Gastro-Intestinal Diseases Flashcards
Definition of dysphagia
Difficulty swallowing
Definition of heartburn
Retrosternal burning, common symptom of acid reflux
Definition of dyspepsia
Range of symptoms referring to upper GI tract including nausea, heartburn, acidity and pain
Definition of flatulence
Passing excess wind (belching, abdominal distention or passing of flatus per rectum)
Definition of vomiting
Stimulation of vomiting centres in lateral reticular formation of medulla. Either from stimulation of chemoreceptor trigger zones in the floor of the 4th ventricle or vagal afferents from the gut.
Nausea and vomiting with pain indicative of
GI origin
Nausea and vomiting without pain indicative of and examples
non-GI origin. Eg, CNS disease (raised intracranial pressures), drugs (chemo) or metabolic agents (uraemia, diabetic ketoacidosis)
Definition of constipation
Mean infrequent passage of stools (<2 per week) or difficulty passage of hard stool
Definition of diarrhea
Increased amounts of loose stool (>250g/day)
Definition of steatorrhoea and cause
Increased passage of pale, bulky stools that contain fat. Indicative of fat malabsorption as a result of small bowel, pancreatic or biliary disease.
Valve between distal end of oesophagus and stomach. How this valve opens/closes. Failure of this valve to open and outcome
Cardiac sphincter. Normally closed. Opens shortly after swallowing. After propelling bolus through peristalsis, the wave shuts it and prevents reflex. Failure of cardiac sphincter to open is known as achalasia. Leads to an accumulation of food in the oesophagus.
4 secretions of the stomach
Gastrin, gastric juice, bile and intrinsic factor
What is absorbed in the stomach
Water, alcohol and aspirin
Relationship of gastrin and gastric juice. Sequence of events after secretion.
Gastrin released from gastric antrum (in response to presence of food) and from duodenum (in response to presence of chyme). Gastrin stimulates secretion of gastric juice.
Increased gastrin leads to increased gastric juice leads to increased pepsin, increased gastric motility, enhancing growth of gastric and duodenal mucosa
What causes stimulation of mucous
Mucosal irritation (mechanical or chemical)
Acid in lumen of stomach
Vagal and sympathetic stimulation
Importance of intrinsic factor
Aids absorption of vitamin B12 from distal ileum
What does gastric motility cause
Mixes stomach contents with gastric juice
Converts to semi-liquid chyme
Propels contents through the stomach and into duodenum
Bile produced, stored and secreted?
Produced in liver, stored and concentrated in gall bladder and released into duodenum
Where does the oesophagus enter the diaphragm
Right and left crus
Common symptoms of problems with the oesophagus
Cough/vomiting (if foods/liquids do not pass normally to the stomach, causing them to reflux back to the pharynx), pain (maybe from acid reflux or spasm) and dysphagia. Sometimes vomiting blood which is known as haematemesis.
Common diseases associated with the oesophagus
Achalasia pharyngeal pouches oesophageal web carcinoma of the oesophagus Peptic ulcer disease/reflux Oesophageal spasm
Anatomy of the pharynx
3 overlapping constrictor muscles: superior, middle and inferior
Inferior constrictors include cricopharyngeus and thyropharyngeus
Name and cause of potential weakness in the oesophagus. Clinical significance
Meeting point of the 2 parts of the inferior constrictor muscles (thyropharyngeus and cricopharyngeus). Called Killian’s dehiscence. Thyropharyngeus pushes food forwards towards stomach (propulsive) but cricopharyngeus acts like a sphicter (constricts normally but then relaxes). If cricopharyngeus fails to relax, a posterior mucosal herniation may occur via Killian’s dehiscence known as Zeneker’s diverticulum or pharyngeal pouch.
