Gastrointestinal Flashcards
1
Q
Treatment for Wilson’s disease (copper accumulation in the eye)
A
- Penicillamine, trentine- chelating agents. It works to treat Wilson’s disease by binding to the extra copper in the body and causing it to leave the body through the urine.
- Avoid high-copper foods
- Liver transplant- last resort
Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.
Autosomal recessive- genetic
2
Q
How should you administer vitamin B12?
A
NICE guidelines suggest that for people with neurological involvement, we initially administer hydroxocobalamin (a type of B12) 1mg IM on alternative days until there are no further improvements in symptoms.
This is called a ‘loading dose’ and it is given as it allows for rapid repletion of B12 levels. This helps reverse the anaemia and neurological symptoms quicker.
Once this loading dose has been given, you give maintenance therapy via 1mg of hydroxocobalamin every 2-3 months IM.
3
Q
Common cause of hepatomegaly?
A
Right heart failure (cor pulmonale)- Common with COPD
Alcohol
Hepatitis A B C
Drug abuse
4
Q
Medication to help PREVENT variceal bleeding?
A
Propranolol.
This is a non-selective beta-blocker which decreases portal venous pressure by reducing cardiac output and splanchnic blood flow.
5
Q
First-line management for non-alcoholic liver disease? Non-alcoholic steatohepatitis (NASH).
A
Weight loss.
Non-alcoholic steatohepatitis (NASH) is a progressive form of non-alcoholic fatty liver disease (NAFLD), which can lead to cirrhosis, hepatocellular carcinoma and liver failure. Weight loss being the most effective intervention.
6
Q
Which drug increases the risk of bacterial infection in GI?
A
PPIs Omeprazole- risk factor for C. difficile infection
7
Q
Which investigation is appropriate for pancreatic cancer?
A
High-resolution CT scanning.
CT scan of the abdomen, which can demonstrate a mass and show a double duct sign caused by dilation of the common bile duct and pancreatic duct in response to the tumour.
If pancreatic cancer is suspected, but CT scan is negative, endoscopic US with biopsy may be indicated.
8
Q
How often is the pneumococcal vaccine given and who will benefit most with a pre-existing GI condition?
A
Once every 5 years
Coeliac disease diagnosed patients
9
Q
Investigations for variceal bleeding?
A
Bloods- FBC, U&E, LTF, G&S coagulation (platelet count/ transfusion, prothrombin)
Endoscopy
CT- liver, portal vein, spleen for signs of cirrhosis
10
Q
Management for variceal bleeding?
A
Variceal bleeding acute-
A-E assessment
2 cannulas
1L 0.9 IV saline
- Endoscopy
- Terlipressin 2mg IV
- Prophylactic antibiotic therapy + blood transfusion
- Rubber band ligation- compressing varices with tight rubber band
- N-butyl-2cyanoscrylate- tissue adhesive solution to treat bleeding (gastric varices)
- Sengstaken- Blakemore tube
- Trans-jugular intrahepatic portosystemic shunts TIPS- if not controlled by band ligation (synthetic vessel that connects hepatic vein and portal vein)
Non-variceal bleeding
Clips
Thermal coagulation with adrenaline
Fibrin/ thrombin with adrenaline
PPIs
11
Q
Investigations for GORD?
A
<55- start with treatment unless red flag symptoms (weight loss, dysphagia, haematemesis, melena, anorexia)
> 55- refer to endoscopy with biopsy and start pH monitoring
12
Q
Management for GORD?
Complications of GORD?
A
Reduce weight
Stop smoking
Reduce alcohol, fatty meals, coffee
Small regular meals
Antacids
H2 antagonists
PPIs- lansoprazole/omeprazole
Laparoscopic fundoplication- if not responded to PPI
Complication: Barret’s oesophagus -> adenocarcinoma
Squamous -> columnar epithelium
13
Q
Investigations for peptic ulcers?
A
Bloods- FBC, CRP, U&E, LFT, clotting factors (PT, platelets)
H. pylori detection- urea breath test, stool antigen test, endoscopy with biopsy
Rapid urease test- CLO (gastric biopsy in urea)
Biopsy- rule out IBD, cancer ect
Endoscopy
14
Q
Management for peptic ulcers?
A
Stop NSAIDS
NSAIDS + H. pylori = 8-week PPI + eradication therapy (clarithromycin, amoxicillin, metronidazole, levofloxacin)
No NSAIDS + no H. pylori = 4-6 weeks PPI
Endoscopy
Stop smoking
Lifestyle change
15
Q
Pathophysiology of oesophageal varices?
A
Oesophageal varices- dilated sub-mucosal veins in lower oesophagus due to portal vein hypertension causing blood to flow into smaller vessels and capillaries causing bleeding/dilation.
Other
Mallory Weiss Tears
Peptic ulcer disease = Gastric cancer Duodenal ulcer
High urea but normal creatinine = upper GI bleed
16
Q
Pathophysiology of GORD?
Complications?
A
Abnormality of lower oesophageal sphincter causing reflux of gastric contents into oesophagus.
Can lead to a change in cell structure of the oesophagus
Squamous cells -> columnar cells = Barrett’s oesophagus (metaplastic= not cancerous)
Epithelial cell change can cause Barrett’s oesophagus due to chronic GORD
GORD -> Barrett’s oesophagus -> invasive adenocarcinoma
17
Q
Pathophsiology of peptic ulcers?
