GI + Liver Flashcards

1
Q

Describe the pathophysiology of acute cholangitis

A

Ascending cholangitis is a bacterial infection (typically E. coli) of the biliary tree. The most common predisposing factors are gallstones and benign/cancerous structures.

Charcot’s Triad : Fever, jaundice RUQ pain (not always present in all patients)

Raised inflam markers will also be present

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2
Q

What are the initial investigation that need to be done to confirm suspicions of acute cholangitis?

A

Bloods: FBC, LFT . Raised LFTs and WBC + CRP

US abdomen, if nothing detected Ct can also be used.

MRCP most accurate method to detect disease (stones and cancer)

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3
Q

What would the management for a patient with acute cholangitis look like?

A

Resus through IV fluids + antibiotics

Gold standard is ERCP (Endoscopic retrograde cholangiopancreatography)

Assessment and management of predisposing cause – for example, if gallstones – consider cholecystectomy. If malignant stricture, this would need further investigation and management as appropriate.

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4
Q

Describe the pathophysiology of cholecystitis

A

Inflammation of the gallbladder. It usually occurs when a gallstone completely obstructs the gallbladder neck or cystic duct.

It typically occurs in critically ill people due to a combination of risk factors that result in bile stasis (due to gallbladder hypomotility/dysmotility) or bile thickening (due to dehydration).

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5
Q

Investigations + management for someone with cholecystitis

A

abdominal US and blood tests (such as a white blood cell count, C-reactive protein, and serum amylase).

Monitoring (for example blood pressure, pulse, and urinary output).

Treatment (may include intravenous fluids, antibiotics, and analgesia)

Surgical assessment for cholecystectomy.

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6
Q

Describe the pathophysiology of acute pancreatitis.

A

Pancreatitis is inflammation of the pancreas.

GET SMASHED:
Gallstones (most common worldwide)
Ethanol (most common cause in Europe)
Trauma
Steroids
Mumps
Autoimmune disease (Polyarteritis Nodosa/SLE)
Scorpion bite
Hypercalcaemia, hypertriglycerideaemia, hypothermia
ERCP
Drugs (Furosemide, Azathioprine/Asparaginase
Thiazides/Tetracycline
Statins/Sulfonamides/Sodium Valproate
Hydrochlorothiazide
Estrogens
Ethanol
Protease inhibitors and NRTIs)

Symptoms include:

Stabbing-like, epigastric pain which radiates to the back that is relieved by sitting forward or lying in the fetal position.

Vomiting

Recent alcohol binge/ history of gallstones

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7
Q

Investigations + management for someone with acute pancreatitis.

A
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8
Q

Describe the pathophysiology of coeliac disease

A

Coeliac disease is a T cell-mediated inflammatory autoimmune disease affecting the small bowel in which sensitivity to prolamin results in villous atrophy and malabsorption.

Gastro Symptoms:
Abdominal pain
Distension
Nausea and vomiting
Diarrhoea
Steatorrhoea

Systemic Symptoms:
Fatigue

Weight loss or failure to thrive in children

General appearance: check for pallor (secondary to anaemia), short stature and wasted buttocks (secondary to malnutrition), and features of vitamin deficiency secondary to malabsorption (e.g. bruising due to vitamin K deficiency).

Dermatological manifestations: dermatitis herpetiformis (pruritic papulovesicular lesions over the buttocks and extensor surfaces of the arms, legs, and trunk).

Abdominal examination: there may be abdominal distension.

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9
Q

Investigations for coeliac disease

A

Basics:

FBC (anaemia)
U&E and bone profile (vit d absorbtion impaired)
LFT (low albumin, malabsorption)
Iron, B12, folate

Anti-TTG IgA antibody measured + IgA level (some patients deficient)
If IgA deficient : check Anti-TTG IgG

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10
Q

Management for coeliac disease

A

Life long gluten free diet
Education on diet restrictions
Regular monitoring to check adherence

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11
Q

What is appendicitis and what are the common presentations?

A

lymphoid hyperplasia or a faecolith → obstruction of appendiceal lumen → gut organisms invading the appendix wall → oedema, ischaemia +/- perforation

Peri-umbilical pain that migrates to the right iliac fossa
Migration of pain to RIF is strongest indicator of appendicitis
Pain worse on coughing/going over speed bumps
Mild pyrexia
Anorexia

On examination rebound and percussion tenderness, guarding and rigidity

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11
Q

Investigations for appendicitis

A

FBC, raised WBC + inflam markers
Neutrophil dominant leucocytosis seen in >80% of patients
Urine analysis to rule out pregnancy in women, renal colic and UTI

No definite rules on the use of imaging and its use is often determined by the patient’s gender, age, body habitus and the likelihood of appendicitis

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12
Q

Management for appendicitis

A

appendicectomy - open/laparoscopic. Laparoscopic treatment of choice

administration of prophylactic intravenous antibiotics reduces wound infection rates

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13
Q

What is ascites and how does it present

A

Ascites is the abnormal accumulation of fluid in the abdomen

The serum ascites albumin gradient (SAAG) can help to determine the cause of ascites.

It is calculated by subtracting the albumin concentration of the ascitic fluid from the serum albumin concentration.

