investigations
Blood tests (FBC, iron studies+ serum folate/B12, CRP and ESR)
Stool tests (Stool cultures including C. difficile toxin assay, faecal calprotectin- raised in active intestinal inflammation
Imaging (*MR enterography* > CT enterography)
Colonoscopy with biopsies (2 from 5 different locations)
Upper GI endoscopy for patients with relevant upper GI symptoms
362
Crohn's disease investigations- blood tests
FBC- Anaemia, leucocytosis, may be thrombocytosis: all signs of inflammation
Iron studies- may be normal, or may demonstrate changes consistent with iron deficiency due to malabsorption or GI bleeding
Raised C-reactive protein (CRP) + erythrocyte sedimentation rate (ESR)- Inflammatory markers
363
Crohn's disease investigations- colonoscopy
Aphthous ulcers, hyperaemia, oedema, skip lesions
Characteristic cobblestone appearance
364
Ulcerative colitis investigations
Blood tests (FBC, ESR + CRP, comprehensive metabolic panel including LFTs)
Stool tests (Stool cultures including C. difficile toxin assay, faecal calprotectin- raised in active intestinal inflammation)
*Endoscopy with mucosal biopsy is gold standard*- flexible sigmoidoscopy/ colonoscopy
Abdominal X-ray- patients in acute severe UC attacks to exclude colonic dilation
365
Ulcerative colitis investigations- blood tests
FBC- may show leukocytosis, thrombocytosis, and anaemia
Raised ESR + CRP- inflammatory markers
Comprehensive metabolic panel- should be checked every 6 to 12 months for surveillance of primary sclerosing cholangitis
366
Ulcerative colitis investigations- flexible sigmoidoscopy/ colonoscopy
rectal involvement, continuous uniform involvement, loss of vascular marking, diffuse erythema, mucosal granularity, fistulas (rarely seen), normal terminal ileum (or mild 'backwash' ileitis in pancolitis)
367
Ulcerative colitis treatment- medical management
Induce/ maintain remission
Aminosalicylate are mainstay treatment- effective at maintaining remission and inducing remission for mild to moderate active disease
368
Ulcerative colitis treatment- refractory/ severe colitis
Investigated to confirm active colitis and exclude infection
Biological therapy with anti- TNF agent/ anti-integrin agent
Corticosteroids- initially oral prednisolone, if ineffective hospitalization with IV hydrocortisone and supportive treatment
If IV steroids ineffective after 3 days, either surgery or salvage medical therapy
369
Ulcerative colitis treatment- surgery
Curative, but reduces QoL
Acute disease- Subtotal colectomy with end ileostomy, preservation of rectum is operative choice
More surgical options available at later date; proctectomy with a permeant ileostomy or ileo-anal pouch (1/3 of patients experience pouchitis)
370
Functional Gastrointestinal Disorders (FGIDS)
Chronic GI symptoms in the absence of organic disease to explain the symptoms
Also termed “disorders of gut-brain interaction”
ie IBS, functional dyspepsia
371
Disorders of Gut-Brain Interaction
A group of disorders, classified by GI symptoms, related to any combination of: visceral hypersensitivity, motility disturbances, altered CNS processing, gut microbiota, mucosal and immune function
372
Irritable Bowel Syndrome (IBS)
Affects 10% of pop
Chronic frequent abdominal pain, Altered bowel habit, Bloating commonly associated
373
Dyspepsia
affects 10% of the population
Functional dyspepsia (~80%)
Organic dyspepsia (~20%)
374
Alarm features or Red Flags for GI disease
* Age >45 years
* Short history of symptoms
* Documented unintentional weight loss
* Nocturnal symptoms
* Family history of GI cancer/IBD
* GI Bleeding
* Palpable abdominal mass or lymphadenopathy
* Evidence of iron deficiency anaemia on blood testing
* Evidence of inflammation on blood/stool testing
375
Faecal Calprotectin
Marker of GI inflammation
Found in UC and CD, not in IBS
376
Wernicke’s encephalopathy
Thiamine (vitamin B1) deficiency with classic triad of confusion, ataxia and ophthalmoplegia (nystagmus, lateral rectus or conjugate gaze palsies)
377
Wernicke’s encephalopathy- causes
Chronic alcoholism, eating disorders, malnutrition, prolonged vomiting
378
Wernicke’s encephalopathy- management
Diagnosis is primarily clinical
Urgent thiamine replacement via IV/IM then oral supplement until no longer at risk
379
Gilbert's syndrome
Common cause of unconjugated hyperbilirubinemia due to decrease UGT-1 activity (enzyme that conjugates bilirubin)
380
Gilbert's syndrome- diagnosis
Mild increased bilirubin, normal FBC and reticulocytes (normal haemolysis)
381
Gilbert's syndrome- presenation
May go unnoticed for years and usually presents in adolescence with intermittent jaundice occurring during illness, exercise or fasting
382
Pancreatic cancer
Most common presentation is at 65-75 years of age with painless obstructive jaundice and weight loss. Generally presents late with advanced disease.
383
Pancreatic cancer- pathology
Mostly ductal adenocarcinoma which metastasize early and present late
Ampullary or islet cell
tumours are rarer but better prognosis
384
Pancreatic cancer- RFs
Smoking, alcohol, carcinogens, DM, chronic pancreatitis, high waist circumference, hight fat/red meat diet
385
Pancreatic cancer- signs
Jaundice + palpable gallbladder, epigastric mass, hepato/ splenomegaly, lymphadenopathy, ascites, weight loss + anorexia
386
Pancreatic cancer- Investigations
pancreatic protocol CT
abdominal ultrasound
LFTs (show degree of obstructive jaundice)
387
Pancreatic cancer- Appearance on abdominal imaging
Pancreatic mass +/- dilated biliary tree +/- hepatic mets
388
Pancreatic cancer- Management
Based on extent of disease, given most present late, a lot of treatment is palliative (ie surgery to relive symptoms, chemo to delay disease progression)
389
Pancreatic cancer- prognosis
Mean survival <6 months
5 years survival is 3%
Prognosis better if clear margins during surgery, use of whipple procedure or if tumour is ampullary or islet cell