A
Most common- H. pylori- causes excessive gastrin production and inhibits somatostatin production leading to increased acid production leading to erosion formation
Causes:
NSAIDS- inhibit COX-1 enzyme production that function to protect the gastric mucosa
Alcohol- irritate and weaken stomach lining -> inflammation
Smoking- inhibits prostaglandin secretion in gastric mucosa -> inflammation -> weakened stomach walls -> acid erosions
Gastric ulcers- pain exacerbated by eating
Duodenal ulcers- pain alleviated by eating and worse 2-3 hours after stomach is empty or at night
18
Q
What is IBS?
Investigations for IBS?
A
GI sensitivity towards stimuli leading to a group of symptoms to occur and persist for a long time and require long-term self-management
Exclude red flag symptoms- weight loss, blood in stool, rectal bleed, >60, FHx of bowel cancer
Rome criteria
Medical history
Blood- rule out coeliac
Faecal-calprotectin
Stool sample- rule out IBD
19
Q
Management for IBS?
A
Lifestyle- physical activity
Regular small meals
Avoid high fibre, carbonated drinks, caffeine
Probiotics
Healthy eating
Psychological support
Laxatives- constipation
Anti-diarrheal- diarrhoea
Adequate sleep
Plenty fluids
20
Q
What is malabsorption?
Conditions that cause malabsorption- These Definitely Cause Absorption Problems (TDCAB)
A
Difficulty of digestion and absorption of nutrients
T- tropical sprue
D- disaccharide deficiency (lactose)
C- coeliac + Crohn’s
A- A-beta lipoproteinemia
P- Pancreatic insufficiency (pancreatitis)
Other:
Short bowel syndrome- small intestine is surgically shortened or damaged and cannot absorb enough nutrients.
Cystic fibrosis- excess mucus plugging lead to malfunction of pancreas enzymes
21
Q
Pathophysiology of coeliac disese?
A
Commonly autoimmune
Associated with HLA-DQ2 haplotype which is present on antigen-presenting cells that initiate an inflammatory cascade
Gliadin peptides in gluten are resistant to digestive enzymes and remain in sub-endothelium of small intestine
Loss of immune tolerance leading to immune response
22
Q
Investigations for coeliac disease?
A
Blood- FBC, U&E, LFT, ESR
Serology- anti-TTG and total IgA
Endoscopy- duodenal biopsy for histology findings
HLA genetic testing- HLA-DQ2
23
Q
Management for coeliac disease?
A
Gluten free diet
Supplements- Fe, Ca
B12 injections
Pneumococcal vaccines- once every 5 years
Psychological help
Yearly GP reviews
Prednisolone- if inflammation continues
Underlaying conditions- SIBO
24
Q
Pathophysiology of Crohn’s?
A
type of chronic IBD causing granulomatous inflammation affecting any part of the GI tract.
Chronic inflammation from T-cell activation leading to tissue injury
Crypt inflammation and abscesses, which progress to tiny focal aphthoid ulcers.
Mucosal lesions may develop into deep ulcers with mucosal oedema, creating a cobblestoned appearance to the bowel.
25
Investigations for Crohn's?
* Observations (temp, RR, BP, SpO2, HR)
* Bloods- FBC, CRP, LFT, U&E, ESR vitamins and electrolytes (B12, folate, K+, Ca+, Na+)
* Stool- cultures, faecal calprotectin
* Imaging- Ileocolonoscopy, biopsy, capsule endoscopy, CT, pelvic MRI (perianal disease- fistulae/ abscess)
* Colonoscopy- cobblestone appearance of GI tract
26
Management for Crohn's?
Step-up apporach
Tier 1: Steroids (e.g. prednisolone, budesonide)
Tier 2: Immunomodulators (e.g. azathioprine, mercaptopurine, methotrexate)- CHECK TPMT
Tier 3: Biologics (e.g. adalimumab, stelara, infliximab)
Maintaining remission
Smoking cessation + lifestyle
Azathioprine + mercaptopurine- post surgery (check TPMT)
Alternative- methotrexate
Surgery
50- 80% require surgery at least once in their lives
Indications for surgery: Drug failure, obstruction, perforation, fistulae, abscesses.
Colectomy, proctocolectomy, ileostomy, fistula removal
Monitoring- for osteoporosis due to vit D deficiency due to small bowel resection
Colorectal cancer surveillance
Perianal disease- oral antibiotics, immunosuppression (azathioprine), surgery (abscess drainage)
27
What is Ulcerative colitis?
Investigations for UC?
Type of IBD- UC causes abnormal reactions of the immune system cause inflammation and ulcers on the inner lining of the large intestine.
Crypt formation- Affects mucosa/ submucosa
Investigations:
* Observations (temp, RR, BP, SpO2, HR)
* Bloods- FBC, CRP, LFT, U&E, ESR vitamins and electrolytes (B12, folate, K+, Ca+, Na+)
* Stool- cultures, faecal calprotectin
* AXR
* Acute- sigmoidoscopy
* Colonoscopy- once controlled with biopsy due to risk of perforation
28
Management for UC?
Follow Truelove and Witts criteria
Acute + bleeding: First line
1. IV corticosteroids
2. Pro-coagulation therapy for bleeding
3. Cyclosporin/ anti-TNFa (immunosuppressant) if unresponsive to steroids
4. Urgent surgery (perforation/ mega colon)
Mild: First line
1. Rectal 5-ASA (aminoacylates- mesalazine)
2. Oral 5-ASA (mesalazine)- if no remission
3. Oral corticosteroids- if no oral-ASA remission
4. Tacrolimus- immunosuppressive agent
Moderate- First line
1. Rectal and oral 5-ASA
2. Oral prednisolone- if no response to 5-ASA
Maintenance- oral/topical 5-ASA, 6-MP (severe exacerbations)
Surgery- Required at some stage by 20%
Subtotal colectomy- removal of most colon but sigmoid left
Completion proctectomy (permanent stoma)- removal of all colon
Ileo-anal pouch
29
What is proctitis?
