GI Flashcards
What are the 2 patterns of movement in the GI tract
Peristalsis - reflex response -result of wall stretch
segmentation - mixes lumen content
Electrical activity of GI tract
spontaneous rhythmic fluctuation with MP -64 and -45
specialised cells aka interstitial cells of cajal
spike potential→ increase tension→ cause contraction
Depo→ ca2+ influx
Repo→ K+ efflux
stimulated by stretch, ACh, Parasympathetic
3 ways GI motility is regulated
- Reflexes from outside the digestive system
- Reflex from inside digestive system (enteric ns)
- GI peptides
The extrinsic nervous system (Sympathetic)
originate between T5 &L2 of the spinal cord
innervated all of GI tract
Nerve ending secrete mainly NE and epinephrine
Stimulation = inhabits GI activity
The extrinsic nervous system (parasympathetic)
divided into cranial and sacral
cranial PN fibres are almost in the vagus nerves except to mouth and pharyngeal
sacral originates from 2-2 sacral segment of spinal cord
it passes through pelvic nerve to distal half of large intestine
stimulation causes increased activity
ENS (layers of cells)
-Lumen
-Mucosa (epithelium, lamina propria, muscularis mucosa)
-Submucosa (submucosal plexus)
- Muscularis propria (circular muscle, myenteric plexus, longitudinal plexus)
- Serosa
6 main polypeptides of GI
Cholecystokinin
Secretin
GIP
GLP-1
Gastrin
Motilin
CCK
- produced by I cells in duodenum and jejunum
- also secreted by neurons in the brain
- stimulates contraction of gall bladder for bile release
- Stimulation of pancreatic enzyme release
- relaxes Sphincter of Oddi
- inhibits gastric emptying by slowing contraction,
- promotes intestinal motility
Secretin
- produced by S cells of upper small intestine mucosa.
- mildly affects gastric emptying,
- promotes pancreatic secretion of HCO3
GIP
- secreted by “K cells” mainly in duodenum
- slows the rate of stomach emptying when SI is overloaded.
GLP-1
- produced by “L cells” in distal small intestine mucosa.
- delays gastric emptying
Gastrin
- released from the gastric antrum G cells by stomach distension.
- increases motility in the stomach
Motilin
- secreted by “M-cells” in the upper small intestine.
- secreted during fasting, and the only known function of this hormone is to increase gastrointestinal motility - migrating motor complex
3 segments of the Oesophagus
cervical
thoracic
Abdominal
Innervation and muscle types of the oesophagus
Proximal 1/3 → striated:
- innervated by somatic motor neurons of vagus nerve
distal 2/3 → smooth muscle
- innervated by visceral motor neurons of vagus nerve
- synapse with postganglionic neurons
Lower oesophageal sphincter (LOS)
- Mainly closed
- ACH causes intrinsic sphincter to contract (closes)
- NO &VIP → inhibitory (opens)
- Function: prevent reflux
3 phases of swallowing
- Oral → voluntary
- Pharyngeal
- Oesophageal
5 features that make up the anti- reflux barrier
- LOS
- normal oesophageal peristalsis
- Crural fibres of the diaphragm
- Length of the abdo oesophagus
- Gravity (small effect)
4 aspects of gastric motility
- Filling
accommodates 20-fold change in its volume by receptive relaxation: - vago-vagal reflex from stomach to brainstem and back; reduces tone of muscular wall.
- the proximal stomach relaxes to store food at low
pressure whilst it is acted upon by acid and enzymes.- Storage
- Mixing
Peristaltic contraction (PC) usually begin in body of stomach down
PC becomes more vigorous as it reaches the antrum.
This propels the chyme forward - Emptying
A small portion of the chyme is pushed through the “partially” open sphincter into the duodenum
When PC reaches the pyloric sphincter, the sphincter closes tightly→ No further emptying
Chyme not delivered into duodenum is forced backward into the stomach – “retropulsion.”
3 parts of the stomach
- Body normally stores food; has weak contraction & numerous oxyntic glands
- Antrum has thick muscularis externa, vigorous contractions & numerous pyloric glands - (secrete gastrin)
- Pylorus regulates passage of chyme into duodenum
Entry of food into duodenum depends on:
- Hypertonic chyme, low pH
- Presence of a.a and peptides
- Fatty acids and monoglycerides → slows gastric emptying
Emesis
- A regulation of the gut motility function following excessive irritation or distension of any part of upper GI
- signals initiating vomiting mainly originate from upper GI - pharynx, oesophagus, stomach and duodenum.
- nerve impulses are transmitted by vagal and sympathetic afferent nerve to v. centre.
- sufficient stimulation of v. centre leads to vomiting act;
- involves forceful expulsion of gastric (and duodenal) contents through the mouth;
- often preceded by salivation, nausea, rapid irregular heart beat, dizziness, retching.
- Vomiting can also be elicited by drugs or by rapid change in direction
- some emetics stimulate duodenal receptors, others act on receptors on floor of 4th ventricles called CTZ
- motion stimulates receptors in vestibular labyrinth centre, then to CTZ.
- It represents a defence reaction to protect the body against intake of dangerous agents.
- Toxins in the GI tract can be recognised either
- before absorption via visceral parasympathetic and sympathetic afferent fibres.
