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Pathology Flashcards

1
Q

How is Liver Disease Classified?

A

Child-Pugh Classification

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2
Q

What aspects does the Child-Pugh classification take into account?

A 
Liver Disease-
Bilirubin
Albumin
PTs (prolonged- DVT)
Encephalopathy
Ascities
A- less 7, B- 7-9, C- Greater 9
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3
Q

What drugs are contraindicated in liver disease?

A

Anticoagulants eg./ warfrin as clotting factors already low
Asprin + NSAIDS- Worsen ascites due to flid retension/ inc bleeding time
Opiates + Benzodiapines- precipitate encephalopathy

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4
Q

What is oesophageal reflux?

A

Reflux of gastric acid back into the oesophagus

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5
Q

What happens to the oesophagus if acid is constantly being refluxed back up into it?

A

Thickens squamous epithelia+ ulceration- Healing by fibrosis= less motility + less solubility of nutrients

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6
Q

What is Barretts Oesophagus?

A

Metaplasia (cells grow abnormally)= premalignant

Squamous Epithelia - Glandular Epithelia- Adenocarcinoma

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7
Q

What are the 2 most common types of oesophageal cancer?

A
  1. Squamous Cell Carcinoma (smoking/ alcohol related in proximal + middle areas)
  2. Adenocarcinoma (barrets, hiatus hernia)
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8
Q

What are the causes of Oesophageal SCC?

A

Smoking
Alcohol
Dietary
In proximal + middle 3rds

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9
Q

What are the causes of Oesophageal Adenocarcinoma?

A 
Oesophageal Reflux (Barrets Metaplasia)
Obesity (hiatus hernia thickens cells)
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10
Q

What are the common presentations of an oesophageal Tumour/ Cancer?

A

Obstruction- Decrease in nutrients + weight
Ulceration- Erodes BV- blood loss- chronic anemia
Perforation- Ulcerates through into thorax- inflammation

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11
Q

What are the causes of gastritis?

A

Autoimmune (T1)
Bacterial (T2). most common
Chemical Injury (T3)

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12
Q

What causes Type 1 gastritis?

A

Autoimmune- atrophy of parietal + intrinsic cells (antibodies against them) = DEC acid secretion + loss of intrinsic factor (B12 deficiency- pernicious anemia)

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13
Q

What causes Type 2 gastritis?

A

Bacterial (most common)- Helicobacter Pylori in gastric surface- acute + chronic inflammatory response= INC acid production

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14
Q

What causes Type 3 gastritis?

A

Chemical Injury- Drugs (eg./ NSAIDS, Asprin); Alcohol + Bile Reflux

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15
Q

What is a Peptic Ulcer?

A

A lesion in the mucosa of the digestive tract caused by the digestive action of pepsin and stomach acid.

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16
Q

Where are peptic ulcers found?

A

1st + 2nd parts of the Duodenum (most common); Lower Oesophagus; Body + Antrum of stomach

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17
Q

What is the most common cause of peptic ulcers?

A

Helicobacter Pylori

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18
Q

How does a peptic Ulcer usually present?

A

Bleeding-Acute- Haemorrhage
- Chronic- Anemia
Perforation- Peritonitis
Obstruction- Heal by Fibrosis

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19
Q

What type of cancer is found in the stomach?

A

Adenocarcinoma

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20
Q

What is the most common reason for an Adenoma forming in the stomach?

A

Helicobacter Pylori

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21
Q

What happens to gastric epithelia in Adenocarcinoma?

A

Mucous Columnar Cells- Intestinal Shape

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22
Q

What is transcoelonic spread?

A

Spread within the peritoneal cavity

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23
Q

What is the usual presentation of gastric Adenocarcinomas?

A

Tiredness

NOTE: There is not weight loss/ pain as no obstruction

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24
Q

Why is gastric cancer hard to pick up?

A

As only general symtoms eg./ tiredness. No weight loss or pain as no obstruction

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25
Q

Acute organic diseases?

A

Allergies + sensitivities

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26
Q

How can an allergy present/ be classified?

A

The pt tends to break out in a rash, hives, throat closing (extreme) and require an epipen.
They can be diagnosed via Radioisotope Allergy Test

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27
Q

What is sensitivity?

A

Pt doesn’t like/ doesn’t sit well as a pose to body reaction

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28
Q

Chronic organic diseases?

A

IBD- Chrons, UC
Surgery- Stomas
Cancers of GI Tracts

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29
Q

What is functional disease?

A

a disease in which there is an abnormal change in the function of an organ, but no structural alteration in the tissues involved

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30
Q

What is organic disease?

A

a disease in which there is a structural alteration

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31
Q

What factors affect functional disease?

A 
Age (tends to be younger pop.)
Motility
Diet
Gut Hormones
Microbiome
Inc Visceral Sensation
Psychological Factors
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32
Q

What is Biliary Disease?

A 
Functional disorder (no structural abnormality) of the GI tract.
Sphincter of Oddi dysfunction- symptoms are general (visceral sensitivity) but examination is normal
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33
Q

Examples of functional diseases of the GI Tract

A

Functional- no structural abnormalities (opposite of organic)

eg. /
1. IBD
2. Biliary Disease
3. Upper GI- reflux, Functional Dyspepsia, Nausea + Vomiting Syndromes

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34
Q

What psychological actions can have an affect on weight gain/loss?

A

Self starvation, self- induced vomiting, compulsive activity, laxative abuse, diet pills, herbal medicines + deliberate cold exposure

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35
Q

What is Binge Eating? Rae

A

Binge + Purge= failure to compensate so weight gain

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36
Q

What is Bulimia Nervosa?

A

Restrict- Binge- Purge= normal weight

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37
Q

What is Anorexia Nervosa?

A

Restriction- OCD- Impaired decision making concerning weight, body dysmorphic, over exercise, amenorrhea (period loss)

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38
Q

What drugs can cause functional GI Disorders?

A

Opiates
Cocaine
Amphetamines (OCD, narcolepsy) Anticholinergics
Antidepressants

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39
Q

What investigations would you carry out for a suspected functional GI disorder?

A 
History- Time Frame, Drugs + Pregnancy 
Physical Exam
Bloods- FBC, Blood Glucose, Pregnancy, Urinalysis
H.Plyori- breath, stool/ blood
CxR, AxR, USS
Endoscope
CT Head
Nutritional- MUST Score
Note: Must rule out possibility of organic disease
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40
Q

How do you treat functional GI Disease?

