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Human Disease > Gastro-Intestinal Diseases > Flashcards

Gastro-Intestinal Diseases Flashcards

1
Q

Definition of dysphagia

A

Difficulty swallowing

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2
Q

Definition of heartburn

A

Retrosternal burning, common symptom of acid reflux

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3
Q

Definition of dyspepsia

A

Range of symptoms referring to upper GI tract including nausea, heartburn, acidity and pain

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4
Q

Definition of flatulence

A

Passing excess wind (belching, abdominal distention or passing of flatus per rectum)

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5
Q

Definition of vomiting

A

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.

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6
Q

Nausea and vomiting with pain indicative of

A

GI origin

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7
Q

Nausea and vomiting without pain indicative of and examples

A

non-GI origin. Eg, CNS disease (raised intracranial pressures), drugs (chemo) or metabolic agents (uraemia, diabetic ketoacidosis)

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8
Q

Definition of constipation

A

Mean infrequent passage of stools (<2 per week) or difficulty passage of hard stool

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9
Q

Definition of diarrhea

A

Increased amounts of loose stool (>250g/day)

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10
Q

Definition of steatorrhoea and cause

A

Increased passage of pale, bulky stools that contain fat. Indicative of fat malabsorption as a result of small bowel, pancreatic or biliary disease.

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11
Q

Valve between distal end of oesophagus and stomach. How this valve opens/closes. Failure of this valve to open and outcome

A

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.

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12
Q

4 secretions of the stomach

A

Gastrin, gastric juice, bile and intrinsic factor

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13
Q

What is absorbed in the stomach

A

Water, alcohol and aspirin

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14
Q

Relationship of gastrin and gastric juice. Sequence of events after secretion.

A

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

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15
Q

What causes stimulation of mucous

A

Mucosal irritation (mechanical or chemical)
Acid in lumen of stomach
Vagal and sympathetic stimulation

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16
Q

Importance of intrinsic factor

A

Aids absorption of vitamin B12 from distal ileum

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17
Q

What does gastric motility cause

A

Mixes stomach contents with gastric juice
Converts to semi-liquid chyme
Propels contents through the stomach and into duodenum

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18
Q

Bile produced, stored and secreted?

A

Produced in liver, stored and concentrated in gall bladder and released into duodenum

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19
Q

Where does the oesophagus enter the diaphragm

A

Right and left crus

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20
Q

Common symptoms of problems with the oesophagus

A

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.

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21
Q

Common diseases associated with the oesophagus

A 
Achalasia
pharyngeal pouches
oesophageal web
carcinoma of the oesophagus 
Peptic ulcer disease/reflux 
Oesophageal spasm
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22
Q

Anatomy of the pharynx

A

3 overlapping constrictor muscles: superior, middle and inferior
Inferior constrictors include cricopharyngeus and thyropharyngeus

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23
Q

Name and cause of potential weakness in the oesophagus. Clinical significance

A

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.

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24
Q

Muscles of the oesophagus
Nervous supply
Lining mucosa

A

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

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25
Q

Process of moving food from mouth to oesophagus and explanation

A

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)

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26
Q

Differential diagnosis for pain in the oesophagus

A

Often poorly localised so can be confused with mediastinal structures (eg the heart)

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27
Q

Causes of dysphagia and examples

A 
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)
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28
Q

Pharyngeal Pouch definition and clinical features

A

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

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29
Q

Fungal infection of oesophagus? Possible reason?

A

Candida oesophagitis. Immunocompromised, transplant patients, HIV infection, chemotherapy

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30
Q

Aetiology and pathophysiology of Achalasia

A

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

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31
Q

Clinical Features of achalasia

A

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

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32
Q

Investigations (and explanation of investigations) and Treatment for achalasia

A

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)
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33
Q

Definition and aetiology of oesophageal spasm

A

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
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34
Q

Distinguishing between oesophageal spasm and achalasia

A

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

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35
Q

In what kind of patients is oesophageal web common, and why is it important despite being rare

A

Chronic anaemics, middle aged women

Premalignant

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36
Q

Clinical features of oesophageal web

A

Glossitis
Iron deficiency anaemia
Dysphagia
Koilonychia

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37
Q

How an oesophageal web forms and investigation(s)

A

Mucosa becomes atrophic (tired and wasted)
Fibrous structure forms at the upper end of the oesophagus
Forms a web, visible on barium swallow

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38
Q

Treatment of oesophageal web

A

Dilatation of the stricture and correction of the iron deficiency. Understand why pt is anaemic
Monitor for recurrence and malignant transformation

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39
Q

Aetiology of GORD

A

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

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40
Q

Clinical features of GORD

A 
symptoms after a meal
reflux most commonly
heart burn
regurgitation
nausea
bloating
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41
Q

Investigations and tx of GORD

A

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

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42
Q

Relationship of GORD and peptic ulcer disease

A

GORD increases chances of peptic ulcer disease

H. Pylori infection not related to pathogenesis of GORD

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43
Q

Peptic Ulcer Disease definition and promoting factors (why these factors increase risk of peptic ulcer disease)

A

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)

