LIVER / GI Flashcards
(116 cards)
1
Q
What does autoimmune hepatitis require for diagnosis
A
Biopsy - presence of plasma cells and lymphocytes in portal tracts
2
Q
Investigations for chronic liver disease
A
1.Bloods:
LFT - can indicate if it is a more liver or biliary picture (biliary alk phos + GGT), prothrombin time
Serology - Hep B, C, EBV, CMV, IgGs - autoimune
FBC - infection, lympocytes
Biochem - tells you metabolic causesIron (haemochromatosis), Cu (wilsons), alpha trypsin 1 deficiency
U&Es - tell you if there are any problems with fluid balance and overload to liver
2.Imaging
Ultrasound to rule out gallstones
Can use CT, MRI to confirm if -ve but suspicion
3.Biopsy
If needed, based on blood results, eg to confirm autoimmune, NAFLD
3
Q
What would you see on biopsy for primary sclerosing cholangitis (PSC)
A
Periductal “Onion skin” fibrosis around the hepatic ducts/ bile duct - see strictures
4
Q
What would you see on biopsy for primary biliary cholangitis (PBC)
A
See granulomas in wall of bile duct
5
Q
What would you see on biopsy for autoimmune hepatitis
A
Lymphoplasmacytic infiltrate (plasma cells around portal tracts)
6
Q
Cause of autoimmune hepatitis
A
Unknown - affects you or middle aged women predominantly. May present with signs of autoimmune disease + hepatitis signs
7
Q
Which autoimmune cause of liver failure overlaps with IBD
A
Primary sclerosing cholangitis - 70% of pt also have colitis. This of this as a vasculitis overlap as well- ANCA associated
8
Q
Which autoimmune disease in liver failure responds to steroids
A
Autoimmune hepatitis
PBC + PSC don’t respond
9
Q
Describe a clinical scenario of primary biliary cholangitis
A
Female, young - middle aged Liver/ Biliary + Autoimmune symptoms, itching, mild jaundice, joint pains, fatigue Bloods - biliary + - alk phos, liver enzymes ok Albumin - normal Raised IgM AMA + (95% of pts) US - normal Serology - no infection Biopsy, granulomas in biliary wall Limited response to steroid
10
Q
Presentation of fatigue & itching
A
Primary biliary cholangitis
11
Q
Treatment of PBC, PSC
A
ursideoxycholic acid
12
Q
Gene associated with haemochromatosis
A
HFE
13
Q
Treatment of haemochromatosis
A
Venesection
14
Q
Before starting anticoagulants or anti-thrombotic drugs what blood test should be done
A
LFT - check the patient isn’t at risk of haemorrhage or that metabolism may be altered
15
Q
Liver cancer most commonly occurs in patients with what liver pathology/ disease stage
A
Cirrhosis Higher risk: Hep B, C (advanced to cirrhosis) Haemochromatosis Lower risk - alcoholic FL, autoimmune diseases
16
Q
What screening should be done on any patient with liver cirrhosis
A
Hepatocarcinoma screening - 50% produce alpha fetoprotein
17
Q
Liver cancer is most commonly primary or secondary
A
Secondary
18
Q
Causes of primary liver cancer
A
Cirrhosis - hepatitis and haemochromatosis causes
19
Q
What is a common asymptomatic chronic liver disease
A
Non alcoholic fatty liver (non alcoholic steatohepatitis)
May pick this up through a routine LFT
20
Q
What is the difference between non-alcoholic fatty liver and non-alcoholic steatohepatitis
A
NAFL is fat deposits and inflammation over the liver. NASH is fat, inflammation and fibrosis (more advanced liver disease than NAFL)
Need to do biopsy to distinguish between these - important clinically as fibrosis means the pt is closer to cirrhosis. NASH important cause of ‘cryptogenic’ cirrhosis.
21
Q
Treatment of non alcoholic fatty liver
A
Weight loss
Few effective drug treatments
22
Q
Pathology of alpha 1-antitrypsin deficiency
A
Enzyme that inhibits protein breakdown, if deficient, get increased protein breakdown, eg like in emphysema.
