Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase2a > GI and liver > Flashcards

GI and liver Flashcards

1
Q

which microorganism is likely to have caused each of the following:

  • 84yr old with diarrhoea after a surgical operation at northern general
  • 36yr old with low volume bloody stools who works in a takeaway
  • 87 year old in a care home with confusion, dehydration, altered consciousness and diarrhoea
  • 2 year old who has recently been to a petting zoo, loss of appetite and loose stools
  • 27 year old student just returned from backpacking around south asia, diarrhoea, flatulence, nausea and abdo pain
A
  • Clostridium difficile
  • shigella
  • norovirus
  • e.coli
  • vibrio cholerae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what should be done if you suspect c.dif infection

A
  • control antibiotic usage
  • isolate patient
  • enteric precautions
  • environmental cleaning
  • treat with metronidazole or vancomycin
  • test stool samples for toxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the at risk groups of diarrhoea

A
  • doubtful personal hygiene
  • children attending preschool or nursery
  • people whose work involves preparing or serving unwrapped/uncooked food
  • HCW/ social care staff working with vulnerable people
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the causes of acute liver injury

A
  • viral (a,b,EBV)
  • drug
  • alcohol
  • vascular
  • obstruction
  • congestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the causes of chronic liver injury

A
  • alcohol
  • viral (B,C)
  • autoimmune
  • metabolic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the presentation of acute liver injury

A
  • malaise
  • nausea
  • anorexia
  • jaundice
  • confusion
  • bleeding
  • liver pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the presentation of chronic liver injury

A
  • ascites
  • oedema
  • varices
  • malaise
  • anorexia
  • easy bruising
  • wasting
  • hepatomegaly
    rarer
  • jaundice
  • confusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the stages of bilirubin metabolism

A

haemoglobin –> haem –> biliverdin –> unconjucated bilirubin –> conjugated bilirubin –> urobilinogen — to either urobilin in urine or stercobilin in faeces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

increase of which compound causes jaundice

A

plasma bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the two types of jaundice and their causes

A

pre hepatic/unconjugated
- haemolysis (over production)
- gilberts syndrome (impaired conjugation)
- drugs (impaired hepatic uptake)
- neonatal jaundice
cholestatic/conjugated
- liver disease - hepatic - hepatitis, ischaemia, immune, alcohol
- bile duct obstruction - post hepatic - gallstone, stricture, blocked stent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does the urine and stools look like in cholestatic jaundice

A

urine - dark

stools - pale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

an increase in which liver enzymes may indicate liver disease

A

ALT

AST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the management of gallstone in the gallbladder and in the bile duct

A 
gallbladder
- laparoscopic cholecystectomy
- bile acid dissolution
bile duct 
- ECRP with spincterectomy and removal (balloon)
- crushing
-stent
- antiemetics 
- NSAIDS
-IV fluid 
NBM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what can drug induced liver injury cause

A
  • acute hepatitis

- acute liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the symptoms of paracetamol poisoning

A
  • vomiting and RUQ pain

- then AKI, jaundice and encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the management of paracetamol poisoning

A
  • N acetylcysteine given by i.v.

- supportive to correct renal failure, encephalopathy, acid base balance, coagulation defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is a poor prognosis from paracetamol poisoning indicated by

A
  • acidosis
  • increased creatinine
  • late presentation
  • increased prothrombin time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is ascites and its causes

A
  • accumulation of protein rich (ascitic) fluid on the abdomen
  • chronic liver disease
  • neoplasia
  • pancreatitis, cardiac causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the symptoms and signs of ascites

A
  • abdominal distension
  • puddle sign
    -shifting dullness
  • flanks fullness
    symptoms
  • distension
    -nausea
  • constipation
  • loss of appetite
  • weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the pathogenesis of ascites

A
  • portal hypertension!
    causes systemic vasodilation, secretion of renin angiotensin, vasopressin, NaD
    leads to fluid retention
  • low serum albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the management of ascites

A
  • low sodium diet
  • bed rest
  • diuretics e.g spironolactone
  • shunts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the difference between exudative and transudative ascites and give examples of conditions that cause each

A

transudative - pushed out by hydrostatic pressure due to decreased protein or increased venous pressure

  • cirrhosis
  • hypoproteinemic states
  • CCF
  • pericarditis

exudative - due to increased capillary permeability due to infection, inflammation or malignancy

  • TB, pneumonia
  • SLE, RA
  • carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is steatosis

A

fat accumulation in hepatocytes, can cause acute or chronic injury to the liver
affects cells with least o2 first - zone 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is cirrhosis

A

chronic irreversible liver damage and loss of hepatocellular architecture

  • hepatic failure
  • varices due to portal hypertension and ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

which cell mediates acute alcoholic hepatitis

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the causes of portal hypertension

A

cirrhosis
fibrosis
portal vein thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the pathology of portal hypertension

A

increased hepatic resistance

increased splanchnic blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the consequences of portal hypertension

A
  • varices - treat with terlopressin (gastric vasoconstrictor) and endoscopic binding
  • splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the complications of chronic liver disease

A
  • constipation
  • GI bleeds
  • hypo: Na, Ka, glycaemia
  • alcohol withdrawal
  • susceptible to infections due to decreased reticuloendothelial function, impaired opsonisation, leukocyte function and permeable gut wall
  • neoplasm development - in macro nodular cirrhosis when nodules regenerate this is prone to errors
  • malnutrition
  • coagulopathy due to decreased coagulation factor synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is spontaneous bacterial peritonitis and treatment

A
  • the commonest infection in cirrhosis
  • diagnosis based on neutrophils in ascitic fluid
  • commonest organisms - e.coli, klebsiella and streptococci
  • infection of the ascitic fluid
    cefotaxime and metronidazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the causes of chronic liver disease

