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Year 3 > GI including liver > Flashcards

GI including liver Flashcards

1
Q

What is IBD (inflammatory bowel disease)?

A

inflammation of bowel caused by genetics/ environment/ poor immune system. (more common in young adults)

  1. Crohns - patchy transmural inflammation of gut mucosa affecting any part of GIT

*genetics (NOD2) , M=F,

  1. Ulcerative colitis- continuous inflammation of superficial mucosa layer from rectum

*genetics (HLA2, HLAB27, p-ANCA)

  • directly linked to primary sclerosing cholangitis
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2
Q

Presenting symptoms of IBD (with history)

A

Crohn’s

  • mainly non-bloody diarrhoea
  • crampy abdominal pain
  • WEIGHT LOSS
  • extreme fatigue

UC

  • more frequent bloody diarrhoea
  • autoimmune: uveitis
  • Primry sclerosing cholangitis

BOTH non-bowel related (autoimmune): arthritis, erythema nodosum (red bumps), jaundice (raised bilirubin + ALP)

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3
Q

Examination findings of IBD

A

UC: usually none but if severe fever, tachycardia, tender/distended abdomen, clubbing, oral ulcers, angular stomatitis, anaemia (visible pallor, conjunctival pallor), jaundice (PSC)

Crohn’s: abdominal tenderness, clubbing, angular stomatitis, skin/joint/eye problems

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4
Q

Investigations + findings of IBD

A

Bedside:

  • Stool microscopy and culture: exclude infective colitis/ GASTROENTERITIS
  • Fecal calprotectin from stool sample - sign of non-specific bowel inflammation

Bloods

  • FBC - low Hb, high platelets (anaemia= chronic disease) high WCC
  • LFTs - low albumin
  • High ESR (suggests chronic inflammation) – inflammatory marker
  • CRP may be high or normal - inflammatory marker

Imaging:

  • AXR: could show evidence of toxic megacolon,
  • Erect CXR: if there is a risk of perforation
  • Colonoscopy/ flexible sigmoidoscopy + biopsy GOLD STANDARD
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5
Q

How to distinguish between crohns and ulcerative colitis (biopsy/ endoscopy)?

A

Crohns: non-caseating granulomas, fistulas, strictures, cobblestone appearance

UC: pseudopolyps, continuous inflammation from rectum

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6
Q

Management for Crohn’s

A

Acute Exacerbation

  • Fluid resuscitation, may also be on oral iron
  • IV/oral corticosteroids
  • 5-ASA analogues (e.g. mesalazine and olsalazine)
  • Analgesia
  • Parenteral nutrition may be necessary

● Monitor markers of disease activity e.g. fluid balance, ESR, CRP, platelets, Hb

Long-Term

  • Corticosteroids (prednisolone/ dexamethosone) - induce remission
  • Immunosuppression: using steroid-sparing agents (e.g. azathioprine, 6-mercaptopurine, methotrexate) reduces the frequency of relapses
  • Anti-TNF agents: (e.g. infliximab and adalimumab)

*Can try liquid therapy diet for Crohn’s/ small kids

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7
Q

Lifestyle changes advised for Crohns

A
  • stop smoking (but smoking better in UC)
  • low fibre diet
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8
Q

Management for UC

A

Acute:

  1. Corticosteroids- hydrocortisone (for SEVERE acute flare ups)
  2. 5-ASA analogues - decreases the frequency of relapses (useful for MILD to moderate disease)
  3. Immunosuppresion (azothioprine)- maintain remission if multiple exacerbations
  4. Biological therapies (anti-TNF therapies)
  5. Surgery=> more for UC - Proctocolectomy with ileostomy – surgical removal of colon, rectum and anal canal
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9
Q

mechanism + side effects of steroids (prednisolone)

A

glucocorticoid receptors interact with specific DNA sequences to increase anti-inflammatory gene produces + reduce pro-inflammatory products.

  • short term: weight gain, Cushing syndrome, mood swings,
  • long term: diabetes, adrenal suppression, osteoporosis, avascular necrosis, thin skin
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10
Q

mehcanism + side effects of immunosupressants (azathioprine)

A

reduce DNA/RNA production of lymphocytes/ interleukins => suppresses immune system => anti-inflammatory

Side effects:

  1. nausea, flu-like
  2. bone marrow suppression
  3. pancreatitis (raised amylase)
  4. hepatotoxicity
  5. increased cancer risk
  6. increased hypersensitivity => skin rashes
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11
Q

mechanism and side effects of biologics (anti-TNFa)

A

monoclonal antibodies against TNFa which reduce disease activity by reducing neutrophil accumulation + granuloma formation and cause cytotoxicity to CD4+ T cells.

Side effects:

  • redness, itching, bruising, pain, or swelling at the injection site
  • headache, fever, rashes
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12
Q

prognosis for IBD

A

IBD patients should have a colonoscopy every 5 years as they are at increased risk of colorectal cancer

Crohns - chronic relapsing condition
● 2/3 of patients will require surgery at some stage
● 2/3 of these patients require more than 1 operation

Ulcerative colitis - normal life expectancy

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13
Q

complications of IBD

A
  • fistulas (narrow passage connecting organs together)
  • malnutrition
  • bowel obstruction
  • colorectal cancer
  • intestinal perforation/ rupture
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14
Q

what is coeliac disease?

A

autoimmune disease triggered by eating gluten. T cells attack small intestine so can’t absorb nutrients.

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15
Q

How to diagnose coeliac disease from history?