- after absorption into the blood via the chemoreceptor trigger zone (CTZ) located in the area postrema.
- Toxins in the GI tract can be recognised either
- Thus CTZ integrates both the afferent signals from the gastrointestinal tract and the chemical signals from the blood.
Motility of the Small intestine (SI)
- SI is 5m in length, has 3 sections
- It takes 2-4 hrs for chyme to traverse it
- Basic electrical rhythm is entirely intrinsic.
- Movements of SI can be
- peristaltic (propulsive contractions)
- mixing (segmentation) contractions
- migrating contractions
- Segmentation is characterised by closely spaced contractions of circular muscles
- Slow waves of smooth muscle causes segmental contractions backed by myenteric nerve plexus.
- Peristaltic contraction progressive, moves content in orthograde direction, about 2 cm/sec
- net movement along SI averages 1cm/min
Regulation of SI
- Peristaltic contraction
- Neural by local reflex mediated via ENS, but can be extrinsic innervation
- Hormonal factors:
- gastrin, CCK, insulin, motilin, and serotonin enhance intestinal motility
- Secretin, VIP and glucagon inhibit
- Drugs such as codeine & other opiates decrease motility
Innervation of large intestine
Parasympathetic
- Vagus: - caecum, ascending & transverse
- Pelvic: - descending, sigmoid rectum anal canal
Sympathetic
- proximal part mainly via sup. mesenteric plexus
- distal – via inf. mesenteric / sup. Hypogastric
- rectum & anal canal – inf. hypogastric plexus
Motility of Large intestine
- Segmental or Haustral contractions
- combined contraction of circular and longitudinal muscle to form bag like sacs - called haustration
- mix and shuttle contents slowly to enhance water and electrolytes absorption.
- progress of colonic content slow, 5-10cm/hr.
- modulated by vagus & pelvic nerves
- Peristalsisslow in comparison to small intestine; 8 -15hrs transit time.Mainly in caecum and ascending colon
- Mass movement
powerful contraction of mid-transverse colon, sweeps colon contents into rectum
occurs usually after first meal of day
associate with gastro-colic reflex
stimulates the urge to defecate
Incontinence
- Faecal incontinence – involuntary or inappropriate passage of stool.
- Continual dribble of faecal matter is prevented by tonic contraction of;
- internal anal sphincter (smooth muscle), which contributes up to 90% of resting anal canal pressure.
- external anal sphincter (striated muscle), voluntary innervation by pudendal nerve, contributes 20% resting anal tone
- puborectal muscle wraps around posterior aspect of anorectal junction.Physiology of incontinence
- Damage to anal sphincters may be associated with dysfunction of;
- smooth muscle: – leads to faecal leakage without awareness.
- Striated muscle: – presents with faecal urgency
The 3 salivary glands
parotid gland - only serous
submandibular gland - both serous and mucinous
Sublingual gland - a mix
2 major components of saliva and what they contain
-Serous component carries out digestive function and has: water, electrolytes,
enzymes, IgA
-Mucinous lubricates; principally contains lubricating glycoproteins mucin.
regulation of salivary secretion
Parasympathetic fibres activation leads to a copious flow of saliva
mediated by Ach activation of acinar cell muscarinic receptors (M1 & M3).
stimulation of mAChRs on salivary acinar cells to lead G proteins activation to increase
intracellular calcium levels.
Sympathetic postganglionic transmitters – noradrenaline acts α1- & β1-
adrenoreceptors
nerves which stimulate mucinous and serous saliva
ACh released at submandibular ganglion of the facial nerve (VII) stimulates muscarinic receptors on
acinar cells & triggers serous and mucinous saliva secretion.
ACh released at otic ganglion of the glossopharyngeal nerve (IX) stimulates muscarinic receptors &
triggers serous saliva secretion
gastric secretion
2 distinctive cell types are involved in gastric secretions:
Parietal cells – HCL, Intrinsic factor
Chief cells – Pepsinogens and gastric lipase
Pancreatic exocrine secretion
Major components are:
HCO3 ions:- making the juice alkaline (pH 7.1-8.2).
Digestive enzymes:
amylases (starch to oligosaccharides)
proteases (trypsin, chymotrypsin, elastase, etc.)
lipases (major triglyceride enzymes)
Activities of these enzymes highest in upper jejunum, declines further
down the intestine.
Phases of secretion
Cephalic phase: nerve signals
from brain causes Ach release in
pancreas.
Gastric phase: nervous
stimulation of enzyme secretion
continues.
Intestinal phase: chyme with low
pH enters intestine; secretin
released in response; pancreatic
secretion is more copious.
Bile secretion
1st secretion by hepatocytes into bile
canaliculi; this contains bile acids,
cholesterol, bilirubin & phospholipids.
2nd stage secretion is made of water,
bicarbonate, NaCl when by ductal
epithelial cells are stimulated by Ach
& Secretin
What is achalasia
- Primary motor disorder of oesophagus; due to inflammatory destruction of inhibitory nitrinergic neurons in oesophagus
- Elevated resting LOS tone (spasm); may be due to
- selective destruction of the n.a.n.c inhibitory neurones
- damage to oesophageal innervation
Risk factors for achalasia
- infection
- autoimmunity
- genetics
Signs and symptom of achalasia
chest pain
Investigations foe achalasia
- Upper GI endoscopy and biopsy of LOS
- Timed barium oesophagram to assess oesophageal emptying; dilated oesophagus appears tapers to beak-like at G-O junction.