Muscles of the oesophagus
Nervous supply
Lining mucosa
Musculo-tendenous tube connecting pharynx to the stomach
Outer longitudinal muscle with an inner circular coat. Upper 1/3 of the oesophagus is striated
Middle 1/3 is mixed
Lower 1/3 is smooth muscle
Motor and sensory from Vagus nerve
Nerve plexi between outer longitudunal and inner circular muscle planes
Lining mucosa= stratified squamous non keratinising
Process of moving food from mouth to oesophagus and explanation
Initial phase of swallow is voluntary
Triggers peristaltic wave
Pushes food bolus to stomach
Stretching gut causes depolarization and propagates creating a wave of muscle relaxation and contraction known as peristalsis
Cardiac sphincter at gastro-oesophageal junction is weak (not a clearly defined anatomical feature- cannot be seen)
Differential diagnosis for pain in the oesophagus
Often poorly localised so can be confused with mediastinal structures (eg the heart)
Causes of dysphagia and examples
Intrinsic Lesion (foreign body, benign/malignant structure, oesophageal web or pharyngeal pouch) Neuromuscular Disorder (Stroke, Bulbar palsy) Motility Disorders (Achalasia, diabetes, scleroderma) Extrinsic lesion compressing the oesophagus (lymphadenopathy, tumours in the neck and mediastinum)
Pharyngeal Pouch definition and clinical features
Herniation of mucosa around Killian’s dehiscence. Pouch hangs down due to gravity and may appear as a swelling in lower neck, usually left sided.
Dysphagia
Undigested food may get regurtitated into mouth
Overflow into lungs may cause respiratory problems
Can go septic, toxic or regurgitate straight into the larynx
Fungal infection of oesophagus? Possible reason?
Candida oesophagitis. Immunocompromised, transplant patients, HIV infection, chemotherapy
Aetiology and pathophysiology of Achalasia
Unknown aetiology but
Loss of ganglia from the intramural plexus leading to failure of relaxation of the smooth muscle of the gastro-oesophageal sphincter
Functional obstruction to oesophageal emptying
Failure of peristalsis leads to progressive dilatation of the oesophagus
Clinical Features of achalasia
Dysphagia
Weight loss if late-stage disease
Retrosternal chest pain
Non-peristaltic contractions may occur
Regurgitation of undigested solids during or shortly after a meal
Respiratory problems sometimes as food or fluid is aspirated into the lungs
Investigations (and explanation of investigations) and Treatment for achalasia
Barium swallow with fluoroscopy and manometry
Fluoroscopy- continuous X ray image like an x ray movie
Manometry- catheter with pressure sensors placed through oesophagus into stomach to measure rhythmic muscle contractions that occur when you swallow
Calcium channel blockers to relax the sphincter (eg, nifedipine, amlodipine) Balloon dilatation (endoscope with a balloon at the end that dilates to open up cardiac sphincter) Cardiomyotomy (muscles of cardiac sphincter cut, allowing food and liquid to pass through to the stomach) Botulinum toxin injections (promote dilation of oesophagus)
Definition and aetiology of oesophageal spasm
Descriptive term for spasm due to a variety of causes
Attacks of dysphagia and pain
Causes include: Atypical achalasia Gastro-oesophageal reflux Motor disorders Symptomatic peristalsis Obstruction at the cardia Neuromuscular disorder
Distinguishing between oesophageal spasm and achalasia
Diagnosed by radiological appearance after a barium swallow or oesophageal manometry
Oesophageal spasm can lead to a corkscrew oesophagus appearance
Pain resembles reflux and heartburn
Regurgitation of meals from less time ago in oesophageal spasms as oesophagus can hold a lot less volume compared to achalasia
In what kind of patients is oesophageal web common, and why is it important despite being rare
Chronic anaemics, middle aged women
Premalignant
Clinical features of oesophageal web
Glossitis
Iron deficiency anaemia
Dysphagia
Koilonychia
How an oesophageal web forms and investigation(s)
Mucosa becomes atrophic (tired and wasted)
Fibrous structure forms at the upper end of the oesophagus
Forms a web, visible on barium swallow
Treatment of oesophageal web
Dilatation of the stricture and correction of the iron deficiency. Understand why pt is anaemic
Monitor for recurrence and malignant transformation
Aetiology of GORD
Multifactoral
Caused by:
Malfunctioning lower oesophageal sphincter (cardiac sphincter) with defective relaxation of the sphincter
Abnormal motility of the lower oesophageal body, resulting in deficient of intermittent inefficiency of peristalsis
Clinical features of GORD
symptoms after a meal reflux most commonly heart burn regurgitation nausea bloating
Investigations and tx of GORD
Endoscopy and barium swallow but both may appear normal in GORD
Protein pump inhibitors eg omeprazole
H2 antagonists eg ranitidine
Antacids to control predisposing factors
Relationship of GORD and peptic ulcer disease
