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4 - Med > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

what is achalasia ? pathology of what ?

A

myenteric plexus degeneration => loss of coordinated peristalsis + lower oesophageal sphincter fails to relax in response to swallowing => dysphagia, regurgitation + weight loss

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2
Q

achalasia px ?

A

dysphagia to solids + liquids, regurgitation, retrosternal pain
(slowly progressive over months or years)
=> weight loss

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3
Q

achalasia Ix ?

A

endoscopy (exclude malignancy)
barium swallow

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4
Q

achalasia Mx ?

A

CCB (verapamil)
- endoscopic balloon dilatation + PPIs

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5
Q

what is dyspepsia ?

A

sx that suggest issue of upper GI issue - epigastric pain, burning, early satiety, bleaching, bloating, nausea, disconfmot
- with no underlying cause
-

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6
Q

when would you do investigations in a patient who presents with dyspepsia ? what investigations ?

A

> 60 or <60 + alarm feature => endoscopy (to rule out malignancy)
<60 => non invasive test for H.pylori

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7
Q

what are the alarm features for dyspepsia ?

A

VBAD
- vomiting
- bleeding
- abdo mass
- dysphagia

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8
Q

what is a peptic ulcer ?

A

break in mucosal lignin of stomach (5cm diameter) to submucosa

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9
Q

what leads to peptic ulcer formation ? kind RF

A
  • factors promoting mucosal damage (gastric acid/pepsin/bile salts, H. pylori, NSAIDs/steroids
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10
Q

what factors protect against peptic ulcer formation ?

A

those promoting gasproduodenal defence
- blood flow
- mucus/mucin
- prostaglandins
- bicarbonate (neutralise acid)

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11
Q

what causes increased stomach acid production ?

A
  • stress
  • alcohol (high alcohol % can be corrosive)
  • excessive caffeine
  • smoking
  • spicy food
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12
Q

what does gastric mucosal ischaemia cause ?

A

(if low blood flow/mucosal ischaemia)
=> mucin barrier not as good => acid can kill cell => attack surrounding cells => ulcer formation

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13
Q

gastric ulcer presentation ?

A
  • epigastric discomfort + pain + tenderness to palpation (often related to hunger)
  • N+V
  • dyspepsia (indigestion)
  • haematemesis
  • coffee ground vomit
  • tarry bloody stools
  • iron deficiency anaemia (due to constant bleeding
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14
Q

how could gastric ulcer cause anaemia ?

A

big ulcer => deeper => hits artery => haemorrhage (into peritoneal cavity) => bloody stool

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15
Q

what investigations for gastric ulcer ?

A
  • endoscopy
  • rapid measure test (CLO test, to check for H.pylori)
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16
Q

gastric ulcer Mx ?

A
  • weight loss, stop dyspepsia-causing drugs
  • PPI
  • if H.pylori: PPI + 2Abx
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17
Q

when would you consider endoscopy in gastric ulcer presentation ?

A

if dysphagia OR >55 plus ALARM Sx => upper GI endoscopy (2WW)

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18
Q

what are the ALARM Sx for peptic ulcer presentaiton ? (6)

A
  • Anaemia (iron deficiency)
  • loss of weight
  • anorexia
  • recent onset/prgoressive sx
  • malaria/haematemesis
  • swallowing difficulties
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19
Q

what is H-pylori ? staining ? found where ? why is it bad ?

A

gram -ve aerobic bacteria that lives in the stomach
- avoids acidic environment by forcing its way into gastric mucosa + releases chemical mediator => increase acid production + inflammatory mediators

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20
Q

how does H.Pylori lead to gastric damage ?

A

lives in gastric mucosa and increases acid production => breaks in mucosa => expose epithelial cells => damage cells => gastritis, ulcers and increase risk of stomach cancer
- also produces ammonia which neuraltises acid but damages gastric epithelial cells

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21
Q

how can H.Pylori be tested for ? what is requirement for these ?

A

(ned 2 weeks without PPI for accurate result)
- urea breath test
- stool antigen test (looks for h pylori antigen
- rapid urease test (done during endoscopy)

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22
Q

what is the urea breath test ? test for what ? explain results

A

H. Pylori testing
- patient drink radio labelled C-13 drunk and if H.PYlori present, it breaks it down and if CO2 exhaled with C-13 then H.PYlori presence confirmed)

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23
Q

H Pylori Mx ?

A

triple therapy with PPI (omeprazole) + 2 Abx (amoxicillin + clarythromycin) (7days)

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24
Q

what is GORD ?

A

it is where acid +/- bile from stomach refuses through lower oesophageal sphincter => irritates oesophageal lining

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25
Q

describe the epithelium in oesophagus vs stomach

A

oesophagus: stratified squamous
stomach: simple columnar

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26
Q

how does GORD present ?

A
  • dyspepsia (indigestion)
  • heartburn
  • acid regurgitation
  • retrosternal pain
  • epigastric pain
  • blasting
  • nocturnal cough (when lying flat)
  • chronic cough
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27
Q

GORD RF ? (6)

A
  • high BMI
  • alcohol
  • smoking
  • CCB (reduces lower oesophageal sphincter pressure)
  • pregnancy
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28
Q

GORD Ix ?

A

clinical dx
- diagnosis confirmed by Mx trial

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29
Q

redid glafs for cancer in a GORD presentaiton ?