- Oesophageal manometry:
- To assess the motor function of the UOS, LOS and oesophageal body
- Assess cause of regurgitation (e.g. reflux of stomach acids into oesophagus)
- Dysphagia (determine cause of swallowing difficulty)
Management for achalasia
- Dilatation, Surgery, Drugs & Botulinum toxin:
- Pneumatic dilatation – to stretch out sphincter.
- Laparoscopic cardiomyotomy – to divide the muscle fibres across the lower oesophageal sphincter; relieves dysphagia in 90% of patients
- Botulinum toxin injection – selectively blocks Ach release.
- Calcium-channel blockers and nitrates to reduce pressure in the LOS.
GORD?
Gastro-intestinal reflux disease (GORD) is a condition characterised by retrosternal, and sometimes epigastric pain, as a result of reflux of the acidic contents of the stomach into the oesophagus
Risk factors for GORD
-Hiatus hernia
-Eating certain foods – fat, chocolate, caffeine
-Smoking
-Obesity
-Dysfunction of the lower oesophageal sphincter (LOS)
-Alcohol
-Helicobacter Pylori
-“Stress”
Pathophysiology of gord
unintentional relaxation of the LOS
Fundic distension due to overeating
delayed gastric emptying secondary to the high-fat western diet and impaired oesophageal defences (e.g. saliva).
distension causes the sphincter to be taken up by the expanding fundus,
o exposing the distal 3cm of squamous epithelium of the oesophagus to gastric juice leads to inflammation.
o Patient compensates by increased swallowing, allowing saliva to bathe the injured mucosa and alleviate the discomfort.
Signs and symptoms of GORD
- heartburn/chest pain
- Acid brash - the feeling of a bitter, acid-like taste in the mouth
- Nausea and vomiting
- Cough
- Dysphagia
Investigation for GORD
Orifice Test
- OGD - endoscopy to visualise the oesophagus is useful to investigate and determine the severity of Oesophagitis.
- If other causes such as malignancy are suspected, biopsies can also be taken.
- Capsule endoscopy can be done as a less invasive alternative
X-ray/Imaging
Barium swallow - if excluding an alternative cause for symptoms, such as malignancy, a barium swallow may be a useful imaging modality
Special Tests
- Manometry - can be useful to investigate motility disorders such as achalasia
Management for GORD
Treatment aims to decrease amount of reflux:
- Lifestyle changes:
- avoiding foods and beverages that can weaken the LOS; e.g. chocolate, peppermint, fatty foods, coffee, and alcoholic beverages.
- eating meals at least 2 to 3 hours before bedtime may lessen reflux.
- stopping smoking
- Drugs: antacids, alginates, H2 receptor blockers, PPI
Complications for GORD
Barret’s oesophagus
Anaemia
Benign oesophageal stricture
gastric volvulus
Webs
4 types of lactose intolerance
primary (the most common) →lactase production falls sharply in adulthood
secondary→ n coeliac dx.
congenital→ in babies born prematurely
developmental. → lack of lactase at birth, inherited.
Risk factors for lactose intolerance
- black, Native American, Asian, Hispanic, or Jewish ethnicity
- adolescence and early adulthood
- family history of lactase deficiency
- enteritis/gastroenteritis
Pathophysiology of lactose intolerance
Lactose intoleranceoccurs when your small intestine doesn’t produce enough of an enzyme (lactase) to digest milk sugar (lactose)
Signs and symptoms of lactose intolerance
Abdominal pain/discomfort
borborygmi
flatulence
skin rashes
Investigation for lactose intolerance
- trial of dietary lactose elimination
- FBC
- lactose hydrogen breath test
- stool culture
- faecal pH
- faecal reducing substance/sugar
Mangement for lactose intolerance
change in diet
Complication for lactose intolerance
Diseases associated with secondary lactose intolerance includeintestinal infection, celiac disease, bacterial overgrowth and Crohn’s disease
What is peptic ulcer disease
Ulcer found in the lower oesophagus, stomach, and duodenum
What causes peptic ulcer disease
caused by infection with helicobacter Pylori
Risk factor for peptic ulcer disease
common in men
poor hygiene
Signs and symptoms for peptic ulcer disease
upper abdominal pian
vomiting
For DU’s, the pain is when you are hungry, and GU’s the pain is when you eat
nausea
weight loss
Investigation for peptic ulcer disease
Urea breath test- test for H. pylori
Serological test for IgG
Stool test
Endoscopy
FBC
U+E
FOB
patient over 55 → straight to endoscopy
Barium meal test
Management for peptic ulcer disease
smoking cessation
First line therapy –Triple therapy –
patients will be treated with a proton pump inhibitor, and two antibiotics
Second line therapy –
Sometimes Tripotassium dicitratobismuthate may be taken (bismuth chelate).
Complication for peptic ulcer disease
Perforation
Haemorrhage
Malignancy
Anaemia
Penetration of adjacent organs
What is Jaundice and what is the normal levels in micromol
Jaundice describes the yellow pigmentation of the skin, sclera, and mucous membrane resulting from raised plasma bilirubin.