A

=> diarrhoea + weight loss

  • STEATORRHEA (fatty stools)
  • fatigue
  • bloating/ gas
  • abdominal pain
  • nausea/ vomiting
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16
Q

Investigations for coeliac disease

A

bloods:

  • FBC (low Hb/ low ferritin/ low b12) ANAEMIA
  • anti-transglutaminase antibody test

=> if high level of suspicion/ positive AB test => duodenal biopsy when on gluten (atrophied tissue)

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17
Q

Management for coeliac disease

A
  1. lifelong gluten free diet
    - can prescribe gluten-free food (biscuits/flour/bread/pasta)
  2. monitor response and repeat tests
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18
Q

complications of coeliac disease (if untreated)

A
  • anaemia
  • dermatitis herpetiformis
  • osteoporosis/ osteopenia
  • infertility
  • hyposplenism (give them flu jabs)
  • increased cancer risk
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19
Q

prognosis of coeliac disease

A

if treated => very good
untreated => fatal

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20
Q

Define IBS

A
  • chronic, relapsing disorder of lower GI tract with recurrent episodes of abdominal pain/ discomfort >6 months

+ altered stool passage
+ abdominal bloating
+ passage of mucus
+ symptoms worse on eating

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21
Q

causes of IBS

A
  • environmental
  • genetic

Trigger symptoms:

  • enteric infection
  • GI inflammation (secondary to IBD)
  • dietary factors (alcohol, caffeine, spicy/fatty foods)
  • Antibiotics
  • stress/ anxiety/ depression (affect brain-gut axis)
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22
Q

presenting symptoms of IBS

A
  • >6 months colicky abdominal pain (pain relieved on defecation)
  • >6 months bloating
  • >6 months change in bowel habit (altered stool consistency, rectal mucus)
  • symptoms worsened by eating
  • other symptoms: lethargy, nausea, back pain, headache, bladder problems, fecal incontinence
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23
Q

Examination signs of IBS

A

usually normal

  • distended abdomen + mildly tender on palpation in illiac fossa
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24
Q

Investigations + findings for IBS

A

*usually diagnosed by exclusion + history

  • Bloods (FBC=> anaemia, ESR/ CRP => inflammatory markers) TFTs
  • Coeliac serology (anti-transglutaminase antibodies - exclude coeliac disease)
  • Stool microscopy, sensitivity and culture (exclude infection)
  • USS (exclude gallstone disease)
  • Sigmoidoscopy
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25
Q

Management of IBS

A
  • Dietary modification (avoid fibre, lactose, fructose, wheat, starch, caffeine, alcohol, fizzy drinks, )

Medical

  • antispasmodics (for bloating)
  • prokinetics (increases GI motility)
  • anti-diarrhoea/ loperamide (for diarrhoea)
  • low dose tricyclic anti-depressants

Psychological therapy:

  • CBT
  • Psychotherapy
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26
Q

complications of IBS

A
  • physical/psychological morbidity
  • colonic diverticulitis
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27
Q

define GORD

A

reflux of stomach contents (acid +/-bile) causing oesophageal inflammation due to failure of anti-reflux barrier

Reflux barrier:

  • folds of stomach
  • intrabdominal portion of oesophagus
  • LOS
  • sling fibres of gastric cardia
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28
Q

causes of GORD

A
  1. lower oesphageal sphincter hypotension
  2. hiatus hernias
  3. oesophageal dysmotility (systemic sclerosis)
  4. increased gastric acid secretion/ delayed gastric empyting
  5. drugs- NSAIDs

Lifestyle:

  • smoking
  • alcohol
  • pregnancy
  • caffeine
  • irregular meals
  • obesity
  • XS excerise => infcreased intra-abdominal pressure
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29
Q

presenting symptoms of GORD

A
  • heart burn/chest pain
  • watery brash (saliva + acid regurgitation)
  • bitter taste on tongue
  • belching/burping
  • odynophagia (pain on swallowing)
  • worse on lying down/ bending, after eating + alcohol

Non-oeosophageal

  • aspiration => wheeze, cough, laryngitis => Resp team
  • hoarseness, sore throat, globus sensation (stuck in throat) => ENT team

RED FLAGS: (malignancy => 2WW)

  • Dysphagia
  • Anorexia
  • Weight loss
  • Odynophagia
  • Iron deficiency Anaemia
  • GI bleeding
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30
Q

examination findings of GORD

A
  • generally normal
  • epigastric tenderness
  • wheeze on auscultation
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31
Q

Investigations for GORD

A

*usually clinical diagnosis

  1. upper GI Endoscopy + biopsy (look at mucosal break - area of erythema separate from normal mucosa + exclude malignancy in >55)
  2. 24hr pH monitoring + manometry- speed of peristalsis (normal =40)

catheter inserted from nose => oesophagus (reflux episodes over 24hrs, how long pH<4.5)

  1. +/- barium swallow (confirm hiatus hernia, oeopshageal peristalsis)
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32
Q

Management of GORD

A
  1. lifestyle (weight loss, stop smoking, less caffeine/alcohol/ spicy foods / citrus fruit, EAT >3hrs before bed, raise bed head)
  2. Medication: PPI (lansoprazole), antacids/ alginates (Gaviscon), , H2 blocker (ranitidine) start high dose=> lower single daily dose
  3. Surgical: antireflux surgery, Nissen’s fundoplication (wrap fundus around lower oesophagus)
  4. regular Endoscopy - keep checking for barrets oeopshagus

Anti-reflux surgery:

  1. reduce hiatus hernia
  2. 2-3 cm of lower oeosphagus
  3. repair fundus defect
  4. wrap gastric fundus around lower oesophagus - prevents reflux (usually 360- Nissens fundoplication, 180- partial wrap)
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33
Q

Indications for anti-reflux surgery

A
  • unresponsive to medical management (check compliance + for duration 12-18 months)
  • complications (Barrett’s, peptic stricture)
  • extra-oeospheageal manifesations (asthma, hoarseness, chest pain)
  • younger patients who don’t want to be on lifelong medication
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34
Q

Complications of GORD

A
  1. oesophagitis
  2. barrets oesophagus => oesophageal cancer
  3. peptic strictures
  4. oesophageal ulceration
  5. laryngitis
  6. anaemia

