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* year 2 Clinical Pathology > GI, pancreas, liver etc > Flashcards

GI, pancreas, liver etc Flashcards

1
Q

what types of cell make up the lining of the oesophagus?

A

squamous epithelial

non-keratinised

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2
Q

what are the sphincters at either end of the oesophagus called?

A

upper end = cricopharyngeal

lower end = gastro-oesophageal

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3
Q

how long is the oesophagus?

how much of the distal oesophagus is lined by glandular (columnar) mucosa? (ie distal to squamo-columnar junction)

what is the normal distance from the incisors to the squamo-columnar junction?

A

25 cm long

distal 1.5-2cm

40cm

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4
Q

what are the three main layers of the lining of the oesophagus?

what are the three sub-layers within the most superficial layer?

A

mucosa:

  • epithelium (stratified squamous) - basal cell layer at bottom!
  • lamina propria
  • muscularis mucosae

submucosa

muscularis propria

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5
Q

oesophagitis:

  • main infectious causes? 3 (with examples)
  • main chemical causes? 2
A

infectious:

  • viral (HSV1, CMV)
  • fungal (candida)
  • bacterial

chemical:

  • reflux of gastric contents (most common!)
  • ingestion of corrosive substances (mainly kids or self-harming adults)
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6
Q

on endoscope examination, what do these oesophageal infections look like:

  • candida?
  • herpes simplex?
A

candida = white plaques

herpes simplex = well-defined ulcers

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7
Q

what are the risk factors for reflux oesophagitis? 6

what is the commonest presenting symptom?

A
  • obesity
  • male
  • defective lower oesophageal sphincter
  • hiatus hernia
  • increased intra-abdominal pressure
  • increased gastric fluid volume (due to gastric outflow stenosis)

‘heart burn’

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8
Q

what is a hiatus hernia

what are the two different types of hiatus hernia?

what do they each tend to present with?

A

abnormal bulging of a portion of the stomach through the diaphragm

sliding hiatus hernia

  • cardia bulges up
  • reflux symptoms

paraoesophageal hiatus hernia

  • fundus bulges up
  • strangulation (can lead to necrosis + perforation)
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9
Q

what do the cells in reflux oesophagitis tend to look like (compared to normal)?

A
  • basal cell hyperplasia
  • increased inflammatory cells

basically more purple nuclei and less squamous cells

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10
Q

what are the potential complications of reflux oesophagitis? 5

A
  • ulceration
  • haemorrhage (at base of ulcers)
  • perforation (if ulcer penetrates through wall)
  • benign stricture
  • BARRETT’S OESOPHAGUS
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11
Q

barrett’s oesophagus:

  • cause?
  • risk factors?
  • macroscopy?
  • histology?
A

cause:
- longstanding gastro-oesophageal reflux

risk factors:
- same as for reflux

macroscopy:
- proximal extension of squamo-columnar junction

histology:
- squamous mucosa replaced by columnar mucosa (called: glandular metaplasia)

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12
Q

what are the two types of barrett’s oesophagus? how do they differ?

A

normal barrett’s oesophagus
- no goblet cells

specialised barrett’s opoesophagus
- presence of goblet cell (norm found in small bowel)

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13
Q

what type of cancer can patient’s with barrett’s oesophagus develop?
- describe the 4 stages of this progression

how is this prevented?

A

adenocarcinoma of oesophagus

  • barrett’s
  • > low-grade dysplasia
  • > high-grade dysplasia
  • > adenocarcinoma

regular endoscopies
- freq determined by height of barrett’s + level of dysplasia

nb vast majority of people with barrett’s won’t get cancer!

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14
Q

what are the 2 main types of oesophageal cancer?

what are the:

  • risk factors?
  • geographical distribution?
  • distribution in oesophagus?
A

adenocarcinoma

  • risk factors: barrett’s, men, (maybe smoking, obesity)
  • mainly caucasians
  • mainly lower oesophagus

squamous carcinoma

  • risk factors:
  • –tobacco (main one)
  • –alcohol
  • –diet
  • –thermal injury (very hot drinks)
  • –human papilloma virus
  • –male
  • –black ethnicity
  • mainly developing world
  • middle + lower third (occasionally upper third)
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15
Q

what are the three different types of macroscopic appearance of oesophageal cancers?

A
  • polypoidal (ie a lump)
  • stricturing
  • ulcerated
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16
Q

what staging system is used for oesophageal cancer?

A

TNM

(tumour, nodes, metastases)

nb in oesophageal cancer, ‘T’ focuses on depth of invasion through oesophageal wall

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17
Q

4 anatomic regions of stomach?

3 histological regions of stomach?

A

anatomic:

  • cardia
  • fundus
  • body
  • antrum

histological:

  • cardia
  • body
  • antrum

nb body and fundus are histologically the same

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18
Q

what are the causes of gastritis due to:

  • ‘increased aggression’? 7
  • ‘impaired defenses’? 5
A

‘increased aggression’:

  • excessive alcohol
  • drugs (esp NSAIDs)
  • heavy smoking
  • corrosive
  • radiation
  • chemotherapy
  • infection

‘impaired defenses’

  • ischaemia (poor blood supply to stomach)
  • shock (poor blood supply to stomach)
  • delayed emptying (due to mass or stricture)
  • duodenal reflux
  • impaired regulation of pepsin secretion
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19
Q

what are the three most common causes of acute gastritis?

what are the possible complications? 2

A
  • drugs (eg NSAIDs)
  • alcohol
  • initial response to helicobacter pylori infection
  • erosion
  • haemorrhage

nb generally heal quickly (if cause is removed)

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20
Q

what are three main causes of CHRONIC gastritis?

A

autoimmune

  • anti-parietal + anti-intrinsic factor antibodies
  • -> atrophy in gastric mucosa

bacterial infection (helicobacter pylori)

  • majority get no disease
  • 2-5% get gastric ulcers
  • 10-15% get duodenal ulcers

chemical injury (NSAIDs, bile reflux, alcohol)

“ABC = causes of chronic gastritis”

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21
Q

what is MALT?

A

mucosa-associated lymphoid tissue

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22
Q

helicobacter pylori:

  • type + shape of bacterium?
  • where found in stomach?
  • what does it result in, in stomach? 3
A
  • gram negative
  • spirillus

more common in antrum than body
- antrum is less acidic

  • glandular atrophy
  • replacement fibrosis
  • intestinal metaplasia
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23
Q

what is the definition of a peptic ulcer?

at which 3 sites are they most common?

A

localised defect extending, at least, into SUBMUCOSA

  • distal oesophagus (DOJ)
  • junction of antral + body mucosa
  • first part of duodenum

basically anywhere on the junction between different cell types

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24
Q

what are the main 5 causes of peptic ulcer disease?

A
  • H.pylori infection
  • duodeno-gastric reflux
  • hyperacidity
  • drugs (NSAIDs)
  • smoking
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25
Q

ACUTE gastric ulcers:

  • what 3 things make up ulcer slough? (which ulcers are covered in)
  • what is found at the floor of the ulcer?
A

ulcer slough

  • necrotic debris
  • fibrin
  • neutrophils
  • granulation tissue
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26
Q

what is the histology of a CHRONIC gastric ulcer?

A
  • clear-cut edges overhanging the base
  • extensive granulation + scar tissue at ulcer floor
  • scarring often throughout the entire gastric wall (with breaching of the muscularis propria)
  • bleeding
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27
Q

what are the 4 major complications of peptic ulcers?