Normal levels are below 21micromol
Normal bilirubin metabolism
Haem→ biliverdin (by haem oxygenase) →Unconj. Bilirubin (by Biliverdin reductase) → Conjugated bilirubin (by glucoronyl- transferase 1)
Urobilin→ urine colour
Stercobilin→ faces colour
Physiology and causes of Pre-hepatic causes of jaundice
Physiology: haem degraded in macrophages, occurs in spleen and liver mainly but can occur in skin and kidneys too. once broken down it is released bound to plasma albumin and transported to the liver to be conjugated and excreted. Unconjugated is water insoluble
Causes:
- Overproduction- Haemolytic anaemia
- Reduced uptake- Gilberts syndrome
- Conjugation defects:
- acquired - neonatal, maternal milk, Wilsons disease
- Inherited- Crigler-Najjar syndrome
- Drugs
Physiology and causes of intra-hepatic causes of jaundice
Physiology: in the liver unconjugated bilirubin is removed from the blood by hepatocytes. it is then conjugated in the hepatocytes with glucuronic acid, and it became soluble to be excreted in bile.
Causes:
- Biliary obstruction
- Intrahepatic cholestasis:
- primary biliary cholangitis
- viral hepatitis
- Hepatocellular injury - Acute or Chronic
Physiology and causes of post-hepatic causes of jaundice
Physiology: conjugated bilirubin is transported through the liver and cystic ducts in bile and stored in the gallbladder or passes into the duodenum. In the intestine, some is excreted in the stool and the rest is metabolised by gut flora into urobilinogen and reabsorbed and excreted by the kidney.
Causes:
- Gallstones
- Surgical strictures
- Extra-hepatic malignancy
- Pancreatitis
- Parasitic infection
RF for jaundice
Alcohol misuse
Factors that increased risk of hepatitis
Travel to high-risk areas
High BMI
Metabolic syndrome
IBD
Pregnancy
FHx
SS for Jaundice
Fever
Abdominal pain
change in skin colour
Dark coloured urine or clay coloured stool
Ix for jaundice
FBC
U+E
LFTs
Clotting screen
Hep a,b,c
Urine dipstick
Complication for jaundice
Most are admitted or referred as it can be indicative of an underlying cause
Whts is acute pancreatitis
Acute pancreatitis refers to inflammation of the pancreas.
The inflammation is believed to occur due to atypical premature activation of pancreatic enzymes inside the pancreas.
Pancreatitis can range from mild to life-threatening
Pathophysiology of acute pancreatitis
- There are a wide variety of causes, with gallstones and alcohol being the two most common.
Theinflammationin acute pancreatitis is typically caused by hypersecretion or backflow (due to obstruction) of exocrine digestive enzymes, which results inautodigestionof the pancreas.
Pancreatic damage can be classified into two major categories:
- Interstitial oedematous pancreatitis: most common, better prognosis
- Necrotising pancreatitis: less common, around 5-10%, more severe
The damage that occurs during acute pancreatitis ispotentially reversible(to varying degrees), whereaschronic pancreatitisinvolves ongoing inflammation of the pancreas that results inirreversible damage.
Chronic pancreatitis is associated withendocrine and exocrine dysfunction, as well as chronic abdominal pain.
Causes of acute pancreatitis
IGETSMASHED
Idiopathic
Gallstones
Ethanol(alcohol)
Trauma
Steroids
Malignancy/mumps
Autoimmune
Scorpion venom
Hypercalcemia or hyperlipidaemia
ERCP examination
Drugs
RF for acute pancreatitis
- Male gender
- Increasing age
- Obesity
- Smoking
- Alcohol
SS of acute pancreatitis
- Abdominal pain which radiates to the back and may be relieved by sitting forward.
- Systemically unwell in a hypovolemic state, and may be pyrexial
- Specific signs to look out for on examination are;
- Cullen’s sign (periumbilical bruising)
- Grey Turner’s sign (Bruising on flanks)
- Nausea and vomiting
- decreased appetite
Ix for acute pancreatitis and one clinical tool
abdo CT scan
MRCP
clinical tool- Glasgow score
Diagnosis of acute pancreatitis
requires 2 of the following:
- Typical history
- Raised serum amylase or lipase more than 3 ULN
- Imaging
Classification of acute pancreatitis
- Mild:most common, no organ dysfunction/complications, resolves normally within a week
- Moderate:initially some evidence of organ failure which improves within 48 hours
- Severe:persistent organ dysfunction for greater than 48 hours, together with local or systemic complications
Immediate management for acute pancreatitis
- IV fluid resus and correction of electrolyte disturbances
- Analgesia
- Anti-emetics
- Nil by mouth
- Control of blood glucose
management for gallstone induced acute pancreatitis
- Endoscopic retrograde cholangiopancreatography (ERCP)
- Cholecystectomy
Management for alcohol induced pancreatitis
- Benzodiazepines to treat withdrawal agitation and seizures
- Thiamine, folate, and vitamin B12 replacement
Early complication for acute pancreatitis
- Necrotising pancreatitis
- Infected pancreatic necrosis occurs when necrosing pancreatic tissue becomes infected, patients require antibiotics and necrosectomy
- Pancreatic abscess: occurs when peripancreatic collections of fluid become infected, urgent drainage is required
- Acute respiratory distress syndrome (ARDS): associated with the SIRS response of acute pancreatitis. Typical CXR appearance of widespread bilateral pulmonary infiltrates
Late complication for acute pancreatitis
- Pancreatic pseudocysts: collections of fluid that are not surrounded by epithelium. They are typically amylase-rich and can become infected, rupture or bleed. Pseudocysts typically accumulate within four weeks after acute pancreatitis. Only 40% resolve spontaneously, therefore intervention is usually advised (drainage/excision).