Inflammation starting at the rectum and not spreading beyond the ileocaecal valve.
Proctitis is the most common disease pattern in UC and is seen in 40-50% of the cases.
Bloody diarrhoea, tenesmus, and mucoid discharge are the presenting features of proctitis.
Inflammation in UC starts as proctitis and does not usually spread beyond the ileocaecal valve.
30
Colorectal cancer investigations?
FIT + CEA tumour marker
Colonoscopy with biopsy
Flexible sigmoidoscopy- if patient is severely unwell
Contrast CT (chest, Abdo, pelvis)- evaluate tumour size/ spread
MRI- pelvic/ liver
31
Ovarian cancer investigation?
History
Bloods- raised CA125 tumour marker
Pelvic exam
Pelvic ultrasound
Pelvic CT
Genetic testing- BRCA1/2 mutation
32
Haemorrhoid treatment?
Increase fluid, fibre
Laxatives
Topical- anusol, anusol
Non-surgical- RBL
Surgical- haemorrhoidal artery ligation or haemorrhoidectomy
33
What is Cholelothiasis?
Gallstone development in gallbladder due to excess bile products (cholesterol).
Liver makes bile -> bile stored in the gallbladder-> excess cholesterol in bile leads to accumulation of cholesterol or bilirubin in the bottom on the gallbladder -> stones grow and harden -> stones travel and get stuck in cystic duct -> biliary colic
Cholesterol gallstones- unpigmented
Calcium-billirubinate gallstones (pigmented and visible on X-RAY)
34
Cholelothiasis management?
No intervention required for asymptomatic
Cholecystectomy: Surgical removal of gallbladder
Carried out if pt is symptomatic and/or gallstones have potential to lead to complications
1. ERCP can be used to remove gallstones before or during surgery
2. Laparascopic cholecystectomy (keyhole surgery) is keyhole surgery with less complications and faster recovery
35
Cholelithiasis investigations?
Bedside: GI exam
Lab:
1. Urinalysis to exclude differentials
2. LFTs to see for raised bilirubin
3. Alkaline Phosphatase (ALP) non-specific marker enzyme originating in liver
4. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) enzymes p
Imaging:
1. Ultrasound is 1st line for symptoms of gallstones (more sensitive than CT scans)
2. MRCP- an MRI scan w/ specific protocol to produce detailed image of biliary system
3. ERCP which involves inserting endoscope down oesophagus, past stomach to duodenum and opening of bile duct
-> helps to see stones, clear them, insert stents to improve bile duct drainage
36
What is cholecystitis?
Causes?
Types?
Inflammation of the gallbladder due to blockage of cystic duct preventing gallbladder from draining
Causes:
Infection
Bile duct obstruction
Tumours
Types:
Calculous cholecystitis: Common in 95% of cases
Gallstones stuck in cycstic duct -> Bile builds up in gallbladder -> distention and gallbladder becomes inflamed
Acute cholecystitis:
Gangrenous cholecystitis: necrosis and perforation of the gallbladder wall as a result of ischemia following progressive vascular insufficiency.
Perforated gallbladder: The gallbladder splits open and can spread infection and lead to peritonitis or abscess
Emergency surgery required for latter two
37
Investigations for cholecytisis?
Labs:
Bloods- CRP and WBC
Bedside: GI exam
Murphy’s sign: placing hand in RUQ and applying pressure. Patient asked to take deep breath in. Gallbladder moves down, comes into contact with hand and results in acute pain and stopping of inspiration
Imaging:
Abdominal ultrasound to see for thickening of gallbladder wall, presence of stones, fluid around gallbladder
MRCP if bile duct stone suspected but not seen on ultrasound scan
38
Management for cholecystis?
- Pain relief
- IV fluids
- Abx initially IV, then oral (as per local guidelines)
- NG tube if necessary for vomiting
- Cholecystectomy which can either be carried out during acute admission within 72 hours of symptoms, or delayed 6-8 weeks after acute episode to allow inflammation to settle
- ERCP to remove stones
If there is gallbladder empyema- gangrenous cholecystitis.
- IV abx
- Cholecystectomy or cholecystostomy if patient is not well enough for surgery
->latter refers to inserting drain into gallbladder to drain infected contents
39
What is MRCP and ERCP?
MRCP- Magnetic resonance cholangiopancreatography type of MRI used to visualise the biliary system, blockages, and tumours. SCAN
ERCP- Endoscopic retrograde cholangiopancreatography used to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas. It combines X-ray and an endoscope. PROCEDURE
ERCP bile duct treatment-bile- balloons and baskets attached to the catheters can be passed into the ducts allowing stone removal.
40
What does Courvoisiers Law state about cholangiocarcinoma?
Patients with jaundice and a palpable gallbladder often have a malignant obstruction of the common bile duct and is unlikely to be a gallstone- 70% of time
41
Cholangiocarcinoma investigations?
GI exam
Bloods- LFT, albumin, bilirubin, ALT, CA19-1 tumour marker
Imaging- CT, MRCP, ERCP, ultrasound
42
Cholangiocarcinoma management?