A
  • dysphagia
  • > 55
  • weight loss
  • upper abdo pain
  • treatment resistant dyspepsia
  • nausea and vomiting
  • low haemoglobin
  • high playlet count
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30
Q

GORD Mx ?

A
  • lifestyle advice
  • antacids: gaviscon, PPIs
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31
Q

describe GORD lifestyle advice

A
  • reduce tea/coffee/acohol intake)
  • weight loss
  • quite smoking
  • smaller meals
  • stay upright after meal
  • avoid eating <3 hrs before bed
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32
Q

GORD complications ?

A
  • stricture
  • Barretts oesophagus
  • oesophageal carcinoma
  • oesphagitis
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33
Q

What is Barretts oesophagus ?

A

log period of acid reflux into oesophagus (through lower oesophageal sphincter) => metaplasia (stratified squamous => simple columnar)

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34
Q

describe why the cellular metaplasia occurs in barrels oesophagus ?

A

stomach cells have neutral mucin buffer to protect but squamous cells delicate => gastric acid kills quick => grow back as glandular epithelium => unstable like this => predisposes to adenocarcinoma

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35
Q

barretss O RF ?

A
  • middle aged
  • white
  • male
  • GORD
  • tobacco smoking
  • obesity
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36
Q

Barretts oesophagus presentation ?

A
  • heartburn
  • regurgitation
  • dysphagia
    (similar to GORD)
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37
Q

Barretts oesophagus Ix ?

A

endoscopy to monitor for adenocarcinoma
- histological diagnosis: endoscopy with mucosal biopsy required

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38
Q

Barretts oesophagus Mx ?

A

PPI (omeprazole)
- ablation treatment (during endoscopy): destroy epithelium so replaced by normal cells

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39
Q

What is a hernia ?

A

protrusion of a viscus through. defect of the walls its containing cavity into an abnormal position (weka point of cavity wall)

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40
Q

what are the 3 complications of hernias ?

A
  • incarceration (hernia is irreducible => obstruction/strangulation)
  • obstruction (BO)
  • strangulation (=> ischaemia, surgical emergency)
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41
Q

abdo hernias general Mx ?

A
  • conservative Mx: leave hernia along (when hernia has wide neck => low risk of complications)
  • tension-free repair (surgical): mesh placed over abdo wall defect
  • tension repaire (surgical): suture muscles + tissue back together
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42
Q

what location is the most common hernia site ?in men ? in women ?

A

inguinal hernia (most common type in M+F)

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43
Q

differential for lump in inguinal region ? (7)

A
  • inguinal hernia
  • femoral hernia
  • lymph node
  • saphena varix
  • femoral aneurysm
  • abscess
  • undescended testes
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44
Q

what are the two types of inguinal hernia ? which most common ?

A
  • indirect (around 80%)
  • direct
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45
Q

describe indirect inguinal hernia ?

A

where bowel herniates through inguinal canal
- can strangulate more easily than direct

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46
Q

what is direct inguinal hernia ? due to weakness where ?

A

occurs due to weakness in th hesselbachs triangle (not along canal or tract)

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47
Q

how to distinguish between direct and indirect inguinal hernias ?

A
  • reduce the hernia and occlude deep (internal) ring
  • ask patient to cough
  • if hernia restrained => indirect
    (gold standard for distinguishing is surgery)
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48
Q

what is the contents of the inguinal canal (in males)

A
  • external spermatic fascia
  • spermatic cord (vas deferens, blood vessels, nerves, lymphatic vessels)
  • ilioinguinal nerve
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49
Q

what is a hiatus hernia ? defect of what

A

herniation of the stomach up through the diaphragm
- diaphragm opening should be at the lower oesophageal sphincter
- opening of diaphragm wider than should be => stomach enter through the diaphragm => contents of stomach can relax into oesophagus

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50
Q

-how many types of hiatus hernia re there ? most common ?

A

4 types
- type 1 - sliding (most common - 80%)

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51
Q

hiatus hernia Ix ?

A

can be intermittent so not always seen on imaging
- CXR
- CT
- Endoscopy

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52
Q

hiatus hernia Mx ?

A
  • lose weight
  • treat GORD
  • consider surgery for treatment resistance sx: laparoscopic fundoplication b
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53
Q

what is an upper GI bleed ?

A

medical emergency
- bleeding from oesophagus, stomach or duodenum

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54
Q

causes of upper GI bleed ? most common

A
  • oesophageal varices
  • mallory weiss tear
  • peptic ulcers (most common), caused by drugs
  • gastritis
  • drugs
  • malignancy
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55
Q

what drugs could cause upper GI bleed ?

A
  • NSAIDs
  • aspirin
  • steroids
  • anticoags
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56
Q

upper GI bleed Presentation ?

A
  • haematemesis
  • coffee ground commit (vomiting digested blood)
  • malaena (tar, black, greasy, stinky stool)
  • haemodynamic instability
  • epigastric pain or dyspepsia (if stomach ulcer cause)
  • weight loss (if cancer)
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57
Q

describe the urea trends with an upper GI bleed ?

A

upper GI bleed associated with increased serum urea (raised urea in proportion to creatinine indicates massive blood meal)
- digestive enzymes break down/digest blood => increase urea absorption

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58
Q

what tool used to estimate risk of upper GI bleed ?

A

glasgow-blatchford score

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59
Q

upper GI bleed Mx ?