- Portal vein/splenic thrombosis: secondary to ongoing inflammation, anticoagulation required
- Chronic pancreatitis:repeated attacks of acute pancreatitis can lead to ongoing inflammation and fibrosis of the pancreas
- Pancreatic insufficiency: the exocrine function of the pancreas is more commonly affected (whilst the endocrine function is typically maintained).
Pathophysiology of chronic pancreatitis
- Chronic pancreatitis has numerous causes namely alcoholism, trauma, congenital (cystic fibrosis), drugs (Steroids, azathioprine), idiopathic, genetics and chronic obstruction secondary to numerous causes.
- All these numerous causes result in pancreatic fibrosis
RF for chronic pancreatitis
- Alcohol intake is the main cause of chronic pancreatitis
- Smoking
- Hypercalcaemia
- Hypertriglyceridaemia
- Autoimmune disease
- Medications (Thiazide diuretics, tetracyclines, oestrogens)
SS for chronic pancreatitis
- Abdominal pain (usually dull, epigastric pain, which may radiate to the back, or localise to RUQ).
- The pain may be relieved by sitting upright and leaning forward
- Pain is made worse by eating, may be chronic or intermittent
- Other symptoms may include: nausea, vomiting, decreased appetite, weight loss, offensive stools/diarrhoea
- Abdominal tenderness (around epigastrium) & guarding
- Abdominal distension
- Signs of malnutrition (assess the BMI)
- Jaundice
- Signs of chronic liver disease
Ix for chronic pancreatitis
Bloods
- FBC/LFT/RFT/Lipase/Amylase/HBA1c/Triglycerides/Calcium
Orifice Test
- PR exam might show slimy faecal matter
X-ray/Imaging
- CT/magnetic resonance cholangiopancreatography
Special Tests
- faecal elastase if malabsorption. Biopsy.
Management for acute pancreatitis
Conservative management
- Reduce alcohol consumption
- Offer smoking cessation
Medical management
- Treat any hypercalcaemia
- Pain management. Opioids typically used
- Malabsorption can be managed with pancreatic enzymes like Creon.
Surgical management
- Utilised if medical management is not effective.
- This may involve ERCP, pancreatic resection
Complication for Chronic pancreatitis
- Diabetes
- Pseudocyst
Pathophysiology of pancreatic cancer
poorly understood
95% mutation in K-RAS2 proto-oncogene, the activation ofwhich leads to increased cell proliferation,loss of the normal response to apoptotic signals, dysplasia and ultimately cancer
RF for pancreatic cancer
- Smoking
- Family history
- Chronic pancreatitis
- Diet (High BMI, red meat)
- Age (above 60s, very rare below 40)
- Diabetes
SS for pancreatic cancer
- Non specific symptoms like epigastric/back pain. Painless progressive jaundice
- Itching
- Dark urine/pale or fatty stools
- Weight loss/reduced appetite
- Abdominal swelling
- Nausea and vomiting if stomach compressed
- Haematemesis
- Ascites
- Lymphadenopathy (virchow’s node)
- Epigastric mass
- Jaundice
Ix Pancreatic cancer
Bloods
- FBC (might show normocytic anaemia or thrombocytopenia), LFTS (raised liver markers), Tumour markers like CA19-9 (good for baseline and follow up but of little diagnostic value), Glucose (hyperglycaemia in the absence of previous diabetes history)
X-ray/Imaging
- Ultrasound abdomen (May show dilated bile duct, lymph nodes but limited by bowel gas). Abdominal CT is the investigation of choice
Management for pancreatic cancer
- Tissue biopsy is important for prognosis and suitability for radiotherapy/chemotherapy. It is also used to determine the histology of pancreatic neoplasm
- Staging is ranked from stage 0 to 4. The TNM staging (Tumour, Node, Metastasis) also used.
- Management includes surgery and chemotherapy/radiotherapy
- Only 10-20% of tumours are resectable. Distal pancreatectomy is used for cancers of the body and tail of the pancreas. Whipple’s procedure is used for proximal pancreatic cancers, this procedure preserves the stomach, pylorus and 4cm of the duodenum.
- About 80% of pancreatic cancers are non resectable. Management plans for the non resectable cancers include stenting of the bile duct to relieve obstruction and palliative radiotherapy/chemotherapy.
- Where pain control is difficult patients should be referred to the palliative team
- Malabsorption can be managed with pancreatic supplements e.g Creon
Complication for pancreatic cancer
- Obstructive jaundice
- Refractory pain
What is cholelithiasis
AKA gallstones
3 types of gallstones:
- Cholesterol
- Mixed
- Pigment stones
Pathophysiology of cholelithiasis
The stones form from concentrated bile in the bile duct, and most are made of cholesterol.
Begins with the secretion of bile, supersaturated with cholesterol from the liver.