Poor prognosis- 12-18 months
Involves MDT
Resectable surgery- if early diagnosis
Chemo/radio therapy
Palliative and end of life treatment
43
First-line treatment for C. difficile infection?
Oral vancomycin is the first-line antibiotic for use in patients with C. difficile infection
44
What drug can increase risk of cholestasis?
Oral contraceptive pill
45
Explain microcytic anaemia
MCV <80 fL/cell (femtolitres)- reduced average size of RBC
Presents as- Low Fe+/ ferritin
Types- iron deficiency, thalassemia, sideroblastic anaemias
High Fe+= thalassemia + sideroblastic
Low Fe+= iron-deficiency
46
Explain normocytic anaemia
MCV= 80/100fL/cell - RBC are normal size and colour- based on reticulocyte count
Presents as- low/high reticulocyte count due to BM function affecting erythropoiesis
Types- aplastic anaemia, chronic, sickle-cell inflammatory disease
High reticulocytes= haemolytic anaemia as the body trying to compensate by making more reticulocytes- sickle-cell, G6PD deficiency, spherocytosis
Low reticulocytes- aplastic anaemia- BM dysfunction not enough RBCs
47
Explain macrocytic anaemia
MCV >100fL/cell- increase in average size of RBC. Based on blood film results
Types/ presents as- megaloblastic/ non-megaloblastic. Folate deficiency- B12/B9
Megaloblastic- large immature RBCs on film (B12/folate deficiency, drug toxicity- methotrexate)
Non-megaloblastic- only large mature RBCs (alcohol abuse, hypothyroidism, pregnancy)
48
Name mechanisms through which anaemias can arise
1. Reduced BM function -> reduced erythropoiesis (aplastic)
2. Hypothyroidism- thyroid hormones essential for healthy RBCs
3. Chronic kidney disease- lack of erythropoietin production in kidney
4. B12/B9/ Fe+ deficiency
5. Blood loss- GI bleed, trauma, heavy periods
6. Microcytic intravascular- (DIC, prosthetic heart valve, incompatible blood transfusion). 7. Microcytic extravascular- sickle-cell, malaria, hypersplenism
49
What is diverticular disease?- Sigmoid colon
Symptoms?
Disease in the large intestine causing the formation of diverticula and these to protrude through weak passages in the mucosa wall that can become inflamed leading to diverticulitis.
Increased pressure in colon-> mucosa protrudes through weak spots mainly near blood vessels -> inflammation and infection -> GI bleeds
LIF colicky pain- relieved by defecation
Change in bowel habit
Flatulence
Sudden fresh red PR bleeding that suddenly stops
50
Diverticular disease investigations.
History
Abdo exam
Bloods- FBC, WBC, Hb, CRP, faecal calprotectin
Abdominal/ pelvic CT scan
AXR
Erect CXR
51
Diverticular disease management.
Asymptomatic- high-fibre diet, fluids, laxatives
Mild- oral antibiotics, corticosteroids
(prednisolone), analgesics
Acute- IV fluids and antibiotics, analgesia
Acute management of rectal bleeding- ABCDE
Surgery- sigmoid colectomy
52
What is the assessment for constipation?
Red flags
Symptoms
History
symptoms
clinically= stool passage less than 3 times a week, requires straining,
Incompletetion, bloating, pain
Red flags- SUDDEN change in bowels, blood, weight loss, abdominal pain, iron deficiency anaemia
History- IBD/IBS, colorectal cancer, certain medications (opiated, iron tablets0
Rule out urinary symptoms- increased frequency or retention
53
Describe difference between acute, chronic constipation and faecal impaction.
Acute- short term
Chronic- 12+ weeks
Faecal impaction- large dry infrequent stool stuck in the rectum (passed 7-10 days)
54
Acute constipation management
Acute
Lifestyle- increase fibre, fluids, activity
1st- line laxatives- bulk-formimg (fybogel, methylcellulose)
2nd-line laxatives- osmotic (macrogol, lactulose)
3rd-line stimulant (senna, bisocodyl)- if soft but hard to pass
Follow-up patient
If not working then do full bloods
Refer to LGI clinic if secondary causes suspected
Refer to GI team if red flag symptoms
55
Chronic constipation management.
Abdominal and DRE exam
1st-line- bulk-forming (fybogel)
2nd-line- osmotic (macrogol)
3rd-line- stimulant (senna)
4th- prucalopride- if 2 laxatives from 2 groups did not work
56
Faecal impaction management.
1. glycerol suppository for hard stools
2. bisacodyl suppository if stools are soft but not being passed
3. Mini enema – such as docusate or sodium citrate (Enemas may need district nursing team or carers to administer)
If unsatisfactory response:
Phosphate enema or arachis oil enema. Can give arachis oil enema first to soften stool and then the phosphate enema the next day.
57
Microorganisms incubation period for gastroenteritis?
Viral- 24hrs
Bacterial toxins- 1-4 hours
Bacterial- 1-4 days
Parasites- 7-10 days
58
Dehydration signs and symptoms
- Feeling listless and lethargic
- Dry mucous membranes
- Sunken eyes
- Decreased skin turgor
- Increased heart rate
- BP may be low – later sign
- Reduced urine output and urine more concentrated and dark in colour.
59
Gastroenteritis investigations?
If confused/ drowsy/ severely dehydrated/?
Admission for IV fluids, bloods and abx
Admission
If lethargic/mild-mod dehydration, managing oral fluids – FBC, U&E, CRP
If distended abdomen/ increasing or severe abdominal pain – A&E for imaging ? Toxic megacolon
60
Gastroenteritis management?