A

IV Fluids, Vitamins, Dietetic Review, NG Tube

Refeeding- correct fluid depletion, give thiamine 30 mins before starting + give 5-10 kcal/kg over 24 hrs

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41
Q

What is refeeding and how is it done?

A

Act of restoring a patients back to nutritional health
Thiamine (30mins before starting)
Correct Fluid Depletion
5-10 kcal/kg over 24 hrs over 1 week

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42
Q

What is refeeding syndrome?

A

If starved and refer too quickly = major electrolyte shift, rapid insulin increase, rapid ATP generation- Ph into cells- hypophophatemia + fluid retension= Anemia, Arrythmia, Cardiac Failure + death

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43
Q

Who is at a hight risk of refeeding syndrome?

A

One of-
BMI < 16kg/m2
> 15% unintentional weight loss (over 3-6mnths)
Little/ No nutritional intake in last 7-10 days
Decreased K,pH/ Mg

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44
Q

What other groups are at a high risk of refeeding syndrome

A

Two of-
BMI < 18 kg/m2
> 10% unintentional weight loss (over last 3-6 months)
Little/ No nutritional intake in last 5+ days
History of alcohol/ drug abuse
History of chemo, diuretics, insulin, antacids

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45
Q

How do you treat an eating disorder?

A

MDT
NG Tube
Liasion with psychiatry

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46
Q

What is a structural disease?

A

One with a detectable pathology

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47
Q

What is an example of a macroscopic disease?

A

Cancer

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48
Q

What is an example of a microscopic disease?

A

Colitis

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49
Q

What has a better prognosis a structural/ organic or a functional disease?

A

A functional disease has a better outcome as no detectable pathology

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50
Q

What causes non- ulcer dyspepsia?

A

Reflux
Delayed Gastric Emptying (ALARM for gastric cancer)
IBS
H. Pylori

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51
Q

What causes Vomiting, Nausea + Retching?

A 
Drugs
Alcohol
Pregnancy
Migrane
Cyclical Vomiting Syndrome
Psychogenic Vomiting Syndrome
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52
Q

What is Cyclical Vomiting Syndrome?

A

Occurs in childhood, recurrent attacks of vomiting, nausea and headaches. No known cause

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53
Q

What is Psychogenic Vomiting Syndrome?

A

Common presentation is young female, no change in appetite but weight loss.
Overlaps with bulimia, stops after admission

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54
Q

What can cause constipation?

A

Organic (structural)- Tumours, Anal Fissure
Functional- Psychosis, Depression
Systemic- Diabetes Mellitus, Hypothyroidism
Neurogenic- Stroke, MS

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55
Q

What are the 3 types of IBS?

A

IBS-C- constipation (less muscular contractions)
IBS-D- diarrhoea
IBS-M- mixed

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56
Q

What is the general presentation of IBS?

A 
Abdominal Pain (radiates to lower back)
Abdominal Bloating
Mucus in stool
Wind, Flatulence
'Awareness' of digestive process
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57
Q

What is the difference between a disease and syndrome?
disease- glands
syndrome- brain

A

A disease is a pathophysiological response to internal or external factors at site
A syndrome is a collection of signs and symptoms associated with a specific health-related cause that goes onto attack a specific function

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58
Q

What causes abdominal pain and bloating in IBS?

A

Abdominal wall muscle reflex

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59
Q

Does IBS occur at night?

A

No as pt is asleep so no trigger/ awareness of digestive process

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60
Q

What investigations would you carry out on a pt of suspected IBS?

A

Bloods- FBC, U+E, LFT (IBD), Ca, CRP (inflammatory marker), TFTs, Coeliac
Stool Culture
Rectal Exam
Colonscopy
Calprotectin (release from inflamed gut mucosa)

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61
Q

How do you treat IBS?

A

Dietetic Review (FOODMAP)
Bloating- Probiotics + Avoid Fibre
Pain- Antispasmotics, Antidepressants (can cause constipation), SSRIs (anxiety related)
Constipation- Laxatives (bulking, osmotic, softness, stimulants)
Diarrhoea- anti motility agents

Psychological Interventions

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62
Q

What general symptoms are presented on a functional GI Disorder?

A

Age (>50) Anorexia
Loss of Weight
Recent Antibiotic use/ onset Rectal Bleeding
Melena/ Mass/ Male

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63
Q

What types of cancer are present in the oesophagus?

A

Adenocarcinoma (barrets)

Squamous Cell Carcinoma

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64
Q

How is adenocarcinoma formed in the oesophagus?

A

Distal oesophagus-

Obesity- Gastro-Oesophageal Reflux- Barretts Metaplasia- Dysplasia- Carcinoma

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65
Q

Where in the oesophagus is adenocarcinoma found?

A

Distal Oesophagus

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66
Q

How is Squamous Cell Carcinoma formed in the oesophagus?

A

In proximal + middle 1/3 of oesophagus

Smoking + Alcohol + low socio-economic status

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67
Q

Presentation of Oesophageal Cancer

A 
Progressive Dysphagia
Odynophagia
Anorexia/ Weight Loss
Chest Pain/ Heartburn
Haematemesis
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68
Q

How would you investigate suspected Oesophageal cancer?

A

Endoscopy- Gold Standard

Contrast Swallow eg./ Barium (will see stricture but not if benign/ malignant)

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69
Q

What equipment is used to stage cancer?

A

CT + TNM

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70
Q

What treatment is available for Oesophageal Cancer Pts with mets/ unfit for surgery?

A

Palliative/ Supportive
Stent
Radiotherapy
Chemotherapy

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71
Q

What treatment is available for Oesophageal Cancer Pts who are fit?

A

EUS- Get T + N Stage
PET CT- Get M Stage
Oesophagectomy- Radical, roof top incision and leave feeding jejunoscopy
- gastric mobilisation- remove stomach + reposition
- oesophageal resection `+ gastric-oesophgeal anastomoses (loose LOS- regurg poss.)
Chemotherapy

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72
Q

How does gastric cancer present?

A

VERY non-specific presentation
Dyspepsia, tiredness
ALARM SYMPTOMS- Weight Loss, Upper Abdomen Mass, Vomiting, GI Blood Loss

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73
Q

What are the ALARM Symptoms?

A 
ALARM SYMPTOMS
Weight Loss
Upper Abdomen Mass
Vomiting
GI Blood Loss
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74
Q

What investigations would you carry out for a suspected stomach cancer?

A

Endoscopy
Contrast Swallow eg./ Barium
Staging (TNM) via CT

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75
Q

What treatment would you offer a Pt with gastric cancer?