Imbalance of cholesterol, phospholipid and bile salt→ precipitation of cholesterol microcrystals → aggregation of microcrystal →formation of cholesterol gallstones
the 4 F’s for RF for cholelithiasis
Fat
Fair
Female
Forty
examples of medication that can cause cholelithiasis
Medication (octreotide, GLP1 analogues, ceftriaxone)
SS of cholelithiasis
majority is asymptomatic
Biliary colic→ intermittent right upper quadrant pain caused by gallstones irritating bile ducts
Pain triggered by meal and last between 30 min -8 hours, may radiate to right shoulder tip.
Vomiting/ Nausea
symptoms can manifest as other complication
LFTS are normal
Ix for cholelithiasis
Stones in gallbladder or cystic duct → unlikely to show abnormal results
stones in common bile duct→ accounts for symptoms and abnormal lab results.
LFTS→ increased bilirubin, ALP and ALT
Ultrasound→ Gold standard
Management of cholelithiasis
1st line, GP, ED and inpatient management
- 1st line → Analgesia:
- intermittent mild- moderate pain → paracetamol or NSAID e.g., diclofenac
- Severe pain - Diclofenac or an opioid
- In GP→ request abdo ultrasound
- In ED→ if pain controlled by analgesia and normal bloods and obs then send home
- Inpatient→ refer to Gen surg
Complications for cholelithiasis
acute cholecystitis
acute cholangitis
pancreatitis
What is acute cholecystitis
Acute inflammation of the gallbladder
Major complication of gallstones
Pathophysiology of acute cholecystitis
impacted gallstones causes complete obstruction of the cystic duct
leads to inflammation within gallbladder wall
RF acute cholecystitis
Gallstones
ss acute cholecystitis
Nausea
Vomiting
Contant RUQ pain lasting more than 8 hrs
Palpable gallbladder
Fever
Raised inflammatory marker WCC+CRP)
Murphys signs
Ix acute cholecystitis
Abdominal ultrasound- gold standard
CT
Management acute cholecystitis
Analgesia
Nil by mouth
IV fluid
Antibiotics
In GP → send patient to ED if suspicions of acute cholecystitis
In secondary care → Referral to General Surgeons for consideration of “Hot Lap Chole”
If not for hot lap chole →routine elective surgery after 6 weeks
Complication for acute cholecystitis
- Sepsis
- Gallbladder empyema
- Gangrenous gallbladder
- Perforation
Chronic cholecystitis
- May occur after one or more episodes of acute cholecystitis.
- Results from chronic irritation or repeated episodes of acute inflammation leading to fibrosis of the gallbladder wall.
- Can initially be asymptomatic and occur from the presence of gallstones in the gallbladder
- Patients may present abdominal pain similar to biliary colic or constant abdominal pain similar to that of acute cholecystitis but less severe and self-limiting
- Gallbladder wall thickening and the presence of gallstones will be seen on imaging.
- Unlike acute cholecystitis – no pericholecystic fluid, no gallbladder distention on imaging.
What is choledocholithiasis
The presence of gallstones migrated from the gallbladder within the bile ducts
SS for choledocholithiasis
Nausea
vomiting
Constant RUQ pain
Pale stools
Dark urine
Afebrile
Bloods→ Inflammatory markers normal in simple choledocholithiasis
- Raised bilirubin/LFTs = OBSTRUCTIVE JAUNDICE
Gold standard Ix for choledocholithiasis
MRCP
Management for choledocholithiasis
Analgesia
Prophylactic Abx
ERCP
What is cholangitis
Acute bacterial infection of the biliary tree in the setting of bile stasis
Predominantly Gram-negative enteric bacteria, most commonly E.coli
HIGH MORTALITY
RF for cholangitis
- age >50 years
- cholelithiasis
- benign stricture
- malignant stricture
SS for cholangitis
Nausea, vomiting
Charcot’s Triad:
- Jaundice, Fever, RUQ pain
pale stool
confusion
dark urine
Ix for cholangitis
Bloods → raised inflammatory marker and deranged LFT
Gold standard→ MRCP
Mangement for cholangitis
ERCP as URGENT to remove the obstruction
Supportive treatment
IV antibiotics, IVF, analgesia, low threshold to refer to ITU for organ support
Complications for cholangitis
Hepatic abscess, portal venous thrombosis
What is meant by acute liver failure
- sudden onset of liver dysfunction
- Absence of prior liver disease
- Resulting in encephalopathy (brain dysfunction) within 8 weeks of onset
Cause and pathophysiology of acute liver disease
causes:
- common→ Paracetamol
- Non paracetamol: e.g. preg, viral, malignancy
Liver injury → liver cell death → loss of critical hepatocyte mass → Failure of liver to perform functions → Multiorgan dysfunction
RF for acute liver disease
- Hepatotoxic drugs
- Contaminated food/water (enteric viruses – Hep A and E)
- Blood borne virus risks (Hep B)
- Unprotected sex
- Tattoos/piercing with unclean equipment
- Recreational drug use – shared paraphernalia
- Recreational drugs – mushrooms, ecstasy
- Threshold for liver injury reduced if underlying liver disease
SS for acute liver failure
- Right upper quadrant pain
- Nausea/Vomiting
- A general sense of feeling unwell (malaise)