Protein cant be transported out of liver.
Build up in liver - get inflammatory response, see eosinophils on histology
Deficiency in blood.
23
Q
Vascular cause of acute liver injury
A
Hepatic vein occlusion due to thombosis
Causes: underlying thrombotic disorder (Budd-Chiari syndrome), chemotherapy (dont know why)
Congestion causes acute or chronic liver injury
Presents with abnormal LFT, ascites, acute liver failure
Treatment - anticoagulation, or shunt
Liver transplant is patient develops liver failure
24
Q
Causes of liver disease
A
Drugs
Alcohol
Virus - hepatitis B, C, D & E, CMV, EBV
Autoimmune - ANA, AMA related
Metabolic - haemachromatosis, wilsons, alpha trypsin one deficiency
Vascular - hepatic vein occlusion
25
Common causes of acute liver disease
```
Adverse drug reaction (30% of all presentations)
Alcohol hepatitis (stand alone, or +CLD)
Viral - hep B or C
Autoimmune hepatitis
Hepatic vein occlusion
```
26
Common causes of chronic liver disease
```
Alcoholic fatty liver
Non-alcoholic fatty liver (metabolic syndrome)
Hepatitis B or C
Autoimmune
Metabolic - haemochromatosis etc
```
27
Presentation (symptoms) of acute liver injury
Jaundice
Malaise
Nausea
Anorexia
28
Presentation (symptoms) of chronic liver injury
Ascites
Malaise
Oedema
Haematesis
29
Signs of chronic liver disease
Spider naevi
Palmar erthyema
Leuconychia - White nails with (from low albumin)
Terry's nails - 2/3 white, distal 1/3 reddened
Clubbing
hepatomegaly
30
Itching is more common with unconjugated or conjugated billirubin
conjugated, t/f more or a sign in obstructive jaundice rather than haemolytic
31
What is cholestatic jaundice
Jaundice with dark urine and pale stools
32
What is biliary pain
Right upper quadrant pain, can radiate to shoulder
| More common after a meal, lasts a couple of hours
33
Define cirrhosis
Irreversible liver damage. Large thick bands of fibrous tissue deposited between portal tracts and central vein - bridging fibrosis. Nodular regeneration in between.
Loss of normal hepatic architecture.
34
Causes of cirrhosis
Alcohol - chronic use
Chronic hepatitis B or C infection
Metabolic genetic disorders - haemochromatosis etc
Hepatic vein events - Budd-Chiari
Non-alcoholic steatohepatitis
Autoimmune - all 3
Drugs - amioderone, methyldopa, methotrexate
35
Signs of liver failure
```
Bleeding - coagulopathy (failure of clotting factor synthesis)
Encephalopathy
Odema
Sepsis
Spontaneous bacterial peritonitis
```
36
Signs of portal hypertension
Ascites
Splenomegaly
Oesophageal varices - umbilical varices
37
Causes of biliary disease
Gallstones - anywhere in biliary tree
| Autoimmune - PBC, PSC
38
Causes compensation in cirrhosis
```
Dehydration
Constipation
Covert alcohol use
Infection
Opiate over use
GI bleed
```
39
GI non diarrhoea disease
Salmonella, Typhoid (enteric fever), gastritis, peptic ulcer disease, acute cholecystitis, peritonitis, amoebic liver abscess
40
What is the secretory antibody of the intestines
SIgA - secretory IgA
41
List some common diarrhoea GI infections
Bacterial - e coli, shigella, cholera, H pylori, whipples, Aeromonas (gram -ve bacteria in water)
Viral - rotavirus, noravirus
Parasite - cryptosporidium (water dwelling), cycospora (fresh fruit)
Worms - schistosomiasis
Travel - travellers diarrhoea
Antibiotics - Clostridium difficile
Whipple's disease - gram positive bacteria
42
Explain how rotavirus damages the body/ is pathogenic. What are its virulence factors
1. Following ingestion, rotaviruses infect the epithelial cells of the small intestine, mainly the jejunum. (Rotaviruses are resistant to acid pH).