A

(assess state and haemodynamic stability of patient (shocked ?))
ABATED
- ABCDE approach (oxy + fluids)
- Bloods (FBC, U+E)
- access (2 large bore cannulas)
- transfusion (or IV fluids while awaiting cross match)
- arrange urgent endoscopy (IV before endo)
- stop drugs (anticoags, NSAIDs)

  • consider terlipressin
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60
Q

why IV PPI before endoscopy in upper GI bleed Mx ?

A

helps blood aggregate so easier to visualise

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61
Q

if you think upper GI bleed is due to varices what do you also give ?

A

Give IV terlipressin (reduces mortality)

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62
Q

after initial upper GI bleed Mx, then what do you do ? after endoscopy (3)

A
  • transfuse to keep Hb > 70 g/L
  • consider FFP if > 4 units transfused
  • Rockall score (after endoscopy): estimates risk of rebreeding
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63
Q

What are oesophageal varices ? form as a result of what ?

A

Dilated collateral blood vessels that develop as consequence of portal hypertension

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64
Q

explain how liver cirrhosis leads to oesophageal varices ? occur where

A

portal HTN and varices
- liver cirrhosis => increased back pressure in portal system (portal HTN) => swelling at anastomoses between portal system + systemic venous system => varices
- occur at gastro-oesophageal, ileocaecal junction, rectum

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65
Q

causes of portal HTN ? (4)

A
  • thrombosis (splenic/portal vein)
  • cirrhosis (80%)
  • RHF
  • constrictive pericarditis
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66
Q

RF for vatical bleeds ? (2)

A
  • increased portal pressure
  • variceal size
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67
Q

oesophageal varices symptoms ?

A

don’t cause symptoms until they start bleeding => bleed out quickly (sig mortality + morbidity)
- active bleeding varices: haematemesis, melaena

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68
Q

managment of stable oesophageal varices ?

A
  • BB - propanolol (reduce bleed risk - prophylaxis)
  • elastic band ligation
  • transjugular intra-hepatic portosystemic shunt (if all fails)
    (prevent bleeding)
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69
Q

management of bleeding oesophageal varicies ?

A

ABATED + terlipressin (vasopressin analogue)
- plus endoscopic variceal band ligation (definitive treatment)

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70
Q

what is mallory Weiss tear ?

A

oesophageal mucosal tear of the mucus membrane => upper GI bleed
- the haemorrhage is self limiting in 80-90% of patients

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71
Q

mallory Weiss tear aetiology ?

A

coughing, retching, chronic cough, heavy alcohol use

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72
Q

mallory Weiss tear presentation ?

A

haematemsis (fresh streaks of blood)
FBC (anaemia)

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73
Q

mallory Weiss tear Ix ?

A

upper GI endoscopy (diagnostic)

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74
Q

mallory Weiss tear Mx ?

A

mostly self limiting, so supportive care
- if actively bleeding: resuscitation and therapeutic endoscopy

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75
Q

how does the type and quantity of bacteria change forms tomach to colon ?

A

(from stomach => colon)
aerobes => anaerobes
small => big quantity

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76
Q

what counts as diarrhoea ?

A

passage of loose watery stools (>3 in last 24 hrs)

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77
Q

name some non-infective causes of diarrhoea ? (5)

A
  • cancer
  • chemical
  • radiation
  • IBD
  • IBS
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78
Q

name some causes of watery infective diarrhoea ?

A
  • bacterial (cholera, E.coli (ETEC), c.diff)
  • virus (morovirus, rotavirus)
  • parasitic (giardia)
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79
Q

name some causes of bloody infective diarrhoea ?

A
  • bacterial (campylobacter, e.coli (EIEC), shigella, salmonella)
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80
Q

what does diarrhoea + low MCV anaemia indicate ? (2)

A
  • coeliac disease
  • colon cancer
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81
Q

what does diarrhoea and high MCV indicate ? (2)

A
  • alcohol abuse
  • or low B12 absorption (coeliac or crohns)
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82
Q

when would you admit someone present with diarrhoea ? (3)

A
  • fever >39
  • clinical dehydration
  • diarrhoea + visible blood > 2 weeks
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83
Q

What is clostridium difficile (c.diff) ? associated with what

A

gram +ve rod shaped anaerobic bacteria
- infection associated with repeated use of Abx, PPIs, healthcare settings
- asymptomattic carriage: 2-5% of all adults

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84
Q

which Abx are most associated with C.diff ? (3)

A
  • clindamycin
  • ciprofloxacin
  • cephalosporins
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85
Q

c.diff Ix and Mx ?

A

stool sample (c.diff antigen)
- Abx: stop causative one, start oral vancomycin

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86
Q

what is gastroenteritis ?

A

acute gastritis is inflam of the stomach and enteritis is inflam of the intestines
- so presents with nausea, vomiting and diarrhoea

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87
Q

what is E.coli ? how is it spread ? how does it present ?

A

normal intestinal bacteria (certain strains cause gastroenteritis)
- spread through contract with infected faces, contaminated water
- E.coli 0157 makes shiga toxin => abdo cramps, bloody diarrhoea, vomiting (+HUS)
- abx should be avoided

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88
Q

what is campylobacter jejuni ? how is it spread ? symptoms ? Mx ?

A

gram -ve bacteria (travelers diarrhoea)
- spread by raw/undercooked poultry, unpasteurised milk
- symptoms: abdo crampes, bloody diarrhoea, vomiting, fever
- abx: azithromycin

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89
Q

complications of diarrhoea ? (4)

A
  • lactose intolerance
  • IBS
  • reactive arthritis
  • Gillian bare syndrome
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90
Q

what is constipation ?