Complications of surgery:

  • dysphagia (odema)-need liquid diet
  • gas bloat/ flatulance- new anti-reflux valve can’t burp/belch
  • convert from laprascopy to open surgery
  • failure to conrol/ reuccurent symptoms
    *
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35
Q

define gastritis

A

inflammation of mucosal lining of stomach

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36
Q

types of gastritis

A
  1. erosive + haemorrhagic gastritis - caused by NSAIDs, trauma, burns
  2. non-erosive/ chronic gastritis- in antrum due to H.pylori
  3. atrophic gastritis => neuroendocrine tumours/ pernicious anaemia
  4. reactive gastritis
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37
Q

Describe pathophysiology of atrophic gastritis

A

autobodies against parietal cells

  1. less HCL => increased gastrin production => gastric epithelial hyperplasia => increased risk of tumours (neuroendocrine)
  2. less IF => less B12 absorption => pernicious anaemia
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38
Q

Define peptic ulcer disease

A

GI ulceration due to increased gastric acid and pepsin. Most commonly gastric/ duodenal (rarer: oesophagus/ Meckel’s diverticulum)

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39
Q

Causes of peptic ulcers

A

imbalance of acid production

  • H-pylori
  • NSAIDs
  • smoking
  • alcohol
  • bisphosphonates
  • RARE: Zollinger-Ellison syndrome (gastrin-secreting tumour/ hyperplasia of pancreatic islet cells => increased acid production)
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40
Q

presenting symptoms of peptic ulcers

A
  • epigastric pain radiating to back
  • relieved by antacids
  • (75%) gastric ulcer - worse after eating
  • (95%) duodenal ulcer- relieved by eating
  • can have haematemesis, melena
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41
Q

examination findings of peptic ulcers

A
  • Usually normal
  • some epigastric tenderness
  • signs of anaemia (conjuctival pallor, koliconichyia)
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42
Q

Investigations for peptic ulcer disease (in <55 with no red flags)

A

Bedside

  • H-pylori breath test/ stool antigen test
  • Stool occult

Bloods

  • FBC- Hb, MCV (anaemia)
  • amylase (exclude pancreatitis)
  • LFTs
  • U&Es- check for dehydration
  • serum gastrin
  • IV Secretin test (for Zollinger-Ellison syndrome)=> secretin causes a rise in gastrin
  • clotting screen

Other

  • GI Endoscopy + biopsy (DIAGNOSTIC)
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43
Q

Gold standard investigation for peptic ulcer (>55 / red flags)

A

Upper GI endoscopy

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44
Q

Different ways to measure H.pylori

A
  1. urea breath test
  2. blood antibody test => presence of IgG against H-pylori
  3. stool antigen test
  4. Campylobacter-like organism test- biopsy + urea + pH indicator, if H-pylori present converts urea=> ammonia (yellow=> red colour change) urease enzyme
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45
Q

Management of peptic ulcer disease

A
  1. IV fluid resus
  2. monitor vitals
  3. Endoscopy- if bleeding => laser coagulation/ electrocoagulation
  4. Surgery - if perforated ulcer

if H.pylori infection=> triple therapy Non H-pylori

=>PPIs/ H2 antagonist

=> stop NSAIDs (if needed use misoprostol)

  • Stop NSAIDs
  • Eradicate H.pylori (Triple therapy- clarithromycin + amoxicillin + PPI-omperazole)
  • Check on gastric ulcer healing with repeat endoscopy 6-8 weeks later
  • If reccurent ulcers think other cause
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46
Q

Complications of peptic ulcer disease

A
  • haemorrhage
  • perforation
  • obstruction/ pyloric stenosis (due to scarring/ penetration)
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47
Q

Define colorectal cancer

A

cancer in bowel

  • most common in sigmoid/ rectum
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48
Q

Presenting symptoms of colorectal cancer

A

Left sided pain

  • fresh red PR bleeding
  • constipation + diarrhoea
  • abdominal mass

Right sided pain (insidious)

  • iron deficiency anaemia
  • weight loss
  • fever
  • diarrhoea
  • bowel obstruction (vomiting, nausea, acute abdomen, shock, distension)

Rectal

  • tenesmus (FEEL MASS haven’t completely gone to loo)
  • PR bleeding
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49
Q

Risk factors for colorectal cancer

A
  • poor diet (fatty, red meat)
  • alcoholics
  • obesity
  • diabetes
  • genetic syndromes (FAP, IBD, lynch syndrome, peutz-jegher)
  • ethnicity (Ashkenazi Jews)
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50
Q

Investigations for colorectal cancer

A

Bedside

  • PR exam
  • Abdo exam
  • ECG
  • Stool culture
  • assess if fit for surgery

Bloods

  • FBC- anaemia
  • LFTs- metastasis
  • U&E- dehydration
  • CRP- inflammation
  • tumour markers - CEA, AFP

Imaging

  • barium enema
  • CT abdo
  • CT CAP +colonoscopy => staging
  • OGD
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51
Q

What would be seen on barium enema of bowel osbtruction/ colorectal cancer?

A

Apple core strictures

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52
Q

Genetic conditions that cause colorectal cancer

A
  • hyperpigmentation of mucosal membranes => peutz-jegher (autosomal dominant)
  • 321 rule - >3 relatives, 2 generations, 1 >50 with CRC => Lynch syndrome (endometrial/gastric/ ovarian cancer risk)
  • >100 polyps => familial adenomatous polyposis (inhibits APC tumour suppressor gene)
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53
Q

How to stage colorectal cancer?