2. Histologically, there is shortening and atrophy of the villi, flattening of the epithelial cells, and denuding of the microvilli.
3. This decreases the surface area of the small intestine, and limits production of digestive enzymes such as the disaccharides, normally synthesized by cells of the brush border.
4. The patient suffers a malabsorptive state in which dietary nutrients such as sugars are not absorbed by the small intestine.
5. This results in a hyperosmotic effect causing profuse diarrhoea
43
How does Rotavirus cause disease to the host
By modification of host cell structure and function of intestinal villi and microvilli.
Shortening and atrophy of villi, flattening of epithelial cells
44
Why is brush border important
Absorption - location of enzymes that catalyse disaccharides (maltose) to glucose for absorption. Na+ channels on enterocytes for secondary transport of glucose.
45
Commonest cause of gastroenteritis in adults
1. Virus - norovirus
| 2. Food poisioning - bacterial, campylobacter jejuni
46
What age group does Rotavirus affect nearly all of?
Children under 4 years
47
What is the most common risk of rota virus vaccine in children
Intussusception
48
Bacteria that causes gastroenteritis from reheated food
Bacillus cereus
49
What is the organism most likely to cause vomitting and diarrhoea <6hours after eating
1. Staph aureus - finger food
| 2. Bacillus cereus - re-heated foods (rice)
50
List the time course of symptoms for common bacterial causes of foodborne diarrhoea
```
Staph A: 6 hours or less
Bacillus cereus: <6 - 16 hours (think would present w/in a day)
Salmonella: 1-3 days
Campylobacter jejuni: 1-3 days
Shigella: 1-3 days
Vibro parahaemolyticus: 1-3 days
E coli (w/ shiga toxin, EHEC): 5 days
```
51
Common food causes of diarrhoea
Dairy, meats (uncooked), salads
Uncooked foods - fruits
Finger foods - staph aureus
52
What foods is EHEC (enterohaemorrhagic e coli; O157) associated with? What symptoms differentiate this from other forms of E Coli infection and what are the complications
Beef & milk.
Bloody diarrhoea. No fever. Adult.
Can develop HUS - haemolytic uremic syndrome
Shiga toxin gets into microvasculature endothelium and damages cells. This promotes thrombi to form. As RBCs pass through damaged microvessles, they are lysed = haemolytic (schistocytes). They are also killed with taken into thombus. Glomerular capillaries are mainly effected = uremic.
Shiga toxin, endothelial injury, thrombi, lyse RBCs, glomerulus capilliaries.
53
Infectious causes of bloody diarrhoea
E Coli 0157
Shigella
Campylobacter jejuni
(ESC)
54
What pathogen is most likely cause of travellers diarrhoea. What are it's virulence factors (toxins) and how does it cause diarrhoea?
1. ETEC - ecoli ; 2. EAEC (enteroaggregative- EAST toxin)
Toxins = heat labile toxin (LT); heat stable toxin (ST); pilli
Both toxins upregulate (stimulate the activation of) the CFRT (cystic fibrosis transmembrane regulator) channel
Get more CRFT channels = increased movement of Cl out of cell into lumen. Electrolyte movement means that water follows.
NB. Cl is transported into enterocyte from circulation with Na+ and K+, so if increase movement of Cl into lumen, get water loss from circulation to provide this.
55
What toxin is associated with EHEC, what is its virulence factor
Shiga like toxin + T3SS (syringe like protein secretion system - basically secretes something - enzymes?, called 'effectors' - that mess up actin & myosin in the enterocyte, and use enterocyte microfilaments to form a pedestal for bacteria to sit on, this gives it really good attachment to lining of the SI.
Attachment with T3SS compromises the lining on enterocytes & ion and nutrient absorption (Na+) = water stays in lumen and more moves in from circulation because of hyperosmolarity in lumen.
Enters endothelium, causes injury and initiates thrombus formation.
NOT invasive. Ecoli remains on surface of enterocyte, system effects caused by Shiga toxin.
56
What group are mainly affected by EIEC - enteroinvasive e coli.
How do these e coli get into enterocytes?