Oral rehydration
Good hygiene – hand washing with soap and warm water, no sharing of towels
No attendance at work or school until >48hrs after last loose stool
Notify Public Health England if stool cultures show a ‘notifiable pathogen’
Small plain meals as tolerated
61
Bowel obstruction investigations?
Bloods FBC, U&E, CRP, G&S, Coag, ABG – lactate and assess for metabolic acidosis
Imaging – abdominal CT or AXR
62
Bowel obstruction management?
Drip and suck’- decompress bowel and give fluids
NG tube- NBM
Cannula and IV fluids
Careful resuscitation and correction of any electrolyte imbalances
Fluid balance chart
Catheter
IV abx if perforation suspected
If ischaemia, peritonism or perforation suspected, or a closed loop obstruction is present – emergency surgery required
If the patient is not fit for surgery a colonic stent may be used – for example in palliative patients
63
Hernia types
Epigastric
Umbilical- women after pregnancy
Incisional- post-surgery created a weakness in abdominal wall
Spigelian- rare, women, maternal abdominal
Inguinal- most common, men
Femoral- most common in women
64
Explain direct and indirect inguinal hernias.
DIRECT- Bowel enters the inguinal canal directly through a weakness in the posterior wall of the canal and does NOT go through the deep inguinal ring
Will bulge out on cough impulse
INDIRECT- Bowel enters the inguinal canal via the deep inguinal ring
Will not bulge out on cough impulse
65
Explain hernia terminology
Reducible
Incarcerated
Irreducible
Obstructed
Strangulated
Reducible- manually manipulated into the original position
Irreducible- hernia unable to be manually manipulated into original position
Obstructed- hernia compressed to the extent that the bowel lumen is no longer free
Strangulated- hernia compressed, prevents blood flow into the tissues, causing ischaemia which may lead to infarction and necrosis.
66
Hernia complication?
Obstruction, strangulation, necrosis
67
Hernia management?
If painful, red, purple- medical emergency-> surgery
Open mesh- for primary inguinal hernias
Laparoscopic mesh- for recurrent inguinal hernias
68
What is the difference between ERCP and MRCP?
ERCP (Endoscopic Retrograde Cholangiopancreatography) and MRCP (Magnetic Resonance Cholangiopancreatography) are both medical imaging techniques used to visualize the bile ducts and pancreatic ducts, but they differ in their approach.
ERCP is an invasive procedure where a flexible tube with a camera is passed through the mouth, esophagus, stomach, and into the duodenum. Contrast dye is then injected, and X-rays are taken to examine the bile and pancreatic ducts.
MRCP, on the other hand, is a non-invasive imaging technique that uses magnetic resonance imaging (MRI) to create detailed images of the bile and pancreatic ducts without the need for a contrast dye or invasive procedures.
In summary, ERCP involves an endoscope and X-rays with contrast dye, while MRCP uses MRI for a non-invasive visualization of the same anatomical structures.
69
What is biliary colic?
Gallstone that is stuck in cystic duct resulting in gallbladder contracting hard to dislodge stone.
Epigastric/ RUQ pain- severe
70
Biliary colic investigations and management?
Investigations:
Bloods - FBC, LFTs, U&Es, CRP, Amylase. Imaging - US Scan.
Management:
Adequate analgesia
Elective cholecystectomy.
71
What is acute cholecystitis and its symptoms?
Inflammation of the gallbladder caused by blockage of bile flow commonly from gallstone obstruction
Symptoms: RUQ pain, guarding, Murphus sign positive, fever
72
Investigations and management of cholecystitis?
Investigations:
Bloods - FBC, LFTs, U&Es, CRP, Amylase. Imaging - US Scan.
Cholestatic blood pattern - bilirubin and ALP may be raised, CRP and WCC also.
Important to rule out a stone in the CBD so MRCP is investigation of choice next.
Management:
NBM, IV Fluids, opiate analgesia, IV antibiotics Laparoscopic Cholecystectomy within 7 days usually.
73
What is acute cholangitis and its symptoms?
Inflammation of the bile ducts caused by gallstones, biliary strictures, bacterial infections
Symptoms:
Charcot’s triad – RUQ pain, Jaundice, Rigors.
May have dark urine, pale stools and pruritis.
74
Investigations and management for cholangitis?
Investigations:
Bloods - FBC (WCC raised) LFTs (Bili, ALP, ALT will be raised), U&Es, CRP (raised), Amylase (can be mildly raised).
Imaging – US scan, MRCP, CT scan, EUS
Management:
NBM, IV Fluids, opiate analgesia, IV antibiotics
ERCP +/- a stent to allow urgent biliary drainage.
Cholecystectomy.
75
What is gallstone ileus and its symptoms?
Gallstone becomes lodged in the small intestine causing bowel obstruction.
Symptoms:
Rigler's triad:
Pneumobilia- air in biliary tree
Small bowel obstruction
Ectopic gallstone- gallstone in abdominal cavity
Nausea/ vomiting
Umbilical pain
Abdo distention
No passage of stool/ gas
Feculent vomiting
76
What is pancreatitis, its symptoms and causes?
Inflammation of the pancreas commonly caused by gallstones, alcohol, trauma/surgery, viral infections.