A

pelvic dysfunction or increased transit time => <2 bowel motions/week

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91
Q

what does constipation + rectal bleeding indicate ?

A

cancer

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92
Q

what does constipation + distension + active bowel sounds indicate ?

A

stricture/GI obstruction

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93
Q

what does constipation + menorrhagia indicate ?

A

hypothyroidism

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94
Q

when would you consider test in constipation ? (4)

A
  • lowing weight
  • abdominal mass
  • PR blood
  • Fe deficiency anaemia
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95
Q

how do bulking agents work ? give example

A

ispagula husk
- increase faecal mass => stimulate peristalsis (take with plenty of fluid, may take a few days to work)

96
Q

how do stimulant laxative work ? give example

A

Senna, sodium pico sulfate
- increase intestinal motility (so DONT use in intestinal obstruction of acute colitis)

97
Q

how do osmotic laxative works ? give example ?

A

lactulose, macrogol
- retain fluid in the bowel

98
Q

name sone drugs that cause constipation ? (5)

A
  • opiates
  • anticholingerics
  • iron
  • diuretics
  • CCB
99
Q

What is IBD ? what conditions ? both involve what ?

A

IBD is umbrella term for 2 main disease that cause inflam of GI tract
- UC + crowns both involve inflam of walls of GI tract + associated with periods of remission + exacerbation

100
Q

what causes raised faecal calprotectin ? what conditions ?

A

released from intestines when inflammation
- Cancer, IBD

101
Q

what investigations for IBD ? diagnostic ?

A
  • bloods (raised CRP, anaemia)
  • faecal calprotectin
  • endoscopy + biopsy (diagnostic)
  • CT or MRI (to look for fistulas, abscesses, strictures)
102
Q

where in GI tract is Crohns disease ? most common ?

A

usually seen in terminal ileum (70%)
- but can be anywhere gum to bum

103
Q

what are skip lesions and what IBD condition associated with them ?

A

Crohns disease
- normal bowel mucosa between diseased parts

104
Q

describe granuloma formation in crohns disease ?

A

lesion starts as inflammatory infiltrate around intestinal crypts => ulceration => inlammation gets deeper => granulomas (collection of histiocytes)

105
Q

what acronym for Crohns disease ? what does it stand for ?

A

Crohn’s (crows) NESTTS
- No blood or mucus (less common)
- Entire GI tract (mouth to anus)
- Skip lesions
- Terminal ileum (most affected)
- Transmural (full thickness of wall)
- smoking (RF - don’t set the nest on fire!)

106
Q

signs and symptoms of crohns disease ? (7)

A
  • chronic diarrhoea
  • weight loss
  • right lower quadrant abdo pain (mimicking acute appendicitis)
  • blood in stool
  • fever
  • fatigue
  • bowel obstruction
107
Q

Crohns disease Mx ?

A
  • induce remission: steroids (during flare up)
  • maintain remission: azathioprine or methotrexate or infliximab
  • surgery: surgical removal (if only affects distal ileum)
108
Q

Crohns disease complications ?

A
  • Intestinal obstrution
  • abscess fomration
  • distal formation
  • reduced QOL
  • sero -ve arthirits, ank spond
109
Q

what is UC ? involves where ?

A

type of IBD, involves rectum and variably extends to colon (can have sharp pathological cut off line)
- potential autoimmune disease initialed by inflammatory response to colonic bacteria

110
Q

UC risk factors ?

A
  • fam history
  • HLA-B27 (identified in most UC patients)
  • infection
111
Q

UC signs and symptoms ? (6)

A
  • rectal bleeding
  • diarrhoea
  • blood in stool
  • abdo pain/tenderness
  • arthritis
  • malnutrition
112
Q

UC accronym and what does it stand for ?

A

CLOSE UP
- Continuous inflam (no skip lesions on endoscopy)
- Limited to colon + rectum
- Only superficial mucosa
- Smoking is protective
- Excrete blood + mucus
- Use aminosalicylates
- Primary sclerosis cholangitis

113
Q

what biopsies are required for UC diagnosis ?

A

2 biopsies forma t least 5 sites along colon
- diagnosis requires endoscopy with biopsy and negative stool culture

114
Q

UC Mx ?

A

induce remission: aminosalicylate (mesalazine) or IV corticosteroids
- ongoing: continue aminosalicylate
- surgery: remove colon + rectum

115
Q

UC complicaitons ?

A
  • toxic megacolon
  • bowel adenocarcinoma
116
Q

What is coeliac disease ?

A

it is an autoimmune condition where exposure to gluten causes autoimmune reaction => inflammation of small bowel
- usually developed in early childhood

117
Q

coeliac disease pathophys ?

A

autoantibodies are created in response to exposure to gluten => target epithelial cells of small intestine => inflam => atrophy of intestinal villi => malabsorption

118
Q

what autoantibodies associated with coeliac ? and what genetic link

A

anti-TTG
anti-EMA
(go up and down with disease activity)
- HLA-DQ2/DQ8 (-ve predicative value of around 100%, but most ppl with these genes do NOT develop coeliac)

119
Q

coeliac disease presentation ? what skin condition associated ?