A
  • haemorrhage (acute and/or chronic -> anaemia)
  • perforation -> peritonitis
  • penetration into an adjacent organ (ie fistula) - liver, pancreas
  • stricturing (due to fibrosis) -> hour-glass deformity
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28
Q

gastric vs duodenal ulcers:

  • relative incidence?
  • acid levels?
  • % caused by h. pylori?
A

duodenal 3 times more common

gastric: normal or low acid levels
duodenal: high or normal acid levels

gastric: 70%
duodenal 95-100%

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29
Q

what is the most common type of gastric cancer?

what are the 3 less common types?

A

adenocarcinoma

  • endocrine tumours
  • MALT lymphomas
  • stromal tumours (GIST)
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30
Q

what is stroma?

A

Stroma is the part of a tissue or organ that has a connective and structural role. It consists of all the parts which do not conduct the specific functions of the organ, for example, connective tissue, blood vessels, nerves, ducts, etc. The other part is the parenchyma, which is the cells that perform the function of the tissue or organ

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31
Q

what are the 5 major causes of gastric adenocarcinoma?

A
  • helicobacter pylori infection (most common)
  • diet (smoked/cured meat or fish, pickled veg)
  • bile reflux
  • hypochlorhydria (ie low gastric acid, allows bacterial growth)
  • hereditary (about 1%)
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32
Q

what are the differing aetiologies of gastric adenocarcinoma of the:

  • Gastro-oesophageal junction (GOJ)?
  • Gastric body/antrum?
A 
GOJ:
- white males
- association with GO reflux
- increasing incidence (due to obesity)
(- no association with H. pylori/diet)
- basically same risk factors as barrett's!
body/antrum:
- association with H. pylori
- association with diet (salt, low fruit + veg)
- decreasing incidence
(- no association with reflux)
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33
Q

what is linitis plastica?

what cause of gastric cancer is this associated with?

A

Diffuse type carcinoma – no distinct mass as cancer spread throughout, entire stomach wall is thickened

hereditary diffuse type gastric cancer (HDGC)
- tend to get gastric cancer in young adults + middle age

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34
Q

coeliac disease:

  • what molecule is this a reaction to?
  • what is the pathophysiology?
A

gliadin (component of gluten)

gliadin induces epithelial cells to express IL-15 (interleukin-15)

-> IL-15 produced by epithelium -> activation/proliferation of CD8+ intraepithelial lymphocytes (IELs)

IELs are cytotoxic + kill enterocytes

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35
Q

define the findings/symptoms in these different types of coeliac patient’s:

  • silent disease?
  • latent disease?
  • symptomatic? 4
A

silent disease:

  • positive serology
  • villous atrophy
  • no symptoms

latent disease:

  • positive serology
  • no villous atrophy
  • no symptoms

symtpomatic disease:

  • anaemia
  • chronic diarrhoea
  • bloating
  • chronic fatigue
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36
Q

coeliac disease:

  • associated extra-GI conditions? 2
  • types of cancer possibly caused by coeliac? 2
  • warning sign (red flag) of cancer?
A 
dermatitis herpetiformis (10% of patients)
- nasty itchy rash

lymphocytic gastritis +/or colitis (less common)
- like coeliac but in stomach/large bowel

  • enteropathy-associated T-cell lymphoma
  • small intestine adenocarcinoma

if symptoms persist DESPITE a gluten-free diet

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37
Q

coeliac disease:

  • possible complications? 4
  • diagnostic tests? 2
  • treatment?
  • histological findings? 4
A
  • anaemia
  • female infertility
  • osteoporosis
  • cancer
  • serology
  • endoscopy w biopsy (before + after GFD is gold standard))

gluten-free diet (GFD)

  • villous atrophy
  • crypt elongation
  • increased intra-epithelial lymphocytes (IELs)
  • increased lamina propria inflammation
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38
Q

what are the 2 different types of diverticulosis?

what’s the difference between them?

which is more common?

A

congenital (eg merkel’s diverticulum)
- all levels of the bowel wall

acquired (‘pseudo’)

  • ONLY mucosa + submucosa
  • more common
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39
Q

what are taenia coli?

A

longitudinal thickenings of muscularis propria

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40
Q

where are acquired diverticulum most commonly found

A

sigmoid colon
- between mesenteric + anti-mesenteric taenia coli

nb this is most common findings but can be found elsewhere

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41
Q

what are the 2 main risk factors for diverticular disease?

A
  • low fibre diet

- increased age

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42
Q

why do diverticular pouches develop?

A

increased intra-luminal pressure

points of relative weakness in the bowel wall

nb connective tissue weakens as you age

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43
Q

what are the clinical features of diverticular disease?

what % develop acute and chronic complications?

A
  • asymptomatic (90-99%)
  • cramping abdominal pain
  • alternating constipation + diarrhoea

10-30% develop complications

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44
Q

name 3 acute complications of diverticular disease

A

diverticulitis (20-25%)

  • due to bacterial overgrowth
  • can develop peridiverticular abscess, causing pyrexia etc - more serious

perforation, can -> peritonitis)

haemorrhage (causes rectal bleeding)

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45
Q

name 4 chronic complications of diverticular disease

A

intestinal obstruction
- due to stricturing (due to repeated infection/inflammation)

fistula
- bladder/vagina/small bowel

diverticular colitis
- infection in lumen around diverticular pouches

polypoid prolapsing mucosal folds
- can cause a bit of bleeding + diarrhoea

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46
Q

what are 4 common causes of acute colitis?

A

infective
- eg campylobacter, shigella, salmonella, CMV

antibiotic
- incl C. diff

drug-induced

acute ischaemic colitis
- transient or gangrenous

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47
Q

what are the 2 most common types of chronic colitis?

what are 6 rarer types?

A
  • chronic idiopathic inflammatory bowel disease
  • ischaemic colitis

less common:

  • diverticular colitis
  • microscopic colitis
  • chronic infective colitis (eg TB)
  • diversion colitis
  • eosinophilic colitis
  • chronic radiation colitis
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48
Q

what are the three different types of chronic idiopathic inflammatory bowel disease?

A

ulcerative colitis

crohn’s disease

unclassified + indeterminate colitis (10-15%)
- half way between UC + crohn’s

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49
Q

does smoking increase or decrease risk of:

  • crohns?
  • UC?

which one does appendectomy protect against?

name two other risk factors for both

A

smoking:

  • crohn’s = bad
  • UC = good

appendectomy protects against UC

  • oral contraceptive
  • FH (of either)
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50
Q

symptoms of UC? 7

A
  • rectal bleeding (>90%)
  • diarrhoea (66%)
  • abdominal pain (30-60%)
  • weight loss (15-40%)
  • anorexia
  • anaemia
  • constipation (2%)
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51
Q

what are the complications of UC? 5

A

toxic megacolon + perforation

haemorrhage

carcinoma

primary sclerosing cholangitis (PSC) aka primary billiary cholangitis (PBC)
- inflammation + fibrosis of bile ducts -> obstructive liver problems (can lead to liver cancer)

strictures (rare, if seen rarely benign)

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52
Q

symptoms of crohns? 9

A
  • diarrhoea (may be bloody)
  • peri-anal disease
  • colicky abdominal pain
  • palpable abdominal mass (thickened bowel due to depper infiltration) - sometimes
  • weight loss (failure to thrive in children) - often
  • anorexia
  • fever
  • anaemia (often)
  • oral ulcers
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53
Q

what are the three commonest areas of the GI tract to be affects by crohns?

