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Year 2 > GI Diseases > Flashcards

GI Diseases Flashcards

1
Q

What is Dsypepsia?

A

It is commonly described as heartburn/ epigastric gnawing, burning or pain.

Dyspepsia is not a diagnosis

It is a group of symptoms which suggest some underlying pathology in the upper GI tract

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2
Q

Symptoms/presentation of Dyspepsia?

A

Oesophageal:

  • Odynophagia
  • Dysphagia
  • Heartburn

Gastric

  • Epigastric pain
  • nausea and vomiting
  • Bloating

General:

  • Weight loss
  • Appetite increase/decrease
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3
Q

Causes of Dyspepsia?

A

Oesophageal causes:

  • GORD
  • Barret’s oesophagus

Gastro-duodenal

  • PUD- gastric and duodenal
  • Gastric cancer
  • Functional dyspepsia

Other causes:

  • Biliary diseases (gall stones)
  • Jaundice
  • Pancreatic diseases
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4
Q

Management of Dyspepsia

A
  • Investigate possible causes for dyspepsia (H pylori, gastric or Oesophageal cancer, Drugs, stress/trauma)
  • Refer for OGD- if meets the criteria
  • Life-style management: Weight loss (if high BMI), Elevate the head while sleeping, Stop smoking, Reduce alcohol consumption
  • Medicinal management: Depends on the cause, Anyone with uninvestigated dyspepsia must be treated with PPI.
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5
Q

WHat is OGD

A

oesophago-gastro-duodenoscopy

sometimes known more simply as a gastroscopy, or endoscopy. This is an examination of your oesophagus (gullet), stomach and the first part of your small intestine called the duodenum

gold standard for investigating dyspepsia.

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6
Q

What is the criteria to be eligible for OGD?

A

>55 years

Dyspepsia

Alarm symptoms:

  • Weight loss- unintentional
  • Persistent GI bleed
  • Difficulty swallowing/ inability to swallow
  • Persistent vomiting
  • Fe deficiency anaemia
  • Epigastric mass
  • Haematemesis
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7
Q

What is the GORD?

A
  • Gastroesophageal reflux disease, also known as acid reflux, is a long-term condition where stomach contents come back up into the oesophagus, resulting in either symptoms or complications. Damage to pylori
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8
Q

Pathology of GORD

A

Three main mechanisms: Poor oesophageal motility decreases clearance of acidic material. A dysfunctional LES allows reflux of large amounts of gastric juice. Delayed gastric emptying can increase the volume and pressure in the reservoir until the valve mechanism is defeated, leading to GORD.

The opening of the LOS results in a backflow/ aspiration of gastric content and acid into the oesophagus causing irritation and inflammation of the lining of the oesophagus. Persistent acid reflux damages the oesophageal mucosa causing complications

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9
Q

Complications of GORD

A

Oesophagitis, Oesophageal stenosis, Barrett’s oesophagus

Hiatus hernia (but note HH does not always cause GORD)

oesophageal adenocarcinoma

ulceration: rarely→haematemesis, melaena,↓F

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10
Q

Symptoms/Presentations of GORD

A
  • Heartburn: related to meals. Worse lying down / stooping, Relieved by antacids
  • Waterbrash
  • Regurgitation
  • May present with odynophagia
  • Nocturnal asthma
  • Chronic cough
  • Laryngitis, sinusitis
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11
Q

Investigations of GORD

A
  • Isolated symptoms don’t need Ix
  • Bloods:FBC
  • CXR:hiatus hernia may be seen
  • OGD if: >55yrs, Symptoms >4wks, Dysphagia, Persistent symptoms despite Rx, Wt. loss, OGD allows grading by Los Angeles Classification
  • Ba swallow:hiatus hernia, dysmotility
  • 24h pH testing ± manometry
    • pH <4 for >4hr
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12
Q

Management of GORD?

A

Lifestyle modifications:

  • Weight loss
  • Stop smoking
  • Reduce alcohol
  • Elevate head while sleeping
  • Small regular meals ≥ 3h before bed
  • Stop drugs: NSAIDs, steroids, CCBs, nitrate

Medications

  • OTC antacids: Gaviscon, Mg trisilicate
  • 1:Full-dose PPI for 1-2mo -Lansoprazole 30mg OD
  • 2:No response→double dose PPI BD
  • 3:No response: add an H2RA -Ranitidine 300mg nocte
  • Control: low-dose acid suppression PR

Surgery

  • Nissen Funoplication : usually laparoscopic approach, mobilise gastric funds and wrap around lower oesophagus. Repai diaphram and close any diaphragmatic hiatus
  • Complications: gast- bloat: inability to belch/vomit. Dysphagia if wrap too tight
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13
Q

Differential Dx for GORD

A
  • Oesophagitis: Infection: CMV, candida, IBD, Caustic substances / burns
  • PUD
  • Oesophageal Ca
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14
Q

What is peptic ulceration?