A
  • asymptomattic
  • failure to thrive
  • diarrhoea
  • tireness
  • weight loss
  • fatigue
  • mouth ulvers
  • anaemia
  • dermatitis herpetiformis (abdo rash)
120
Q

how is coeliac disease diagnosed ? (3)

A

investigations must be carried out on gluten containing diet
- check total IgA levels (to exclude IgA deficiency)
- raised anti-TTG antibodies
- Endoscopy + intestinal biopsy (crypt hypertrophy + villous atrophy)

121
Q

with what other conditions is coeliac associated with ? (4)

A

autoimmune conditions
- T1DM
- thyroid disease
- primary biliary cirrhosis
- primary sclerosis cholangitis

122
Q

coeliac disease complications ? (4)

A
  • vit d deficiency
  • anaemia
  • osteoporosis
  • NHL
123
Q

coeliac disease Mx ?

A

life long gluten free diet is curative

124
Q

What count as functional gut disorders ? (2)

A
  • IBS
  • functional dyspepsia
125
Q

what are functional gut disorders ?

A

chronic GI symptoms in the absence of organic disease to explain the symptoms (>6 months)

126
Q

What is IBS ? characterised by ?

A

chronic condition characterised by abdo pain, bowel dysfunction, pain relieved on defecation, abdo bloating

127
Q

IBS pathosphsy ?

A

altered gut reactivity (motility + secretion) in response to stimuli (environment, person life stress/abuse) or luminal (certain foods, toxins, inflammation) =? pain, constipation, diarrhoea
- dysregulation of the gut-brain axis

128
Q

IBS Ix ?

A
  • FBC: normal (anaemia suggests non IBS cause)
  • serology for coeliac
129
Q

IBS Mx ?

A
  • aim to reduce severity of symptoms, life style changes, reduce stress, reduce potential precipitating food (caffeine, lactose, fructose), low FODMAP diet, probiotics, laxative, antispasmodics (if experiencing pain and bloating)
130
Q

What is chronic pancreatitis ? most common cause

A

chronic inflammation in pancreas => fibrosis (irreversible) = reduced function
- alcohol is most common cause

131
Q

chronic pancreatic presentation ?

A

Similar to acute but less intestinal and longer lasting (sx release and worsen)

132
Q

chronic pancreatitis complications ?

A
  • chronic epigastric pain
  • loss of exo + endocrine function (=> diabetes, steatorrhoea, malnutrition)
  • abscess
  • pseudocyst formation
133
Q

chronic pancreatitis RF ? (4)

A
  • alcohol
  • smoking
  • FHx
  • coeliac disease
134
Q

chronic pancreatitis Ix ? what confirms Dx ?

A
  • US +/- CT
  • pancreatic calcifications confirm the dx
135
Q

chronic pancreatitis Mx ? (6)

A
  • stop smoking + alcohol
  • analgesia
  • replacement of pancreatic enzymes (creon)
  • sub cut insulin
  • ERCP withs tenting (Hilary obstruction)
  • surgery
136
Q

most common aetiology of carcinoma of the pancreas ? most arise where anatomically ?

A
  • mostly ductal adenocarcinoma
  • 60% arise from pancreatic head
137
Q

pancreatic cancer RF ?

A
  • smoking
  • alcohol- DM
  • chronic pancreatitis
  • 95% have mutation in KRAS2 gene
138
Q

pancreatitis cancer px ?

A

epigastric apin (radiates to back and relieved by sitting forward)
- similar to pancreatitis presentation

139
Q

pancreatic cancer Ix ? what would be seen

A
  • imagine: US/CT (pancreatic mass +/- dilated biliary tree +/- hepatic metastases)
140
Q

pancreatic cancer prognosis ?

A

v poor (mean survival < 6 months)

141
Q

what are carcinoid tumours

A

tumours of enterochromaffin cells (can be many locations)
- 80% of tumours > 2cm will metastasise

142
Q

carcinoid syndrome mx ?

A
  • octreotide (somatostatin analogue)
  • surgery: resection is the only cure for carcinoid tumours (whipples - removes head of pancreas)
143
Q

what is chronic liver disease ?

A

progressive deterioration of liver function for more than 6 months

144
Q

what is liver failure ?

A

development of coagulopathy ( INR>1.5) and encephalopathy + jaundice

145
Q

prescribe in liver failure: avoid what drugs ?

A
  • avoid drugs that constipate (antimuscarinics, opioids)
  • sedating meds (opioids, benzos, hypnotics)
    (=> increase risk of encephalopathy)
146
Q

liver failure symptoms + signs ? (9)

A
  • yellowing skin and eyes (jaundice)
  • abdominal pain + swelling (ascites)
  • swelling in legs + ankles
  • itchy skin
  • dark urine
  • pale stool
  • chronic fatigue
  • bruise easily
  • astarixis
147
Q

causes of liver failure ? (7)

A
  • viral hep (B, C, CMV)
  • leptospirosis
  • paracetamol overdose
  • alcohol
  • fatty liver disease
  • primary biliary cholangitis
  • primary sclerosing cholangitis
148
Q

what is liver cirrhosis ? what does this lead to ?

A

(end stage of any liver disease)
- cirrhosis is the fibrosis and conversion to abnormal nodules (regenerative nodules) => this leads to portal hypertension, liver failure, HCC

149
Q

CLD and liver failure RF ? (7)

A
  • heavy alcohol consumption
  • obesity
  • T2DM
  • tattoos and piercings
  • sharing needles
  • unprotected sex
  • FHx of liver disease
150
Q

what is ascites ? explain. caused by what ?