Symptoms:
Epigastric pain, boring through to the back, prominent
Nausea/ vomiting
Signs in severe necrotising pancreatitis – digestive enzyme release into tissue-> breakdown of blood cells and pigment deposition
Cullen’s sign- umbilical bruising
Grey turner’s sign- flank bruising
Tachycardia, hypotension, oliguric.
77
Investigations and management for pancreatitis?
Investigations:
Bloods - FBC, LFTs, U&Es, CRP (>150mg/L at 36hr predictor of severe pancreatitis, Amylase (falls back to normal over 3-5 days),
ABG, Blood glucose.
Imaging – AXR, Erect CXR, US- scan, CT scan (will have repeated scans to monitor progress). MRCP, ERCP, Lap Chole if gall stones are the cause.
Management:
NBM, NJ Feed, IV fluids–catheter,
Analgesia
Ocreotide treatment considered- synthetic version of somatostatin
Stop alcohol
Gallstone removal- if gallstone
Can be a long, long road to recovery.
78
Colorectal cancer investigations and management?
Investigations:
Abdominal exam- masses
FIT and FOBT
Bloods- FBC, LFT, CRP, U&E, CEA marker
Colonoscopy with biopsy
CT-pelvis
Management:
Chemotherapy- neoadjuvant/ adjuvant
Radiotherapy- local neoadjuvant to shrink the tumour and then adjuvant to kill remaining cells
Surgery- tumour resection, lymph node removal, colostomy
Targeted therapies- EGFR inhibitors and mabs
Immunotherapy
Palliative care
79
Investigations for Wilson's disease?
Bloods-FBC, U&E, LFT, CRP, caeruloplasmin
Check 24hr urinary copper excretion
Liver biopsy
80
What is haemochromatosis?
Symptoms?
Genetic disorder causing excess iron deposition throughout body.
Associated with type-1 diabetes due to insufficient insulin secretion due to excess iron deposition in pancreatic beta islet cells.
HFE gene mutation causes low production of iron-regulating hormone hepcidin which controls iron absorption in the gut by inhibiting iron channels. Down-regulation of hepcidin increases gut iron absorption -> excess accumulation.
Symptoms:
* Fatigue- endocrine= diabetes
* Joint pain
* Abdominal pain
* Heart problems- arrhythmias
* Liver dysfunction- hepatomegaly, cirrhosis
* Bronzing of the skin- haemosiderin deposition and melanocyte activation
81
Investigations and management for haemochromatosis?
Investigations:
* Bloods- FBC, U&E, LFT, CRP, ferritin, transferrin, serum iron, TIBC, Hb, Hct
* Genetic testing for HFE mutation
* ECG/ echo- heart problems/ arrhythmias
* Liver MRI/ biopsy- cirrhosis, levels of iron in liver
Management:
* Low iron diet- avoid Vit-C, tea, alcohol
* Regular venesection to get rid of excess blood iron
* Chelation therapy- administration of chelating agents to remove heavy metals (iron) and excreted in urine/ faeces. Done if venesection is not tolerated.
* Regular monitoring- LFTs/ iron markers
* Genetic counselling/ screening
* Liver transplant- end stage
82
What is:
Cholelithiasis
Cholecystitis
Cholangiocarcinoma
Cholangitis
Biliary colic
Cholestasis
Primary sclerosing cholangitis
Cholelithiasis- formation of gallstones in the gallbladder due to excess bile (cholesterol)
Cholecystitis- inflammation of gallbladder due to blockage of cystic duct/ inadequate drainage
Cholangiocarcinoma- biliary tree cancer
Cholangitis- inflammation of bile ducts (bacterial)
Biliary colic- gallstone stuck in the cystic duct leading to gallbladder contracting hard to dislodge stone leading to epigastric severe pain
Cholestasis- reduction/ blockage of bile flow from liver (extra or intrahepatic)
Primary sclerosing cholangitis- biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts. Associated with ulcerative colitis
83
What is diverticulitis?
Symptoms?
Complications?
Formation and inflammation of diverticula which are out-pouching’s along walls of colon.
Caused by low-fibre diet which increases stool transit time and makes stool smaller which increases intra-luminal pressure for passage. Weakened areas are susceptible to herniation and diverticular formation.
Symptoms:
* LIF pain
* Asymptomatic
* Abrupt intermittent PR bleeding that stops on its own
Complications:
* Bowel obstruction
* Perforation
* Abscesses/ peritonitis
84
Investigations and management for diverticulitis?
Investigations:
* Abdo exam
* Bloods- FBC, LFT, U&E, CRP
* Stool- Faecal calprotectin
* CT- abdo
* Endoscopy
Management:
* High fibre diet
* Non-systemic= painkillers, abx
* Systemic- IV fluids, IV Abx
* Acute/ perforation- control bleed, coagulation therapy/ clips
85
What is appendicitis?
Symptoms?
Inflammation of the appendix which is serious and can lead to rupture, abscess
Symptoms:
* Pain starts in umbilical area -> RIF
* Nausea/ vomiting
* Loss of appetite
* Fever
* Rovsing’s sign- pressing on left side of abdomen and pain felt in right side
86
Investigations and management for appendicitis?
Investigations:
* Abdo exam
* Bloods- FBC, LFT, U&E, CRP, high WBC
* Ultrasound
Management:
* 1st-line: IV fluids, Abx, analgesia
* Surgery- laproscopic appendectomy
87
What is an ectopic pregnancy?
Symptoms?
Fertilisation and implantation of egg outside of uterus in the fallopian tubes. Medical emergency and requires surgery. Risk of perforation
Symptoms:
* Severe LIF/ RIF pain
* Vaginal bleeding
* Shoulder pain
* Weakness/ dizziness
* Rectal pressure
* Nausea/ vomiting
88
Investigations and management of ectopic pregnancy?