A
  • ileocolic (junction of terminal illeum + caecum)
  • small bowel
  • colon (hard to distinguish from UC)
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54
Q

what are the complications of crohns? 7

A
  • toxic megacolon
  • perforation
  • fistula
  • stricture (common)
  • haemorrhage
  • carcinoma
  • short bowel syndrome
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55
Q

what is short bowel syndrome?

A

malabsorption disorder caused by a lack of functional small intestine

caused by repeated surgical resections of small bowel

primary symptom is diarrhea, which can result in:

  • dehydration
  • malnutrition
  • weight loss
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56
Q

what are the 3 major and 4 minor risk factors for UC developing into colorectal cancer?

A

major:

  • early age of onset
  • duration of disease >8-10 years
  • total/extensive colitis (ie beyond splenic flexure)

minor:

  • presence of PSC (primary sclerosing colangitis) aka PBC
  • FH of colorectal cancer
  • severity of inflammation
  • presence of dysplasia
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57
Q

name difference between UC and crohn’s.

  • spread in GI tract?
  • effect of smoking?
  • likelihood of rectal bleeding?
  • likelihood of strictures?
  • layers of bowel wall affected?
  • presence of granulomas?
  • peri-anal disease?
A

spread:

  • UC: continuous from rectum up
  • crohn’s: patchy, anywhere in GI tract (‘skipped lesions’)

smoking:

  • UC: makes better
  • crohn’s: makes worse

rectal bleeding:

  • UC: highly likely
  • crohn’s: less likely

strictures:

  • UC: rare
  • crohn’s: common

layers affected:

  • UC: just mucosa
  • crohn’s: deeper infiltration

granulomas:

  • UC: absent
  • crohns: present in 50%

peri-anal disease:

  • UC: don’t get
  • crohn’s: more likely

nb both UC + crohn’s are relapsing/remitting conditions!!

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58
Q

what is offered to reduce risk of cancer developing?

A

regular colonoscopies

(after having had disease for more than 10 years)

frequency dependent on other risk factors

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59
Q

what is ischaemic colitis?

what are the 2 subtypes?

what conditions is it associated with?

A

colonic injury secondary to an acute, intermittent of chronic reduction in blood flow

  • occlusive (blood flow blocked completely)
  • non-occlusive (blood flow reduced)

nb varies from mild (80%) to severe (15%)!!

other vascular diseases, eg:

  • hypertension
  • peripheral vascular disease
  • coronary artery disease
  • diabetes mellitus
  • chronic renal failure
  • COPD
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60
Q

what are the symptoms of ischaemic colitis? 3

A
  • acute onset cramping abdominal pains
  • urge to defecate
  • bloody diarrhoea/ rectal bleeding

nb in majority (mild) symptoms improve within 48hours (completel recovery within a fortnight)

nb 20% require surgery for colonic infarction

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61
Q

where in the large bowel are you most likely to get ischaemic colitis? why?

A

just distal/proximal to the splenic flexure

as this is a watershed between the superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA)

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62
Q

when do haemorrhagic infarctions occur?

A

when there’s a blockage in a large vein so blood backs up, pressure builds -> haemorrhage

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63
Q

what is a colorectal polyp?

what is it called when there are multiple?

what are the 3 morphological types?

A

a mucosal protrusion

polyposis

  • pedunculated (have a stalk, bit like mushroom)
  • sessile (no stalk)
  • ‘flat’
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64
Q

what are 6 types of non-neoplastic polyps?

A
  • hyperplastic polyps (most common)
  • hamartomatous polyps
  • polyps related tomucosal prolapse
  • post-inflammatory polyps (see in IBD after inflammation)
  • inflammatory fibroid polyp
  • benign lymphoid polyp
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65
Q

hyperplastic polyps:

  • where common in GI tract?
  • what subtype may give rise to cancer?
A

rectum + sigmoid colon

  • 1-5mm in size
  • often multiple

sessile serrated lesions

  • large
  • found on RIGHT colon
  • can give rise to microsatellite unstable carcinoma
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66
Q

juvenile polyps:

  • type of polyp?
  • morphology of polyp?
  • where occur in GI tract?
  • cancer risk?
  • presentation?
A

hamartomatous

pedunculated (+ spherical head)

rectum + distal colon

sporadic: no malignant potential
genetic: increased risk of cancer (=juvenile polyposis)

  • diarrhoea + rectal bleeding

nb commonest type of polyp in children

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67
Q

peutz-jeghers syndrome:

  • type of polyp?
  • where occur in small bowel?
  • inheritance?
  • symptoms? 4
  • cancer risk?
A

hamartomatous

predominately small bowel

autosomal dominant

  • abdo pain
  • GI bleeding
  • anaemia
  • brown freckles around lips/oral mucosa (+ fingers?)

increased likelihood of cancers of:

  • pancreas
  • liver
  • lung
  • breast
  • uterus
  • ovaries
  • testes
  • and others

nb polyps rarely develop into cancer but mutation that causes them causes cancers in other parts of body

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68
Q

what are the risk factors for an adenoma (a type of neoplastic polyp) progressing into adenocarcinoma? 5

A
  • flat adenomas (as opposed to sessile or pedunculated)
  • large (>10mm)
  • villous or tubulo-villous (as opposed to tubulus)
  • high grade dysplasia
  • if patient has lynch syndrome
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69
Q

colorectal cancer:

  • risks? 8 (excluding lynch + FAP)
  • protective things? 4
A

risks:

  • diet high in fat
  • diet high in red meat
  • obesity/lack of physical activity
  • alcohol
  • HRT + oral contraceptives
  • schistomiasis
  • pelvic radiation
  • IBD (UC + crohns)

protective:

  • high fibre diet
  • high folate diet
  • high calcium diet
  • NSAIDs + aspirin
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70
Q

what is FAP?

  • inheritence?
  • genetic mutation?
  • colonoscopy finding?
  • cancer risk?
A

familial adenomatous polyposis

autosomal dominant
- mutation in APC tumour suppressor gene

multiple (100s/1000s) of benign adenomatous polyps in colon

100% lifetime risk of colorectal cancer (norm get in 30s/40s)
- increased risk of other cancers too

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71
Q

lynch syndrome:

  • another name for it?
  • inheritance pattern?
  • genetic mutation?
  • cancer risk?
A

HNPCC - hereditary non-polyposis colorectal cancer

autosomal dominant
- mutations in DNA mismatch repair genes

50-70% lifetime risk of colorectal cancer

increased risk of:

  • endometrial
  • ovarian
  • gastric
  • small bowel
  • urinary tract
  • billary tract
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72
Q

what type of cancers are the vast majority of colorectal cancers?

A

adenocarcinomas (>95%)

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73
Q

what are the 5 ways in which colorectal cancers spread?

A
  • direct invasion of adjacent tissue
  • lymphatic metastasis
  • haematogenous metastasis (norm to liver + lung)
  • transcoelimic (peritoneal) metastasis
  • iatrogenic spread (ie during biopsies etc)
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74
Q

what two staging systems are used for staging colorectal cancer?