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44
Q

Peptic v gastric ulcers

A

Peptic ulcers can affect oesophagus, stomach or duodenum (anywhere the acid can get to)
Gastric ulcers is in the stomach only

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45
Q

Clinical features of PUD

A 
Pain 
Vomitting 
Haematemesis- blood with vomiting
Ulcers with scarring 
Spasm
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46
Q

Likely sites for ulcers to appear in the upper GI tract

A

Lower oesophagus, lesser curve of stomach, first part of the duodenum

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47
Q

Investigtions and treatment of PUD

A

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

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48
Q

Tx for H.Pylori infection

A

Quadruple therapy
Proton pump inhibor eg omeprazole
Bismuth-based (pepto-bismol)
2 antibiotics (amoxicillin and clarithromycin)

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49
Q

How can peptic ulcer disease cause acute upper GI bleeding

A

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

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50
Q

Complications of cardiac sphincter failure

A

Barett’s oesophagus, GORD, Achalasia, PUD

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51
Q

Barett’s oesophagus definition and importance

A

Acid from stomach changes oesophageal lining due to failure of the cardiac sphincter
Pre-malignant

52
Q

Hiatus Hernia definition and clinical features

A

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

53
Q

Investigations and tx of hiatus hernia

A

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
54
Q

Risk factors for carcinoma of the oesophagus

A 
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)
55
Q

Clinical features ??

A

End stage dysphagia
Pain
Haematemesis
Weight loss, malaise, anorexia

56
Q

Types of oesophageal cancer

A

Majority squamous cell carcinoma (upper two-thirds of the oesophagus)
Lower 1/3 of oesophagus may be adenocarcinoma (due to ectopic gastric mucosa)

57
Q

Where is a tumour in the oesophagus likely to spread

A

Fungate into lumen
Infiltrate adjacent structures in the mediastinum
Lymph nodes
Liver

58
Q

Investigations of carcinoma of the oesophagus

A

Endoscopy, biopsy and barium swallow to establish diagnosis

CXR, ultrasound and CT scan used to stage tumour

59
Q

Difference in mucosa throughout the oesophagus

A

Upper 2/3s stratified squamous non keratinizing epithelium

lower 1/3 can be ectopic gastric columnar `

60
Q

Treatment for oesophageal carcinoma

A

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

61
Q

Dental relevance of peptic ulcer disease and oesophageal reflux

A

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

62
Q

Dental relevance of oesophageal cancer

A

If pt presents with dysphagia, take a careful history of it

Examination of neck may reveal cervical lymphadenopathy

63
Q

Acute v chronic duodenal ulcer in terms of structure

A

Acute ulcers just penetrate the submucosa

Chronic ulcers go deep into the muscular coat so are harder to cure

64
Q

Clinical significance of pyloric stenosis

A

Caused by stenosis of the pyloric sphincter

Paediatric projectile vomiting. Cycle of eat, full, throw up and cry cos im hungry

65
Q

List the substructures of the bowel (small intestine) and colon (large intestines) in order

A

Duodenum
Jejunum
Ileum

Cecum
Sigmoid
Rectum
Anal Canal

66
Q

Definition and aetiology of coeliac disease

A

chronic autoimmune-mediated disease of the small intestine caused by a sensitivity/intolerance to gluten

genetic, associated with HLAB8

67
Q

Pathogenesis of coeliac

A

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

68
Q

Clinical features of coeliac

A

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

69
Q

Diagnosis of coeliac

A 
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
70
Q

Treatment for coeliac

A

Gluten-free diet

71
Q

Dental relevance of coeliac disease

A
  • 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
72
Q

Definition of Crohn’s Disease

A

Chronic inflammatory disorder that can affect any part of the GI tract from mouth to anus
Peak age of incidence from 20-60 years

73
Q

Aetiology of Crohn’s

A

Strong family history (Genetic)

Environmental factors such as smoking and diet

74
Q

Clinical features of Crohn’s

A
  • Diarrhea
  • Abdominal pain
  • Decreased apetite
  • Rectal bleeding
  • Weight loss
  • Fever
  • Fistula and perianal sepsis
75
Q

Pathology of Crohn’s Disease

A
  • 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
76
Q

3 phenotypes of Crohn’s Disease

A

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

77
Q

Diagnosis of Crohn’s

A

Barium enema showing rose thorn, skip lesions, string sign

Signmoidoscopy and biopsy, colonoscopy

78
Q

Differential Diagnosis of Crohn’s

A

Tuberculosis or sarcoidosis

79
Q

Treatment of Crohn’s

A

Corticosteroids eg prednisone or budenoside
Immunomodulators
Biologics

Surgical treatment includes intestinal resection

80
Q

Dental Relevance of Crohn’s

A
  • 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
81
Q

Orofacial Granulomatosis definition, relationship to other inflammatory diseases, clinical features and tx

A
  • 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
82
Q

Types of inflammatory bowel disease

A

Ulcerative Colitis and Crohn’s Disease

Coeliac disease is autoimmune

83
Q

Ulcerative Colitis definition

A
  • Chronic inflammatory bowel disease
  • Rectum always involved
  • Sometimes ascends up to proximal colon (caecum) and terminal ileum
  • Remit and relapse disease
84
Q