A

Surgical
Total gastrectomy + Route en Y Reconstrction- Stomach out and plug in a bit of small bowel
Subtotal gastrectomy- Partial Removal
+ Chemo before and after operations

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76
Q

What is Gastro-Oesophageal Reflux Disease caused by?

A

Hiatus Hernia

  1. Sliding- High Pressure zone in chest, causes reflux
  2. Paraoesophageal- Stomach flipped into chest, retrosternal pain
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77
Q

What is the main clinical feature of a sliding gastric hiatus hernia?

A

Reflux

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78
Q

What is the main clinical feature of a paraoesphgeal gastric hiatus hernia?

A

Retrosternal Pain

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79
Q

What are the risk factors for GORD/ Hiatus Hernia?

A

obesity
smoking
alcohol excess

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80
Q

What are the symptoms of GORD?

A

Heart Burn
Water Brash- Regurgitation
Cough

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81
Q

How would you investigate possible GORD?

A

Endoscopy

Oesophageal pH + Manometry (if pH>4.2= pathological)

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82
Q

How do you treat GORD?

A 
Life Style Management
PPI Therapy (eg./ omeprazol + gaviscon) for reflux
Laprascopic Hiatus Repair + Fundoplication (funds wrapped around oesophagus- can cause dysphagia, bloating, flatulence + diarrhoea)
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83
Q

What is a Fundoplication and what are the possible consequences?

A

Wrapping funds around oesophagus (tightens LOS)

Can cause dysphagia, bloating, flatulence + diarrhoea

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84
Q

What makes someone a candidate for Bariatric Surgery?

A

Some genetic components but mostly diet and exercise

IF risk of death/ shorter life expectancy

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85
Q

Give examples of restrictive bariatric surgery

A

Restrictive- Dec stomach size= Inc satiety

  1. Laparoscopic Adjustable Gastric Band- Silicon band tightened / loosed on demand with isotonic fluid
  2. Laparoscopic Sleeve Gastrectomy- remove most of stomach, Dec size, removes funds (grenlin) so less hungry
86
Q

What is Laparoscopic Adjustable Gastric Band Surgery and what are the pros + cons?

A

RESTRICTIVE Laparoscopic Adjustable Gastric Band- Silicon band tightened / loosed on demand with isotonic fluid.
+ve= Minor, Reversible, Low Mortality
-ve= Can cheat by changing band size, risk prolapse/ slip/ more surgery

87
Q

What is Laparoscopic Sleeve Gastrectomy and what are the pros + cons?

A

RESTRICTIVE Laparoscopic Sleeve Gastrectomy- remove most of stomach, Dec size, removes funds (grenlin) so less hungry
+ve= No dumping syndrome, no foreign body, no manipulation
-ve= More invasive, Long staple line, short pedigree

88
Q

Give examples of Malabsorbitive Bariatric Surgery

A

Bypass segments to encourage malabsorption

1. Laparoscopic Gastric Bypass- patch to restrict food intake + Y Shaped SI attached- food goes to lower stomach

89
Q

What is Laparoscopic Gastric Bypass and what are the pros + cons?

A

MALABSORBITIVE Laparoscopic Gastric Bypass- patch to restrict food intake + Y Shaped SI attached- food goes to lower stomach
+ves= Quick, Dramatic Weight Loss, Dumping Syndrome
-ves= More Invasive, life-long supplements, more complex if requires revision, highest mortality

90
Q

What is combination bariatric surgery + what are its complications?

A

Combination of restrictive and malabsorption surgery
Roux en Y Gastric Bypass is gold Standard
Complications include anastomotic leak, DVT/PE, Infection, malnutrition, mineral/ vitamin deficiency, hair loss + excess skin

91
Q

What is Dysphagia?

A

Difficultly Swallowing

92
Q

What 5 questions would you ask a patient presenting with dysphagia?

A
  1. Was there difficulty swallowing solids and liquids from the start-
    Yes- Motility Disorder
    No- Stricture (benign/ malignant)
  2. Is it difficult to make the swallowing movement?
    Yes- Suspect bulbar palsy esp. if coughing on swallowing
  3. Is swallowing painful (odynophagia)?
    Yes- Suspect Cancer, oesophageal ulcer (benign/ malignant), candida (inhaler/ immunocompromised), spasm
  4. Is the dysphagia intermittent or constant and getting worse?
    Intermittent- Oesophageal Spasm
    Constant + worsening- malignant stricture
  5. Does the neck bulge or gurgle during drinking?
    Yes-pharyngeal pouch
93
Q

What are the common causes of acid reflux?

A 
Alcohol
Nicotine
Dietary Xanthines (reduce LOS Pressure)
Persistent- GORD (long term complications)
Stricture (benign/ malignant)
Motility Disorders (Achalasia, Presbyoesophagus)
Eosinophilic oesophagus 
Extrinsic Compression
94
Q

What is Odynophagia?

A

Pain with swallowing

95
Q

What is Eosinophilic Oesophagus?

A

Inflammatory Allergic Disorder affecting the oesophagus causing dysphagia

96
Q

What would cause an extrinsic compression of the oesophagus?

A

Lung Cancer would push on the oesophagus causing dysphagia

97
Q

What investigations would you perform on a patient presenting with dysphagia?

A

Endoscopy- If dysphagia/ Reflux + ALARM
Contrast Swallow eg./ Barium if high up dysphagia eg./ pharyngeal pouch
Manometry- motility disorder
pH- refractory heartburn/ reflux over time

98
Q

What investigation would you perform to confirm clinical suspicion of a pharyngeal pouch?

A

Contrast eg./ Barium Swallow

99
Q

What investigation would you perform to confirm clinical suspicion of a motility disorder? And how would this look?

A

Manometry/ Barium Swallow

1. Hypermotility- Corkscrew Appearance on BS and exaggerated, uncoordinated, hypertonic contraction on manometry

100
Q

What is the classical presentation of hyper motility?

A

Severe episodic chest pain +/- dysphagia

Confused, Angina, MI

101
Q

What is the cause of hypomotility?

A

Connective Tissue Disease, Diabetes, Neuropathy, LOS Failure (heartburn + reflux)

102
Q

What is the cause of hypermotility?

A

Diffuse Oesophageal Spasm, Idiopathic (functional)

103
Q

What is the classical presentation if the LOS fails?

A

Reflux- Heart Burn

Hypomotility

104
Q

What can cause dysphagia?