A

TNM

dukes

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75
Q

angular chelitis:

  • what is it?
  • cause?
  • most common in?
A

acute or chronic inflammation of the skin + next door mucosa at the corners of the mouth
- normally bilateral lesions, may be painful

excessive moisture from saliva -> maceration (breakdown of tissue from too much liquid) + secondary infection with Candida albicans (less commonly staph aureus)

  • older people with dentures
  • young children
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76
Q

dental infections

  • what are caries?
  • what is pulpitis?
  • cause? (incl 2 organisms)
  • diagnosis?
  • management?
A 
caries = tooth decay
pulpitis = infection/inflammation of pulp of the tooth (where blood + nerves are) secondary to decay

acid produced by bacteria

  • streptococcus mutans - “MUTAte your teeth!”
  • lactobacillus spp
  • examination
  • dental x-rays
caries = fillings
pulpitis = root canal procedure
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77
Q

oral hairy leucoplakia

  • signs/symptoms?
  • cause?
A

white plaques on tongue

epstein barr virus (norm give glandular fever)
- only really seen in HIV patients

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78
Q

bilary tract infection (cholangitis)

  • charcot’s triad?
  • causes? 5
  • abnormal LFT test results? 3
  • normal bacterial pathogen involved?
  • treatment?
A

charcot’s triad = classical presentation of cholangitis:

  • fever
  • abdominal pain
  • jaundice

causes:

  • gall stones
  • stenosis
  • stents
  • surgery
  • cancer

elevations in:

  • alkaline phosphatase (ALP)
  • gamma-glutamyl transpeptidase (GGT)
  • bilirubin (mainly conjugated)

enterobacteriacae (esp enterococcus spp.)

antibiotics +/- surgery

79
Q

quinsy:

  • what is it?
  • another name for it?
  • symptoms? 3
  • signs? 4
  • treatment? 2
A

complication of tonsilitis
- abscess forms between your tonsils and wall of throat

peritonsillar abscess

symptoms:

  • painful swallowing
  • unilateral sore throat
  • ear ache

signs:

  • muffled voice
  • trismus (lock jaw)
  • unilateral deviation of uvula (to unaffected side)
  • soft palate fullness/oedema
  • surgical drainage
  • antibiotics
80
Q

oral candidiasis

  • two types?
  • appearance of each?
  • symptoms?
A

aka thrush

pseudomembranous

  • most common
  • white plaques (that you can scrape off) on mucosa + tongue etc
atrophic form (aka denture stomatitis)
- found under upper dentures + characterised by erythema without plaques

most are asymptomatic

  • cottony feeling in mouth
  • loss of taste
  • pain (most common in atrophic)
81
Q

boerhaave syndrome:

  • what is it? + cause?
  • what can it lead to?
  • immediate symptom? 1
  • later symptoms/signs? 4
  • management? 4
A

effort rupture of the oesophagus
- spontaneous perforation of the oesophagus resulting from severe straining or vomiting (but not in about 1/3!)

contamination of the mediastinal cavity with gastric contents
-> chemical mediastinitis w mediastinal emphysema + inflammation
-> bacterial infection + necrosis
can -> sepsis!!!

  • excruciating retrosternal chest pain

after about an hour:

  • crepitus on chest wall (due to subcutaneous emphysema)
  • mediastinal crackling (on auscultation)
  • pain on swallowing (odynophagia)
  • dyspnoea

management:

  • avoidance of all oral intake (nutritional support norm parenteral)
  • antibiotics
  • intravenous proton pump inhibitor
  • drainage of fluid collections/infected + necrotic tissue
82
Q

mucositis:

  • what is it?
  • who normally gets it?
  • prevention? 2
  • complication? 1
A

inflammation of mucous membranes of the GI tract (normally in mouth +/or intestines)

chemotherapy patients
(about 2 wks after stopping chemo)

  • prophylactic antibiotics for neutropenic cancer patients
  • dental review before chemo (caries/peridontal disease increase risk)

bacteraemia

83
Q

how does helicobacter pylori cause stomach ulcers?

A

bacterial urease hydrolyses gastric luminal urea to form ammonia that neutralises gastric acid, forming a protectiv cloud around the bacteria, enabling it to penetrate the gastric mucosa layer

84
Q

oesophageal candidiasis:

  • who gets it?
  • appearance on endoscopy?
  • symptom?
A

immunosuppressed patients, esp HIV
- it’s an AIDS-defining illness

small white plaques in oesophagus

pain on swallowing (odynophagia)

nb cytomegalovirus (CMV) + herpes simplex virus can cause oesophagitis in immunosuppressed patients

85
Q

ludwigs angina:

  • what is it?
  • treatment?
  • potential complications?
A

bilateral infection of the submandibular space

  • antibiotics
  • surgical drainage (if abscess forms)
  • airway obstruction causing asphyxia
  • aspiration pneumonia

nb angina means stranguling

86
Q

definition of a gastric ulcer?

A

lesion in stomach which spans, at least, the full depth of the mucosa

nb if shallower then called an erosion

87
Q

what is murphy’s sign?

A

Murphy’s sign. a test for gallbladder disease in which the patient is asked to inhale while the examiner’s fingers are hooked under the liver border at the bottom of the rib cage. The inspiration causes the gallbladder to descend onto the fingers, producing pain if the gallbladder is inflamed.

88
Q

bacterial overgrowth in the small bowel:

  • symptoms? 2
  • causes? 5
  • treatment? 4
A

symptoms:

  • malabsorption
  • chronic diarhoea

causes:

  • achlorhydria (low HCl, eg after gastric surgery)
  • impaired bowel motility
  • blind loops of bowel
  • surgery
  • radiation damage

treatment:

  • dietary changes
  • surgical
  • motility
  • non-absorbable antibiotics (aren’t absorbed into circulation, just act on GI bacteria)
89
Q

whipple’s disease:

  • causative agent?
  • symptoms? 4
  • diagnosis?
A

bacterium Tropheryma whipplei

  • arthralgia
  • chronic diarrhoea
  • malabsorption/weight loss
  • abdo pain

nb symptoms present slowly over many years (arthralgia comes first)

nb there are many more common causes of these symptoms so exclude these first before looking for whipples

  • upper GI endoscopy +biopsy of small intestine
  • PCR the organism
90
Q

liver abscess:

  • ways in which infection can spread to liver? 4
  • LFT results? 3
A
  • ascending bilary tract infection
  • via portal vein (after peritonitis or colonic perforation)
  • haematogenous spread (eg endocarditis)
  • entamoeba histolytica
  • ALP raised (67-90%)
  • AST raised (50%)
  • bilirubin raised (50%)

nb AST = aspartate aminotransferase

91
Q

hepatosplenic candidiasis:

  • who does it occur in?
  • pathogenesis?
A

seen almost entirely in patients with hematologic malignancies who have just recovered from an episode of neutropenia.

Candida overgrows in bowel and then (since immunosuppressed, due to chemo) spread via lymph to liver then immune system starts to work again (after chemo done) and attack candida in liver, causing symptoms

92
Q

entamoeba histolytica:

  • 2 forms?
  • route of infection?
  • what does it cause?
A
  • cyst stage (the infective form)
  • trophozoite stage (form that causes disease)

faecal-oral, norm spread via contaminated food/water (ingest cyst)

nb found in developing world

liver abscesses

93
Q

TB in the GI tract

  • possible localised symptoms? 3
  • most common site?
A
  • non-healng oral ulcers
  • gastric ulcers
  • enterocutaneous fistula (between skin + GI tract)
  • ileo-caecal (nb may be confused with a colonic malignancy)
94
Q

what is necrotising pancreatitis?

A

Pancreatic necrosis is a serious infection usually associated with acute pancreatitis. During recurring attacks of pancreatitis, tissue within the pancreas may die (necrotize) and later become infected. This condition is called acute necrotizing pancreatitis.

95
Q

what is the definition of a complicated intra-abdominal infection?

A

Defined as infection that extends beyond the hollow viscus of origin into the peritoneal space and is associated with either abscess formation or perforation -> peritonitis.