What are the symptoms?
Children
Get in using T3SS and invasins - invasin is an effector that causes ulceration and allows e coli to move into cell.
Occure in large intestine, not small intestine.
Symptoms - dysentery. Bloody diarrhoea, fever, abdo pain.
57
What group is EPEC most common in, what is its virulence factor and symptoms
Common in children < 1 year
Virulence = T3SS, adhesion
Symptoms = watery diarrhoea
58
List the different types of E Coli that cause gastroenteritis
ETEC (enterotoxigenic) - travellers
EHEC (enterohaemorrhagic) - food borne, milk beef
EIEC (enteroinvastive) - Large intestine, children, dysentry
EAEC (enteroaggregative) - travellers
EPEC (enteropathogenic) - P = paediatric, children <1
DAEC
UPEC - uro-pathogenic - UTI, mainly women
59
List some causes of gallstones
Depends where the gallstones are.
If in hepatic ducts - could be because of too much cholesterol (bile is made up of water, fats - cholesterol, bilirubin, and bile salts - any imbalance in these could cause a stone).
Too much bilirubin - think of haemolytic (pre-hepatic) and hepatic causes - cirrhosis, fatty liver etc
If in bile duct, could be because of primary biliary cholangitis or primary sclerosing cholengitis, bc of obstruction in the bile duct and stasis.
60
What are the commonest compositions of gallstones
Cholesterol
| Calcium carbonate
61
Common pathogens of peritonitis
Surgical
2° bacterial peritonitis due to to perforation or trauma; polymicrobial with gut flora
Spontaneous bacterial peritonitis (SBP)
complication of ascites in cirrhosis, E coli and other GNB, S. pneumoniae,
Paediatric in absence of ascites
S. pneumoniae and other streptococci
Infection 2° peritoneal dialysis
with Staph. aureus , coagulase negative staphylococci or other skin flora, E. coli, , P. aeruginosa or other gram negative bacteria
Pelvic inflammatory disease (PID)
As complication of chlamydial or gonococcal sexually transmitted infection (STI) in young women
Tuberculous
62
What is charcot's triad
Fever
RUQ Pain
Jaundice
63
List some examples of non-infectious causes of peritonitis
Foreign body post surgical
endometriosis
pancreatitis
64
What is Reynolds pentad
Charcot's triad, plus:
Hypotension
Confusion/altered mental state
65
What does MRCP stand for
| What does ERCP stand for
Magnetic resonance cholangiopancreatography
| Endoscopic retrograde cholagiopancreatography
66
When is an MRCP or ERCP used
Looking for gallstones
| Use if ultrasound not shown anything but have clinical suspicion
67
What investigations should be done in a patient who you suspect has ascending cholangitis
Abdominal ultrasound
MRCP, ARCP if ultrasound -ve or unclear
Bloods - LFTs
68
What is the management of ascending cholangitis
```
IV fluid
IV antibiotics
ERCP to remove stone
Stenting
Laproscopic cholecystecomy
Open surgical exploration/drainage/percutanous cholangiography
```
69
Is bile sterile
Yes
Commensal bacteria of the gut is prevented from infecting bile by flow
When flow is partially or fully obstructed by gallstone then gut bacteria can colonise bile, cause cholangitis and ascend biliary tree to liver
70
What would be the signs and symptoms of biliary sepsis
```
RUQ pain
Jaundice
Fever
Hypotension
Confusion/ altered mental state
```
71
What are the signs and symptoms of acute cholecystitis, how does this clinical presentation differ from biliary colic (gallstones) and ascending cholangitis
RUQ pain
Fever - would differentiate from gallstones
Bloods - LFT, FBC - raised inflammatory markers - differentiate from gallstones
No jaundice - if ascending cholangitis would have jandice
72
Risk factors for acute cholecystitis
Diabetes
| Obesity
73
Common bacterial cause of gastritis and peptic ulcers
| Risk factor for gastric carcinoma
Helicobacter Pylori
74
What are the pathogenic mechanisms of H Pylori
Synthesizes urease which produces ammonia. Ammonia damages the gastric mucosa = ulcer.