A
  1. Diffuse oesophageal spasm- corkscrew barium
  2. Achalasia- LOS fails to relax (due to degeneration of myenteric plexus)
  3. Benign Oesphageal Stricture
  4. Oesophageal Caner
105
Q

Where is the myenteric plexus located?

A

In the muscularis propria between the circular and longitudinal muscle layers

106
Q

What is Achasia? What is its common presentation? What tests would you preform to determine your clinical suspicion? How would you treat this?

A

LOS fails to relax (due to degeneration of myenteric plexus)
Presentation- dysphagia, regard, cramps + decrease weight
Investigation- Barium Swallow
Treat- Endoscopic Balloon dilatation, PPI, Botulinum Toxin Injection, CCBS

107
Q

What clinical circumstance would Botulinum Toxin be used as treatment?

A 
Stops contraction of the muscle cells allowing them to become less stiff
achalasia
diffuse esophageal spasm
gastroparesis
sphincter of Oddi dysfunction
anal fissures
108
Q

A pt presents with nausea + vomiting. What tests would you run + questions would you ask?

A

Coffe grounds- GI bleeding
Recognisable food- gastric stasis
Feculent- small bowel obstruction/ bacterial overgrowth

109
Q

How do you test for Helicobacter Pylori invasively and non-invasively? How do you treat it?

A 
Test-
1. Non- Invasive- Give 13C (food source)- Test for urea.
ELISA on stool sample
2. Invasive- endocopy and culture sample
Treat- eradication therapy. Triple therapy for 7 days-
Clarithromyocin
Amoxycillin
PPI
(test again unless resistant strain)
110
Q

What are the 3 classes of gastritis?

A

A-autoimmune
B- bacterial
C- chemical

111
Q

What affects does alcohol have on metabolic process’?

A 
Disrupts
Gluconeogenesis
Acidosis- build up of pyretic acid
Ketosis- CAC disruption (DKa)
Lipid metabolism - hyperlipidemia- atherosclerosis
112
Q 
A Pt presents with
Spider Naevi
Palmar Erythema
Ascites
Encephalopathy
Jaundice
Muscle Wasting
What could this be an advanced/ chronic presentation of? How would you test to confirm this/ rule out anything malignant?
A 
Alcohol abuse
AAT>ALT
Gammaglutamyltransferase (raised)
Low Platlets
USS- Fatty Liver
113
Q

What is hepatic encephalopathy? When does it occur? What can cause it? How do you treat it?

A

Liver Fails- Nitrogenous waste (eg./ ammonia) builds up in the system - brain, astrocytes work to clear it- clearing converts glutamate- glutamine- osmotic imbalance
=cranial oedema (confusion, slurred speech), flapping tremor
Infection, Drugs, Constipation, GI bleed
(if looking for a GI cause exclude infection, hypoglycaemia + inter cranial bleed)
Treat- Clear out bowel (lactose, enemas) + antibiotics + 20 degree angle

114
Q

How is liver failure graded?

A

1(mild confusion)- 4 (coma)

115
Q

How is spontaneous bacterial peritonitis defined? How do you treat?

A

Neutrophil count >0.25x10,9/L
Protein <25g/L
+ abdominal pain, fevers, rigors, sepsis (tacky, high temp), renal impairment

Treat-
IV antibiotics, Ascitic fluid drainage (culture), IV albumin infusion

116
Q

How does alcoholic hepatitis present? How do you treat it?

A

Jaundice (raised bilirubin), Encephalitis, Infection (common), Decompensated Hepatic function (Plasma LFTS raised, low albumin + Inc prothrombin) Alcohol history (inc GGT)
Treat- mostly supportive (poor prognosis) Can treat infection (antibiotics), encephalopathy (clear out bowels), steroids (if GCS >9 but watch for GI bleed)

117
Q

What are the 2 types of fatty liver? How are they diagnosed and treated?

A

NAFLD- non-alcoholic fatty liver disease- fibrosis + cancer
NASH-non-alcoholic steatohepatitis (fat + inflammation related to diabetes, obesity, hypercholestrolaemia) +/- fibrosis= cirrhosis.
Diagnose via inflammatory markers (ELF, cytokeratin 18), US, Fibroscan, CT, MRI Spectrroscopy (quantify fat), biopsy.
Treat via diet + exercise + insulin sensitisers + vit E

118
Q

What happens in chronic liver failure?

A

6mnth history
Alcohol/ Hepatitis (B+C)/ Autoimmune/ NAFLD/ Drugs, CF/ Portal Hypertension/ Sarcodosis
Normally sinusoid fenestrations allow free passage of nutrients + toxins into the liver, cirrhosis blocks this not allowing cells in so increases pressure + toxin build up systemically
= jaundice, hepatic encephalopathy (flap), ascites, Inc JVP

119
Q

What are variceal haemorrhages? When do they occur and how do you treat them?

A

Inc in portal tension (ascites, liver failure)
See caput medusa (belly), oesophageal, rectal and gastric manifestations
EMERGENCY if burst- IV, resuscitate, transfusion, endoscopy (band lesion + TIPPS to stop further bleeding)

120
Q

What is the most common carcinoma of the liver?

A

Hepatocellular carcinoma (Hep B+C association)
AFP tumour marker, US, MRI (staging) biopsy is rare
Resect- Transplant

121
Q

What are the 3 types of jaundice + how are they caused?

A

Jaundice- yellowing of skin, sclera + urine- due to excess bilirubin- 34µmol/L (double normal)

  1. Prehepatic-unconjugated, inc quantity of bilirubin. Splenomeagly, anemia, choleric jaundice
  2. Hepatic- conjugated, defective uptake. Ascites, gynacomastia, encephalopathy (liver disease)
  3. Post- Hepatic- conjugated, defective transport via biliary ducts. Palpable gallbladder (abdominal pain), cholestasis (puritis, pale stools, coloured urine)
122
Q

What is a differential diagnosis for jaundice? How can you tell them apart?

A

Carotenimia,no yellow sclera

123
Q

What is alcholuric jaundice? When does it occur?

A

Jaundice due to high levels of UNCONJUGATED bilirubin (hasn’t been conjugated by liver) so no bile pigments, associated with splenomegaly + anaemia

124
Q

A Pt presents jaundiced with an enlarged spleen. What LFTs would you concentrate on and what would you expect to see to confirm your clinical diagnosis?
What’s your differential CLINICAL diagnosis?