96
Q

diverticulitis:

  • treatment if complicated?
  • treatment if uncomplicated?
A

complicated:
- antibiotics + surgery (eg abscess drainage, resection of affected bowel)

uncomplicated:
- supportive treatment (NOT antibiotics)

97
Q

intra-peritoneal abscess:

  • predisposing factors? 7
  • treatment?
A
  • perforation of peptic ulcer
  • perforated appendix
  • perforated diverticulum
  • mesenteric ischaemia/bowel infarction
  • pancreatitis/pancreatic necrosis
  • penetrating trauma
  • postoperative anastomotic leak

treatment:
- surgical drainage + antibiotics

98
Q

intraperitoneal abcess:

  • symptoms? 5
  • symptoms of subphrenic abscess (ie below diaphragm)? 5
  • symptoms of pelvic abscess? 2
A

nb very non-specific presentation

  • sweating
  • anorexia
  • wasting
  • swinging pyrexia
  • localising features

subphrenic abscess:

  • pain in ipsilateral shoulder
  • persistant hiccup
  • intercostal tenderness
  • apparent hepatomegaly (liver displaced downwards)
  • ipsilateral lung collapse (with pleural effusion)

pelvic abscess:

  • urinary frequency
  • tenesmus (feel like you need to poo all the time but nothing/little comes out)
99
Q

spontaneous bacterial peritonitis (SBP):

  • definition?
  • pathogenesis?
  • diagnosis?
  • treatment?
  • what do most patients with SBP have before they get SBP?
A

ascitic fluid infection without an evident intra-abdominal surgically treatable source

bacteria within GI lumen -> mesenteric lymph nodes (called translocation)
- lymphatics carrying the contaminated lymph ruptures (due to high flow + high pressure, associated with portal hypertension)

  • positive ascitic fluid bacterial culture
  • elevated ascitic fluid leukocyte count
  • antibiotics (nb prophylactic antibiotics may be given to those at risk)

The vast majority of patients with SBP have advanced liver cirrhosis with ascities

100
Q

which bacteria often causes bacteraemia in bowel cancer patients?

what else can it cause?

A

streptococcus bovis (aka S. gallolyticus)

endocarditis

nb don’t know why there is a link but there is

101
Q

what is the definition of diarrhoea?

A

3 or more loose stools per day

type 5-7 on bristol stool chart

102
Q

what is the treatment for gastroenteritis?

A

oral rehydration solution
- generally avoid Abx

except in:

  • very young + very old
  • immunosuppressed
  • bacteraemia (eg typhoid)
103
Q

pancreas:

  • what % is exocrine?
  • what % is endocrine?
  • which digestive enzyme activates the others?
  • what prevents autodigestion of pancreas?
A

85% exocrine
1-2% endocrine

  • trypsin activates others (by proteolytically cleaving them)
trypsin inhibitors (found in cells of pancreas)
- inhibit any active trypsin in pancreas (trypsinogen is activated in duodenum)
104
Q

pancreatitis:

  • acute definition?
  • chronic definition?
  • what’s normally damaged?
A

acute
- gland can revert back to normal, if underlying cause removed

chronic
- irreversibvle loss of pancreatic tissue

nb not two distinct conditions but a continum from acute to chronic

exocrine parenchyma
- islets of langerhan are much more resistant to infection/inflammation, only get injured when it’s really bad!

105
Q

which blood vessels pass between the neck and uncinate process of the pancreas?

A

superior mesenteric artery and vein

106
Q

acute pancreatitis:

  • symptoms? 3
  • blood test? 1
  • common causes? 3
  • rare causes? 5
A

symptoms:

  • severe abdo pain, radiating to back
  • nausea
  • vomiting

blood test:
- raised serum amylase/lipase (>3x normal)

common causes:

  • gallstones (50%) - esp women
  • alcohol (25%) - esp men
  • idiopathic (10%)

rare causes (<5%):

  • vascular insufficiency
  • viral infections (mups, coxsackie B)
  • hypercalcaemia
  • ERCP (Endoscopic retrograde cholangiopancreatography)
  • hereditary

nb ERCP is endoscopy + radiological diagnostic procedure to access bile duct and pancreas

107
Q

Hereditary pancreatitis:

  • presentation?
  • known causative mutations? 2
A

recurrent attacks of severe pancreatitis

  • usually begins in childhood
  • normally progresses to chronic pancreatitis with 30-40% lifetime risk of pancreatic cancer
PRSS1 mutation (autosomal dominant)
- unknown mechanism

SPINK 1 gene (autosomal recessive)

  • serine protease inhibitor Kazal-type 1
  • means there is less inhibition of intra-pancreatic trypsin -> slow autodigestion

“pancreas is PINK, so a Sick pancreas is SPINK”

108
Q

what is Grey Turner’s sign? (incl cause)

A

bruising of the flanks

sign of retroperitoneal haemorrhage into subcutaneous tissue of flank
- norm caused by severe acute pancreatitis

109
Q

what is cullen’s sign?

- causes? 4

A

superficial oedema and bruising in the subcutaneous fatty tissue around the umbilicus.

“bleeding around where you CUt the LINe that connects mother to baby”

causes:

  • acute pancreatitis
  • bleeding from blunt abdominal trauma
  • bleeding from aortic rupture
  • bleeding from ruptured ectopic pregnancy
110
Q

what are the complications of acute pancreatitis? 4

A
  • shock
  • intravascular coagulopathy (eg DIC)
  • haemorrhage
  • pseudocysts
111
Q

what are pancreatic pseudocysts?

A

collections of pancreatic juice secondary to duct rupture

called pseudocyst as does not have epithelial lining (true cysts do!)

112
Q

what are the causes of chronic pancreatitis? 13

which 3 are most common causes?

A
  • alcohol
  • cigarette smoking
  • drugs
  • hypercalcaemia
  • hyperparathyroidism
  • cystic fibrosis
  • PRSS1, SPINK mutations

obstruction of main duct:

  • cancer
  • scarring
  • recurrent acute pancreatitis
  • infection
  • autoimmune
  • idiopathic

most common causes are alcohol, smoking + idiopathic

TIGARO

  • toxins (alcohol, smoking)
  • idiopathic
  • genetic (PRSS1, SPINK, CF)
  • autoimmune
  • recurrent acute
  • obstruction
113
Q

symptoms of chronic pancreatitis? 3

A
  • intermittent abdo pain
  • back pain
  • weight loss (due to malnutrition)

nb symptoms often mistaken for cancer

114
Q

complications of chronic pancreatitis? 5

A

malabsorption of fat (due to lack of lipases)

  • steatorrhoea
  • lack of fat soluble vitamins (DAKE)
  • diarrhoea, weight loss + cachexia

diabetes (late feature)

pseudocysts (10% of patients)

stenosis of common bile duct/duodenum

pancreatic cancer

115
Q

what is a calculus (pl. calculi)?

A

often called a stone, is a concretion of material, usually mineral salts, that forms in an organ or duct of the body.

ie kidney stones, gallstones etc

116
Q

what is the most common type of pancreatic cancer?

what are the 3 most common causes?

where in the pancreas do they normally occur?