A

Dukes criteria

  • A- mucosa + submucosa involvement
  • B- muscle layer involvement
  • C- lymph node metastasis
  • D- distant metastasis
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54
Q

Management of colorectal cancer

A
  • A+B => surgery
  • C => surgery + adjuvant chemo
  • D => chemo +/- surgery +/- radiotherapy
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55
Q

Types of surgery for colorectal cancer

A
  • right sided=> right hemicolectomy
  • left sided => left hemicolectomy
  • transverse colon => extension hemicolectomy
  • sigmoid => Hartmann’s
  • rectal => create anal stump
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56
Q

Management for emergency bowel obstruction + colorectal cancer risk

A

defunctioning stoma - cut ileum and create stoma to allow large bowel to rest

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57
Q

Define oesophageal carcinoma

A

malignant tumour of the oesophagus. 2 histological types:

  • squamous cell carcinoma (more common in LEDC)
  • adenocarcinoma (more common in western world)
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58
Q

Causes of oesophageal carcinoma

A

SCC

  • alcohol
  • achalasia
  • scleroderma
  • tumours
  • Plummer-wilson
  • nutritional deficiencies

Adenocarcinoma

  • GORD
  • Barrett’s oeosphagus
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59
Q

Presenting symptoms of oesophageal carcinoma

A
  • can be asymptomatic
  • progressive dysphagia (initially worse for solids => liquids)
  • hoarseness
  • weight loss
  • fatigue
  • odynophagia (painful on swallowing)
  • cough
  • regurgitation
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60
Q

Examinations findings of oesophageal carcinoma

A
  • usually no signs
  • metastatic disease => supraclavicular lymphadenopathy, hoarseness, hepatomegaly
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61
Q

Investigations for oesophageal cancer

A

Imaging

  • OGD + biopsy
  • CXR - exclude perforation
  • Barium swallow (can see shouldering)
  • Staging: CT CAP, PET, endoscopic ultrasound

Other: bronchoscopy, blood gas, lung function tests

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62
Q

Management of oesophageal carcinoma

A
  • early stage => surgery (oesophagectomy/ oesophagogastrectomy) + adjuvant chemo/radiotherapy
  • late/ metastatic => palliative chemo, stent, laser treatment for lesion
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63
Q

Define pancreatic cancer

A

malignancy of the exocrine/endocrine tissues of the pancreas

*most tumours in head of gland + exocrine tissue

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64
Q

causes of pancreatic cancer

A
  • UNKNOWN
  • some hereditary (FAP, HNPCC, MEN, Von-hippel Lindau syndrome)
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65
Q

Risk factors for pancreatic cancer

A
  • older age (>60)
  • smoking
  • alcohol
  • chronic pancreatitis
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66
Q

Presenting symptoms of pancreatic cancer

A
  • non-specific symptoms
  • FLAWS - fever, lethargy, anorexia, weight loss, nausea
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67
Q

Examination findings of pancreatic cancer

A
  • jaundice
  • Epigastric tenderness/ mass
  • palpable gallbladder + painless
  • If metastatic => hepatomegaly, splenomegaly, lymphadenopathy
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68
Q

Investigations for pancreatic cancer

A

Bloods

  • Tumour markers (Ca-19-9, CEA)
  • LFTs (obstructive => high GGT, ALP, bilirubin)

Imaging:

  1. CT scan (within 2 weeks) + Staging CT CAP
  2. USS abdomen- exclude gallstones/ only if CT not possible
  3. MRCP - look for blocked bile/pancreatic duct, ERCP - biopsy, tissue diagnosis, stenting
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69
Q

Management of pancreatic cancer

A
  • early (surgery + adjuvant chemo)
  • late (palliative chemo +/- surgery +/- raiotherapy)
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70
Q

Label ERCP

A

A- endoscope

B-duodenum

C- leads

D-common bile duct

E- dilated intrahepatic duct

F- sternotomy clip

G- ampullary stricture

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71
Q

complications of pancreatic cancer

A
  • diabetes
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72
Q

Define gastric cancer

A

Malignancy of the stomach

  • adenocarcinoma (most common)
  • leimyosarcoma
  • stromal tumours
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73
Q

risk factors for gastric cancer

A
  • genetic (FAP)
  • poor diet (processed foods, salt, low vit C)
  • smoking
  • alcohol
  • atrophic gastritis
  • pernicious anaemia
  • H. pylori infection
  • post-gastrectomy
  • blood group A
  • hypogammaglobulinanaemia
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74
Q

presenting symptoms of gastric cancer

A

early

  • appetite loss
  • epigastric discomfort
  • indigestion
  • nausea
  • heart burn

Late

  • Haematemesis
  • weight loss
  • stomach pain
  • dysphagia
  • jaundice (metastasis)
  • ascites (metastasis)
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75
Q

examination findings of gastric cancer

A
  • epigastric mass
  • abdominal tenderness
  • ascites/ jaundice (metastasis)
  • conjunctival pallor (anaemia)
  • virchow’s node
  • sister mary joesph nodule (metastatic node in umbilicus)
  • krukenburg’s tumour (ovarian mass due to metastasis)
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76
Q

investigations for gastric cancer

A
  • bloods - FBC (anaemia), LFTs (metastasis)
  • Upper GI endoscopy + biopsy
  • CT CAP- for staging
  • Endoscopic USS
  • Liver ultrasound + bone scan - for tumour staging
  • Laprascopy
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77
Q

Management of gastric cancer

A
  • SURGERY (fit/ early) = subtotal/ total gastrectomy
  • Endoscopic mucosal resection (early stages)
  • Chemo- metastatic
  • Radiotherapy
  • Monoclonal antibodies (Trastuzumab- blocks HER2 - blocks growth signals to gastric cancer cells)*stage IV
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78
Q

Define biliary colic

A

gallstone causing obstruction in gallbladder/ common bile duct causing biliary tree contraction to relieve obstruction

*x3 more common in females

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79
Q

types of gallstones

A
  • mixed (cholesterol, calcium bilirubinate, phosphate, protein)
  • pure cholesterol stones
  • pigment stones- black (calcium bilirubinate), brown (bile duct infestation)
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80
Q

risk factors for gallstones (6Fs)