A

Pre-hepatic jaundice
Bilirubin levels normal- Non-conjuagated as hasn’t passed liver
Platlet Count- low as splenomegaly so platelets stuck
Treat via splenectomy
Differential- carotemia (sclera won’t be jaundice)

125
Q

What liver cells does hepatitis attack?

A

Hepatocytes- destroys liver function

126
Q

What are the types of hepatitis and how are they classified?

A

A + E= Return to normal
B+C= progression to chronic liver failure
D= only in presence of B

127
Q

What can cause acute liver failure?

A

Hepatitis
Drugs eg./ Paracetamol
Alcoholic Liver Disease (excess alcohol- fatty change- inflammation- cell death- failure/ cirrhosis
Jaundice (Inc in circulating bilirubin)

128
Q

How is haemoglobin broken down?

A

In the SPLEEN- Haem + Globin
Haem- Bilirubin- Circulation(prehepatic) - uptake by hepatocytes in LIVER- conjugated by hepatocytes (more water soluable)- BILIARY SYSTEM- breakdown INTESTINE (post hepatic)- enterohepatic circulation- reabsorped

129
Q

What can cause pre-hepatic jaundice?

A

Inc release of haemoglobin (haemolysis)

130
Q

What can cause hepatic jaundice?

A

Conjugated

  1. Cholestasis- accumulation of bile in ducts/ hepatocytes (hep, alcohol, drugs)
  2. Intra-Hepatic Biliary Obstruction
  3. Primary Biliary Cholangitis- autoimmune (serum alkaline) granulomatous inflammation- cell death- failure/cirrhosis
  4. Primary Sclerosing Cholangitis- Chronic inflammation + fibrosis of bile ducts- loss- cirrhosis- cholingocarcinoma (at risk if IBS)
  5. Hepatic Cirrhosis- End stage of chronic liver disease (hep B+C, alcohol, obesity, autoimmune, DM, Inc iron + copper) replaces normal liver structure, altered liver function- failure; abnormal blood flow- portal hypertension (varices, splenomegaly) Inc risk of hepatocellular carcinoma
  6. Tumours- hepatocelluar carcinoma (malignancy of hepatocytes), cholangiocarcinoma (malignancy of bile duct epithelia), mets
131
Q

What can cause post- hepatic jaundice?

A
  1. Cholethasis (gallstone)- obesity, diabetes

2. Extrahepatic Bile Duct Obstruction

132
Q

What is Cholethiasis? What are the risk factors? How does it present acutely + chronically?

A

Gallstones- Female, Fat, Fertile + Forty. Cholesterol (obesity, CF, low fat diet)
ACUTE
Inflammation- perforation- biliary peritonitis
PROGRESS
CHRONIC
Chronic inflammation- fibrosis and destruction of gallbladder
Causes post hepatic jaundice

133
Q

What is Extrahepatic Biliary Obstruction?

A 
Obstruction of common bile duct due to-
Cholethiasis
Duct tumour eg./ cholangiocarcinoma
Benign stricture
External compression
No bile excreted into duodenum 
Get infection of bile proximal to obstruction- ascending cholangitis- into liver- secondary biliary cirrhosis
134
Q

What are gallstones commonly made of?

A

Cholesterol +/- a pigment (if haemolytic anaemia/ bile infection eg./ e.coli)

135
Q 
A Pt presents with
Biliary Colic + Back radiating pain
Obstructive Jaundice
Dyspepsia (flatulence)
What are they most likely to have? What investigations would you carry out to confirm your diagnosis?
A

Cholethiasis

Bloods- LFTs. USS/ EUS (sensitive), CT if obstructive jaundice as may block stones

136
Q

What is gallstone illeus?

A

Stone wedged in illeum

137
Q

What is obstructive jaundice?

A

jaundice resulting from blockage of the bile ducts or abnormal retention of bile in the liver.

138
Q

You have diagnosed a Pt with cholethiasis through clinical signs + an USS. How would you now treat them?

A
  1. Non-operative- dissolution acid drink (elderly, for life). Liprotripsy shock waves to break stone (risk of pancreatitis if big/ obstruction)
  2. Operation- open/ mini/ laparoscopic/ sigle-port cholecystectomy (remove gallbladder)
    + drain + IV antibiotics
139
Q

What is biliary atresia?

A

Congenital. Bile/ Cystic/ Both ducts fail to preform- jaundice- need transplant

140
Q

What are choledochal cysts?

A

Congenital cystic dilation of bile ducts (risk of cancer malformation)

141
Q

What is a binary enteric fistula?

A

Between gallbladder and surrounding organs- bile enters- inflammed

142
Q

What 3 tumours can be found the the gallbladder/ biliary apparatus?

A
  1. Choleangiocarcinoma
  2. Gallbladder Cancer
  3. Ampullary Tumour
143
Q

How does choleangiocarcinoma present?

A

Rare, elderly, PSC
Causes: Obstructive jaundice, itching, weight loss etc.
Extrahepatic/ Intrahepatic

144
Q

How would you investigate a suspected biliary cancer?

A

US, EUS, PET CT, MRCP, Angiograph, Cholangioscopy

145
Q

How does gallbladder cancer present?

A

rare + existing gallstones, aggressive

146
Q

How do do you treat ampullarf tumours?

A

In ampulla of vater (opening for common bile duct into duodenum)
Endoscopic excision- pancreatic-duodenal excision

147
Q

What can cause pancreatitis?

A 
Alcohol abuse + Gallstones
Trauma (operative/ ERCP)
Drugs- steriods, diuretics
Virus'- mumps, HIV
Metabolic- Inc calcium, triglycerides, temp
Carcinoma
Autoimmune
Scorpion venom
148
Q

What is the aetiology of acute pancreatitis?

A

Insult- exocrine releases activated pancreatic enzymes- autodigestion- oedema + haemorrhage

149
Q 
A Pt presents with 
Abdominal Pain
Vomiting
Tachycardia
Jaundice
Hypoxia
Hyperlipidemia
Hyperglycaemia + hypovolaemic shock
After an injury to the left hypogastric area.
What is your clinical diagnosis and how would you investigate this?
A

Acute Pancreatitis
Bloods- Amalyase, Lipase, Glucose, Blood Gases, Lipids
AxR (isles) + CxR (pleural effusion)
Abdominal US- pancreatic oedema, gallstones, pseudocyst
CT (contrast enhanced if no renal problems)-shows necrosis

150
Q

How do you treat acute pancreatitis?