Ulcerative Colitis pathogenesis

A
  • 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
85
Q

Ulcerative Colitis aetiology

A

Unknown

  • Hypothesis is that there is a dysregulated interaction between mucosal immunology and intestinal microflors
  • Along with a genetic disposition (strong jewish family history)
86
Q

Ulcerative Colitis clinical features

A
  • 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
87
Q

Investigations and Diagnosis for UC

A

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
88
Q

Tx for UC

A
  • High protein, high fibre diet
  • 5-aminosalicyclic acid
  • Sulphasalazine
  • Corticosteroils eg prednisolone
  • Mesalazine
  • Thioprines
  • Surgery if perforation, haemorrhage, severe complications or repeated relapse
89
Q

Risks of Inflammatory Bowel Diseases

A

-Increased risk of colorectal cancer

90
Q

Dental Relevance of UC

A

-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
91
Q

Differentiating between UC and CD

A

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
92
Q

Aetiology of carcinoma of the colon. Predisposing factors

A

Environmental factor and family history

Predisposing factors include previous cancer, neoplastic familial polyposis coli and UC fam history

93
Q

Common sits for carcinoma of the colon

A 
Rectum
then 
Sigmoid 
then
Caecum
94
Q

Presentation/clinical features of colon cancer

A

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
95
Q

Types and definition of functional bowel disorders

A

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
96
Q

Blood supply of the liver

A
  • 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
97
Q

Describe the biliary tree

A
  • 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
98
Q

Functions of the liver

A
  • 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
99
Q

Causes of liver disease

A

-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

100
Q

Compensated v Decompensated Liver disease

A

Compensated- liver coping with working at reduced capacity

Decompensated- liver failing to cope with its functional demands

101
Q

Clinical features of acute liver disease

A

Loss of appetite
Jaundice
Weight loss

102
Q

Clinical features of chronic liver disease

A
  • More than 3 spider naevi (telangiectasis- swollen blood vessels)
  • Palmar erythema
  • Finger clubbing
  • Jaundice
  • Oedema/ascites
103
Q

What is jaundice and what are the causes/types

A

-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)
104
Q

A patient has normal liver function and normal bile production. What type of jaundice do they have?

A

Pre-hepatic jaundice

105
Q

Symptoms of liver failure

A

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)

106
Q

Cirrhosis definition

A
  • Necrosis of liver cells followed by fibrosis and nodule formation
  • Leads to interference of blood flow through the liver and loss of liver function
107
Q

Diagnosis for cirrhosis

A

Liver biopsy shows decreased liver size and histology shows scars contracting together

108
Q

Causes of cirrhosis

A
  • Common causes include Alcohol and viral (Hep B and C)

- Less commonly, autoimmune diseases, drugs, haemochromatosis and Wilson’s disease

109
Q

Investigations of Cirrhosis

A

-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

110
Q

Alcohol-related liver disease definition, treatment and complications

A
  • Term that encompasses liver manifestations of alcohol overconsumption
  • No treatment
  • Complications include alcoholic hepatitis and cirrhosis
111
Q

Signs and symptoms of alcohol-related liver disease

A
  • 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)
112
Q

Difference between non-alcoholic fatty liver disease and alcoholic fatty liver disease

A
  • 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

113
Q

4 stages on NAFLD

A
  • Steatosis (reversible)
  • Non-alcoholic steatohepatitis
  • Fibrosis
  • Cirrhosis
114
Q

Gallstones definition

A
  • Stone formed within the gall bladder out of bile components
  • Can block bile duct
115
Q

Risks for gallstones

A 
Female
Forty
Fertile
Fat
Fair
116
Q

Signs and symptoms of gallstones

A

Central abdominal pain (intermittent or persistent)
Jaundice
Fever

117
Q

Diagnosis of gallstones

A
  • Can be suspected based on symptoms
  • Confirmed by ultrasound scan or other imagine
  • Complications may be detected on blood tests
118
Q

Differential diagnosis of gallstones

A
  • Sludge in bile duct
  • Bile duct wall mass
  • Mass pressing on bile duct from adjacent anatomy
  • Carcinoma of head of the pancreas
119
Q

Tx of gallstones

A

Depends on severity of disease

  • If asymptomatic, no tx needed
  • If pain, then surgery (cholecystectomy)
120
Q

Hep B definition, spread and significance

A
  • 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
121
Q

Prevention of Hep B

A

Safe and effective vaccine

122
Q

Definition, significance and spread of Hep C

A
  • Acute and chronic
  • 80% asymptomatic
  • Viral hepatitis
  • Contact with blood or other body fluids of an infected person
  • Occupational hazard (most people asymptomatic)
123
Q

Prevention of Hep C

A

-No vaccine available but antiviral meds can cure approximately 90% of people with Hep C infection

124
Q

Symptoms of Hep B and C

A
  • Flu-like symptoms
  • Feeling and being sick
  • Lack of appetite
  • Jaundice
125
Q

Dental Relevance of Liver Disease

A

-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

Human Disease (19 decks)

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