A

increased extravascular fluid pressure => fluid accumulation in anterior peritoneal cavity
- caused by systemmic vasodilation and increased intrahepatic resistance

151
Q

ascites Mx ? (4)

A
  • restrict fluid
  • low salt diet
  • weigh daily
  • dietetics (spironolactone)
152
Q

what are some of the complications of liver failure ?

A
  • cerebral oedema
  • ascites
  • bleeding
  • encephalopathy
153
Q

treating liver failure complications: cerebral oedema ?

A
  • 20% mannitol
  • hyperventilate
154
Q

how does liver failure lead to cerebral oedema ?

A

nitrogenous waste (ammonia) build up => osmotic imbalance => fluid shift into astrocytes (cerebral oedema(

155
Q

treating liver failure complications: bleeding ? (3)

A
  • IV vit K
  • platelets
  • FFP + blood as needed
156
Q

how does liver failure cause encephalopathy ? explain the ammonia

A

ammonia is produced when intestinal bacteria break down protein => absorbed into gut => enter blood stream
- ammonia builds up as liver cells no function properly => not metabolised right
- colateral vessels between portal + systemic system mean liver bypassed
- leads to brain exposure to ammonium (neurotoxin)

157
Q

hepatic encephalopathy presentation ?

A

vary, mild alteration in mental state to coma (often reversible with treatment)
- mood/sleep/motor disturbances

158
Q

hepatic encephalopathy diagnosis ?

A
  • based on neurological defects + lab abnormalities showing liver dysfunction
  • head CT (fuel out differential, may show oedema)
159
Q

hepatic encephalopathy Mx ?

A
  • 20 degree head up tilt in ITU
  • correct electrolytes
  • laxatives (lactulose), promote ammonia excretion
  • nutritional support
  • Abx (rifaxamine) => reduce number of intestinal bacteria that produce ammonia
160
Q

what is hepatorenal syndrome (HRS) ?

A

cirrhosis + ascites + renal failure
- life threatening condition that consist of rapid deterioration of kidney

161
Q

what are the 3 main features of liver cirrhosis ?

A
  • jaundice
  • ascites
  • encephalopathy
162
Q

what is liver cirrhosis ?

A

it is the result of chronic inflam + damage to liver cells (pathological end stage of CLD)
=> fibrosis and nodular degeneration
- damaged liver cells replaced with scare tissue (fibrosis) which forms nodules within liver

163
Q

how does the fibrotic change affect liver ?

A

fibrosis affects liver blood flow and increase resistance in vessels leading to liver (portal hypertension)

164
Q

causes of liver cirrhosis ? (10)

A

(any CLD)
- alcohol liver disease
- NAFLD
- hep B/C
- autoimmune hep
- primary biliary corrhosis
- haemochromatosis
- Wilsons disease
- alpha 1 antitrypsin disease
- CF
- drugs (amiodarone, methotrexate)

165
Q

signs of liver cirrhosis ?

A
  • juandice
  • hepatomegaly (only early on)
  • splenomegaly (due to portal HTN)
  • spider naval
  • bruising (due to low clotting factors)
  • ascites
  • asterixis
  • leukonychia (from hypoalbuminaemia)
166
Q

what would US show in liver cirrhosis ?

A

modularity of liver, enlarged portal vein, ascites, splenomegaly

167
Q

how confirm liver cirrhosis diagnosis ?

A

liver biopsy

168
Q

what can be used as marker for HCC

A

alpha-feto protein is tumour marker for HCC

169
Q

what scoring tool assess severity of liver cirrhosis ?

A

child Pugh score (5 -15)
- bilirubin, INR, ascites, encephalopathy

170
Q

liver cirrhosis general Mx ? what ongoing monitoring ? how often ?

A

US + alphafetoprotein every 6 months to screen for HCC
- endoscopy every 3 years in patients with known clarifies
- high protein, low salt diet
- MEDL score every 6 months to assess mortality + need for liver transplant
- treat underlying cause and complications

171
Q

liver cirrhosis complications ?

A
  • hepatic failure: coagulopathy, encephalopathy, hypoalbuminaemia (oedema), sepsi (pneumonia), spontaneous bacterial peritonitis (SBP), hypoglycaemia
  • portal HTN: ascites, splenomegaly, oesophageal varices
172
Q

what should you suspect in patient with ascites who deteriorates ? most common cause ?

A

spontaneous bacterial peritonitis (SBP)
- e.coli, klebsiella

173
Q

what are the most common aetiology of liver tumours ?

A

90% are metastases
(from stomach, lung, colon, breast)

174
Q

What is hepatitis ? when does it count as chronic ?

A

it is inflammation of liver
- can vary form chronic low level to severe inflam => necrosis + liver failure
(>6 months: chronic)

175
Q

hepatitis presentation ?

A
  • asymptomattic
  • abdo pain
  • fatigue
  • pruritus
  • muscle + joint aches
  • N&V
  • jaundice
  • fever
176
Q

name some infective causes of acute hepatitis ?

A
  • viral (hep A, B+/- D, C, E), HPV
  • non-viral: syphillus, TB
177
Q

name some non-infective causes of acute hepatitis ?

A
  • alcohol, drugs, toxins
  • NAFLD
  • pregnancy
  • autoimmune hepatitis
178
Q

which viral hepatitis can lead to chronic hepatitis ?

A

hep B+/-D, C (+E)

179
Q

hepatitis A:
- what type of virus ?
- how transmitted ?

A

most common worldwide (but rare in UK), problem for travellers
- RNA virus
- transmitted via faeco-oral route (contaminated food + water)

180
Q

Hep A Px ?