GORD increases chances of peptic ulcer disease
H. Pylori infection not related to pathogenesis of GORD
Peptic Ulcer Disease definition and promoting factors (why these factors increase risk of peptic ulcer disease)
Failure of the cardiac sphincter
Leads to acid reflux in oesophagus
Decreased mucosal protection coat:
Smoking (decreased vasculation and mucosal impairment)
NSAIDs and Aspirin (block cyclooxygenase and prostaglandin production, impairing mucosal production)
Steriods (same)
H.pylori infection (colonises mucous)
Peptic v gastric ulcers
Peptic ulcers can affect oesophagus, stomach or duodenum (anywhere the acid can get to)
Gastric ulcers is in the stomach only
Clinical features of PUD
Pain Vomitting Haematemesis- blood with vomiting Ulcers with scarring Spasm
Likely sites for ulcers to appear in the upper GI tract
Lower oesophagus, lesser curve of stomach, first part of the duodenum
Investigtions and treatment of PUD
Barium meal and endoscopy
Endoscopy most reliable. Cells taken for biopsy and culture
Proton pump inhibitors eg omeprazole
H2 antagonists eg ranitidine
Control predisposing factors using antacids
Treatment of H.pylori infection
Surgery includes inspection/ligation of bleeding vessels, transfusion and repair but surgical tx declined recently
Tx for H.Pylori infection
Quadruple therapy
Proton pump inhibor eg omeprazole
Bismuth-based (pepto-bismol)
2 antibiotics (amoxicillin and clarithromycin)
How can peptic ulcer disease cause acute upper GI bleeding
PUD either leads to scarring (may lead to stricture or obstruction) or
Healing (local scarring healed by secondary intent)
If it spreads through the gut wall, perforation and bleeds
Complications of cardiac sphincter failure
Barett’s oesophagus, GORD, Achalasia, PUD
Barett’s oesophagus definition and importance
Acid from stomach changes oesophageal lining due to failure of the cardiac sphincter
Pre-malignant
Hiatus Hernia definition and clinical features
Upper part of stomach moves into the chest through a hole (hiatus) in the diaphragm
Burning pain which occurs after meals and on lying down
Reflux of fluid, foul taste of waking
Bloating, frequent belching and dysphagia
Investigations and tx of hiatus hernia
Barium swallow and possible endoscopy
Large meals avoided No food 2-3 hours before bed Bending avoided Lose weight Antacids, H2 antagonists and protein pump inhibitors
Risk factors for carcinoma of the oesophagus
Male Barrett's oesophagus Iron Deficiency (oesophageal web) Achalasia of cardia Pharyngeal pouch Smoking (5 times risk) Heavy alcohol use (20 times risk) Coeliac disease (malabsorption)
Clinical features ??
End stage dysphagia
Pain
Haematemesis
Weight loss, malaise, anorexia
Types of oesophageal cancer
Majority squamous cell carcinoma (upper two-thirds of the oesophagus)
Lower 1/3 of oesophagus may be adenocarcinoma (due to ectopic gastric mucosa)
Where is a tumour in the oesophagus likely to spread
Fungate into lumen
Infiltrate adjacent structures in the mediastinum
Lymph nodes
Liver
Investigations of carcinoma of the oesophagus
Endoscopy, biopsy and barium swallow to establish diagnosis
CXR, ultrasound and CT scan used to stage tumour
Difference in mucosa throughout the oesophagus
Upper 2/3s stratified squamous non keratinizing epithelium
lower 1/3 can be ectopic gastric columnar `
Treatment for oesophageal carcinoma
Survival limited
Curing requires surgery, which requires copious tissue removal (tumour +5cm around it)
Palliate is to make it less severe without curing (radiotherapy and surgery)
Stent can be used to force the oesophagus open, accepting the tumour around it
Dilatation endoscopy
Dental relevance of peptic ulcer disease and oesophageal reflux
Avoid NSAIDs
Steroidal complications
Blood loss may result in iron deficiency anaemia with consequent sore mouth
Oral features are sore mouth, glossitis and angular cheilitis
Dysphagia may present problems with GA
Dental relevance of oesophageal cancer
If pt presents with dysphagia, take a careful history of it
Examination of neck may reveal cervical lymphadenopathy
Acute v chronic duodenal ulcer in terms of structure
Acute ulcers just penetrate the submucosa
Chronic ulcers go deep into the muscular coat so are harder to cure
Clinical significance of pyloric stenosis
Caused by stenosis of the pyloric sphincter
Paediatric projectile vomiting. Cycle of eat, full, throw up and cry cos im hungry
List the substructures of the bowel (small intestine) and colon (large intestines) in order
Duodenum
Jejunum
Ileum
Cecum
Sigmoid
Rectum
Anal Canal
Definition and aetiology of coeliac disease
chronic autoimmune-mediated disease of the small intestine caused by a sensitivity/intolerance to gluten
genetic, associated with HLAB8
Pathogenesis of coeliac
Wheat consists of endosperm proteins (white flour), which consists of albumin, globulins and gluten. Gluten contains gliadin, which is toxic to the mucosa.