A

Ulcer in stomach or duodenum - most benign but gastric ulcers can be malignant

  • It is a defect of the gastric/ duodenal mucosa which extends to the muscularis mucosa
  • Gastric ulcer: defect of the gastric mucosa that is >0.5cm and extends to the muscularis mucosa
  • Duodenal ulcer: defect of the duodenal mucosa extending to the muscularis mucosa
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15
Q

Causes of PUD?

A

H pylori infection

H pylori

NSAIDs and aspirin

Stress- also called curling ulcers

Neuroendocrine tumors- Zollinger Ellison tumour

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16
Q

How does H pylori and NSAIDS/aspirin cause PUD?

A

H pylori infection

H pylori🡪 produces Urease🡪 breakdown urea into NH3🡪 creates an alkaline environment that favors bacterial colonization🡪 release of bacterial cytotoxins 🡪 cause damage to the mucosa lining of the stomach

NSAIDs and aspirin

Inhibition of COX 1 and COX2🡪 decreased prostaglandins🡪 decreased mucosal blood flow, inhibition of mucosal epithelium proliferation, decreased HCO3-🡪 Damage to the mucosa–> ulcer

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17
Q

PUD complications?

A

Bleeding from the ulcer is a common and potentially life threatening complication.

Perforation resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).

Scarring and strictures of the muscle and mucosa. This can lead to a narrowing of the pylorus (the exit of the stomach) causing difficulty in emptying the stomach contents. This is known as pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting, particularly after eating.

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18
Q

What is Barret’s oesophagus/metaplsia?

A

when the epithelium is continuously damaged and replaced, the new epithelium of the lower esophagus is gradually replaced by a single layer of columnar cells instead of stratified squamous

It is caused due to chronic acid reflux: acid reflux🡪 damage to the mucosa of the distal oesophagus🡪 intestinal metaplasia

Can be caused due to prolonged bile exposure too

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19
Q

Presentation of Barret’s metaplasia?

A

Appears red as compared to the adjacent pink squamous cell mucosa of the oesophagus

The transition zone (Z line) is shifted upwards

The physiological transformation zone separating the squamous cells from the columnar cells

Pre-malignant change- requires close monitoring

Increased risk of Oesophageal adenocarcinoma

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20
Q

Treatment for Barret’s Oesophagus?

A

PPI

Biopsies to rule out dysplasia and cancer

Low grade dysplasia= need radio-ablation or endoscopy every 6-12 months taking biopsies every 1cm

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21
Q

Investigations for Oesophageal adenocarcinoma

A

Endoscopy

Biopsy

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22
Q

Oesophageal squamous cell carcinoma

  • Oesophageal squamous-cell carcinomas may occur as ______ ________tumors associated with _____ and ______ cancer, due to field cancerization
  • Primary oesophageal cancer however is more commonly an _________
  • Anal cancers are normally ________ _______ ________
A
  • Oesophageal squamous-cell carcinomas may occur as second primary tumors associated with head and neck cancer, due to field cancerization
  • Primary oesophageal cancer however is more commonly an adenocarcinoma
  • Anal cancers are normally squamous cell carcinomas
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23
Q

Adenocarcinoma

  • Stomach is lined by ______ ________ normally
  • Risk factors for cancer = ________, diet, __ ______ ______
  • Two types of gastric adenocarcinoma: _______ vs _______
  • Intestinal type forms glands (polypoid)
A
  • Stomach is lined by glandular epithelium normally
  • Risk factors for cancer = smoking, diet, H pylori infection
  • Two types of gastric adenocarcinoma: Intestinal vs Diffuse type
  • Intestinal type forms glands (polypoid)
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24
Q

Oesophageal adenocarcinoma Pathology?

A
  • It is associated with Barret’s oesophagus
  • Intestinal metaplasia- Tumour produces mucins
  • Tumour mutations in TP53
  • It occurs in the distal colon
  • Hence lymph node spread- gastric and coeliac nodes
  • Usually presents after lymph node metastasis and hence poor prognosis as compared to squamous cell carcinoma
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25
Q

Presentation of Oesophageal ademocarcinoma?