A
  • alcohol
  • non alcoholic steatohepatitis
  • viral hepatitis (B,C)
  • immune - autoimmune hepatitis (AIH)
    - primary biliary cirrhosis/cholangitis (PBC)
    - primary sclerosing cholangitis ( PSC)
  • metabolic -haemochromatosis
    - wilsons
    - a1-antitrypsin deficiency
  • vascular - Budd - Chiari
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what tests can be used in diagnosis of chronic liver disease

A
  • viral serology - Hep B surface antigen/Hep C antibody
  • biochem - copper and iron studies
  • radiological
  • immunology - autoantibodies, immunoglobulins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the tests for autoimmune hepatitis

A
  • liver biopsy - lymphocytes and plasma cells within portal tracts and lobular parenchyma
  • -resultant damage causes apoptosis causing necrosis
  • serum bilirubin, ALT, AST and ALP all usually increased
  • hypergammaglobulinaemia
  • positive autoantibodies (ASMA +ve in 80%, ANA +ve in 10%)
  • increased IgG in 97%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the management of autoimmune hepatitis

A
  • immunosuppressants - prednisolone shows good response

- liver transplant if liver has cirrhosis (30% have at presentation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is primary biliary cirrhosis/cholangitis (PBC)

A
  • immune damage of the small bile ducts
  • granulomas may be present
  • eventual bile duct and branch destruction
  • treat with ursocleoxycholic acid - improve enzymes, reduce inflammation, decrease portal pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the presentation of PBC

A
  • itching/fatigue
  • dry eyes
  • joint pains
  • varicael bleeding
  • ascites
  • jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is primary sclerosing cholangitis

A

progressive cholestasis (reducing or stopping or bile flow) with bile duct inflammation and strictures

  • over 50% have IBD
  • presents - itching, pain, jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

list three causes of metabolic liver disease

A
  • alpha1 antitrypsin deficiency
  • wilsons disease
  • haemochromatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is the pathogenesis of haemochromatosis

A
  • mutation in HFE gene
  • autosomal recessive disorder
  • leading to uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas
  • increased ferritin and transferring saturation
  • iron removal may lead to regression of fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the pathogenesis of alpha 1 antitrypsin deficiency

A

A1AT is a glycoprotein made in the liver that controls inflammatory cascades
- inability to export it from liver
-can lead to liver disease (protein retention in liver)
-emphysema (protein deficiency in blood)
-cholestatic jaundice
treat with smoking cessation, vaccination against infection and transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is wilsons disease

A

metabolic liver disease - rare inherited disorder (autosomal recessive)

  • copper excretion with excess deportation in liver and CNS
  • children present with liver disease and adults usually with CNS signs - tremor, dysarthria, dysphagia, dementia
  • urine copper excretion high and increased on liver biopsy
  • management - decreased copped diet, lifelong pencillamine, liver transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

describe one vascular cause of liver disease, its presentation and treatment

A
  • Budd-chiari - hepatic vein occlusion by thrombosis or tumour causes congestive ischaemia and hepatocyte damage
  • presents as: ascites, acute liver failure, abnormal tests
  • treatment - anticoagulation, transjugular intrahepatic portosystemic shunt transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are the symptoms of alcoholic liver disease

A
  • malaise
  • anorexia
  • D&V
  • tender hepatomegaly
  • jaundice
  • bleeding
  • ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what may be found on a blood test of a pt with alcoholic liver disease

A
  • increased WCC
  • decreased platelets (toxicity)
  • increased INR (prothrombin time)
  • increased AST
  • increased GGT
  • increased MCV
  • increased urea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the management if alcoholic liver disease

A
  • screen for infections and ascitic fluid tap
  • stop alcohol consumption, for withdrawal chloradiazepoixide
  • vitamin K iv
  • optimise nutriton
  • high protein diets
  • steroids may confer benefit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is NAFL/ NASH

A

NAFL - non alcoholic fatty liver - increased fat in hepatocytes (steatosis)
if inflammation also present = non alcoholic steatohepatits (NASH) in which inflammation also causes damage to cells ( increased LFT and ALT) - NASH can progress to cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are the risk factors and treatment for NAFL

A
  • obesity
  • hyperlipidaemia
  • diabetes
    treatment
    -weight loss
    -decreased alcohol consumption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how is hep B spread

A
  • blood products
  • sexual
  • IVDU
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how long is the incubation period of HepB

A

1-6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what are the signs of a hep B infection

A
  • fever
  • arthragia
  • jaundice
  • malaise
  • nausea
  • hepatosplenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is in a hepB vaccine? what other management methods can be used

A

inactivated HBsAg (surface antigen)

  • refer anyone with chronic inflammation or cirrhosis for anti viral
  • avoid alcohol
  • immunize sexual contacts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are the tests for Hep B

A

HBsAg present 1-6 months after exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what type of virus is Hep C

A

RNA flavivirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the treatment of Hep C

A
  • inhibition of non structural viral proteins e.g sofofbuvir
  • pegylated interferon injection
  • ribacvarin for harder to treat genotypes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

when can Hep D occur

A

in the presence of Hep B virus, increases the severity of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is gastritis

A

inflammation of the lining of the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what are the risk factors of gastritis

A
  • alcohol
  • NSAIDS
  • H. pylori
  • reflux/hiatus hernia
  • granulomas e.g crohns
  • CMV (cytomegalovirus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what are the symptoms of gastritis

A
  • epigastric pain

- vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what are the tests for gastritis

A
  • upper GI endoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

which organism most commonly causes peptic ulcer disease

A
  • helicobacter pylori
  • gram negative rod
  • urease virulence generates ammonium that buffers stomach acid
  • in absence of NSAIDS or zollinger- ellison syndrome 90% of duodenal ulcers are associated with helicobacter pylori
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is the pathogenesis of peptic ulcer disease by helicobacter pylori