- Sweet smelling/musty breath (fetor)
- Disorientation, confusion, agitation, sleepiness, flapping tremor (features of encephalopathy)
Ix for acute liver failure
- liver function tests
- prothrombin time/INR
- basic metabolic panel
- FBC
Management for acute liver failure
REsus
NAC
Empirical antibiotic
Complication for acute liver failure
coagulopathy
Infection
renal failure
Paracetamol metabolism
see notes
RF for paracetamol overdose
- High doses
- chronic alcohol consumption
- Drugs→ anti-seizure, opioids
- Advanced age
- Malnutrition
- Chronic liver disease
What is Acute hepatitis
- Acute inflammation of the liver, of any cause, causing sudden increase in liver tests
- Usually manifests as an increase in aminotransferases (ALT and AST)
- Intracellular enzymes
- Released in the setting of liver inflammation causing disruption/death of hepatocytes
- Could be interchangeably referred to as acute liver injury
- In some cases, if ongoing hepatocyte necrosis and loss of critical liver cell mass, can lead to acute liver failure
Some examples of drugs that cause acute hepatitis
-Paracetamol
- NSAIDS
- Amiodarone
- Anabolic steroids
- Chlorpromazine
- statins
other causes of acute hepatitis
- Viral
- (Drugs)
- Autoimmune
- Genetic/inherited
- (Alcohol)
- Ischaemic
- (Pregnancy)
- Malignancy
Ix for acute hepatitis
- FBC, U&E, LFT, GGT, blood clotting, glucose
- ABG
- Blood cultures
- Arterial blood gases
- Blood cultures
- ultrasound
- ct
- biopsy
Difference between acute and chronic hepatitis
see notes
What is Cirrhosis
Chronic liver disease is continual destruction of the liver parenchyma and its gradual substitution with fibrous tissue. It is a long-term process (>6 months)
This process ultimately leads to liver cirrhosis
Cirrhosis → Irreversible distortion of liver architecture by scar tissue and nodule formation
This affects the liver’s synthetic, metabolic and excretory actions
Causes of cirrhosis
- Commonest cause worldwide = chronic viral hepatitis B and C
- Commonest causes in Western world
- Alcohol, chronic viral hepatitis B and C, MAFLD
Compensated vs decompensated
- Compensated— when the liver can still function effectivelyand there are no, or few, noticeable clinical symptoms
- Decompensated— when the liver is damaged to the point that it cannot function adequately, andovert clinicalcomplications(such as jaundice, ascites, variceal haemorrhage, and hepatic encephalopathy) are present. Events causing decompensation include infection, portal vein thrombosis, and surgery.**
RF for cirrhosis
alcohol misuse
HEP b and c infection
Obesity
type 2 diabetes
autoimmune liver disease
SS for cirrhosis
- suspect in high-risk groups if they have malaise, fatigue, anorexia, nausea, weight loss, muscle wasting or Abdo pain
- hepatomegaly
- chronic liver disease→ spider naevi, palmar erythema, white nails, muscle wasting.
- signs of decomp liver disease →jaundice, abnormal bruising, peripheral oedema, ascites, sepsis, variceal bleeding, encephalopathy
Ix for Cirrhosis
FBC → Low platelet count
LFT → high AST to ALT ratio, high bilirubin, low albumin, increase prothrombin time and INR
transient elastography
Management for Cirrhosis
REFER
Lifestyle changes
Alcohol cessation
Complications for Cirrhosis
Portal HTN
Ascites
Hepatic encephalopathy
Haemorrhage from oesophageal varices
infection
Some withdrawal symptoms of alcohol
- Tremors
- Sweating
- Fever
- Nausea, vomiting
- Anxiety
- Agitation
- Anorexia
- Insomnia
Management for alcohol related liver disease and withdrawal
Benzodiazepines
Whts is oesophagitis
Inflammation of the oesophagus
Causes of oesophagitis
- GORD
- Medications- NSAIDS, bisphosphonates, tetracycline antibiotics)
- immune mediated- eosinophilic oesophagitis
RF for oesophagitis
Eating just before bed
Excessive alcohol, caffeine, chocolate
Greasy or spicy food
Cigarette smoking
Obesity
Hiatus hernia
Certain medications
SS of oesophagitis
Epigastric or chest pain
Burning (“hearburn”)
Acidic/sour taste
Dysphagia
Odynophagia
Hoarseness
Persistent cough
Epigastric abdominal tenderness to
palpation
Ix for oesophagitis
Oesophagogastric duodenoscopy (OGD) with oesophageal biopsies
Management for reflux oesophagitis
- Avoid greasy/spicy foods, citrus, chocolate, peppermint, caffeine, alcohol
- Smoking cessation
- Weight loss
- PPI
Management for eosinophilic oesophagitis
- Refer to allergist
- Avoidance of food allergies
- Daily PPI
- Topical steroids
- Fluticasone MDI without spacer
- Sprayed into patient’s mouth, then swallowed
- Fluticasone MDI without spacer
Management for drug induced eosophagitis
- Discontinue offending medication, if possible
- Offer alternative
- Remain upright 30 minutes after consuming
- Liquid version
Complications of oesophagitis
Strictures
Barrett’s oesophagus
- Abnormal cellular changes of oesophagus
- ~1% progress to oesophageal cancer
Oesophageal cancer
What is anal fissure and what are the 2 classifications