Causes influx of lymphocytes in duodenal epithelium, subsequent villous atrophy and a decreased absorptive surface of the duodenum
Can lead to malabsorption
Clinical features of coeliac
May be asymptomatic and diagnosis frequently delayed
Common features include:
In children- abdominal bloating, diarrhoea, short stature, anaemia, anorexia and vomiting
In adults- glossitis, clubbing of fingers
Pts often present with a change of bowel habit. Pale, bulky offensive greasy stool
Diagnosis of coeliac
Serology- Antibodies to gliadin, endomysium and transglutinase Biopsy of small intestine to show mucosal atrophy (ranging from mild blunting to total absence of villi), infiltration of intraepithelial lymphocytes and lamina propria infiltrated with plasma cells
Treatment for coeliac
Gluten-free diet
Dental relevance of coeliac disease
- Malabsorption of ferritin (iron) leads to anaemia so pt may present with glossitis
- Malabsorption of folate, vitamin B12 may lead to angular chelitis and glossitis
- May present with other autoimmune disease such as hypothyroidism and diabetes which may lead to increased chance of oral candidasis
- Malabsorption of vitamin K may lead to increased bleeding
- Malabsorption of vitamin D may lead to increased rickets in children and osteomalacia
- Increased risk of oral carcinoma in patients with coeliac
- Dermatitis herpetiformis may occur in pts
Definition of Crohn’s Disease
Chronic inflammatory disorder that can affect any part of the GI tract from mouth to anus
Peak age of incidence from 20-60 years
Aetiology of Crohn’s
Strong family history (Genetic)
Environmental factors such as smoking and diet
Clinical features of Crohn’s
- Diarrhea
- Abdominal pain
- Decreased apetite
- Rectal bleeding
- Weight loss
- Fever
- Fistula and perianal sepsis
Pathology of Crohn’s Disease
- Patchy, discontinuous distribution of skip lesions
- Usually occurs in distal ileum and proximal caecum but can occur anywhere in the GI tract
- Apthous ulceration (recurrent round/oval ulcers inside the mouth or an area where skin is not tightly bound to bone
- Oral and mucosal involvement
- Transmural inflammation (through all mucosal layers) but predominantly submucosa
- Inflammatory infiltrate (lymphocytes, macrophages and plasma cells)
- Leads to 3 phenoypes of Crohns
3 phenotypes of Crohn’s Disease
Stricturing: gradual thickening of the intestinal wall. Leads to obstruction/stenosis
Penetrating: intestinal fistulas develop between GI tract and other organs
Non-penetrating: anal fistulas and absecces
Diagnosis of Crohn’s
Barium enema showing rose thorn, skip lesions, string sign
Signmoidoscopy and biopsy, colonoscopy
Differential Diagnosis of Crohn’s
Tuberculosis or sarcoidosis
Treatment of Crohn’s
Corticosteroids eg prednisone or budenoside
Immunomodulators
Biologics
Surgical treatment includes intestinal resection
Dental Relevance of Crohn’s
- Oral manifestations appear in children more than adules (may be the first clinical feature of systemic disease in kids)
- Still occurs in adults at least once during their life
- Precedes or coincides with intestinal disease
- Oral manifestations can be specific or non-specific
- Specific manifestations include cobblestoning, diffuse labial and buccal swellings, mucosal tags, linear ulcers, mucogingivitis and granulomatous cheilitis
- Non-specific manifestations include caries, periodontitis/gingivitis, glossitis, angular cheilitis, apthous ulcers
- Patients may be perscribed corticosteroilds for treatment
- Oral soreness so potential difficult OH
- Regular hygienist appointment necessary
- Potential malabsorption of ferritin (iron), folate and Vit B12 and subsequent oral affects
Orofacial Granulomatosis definition, relationship to other inflammatory diseases, clinical features and tx
- Condition characterized by persistent enlargement of the soft tissues of the mouth, lip and area around the mouth on the face