A
  1. in antrum H pylori decreases somatostatin release by D cells - loss of inhibition of gastrin release
  2. G cells now produce more gastrin in the stomach
  3. increased gastrin = increased acid output
  4. in duodenum increases acidity leads to gastric metaplasia
  5. H. pylori then able to colonise duodenum and causes further damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what are the investigations for peptic ulcer disease

A
  • serology
  • stool antigen for H.pylori (1st line)
  • urea breath test
  • endoscopy with urease test, histology and culture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what is the treatment peptic ulcer disease

A
  • stop drugs causing dyspepsia e.g NSAIDS
  • lifestyle changes (GORD)
  • over the counter antacids e.g magnesium trisilicate
    if no improvement test for H.pylori - if negative:
    acid suppressants - PPI’s e.g lanzoprazole/omeprazole
    for 4 weeks DU or 8 weeks GU

if positive:
- h pylori eradication drugs - amoxicillin +clarithryomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is gastroenteritis

A

diarrhoea with vomiting due to enteric infection with viruses, bacteria or parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how can bacteria cause diarrhoea and give examples

A
  • toxin production - bloody if shiga toxin producing e.coli (STEC), enterotoxigenic e.coli (ETEC) - travellers diarrhoea
  • invasive - enteroinvasive e.coli (EIEC) - dysenteric
  • adherent - enteropathogenic e.coli (EPEC) - attach and efface surface epithelium- infantile diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

which bacteria most commonly causes travellers diarrhoea

A

ETEC - enterotoxigenic e.coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what are the features of c.dif infection and how is it diagnosed

A
  • abdo pain
  • watery diarrhoea
  • increased WCC

diagnoses

  • GDH screen in stool
  • tissue culture cytotoxicity assay
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is the prevention and treatment of c.dif infection

A

prevention
- antimicrobial stewardship - limit use of cephalosporins, fluroquinolones
- effective cleaning of rooms with sporicidals
treatment
- metronidazole
- vancomycin for relapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what is cholangitis and charcots triad of symptoms

and the treatment

A
  • bile duct infection
  • RUQ pain, jaundice, fever with rigors/increased WCC
  • treatment -i.v antibiotics and fluids, ERCP and spinchterectomy for stone removal, may stent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what is acute cholecystitis, symptoms and treatment

A
  • stone impactation in the neck of gallbladder
  • RUQ pain, abdominal tenderness, fever, increased WCC
  • treat with amoxicillin, pain relief, i.v fluids, early cholecystectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what is biliary colic, symptoms and treatment

A
  • gallstones symptomatic with cystic duct obstruction or if passed into common bile duct
  • RUQ pain
  • analgesia, rehydrate, elective laparoscopic cholecystectomy
  • do urinalysis, CXR and ECG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what are the symptoms of peritonitis

A
  • pain, tenderness and guarding of abdo wall
  • rebound
  • rigidity
  • fever
  • nausea
  • chills
  • rigor
  • dizziness
  • weakness
  • pyrexia
  • tachycardia
  • pts lie still - washboard rigidity
  • lack of bowel sounds
  • CXR - air under the diaphragm - perforated bowel
  • serum amylase - pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what are the causes of peritonitis

A
  • surgical
  • spontaneous bacterial peritonitis - complication of ascites in cirrhosis - e.coli, s.pneumoniae
  • infection secondary to peritoneal dialysis with staph aureus
  • PID - as a complication of STI
  • TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what percent of liver tumours are metastases? where can these metastases be from

A

90%

- breast, bronchus, GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what are the symptoms and signs of liver tumours

A
  • fever
  • malaise
  • anorexia
  • weight loss
  • RUQ pain
  • jaundice late except for with cholangiocarcinoma
    signs
  • hepatomegaly
  • signs of chronic liver disease
  • ascites/jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what are the tests for liver tumours

A
  • FBC
  • CT to identify lesions and grade biopsy
  • ERCP
  • MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what are the causes of a hepatocellular carcinoma

A
  • HBV
  • cirrhosis
  • NAFLD
  • AIH
  • anabolic steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what is the treatment/prevention of a hepatocellular carcinoma

A 
prevention 
-HBV vaccine
- dont reuse needles
-screen blood
treatment 
-transplant
-resecting solitary tumours
- tumour embolisation 
- sarafenib
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what are the causes of cholangiocarcinoma

A
  • flukes
  • cysts
  • HBV
  • HCV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what are the patient symptoms and signs of cholangiocarcinoma

A
  • fever
  • abdo pain
  • ascites
  • malaise
  • increased bilirubin
  • jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what is the management of cholangiocarcinoma

A
  • 70% in operable at time of presentation
  • palliative care
  • prognosis about 5 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what are the causes of liver failure

A
  • infections - viral hepatitis, yellow fever
  • vascular - budd chiari syndrome
  • alcohol, FLD, PBC, AIH, a1 antrypsin deficiency, wilsons disease, malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what are the signs of liver failure

A
  • jaundice
  • hepatic encephalopathy
  • asterixis/flap
  • construction apraxia - difficulty motor planning tasks
  • fetor hepaticus - breath of the dead- portosystemic shunting allows thiols to pass directly into the lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what are the tests for liver failure

A
  • FBC
  • U+E
  • clotting
  • glucose
  • CMV and EBV serology
  • ferritin
  • a1 antitrypsin
  • cultures
  • CXR
  • ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what is acute pancreatitis

A
  • self perpetuating pancreatic enzyme mediated auto digestion
  • hypovolaemia as ECF trapped in gut
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what are the causes of acute pancreatitis

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom 
Hyperlipidaemia, hypothermia, hypercalcaemia 
ERCP + emboli
Drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what are the symptoms and signs of acute pancreatitis