A

Hypovolemic- IV Fluids, O2, blood transfusion
Hyperglycemia- insulin
Jaundice (post hepatic)- Cholecystectomy if gallstone + ERCP (risk of precipitating another attack/ chronic)
Necrosis- CT guided aspiration/ necrosectomy
Hyperlipidemia- lipid lower drugs eg./statin

151
Q

What is the difference in symptoms between chronic and acute pancreatitis?

A 
Chronic (staged further)
PAIN (epigastric, bores into back)
Steatorrhea (dec in fat sol vitamins)
Weight loss
Diabetes
152
Q

Main treatment for chronic pancreatitis in Kaush-Whipple procedure. What is this?

A

Anastamoses of let over pancreas and stomach

153
Q

What are the most common carcinomas of the pancreas? How do they present? How are they best investigated and treated?

A

Duct Cell Adenocarcinoma (most common), Carcinosacroma, Cystadenocarcinoma.
Epigastric pain, weight loss, malaise, sterattorhea, subcutaneous fat nodules (tender, mets), jaundice.
Investigate via USS, CT, EUS (fine needle aspiration)
Treat- If mass + jaundice= ERCP + stent- cholesectomy
If Mass - jaundice= EUS (biopsy)- pancreatoducodenectomy (whiles)

154
Q

What is the anatomical landmark that marks ups to lower GI bleeds?

A

Ligament of treiz (suspensory ligament from diaphragm to duodenum)

155
Q 
A Pt presents with
Haematemisis
Malena
Dyspepsia
Reflux
Epigastric Pain
Where is their problem located? What are the common causes of this?
A 
Upper (above ligament of triez)
Cause-
1. Ulcers (peptide most common)
2. Gastritis + Duodenitis
3. Oesophagitis
4. Oesophgeal Varices
5. Malignancy eg./ oesophageal/ gastric cancer
6. Mallowy- Weiss Tear
7. Dieulafoy
8. Angiodysplasia
156
Q

What is the risk factor for ulcers?

A

Peptic most common
Seen anywhere (most common in duodenum)
Risk Factors- H. Pylori, NSAIDS, Smoking + Alcohol
NOTE: Zollinger Ellisons Syndrome is a gastrin secreting pancreatic tumour- causes recurrent duodenal ulcers (endoscopy after 8 weeks)

157
Q

How does osophagitis occur?

A

Bleed in the context of abnormal clotting eg./ Hiatus hernia, alcohol, reflux

158
Q

How do oesophageal varies occur?

A

Liver cirrhosis- portal hypertension- oesophageal, gastric, splenic + rectal

159
Q

What is a Mallowy- Weiss tear?

A

Linear tear at oesophageal- gastric junction (normal heals itself)

160
Q

What is a dieulafoy?

A

large torturous arteriole in stomach wall (usually)

161
Q

What is a angiodysplasia?

A

Small vascular malformation- anywhere. Caused by anticoagulation/ platelets. Chronic occult bleeding eg./ heart valve replacements

162
Q

What can cause a lower GI Bleed?

A

Below ligament of triez

  1. Diverticular Disease
  2. Haemorrhoids
  3. Angiodysplasia
  4. Neoplasia (colonic)
  5. Ischamic Cholitis
  6. Radiation Radiotherapy Protitis
  7. IBD
163
Q

What is Diverticular Disease?

A

Lower GI bleed
protrusion of inner mucosal lining through outer muscle layer- pouch
diverticulosis- presence
diverticulitis- inflammation (can bleed ut usually self limiting)

164
Q

What are haemorrhoids?

A

Enlarged vascular cushions around the anal canal- thrombosed (staining, high fibre diet)- PAINFUL if rupture

165
Q

What kind of neoplasm is commonly seen in the GI tract? What is the first sign of it?

A

Colonic Polyps (usually benign) cause GI bleeding iron deficient anaemia is the first sign

166
Q

What is ischamic colitis?

A

Disruption of blood supply to colon- cramps abdominal pain

Can cause gangrene/ perforation

167
Q

What is radiation radiotherapy parotitis?

A

Radiotherapy (cervical/ prostate cancer)- bleeding + chronic blood loss

168
Q

What is Meckles Diverticulum? Where is it found?

A

Small Bowel

Reminent of vitelline duct/yolk sac bulges into small intestine

169
Q

How do yo manage a major Gi Bleed/ Haemorrhage?

A

Airways
Breathing
Circulation-Transfusion if Hb<7g/L/activebleed
Disability
Exposure- withhold adv medicines eg./ warfrin

170
Q

What is SHOCK?

A

Circulatory collapse resulting in inadequate tissue- oxygen perfusion= global hypo perfusion + tissue hypoxia

171
Q

At what age has your small intestine fully developed?

A

By 11 years of age (250-450cm varies depending on size of individual)

172
Q

List the functions of the small intestine

A
  1. Large surface area- villous (stem cells produced in crypts- migrate to top- drop off into gut
  2. Barrier- immune sampling via Peyers Patches (translocation + monitoring of pathogen) + low bacteria pop (enzymes + bile salts are toxic)
  3. Digestion + Absorption- break down food- pass on nutrients via salivatory amylase and pepsins
173
Q

What enzymes cause breakdown in the small intestine? What are proteins + fats broken down to?

A

Salivatory amalyase + pepsins
Proteins- oligopeptides + aas- absorbed at the brush border via trypsin hydrolysis
Fat- pancreatic lipase- glycerol + free FA- absorbed via lacteal + lymphatic system
Carbs- pancreatic amylase- disaccharides digested at brush border

174
Q

What typical presentation would you see in a Pt with malabsorption/ small bowel disease?

A

Weight Loss
Increased Appetite
Sterratorrhea (pale, foul, floats)
Clubbing + Aprithous (mouth ulcers)- chrons + coeliac

175
Q 
A Pt presents with
Weight Loss
Increased Apetite
Sterratorrhea
Where do you think their problem is located? How would you investigate it?
A

Small Bowel
Bloods- Iron, B12, Folate, Ca, Mg + Vit D
SB Biopsy, MRI enterography (vascularity/ inflammation) OR capsule enterography, CT (functionality)

176
Q

What is Coeliac Disease?

A

Sensitivity to wheat, rye + barley
T Cell autoimmune inflammatory response
Gives diarrohea + constipation, Wind, steratorrhea, nausea/ vomiting, anaemia, ulcers, neurological (coordination), angular stomatis
Diagnosed via Bloods- Antibodies (⍺gliadintransglutamase) + Distal Duodenal Biopsy (gold-standard- see villi thinning)
Treatment is withdrawing gluten from diet (difficult, dietician needed).
VITAL to control gluten as side effects include small bowel lymphoma/ adenocarcinoma, oesophageal carcinoma, colon cancer

177
Q

What can cause malabsorption in a Pt?