- Mechanism of enlargement is granulomatous inflammation
- Some sort of relationship with Crohn’s
- Orofacial signs and symptoms similiar to Crohn’s
- Benzoate and cinammon-free diet effective in most
Types of inflammatory bowel disease
Ulcerative Colitis and Crohn’s Disease
Coeliac disease is autoimmune
Ulcerative Colitis definition
- Chronic inflammatory bowel disease
- Rectum always involved
- Sometimes ascends up to proximal colon (caecum) and terminal ileum
- Remit and relapse disease
Ulcerative Colitis pathogenesis
- Diffuse, continuous mucosal inflammation of the colon
- Fine ulceration but only in the mucosa
- Neutrophils, plasma cells and eosinophil cellular infiltrate
- Mucin depletion, gland destruction
Ulcerative Colitis aetiology
Unknown
- Hypothesis is that there is a dysregulated interaction between mucosal immunology and intestinal microflors
- Along with a genetic disposition (strong jewish family history)
Ulcerative Colitis clinical features
- Painless, bloody diarrhoea with mucus
- Either single mild episode or acute episodes of severe bloody diarrhoea
- Associated fever
- Remissions to near normal
- Abdominal pain
-Oral manifestations include Pyostomatitis vegetans (beinign, multiple small white and yellow pustules) that can be snail track ulcers, commonly appearing on labial attached gingiva, palate and buccal mucosa Apthous ulcers Pyoderma gangrenosum (painful nodules become ulcers that progressively grow) Gingivitis Periodontitis Halitosis Acidic taste
-Cutaneous manifestations include Erythema nodusum (Swollen fat patches under the skin) Pyodermatitis vegetans Pyoderma gangrenosum Vasculitis
Investigations and Diagnosis for UC
Colonoscopy and biopsy
-Look for exudates, ulceration, loss of vascular pattern, continuous granularity and superficial inflammation with loss of hasturation (hastura= small pouches caused by sac formation giving colon segmented appearance)
- Sigmoidoscopy appearance will depend on the disease type:
- If quiescent disrase, surface mucosa will appear granular
- In active disease, there is pus and blood and the mucosa looks red
- In an acute episode of active disease, there is pus and blood with ulceration and contact bleeding
Tx for UC
- High protein, high fibre diet
- 5-aminosalicyclic acid
- Sulphasalazine
- Corticosteroils eg prednisolone
- Mesalazine
- Thioprines
- Surgery if perforation, haemorrhage, severe complications or repeated relapse
Risks of Inflammatory Bowel Diseases
-Increased risk of colorectal cancer
Dental Relevance of UC
-Severe UC pts may need to constantly shit so appointment times may be difficult
-Oral manifestations include Pyostomatitis vegetans (beinign, multiple small white and yellow pustules) that can be snail track ulcers, commonly appearing on labial attached gingiva, palate and buccal mucosa Apthous ulcers Pyoderma gangrenosum (painful nodules become ulcers that progressively grow) Gingivitis Periodontitis Halitosis Acidic taste
- Dental hygienest due to associated perio and gingivitis
- Nutritional issues may result in glossitis
Differentiating between UC and CD
Clinical Features:
- Bloody diarrhoea common in UC but not in CD
- Painless in UC but abdominal pain/distention in CD
- Signs of malabsorption not seen in UC, but common in CD
Radiological Features:
- Rectal involvement invariable in UC but uncommon in CD
- Continuous distribution in UC but segmental and discontinuous in CD
- Fine ulceration in UC but cobblestone, rose thorn ulcers in CD
- Strictures and fistulas uncommon in UC but may occur in CD
Histological Features:
- Mucosal in UC but transmural in CD
- Neutrophils, plasma cells and eosinophils in UC but lymphocytes, plasma cells and macrophages in CD
- Mucin depletion, gland destruction and crypt destruction in UC but gland preservation in Crohn’s