A
  • gradual or sudden sever epigastric or central abdo pain
  • vomiting prominent
    signs
  • tachycardia
  • fever
    -jaundice
  • shock
  • rigid abdomen
  • permiumbilical or flank bruising
88
Q

what are the tests for acute pancreatitis

A
  • serum amylase/lipase increased
  • ABG to monitor oxygenation and acid base status
  • AXR - no psoas shadow (increased retroperitoneal fluid)
  • CT
  • CXR to eliminate perforation
89
Q

what is the management of acute pancreatitis

A
  • Nil by mouth (decrease pancreatic stimulation)
  • analgesia
  • hourly vital signs
  • ERCP + gallstone removal may be needed
90
Q

what are the symptoms of chronic pancreatitis

A
  • epigastric pain bores through the back relieved by sitting forward
  • bloating
  • steatorrhoea
  • weight loss
  • brittle diabetes

examination

  • guarding
  • reduced or absent bowel sounds
  • periumbilical bruising - cullens sign
  • flank bruising - grey turners sign - released lipases causes fat necrosis within abdomen
91
Q

what are the causes of chronic pancreatitis

A

-alcohol
- smoking
-autoimmune
rarely
-CF
-familial
-pancreatic duct obstruction

92
Q

what are the tests for chronic pancreatitis

A
  • ultrasound
  • CT - calcifications
  • MRCP
  • AXR - speckled calcification
93
Q

what is the treatment of chronic pancreatitis

A
  • analgesia
  • no alcohol
  • low fat
  • surgery - pancreatectomy or pancreaticojejunostomy (drainage) for unremitting pain, narcotic abuse and weight loss
  • Lipase e.g creon
94
Q

what are the causes of GI malabsorption

A
  • coeliac
  • crohns
  • chronic pancreatitis
  • decreased bile
  • pancreatic insufficiency
  • infection
95
Q

what are the symptoms and signs of GI malabsorption

A 
symptoms 
- diarrhoea
- weight loss
- lethargy
-steatorrhoea
-bloating
signs
- anaemia (decreased Fe, B12, folate)
- bleeding disorders (decreased Vit K)
- oedema (decreased protein)
- metabolic bone disease ( decreased Vit D)
96
Q

what are the tests for GI malabsorption

A
  • FBC
  • ;lipid profile
  • coeliac tests
  • stool sudan stain for fat globules + microscopy (infestation)
  • endoscopy and small bowel biopsy
97
Q

what is the pathology of GI malabsorption

A
  1. insufficient intake
  2. defective intraluminal digestion
    - pancreatic insufficiency - pancreatitis, CF
    - defective bile secretion - biliary obstruction, ileal restriction ( decreased bile salt uptake)
    - bacterial overgrowth
  3. insufficient absorptive area
  4. lack of digestive enzymes e.g lactose intolerance + disaccharidase deficiency
  5. defective epithelial transport - primary bile acid malabsorption (mutations in transporter protein)
  6. lymphatic obstruction - lymphoma, TB
98
Q

which two conditions does inflammatory bowel disease encompass

A
  • crohns disease

- ulcerative colitis

99
Q

where is the most proximal point that ulcerative colitis spreads to

A

the ileocaecal valve

100
Q

what is the pathology of ulcerative colitis

A
  • inappropriate immune response to clinic mucosa
  • hyperaemic/haemorrhagic colonic mucosa with or without pseudopolyps formed by inflammation
    -punctuate ulcers may extend deep into the lamina propria
    differentiated from crohns by the fact it is continuous inflammation limited to the mucosa
101
Q

what are the symptoms and signs of UC

A
  • episodic or chronic diarrhoea and blood and mucus
  • crampy abdo discomfort (RLQ)
  • bowel frequency released to severity
    signs
  • fever
  • tachycardia
  • tender, distented abdomen
  • clubbing
    -oral ulcers
102
Q

what are the tests for UC

A 
FBC
ESR
U+E 
cultures
stool
faecal calprotectin - simple non invasive test for GI inflammation with high sensitivity 
AXR - no faecal shadows, mucosal thickening, colonic dilation
lower GI endoscopy
103
Q

what is the treatment for UC

A
  • 1st line e.g mesalazine - 5ASA
  • oral or parenteral steroids for those with more extensive disease e.g methotrexate
  • topical steroid management for patients with active disease e.g with proctitis (inflammation in the rectum living)/distal disease - leukophoresis (removal of leukocytes from blood)
  • surgery e.g colerectomy
    severe = IV hydrocortisone
104
Q

what is the pathology of crohns disease

A
  • chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus
  • unlike UC there is unaffected bowel between areas of active disease (skip lesions)
  • inappropriate immune response to normal gut mucosa
105
Q

what are the symptoms and signs of crohns

A 
symptoms 
- diarrhoea
- abdo pain 
- weight loss
-anorexia
- fatigue
-malaise
- fever
signs
- bowel ulceration
- abdominal tenderness
- perianal abscess
- anal strictures
-clubbing
- skin, joint and eye problems 
-ORAL ULCERS
106
Q

what tests for crohns disease

A
  • FBC
  • ESR
  • U+E
  • ferritin
  • B12
  • stool
  • Faecal calprotectin
  • colonoscopy and biopsy
  • capsule endoscopy
107
Q

what is the treatment of crohns disease

A
  • opsonise nutrition
  • stop smoking
  • 1st line steroids e.g prednisolone tablets or hydrocortisone injections
  • 2nd line immunosuppressants e.g methotrexate
  • monoclonal antibodies e.g infliximab target TNFa which is believed to be responsible for the inflammation
  • surgery - resection (remove inflamed area), ileostomy (direct digestive waste away form the inflamed colon)
  • aim of treatment = remission
108
Q