A
  • Usually presents after lymph node metastasis and hence poor prognosis as compared to squamous cell carcinoma
  • The tumour may spread to the gastric cardia
  • Patients usually present with dysphagia, chest pain, progressive weight loss and vomiting
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26
Q

Epidemiology of squamous cell carcionoma

A

Male > female (4:1)

More seen in the African American population

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27
Q

Epidemiology of Oesophageal Adenocarcinoma?

A

Male > female (7:1)

More seen in the Caucasian population

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28
Q

IBD is typically divided into 2 categories:

A

Crohn’s disease and Ulcerative Colitis

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29
Q

Which one is more common UC or Crohns

A

UC is more common than Crohn’s. Common in western/developed countries. Common in young adults

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30
Q

Risk Factors for IBD

A

Smoking (for Crohn’s only),

Family history, NSAID use, Hygiene hypothesis (Reduced biodiversity of commensal bacteria), Oral contraception, White ethnicity

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31
Q

What is Crohn’s disease?

A

Inflammation that can involve one small area of the gut, or multiple areas with normal bowel in between: SKIP LESIONS

AKA Cobblestone appearance

Commonly affects the terminal ileum and ascending colon- resulting in RLQ pain

Transmural Inflammation: Damage extends beyond the submucosal layer and through the depth of the entire intestinal wall (unlike UC)

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32
Q

Patho of Crohns

A

Uncontrolled and unregulated immune response to GIT pathogens, leading to tissue destruction and inflammation

Unregulated inflammation means lots of proteases, platelet activating factor, and free radicals floating around the gastrointestinal tissue which ultimately causes destruction of healthy tissue

It is an immune related disorder. In Crohn disease, the immune system is thought to be triggered by some foreign pathogen in the gastrointestinal tract. Several pathogens have been implicated, like Mycobacterium paratuberculosis as well Pseudomonas and Listeria species

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33
Q

Symptoms of Crohns?

A

Crampy abdo pain (RLQ), watery diarrhoea, steatorrhea, fatigue, fever, weight loss, dysphagia

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34
Q

Complications of Crohns

A

fistulae, abscess, bowel obstruction, perforation, toxic megacolon, kidney stones, Bowel cancer (adenocarcinoma), gallstones

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35
Q

What is Ulerative Colitis?

A

Inflammation will occur in the rectum first, and ascend proximally towards the rest of the colon- leading to LLQ pain

The pattern of inflammation is: circumferential and continuous (goes around the whole lumen)

The degree of inflammation is superficial (affecting the mucosa and submucosa layers only)

It is an autoimmune condition.

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36
Q

Patho fo UC

A

AUTOIMMUNE Th2 mediated rxn, where cytotoxic T cells target abnormal gut bacteria or p-ANCA antibodies, thus eroding the lining of the intestines, and ulceration

The circumferential inflammation can destroy the haustras of the colon leading to a smooth section of colon which is called the “lead pipe” sign.

Prevalent in non-smokers/ex-smokers*

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37
Q

Symptoms of UC?

A

Bloody diarrhoea, LLQ pain, mucus/pus in stool, tenesmus/urgency, pseudopolyps

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38
Q

Classifications of UC

A
  • Proctitis: Just the rectum
  • Proctosigmoiditis: Involves the rectum and sigmoid colon
  • Left sided Colitis: Involves the descending colon up to the splenic flexure
  • Extensive Colitis: Extending to the hepatic flexure
  • Pancolitis/Universal colitis: The entire colon is affected, associated with Backwash Ileatis (inflammation of the terminal ileum)
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39
Q

IBD investigations

A

Bloods

  • Anemia
  • Raised ESR and CRP, WBC, Platelets (same as UC)
  • Hypoalbuminemia
  • B12, iron studies: LOW
  • pANCA- POSITIVE in UC

Stool

  • Faeceal Calprotectin- RAISED
  • released by the intestines when inflamed, and is a useful screening test (> 90% sensitive and specific to IBD in adults)

Other:

Colonoscopy, Sigmoidoscopy, PR exam, US, CT, Barium Enema, Rectal biopsy

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40
Q

Difference between Crohns and UC

A
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41
Q

Tretament for Crohns?

A

Surgery does NOT cure the disease, because the whole GI tract can be involved

Conservative management (smoking cessation for Crohn’s) Pharmacological treatment (don’t need to know this year), Faecal transplantation

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42
Q

Treatment for UC

A

A colectomy or proctolectomy can be curative

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43
Q

What is Diverticulitis?

A

Inflammation of abnormal pouches called diverticula (can develop on the walls of the large intestine, or any other hollow structure). Usually 0.5c,-1cm large

True Diverticula: involve all layers of the intestine

Pseudo diverticula: Muscle layers are not included MOST COMMON

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44
Q

When abdominal outpouching occurs without inflammation, it is called ________

A

diverticulosis

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45
Q

Risk factors for Diverticulitis?

A

Obesity, lack of exercise, low fibre diet, Smoking, Connective tissue disorders (genetic), Family history, NSAIDs, Common in the western world, Elderly, Females

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46
Q

Symptoms of Diverticulitis?

A

Symptoms: MOST CASES ARE ASYMPTOMATIC

  • Lower abdominal pain (sudden onset)- mostly affects the Sigmoid colon- LLQ pain and tenderness
  • Erratic bowel habits
  • Symptoms of infection (fever, tachycardia), Nausea, Diarrhea, Constipation, Fever, blood/mucus in the stool
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47
Q

Investigations and Treatment for Diverticulitis?

A

Raised CRP and ESR, USS, CT, Barium enema, Sigmoidoscopy

Treatment

If less severe: analgesia, Fibre, Antibiotics, Fluid resus

Surgical resection if acutely unwell

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48
Q

What is Coeliac’s disease?

A

An AUTOIMMUNE DISORDER where exposure to gluten causes an autoimmune reaction that causes inflammation in the small bowel. It usually develops in early childhood but can start at any age.

1 in 100 people have it. Family History increases risk to 1 in 10.

49
Q

Pathophysiology of Coeliac’s Disease

A

Gluten is a large molecule, that is broken down to smaller ones in the gut, and it is the breakdown products that are toxic (gliadins). The main toxic peptide is α-Gliadin.

Autoantibodies are created in response to exposure to gluten, which target the epithelial cells of the intestines, leading to inflammation in the small bowel (particularly jejunum)

It causes atrophy of the intestinal villi, and crypt hypertrophy, so the surface of the bowel becomes flattened, and the surface area for absorption becomes greatly reduced (malabsorption)

50
Q

Important antibodies to know for coeliac disease?

A
  1. Anti-TTG (anti-tissue transglutaminase)- attacks TTG, which is responsible for gluten breakdown
  2. Anti-EMA (Anti-endomysial)
  3. DGP (deaminated gliadin peptide)
51
Q

Clinical features of Coeliac Disease

A

Often asymptomatic (can be mistaken for IBS), Steatorrhea, failure to lose/gain weight, abdo pain, cramps, bloating, distension, diarrhoea, fatigue, mouth ulcers, anaemia, dermatitis herpetiformis, osteomalacia, Vit D and calcium deficiency, neurological (ataxia, epilepsy)

52
Q

Coeliac disease diagnosis?

A

Check for total IgA levels whilst on gluten diet

  • Raised Anti-TTG antibodies serology (FIRST LINE)
  • Raised anti-endomysial antibodies
  • deaminated gliadin peptide (DGP) – in cases of patients who have a IgA deficiency

Duodenal Biopsy to confirm

Genetic testing for HLADQ2 and HLADQ8

53
Q

What is IBS?

A
  • Irritable bowel syndrome (IBS) is a group of symptoms—including abdominal pain and changes in the pattern of bowel movements without any evidence of underlying damage (like inflammation, ulcers etc).
  • It has been classified into four main types depending on whether diarrhoea is common, constipation is common, both are common, or neither occurs very often
54
Q

IBD vs IBS?

A

IBD has structural damage to the bowel (ie inflammation, ulceration) in ADDITION to IBS symptoms

55
Q

Diagnosis of IBS

What is the criteria used called

A

Other pathology should be excluded:

  • Normal FBC, ESR and CRP blood tests
  • Faecal calprotectin negative to exclude inflammatory bowel disease
  • Negative coeliac disease serology (anti-TTG antibodies)
  • Cancer is not suspected or excluded if suspected

Symptoms should suggest IBS:

Abdominal pain / discomfort pain for ≥12wks which has 2 of:

  • Relieved by defecation
  • Change in stool frequency (D or C)
  • Change in stool form: pellets, mucu

AND 2 of:

  • Abnormal stool passage: incomplete/urgency
  • Bloating/Distention
  • Worse symptoms after eating
  • PR mucus

ROME CRITERIA

56
Q

Risk factors for IBS

A

Female, stress, gastroenteritis (nota/rotavirus)

57
Q

Treatment for IBS?

A
  • A low FODMAPS diet:

F- fermentable

O- oligosaccharides 🡪 sucrose (Wheat, rye, legumes and various fruits and vegetables, such as garlic and onions.)

D- disaccharides 🡪 lactose (Milk, yogurt and soft cheese)

M- monosaccharides 🡪 fructose (Various fruit including figs and mangoes, and sweeteners such as honey

Andmitriptyline

P- polyols 🡪 sugar free sweeteners ( Certain fruits and vegetables including blackberries and lychee, as well as some low-calorie sweeteners like those in sugar-free gum.)

  • Avoid caffeine and alcohol
  • Probiotics, regular small meals, reduced processed food, physical activity, for constipation: soluble fibres, laxatives, stool softeners, for pain: anti-diarrhoeals (ie loperamide), antimuscarinics, antispasmodics (mebeverine)
  • Manage stress, anxiety and depression- CBT
  • Amitriptyline
58
Q

First, Second and Third line Medication for IBS

A

First Line Medication:

  • Loperamide for diarrhoea
  • Laxatives for constipation. Avoid lactulose as it can cause bloating. Linaclotide is a specialist laxative for patients with IBS not responding to first-line laxatives
  • Antispasmodics for cramps e.g. hyoscine butylbromide (Buscopan)

Second Line Medication:

  • Tricyclic antidepressants (i.e. amitriptyline 5-10mg at night)

Third Line Medication:

  • SSRIs antidepressants
59
Q

Genetic connections with coeliac disease

A

Genetic connections:

HLA-DQ2 gene (90%)

HLA-DQ8 gene

60
Q

What are Gallstones?

Incidence?

RF?

Symptoms

A

Formation of hard stones in the gallbladder

Incidence increases with age. More common in women.

F – Fat

F – Fair

F – Female

F – Forty

Most are asymptomatic and are discovered when they cause biliary colic etc

61
Q

What are the types of gallstones?

A
  • Cholesterol gallstones are the most common stones -supersaturation of bile with cholesterol –Gallbladder stasis -cannot been seen on X-RAY . However if they have enough CaCO3
  • Bilirubin gallstones are the 2nd most common stones: AKA pigmented
  • can be seen on X-RAY as the bilirubin binds to calcium

–associated with : hemolytic disease, E.coli

62
Q

How do Cholesterol stones form?

A
  1. Supersaturated with cholesterol- bile salts and phospholipids cannot handle the cholesterol so they become free flowing in bile causing it to solidify and precipitate out.
  2. To little bile salts and phospholipids- cant break down the cholesterol
  3. Gallbladder stasis- inactivity of bile can separate the cholesterol from the bile solution= solidify
63
Q

How do pigmented stones form?

A
  1. Too much unconjugated (in a form where you cant remove it/absorb it in body) bilirubin- binds to calcium in bile sol and forms calcium bilirubinate

Increase bilibrum is due to increase extravascular haemolysis (macrophages engulf rbc and release unconjugated bilirubin

64
Q

What if the stones are brown in colour?

A
  • sign of infection (caused by bacteria Ecoli)
  • causes calcium + UBC
  • browness is due to hydrolysed phospholipid too in it.
65
Q

What is biliary colic? and where would you find pain?

A

Biliary colic, also known as symptomatic cholelithiasis, a gallbladder attack or gallstone attack, is when a colic (sudden pain) occurs due to a gallstone temporarily blocking the cystic duct.

  • Intermittent RUQ pain that comes in waves
  • Pain MAY radiate to R shoulder tip
  • Typically starts in the evening and lasts till the morning
  • Recurring condition, usually managed with diet adjustment
66
Q

What is Cholecystitis? and where would you find pain?

A
  • Inflammation of the cystic duct due to gallstone obstruction
  • Prolonged colicky pain which MAY radiate to the shoulder tip
  • Inflammation->Fever + leucocytosis
  • Murphy’s Sign. There will be RUQ pain that is usually worse on inspiration.
67
Q

What is Choledocholithiasis? where would you get pain?

A
  • Common bile duct obstruction
  • No inflammation -> no fever or leucocytosis
  • Obstructive jaundice
  • Dilated hepatic ducts
  • RUQ pain> 6h
68
Q

What is Cholangitis? where would you get pain?

A

Infection of the gallbladder and CBD

Charcot triad-> fever, jaundice and RUQ pain

Reynolds triangle -> hypotension (shock) +altered mental status + Charcoat triangle. This occurs when the infection becomes more advanced

RUQ pain

Murphy sign

69
Q

Complications of gallstones?

A
  • Cholecystitis , Acute cholangitis + Mirizzi syndrome
  • Empyema +perforation
  • Jaundice -> obstructive jaundice
  • Acute pancreatitis -> epigastric pain, radiates to the back , curling makes it better
  • Cancer of the gallbladder
  • Gallstone ileus

A bowel obstruction requires immediate medical treatment. If it’s not treated, there’s a risk that the bowel could split open (rupture).

70
Q

What is PRIMARY SCLEROSING CHOLANGITIS

A

Primary (not caused by something else)

Sclerosing (hardening/fibrosis of tissue)

Cholangitis (inflammation of bile ducts)

Disorder caused due to the chronic inflammation of the intra hepatic and extra hepatic bile ducts leading to fibrosis

More commonly occurs in males (around 30-50 years)

71
Q

Causes of PRIMARY SCLEROSING CHOLANGITIS

A

The exact cause is unknown but it has a strong association with autoimmune disesases, especially inflammatory bowel disease (most commonly UC).

In most patients, there is presence of antibodies such as pANCA and ANA antibodies but these are not specific for the disease.

It is linked to HLA DR3 and HLA B8

72
Q

Symptoms and signs of PSC

A

Symptoms

  • Jaundice
  • Pruritus and fatigue
  • Abdo pain

Signs

  • Jaundice: dark urine, pale stools
  • HSM
73
Q

Complications of PSC

A

Bacterial cholangitis

↑Cholangiocarcinoma

↑CRC

74
Q

Ix for PSC

A
  • LFTs:↑ALP initially, then↑BR
  • Abs:pANCA (80%), ANA and SMA may be +ve
  • ERCP/MRCP:“beaded” appearance of ducts
  • Biopsy:fibrous, obliterative cholangitis
75
Q

Associated diseases for PRIMARY SCLEROSING CHOLANGITIS

A

UC

Crohn’s (much rarer)

AIH

HIV

76
Q

WHat is PRIMARY BILIARY CHOLANGITIS?

A

Disorder caused due to the chronic inflammation of the intra hepatic bile ducts leading to fibrosis

More commonly occurs in females (around 30-65 years)

77
Q

Presentation of PRIMARY BILIARY CHOLANGITIS

Think of PPBBCCS

A
  • Often asympto and Dx incidentally (↑ALP)
  • Jaundice occurs late
  • Pruritus and fatigue
  • Pigmentation of face
  • Bones: osteoporosis, osteomalacia (↓vit D)
  • Big organs: HSM
  • Cirrhosis and coagulopathy (↓vit K)
  • Cholesterol↑: xanthelasma, xanthomata
  • Steatorrhoe
78
Q

Sclerosing Cholangitis vs Biliary Cirrhosis

A
79
Q

What is appendicitis?

causes?

A

Inflammation of the appendix

Can occur at any age but most commonly in the elderly or in the 2nd decade of life.

It is due to the obstruction of the appendix lumen by hyperplasia of the lymphoid tissue, feces, worms, foreign body etc.

80
Q

Patho of appendicitis?

A

Once the lumen is obstructed, it can lead to bacterial overgrowth, ischemia, inflammation etc.

If untreated, it can lead to necrosis, peritonitis, gangrene, perforation etc

81
Q

Pain in Appendicitis?

Visceral pain

A

n the early stages, the pain will be poorly localized to the periumbilical or epigastric region. This is because the organ is poorly innervated by the lesser splanchnic nerves which localise the pain to the centre of the abdomen.

82
Q

Pain in Appendicitis?

Somatic pain

A

In the later stages, as the inflammation becomes worse, it spreads to the parietal peritoneum in that area, so the pain can be localized. This is because the peritoneum is supplied by the same nerve as the respective dermatome.

So, initial pain will be in the periumbilical region and then will localize to the RIF as the inflammation becomes worse

83
Q

How is the pain in appendicitis described?

A

It is described as constant and sharp

84
Q

What is Mcburney’s point?

A

2/3’s of the way along an imaginary line from the umbilicus to the anterior superior iliac spine on the right hand side

85
Q

What is Rovsing’s Sign?

A

pain felt in the LRQ when the LLQ is palpated

86
Q

Psoas sign –

A

increased pain during passive extension of the right hip

87
Q

Obturator sign

A

pain felt on passive internal rotation of the flexed hip

88
Q

what does Washboard ridgidity

A

This shows that there is peritonitis. the pain is exacerbated by the slightest movement (e.g. rolling, coughing, even breathing) as this moves the peritoneum.

89
Q

Characteristics fo autoimmune hepatitis?

A
  • Increased IgG levels
  • Antibodies against:

Liver specific proteins

Non-live specific proteins

Mononuclear infiltrate within the liver:

Monocytes, macrophages, lymphocytes, plasma cells, macrophages and mast cells

90
Q

Key definitions relating to gallbladder and gallstones?

  • Cholestasis
  • Cholelithiasis:
  • Choledocholithiasis:
  • Biliary colic:
  • Cholecystitis:
  • Cholangitis:
  • Gallbladder empyema:
  • Cholecystectomy:
  • Cholecystostomy:
A
  • Cholestasis: blockage to the flow of bile
  • Cholelithiasis: gallstone(s) are present
  • Choledocholithiasis: gallstone(s) in the bile duct
  • Biliary colic: intermittent right upper quadrant pain caused by gallstones irritating bile ducts
  • Cholecystitis: inflammation of the gallbladder
  • Cholangitis: inflammation of the bile ducts
  • Gallbladder empyema: pus in the gallbladder
  • Cholecystectomy: surgical removal of the gallbladder
  • Cholecystostomy: inserting a drain into the gallbladder
91
Q

atients with gallstones and biliary colic are advised to avoid fatty foods to prevent CCK release and gallbladder contraction.

TRUE OR FALSE

A

TURE

92
Q

Ix for gallstones

A

LFTs- raised bilirubin, ALP

USS- first line

93
Q

In a raised ALT and AST with higher rise in ALP , this suggest?

A

cholestasis an”obstructive picture”

94
Q

If ALT and AST are high compared with the ALP level, this is more indicative of…

A

a problem inside the liver with hepatocellular injury “a hepatitic picture”

95
Q

A raised ALP is consistent with ______ ___________ in presence of right upper quadrant pain and/or jaundice.

A

A raised ALP is consistent with biliary obstruction in presence of right upper quadrant pain and/or jaundice.

96
Q

What is (MRCP)

A

A magnetic resonance cholangio-pancreatography (MRCP) is an MRI scan with a specific protocol that produces a detailed image of the biliary system. It is very sensitive and specific for biliary tree disease, such as stones in the bile duct and malignancy.

MRCP is used in a number of scenarios for gaining a detailed picture of the biliary system, such as identifying biliary strictures or congenital abnormalities.

With gallstone disease, MRCP is typically used to investigate further if the ultrasound scan does not show stones in the duct, but there is bile duct dilatation or raised bilirubin suggestive of obstruction.

97
Q

What is ERCP

Complications

A

An endoscopic retrograde cholangio-pancreatography (ERCP) involves inserting an endoscope down the oesophagus, past the stomach, to the duodenum and the opening of the common bile duct (the sphincter of Oddi). This gives the operator access to the biliary system.

The main indication for ERCP is to clear stones in the bile ducts.

Key complications of ERCP are:

  • Excessive bleeding
  • Cholangitis (infection in the bile ducts)
  • Pancreatitis
98
Q

Complications of cholecystectomy include:

A
  • Bleeding, infection, pain and scars
  • Damage to the bile duct including leakage and strictures
  • Stones left in the bile duct
  • Damage to the bowel, blood vessels or other organs
  • Anaesthetic risks
  • Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
  • Post-cholecystectomy syndrome
99
Q

What is Post-cholecystectomy syndrome

A

Post-cholecystectomy syndrome involves a group of non-specific symptoms that can occur after a cholecystectomy. They may be attributed to changes in the bile flow after removal of the gallbladder. Symptoms often improve with time. Symptoms include:

  • Diarrhoea
  • Indigestion
  • Epigastric or right upper quadrant pain and discomfort
  • Nausea
  • Intolerance of fatty foods
  • Flatulence
100
Q

What is Wilson Disease?

How is it inherited?

What gene and what chromosome?

A

Wilson disease is the excessive accumulation of copper in the body and tissues. It is caused by a mutation in the “Wilson disease protein” on chromosome 13. The Wilson disease protein also has the catchy name “ATP7B copper-binding protein” and is responsible for various functions, including the removal of excess copper in the liver. Genetic inheritance is autosomal recessive.

101
Q

Patho of Wilson’s Disease

A
  • Mutation of Cu transporting ATPase
  • Impaired hepatocyte incorporation of Cu intocaeruloplasmin and excretion into bile.
  • Cu accumulation in liver and, later, other organ
102
Q

Clinical Features of Wilson disease?

think of CLANKAH

A

Cornea

  • Kayser-Fleischer rings (70%, may need slit-lamp)

Liver Disease

  • Children usually present c̄acute hepatitis.
  • Fulminant necrosis may occur
  • →cirrhosis

Arthritis

  • Chondrocalcinosis
  • Osteoporosis

Neurology

  • Parkinsonism:bradykinesia,tremor, chorea, tics
  • Spasticity, dysarthria, dysphagia
  • Ataxia
  • Depression, dementia, psychosis

Kidney

  • Fanconi’s syn. (T2 RTA)→osteomalacia

Abortions

Haemolytic anaemia

  • Coombs’ negative
103
Q

Copper deposition in the liver leads to ____ _____ and eventually liver cirrhosis. Copper deposition in the ______ _____ ______ can lead to neurological and psychiatric problems.

A

Copper deposition in the liver leads to chronic hepatitis and eventually liver cirrhosis. Copper deposition in the central nervous system can lead to neurological and psychiatric problems.

104
Q

Ix of Wilson Disease?

A
  • Bloods:↓Cu,↓caeruloplasmin

NB. Caeruloplasmin is an acute-phase protein and maybe high during infection. It may also be low protein-deficient states: nephroticsyndrome, malabsorption

  • ↑24h urinary Cu
  • Liver biopsy:↑hepatic Cu
  • MRI:basal-ganglia degeneration
105
Q

Management for wilsons disease

A

Treatment is with copper chelation using:

  • Penicillamine (lifelong)
  • Trientene
106
Q

eating typically worsens the pain of ______ ulcers and improves the pain of _________ ulcers.

A

eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

107
Q

Management for peptic ulcer?

A

Peptic ulcers are diagnosed by endoscopy. During endoscopy a rapid urease test (CLO test) can be performed to check for H. pylori. Biopsy should be considered during endoscopy to exclude malignancy as cancers can look similar to ulcers during the procedure.

Medical treatment is the same as with GORD, usually with high dose proton pump inhibitors. Endoscopy can be used to monitoring the ulcer to ensure it heals and to assess for further ulcers

108
Q

What is hiatus hernia

A

A hiatus hernia is when part of your stomach moves up into your chest. It’s very common if you’re over 50. It does not normally need treatment if it’s not causing you problems

109
Q

Explain the classification of Hiatus Hernia?

A

Sliding (80%)

  • Gastro-oesophageal junction slides up into chest
  • Often assoc. c̄GORD

Rolling (15%)

  • Gastro-oesophageal junction remains in abdomen but abulge of stomach rolls into chest alongside theoesophagus
  • LOS remains intact so GORD uncommon
  • Can→strangulation

Mixed (5%)

110
Q

Ix for Hiatus Hernia

A
  • CXR:gas bubble and fluid level in chest
  • Ba swallow: diagnostic
  • OGD: visualises the mucosa but can’t exclude hernia
  • 24h pH + manometry:exclude dysmotility or achalsia
111
Q

Tx for Hiatus Hernia

A
  • Lose wt.
  • Rx reflux
  • Surgery if intractable symptoms despite medical Rx.-Should repair rolling hernia (even if asympto) as it may strangulate
112
Q

What is hereditary haemochromatosis

How is it inherited

What gene on what chromonsome:

A

Hereditary hemochromatosis (he-moe-kroe-muh-TOE-sis) causes your body to absorb too much iron from the food you eat. Excess iron is stored in your organs, especially your liver, heart and pancreas. Too much iron can lead to life-threatening conditions, such as liver disease, heart problems and diabetes

AR

HFE gene (High FE) on Chr6 (C282Y

113
Q

Patho haemochromatosis

A
  • Inherited, multisystem disorder resulting from abnormaliron metabolism.
  • ↑intestinal Fe absorption (↑enterocyte DMT +↓hepatocyte hepcidin)→deposition in multiple organ
114
Q

Clinical features of Haemochromotosis

A

Myocardial

  • Dilated cardiomyopathy
  • Arrhythmias

Endocrine

  • Pancreas: DM
  • Pituitary: hypogonadism→amenorrhoea, infertility
  • Parathyroid: hypocalcaemia, osteoporosis

Arthritis

  • 2ndand 3rdMCP joints, knees and shoulders

Liver

  • Chronic liver disease→cirrhosis→HCC
  • Hepatomegaly

Skin

  • Slate grey discolouration
115
Q

Ix of Haemochromatosis

A
  • Bloods:↑LFT,↑ferritin,↑Fe,↓TIBC, glucose, genotype
  • X-ray:chondrocalcinosis
  • ECG, ECHO
  • Liver biopsy:Pearl’s stain to quantify Fe and severity
  • MRI:can estimate iron loading
116
Q

Treatment for haemochromotosis

A

Iron removal

  • Venesection: aim for Hct <0.5
  • Desferrioxamine is 2ndline

General

  • Monitor DM
  • Low Fe diet

Screening

  • Se ferritin and genotype
  • Screen 1stdegree relatives

Transplant in cirrhosis

117
Q

Associated diseased with primary bilary cirrhosis ?

A

rimary biliary cholangitis is associated with metabolic or immune system disorders, including thyroid problems, limited scleroderma (CREST syndrome), rheumatoid arthritis, and dry eyes and mouth (Sjogren’s syndrome)

118
Q
A

Year 2 (33 decks)

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