Tear or ulcer in lining of anal canal
Classification:
- acute - less than 6 weeks
- Chronic- more than 6 weeks
RF for primary anal fissure
Trauma secondary to hard or loose stools
RF for secondary anal fissure
- IBD
- STIs (HIV, syphilis, HSV)
- Colorectal cancer
- Psoriasis
- Bacterial, fungal, viral skin infections
- Anal trauma (previous anal surgery or anal sex)
- Pregnancy, childbirth
SS for anal fissure
Anal pain on defecation
Tearing sensation on passing stool
Bright red blood on stool or toilet paper
Fissure visible on anal exam
Sentinel pile
Examination finding on acute anal fissure
Superficial with well-demarcated edges
Examination finding on chronic anal fissure
- Wider and deeper with muscle fibres visible in the base
- Edges often swollen
- +/- skin tag
Examination finding on primary anal fissure
- Singular
- Posterior midline of anus
Examination finding on secondary anal fissure
- Multiple
- Irregular outline
- Location may be lateral
Management for Anal fissure
Ensure stool is soft
Treat constipation (if indicated)
Increased fluid intake and dietary fibre
Keep anal area dry and clean
Manage pain (Paracetamol or ibuprofen)
Sitz bath
lidocaine -apply prior to defecation
if symptoms persist for more than week then rectal GTN ointments and consider secondary causes
Complications of anal fissure
Anorectal fistula
Infection / abscess
What is anorectal abscess
Infection of soft tissue around the anus or rectum
May cause sepsis
RF for anorectal abscess
Immunodeficiency
Diabetes
Receptive anal intercourse
Crohn’s disease
SS for anorectal abscess
perianal pain
erythema
discharge
fever
bleeding
Malaise
Swelling
Perianal fluctuance
Purulent discharge
Ix for anorectal abscess
Clinical diagnosis by digital rectal exam and other signs
Ultrasound, MRI
Culture and sensitivity of discharge
Management for anorectal abscess
Prompt drainage of abscess
perianal - outpatient incision & drainage
Perirectal - surgical drainage
Sitz bath
Antibiotic (cover anaerobes and gram neg)
Ampicillin/sulbactam or cefoxitin + metronidazole or ciprofloxacin or clindamycin
What are colorectal polyps
Projections arising from colonic mucosal surface
(Most commonly adenomatous polyps)
What genetic condition predispose someone to colorectal polyps
Familial adenomatous polyposis (FAP) syndrome
Autosomal dominant
- Hundreds to thousands of colorectal adenomas
- Near100% risk for colorectal cancer by age 4
4 types of colorectal polyps
Tubular
Serrated
Tubulovillous
Villous
SS for colorectal polyps
Usually asymptomatic
Rectal bleeding
Frank red blood, melaena
Mucus discharge
Tenesmus
Post-defecation sensation that rectum was incompletely evacuated
Change in bowel habits
Diagnosis for colorectal polyps
May be found incidentally on colonoscopy
Colonoscopy with biopsy/excision of polyp
Ordered if concern for colorectal cancer
- Iron deficiency anaemia in persons age ≥60, positive faecal occult blood test, change in bowel habit etc
What is the management for adenomatous polyps
Removed endoscopically
Surveillance - colonoscopy frequency dependent upon number/size of polyps, family history, patient age
What is the management for hyperplastic/ metaplastic polyps
No action required
management for familial adenomatous polyposis syndrome
colectomy
RF for colorectal cancer
Increasing age
Genetics
FHx
Inflammatory bowel disease
Obesity
alcohol
SS for colorectal cancer
Increase freq and looser stools (change in bowel habits)
bleeding
distension
pain
weight loss
appetite loss
unexplained fever
conjunctival pallor palpable lymp nodes
When to give urgent 2 ww referral (4 pts , colerectal cancer)
- Positive faecal occult blood test
- Age ≥40 with unexplained weight loss and abdominal pain
- Age ≥50 with unexplained rectal bleeding
- Age ≥60 with:
- Iron-deficiency anaemia or
- Change in bowel habit
Ix for colorectal cancer
colonoscopy with biopsies
Management for colorectal cancer
Surgical resection
Chemoradiotherapy
Chemotherapy
What is coeliac disease
Chronic, autoimmune systemic disorder triggered by gluten exposure
Pathophysiology of coeliac disease
Genetic predisposition (human leukocyte antigen (HLA) alleles found)
Gluten presence triggers immune activation within small bowel epithelium → Deveolpment of coeliac-specific autoantibodies + intraepithelial lymphocytosis →villous atrophy →small bowel enteropathy with systemic symptoms
SS for coeliac disease
Diarrhoea
steatorrhea
Constipation
Weight loss
Heartburn
pain
Bloating
Flatulence
Fatigue
Rash
Tenderness
dermatitis herpetiformis
Diagnosis for coeliac disease
Serum IgA tissue transglutaminase antibody (tTGA) and serum total IgA
Endoscopy intestinal biopsy (confirms diagnosis and only done if indicated by positive serology)
Coeliac disease management
Gluten-free diet
supplement for any nutritional deficiency
annual FBC monitoring
Complication for coeliac disease
reduced qualy
depression and anxiety
delayed puberty
Nutrional deficiency
Hypersplenism