Swollen abdomen, shifting dullness

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14
Q

Causes of high SAAG (>11g/L)

A

PORTAL HYPERTENSION

cirrhosis/alcoholic liver disease
acute liver failure
liver metastases

right heart failure
constrictive pericarditis

Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema

A high SAAG suggests that the cause of the ascites is due to raised portal pressure. Raised hydrostatic pressure forces water into the peritoneal cavity whilst albumin remains within the vessels, thus resulting in a higher difference in the albumin concentration between the serum and ascitic fluid.

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15
Q

Causes of low SAAG (<11g/L)

A

Hypoalbuminaemia -

nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)

Malignancy -
peritoneal carcinomatosis

Infections -
tuberculous peritonitis

Other causes -
pancreatitis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases

16
Q

Management of ascites

A
  • reducing dietary sodium
  • fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
  • aldosterone antagonists: e.g. spironolactone
  • drainage if tense ascites (therapeutic abdominal paracentesis)

Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved

17
Q

What is gastric carcinoma and how does it present

A

Cancer of the stomach. Can be split into 2 types, intestinal and diffuse.

Intestinal -

Associated with H. pylori, tobacco smoking, achlorhydria and chronic gastritis.
Commonly on lesser curvature of the stomach

Diffuse -
Not associated with H. pylori
Associated with signet cells

Presentation-

abdominal pain - vague epigastric pain
weight loss and anorexia
nausea and vomiting
dysphagia: particularly if the cancer arises in the proximal stomach
if lymphatic spread:
left supraclavicular lymph node (Virchow’s node)
periumbilical nodule (Sister Mary Joseph’s node)

18
Q

What is the investigation + management for gastric carcinoma

A

Investigation -

oesophago-gastro-duodenoscopy with biopsy

URGENT 2 week referral if :
Dysphagia
Aged 55 and over with weight loss AND –
Upper abdominal pain OR reflux OR dyspepsia
Upper abdominal mass consistent with stomach cancer

CT scan to assess stage then MRI if suspected liver met

Management -
surgical options depend on the extent and side but include:
endoscopic mucosal resection
partial gastrectomy
total gastrectomy
chemotherapy

19
Q

What is the pathophysiology of oesophageal cancer and its presentations?

A

Two types, Adenocarcinoma (most common) and squamous cell

Adenocarcinoma effects lower third of oesophagus
Risk factors -

GORD
Barrett’s oesophagus
smoking
obesity

Squamous effect upper 2/3rds
Risk factors - smoking ,alcohol ,achalasia ,Plummer-Vinson syndrome and diets rich in nitrosamines

Features

dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough

20
Q

What is the pathophysiology of oesophageal cancer and its presentations?

A

Two types, Adenocarcinoma (most common) and squamous cell

Adenocarcinoma effects lower third of oesophagus
Risk factors -

GORD
Barrett’s oesophagus
smoking
obesity

Squamous effect upper 2/3rds
Risk factors - smoking ,alcohol ,achalasia ,Plummer-Vinson syndrome and diets rich in nitrosamines

Features

dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough

21
Q

What are the investigations used in suspected oesophageal cancer

A

Upper GI endoscopy with biopsy
Endoscopic ultrasound is used for locoregional staging
CT scanning of the chest, abdomen and pelvis is used for initial staging then FDG-PET CT

22
Q

How is oesophageal cancer treated

A

Operable disease is managed by surgical resection - the most common procedure is an Ivor-Lewis type esophagectomy

Adjuvant chemo may also be considered in some patients

23
Q

How does pancreatic cancer present and what are the risk factors?

A

Over 80% of pancreatic tumours are adenocarcinomas which typically occur at the head of the pancreas.

classically painless jaundice
pale stools, dark urine, and pruritus
cholestatic liver function tests
Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
however, patients typically present in a non-specific way with anorexia, weight loss, epigastric pain
loss of exocrine function (e.g. steatorrhoea)
loss of endocrine function (e.g. diabetes mellitus)
atypical back pain is often seen
migratory thrombophlebitis (Trousseau sign) is more common than with other cancers

24
Q

What is the investigation for suspected pancreatic cancer?

A

ultrasound has a sensitivity of around 60-90%
high-resolution CT scanning is the investigation of choice if the diagnosis is suspected
imaging may demonstrate the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts

25
Q

How is pancreatic cancer managed?

A

a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas. Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease

adjuvant chemotherapy is usually given following surgery

ERCP with stenting is often used for palliation

26
Q

What is Gastro-oesophageal reflux disease?

A

Gastro-oesophageal reflux disease (GORD) is a medical condition that occurs when stomach contents flow back into the oesophagus, causing symptoms such as dyspepsia, heartburn, or acid reflux. This condition is caused by a weakened lower oesophageal sphincter, and it is diagnosed based on the presence of these symptoms.

Common symptoms include:

Dyspepsia (“heartburn”)
Sensation of acid regurgitation

27
Q

Investigation + Management for GORD

A

Diagnosis is clinical.

First line treatment is PPI
If alarming symptoms present, OGD is used
Additionally manometry (looking at motility) may be used

28
Q

What is diverticular disease and its presentations?

A

Herniation of colonic mucosa through the muscular wall of the colon. The usual site is between the taenia coli where vessels pierce the muscle to supply the mucosa. For this reason, the rectum, which lacks taenia, is often spared.

Presents with:

Altered bowel habit
rectal bleeding
LLQ Abdominal pain