Ammonia can also increase (neutralise) pH making stomach more hospitable to other pathogens
75
What is the treatment for H Pylori infection
PPI to lower acid level that is irritating ulcers - eg. omeprazole
Antibiotics - H Pylori is a gram negative rod
Clarithromycin (macrolide, ribosome inhibitor)
+ Amoxicillin (bacterial cell wall inhibitor)
76
Risk factors for H Pylori infection
Age - more likely to have living as commensal
77
Describe the routes of parthenogenesis of H Pylori infection and possible outcomes
1. Normal/ slightly increased gastric acid = no disease (due to differences in bacterial strain and/ or genetics) H pylori is not a harmful commensal
2. Increased gastric acid production - bc of ammonia and drive to change ph (dont really know if true)
- > causes peptic ulcers
3. Lower ph bc of ammonia
- >causes gastric cancer
78
What is diverticulitis
Infection of diverticula - out pouchings of the colon, these alone arent a disease or may not cause problems, they from because of weak spots in the colon wall. When they become infected = diverticulitis
79
Causes of peptic ulcer disease
H Pylori
NSAIDs (cox-1 inhibitors, = inhibit prostaglandin synthesis, required for mucus production, decreased = reduced mucosal barrier = ulcer).
Bile salts - duodenal reflux
80
GI infections that cause dysentery (diarrhoea + blood)
```
C Diff
Campylobacter jejuni
Amoebic dysentery
Shigella
E coli - EHEC & EIEC
Yersinia entrocolitis
```
81
List some non diarrhoeal GI infections
```
Gastritis - H pylori infection
Staph A - finger food
Bacillus cereus - finger food
Yersinia entercoliticia
Ascending cholangitis - risk of biliary sepsis
Cholecystitis
Amoebic liver abscess
Peritonitis
```
82
Signs of ascending cholangitis
Charcots triad
83
What empirical antibiotics would you give for appendicitis
Co-amoxiclav or cephalosporin (if penicillin allergy, eg cefuroxime): cell wall target
+ Metronidazole: intracellular target
84
What empirical antibiotics would you give for ascending cholangitis
IV Co-amoxiclav - dont know why
85
What foods is salmonella associated with
Chicken & eggs
86
What food is campylobacter associated with
meats
87
What food is EHEC associated with
beef
| milk
88
What foods is staph A associated with
any finger food
89
what advice would you give to a patient who has diarrhoea and is taking the oral contraceptive pill
To count the days she has diarrhoea as missed pill day and to use alternative contraception
90
Which IBD condition is associated with an increased risk of uveitis, iritis, episcleritis and ankylosing spondylitis
Ulcerative colitis
91
Name some pathological differences between Crohn's and UC
Crohn's can affect whole GI tract
UC - large bowel only
Crohn's has patchy distribution across mucosa and is transmural, non caseating granulomas
UC - continuous distribution with ulcers, only usually affects mucosea and submucosa
Crohns' - malabsorption syndrome bc it mainly affects SI
UC - electrolyte imbalances bc affects large bowel
92
Which IBD has the most systemic complications
```
Ulcerative colitis
Liver - inflammation & PSC
Skin - skin abscesses
Eyes - uveitis etc
Joints - ank sponds
```
93
Commonest cause of infectious gastritis
H Pylori
94
Causes of gastritis
Acute = alcohol (binge), NSAID, asprin, reflux (duodenal), stress (ischemia)
Chronic = H Pylori, autoimmune (pernicious aneamia), chemical - NSAIDS, asprin, corticosteroids, bile reflux (secondary to gastrectomy - bilous vomitting)
Others: Coeliac gastritis, Eosinophillic - associated with Scleroderma and Lupus, Granulomatous - associated with crohns
95
What are the two commonest causes of peptic ulcers, what are the commonest sites of peptic ulcers and age groups
Causes - H Pylori, NSAIDS
Duodenal (most common)
Gastric (less common, more common in elderly)
Peptic ulcers more common in elderly
96
Complications of peptic ulcers
Haemorrhage- posterior surface of duo & gastroduodenal artery commone place. If haemorrhage in stomach = haematemesis, if duodenum = melaena