what is the pathology of coeliac disease

A
  1. gluten peptides taken up by epithelial cells
  2. deaminated by enzyme tissue transglutaminase in sub epithelial layer
  3. APC presents compound to CD4+ T cells
  4. immune response triggered with generation of pro inflammatory cytokines (IL1, IFN-y, TNFa)
  5. lymphocytes infiltrate the lamina propria causing crypt hyperplasia and villous atrophy
109
Q

what is the prevalence of coeliac disease

A

1/100-300

110
Q

what is the presentation of coeliac disease

A
  • steatorrhoea
  • diarrhoea
  • weight loss
  • abdominal pain
  • failure to thrive
  • nausea and vomiting
  • fatigue
  • osteoporosis
  • iron deficiency anaemia
  • dermatitis herpitiformis (blistering of the skin)
111
Q

what are the tests for coeliac disease

A
  • gastroscopy and biopsy of the small intestine - villous atrophy on histology
  • serology - antitransglutaminase, anti endomysial, anti alpha gliadin
  • decreased Hb, B12, ferritin
  • must be on a gluten diet whilst testing - gluten in ,more than one meal everyday for at least 6 weeks
112
Q

what is the management of coeliac disease

A
  • gluten free diet
  • dietician review
  • DEXA scan for osteoporosis risk
  • 10% risk in first degree relatives
  • pneumococcal vaccine
  • supplements
  • iron for anaemia
113
Q

what are the complications of coeliac disease

A
  • osteoporosis
  • anaemia
  • increased risk of malignancy
  • dermatitis herpetiformis
114
Q

what is the prevalence of IBS

A

10-20%

115
Q

how is IBS diagnosed

A

at least 2 of:

  • relief by defecation
  • altered stool form
  • altered bowel frequency ( constipation/diarrhoea)
116
Q

what are the symptoms of IBS

A
  • relief by defecation
  • altered stool form
  • altered bowel frequency ( constipation/diarrhoea)
  • urgency
  • abdo bloating
  • worse symptoms after food
  • incomplete defecation
  • mucus PR
  • chronic
  • exacerbated by stress
117
Q

what is the management of IBS

A

diet
- low FODMAP diet (short chains that are poorly absorbed)
- 8 cups of fluid per day
- less alcohol, caffeine
- less high fibre foods
- avoid missing meals or long gaps between eating
- regular meals
physical activity
first line pharmacological
- laxatives for constipation e.g sodium picosulfate, senna
- anti motility for diarrhoea e.g loperamide
second line
- antidepressants and selective serotonin reuptake inhibitor e.g sertraline
psychological interventions
- CBT
-hypnotherapy
- psychological therapy

118
Q

what is GORD

A

Gastro-oesophageal reflux disease

- reflux of the stomach contents and bile

119
Q

what are the causes of GORD

A
  • lower oesophageal sphincter hypotension
  • hiatus hernia - GO junction slides up the chest
  • obesity
  • gastric acid hyper secretion e.g zollinger ellison syndrome due to gastrinoma secreting gastrin
  • delayed gastric emptying e.g due to drugs - codeine, amitriptyline, anti cholinergics
  • smoking
  • alcohol
  • pregnancy
120
Q

what are the symptoms of GORD

A
  • heartburn
  • belching
  • acid brash (regurgitation)
  • water brash
  • nocturnal asthma
  • ## sinusitis and laryngitis
121
Q

what are the complications of GORD

A
  • oesophagitis
  • barrett’s oesophagus (squamous —> columnar by metaplasia)
  • ulcers
  • oesophageal cancer
122
Q

what are the tests for GORD

A
  • endoscopy if dysphagia

- PH monitoring

123
Q

what is the treatment for GORD

A 
lifestyle
- lose weight
- smoking cessation
-less hot drinks
-less alcohol
- small regular meals
drugs 
-antacids
- H2 receptor antagonist - renitodine
-PPI's e.g lanzoprazole
- stop drugs affecting oesophageal/gastric motility (nitrates, CCB, anticholinergics) or damage mucosa (NSAIDS, bisphosphonates)
-surgery to increase lower oesophageal sphincter pressure
124
Q

what are the risk factors for oesophageal cancer

A
  • smoking
  • diet
  • alcohol excess
  • GORD
125
Q

what is the presentation of oesophageal cancer

A
  • weight loss
  • retrosternal chest pain
  • hoarseness - due to tumour pressing on recurrent laryngeal nerve
  • cough
126
Q

what are the tests for oesophageal cancer

A
  • oesophagoscopy with biopsy
127
Q

what is the treatment of oesophageal cancer

A
  • oesophagoectomy

- chemoradiotherapy

128
Q

what are the risk factors of stomach cancer

A
  • pernicious anaemia (b12 deficiency anaemia)
  • blood group A
  • H.pylori
  • adenomatous polyps
  • lower social class
  • smoking
  • diet
  • atrophic gastritis
129
Q 
put in order 
dysplasia
invasive carcinoma
normal gastric mucosa
intestinal metaplasia 
intramucosal carcinoma
A 
normal gastric mucosa
intestinal metaplasia
dysplasia
intramucosal carcinoma
invasive carcinoma
130
Q

what is the difference between early gastric cancer and late gastric cancer

A

early - mucosa and submucosal layers

late - invaded into muscular wall and lymph nodes

131
Q

what are the symptoms and signs of gastric cancer

A 
symptoms 
- dyspepsia
- weight loss
- vomiting
- dysphagia
- anaemia
signs
- epigastric mass
- hepatomegaly 
- jaundice
-ascites
132
Q

what are the tests for gastric cancer

A
  • gastroscopy
  • biopsy all gastric ulcers
  • CT/MRI - staging
  • endoscopic ultrasound - depth of invasion
133
Q

what is the treatment of gastric cancer

A
  • resection
  • gastrectomy
  • combination chemo
  • targeted therapies e.g for Her2 positive tumours
134
Q