A
  • N&V
  • anorexia
  • jaundice
  • cholestasis
  • hepatomegaly
  • dark urine
  • pale stools
181
Q

Hep A Ix ?

A
  • Serological markers: IgM anti hepatitis A virus serology (+ve)
  • deranged LFTs
  • raised bilirubin
  • prolonged PTT
  • raised serum creatinine
182
Q

Hep A Mx ? prognosis ?

A

usually resolves by itself in 1-3 months
- so supportive mx (+analgesia)
- avoid alcohol
- have immunity after infection (can’t get infected twice)
- public health notifiable disease

183
Q

Hep B
- what type of virus is it ?
- how is it transmitted ?

A

DNA virus
- transmitted by blood or body fluid (sex, shared needles, vertical transmission)

184
Q

hep B RF ? (6)

A
  • prenatal exposure
  • multiple sexual partners
  • MSM
  • IVDU
  • born in endemic area (Asia, Africa)
  • harm-dialysis
185
Q

hep B prognosis ?

A

most people recover within 2 months but 10% => chronic hep B carriers (viral DNA has integrated into own DNA => continue to produce viral proteins => cirrhosis, hepatocellular cancer, decompensation)

186
Q

acute hep B Mx ? whole approach/ what. else other than medicine (6)

A
  • antiviral meds (entecavir): to slow progression and reduce infectivity
  • test for complications (fibroscan for cirrhosis, USS for HCC)
  • screen at risk patients for hep B?C, HIV
  • notify public health
  • stop smoking + alcohol (minimise liver damage)
  • inform and immunise sexual contacts
187
Q

what hep B screening ?

A
  • antenatal screening
  • universal blood product screening
188
Q

describe the hep B vaccination ?

A
  • involves infecting hep B surface antigen (which triggers immune response => hep B surface Abs)
  • vaccinated patients are tested for hep B Ab to confirm response to vaccine
189
Q

Hep C
- what type of virus
- how transmitted ?

A
  • RNA virus
  • spread by blood and bodily fluids
190
Q

hep C prognosis ?

A

1/4 make full recovery (without treatment)
3/4 => chronic hep C
(no available vaccination but is now curable with direct acting anti-viral meds)

191
Q

hep C Px ?

A
  • often asymptomattic
  • fatigue
  • joint stiffness
  • jaundice
192
Q

how hep C diagnosed ?

A
  • hep C antibody test
  • if +ve: hep C RNA PCR test (confirm diagnosis + viral load)
193
Q

hep C Mx ?

A

(same as hep B)
- antiviral med (glecaprevir) to slow progression and reduce infectivity
- test for complications (fibroscan, USS)
- screen at risk patients for Hep B/C + HIV
- notify public health
- stop smoking + alcohol (minimise liver damage)

194
Q

Hep D
- what type of virus
- transmission ?

A

RNA virus
- only present in patients with hep B infection. attaches to hep B surface antigen (required to survive)
- blood Bourne

195
Q

Hep D Ix and Mx ?

A
  • hep D antibody
  • treat: pegylated interferon alpha
  • B + D increases risk of complications, more severe disease (cirrhosis, decompensation)
196
Q

Hep E
- what type of virus ?
- transmission ?

A
  • RNA virus
  • transmitted by faecal-oral route
    (rare in the UK)
197
Q

hep E prognosis ?

A

usually mild illness, cleared within a months
- no treatment required
- rarely can progress to chronic hep and liver failure (but can in immunocompromised)

198
Q

hep E Ix ?

A

viral serology: initially anti-HEV IgM and then anti-HEV IgG

199
Q

hep E Mx ? acute ? chronic ?

A

acute: supportive, monitor for fulminant hep (severe liver impairment)
- chronic: reverse immunosuppression
- notify public health

200
Q

what is autoimmune hepatitis ? characterised by what ?

A

inflam liver disease of unknown cause (possible environmental factor)
- characterised by abnormal T-cell function + autoantibodies directed against hepatocyte surface antigens
=> liver cirrhosis => liver failure

201
Q

autoimmune hepatitis Px ?

A
  • fatigue
  • malaise
  • anorexia
  • abdo pain
  • hepatomegaly
  • jaundice
  • amonrrhoea
202
Q

autoimmune hepatitis Ix ? Dx ?

A
  • raised transaminases
  • high IgG levels
  • autoantibodies
  • Diagnosis: confirmed with liver biopsy (and positive autoantibodies)
203
Q

autoimmune hepatitis Mx ?

A
  • high dose steroids (prednisolone), other immunosuppressant (azathioprine)
  • life long immunosuppression (remission achievable in 80% patients)
  • if advanced liver disease => liver transplant
204
Q

what are cholelithiasis ? when do they cause symptoms ?

A

gallstones: presence of stones in gall bladder that may exit into bile ducts
- cause symptoms when stone obstruct cystic duct, common bile duct, pancreatic duct

205
Q

what is purpose of gall bladder ? what makes it contract ?

A

stores bile waiting for signal form stomach that there is fat (CCK) => gallbladder contract

206
Q

what are the main constituents of gallstones ?

A

> 90% consist of cholesterol and bile pigment
( cholesterol supersaturation and increased haemoglobin breakdown => stone formation)

207
Q

gall stone RF ? (5)

A
  • female
  • fat
  • forties
  • fertile (pregnancy)
  • rapid weight loss
208
Q

gall stones Px ?