A
  1. IBS + IBS
  2. Coeliac
  3. HIV
  4. Whipples (infectious)
  5. Giardia Lamblia- Infectious water parasite
  6. Gastric Surgery/ bypass, short bowel syndrome
  7. Sclerosis + Diabetes (impaired motility)
  8. Pancreatitis/ CF
178
Q

What are inflammatory bowel diseases? Name the 4 of them

A

Chronic inflammation via inappropriate and persistent action of mucosal immune system driven by normal intraluminal flora

  1. IBS- UC + Chrons
  2. Radiation Colitis
  3. Appendicitis
  4. Ischaemic Colitis
179
Q

What is Ulcerative Colitis?

A

IBD- HLA gene thinning Inflammation of rectum (proctitis), one side of colon (left sided colitis) or whole colon (pancolitis)
presents as bloody diarrhoea, abdominal pain + weight loss.
Thinning, ulcers, pseudopolyps, cryptitis (no crypts, submucosal fibrosis), high/ low grade, cobblestone mucosa.
dysphasia- adenoma- carcinoma, perforation + Bleeding are 2 serious dangers
NOTE: Inflammation contained to inside so serosa not damaged
Test- Bloods (FBC, ESR, CRP, culture), Stool (to exlude pathogenic cause), AxR, Erect CxR (perforation), Ba Enema (not diagnostic/ used in severe attacks), Colonoscopy (progression)

180
Q

What is Chrons Disease?

A

IBD- Patchy thickening inflammation anywhere in GIT
Presents as diarrhoea (may be blood depending on where is affected), abdominal pain, weight loss, malabsorption
Thickened, oedematous + fibrotic mesentery due to wrapping fat; narrowed lumen; ulcerations (cobblestone appearance); Cryptitis + abscess’; ulceration; non-caseating granulomas + fibrosis.
Long term= strictures, fistulas, perforation + abscess’ (inc cancer risk)
Test- Bloods FBC, ESR, CRP, ferritin, culture), Colonscopy + rectal biopsy, small bowel enema, barium enema but colonoscopy preferred (asses progression/ extent), MRI

181
Q

What is ischaemic enteritis?

A

Acute arterial occlusion= 02 supply does not meet tissue supply (is gradual occlusions but little effect due to anastomosic circulation)
Atherosclerosis, vasculitis, oral contraceptive and cardiac vegetation (arterial embolism, atherosclerosis/cholestroembolism)
chronically can cause fibrosis and stricturing

182
Q

What is radiation colitis?

A

rectal/ pelvic radiotherapy causes abdominal irritation
Diarrhoea, malabsorption
Impares normal proliferative bowel epithelia (BV + crypts)
Need biopsy to rule out IBD
inflammation- ulcerating necrosis- haemorrhage- perforation- BV destroyed (ischemia- infarction)

183
Q

What is appendicitis?

A

Acute inflammation of the appendix- ischamia due to obstruction
Wall inflammation- pus in lumen- fibropurulent exudate- acute gangrenous (full thickness gangrene + necrosis)

184
Q

Describe the process of cancer of the small bowel

A
  1. Neoplasia
    - Low grade- inc nucleus number + size, dec in muffins
    - High grade- carcinoma in situ (not invasive yet)
  2. +Genetics eg./ FAP, HNPCC + lifestyle + FH + IBD
  3. Colerectal Adenocarcinoma
185
Q

Describe the differences in symptoms between an adenocarcinoma of LHS and RHS of the large bowel

A

RHS-Ascending Colon= anaemic (vague pain, weak + obstruction)
LHS- Descending colon, sigmoid colon, rectum= pass fresh blood, altered bowel habit, difficulty passing stools (due to obstruction)

186
Q

What is the aetiology of IBD?

A 
2 hit hypothesis- environmental trigger + gene susceptibility (GWAS)
Easy test is faecal calprotectin 
< 50 normal
50-200 equivocal
>200 elevated/ inflammation
187
Q

What are the common extra intestinal manifestations of IBD?

A

Eyes- uveitis, conjunctivitis
Joints- Sacrolitis, arthritis, spondylitis
Renal- calculi (chrons only)
Liver- fatty change
Biliary- gallstones, sclerosing cholnagitis
Skin- gangrene, erythema nodosum

188
Q

Colonic Carcinoma is a possible complication of IBD/ Colitis. How do we ensure this doesn’t occur?

A

Survellaince Colonscopy (+ dye spray)
<30 years- 3 yearly
30-40- 2 yearly
>40- annually

189
Q

How do you treat IBD?

A
  1. Aminoglycosides (5ASAs) in maintenance of remission of UC + Chrons (may introduce remission)
  2. Steroids eg./ Prednisolone (4 weeks then 4-8 weeks wean off) in mild/ induce remission
  3. Thiopurines eg./ Azothioprine (maintenance + is steroid sparing. Hepatotoxic so monitor every 8 weeks)
  4. Methotrexate (chrons
  5. Immunosupressants
  6. Biologics
  7. Antibiotics
  8. Elemental feeding-can be as effective as steroids (kids comply, adults don’t)
  9. Surgery- Total Colectomy/pouch surgery
190
Q

What is peritonitis?

A

Perforation of GI/ Biliary Tract/ female genital tract/ abdominal wall/ haemotogenous spread
Leads to a breach of the peritoneum- Infection- Transudates (Inc venous + Fluid pressure) OR exudates (inflammation) entry causing Generalised (rapid, persistent contamination) or Localised (anaerobic growth)

191
Q

How do the symptoms differ depending if the intestinal obstruction is proximal or distal?

A

Proximal ( after stomach)- vomit only (will die before other symptoms)
Distal- (large bowel obstruction)- change in bowel habit, bloating, noise, pain, sick

192
Q

How is abdominal pain characterised?

A

Visceral- poorly localised, systemic upset
Somatic- body wall, torn muscle (sport), accurate localisation as parietal peritoneum.
Reffered- felt in other part of body away from source eg./ McBurneys point in appendicitis
NOTE: Abdominal pain tends to be defined in episodes

193
Q

A Pt presents with episodic abdominal pain. How would you investigate this?

A

Urine, FBC, U+E, LFT

Radiology- US + CT

194
Q

What is the most common cause of colerectal cancer? Where is it most likely to be found? What puts an individual at risk + what is the normal aetiology?