Investigations:
* Pregnancy test
* Abdominal exam
* Bloods- measure hCG hormone levels as they rise more slowly than in a normal pregnancy
* Ultrasound
Management:
* 2 large bore IV cannula for urgent bloods, clotting, G&S and crossmatch 4-6 units.
* Give rapid IV fluids
* Analgesics
* Catheterise and monitor urine output.
* Monitor vital signs every 15 minutes.
* Emergency surgery – laparoscopy preferred, if healthy contralateral fallopian tube salpingotomy (incision in fallopian tube to remove ectopic pregnancy) is preferred management rather than salpingotomy (removal of 1 fallopian tube)
89
What is acute mesenteric ischaemia?
Causes?
Symptoms?
Sudden loss of blood flow to intestines leading to inadequate oxygen supply. Leads to necrosis of small and large intestines and sepsis and death. Medical emergency.
Causes:
* Atherosclerosis
* Acute- embolism (travel from heart) or thrombus (form in mesenteric arteries)
* Vasculitis- inflammation of vessels
Symptoms:
* Severe central/ RIF pain
* Bloating
* Nausea/ vomiting
90
Investigations and management for acute mesenteric ischaemia?
Investigations:
* Bloods- FBC, U&E, LFT, CRP, amylase
* ABGs
* CT with IV contrast
Management: The location, timing, and severity of the mesenteric ischaemia, among other factors, will determine the surgical intervention performed:
* IV fluids, IV Abx, catheter
* Excision of necrotic or non-viable bowel
* Revascularisation of the bowel- removal of thrombus/ emboli
91
What is an abdominal aortic aneurysm (AAA)?
Risk factors?
Symptoms?
Enlargement/ bulging of the aorta in the abdomen.
Risk factors:
* Atherosclerosis
* Older aged men
* Tobacco
* Hypertension
* Inflammatory diseases
* TIA- temporary disruption of blood flow to the brain
Symptoms:
* Sudden severe mid/low back pain
* Severe umbilical pain
Pulsating abdominal mass
* Sudden weakness- on one side of body
* Loss of balance
Tachycardia/ sweating
92
Investigations and management for an abdominal aortic aneurysm (AAA)?
Investigations:
Bloods- FBC, Hb, amylase troponin, G&S, coagulation, LFT, U&E, TFT, CRP
Obs
Abdominal ultrasound- best if unstable
CT-scan with contrast- best if uncertain
ECG- check for irregular heart rhythm
CT- rule out bleeding in brain
Management: depends on size of aneurysm and rate of growth
* Less than 5.5cm- monitoring and lifestyle changes
* Medication to control high BP and cholesterol
* Endovascular repair- stents
* Open surgical repair- large aneurysms
Acute- surgical emergency, 2 large bore IV cannulae, IV fluids, analgesics, urgent bloods G&S and crossmatch, catheterise and monitor urine output. Surgery to repair AAA
93
What is gastroparesis?
Symptoms?
Paralysis of nerves and muscles in the stomach leading to weaker and slower contractions. Leads to delayed emptying of contents into small intestine.
Symptoms:
* Vomiting/ Nausea
* Abdominal bloating
* Abdominal pain
* A feeling of fullness after eating just a few bites
* Vomiting undigested food eaten a few hours earlier
* Acid reflux
* Changes in blood sugar levels
94
Investigations and management for gastroparesis?
Investigations:
* Bloods- FBC, CRP, LFT, U&E, amylase
* Gastric emptying scintigraphy/ smart-pill- tracks movement of radioactive material through stomach to check emptying
* Upper endoscopy- inspect lining and rule out others
* EGG- electrogastrography
* CT
Management:
* Eat smaller meals
* Prokinetic medications- promote stomach motility
* Botulinum injection- injected into pyloric sphincter to improve emptying
* Parenteral nutrition
95
What is acute pancreatitis?
Causes?
Symptoms?
Acute inflammation of exocrine pancreas due to acute insult commonly caused by gallstones and alcohol. Activation of digestive enzymes leads to autodigestion of pancreas. Reversible.
Causes: GET SMASHED
G- gallstones
E- ethanol
T- trauma
S- steroids
M- mumps and infection
A-autoimmune
S- scorpion venom
H- hyperlipidaemia/calcaemia
E- ERCP induced (increases pressure in pancreatic duct -> inflammation -> necrosis)
D- drugs (azathioprine, diuretics, valproate)
Symptoms:
* Severe epigastric pain that radiates to the back
* Nausea/ vomiting
* Cullen’s and Grey turners signs
96
Investigations and management for acute pancreatitis?
Complications?
Investigations:
* Bloods- FBC, CRP, WBC, elevated amylase and lipase, U&E, Ca+, albumin, LFT (raised ALP + GGT)
* ABGs- hypoxia
* Abdominal ultrasound
* Abdominal CT with contrast
* AXR- rule out perforation
Management:
Initial resus
ABCDE, NBM, anti-emetics, analgesia, IV fluids, catheterisation and urine output observations, VTE prophylaxis, glucose monitoring and management with insulin, escalate to ICU if multiorgan failure
Interventional
* ERCP for gallstone extraction (within 24hrs)
* Routine MRCP/ ESU- loos for residual stones
* Urgent laparoscopic cholecystectomy (within 2 weeks)
Complications:
* Haemorrhage
* DIC- disseminated intravascular coagulation
* ARDS
* Multiorgan failure/ Necrosis
97
What is chronic pancreatitis?