what are the risk factors for colorectal cancer

A
  • neoplastic polyps
  • IBD
  • genetics - e.g familial adenomatous polyposis
  • smoking
  • alcohol
  • diet, low fibre, red meat
135
Q

what is the presentation of colorectal cancer

A 
right sided
-weight loss
-low hb 
-abdo pain
left sided
- bleeding/mucus PR 
- Altered bowel habit
- obstruction 
- mass PR 
either 
- perforation 
- haemorrhage
- fistula
136
Q

what are the tests for colorectal cancer

A
  • FBC - microcytic anaemia
  • sigmoidoscopy
  • colonoscopy
  • LFT
  • liver MRI/US
  • TNM for staging
  • dukes colorectal
137
Q

what is the treatment for colorectal cancer

A
  • surgery - keyhole/laproscopic
  • endoscopic stenting
  • chemotherapy + biological therapies
  • radiotherapy
  • palliative care - for metastatic colorectal adenocarcinoma
138
Q

who is colorectal cancer screening offered to and what does it test for

A
  • those aged 60-75 years
  • tests first for faecal occult blood in stools (blood that is not visibly apparent)
  • then colonoscopy offered for all that test positive
139
Q

what are the risk factors for pancreatic cancer

A
  • > 70yrs
  • smoking
  • alcohol
  • carcinogens
  • chronic pancreatitis
  • increased waist circumference
  • high fat diet
  • 95% have mutations in KRAS2 gene
140
Q

what is the most common type of pancreatic cancer

A
  • most ductal adenocarcinoma- 60% in head, 25% body, 15% tail
  • a few in ampulla of vater
  • pancreatic islet cells
141
Q

what are the symptoms and signs of pancreatic cancer

A
  • painless obstructive jaundice if in head of the pancreas
  • body and tail = epigastric pain radiating to the back and relieved by sitting forward
  • anorexia
    -weight loss
    -diabetes
    -acute pancreatitis
    signs
  • jaundice
  • palpable gallbladder
  • epigastric mass
  • hepatosplenomegaly
  • ascites
  • lymphadenopathy
142
Q

which vessels run between the neck and tail of the pancreas

A
  • superior mesenteric vein and artery
143
Q

what are the tests for pancreatic cancer

A
  • blood - cholestatic jaundice

- US/CT - pancreatic mass + dilated biliary tree + hepatic metastases

144
Q

what is the treatment for pancreatic cancer

A
  • resection
  • post op them
  • opiates for pain
  • stent for jaundice and anorexia management
145
Q

what is the lifetime incidence of appendicitis

A

6%

146
Q

what is the pathogenesis of appendicitis

A
  • gut organisms invade the appendix wall after lumen obstruction by lymphoid hyperplasia, stricture (faecolith) or filarial worms
  • leads to oedema, ischameic necrosis and perforation
147
Q

what is the surface anatomy of the appendix

A

2/3 of the way from the umbilicus to the anterior superior iliac spine ( mcburneys point)

148
Q

what is the presentation of appendicitis

A
  • periumbilical pain that moves to the right iliac fossa
  • Rovsings sign - pain > in RIF than LIF if LIF pressed
  • Psoas sign - retrocaecal appendix pain on extending hip
  • Cope’s sign - pain on flexion and internal rotation of right hip if appendix in close relation to obturator externus
  • constipation/diarrhoea
  • anorexia
  • rebound tenderness
149
Q

what are the tests for appendicitis

A
  • blood - increased CRP, neutrophilia

- CT high diagnosis accuracy

150
Q

what is the treatment of appendicitis

A
  • prompt appendicectomy
  • antibiotics to reduce wound infections - metronidazole and cefotaxime
  • laparoscopy - not recommended in gangrenous perforation
151
Q

what are the complications of appendicitis

A
  • perforation
  • abscess
  • appendix mass- inflamed appendix becomes covered by omentum
  • ischaemia as a result of exudate build up and toxic damage to the blood vessels - leads to gangrene and causes peritonitis, septicaemia
152
Q

give examples of intestinal obstruction within lumen, in wall and outside lumen

A

in lumen

  • tumour
  • diaphragm disease caused by NSAIDS
  • meconium ileus (sticky ileus) - dont pass first stool in baby
  • gallstone ileus - gallstone erodes into small bowel when gallbladder is inflamed
in wall
- crohns, diverticular disease (strictures), tumours
outside
-tumour pressing on intestine
- adhesions
-volvus
153
Q

what is the pathology of diverticular disease

A
  • low fibre diet
  • increased pressure in lumen as nothing to squeeze
  • pushes through layers of intestine
154
Q

what are the four types of intestinal obstruction

A
  1. volvus - twist - mesenteric bowel - rotation by 360 degrees proximal limb around distal, cutting off blood supply
  2. adhesions - sticking together/to omentum/to organs/to wall
  3. intersussuption - telescoping - one hollow structure into its distal hollow structure. a mass acts as a lead point or disorganised pattern of peristalsis
  4. atresia - absence of opening or failure of development of hollow structure
155
Q

what is the pathophysiology of bowel obstruction

A
  1. obstruction of bowel
  2. increased secretions and swallowed air (SBO) or bacterial fermentation (LBO)
  3. more dilation, less absorption - mucosal wall oedema
  4. increased pressure - intramural vessels compressed - ischaemia - perforation
  5. increased secretions + distention cause: anorexia, nausea, vomiting, fluid and electrolyte balance change, hypovolaemia, bacterial overgrowth faeculant vomiting
156
Q

what are the causes of small bowel obstruction

A 
adults
-adhesions - previous surgery 
- hernia 
- crohns
- malignancy 
children 
- intersussption 
- appendicitis
-volvulus 
-atresia
- pyloric stenosis
157
Q

what is a hernia

A

abnormal protrusion of viscus through normal or abnormal defects of body cavity, presenting as a lump and pain
if left untreated - strangulation