A
  • mostly asymptomattic
  • binary colic pain (often after eating)
  • RUQ tenderness + pain
  • jaundice
209
Q

what is the scan of choice for suspected gallstones ?

A

abdominal US (shows presence of stones in GB, dilated CBD

210
Q

what could raised WCC in biliary colic presentation suggest ?

A

consider acute cholecystitis

211
Q

biliary colic Mx ?

A
  • Analgesia (NSAID, paracetamol)
  • rehydrate
  • NBM
  • elective laparoscopic cholecystectomy (early or delayed)
212
Q

complications of gallstones ? (4)

A
  • biliary colic
  • acute and chronic cholecystitis
  • acute cholangitis
  • acute pancreatitis
213
Q

What is acute cholecystitis ? caused by what ?

A

it is inflammation of gall bladder caused by blockage of cystic duct or neck of GB => prevent GB drainage
- key complications of gall stones

214
Q

how do gall stones cause acute cholecystitis ?

A

trapped gallstones => irritation + pressure => inflammation

215
Q

acute cholecystitis Presentaiton ?

A
  • pain in RUQ, radiating to R shoulder
  • fever
  • nausea
  • vomiting
  • tachycardia
  • tachynpiena
  • Murphys signs
  • raised WCC

(no jaundice )

216
Q

acute cholecystitis Ix ? what would they show ?

A
  • abdo US (thickened GB wall, stones (main cause), fluid around GB)
  • MRCP (if bile duct stone suspected but not seen on US)
217
Q

acute cholecystitis Mx ? (5)

A
  • bit by mouth (rest gall bladder)
  • IV fluids
  • IV Abx (co-amox)
  • ERCP (remove sones trapped in CBD)
  • laparoscopic cholecystectomy (GB removal)
218
Q

what is charcots triad ? what does it indicate ?

A

Acute cholangitis
- RUQ pain
- Fever/raised WCC
- Jaundice

219
Q

what is Acute cholangitis ?

A

infection and inflammation in the bile ducts
- surgical emergency

220
Q

what causes Acute cholangitis ?

A

caused by obstruction in bile ducts (gallstones) or infection introduced in ERCP (e.coli, klebseilla, enterococcus)
- can quickly become acute, septic life threatening disease

221
Q

Acute cholangitis RF ? (4)

A
  • > 50
  • cholelithiasis
  • benign or malignant stricture
  • prev ERCP procedure
222
Q

Acute cholangitis presentaiton ?

A
  • Charcot’s triad (RUQ pain, fever, jaundice)
  • pale stools (jaundice), pruritus (high bile acids)
223
Q

Acute cholangitis Mx ? (6)

A

(surgical emergency)
- NBM
- IV fluids
- Analgesics
- Sepsis screen
- Start IV Abx
- ERCP: required to investigate and remove the stones blocking bile duct

224
Q

What is primary biliary cirrhosis ? what does it lead to ?

A

immune system attacks small bile ducts in liver (first affecting interlobular ducts) => obstruction of outflow of bile => cholestasis => increase back pressure => fibrosis => cirrhosis => liver failure
(progressive bile duct damage => eventual loss)

225
Q

explain PBC pathophys ? how does it explain the symptoms ?

A
  • obstruction to outflow => increase bile acids, bilirubin and cholesterol in blood => pruritus, jaundice + xanthelasma (cholesterol deposits in skin)
  • lack of bile in gut (usually helps digest fat) => GI disturbances, fat malabsorption, greasy stools (steatorrhoea)
226
Q

PBC presentation ? (8)

A
  • fatigue
  • pruritus
  • GI disturbance
  • abdo pain
  • jaundice
  • pale stools
  • xanthelasma
  • signs of cirrhosis and liver failure (ascites)
227
Q

how is primary biliary cirrhosis diagnosed ?

A
  • presence of autoantibodies (antimitochondiral Ab)
  • raised ALP
  • liver biopsy (for diagnosing and staging)
228
Q

primary biliary cirrhosis Mx ? (5)

A
  • bile acid analogue (ursodeoxycholic acid)
  • immunosuppression (prednisolone)
  • antipuruitic (cholecystamine)
  • vitamin supplementation (ADEK)
  • if end stage liver failure: liver transplant
229
Q

what is primary sclerosing cholangitis ?

A

it is condition where intra + extra hepatic ducts become structured and fibrotic (narrowing + hardening) => obstruction to flow of bile out of liver into intestines
(progressive disease)

230
Q

what doesprimary sclerosing cholangitis lead to ?

A

chronic obstruction of bile => back pressure of bile into liver => hepatitis => fibrosis => cirrhosis

231
Q

which bile duct condition is UC associated with ?

A

primary sclerosing cholangitis

232
Q

primary sclerosing cholangitis px ?

A
  • jaundice
  • chronic RUQ pain
  • prurits
  • fatigue
  • hepatomegaly
233
Q

primary sclerosing cholangitis Ix ? Dx ?

A
  • LFTs (cholestatic picture: deranged ALP, high bilirubin, deranged transaminases)
  • diagnosis: MRCP (gold standard) would show bile duct lesions or strictures
234
Q

primary sclerosing cholangitis complications ? (3)

A

acute bacterial cholangitis
cirrhosis
liver failure

235
Q

primary sclerosing cholangitis Mx ? (3)

A

liver transplant is only curative option (but not always best)
- ERCP (dilate + stent strictures
- cholesytamine (improve pruritus)

4 - Med (12 decks)

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