Causes?
Symptoms?
Structural integrity of pancreas is permanently altered and results in chronic inflammation, abdominal pain, destruction of exocrine pancreas- 80% caused by alcohol and is irreversible.
Causes- CAMP
C- cystic fibrosis
A-autoimmune
M- malabsorption
P- pancreatic duct obstruction
Symptoms:
* Epigastric pain radiating to the back
* N&V
* Steatorrhea/ diarrhoea
* Weight loss
98
Investigations and management for chronic pancreatitis?
Investigations:
* CT pancreas with contrast
* MRCP/ EUS
* Pancreatic function- serum glucose, faecal elastase reduced
Management:
* Alcohol cessation and low-fat diet
* NSAIDs
* Vitamin supplements- A, D, E, K
* PPIs
* Glycaemic control for diabetes
99
What is toxic megacolon?
Causes?
Symptoms?
Severe acute inflammation and dilation of the colon with presence of acute colitis and systemic toxicity.
Causes:
* IBD- UC or Crohn’s
* Infections/ pseudomembranous colitis- antibiotics and overgrowth of C. diff
* Ischemic colitis- reduced blood flow to colon due to blocked vessel
Symptoms:
* Abdominal pain/ distention
* Fever- inflammation or distention
* Tachycardia
* Dehydration
* Change in bowel habits
* Confusion- due to toxins released by inflamed colon
100
Investigations and management for toxic megacolon?
Investigations:
* Abdominal xray- extent of dilation/ if perforation
* Chest/pelvis CT
* Bloods- FBC, U&E, LFT, CRP, amylase, WBC, Hb, electrolytes for dehydration, albumin, lactic acid
* Stool cultures- infection
* Colonoscopy/ sigmoidoscopy
Management:
* IV fluids and abx
* Bowel rest- NBM and IV nutrition to reduce bowel inflammation
* NG tube to decompress stomach
* Corticosteroids and immunosuppressants (infliximab)- UC patients
* Surgery- subtotal colectomy with ileostomy and either a Hartmann pouch, sigmoidostomy, or rectostomy.
101
What stool consistency does gardia lamblia cause?
Giardia causes fat malabsorption, therefore greasy stool can occur. It is resistant to chlorination, hence risk of transfer in swimming pools.
102
What is the treatment for severe alcoholic hepatitis?
Corticosteroids are used in the management of severe alcoholic hepatitis (prednisolone)
103
What cancer is coeliac disease associated with?
T-cell lymphoma
This is due to the neoplastic transformation of intraepithelial T lymphocytes in coeliac patients. Risk factors include poor adherence to a gluten-free diet and late diagnosis of coeliac disease.
104
What does a high serum-ascites albumin gradient (SAAG) suggest and what does it present with?
Ascites: a high SAAG gradient (> 11g/L) indicates portal hypertension
This is because increased hydrostatic pressure forces fluid out of the vascular spaces, concentrating serum albumin.
105
How is a C. difficile infection treated?
In life-threatening C. difficile infection treatment is with ORAL vancomycin and IV metronidazole
IV vancomycin is less effective at treating enteric infections
106
How does pancreatic cancer present on a abdominal CT?
Simultaneous dilatation of the common bile duct and pancreatic ducts- double duct
107
Before peptic ulcer endoscopy what is the line of management?
No intervention required
This approach avoids the premature use of PPIs which, whilst they may decrease the visibility of recent haemorrhage, have not consistently been shown to improve clinical outcomes prior to endoscopic evaluation.
Their use is more strategically applied post-endoscopy, particularly when high-risk lesions are identified, to provide targeted therapy that can lead to improved clinical outcomes, including reduced rates of re-bleeding and surgery.
108
Common epigastric conditions?
Peptic ulcer disease
Cholecystitis
Pancreatitis
MI
Gastritis
109
Common RUQ coniditions?
Cholecystitis/ cholangitis
Pyelonephritis
Biliary colic
Hepatitis
Bowel obstruction
Constipation
Ureteric stone
110
Common LUQ conditions?
Splenomegaly
Gastritis
Splenic infarct
Pyelonephritis
Bowel obstruction
Ureteric stone
111
Common umbilical pain causes?
Pancreatitis
Early appendicitis- McBurney's point
Umbilical hernia
AAA
Bowel obstruction
Constipation
112
Common RLQ/ RIF conditions?
Appendicitis
Ectopic pregnancy
Ovarian cyst/ torsion
Hernia
PID
113
Common LLQ/ LIF conditions?
Diverticulitis
Ectopic pregnancy
Hernia
Constipation
114
Name 2 types of bowel obstruction.
Mechanical- contents cannot pass through due to physical block. Completely or partially
Paralytic- contents cannot pass due to cessation of normal gut peristalsis (paralysis)
115
Large bowel obstruction causes?
Colorectal cancer
Diverticular strictures
Sigmoid volvulus- intestine twists around on itself
116
Causes of air bubbles in urine in diverticulitis?
Colovesical fistula
117
what is pilonidal disease?
infection of the small hole at the top of the bottom between the buttocks resulting in a pus-filled skin abscess
causes: unclear cause
dermatological issues
pressure
friction
hair entering the pilonidal sinus and blocking it
> in hairier men
prolonged sitting
symptoms: small bump that's bleeding, pus or painful
management:
NSAIDs
Abx
incision and drainage
surgery to remove sinus