Aetiology of carcinoma of the colon. Predisposing factors
Environmental factor and family history
Predisposing factors include previous cancer, neoplastic familial polyposis coli and UC fam history
Common sits for carcinoma of the colon
Rectum then Sigmoid then Caecum
Presentation/clinical features of colon cancer
Depends on the site of the carcinoma
- If left, then bleeding rectum and teresmus
- If right then anaemia, weight loss and abdominal pain
- If both then obstruction, perforation, haemorrhage or fistula
Types and definition of functional bowel disorders
Divericulum Disease:
- Condition of having multiple inflamed patches in the colon
- Herniation of the bowel mucosa through the bowel wall
- Treatment is a high fibre diet with or without surgery
Irritable Bowel Syndrome:
- No inflammation
- Intermittant diarrhoea, abdominal pain and bloating
- Relieved by bowel action
- Psychological factors important
- Some cases relate to food intolerances
Blood supply of the liver
- Hepatic Portal Vein delivers 75% of liver’s blood supply, carrying venous blood from spleen and GI tract
- Hepatic artery delivers the remaining 25% of the blood from the heart
- Blood flows through the liver sinusoids and empties into the central vein of each lobule
- Central veins coalesce into the hepatic vein, which leaves the liver and drains into the inferior vena cava
Describe the biliary tree
- Biliary tree is the path by which bile is secreted from the liver to the duodenum
- Bile is produced in the liver and collected in the canaliculi
- Canaliculi radiate to the edge of the liver lobule where they merge to form bile ducts in the liver
- Intrahepatic ducts eventually drain into the right and left hepatic ducts
- These drain into the common hepatic duct
- Cystic duct from the gall bladder joins the common hepatic duct to form the common bile duct
Functions of the liver
- Metabolism, breakdown and excretion of drugs and endogenous products (ammonia, urea, bilirubin, hormones and alcohol)
- Production of albumin, blood clotting factors (II, VII, IX and X), complement, transporter proteins, cholesterol and bile components
- Storage of substances (glycogen, fat-soluble vitamins eg Vitamin D, E, A, K, vitamin B12 and folate, minerals such as iron and copper)
- Maintenance of body homeostasis by regulating the glucose and cholesterol blood levels
Causes of liver disease
-Over 100 different causes
-Infections
Viral (Hep A, B, C, D, E; Epstein Barr Virus; Cytomegalovirus)
Bacterial (TB, syphilis)
Parasitic (malaria)
-Toxic and drugs
Drug misuse (paracetemol and ecstasy)
Alcohol
-Metabolic
Non-alcoholic fatty liver disease (obese, type II diabetes, high blood pressure, hypercholesterolaemia)
Wilson’s disease
Haemochromatosis
-Autoimmune
Systemic lupus erythematosus
Primary biliary cirrhosis
Compensated v Decompensated Liver disease
Compensated- liver coping with working at reduced capacity
Decompensated- liver failing to cope with its functional demands
Clinical features of acute liver disease
Loss of appetite
Jaundice
Weight loss
Clinical features of chronic liver disease
- More than 3 spider naevi (telangiectasis- swollen blood vessels)
- Palmar erythema
- Finger clubbing
- Jaundice
- Oedema/ascites
What is jaundice and what are the causes/types
-Yellowing of the skin and sclera due to a build up of bilirubin in the blood and body’s tissues
- Pre-hepatic jaundice occurs due to a breakdown of red blood cells (sickle cell anaemia, thalassaemia)
- Intra-hepatic jaundice occurs due to liver disease itself, resulting in less breakdown of bilirubin (hepatitis, alcohol, drug misuse, cirrhosis)
- Post-hepatic occurs when the excretion pathway is blocked so you can’t get rid of the bilirubin (gallstones and tumours)
A patient has normal liver function and normal bile production. What type of jaundice do they have?