158
Q

what is the presentation of a SBO

A
  • vomiting - projectile, faeculant (dirty)
  • constipation - late, -obstipation - absence of faeces or flatus
  • pain - colicky to constant, tenderness
  • distension
  • strangulation
159
Q

what makes up 90% of LBO’s in the UK

A

colorectal malignancy

160
Q

what may cause a paediatric LBO

A
  • imperforate anus

- Hirshspring disease (congenital absence of ganglionic cells in bowel wall)

161
Q

what is the management of a bowel obstruction

A
  • pain control
  • NGT - nasogastric feeding tube to decompress small both, NBM
  • catheter
  • surgery - strangulation needs emergency surgery, endoscopic stunting can be used for obstruction by large bowel malignancy
  • conservative vs operative
162
Q

what is the 3-6-9 rule of a normal abdominal X-ray

A
  • small bowel < 3cm wide, only seen if contains gas
  • large bowel <6cm wide
  • caecum and sigmoid up to 9cm wide
  • contains faeces - mottled appearance
163
Q

what is a diverticulum

A
  • out pouching of the gut wall, usually at sites of perforating arteries
  • high intraluminal pressure causes mucosa to herniate through the muscles layers of the gut at weak points adjacent to vessels
164
Q

what is diverticulitis

A

inflammation of a diverticulum

165
Q

what are the symptoms of diverticulitis

A 
- diverticular disease symptoms 
\+
- fever
- inc WCC
-inc CRP/ESR
- tender
colon
- altered bowel habit + left sided colic relieved by defectation 
- nausea
- flactulence
166
Q

what are the complications of diverticulitis

A
  • perforation
  • strangulation
  • haemorrhage
  • fistulae
  • abscesses
  • post infective strictures
167
Q

what are the common causes of haematemesis

A
  • peptic ulcers
  • Mallory- Weiss tear - tear when oesophagus meets stomach due to persistent vomiting/retching
  • oesophageal varices
  • gastritis
  • drugs
  • oesophagitis
  • malignancy
168
Q

what are the signs of haematemesis

A
  • of chronic liver disease
  • cool/ clammy peripheries
  • capillary refill time > 2s
  • urine output < 0.5mL/kg/h
  • tachycardia
169
Q

what is the management of haematemesis

A
  • protect airway
  • high flow O2
  • take FBC, LFT, clotting and crossmatch
  • IV fluids
  • catheter
  • CXR, ECG and ABG
  • Endoscopy
170
Q

what are the three types of bowel ischaemia

A
  1. acute mesenteric - small bowel following superior mesenteric artery thrombosis or embolism - severe abdo pain, rapid volemia —> shock
  2. chronic mesenteric ischaemia - intestinal angina - colicky pain and weight loss
  3. chronic colonic ischaemia - low flow in inferior mesenteric - blood diarrhoea and lower sided abdo pain
171
Q

what are the two types of hiatus hernia

A
  • sliding hiatus hernia - GO junction slides up the chest

- rolling hiatus hernia/paraoesophageal hernia - stomach herniates into the oesophagus

172
Q

what is meant by a direct and indirect inguinal hernia

A

direct - due to a weakness in the muscle wall and travel through the muscle wall
- direct = medial to inferior epigastric artery
indirect - due to a birth defect and travel through the inguinal canal
- indirect = lateral to inferior epigastric artery

173
Q

what is an anal fistula

A

An anal fistula is a small channel that can develop between the end of the bowel and the skin near the anus. An anal fistula can cause bleeding and discharge when passing stools - and can be painful. An anal fistula can occur after surgery to drain an anal abscess.

174
Q

what is an anal fissure

A

a tear in the squamous lining of the lower anal canal, most due to hard faeces

175
Q

what is a perianal abscess

A

a shallow collection of pus under the skin surrounding the anus, caused by gut organisms
- treat with drainage under GA

176
Q

what is a pilonodal sinus/abscess

A
  • obstruction of natal cleft hair follicles 6cm above the anus
  • excites a forge in body reaction and may cause second tracts to open laterally +/- abscess
177
Q

what are haemorrhoids

A

Haemorrhoids, also known as piles, are swellings containing enlarged blood vessels found inside or around the bottom (the rectum and anus).
causes bleeding after passing a stool, itchy bottom, a lump hanging outside of anus, a mucus discharge, soreness, redness and swelling
usually due to prolonged straining during constipation
treat with lifestyle changes e.g decrease weight, or by topical treatment of anus

178
Q

what is the treatment of diverticulitis

A
  • metronidazole
179
Q

what is the treatment of food poisoning (salmonella/shigella)

A
  • ciprofloxicin
180
Q

what are the differentials of peptic ulcer disease

A
  • non ulcer dyspepsia
  • duodenal crohns
  • TB
  • lymphoma
  • pancreatic cancer
181
Q

what is the mean age of diagnosis of crohns disease

A

26

182
Q

does smoking protect against UC or crohns

A

ulcerative colitis

183
Q

give some extraintestinal features of IBD

A
  • arthritis
  • conjunctivitis
  • scleritis
  • anterior uveitis
  • pyoderma gangrenosum - necrotic patches on skin
  • erythema nodusum
  • primary sclerosing cholangitis and uveitis = UC
184
Q

what is the appearance of crohns and ulcerative colitis on a barium swallow

A
  • crohns = cobblestone

- UC = loss of haustrations and drain pipe colon

185
Q

what are the complications of crohns

A
  • anaemia
  • osteoporosis
  • obstruction
  • fistula
  • malignancy
  • adenocarcinoma of distal ileum
186
Q

which scale is used for severity of IBD

A

True love and witts criteria
mild - <4 bowel motions per day and small amount of rectal bleeding
moderate - 4-6 bowel motions and moderate bleeding
severe - >6 bowel motions and severe bleeding