A

2nd leading cause of cancer in western world
95% adenocarcinomas
Most found in colon
Most are sporadic, IBD, diet (dec fibre + calcium, inc alcohol + smoking + red meat), DM but can have hereditary factors
1. FAP- early age
2. HNPCC- 40s non-polyposis (not from existing polyps), mets
3. CRC
Oncogene (K-ras, C-myc) activation- prebenign/malignant colorecatl polyps (loss of tumour suppressor gene FAP + micro satellite instability HNPCC- tubular, villous, indeterminate tubuovillous dysplasia

195
Q

A Pt presents with
Rectal Bleeding
History of altered bowel opening with recent acute obstruction
Iron Deficient anaemia
Weight Loss
Palpable right lower lilac/ hypogastric mass.
What are your differentials and most likely diagnosis? What investigations would you carry out to confirm this?

A

Differentials
R sided obstruction due to iron deficient anemia + mass
Altered bowel habit + acute presentation= growing mass
weight loss= malignant
Most likely colonic adenocarcinoma
Investigate via colonoscopy- therapeutic (polypectomy) + Diagnostic (biopsy- risk of perforation esp if laxative does not clear bowels)
OR Radiological Imaging- Barium enema + CT colonoscopy- diagnostic (cant biopsy)

196
Q

How is a cancer staged?

A 
T1-4= local invasion
N0-N1= lymph node involvement
M0-M1= distant mets
OR
Dukes
A- confined to mucosa
B- muscosa- muscle layer- wall
C- Lymph node involvement
D- distant mets
197
Q

How do you treat colorectal cancer?

A

Adenocarcinoma, colon more common (FAP, HNPCC, CRC
Endoscopic/ local resection- colostomy (stoma needed + take lymph for analysis)
+ chemotherapy (mop up mets/ palliative care)
+ radiotherapy (if rectal)
OR colonic stenting (palliative) to stop obstruction

198
Q

What screening is available to prevent bowel cancer in Scotland?

A

Scottish Bowel Screening
50-74 FOBT(yearly)-+ve-colonscopy
If
FAP- annual colonoscopy from 10y + proctocolectomy (remove rectum + colon) over 16
HNPCC- at 25, 2 yearly colonoscopy
CRC- 5 yearly colonoscopy, then 1 more over 55
IBD- 10 year post diagnosis colonoscopy

199
Q

What congenital ano-rectal condition causes disinhibition of the internal anal sphincter?

A

Hirschprings Myenteric Plexus Deficency

200
Q

A Pt presents with painless fresh blood in stools with no other symptoms
What is your clinical diagnosis? How would you treat this?

A

Haemorrhoids- swollen veins at bottom of rectum + anus
Treat via-
1. Haemorrhoidectomy- can be pain + recurrence
2. Haemorrhoids Artery Ligation- use Us to find arteries supplying + suture closed. Quicker recovery, less pain, lower bleeding risk
3. Stapled Anopexy- staple ano-rectum, used in prolapse, fistula to vagina/ rectal perforation possible

201
Q

A Pt presents with painful fresh blood in their stools.

What is your clinical diagnosis? How would you treat this?

A

Anal fissure- tear/ ulcer in lining of anal canal acute/ chronic >6weeks. Ischaemia is possible
Treat via-
1. GTN cream (suppository, 4-6weeks)
2.CCB to relax sphincter
3. Botulinum Toxin- paralyse sphincter
4. Internal Lateral Sphincterotomy- cut into sphincter to reduce tension in anal canal (if cut too much= incontenence)
5. Anal Flaps- repair fissure with tissue from another body area (chronic treatment/ after childbirth)

202
Q

A Pt presents with back passage pain, swelling + discharge/pus.
What is your clinical diagnosis? How would you treat this?

A

Peri-Anal Abscess
Treat Via-
Incision and drainage- sepsis/ bacteria/ endocarditis are possible side effects

203
Q

How do you treat an anal fistula?

A

Anus- vagina/ bladder/ skin
Treat Via-
Fistulotomy- fistula tract laid open to heal
Fistulectomy- cut out fistulus tract
Seton Suture- silicon string in
Cook SIS- animal tissue to block internal opening of fistula

204
Q

Cancers of the anus are
1. Anal squamous cancer
2. Rectal adenocarcinoma
How are they treated?

A
  1. Anal squamous cancer- radiotherapy

2. Rectal adenocarcinoma- neo-adjuvant chemo + radical laparoscopic resection

205
Q

How is continence controlled? How can it be medically produced?

A 
Pelvic floor (S2,3 + 4) + ano-rectal angle control
Artificial sphincter (inflatable cuff)  OR
Sacral nerve stimulation surgery
206
Q

What is visceral pain?

A

Pain in receptors of smooth muscle, poorly localised

207
Q

What differentiates high from low risk rectal bleeding?

A

Low Risk- <6weeks (transient), <40y/o. Watch + wait

High Risk- >6weeks, bleeding without anal symptoms, abdominal mass, iron deficient anaemia

208
Q

A Pt presents with rectal bleeding. How would you proceed?

A 
Determine if high or low grade (<6weeks, <40)
Endoscopy- colonoscopy + biopsy
Barium Enema
CT/ CT colonography
MRI (mets)
209
Q

Laparotomy vs laparoscopic?

A

Laporotomy is open whereas laporoscopic is keyhole/ port so less invasive + shorter recovery time

210
Q

Briefly describe the different sub-types of hepatitis

A

A- Via FO, sex, blood, DNA virus, enteric. Young, asymptomatic, fever, unwell + jaundice (self limiting). IgM Antibody diagnosis
B- Via parental, blood. Chronic. Causes liver inflammation + cirrhosis. Test via HBsAGinactive form- then IgM/ anti-HBE to see if acute (IgM) or chronic (IgG)
C- Via parental, blood, RNA virus. Chronic. Causes liver cirrhosis
D- Via parents, blood, RNA. Chronic. Faculative (need hep B to get) . Resistant to treatment
E- Via animals eg./ pork. Self limiting
Herpes Simplex- rare, severe acute hepatitis

211
Q

What is autoimmune hepatitis?

A

Inflammatory liver disease (due to T cells directed against autoantibodies)
Autoimmune presentation- fever, malaise, urticarial rash, polyarthritis, pleurisy, glomerulonephritis/ gradual onset jaundice
Investigations- serum bilirubin, Autoantibodies,AST, ALT, alk phos
Treat via- immunosupressions eg./ prednisone and transplant

GI (6 decks)

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