A

pancreatic adenocarcinoma (90% of all pancreatic cancers)

  • smoking
  • alcohol
  • family history/hereditary

head (60-70%)

117
Q

pancreatic adenoma carcinoma signs + symptoms? 8

A
  • epigastric pain, radiating to back
  • weight loss
  • painless jaundice
  • pruritis
  • nausea
  • trousseau’s syndrome (migratory thrombophlebitis)
  • diabetes (increases risk + can be a presenting complaint)
  • courvoisier’s sign (palpable gall bladder without pain)

nb patients with gall stones often have small, shrunken, painful gall bladders

118
Q

pancreatic adenocarcinoma:

  • where most likely to metastasise to? 3
  • prognosis?
  • treatment?
A
  • liver
  • peritoneum
  • lung
  • 4% survival at 5 years (ie almost always fatal)

nb cancer is normally symptomatically silent for about 10 years before detected

surgery (but only 10-20% are operable at diagnosis)

119
Q

what does pancreatic adenocarcinoma look like histiologically?

A

lots of fibrotic desmoplastic stroma and only a few malignant glands

nb islets of langerhans tends to survive for a long time

120
Q

what is the commonest way in which pancreatic adenocarcinoma invades surrounding tissue?

A

perineural invasion
- ie via the fatty tissue that surrounds nerves

this then spreads to fatty tissue around pancreas

121
Q

pancreatic neuroendocrine tumours:

  • cells derived from?
  • 2 genetic cancer syndromes which increase risk?
  • age of onset?
A

islet cells

  • MEN1 (multiple endocrine neoplasia type 1)
  • von Hippel Lindau

20-60 years

nb huge variation in presentation and malignancy etc

122
Q

what are the 6 different types of functioning (ie producing hormones) pancreatic neuroendocrine neoplasms (PENs)?

  • cell derived from?
  • syndrome caused?
  • clinical findings?

which is most common?

A

insulinoma

  • B cells
  • insulinoma syndrome
    • hypoglycaemia

glucagonoma

  • a cells
  • gluganoma syndrome
    • stomatitis (inflammation of mouth + lips)
    • rash
    • diabetes
    • weight loss

gastrinoma

  • G cells
  • zollinger-ellison syndrome
    • peptic ulcer
    • diarrhoea

stomatostatinoma

  • delta cells
  • somatostatinoma syndrome
    • diabetes
    • cholelithiasis (gall stones)
    • hypochlorhydria

VIPoma

  • unknown cell type
  • verner-morrison syndrome
    • diarrhoea
    • hypokalaemia
    • achlorhydria

PP-cell PEN

  • PP cells (panccreatic polypeptide)
  • no syndrome
  • no clinical findings

insulinoma is most common type
- also only type which is definitely benign (other can start benign but potential to become malignant)

123
Q

describe the tumours found in pancreatic neuroendocrine cancers

A
  • usually well-circumscribed, sometimes encapsulated
  • solid
  • occur anywhere in pancreas
  • can be multiple
  • white or yellow in colour
124
Q

what are the differential diagnoses for a 65 year old man with long-standing heartburn + occasional difficulty swallowing? 7

A
  • gastro-oesophageal reflux disease (+ subsequent barrets dysplasia)
  • hiatus hernia
  • achalasia
  • oesophageal cancer
  • peptic ulcers
  • gastritis (acute or chronic)
  • cardiac chest pain
125
Q

What is achalasia?

A

failure of smooth muscle fibers to relax, which can cause a sphincter to remain closed and fail to open when needed `

126
Q

what is pleurisy?

A

inflammation of the lung pleura (aka pleuritis)

127
Q

what is metaplasia?

A

The replacement of one differentiated cell type with another. This may be
physiological (transition between squamous and columnar epithelium in the cervix) or
pathological (e.g. bronchial squamous metaplasia in response to cigarette smoking).

128
Q

what are the possible causes of gastric ulcers? 4

A
  • helicobacter pylori infection
  • NSAIDs
  • gastrin-secreting tumour in pancreas (Zollinger-Ellison syndrome)
  • gastric cancer
129
Q

what is the treatment for gastric ulcers caused by helicobacter infection?

A

triple therapy

- 2 antibiotics + PPI (proton pump inhibitor)`

130
Q

what conditions can cause granulomas in the bowel? 4

what are granulomas?

A
  • crohns disease
  • TB
  • sarcoidosis
  • certain parasitic infections

is a collection of macrophages. Granulomas form when the immune system attempts to wall off substances it perceives as foreign but is unable to eliminate

131
Q

what is the treatment for crohn’s? 3

when is surgery indicated?

A
  • oral sulphasalazine
  • steroids (acute attacks)
  • elemental diet

surgery indicated:

  • failure of medicaal treatment
  • complications
  • failure to grow in children
132
Q

what are multiple adenomas in the liver called?

what are they often caused by? 2

complication?

A

adenomatosis

exogenous steroids

  • oral contraceptive pill (specifically the oestrogen)
  • anabolic steroids

may rupture -> haemoperitoneum

133
Q

bile duct adenomas:

  • aka?
  • what are they?
  • what do they looks like?
  • often confused with?
A

aka von meyenberg complex

benign proliferation of bile duct cells

tiny white nodules on liver

look like metastases
- have to look microscopically to tell difference

134
Q

what % of people have haemangiomas in the liver?

how are these often discovered?

A

1%

incidental finding

135
Q

focal nudular hyperplasia of liver:

  • what is it?
  • who gets it?
A

a regenerative, arterialised nodule

young females (20-40)

136
Q

key diagnostic test for malignant liver cancer?

A 
raised AFP
(alpha-fetoprotein)

a lot of liver cancers secrete AFP
- cirrhosis can also cause it to raise though

137
Q

malignant tumour of bile duct cells:

  • name?
  • risk factors? 2
  • prognosis
A

cholangiocarcinoma

chronic inflammation:

  • primary scelosing cholangitis (PSC) - associated with IBD
  • liver fluke (clonorchis sinensis)

nb most patients have no risk factors though

not great, aggressive tumout that is difficult to resect

138
Q

tumour of blood vessels:

  • name?
  • causes? 2
A

angiosarcoma

(nb sarcoma is cancer of connective tissue, carcinoma is of epithelial cells)

strongly associated with toxins:

  • vinyl chloride (used in making of vinyl records)
  • thorotrast (an old contrast agent)
139
Q

what are the cancers which most commonly metastasise to the liver? 4

A
  • lung
  • breast
  • colon
  • pancreas
140
Q

gall stones:

  • risk factors? 3
  • clinical features?
  • complications? 5
A
  • female
  • middle-aged
  • overweight

80% asymptomatic
- others get crampy pain (‘bilary colic’)

  • obstruction at neck -> pain
  • obstruction at common bile duct -> jaundice
  • chronic cholecystitis
  • perforation
  • obstruction at level of pancreas -> pancreatitis
141
Q

chronic cholecystitis:

  • pathophysiology?
  • symptoms? 3
  • diagnosis?
  • treatment?
A

inflammation of gall bladder -> fibrosis + ulceration of gall bladder

  • pain (RUQ)
  • fever
  • jaundice

ultrasound (only 25% visible on x-ray)

cholecystectomy (only treatment!)

142
Q

what is trauma?

A

an injury or wound to living tissue caused by an extrinsic agent

includes things like:

  • RTAs
  • stabbing/gunshot
  • burns
  • any surgeries/amputations etc
143
Q

possible features of physical trauma:

  • immediate? 4
  • later? 3
A

immediate:

  • intravascular fluid loss
  • extravascular volume
  • tissue destruction
  • obstructed/impaired breathing

later (as above, plus):

  • starvation
  • infection
  • inflammation
144
Q

what are the consequences of a trauma which leads to blood loss, impaired breathing + infection barrier penetration?