187
Q

what is found on histology for crohns

A
  • non caseating granuloma
  • transmural
  • skip lesions
  • goblet cells increase
188
Q

what is found on histology for ulcerative colitis

A
  • goblet cells decrease
  • continuous
  • mucosal layer only
189
Q

what is it called when UC goes proximal to ileocaecal valve

A
  • backwash ileitis
190
Q

what is found on histology for coeliac

A
  • crypt hyperplasia

- villous atrophy

191
Q

which scale is used to determine the likelihood of surgery of appendicitis

A
  • alvarado score
192
Q

what are the symptoms of gastric ulcer

A
  • gastric worse on eating
  • duodenal worse when hungry
  • duodenal worse at night
  • epigastric burning, gnawing pain
  • weight loss
  • lethargy
  • radiates to back
  • melena (dark black stool associated with upper GI bleeding)
193
Q

what is the triple therapy for H.pylori eradication

A
  • omeprazole
  • clarithryomycin
  • metronidazole or amoxicillin
194
Q

what is the management of diverticulitis

A
  • diet more fibre
  • smooth muscle relaxants
  • cephalosporin and metronidazole
  • NBM
  • fluids
  • analgesia
195
Q

what are the complications of pancreatitis

A
  • malabsorption
  • diabetes - destruction of islets of langerhans
  • acute respiratory distress in acute pancreatitis ( circulating digestive enzymes - trypsin and phospholipase A2) loss of surfactant = ARDS and pleural effusion
196
Q

which scoring system is used for severity of pancreatitis

A

Glasgow scoring system

PaO2
Age
Neutrophilia
Calcium 
Renal urea
Enzymes lactate dehydrogenase/aspirate transaminase 
Albumin
Sugar glucose
197
Q

What are the two types of oesophageal cancer and where do they affect

A
  • SCC - upper 2/3 of oesophagus

- Adenocarcinoma - lower 1/3 of oesophagus

198
Q

what is the difference between irreducible, incarcerated, obstructed and strangulated hernia

A
  • irreducible - hernia cannot be pushed back in
  • incarcerated - contents of the hernia are stuck inside it
  • obstructed - bowel is obstructed by the hernia
  • strangulated - ischaemia of the tissue inside the hernia
199
Q

In which conditions are AST and ALT (transaminases) likely to be raised

A
  • parenchymal liver disease e.g NAFLD, cirrhosis, hepatitis
200
Q

when is GGT likely to be raised on a LFT

A
  • alcohol involvement
201
Q

when GGT and ALP are raised what does this indicate

A
  • an obstructive picture e.g gallstones, cholangitis, PBS
202
Q

what reasons other than bile duct damage may ALP be raised

A
  • muscle breakdown

- pregnancy

203
Q

How is hep A spread

A

faecal oral route

  • food preperation
  • shellfish
  • water
204
Q

when would Anti-HBc be positive

A
  • you have made antibodies to the core protein - had an infection and cleared it
205
Q

when would anti HBs be positive

A

in vaccinated people- antibodies to the surface antigen

206
Q

what are the complications of viral hepatitis

A
  • hepatocellular carcinoma
  • liver failure
  • cholangiocarcinoma
  • hep d, hep c
207
Q

describe murphys sign and when it is positive

A
  • push on RUQ and when they inspire it will be painful
  • gallstones/gall bladder problems
  • in peritonitis it hurts on both sides (negative murphys sign)
208
Q

what are the tests for gallstones

A
  • CRP increased
  • MRCP first line - MRI of cholangiopancreatic area
  • US abdomen - stones or dilated common bile duct, gallbladder small and shrunken with a thick wall
  • ERCP - can be used to test or remove
209
Q

what is reynolds pentad

A
  • charcots triad - fever/inc WCC, jaundice, RUQ pain with shock (low BP, tachycardia) and an altered mental state
  • it happens when ascending cholangitis leads to sepsis
210
Q

what are the tests for cirrhosis

A
  • bloods - increased AST and ALT

- US abdomen - small liver, focal liver lesions, portal venous thrombosis

211
Q

what drugs can cause cirrhosis

A
  • methotrexate
  • rifampicin
  • methyldopa
212
Q

what are the signs of cirrhosis

A
  • ascites
  • easy bruising
  • clubbing
  • asterixis flap
  • jaundice
  • leukonychia - due to hypoalbuminemia
  • terrys nails (white in proximal, red in distal)
  • clubbing
  • palmar erythema
  • Dupuytren’s - finger fixed in permenant flexed position
  • hyperdynamic circulation (bounding pulse)
  • spider angioma - red spots with branches coming out of them - >5 abnormal
  • gynecomastia - boys with boobs, loss of body hair, atrophic testes
213
Q

what is the 1st and 2nd line Abx for C.diff infection

A
  1. metronidazole

2. vancomycin

214
Q

which organisms cause pyogenic and amoebic liver abscess and what is the treatment

A
  • pyogenic - e.coli
    treat with cephalosporin and metronidazole
  • amoebic - entamoeba histolytica
    treat with metronidazole
215
Q

what is the triad of symptoms of budd chiari syndrome

A
  • ascites
  • hepatomegaly
  • abdominal pain
216
Q

what are the triggers of gilbert’s syndrome

A 
being dehydrated
going without food for long periods of time (fasting)
being ill with an infection
being stressed
physical exertion
not getting enough sleep
having surgery
in women, having their monthly period
217
Q

what are the stages of dukes colorectal cancer

A

A- tumour confined to mucosa
B1 - into muscularis propria
B2 - into muscularis propria and serosa (fully through bowel wall)
C1 - involving lymph nodes (not through bowel wall)
C2 - involving lymph nodes (through bowel wall)
D - distant metastases

Phase2a (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions