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BDS2 > GI & Hepatology > Flashcards

GI & Hepatology Flashcards

1
Q

How is formed acid eliminated in upper GI disease?

A

By drugs called antacids - most are alkaline so neutralise the stomach dyspepsia, non-systemic-, calcium, magnesium and aluminium based, systemic- sodium bicarbonate

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2
Q

How is acid secretion reduced in upper GI disease?

A

By drugs such as
- H2 receptor blockers (dines - e.g cimetidine, ranitidine) - reduce acid production as antagonist to histamine h2 receptor, ACh and gastrin pathways still produce acid

  • Proton pump inhibitors (zoles - omeprazole, lansoprazole) - block the ACh, gastrin and histamine pathways to the H+/K+ ATPase proton pump which catalyses the final step in gastric acid
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3
Q

What are a few oral diseases of GI nature?

A

Recurrent oral ulceration

Lichen Planus - chronic
inflammatory autoimmune disease which results in white lacy patches and sores

Orofacial granulomatosis - resulting in cobblestoning and fissuring of the oral mucosa, it is an oral manifestation of crohn’s disease

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4
Q

What are 5 oesophageal disorder?

A 
Dysphagia
GORD
Barrett's Oesophagus
Hiatus Hernia
Peptic ulcer disease
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5
Q

What is dysphagia in relation to the oesophagus?

A

Compression of the oesophageal wall

Functional dysphagia is the sensation of solid/liquid foods sticking, lodging or passing abnormally through the oesophagus - oesophagitis, carcinoma of oesophageal wall, stricture

dysmotility - stroke, achalisa (failure of peristalsis and lower oesophageal sphincter relaxation)

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6
Q

What is GORD?

A

Gastro-oesophageal reflux disorder

Caused by defective oesophageal sphincter, impaired lower clearing, impaired gastric emptying

Causes ulceration, inflammation and metaplasia

Signs/symptoms - epigastric burning (worse lying down, bending, pregnancy), dysphagia, GI bleeding, severe pain (oesophageal muscle spasm, mimics MI pain)

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7
Q

What is barrett’s oesophagus?

A

Reccurrent acid reflux, lower oesophagus
Metaplasia of oesophageal lining (stratified squamous to simple columnar)
Adenocarcinoma results in some cases

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8
Q

What is hiatus hernia?

A

Part of stomach goes up diaphragm into thorax
Symptoms like GORD
More common in women
Classed as sliding (up/down) or rolling (paraoesophageal)

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9
Q

What is peptic ulcer disease?

A

any acid affected site
causes - high duodenal acid secretion, normal acid secretion, NSAIDs/Steroids
Helicobacter pylori eats away at mucosal layer forming a gatric ulcer
Perforated ulcer - GI bleed
Chronic inflammation can lead to gastric lymphoma
Often asymptomatic
Can lead to systemic anaemia, investigated by FOB (faecal occult blood test)
Treated by surgery/lifestyle change
Treated with medications, triple therapy; antibiotics (amoxycillin, metronidazole) and PPI - omeprazole, bismuth salts

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10
Q

What is a commensal bacteria and what are examples in GI infections?

A

Commensal - living in a relationship in which one organism derives food or other benefits from another organism without hurting it, commensal bacteria are normal flora in the mouth.

Bacteroides Fragilis - fermentation of carbohydrates, utilisation of nitrogenous substances, and biotransformation of bile acids and other steroids

Escherichia coli (vitamin K production)

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11
Q

What is an example of a pathogenic bacteria in GI infections?

A

Helicobacter Pylori - duodenal ulcers, gastric ulcers, increased risk of adenocarcinoma, PUD

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12
Q

What is gastroenteritis and what are the 3 ways it can occur?

A

Inflammation of the GI tract - the stomach and small intestine.

Can occur virally (rotavirus, norovirus, calicivirus) - if viral may experience cramps, vomiting, watery diarrhoea, myalgias (muscle pains), fever or headaches.

Can occur due to bacteria (salmonella, shigella, campylobacter, clostridium difficile) - small volume stools, fever, tenesmus (feeling of incomplete defaecation), bloody mucoid stools, suprapubic pains.

Can also occur due to parasitic origin (Giardia lamblia, entamoeba, cryptospordium)

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13
Q

What are the signs and symptoms of salmenellosis?

A
  1. gastroenteritis
  2. enteric fever (typhoid fever)
  3. bacteraemia

Caused by eating food from infected animals

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14
Q

What is pseduomembranous colitis, how does the disease process work and what is the treatment plan?

A

Inflammation of the large instestine (colon) due to overgrowth of C.difficle.

  1. antibiotic therapy
  2. alteration of colonic microflora
  3. c.difficile exposure and colonisation
  4. release of toxin A+B
  5. colonic mucosal injury and inflammation
  6. Pseudomembranous colitis

Treatment:

  • ORT
  • Antibiotics (vancomycin, metronidazole)
  • Probiotics
  • Colectomy
  • Faecal transplants
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15
Q

What is the aetiology of Crohns disease?

A

Granulamotous inflammation (food intolerance, persisting viral/immune process)

Johne’s disease - infection w/ mycobacteria (M. paratuberculosis)

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16
Q

What are the symptoms of crohn’s disease?

A

Colonic disease - same as UC

Small bowel disease - pain, malabsorption, obstruction, anal disease

Mouth - OFG (w/ severe gingivitis)`

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17
Q

Where does crohn’s disease affect?

A

Anywhere from the mouth to the anus

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18
Q

What are the features of crohn’s disease?

A
  • Discontinous
  • Rectum 50%
  • Anal fissures 75%
  • Ileum 30%
  • Mucosal cobbing + Fissures
  • Narrowed lumen, thickened wall
  • Non vascular
  • Serosa inflamed
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19
Q

What are the microscopic features present in crohns disease?

A

Transmural (present along full wall of an organ)

Oedematous

Granulomas

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20
Q

What are the sites of ulcerative colitis and what is the condition called?

A

Proctitis - rectum only

Proctosigmoiditis - Rectum and sigmoid colon (lower colon before rectum sigmoid shape)

Distal colitis - full left side of the colon up to transverse colon

Pancolitis - involves entire colon

Backwash Ilietis - involves distal ileum of small bowel

21
Q

What are the symptoms of ulcerative colitis?

A
  • Abdominal sounds
  • Diarrhoea
  • Fever
  • Weight loss
  • Malnutrition
  • Dehydration
22
Q

What are the microscopic features of ulcerative colitis?

A
  • Mucosal only
  • Vacular
  • Mucosal abcesses
23
Q

What are the features of ulcerative colitis?

A
  • Continuous
  • rectum always involved due to colonic primary
  • anal fissures 25%
  • ileum 10%
  • mucosal granulomatosis +_ ulcers
  • vascular
  • serosa normal
24
Q

What is the treatment for ulcerative colitis?

A

IBD treatment:

Systemic steroids (prednisalone)

Local steroids - rectal disease, colorectal

AIDs (zines - mesalazine, sulphalazine) - 5-ASA based

NS immunosuppressants - Azathioprine, methotrexate

Anti-TNF alpha therapy (Mabs - infliximab, adalimumab)

25
Q

What are the main issues involved with the liver?

A

Viral liver disease
Jaundice
Cirrhosis
Liver failure

26
Q

How does the hepatobiliary system work?

A

Bile made in the liver
Secreted into the canaliculi, through liver biliary tree
Merge to common hepatic duct
CHD joins cystic duct from gall bladder = common bile duct
Pancreatic duct + CBD = ampulla of vater
Enters duodenum

27
Q

What is jaundice?

A

Accumulation of bilirubin in the skin
Bilirubin is one of the end products of haem catabolism
Usually conjugated in the biliary tree
Passed out as stercobillin (gives faeces its colour)

28
Q

What are the featurs of pre-hepatic jaundice?

A

Increased haem load

Excessive bilirubin from either haemolytic anaemia, post blood transfusion where the match is poor, or induced neonatally from maternal RBCs

Difficult for bile to conjugate all bilirubin

  1. Haemolytic - increased bilirubin beyond the livers ability to conjugate it
  2. Gilbert’s disease - decreased bilirubin uptake by liver cells, therefore less is conjugated than normal
29
Q

What are the features of hepatic jaundice?

A

Due to liver failure
Drug induced liver dysfunction, prevents metabolism of RBC products

  1. Impaired enzyme action - unconjugated bilirubin doesnt get metabolised by liver cells but instead continues to pass through systemic circulation and not through biliary tree
  2. Secretion failure - unconjugated bilirubin is metabolised by liver cell enzymes, but cannot be secreted into biliary tree canaliculi, meaning conjugated bilirubin passes into the systemic circulation
30
Q

What are the features of post-hepatic jaundice (obstructive jaundice)?

A

Bilirubin conjugated as normal through liver cells from blood, but when they flow into canaliculi there is an obstruction which causes backflow of conjugated bilirubin into blood

Pale stool and dark urine often indicative of post hepatic jaundice

Can be either intra or extra hepatic

31
Q

What are the features of neonatal jaundice?

A
  • Haemolytic jaundice (rhesus incompatability)

- Crigler-Najjar syndrome (caused by kernicterus, brain and nerve damage by hyperbilirubinaemia)

32
Q

What are the clinical features of jaundice?

A
  • Conjugated bilirubin in urine and faeces

- Appear normal in haemolytic jaundice as bilirubin unconjugated

33
Q

What is the treatment for jaundice?

A
  • cholecystectomy
  • ursodeoxycholic acid and low calorie/cholesterol diet to reduce bile acid
  • Colerstyramine (prevents bile acid reabsorption from GI tract)
34
Q

What are gall stones?

A
  • Gall stones
  • Can block biliary tree
  • Form within the gall bladder
  • Inflammation (acute cholecystitis)
  • Can move out of biliary tree
35
Q

What are the symptoms of gallstones?