A

decreased circulating volume

  • > low RBCs -> low O2 sat
  • > low leucocytes -> low immune response
  • > low cardiac output/BP -> low organ perfusion -> poor energy distribution to cells/tissues
  • > major organ dysfunction (GI, heart/brain/renal etc)
  • > infection barrier penetration -> sepsis
145
Q

what is shock?
signs? 4
types? 5

A

condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function.

typical signs of shock:

  • low BP
  • rapid heart rate
  • weak pulses
  • signs of poor end-organ perfusion (i.e.: low urine output, confusion, or loss of consciousness)

types:
- Cardiogenic shock (due to heart problems)
- Hypovolemic shock (caused by too little blood volume)
- Anaphylactic shock (caused by allergic reaction)
- Septic shock (due to infections)
- Neurogenic shock (caused by damage to the nervous system)
“SHANC - is someone shanks you, you get shocked”

nb shock is often more than one type

146
Q

what are the 3 phases that the body goes through after severe trauma?

A

phase 1 = clinical shock

phase 2 = hypercatabolic state

phase 3 = recovery (anabolic state)

147
Q

what is the difference between anabolism + catabolism?

A

Catabolic reactions usually release energy that is used to drive chemical reactions. Anabolism refers to chemical reactions in which simpler substances are combined to form more complex molecules. Anabolic reactions usually require energy. Anabolic reactions build new molecules and/or store energy.

“anabolic steroids build people up”

148
Q

phase 1 - clinical shock:

  • clinical signs? 4
  • what secreted into blood? 3
  • primary medical aims in this phase? 2
A

signs:

  • tachycardia
  • hyperpnoea
  • low BP (due to hypovolaemia)
  • peripheral vasoconstriction

secreted:

  • cytokines
  • catecholamines (adrenaline, noradrenaline, dopamine)
  • cortisol

aims:

  • stop bleeding
  • prevent infection
149
Q

phase 2 - catabolic state:

  • what secreted into blood? 3
  • what occurs? 5
  • primary medical aims? 2
A
  • catecholamines
  • glucagon
  • cortisol

increased:

  • O2 consumption
  • metabolic rate
  • skeletal muscle breakdown (negative nitrogen balance)
  • glycolysis
  • lipolysis

aims:

  • avoid sepsis
  • provide adequate nutrition
150
Q

what is the main risk during phase 3 (anabolic state)?

how do you minimise this?

A

refeeding syndrome risk
- during catabolic phase, loose lots of micronutirients from cells into blood, fast refeeding triggers them to go back into cells but this means low levels in blood which can cause lots of problems (eg low blood K -> arrythmias)

  • therefore refeed slowly and monitor blood electrolyte/vitamin levels
151
Q

what is the obesity paradox?

A

that you do better after severe trauma if you’re obese due to increased energy reserves

152
Q

what happens in a systemic capillary leak?

A

injury causes inflammatory mediator release
-> capillaries become ‘leaky’

-> loss of:
– water
– salts
– albumin
– energy substrates
from blood into tissues

153
Q

5 signs of inflammation?

A
  • heat
  • redness
  • swelling
  • pain
  • loss of function
154
Q

which of these are catabolic hormones + which are anabolic:

  • ACTH (-> cortisol)
  • catecholamines
  • insulin
  • glucagon
  • growth hormones
A

catabolic:

  • ACTH (-> cortisol)
  • catecholamines
  • glucagon

anabolic:

  • insulin
  • growth hormone
155
Q

what is gluconeogenesis?

A

breakdown of amino acids -> glucose

156
Q

what is ketogenesis?

A

production of ketone from fatty acids of lipids

nb ketones are acids + cause diuresis (with consequent loss of H20 + electrolytes)

157
Q

what are the 2 mechanisms by which inadequate oxygen causes cell death?

A

increased anaerobic resp

  • > lactic acid production
  • -> metabolic acidosis
  • –> cell death

increased anaerobic resp

  • > inadequate energy production
  • -> metabolic failure
  • –> cell death

nb failure of blood lactate to return to normal following trauma resuscitation carries a poor prognosis (should be <1mmol/L)

158
Q

why won’t increased calorific intake prevent muscle wasting in trauma/sepsis patients? (when it does in starvation)

what can resp muscle wasting lead to?

A

because the primary stimulation for protein breakdown in trauma/sepsis is CYTOKINE SECRETION from activated macrophages

resp muscle meakness -> poor cough -> retention of secretions -> pneumonia

159
Q

what is:

  • primary malnutrition? 2
  • secondary malnutrition? 3
A

primary:

  • too few calories ingested (starvation)
  • dietary deficiency of specific micronutrients

secondary:

  • nutrients present in adequate amounts but appetite is suppressed
  • nutrients present in adequate amounts but absorption + utilisation are inadequate (eg short bowel syndrome, coeliacs)
  • increased demand for specific nutrients to meet physiological needs
160
Q

what is nitrogen balance?

what causes:

  • positive nitrogen balance? 4
  • negative nitrogen balance? 4
A

Nitrogen balance is a measure of nitrogen input minus nitrogen output

Nitrogen Balance = Nitrogen intake - Nitrogen loss

positive:

  • periods of growth
  • tissue repair
  • pregnancy
  • hypothyroidism

negative:

  • fasting
  • burns
  • serious tissue injuries
  • hyperthyrpoidism

basically positive means gaining muscle mass, negative means loosing it

161
Q

what is the mechanism by which CFTR dysfunction causes lung damage in CF patients?

A 
viscous mucous due to poor CFTR function
-> poor mucus clearance
-> increased bacterial colonisation
-> neutrophils accumulate
-> elastase is secreted
-> this digests lung proteins 
-> tissue damage
dead neutrophils release DNA -> increased viscosity of sputum -> (repeat)
162
Q

cystic fibrosis:
what is used to treat:
- resp disease? 6
- GI disease? 5

A

resp disease:

  • physiotherapy
  • exercise
  • bronchodilators
  • antibiotics (oral/nebuliser/IV)
  • steroids
  • mucolytics (DNAse)

GI disease:

  • pancreatic enzyme replacement (creon)
  • nutritional supplements
  • fat soluble vitamins
  • high calorie diet
  • ursodeoxycholic acid (secondary bile acid, helps absorb fat)
163
Q

what are the functions of the liver to do with:

  • carbohydrates? 2
  • proteins? 4
  • lipids? 3
  • excretion/detoxification? 3
  • miscellaneous? 2
A

carbs:

  • glycogen synthesis + storage
  • glycolysis + gluconeogenesis

proteins:

  • synthesis + catabolism
  • clotting factors
  • amino acid metabolism
  • urea synthesis

lipids:

  • lipoprotein + cholesterol synthesis
  • fatty acid metabolism
  • bile acid synthesis

excretion/detoxification:

  • bile acid + bilirubin excretion
  • drug detoxification + excretion
  • steroid hormone inactivation + excretion

miscellaneous:

  • iron storage
  • vit A, D, E + B12 storage + metabolism
164
Q

what are the causes of liver disease? 8

A
  • alcohol
  • drugs
  • poisoning
  • fatty liver
  • infection (viral + non-viral)
  • autoimmune
  • metabolic
  • tumours + metastases
165
Q

give 5 examples of metabolic causes of liver disease.