A
  • fat
  • forty
  • fertile
  • female
  • family history
  • fair (caucasian)
  • diabetes
  • drugs: ocreotide/ OCP
  • haemolytic disorders (sickle cell, hereditary spherocytosis, thalassemia) => pigment stones
  • crohn’s (due to poor enterohepatic recycling of bile salts)
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81
Q

presenting symptoms of biliary colic

A
  • sudden severe constant RUQ pain => radiating to right scapula
  • pain usually after fatty meals
  • nausea
  • vomiting
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82
Q

examination findings of biliary colic

A

RUQ/ epigastric tenderness

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83
Q

investigations for biliary colic

A

Bloods

  • FBC (raised WCC)
  • LFTs
  • amylase (exclude pancreatitis)
  • blood culture

Bedside

  • urinalysis
  • ECG

Imaging

  • Abdo + biliary tree USS
  • Abdo X-ray (only 10% of stones = opaque)
  • Extra: MRI, ERCP, MRCP
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84
Q

Management for biliary colic

A
  • conservative => low fat-diet
  • remove symptomatic stones in CBD using ERCP then check LFTs are normal => cholecystectomy
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85
Q

complications of gallstones

A

In gallbladder:

  • biliary colic (obstruction of gallbladder/common bile duct)
  • acute cholecysitits (inflamed gallbladder)
  • gallbladder cancer
  • gallbladder empyema (pus)

Outside gallbladder:

  • acute cholangitis (infection of bile duct)
  • obstructive jaundice
  • gallstone ileus
  • Mirizzi syndrome= common hepatic duct obstruction due to stone in gallbladder/ cystic duct
  • Bouveret syndrome- gastric outlet obstruction

*cholelithiasis (presence of gallstones in gallbladder)

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86
Q

Define cholecystitis

A

gallbladder inflammation usually due to stone/ sludge formation in the gallbladder neck.

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87
Q

Presenting symptoms of cholecystitis

A
  • unwell, fever
  • prolonged RUQ pain => radiating to shoulder (irritates diaphragm C3-5)
  • pain worse after eating fatty foods
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88
Q

Examination signs of acute cholecystitis

A
  • tachycardia
  • +ve Murphy’s sign
  • pyrexia
  • RUQ/ epigastric tenderness
  • local peritonism (guarding + rebound tenderness)
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89
Q

Investigations for acute cholecystitis

A

Bedside:

  • urinalysis - check for haematuria (renal colic)

Bloods

  • FBC- raised WCC (cholecystitis/cholangitis)
  • LFTs - exclude cholangitis (high GGT +ALP)
  • Blood cultures
  • amylase - exclude pancreatitis

Imaging

  • US of billiary tree/ abdomen - thickened gallbladder wall, calculi (only 20% of stones are opaque)
  • CXR - exclude perforated viscus
  • MRCP - only for complicated gallstone disease
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90
Q

Management of acute cholecystitis

A

Medical:

  • NBM
  • IV fluids + analgesia
  • Antibiotics
  • If symptoms persist (abscess/empyema) => drainage

Surgical:

  • Laprascopic cholecystectomy
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91
Q

Complications of acute cholecystitis

A
  • empyema
  • abscess
  • cancer?

cholecystectomy

  • infection
  • bleeding
  • bile leak
  • fat intolerance (no gallbladder => no bile)
  • post-cholecystectomy syndrome (dyspepsia, nausea, RUQ pain)
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92
Q

Define acute cholangitis

A

infection of the bile duct

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93
Q

Causes of acute cholangitis

A
  • gallbladder/ bile duct obstruction by stones
  • ERCP
  • tumours (pancreatic, cholangiosarcoma)
  • parasites (ascariasis)
  • bile duct stricture/ stenosis
  • cholecystectomy => dilate common bile duct
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94
Q

presenting symptoms of acute cholangitis

A
  • Charcot’s triad (fever, RUQ pain=> spread to right shoulder, jaundice)
  • Reynold’s pentad (charcot’s + mental confusion + septic shock/hypotension)
  • pruritus (itching)
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95
Q

Examination signs of acute cholangitis

A
  • fever
  • RUQ pain
  • jaundice
  • mental confusion
  • sepsis
  • hypotension
  • tachycardia
  • mild hepatomegaly
  • Murphy’s sign +ve
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96
Q

investigations for acute cholangitis

A

Bloods

  • FBC- high WCC
  • high CRP
  • LFTs - obstructive picture (raised GGT + ALP)
  • U&Es- check for renal dysfunction
  • slightly elevated amylase if stone in lower CBD
  • blood culture- check for sepsis

Imaging

  • US KUB- check for stones
  • Abdominal ultrasound - check for gallstones/ biliary tree dilation/obstruction
  • CXR- exclude perforation
  • contrast CT/MRI - check for cholangitis
  • MRCP- check for non-calcified stones
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97
Q

Management of acute cholangitis

A

Immediate

  • ABC
  • analgesia, IV fluid, antibiotics
  • endoscopic billiary drainage

Surgical

  • ERCP (Endoscopic retrograde cholangiopancreatography) + sphincterectomy
  • Open bile duct exploration is a last resort due to a high mortality risk
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98
Q

complications of ERCP

A
  • infection
  • pancreatitis
  • aspiration pneumonia
  • duodenal perforation
  • haemorrhage
  • ascending cholangitis
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99
Q

Complications of acute cholangitis

A
  • liver abscess
  • liver failure
  • AKI
  • septic shock => organ dysfunction

endoscopic drainage can lead to=> Intra-abdominal or percutaneous bleeding, sepsis, fistulae and bile leakage

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100
Q

Define Vitamin B12 deficiency

A

inadequate vitamin B12 to meet demand

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101
Q

Causes of vitamin B12 deficiency

A
  • atrophic gastritis => autoantibodies destory parietal cells =>less IF => less B12 absorption
  • gastrectomy
  • terminal ileum resection (where B12 absorbed)
  • reduced intake (vegans, vegetarians - B12 in red meat)
  • malabsorption (crohn’s)
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102
Q