Pre-hepatic jaundice
Symptoms of liver failure
Bleeding/bruising due to lack of synthesis of clotting factors II, VII, IX and especially X
Hypoglycaemia
Infections
Ascites (fluid in the stomach due to pressure from the hepatic portal vein)
Encelopathy (brain damage, disease or malfunction as you cannot detoxify anything after you’ve eaten anything, so toxins can enter the IVC and then the brain)
Cirrhosis definition
- Necrosis of liver cells followed by fibrosis and nodule formation
- Leads to interference of blood flow through the liver and loss of liver function
Diagnosis for cirrhosis
Liver biopsy shows decreased liver size and histology shows scars contracting together
Causes of cirrhosis
- Common causes include Alcohol and viral (Hep B and C)
- Less commonly, autoimmune diseases, drugs, haemochromatosis and Wilson’s disease
Investigations of Cirrhosis
-Gold standard for diagnosis is histological appearance through liver biopsy
-Liver function tests (group of blood tests) to show:
Alanine transaminase
Aspartate transaminase
Gama-Glutamil transfererase
Bilirubin (jaundice test)
Albumin (remember the liver synthesises albumin)
-Imaging tests:
Ultrasound Scan
Compued Tomography scan
Magnetic Resonance Imagine scan
Alcohol-related liver disease definition, treatment and complications
- Term that encompasses liver manifestations of alcohol overconsumption
- No treatment
- Complications include alcoholic hepatitis and cirrhosis
Signs and symptoms of alcohol-related liver disease
- Feeling sick
- Weight loss
- Loss of appetite
- Jaundice
- Swellings in the ankles and the stomach
- Confusion or drowsiness
- Vomiting blood or passing blood in the stools (due to back pressure of the portal system)
Difference between non-alcoholic fatty liver disease and alcoholic fatty liver disease
- Very similiar
- NAFLD due to a build-up of fat within the liver cells
- Due to overweight/obese, type II diabetes, HBP, hypercholesterolaemia
-Basically liver ultimately ends up scarring but on the way it turns into fat
4 stages on NAFLD
- Steatosis (reversible)
- Non-alcoholic steatohepatitis
- Fibrosis
- Cirrhosis
Gallstones definition
- Stone formed within the gall bladder out of bile components
- Can block bile duct
Risks for gallstones
Female Forty Fertile Fat Fair
Signs and symptoms of gallstones
Central abdominal pain (intermittent or persistent)
Jaundice
Fever
Diagnosis of gallstones
- Can be suspected based on symptoms
- Confirmed by ultrasound scan or other imagine
- Complications may be detected on blood tests
Differential diagnosis of gallstones
- Sludge in bile duct
- Bile duct wall mass
- Mass pressing on bile duct from adjacent anatomy
- Carcinoma of head of the pancreas
Tx of gallstones
Depends on severity of disease
- If asymptomatic, no tx needed
- If pain, then surgery (cholecystectomy)
Hep B definition, spread and significance
- Inflammation of the liver
- Acute and Chronic
- Hepadnavirus can survive outside the body for at least 7 days (dry bloods, fluids)
- Transmitted through contact with the blood or other body fluids of an infected person
- Occupational hazard
- Causes viral hepatitis
Prevention of Hep B
Safe and effective vaccine
Definition, significance and spread of Hep C
- Acute and chronic
- 80% asymptomatic
- Viral hepatitis
- Contact with blood or other body fluids of an infected person
- Occupational hazard (most people asymptomatic)
Prevention of Hep C
-No vaccine available but antiviral meds can cure approximately 90% of people with Hep C infection
Symptoms of Hep B and C
- Flu-like symptoms
- Feeling and being sick
- Lack of appetite
- Jaundice
Dental Relevance of Liver Disease
-Cross infection risk
Hep B and C have the highest risk of transmission of blood-borne viruses from pt to healthcare worker
Sharps injury
- Altered drug metabolism
- Post-operative haemorrhage (vitamin K and clotting factor deficiencies)
- Delayed wound healing
- LA safe, relative anaesthesia preferable to IV sedation with benzodiazepine
- Liase with GP, gastroenterologist and liver specialist
-Liver disease due to SLE:
Oral lichenoid reaction
Sjorgen’s syndrome
-Liver disease due to Primary Biliary Cholangitis
Sjorgens syndrome
-Liver disease due to NAFLD
T2 diapetes or HBP
-Dental hypoplasia and greenish discoloration of teeth due to an early rise in conjugated bilirubin serum levels