Perforation - peritonitis
97
Causes of peptic ulcers
Blood supply - ischemia
Acid production - H Pylori
Mucin production - NSAIDs, asprin, H Pylori
98
Cause of coeliac's disease
Adenovirus type 12 infection + genetic susceptibility (HLA dq2, dq8, B8)
99
What auto-antibodies are associated with coeliacs disease
Anti-gliadin, Anti-transglutaminase, Anti-endomysial in 90% of patients
100
What are the pathological changes of coeliacs disease
Villus atrophy
| Crypt hyperplasia
101
How is coeliac's diagnosed
Bloods - auto antibodies (90% of pts)
Biopsy - histological changes
Response to gluten free diet - clinical improvement can be achieved within 48 hours of diet change and full remission can be achieved
102
What are the symptoms/ features of malabsorption
Weight loss
Changes in bowel habit/ stools
Anaemia
103
List the different pathology of malabsorption
1. Insufficient intake
2. Problem with intraluminal digestion (pancreas problem, biliary obstruction)
3. Insufficient surface area (coeliacs, crohns - resection, Giardia)
4. Deficiency in digestive enzymes - lactose intolerance, bacterial overgrowth (brush boarder)
5. Defective epithelial transport - bile reabsorption
6. Lymphatic obstruction - lymphoma, TB
104
Symptoms of coeliac's disease
Malabsoption symptoms if severe, if milder, bloating and indigestion
105
Risk factors for GORD
```
Obesity
Hiatus hernia
Increased gastric fluid volume
Smoking
Alcohol
Hot drinks
Caffeine
Patient age
```
106
Pathology of GORD
Anything that increases abdominal pressure relative to lower oseophageal pressure.
Obesity, pregnancy, delayed gastric emptying, hiatus hernia.
Lower sphincter opens - acid, pepsin reflux - squamous epithelium damaged - inflammation - repair - fibrosis - may get metaplasia to goblet cells - Barrett's oseophagus - 1% lifetime risk of adenocarcinoma.
107
What is bacterial overgrowth
Upper small intestines are sterile. Stasis of luminal contents (eg in systemic sclerosis) gives bacterial in lower intestines more opportunity to grow. Impairs brush border enzymes = malabsorption
108
What is the most common type of volvulus
Sigmoid, then cecal
109
What are the commonest types of bowel obstruction and their causes
1. Small intestine adhesion - cause previous surgery
2. Small intestine inflammation - cause crohn's, inflammation - stricture - obstruction
3. Large bowel obstruction - colorectal cancer - most often in rectum
110
What are the most common cancers in the UK
Breast
Prostate
Lung
Bowel
111
What is the main type of colorectal cancer
Adenocarcinoma
112
What stages do cells go through before coming cancerous
hyperplasia - metaplasia (change to other differentiated cell, eg goblet to squamous) - dysplasia - change to undifferentiated (abnormal) cells - carcinoma in situ - invasion - metastasis
113
What investigations should you do for peritonitis
Bloods - FBC, U&E, LFT, culture
Imaging - ARX, CT
In primary - sample ascities fluid and culture
114
What measure in ascities fluid is 100% indicative of SPB
ascities lactate >250 mg/dL
115
What is the pathology of haemochromatosis
Human haemochromatosis protein mutation (HFE gene). This protein regulates expression of hepcidin (with some interaction of transferrin gene as well)
Basically, the mutation leads to decreased expression of hepcidin, which = unregulated absorption of Iron = increased serum irom = deposit in tissues, heart, pancrease, liver etc = fenton reactions (generate free radicals) = tissue damage = organ failure. Main one to think about is heart failure and liver failure.
116
Describe iron metabolism
Absorption into enterocytes via haem transporters or metal transporter (Fe2+), movement out of enterocyte via ferroportin (hepcidin regulated) -> binds to transferrin -> liver or macrophage for storage -> taken in by transferrin receptor. Released from macrophage or liver cell by ferroportin (hepcidin regulated).