Presenting symptoms of b12 deficiency

A
  • fatigue
  • lethargy
  • dyspnoea
  • headaches
  • palpitations
  • fainting
  • neurological - numbness, parathesia, cognitive/ visual changes
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103
Q

Examination findings of b12 deficiency

A
  • anaemia signs (conjuctival pallor, glossitis, angular stomatits)
  • neurological (peripheral neuropathy, degeneration of spinal chord)
  • psychiatric (dementia, irirtability, depression)
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104
Q

Investigations for b12 deficiency

A
  • plasma total Homocysteine
  • plasma methymalonic acid
  • Serum b12 - less relaible
  • Bloods- FBC (hypersegmented neutrophils, oval macrocytes

Tests for perniciosu anaemia

  • anti-intrinsic factor antibodies
  • anti-parietal cell antibodies
  • shilling test
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105
Q

Management of B12 deficiency

A
  • neurological symptoms => hydroxocobalamin
  • no neurological symptoms + diet related => hydroxocobalamin
  • no neurologicl symptoms + non-diet related => cyanocobalamin

advise more B12 in diet (eggs, soya, red meat, dairy)

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106
Q

Define haemorrhoids

A

Cushions of vascular rich connective tissue located in the anal canal.

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107
Q

Risk factors for haemorrhoids

A
  • Constipation/ increased straining
  • pregnancy
  • 45-65 age
  • portal hypertension
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108
Q

Classification of haemorrhoids

A
  • Internal- superior haemorrhoidal plexus, above dentate line
  • External = below dentate line

*dentate line = line divides the upper 2/3 anal canal from lower 1/3

  • Grade 1- no prolapse
  • Grade 2- prolapse with defecation but reduces by itself
  • Grade 3- prolapse + manually reducible
  • Grade 4- proplapse + can’t reduce
    *
109
Q

Presenting symptoms of haemorrhoids

A
  • bright red PR bleeding- on wiping
  • Sudden perinatal discomfort
  • anal pruitus
  • tender anal mass
  • Painless (no sensory fibres) unless external => thrombosed
  • NO ALARM SYMPTOMS
110
Q

Examination signs of haemorrhoids

A
  • grade 1/2 can’t be seen on external inspection
  • internal haemorrhoids can’t usually be palpated on DRE
111
Q

Differentials for haemorrhoids

A
  • anal fissure
  • anal tags
  • polyps
  • rectal prolpase
  • tumour
112
Q

Investigations for haemorrhoids

A
  • Abdo exam
  • DRE- can see prolapsed haemorrhoids
  • Protoscopy- can see internal haemorrhoids
  • Rigid/ flexible sigmoidoscopy
113
Q

Management of haemorrhoids

A
  • 1st degree = conservative
  • 2/3rd degree = non-surgical (banding, sclerotherapy)
  • 4th degree = surgery

Conservative

  • Laxatives
  • High fibre diet
  • high fluid intake

Banding- applied proximal to haemorrhoids (will fall off after a few days)

Sclerotherapy- fibrosis of dilated veins

Surgery- Morgan- Milligan haemorrhoidectomy

114
Q

complications of haemorrhoids

A
  • bleeding
  • prolapse
  • thrombosis
  • gangrene
115
Q

Define ascites

A

fluid collection in peritoneal cavity

116
Q

Causes of ascites

A
  • CIRRHOSIS
  • portal hypertension (congestive heart failure, pericarditis, fulminant hepatits- XS Paracetamol, Budd-chiari syndrome, alcoholic liver disease)
  • hypoalbumin-anaemia (nephrotic syndrome)
  • Malignancy , liver metastasis
  • infectious peritonitis
117
Q

presenting symptoms of ascites

A
  • abdominal distension
  • risk factors for heart failure (smoking, diabetes, hypertension, high cholesterol, elderly, family Hx)
  • history of alcohol consumption (alcoholic liver disease)
  • risk factors for hep C (drug user, blood transfusion)
  • family Hx (liver disease, autoimmune heaptitis)
  • Symptoms of heart failure (SOB +/- odypnoea)
  • toxins (paracetamol overdose)
118
Q

examination findings of ascites

A
  • abdominal distension
  • shifting dullness
  • abdominal thrills
  • signs of liver disease (palmar erythema, leuconycia, jaundice, hepatomegaly)
  • raised JVP => congestive HF
  • pitting oedema => nephrotic syndrome
119
Q

Investigations for ascites

A

Bloods

  • FBC (thrombocytopenia => portal hypertension)
  • LFT (raised bilirubin)
  • U&Es (monitor for hepatorenal syndrome)
  • Viral serology (hep A/B/C)

Imaging

  • ultrasound
  • CT abdo
  • MRI abdo
  1. Abdominal parentesis - check serum albumin levels (cirrhosis)
  2. Blood culture if non cirrhosis
  3. Liver biopsy - identify cause
120
Q

managment of ascites

A
  • diuretics
  • abdominal paracentesis- drain fluid
  • insertion of a transjugular intrahepatic portosystemic shunt (for portal hypertension)
  • Prevent development of spontaneous bacterial peritonitis

Lifestyle

  • stop drinking
  • reduce fluid intake
  • treat cause
121
Q

Define gastroenteritis (infectious colitis)

A

acute inflammation of GIT lining

  • dysentry = type of gastroenteritis with bloody diarrhoea
122
Q

Causes of gastroenteritis

A

caused by toxins, viruses, bacteria, protozoa in contaminated food/ water

Dystentry (bloody gastroenteritis) causes: CHESS

  • Campylobacter jejuni
  • Haemorrhagic E.coli
  • Entomoeba histolytica
  • Salmonella
  • Shigella
    *
123
Q