A
  • haemachromatosis (congenital or acquired through transfusions)
  • anti-trypsin deficiency
  • wilson’s disease (copper metabolism)
  • diabetes
  • inborn errors of metabolism
166
Q

what are typical systemic signs of liver disease? 13

A
  • jaundice
  • itchy skin
  • gynaecomastia (dt excess oestrogen)
  • testicular atrophy (dt excess oestrogen)
  • palmar erythema
  • spider naevi
  • ascites
  • peripheral oedema
  • clubbing
  • bruising
  • encephalopathy
  • fatigue
  • osteomalacia/osteoporosis (dt reduced vit D)

nb liver has a lot of ‘spare capacity’ so can get quite damaged before signs/symptoms start to show

167
Q

what are the routine LFTs? 7

what can they mean if abnormal?

A

ALP (alkaline phosphatase)

  • bile duct problem/blockage
  • high bone turnover
  • also intestines + placenta

ALT (alkaline aminotransferase)
- indicative of liver damage (esp hepatitis)

AST
- raised in liver, skeletal muscle + RBC problems

Bilirubin

  • high direct (conjugated) = post-hepatic/obstructive
  • high indirect (unconjugated) = hepatic or pre-hepatic

Albumin

  • diarrhoea
  • liver disease
  • poor diet
  • iron deficiency
  • infection

GGT (gamma-glutamyl transferase)
- raised in bile duct probs

INR

  • liver not producing clotting factors/storing vit K
  • also altered by blood thinners + other stuff
168
Q

what is a tumour marker which is often raised in primary hepatocellular carcinoma?

A

alpha-fetoprotein

169
Q

what is used to treat paracetamol overdose? 2

A

activated charcoal
- gets patient to throw up any unabsorbed stuff

acetyl-cysteine
- acts as a precursor to glutathione

170
Q

if there was bilary tract damage, which LFTs would be raised? 3

A
  • CONJUGATED bilirubin
  • ALP
  • GGT
171
Q

what doyou do if there is no clinically obvious cause of raised ALP?

A

use electrophoresis to seperate out the different isoenzymes of ALP (from different sites of the body) to find out where the ALP is coming from

172
Q

what can produced a raised gamma glutamyltransferase (GGT)? 8

A
  • bile duct obstruction/problem
  • fatty liver (dt alcohol, diabetes or obesity)
  • alcohol
  • enzyme inducing agents (eg anti-epileptics)
  • pancreatic disease (acute + chronic pancreatiti, cancer)
  • heart failure
  • prostatic disease
  • kidney damage (AKI, nephrotic syndrome, rejection)
173
Q

primary sclerosing cholangitis (PSC):

  • what is it?
  • who gets it?
  • treatment?
A

inflammation and obliterative fibrosis of bile ducts inside and/or outside of the liver. This pathological process impedes the flow of bile to the intestines and can lead to cirrhosis of the liver, liver failure, and other complications, including bile duct and liver cancer.

75% of people with PSC have IBD (norm UC)

steroids/immunosuppresants
- only long term treatment is liver transplant

174
Q

jaundice:

  • medical name for it?
  • pre-hepatic causes? 2
  • post-hepatic causes? 4
A

hyperbilirubinaemia

pre-hepatic:

  • haemolysis (eg Rh incompatibility)
  • ineffective erythropoiesis (eg spherocytosis)

post-hepatic:

  • gallstones
  • cholangitis
  • biliary stricture
  • cancer (ie cholangiocarcinoma, head of pancreas)
175
Q

six hepatic causes of jaundice?

A
  • hepatitis
  • alcoholic liver disease
  • non-alcoholic fatty liver disease
  • cancer
  • inherited disorders of conjugation (unconjugated)
  • inherited disorders of excretion (conjugated)
176
Q

name two inherited disorders of bilirubin conjugation.

name two inherited disorders of bilirubin excretion.

A

conujugation:

  • gilbert’s
  • crigler-najjar

excretion

  • dubin-johnson
  • rotor
177
Q

if AST/ALP ratio is elevated with a normal ALP, what is the likely diagnosis?

A

hepatitis (90%)

178
Q

if AST/ALP ratio is normal with an elevated ALP, what is the likely diagnosis?

A

obstructive jaundice (90%)

179
Q

what would the colour of the urine and stools be in someone with:

  • pre-hepatic jaundice?
  • heptic jaundice?
  • post-hepatic jaundice?
A

pre-hepatic:

  • normal urine
  • normal stools

hepatic:
- variable (urine can be dark)

post-hepatic:

  • dark urine
  • pale stools

nb these are in general!

180
Q

specific tests in liver disease:

  • viral hepatitis? 1
  • chronic, active + autoimmune hepatitis? 4
  • primary biliary cirrhosis? 1
  • hepatocellular cancer? 1
A

viral hepatitis
- serology (hep A, B, C, D, E, CMV, HIV)

chronic, active + autoimmune hepatitis:

  • anti-smooth muscleantibodies
  • anti liver/kidney antibodies
  • anti microsomal antibodies
  • anti nuclear antibodies

primary biliary cirrhosis:
- anti-mitochondrial antibodies

hepatocellular cancer
- AFP tumour marker

181
Q

specific tests in liver disease:

  • hereditary haemachromatosis? 4
  • wilson’s disease? 4
  • a1-antitrypsin deficiency? 2
A

hereditary haemachromatosis:

  • ferritin
  • transferrin saturation
  • liver biopsy
  • genetic testing

wilson’s disease:

  • caeruloplasmin (carries copper in blood)
  • urine copper
  • plasma copper
  • liver biopsy

a1-antitrypsin deficiency:

  • a1-antitrypsin
  • genetic testing
182
Q

what common drug alters LFTs?

A

statins

183
Q

what does TATT stand for?

what can it indicate?

A

tired all the time

liver disease

184
Q

at what level of bilirubin does jaundice become visible?

A

> 40umol/L

185
Q

what can be found in a liver biopsy of someone with obstructive jaundice? 3

A
  • bile pigment visible in canaliculi
  • swelling + irregularity of hepatocytes
  • increased activity of kupffer cells (macrophages)
186
Q

what is it called when all hepatocytes, in an area of liver, have died?

A

confluent panacinar necrosis

187
Q

what are the 4 histological stages of liver disease seen in hepatitis?

A

normal

portal fibrosis

bridging fibrosis

cirrhosis

188
Q

what are the 3 histiological stages seen in alcoholic liver disease and NAFLD?

A
  • fatty change (steatosis)
  • alcoholic steatohepatitis (fatty change + hepatocyte injury, ballooning, inflammation, fibrosis)
  • cirrhosis
189
Q

what are the two different types of drug-induced liver injury?

A

intrinsic (eg paracetamol)
- anyone taking this drug is likely to get liver damage, predictable

idiosyncratic (eg some antibiotics)
- depends on individual susceptability, rare + can be severe

190
Q

what are the histological liver findings in paracetamol OD? 3

A
  • uniform zonal necrosis of hepatocytes
  • areas around portal trcts are spared
  • no inflammation seen
191
Q

in hereditary haemochromatosis, which 5 organs does iron build up in?

what effects does this have on each organ?

A

liver - cirrhosis

pancreas - diabetes

skin - hyperpigmented

joints - arthritis

heart - cardiomyopathy

“bornzed diabetes”

192
Q

what stain is used to find iron deposits in the liver? what colour does iron go with this stain?

A

perl’s stain

blue

193
Q

in wilson’s disease, which 3 organs does copper accumulate in, what affects does this have on each organ?

A

liver - cirrhosis

eyes - kayser-fleischer rings

brain - ataxia etc

194
Q

what effects does alpha-1-antitrypsin deficiency have on the body? 2

A

liver cirrhosis
- dt build up of abnormal protein

emphysema/COPD
- dt failure to inactivate neutrophiil enzymes

* year 2 Clinical Pathology (11 decks)

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