A
  • Pain in shoulder tip
  • RHS abdo pain (through to back)
  • Fatty food triggers pain (contraction of gall bladder)
  • Cholangiocarcinoma in rare patients
36
Q

What population is gallstones likely to affect?

A
  • Fair
  • Fertile
  • Female
  • Fat
  • Forty
37
Q

How do we treat gallstones?

A

Endoscopic retrograde cholangiopancreatography (ERCP) is a procedure that combines upper gastrointestinal (GI) endoscopy and x-rays to treat problems of the bile and pancreatic ducts.

38
Q

What are the features of pancreatitis and Cystic Fibrosis?

A

Oral enzyme supplements can be used to treat (pancreatic amylase, trypsin, lipase, nuclease, nucleosidase)
Alcohol prominent in aetiology
Mumps virus can cause pancreatitis
Diabetes consequence of chronic pancreatitis disease (pancreatitis = reduced insulin output = hyperglycaemia)

39
Q

What are the clinical features of acute liver failure?

A
  • URHS abdo pain
  • Jaundice
  • Abdo swelling
  • Peripheral oedema

Usually arises from paracetemol poisoning

Acute-on-chronic - chronic liver failure that has decompensated

Fulminant hepatic failure - encephalopathy after 8 weeks

40
Q

What are types of chronic liver failure?

A

Cirrhosis - arises from alcohol, primary biliary cirrhosis, chronic active/autoimmune hepatitis, haemoachromatosis, cystic fibrosis

Primary liver cancer
Secondary liver cancer (metastases)

Loss of function - Synthetic/Metabolic

41
Q

What are the signs and symptoms of chronic liver failure

A

Signs - often none - large/small liver, portal hypertension (inc venous pressure due to vascular resistance from cirrhosis) - ACUTE BLEED

  • Jaundice
  • Ascities
  • Peripheral oedema
  • Encephalopathy
  • Spider Naevi + Palmar Erythema (from portal hypertension)
  • Oesophageal varices (from portal hypertension)
42
Q

How do synthetic and metabolic loss of function of the liver differ?

A

Synthetic :

Plasma proteins
- Transport protein reduced, imporant in drug doses
- Immunoglobulins (reduced) infection risk increased
Clotting factors
- Increased bleeding tendency

Metabolic:

  • Drug metabolism (esp 1st pass) drug just keeps circulating
  • Detoxification
  • Conjugation of RBC breakdown products
43
Q

What are things to note in terms of hepatology in relation to dentistry?

A

*INR of 1.1-1.3 abnormal for liver disease patients
Platelets - make sure normal
Reduce drug dosage
Antifungals - miconazole, erythromycin, tetracycline
Analgesics - paracetemol safest, NSAIDs increase bleed risk
IV sedation - avoid, liver cant clear sedative property so continues to circulate
LA - OK as metabolised in plasma not liver

44
Q

What is coeliac disease?

A

Sensitivity to the alpha-gliaden component

Caused by

  • Genetic causes (DQW2 allele)
  • T lymphocytes (autoimmune infiltration of crypts of leiberkuhn)
  • Villous atrophy and crypt hyperplasia of small colon from T lymphocytes
  • Results in malabsorption = due to reduced surface area

Oral ulceration can also occur coccurently w/ coeliac disease

45
Q

What are the symptoms of coeliac disease?

A
  • Weight loss
  • Lassitude/weakness
  • Apthae/Glossitis
  • Steatorrhea
  • Dysphagia
  • Diarrhoea
  • Abdominal pain/swelling
46
Q

How does a gluten free diet affect coeliac disease?

A

Reverses jejunal atrophy
Improved wellbeing
Reduced risk of lymphoma

47
Q

What is dermatitis herpetiformis and how is it associated w coeliac disease?

A

DH is an autoimmune skin condition linked to coeliac disease
Has oral manifestation
Granular IgA deposit in skin and mucosa

48
Q

What is apthae and how is it associated w coeliac disease?

A

a small ulcer occurring in groups in the mouth or on the tongue.

haematinic assay to detect deficiency
Ferritin and folate def. may mean anaemia and or coeliac

49
Q

What are the features of bowel cancer (colonic cancer)?

A
  • Colo-rectal Adenocarcinoma
  • FOB, Barium, Endoscopy over 50
  • Intestinal Polyposis
    • Pedunculated or flat, Bleeding (irritation/trauma) take around, 5 years to become malignant
    • Small intestine (LOW RISK MALIGNANCY)- Peutz-Jehger syndrome (GI tract polyps, hyperpigmented macules on the lips,
    melanosis of mucosa)
    • Large Intestine (HIGH RISK MALIGNANCY)- Gardener’s Syndrome (GI polyps, multiple osteomas, and skin and soft tissue
    tumors), Cowden’s syndrome (multiple benign hamartomas, which typically are found in the skin, mucous membranes
    (mouth, GIT)

BDS2 (8 decks)

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