Typical causes of gastroenteritis

A
  • elderly with antibiotics overuse = C. Difficile
  • young children/ D+V hopsital incident = Norovirus
  • Uni student with watery diarrhoea= Campylobacter jejuni
  • Travellers diarrhoea = E. coli
  • Diarrhoea after meals = S. aureus

Contaminated food

  • uncooked meat= stap. aureus, C. perfiringens
  • milk + cheese = Listeria, campylobacter
  • Eggs + poultry= salmonella
  • canned food = botulinum
124
Q

Presenting symptoms of gastroenteritis

A
  • SUDDEN nausea, vomiting
  • DIARRHOEA (watery/ bloody)
  • SUDDEN anorexia
  • fever + malaise
  • SPECIFIC: botulinum (paralysis), mushrooms (renal failure)

Symptoms present:

  • toxins (<24hrs)
  • virus/bacteria/protozoa (12+hrs)

Ask about

  • recent travel history
  • antibioitc use
  • any close contacts with diarrhoea/vomiting
  • recent meals (takeouts/ raw foods/ how food was prepared)
125
Q

Examination findings of gastroenteritis

A
  • abdominal tenderness
  • abdominal distension
  • XS nausea/diarrhoea=> dehydration
  • hypotension (low bp)
  • fever
126
Q

Investigations for gastroenteritis

A

Bedside

  • stool culture (MC&S)- C.diff => pseudomembranous colitis

Bloods

  • FBC
  • U&Es- dehydration
  • blood culture

Imaging

  • AXR/ ultrasound - exlcude perforation (could cause abdo pain)
  • Sigmoidoscopy (if IBD suspected)
127
Q

Management of gastroenteritis

A

Mild/moderate dehydration

  • Bed rest - 48hrs
  • Oral rehydration soloution (fluids + electrolytes)
  • +/- anti-emetics (ondansetron)
  • +/- anti-diarrhoeal (ioperamide) avoid in bloody/infectious diarrhoea as can prolong infection

Severe dehydration

  • IV fluids
  • +/- anti-emetics
  • +/- anti-diarrhoeal

*Only give antibiotics - if SEVERE infection

128
Q

Specific treatment for C. diff infecitons

A
  1. Isolate
  2. Metronidazole (antibiotic)
  3. if returns, vancomycin
129
Q

Complications of gastoenteritis

A
  • dehydration
  • electrolyte imbalances
  • prerenal failure (dehydration)
  • Haemolytic uraemic syndrome (E.coli toxin)
  • respiratory muscle weakness (botulinum)
    *
130
Q

Define Haemochromatosis

A

autosomal recessive genetic disorder that causes increased iron absoprtion in the small intestine

*defect in HFE gene

131
Q

Presenting symptoms of haemochromatosis

A

usually asymptomatic and present in later stages:

Early

  • weakness
  • fatigue
  • arthralgia (joint disease)
  • erectile dysfunction

Later

  • Diabetes
  • Hypogonadism => loss of libido, impotence
  • bronzed skin
  • arrythmias
132
Q

Examination findings of haemochromatosis

A
  • hepatomegaly (associated cirrhosis)
133
Q

Investigations for haemochromatosis

A

Bedside:

  • ECG (not diagnostic)

Bloods

  • Haematinics: serum ferritin (HIGH), transferrin (LOW), transferrin saturation (HIGH) *not specific
  • LFTs/ CRP (exclude other causes for high ferritin)
  • fasting blood glucose
  • testosterone/ LH/FSH assay (check for hypogonadism)

Imaging

  • Liver MRI- check for Fe overload
  • Echo (check for cardiomyopathy)

Other:

  • Genetic testing (HFE mutation)
  • Liver biopsy
134
Q

Management for haemochromatosis

A

Stage 0

  • 3yr follow up
  • lifestyle changes (reduce iron/vit C in diet + supplements, stop alcohol)
  • Hep A/B vaccines

Stage 1

  • 1yr follow up
  • lifestyle changes
  • Hep A/B vaccines

Stage 2-4

  1. Phlebotomy (remove blood to stimulate new RBC production using stored iron) + lifestyle modifications +/- Hep A/B vaccines
  2. Iron chelation (deferasirox) + lifestyle modification +/- Hep A/B vaccines

*2nd line treatment for patients who can’t give blood- anaemia, severe heart disease, difficult venous access

135
Q

Why should vit C be avoided in patients with haemochromatosis?

A
  • increases absorption of dietary iron in small bowel
  • but can be given in small doses with iron chelation (to increase iron for chelation)
136
Q

Define peritonitis

A

inflammation of the peritoneal lining of the abdominal cavity

  • Localised (usually resolves with treatment)
  • Specialised bacterial peritonitis
  • Generalised (worse prognosis)
  1. Primary- RARE, most common in females- usually resolves with ABs
  2. Secondary
137
Q

Causes/ risk factors of peritonitis

A

Localised

  • appendicitis
  • cholecysitis
  • diverticulitis
  • post-surgery

Generalised

  1. Primary - bacterial cause, ascites, nephrotic syndrome, UTI
  2. Secondary - bacterial, non-bacterial spillage of bowel contents/blood/bile (e.g. perforated peptic ulcer)

Localised/ secondary generalised common post surgery

138
Q

Presenting symptoms of peritonitis

A
  • continuous, sharp, stabbing abdominal pain
  • pain worsened by movement so patient usually lying still
  • vague symptoms if patient has liver disease (confusion from encephalopathy)
139
Q

Examination findings of peritonitis

A

Localised

  • abdomen tenderness
  • rebound tenderness
  • guarding

Generalised (worse)

  • unwell patient
  • signs of sepsis (fever, tachycardia + dehydration)
  • patient lying still
  • rigid abdomen
  • shallow breathing
  • generalised abdomen tenderness
  • may have reduced bowel sounds (due to paralytic ileus)
140
Q

Investigations for peritonitis

A

Bedside:

  • pregnancy test
  • urine dipstick

Bloods:

  • FBC - raised WCC
  • U&Es- check for dehydration => AKI (raised urea/creatinine)
  • LFTs
  • amylase (exclude pancreatitis)
  • CRP - bowel inflammation
  • blood cultures
  • clotting screen
  • group & save
  • ABG?

If ascities is present

  • ascitic tap (exclude SBP- >250mm^3 neutrophils)
  • gram stain + culture

Imaging:

  • CXR- exclude perforation
  • AXR- exclude bowel obstruction
  • USS- exclude stones
141
Q

Management of peritonitis

A

Localised

  • identify and treat cause (surgery for appendicectomy/ antibiotics for salpingitis)

Generalised

  • RESUS: treat sepsis/ shock
  • IV fluids
  • IV antibiotics (PRIMARY)
  • Urinary catheter
  • NGT
  • central venous line (monitor fluid input)
  • Laparotomy (remove infected tissue + drainage)

Specialised bacterial peritonitis (SBP)

  • quinolone antibiotics
  • cerufoxime + metronidazole
142
Q

Complications of peritonitis

A

Early

  • sepsis
  • resp failure
  • multi-organ failure
  • paralytic ileus
  • abscess
  • wound infection

Late

  • incisional hernia
  • adhesions
143
Q

define hyposplenism

A
  • dysfunctional spleen or spleen removed during splenectomy
144
Q

Causes of hyposplenism

A
  • splenectomy (due to spleen trauma, cysts)
  • Bone marrow transplant (Graft Vs host disease, splenic irradiation)
  • congenital asplenia (missing spleen)

functional hyposplenism

  • sickle cell anaemia
  • thalassemia major
  • Hodgkins Lymphoma
  • Coeliac disease
  • IBD
145
Q

Indications for splenectomy

A
  • trauma
  • spontaneous rupture
  • hypersplenism
  • neoplasia (leukaemia/ lymphoma infiltration)
  • splenic cysts
  • splenic abscess
146
Q

Investigations for hyposplenism

A
  • Blood film (howel-jolly bodies, Pappenheimer bodies, irregularly contracted cells, target cells)
  • Ultrasound/ CT/ MRI imaging
147
Q

Management for hyposplenism

A
  • vaccines (S. pneumoniae, N. meningitidis, H. influenzae type b and influenza virus)
  • antibiotic prophylaxis (1-2yrs after splenectomy)- for patients high risk for penumococcal infections (macrolides)

High risk=

  • <16, >50
  • don’t respond to pneumococcal vaccine
  • immunosuppressed
  • haemotological malignancies
148
Q

Complications of hyposplenism/ splenectomy

A
  • Thrombocytosis (high platelets)

RISK OF INFECTIONS:

  • S. pneumoniae (pneumoccocus)
  • N. meningitidis
  • H. infleunzae type B
  • E.coli
  • Malaria
149
Q

define perianal abscess and fistula

A

perianal abscess= collection of pus

perianal fistulae= abnormal connection between perineal skin and anal canal/rectum

150
Q

causes of perianal abscess + fistula

A
  • bacterial infection => abscess
  • IBD
  • Diabetes
  • Malignancy

Fistula

  • complication of an abscess
  • complication of Crohn’s (IBD)- multiple perianal fistuae (pepper pot)
151
Q

presenting symptoms of perianal abscess / fistula

A
  • throbbing pain in perianal region
  • intermittant dishcarge (mucus/ faecal)
  • Family Hx of IBD
152
Q

Examination findings of perianal abscess / fistula

A
  • tender mass (can be fluctuant)= abscess
  • small skin lesion near anus (opening of fistula)
  • DRE = thickened area (but can’t always be done due to pain/ anal sphincter spasm)

To determine pathway of fistula=> GOODSALL’S rule

  • external opening is anterior to transverse line across anus => straight radial tract to anteriorly
  • external opening is posterior/ 3cm away => curved tract to midline posteriorly
153
Q

Investigations for perianal abscess / fistula

A

Bloods:

  • FBC
  • CRP
  • ESR
  • blood culture

Imaging

  • MRI
154
Q

Management of perianal abscess / fistula

A

SURGICAL TREATMENT

  • drainage of abscess
  • low Fistula=> laying open (fistulotomy)- minimal damage to anal sphincter =>reduce INCONTINENCE
  • High fistula => Seton (non-surgical thread keeping tract open and allows drainage)
  • ANTIBIOTICS

external sphincter - voluntary defecation

internal sphincter - involuntary

155
Q

Complications of perianal abscess / fistula

A
  • RECURRENCE (if not fully excised)
  • Incontinence (damage to internal anal sphincter)
  • perisiting pain
156
Q

Define viral gastroenteritis

A

inflammation of the lining of GIT due to enteropathogenic viruses

viruses damage enterocytes => structural changes to mucosa => malabsorption + loss of brush border enzymes (food intolerance)

*usually spread person-person, food/water borne

157
Q

causes of viral gastroenteritis

A

Rotaviruses- airborne

noroviruses- children/elderly high risk (fecal-oral route)

caliciviruses

astroviruses

coronaviruses

enteric adenoviruses

158
Q

presenting symptoms of gastroenteritis

A
  • mild fever
  • nausea + vomiting
  • frequent, watery diarrhoea
  • abdominal pain
  • anorexia (appetite loss)
159
Q

examination findings of gastroenteritis

A
  • high temp
  • dehydrations signs- tachycardia, hypotension, dry mucous membranes
  • mild abdominal pain + tenderness
160
Q

investigations for viral gastroenteritis

A

bedside:

  • urine dip (UTI, infection-glucose)
  • pregnancy test
  • stool culture - MC&S

bloods

  • FBC- Hb (anaemia= chronic cause), raised WCC- infection,
  • U&Es- raised urea:creatinine ratio (AKI/ dehydration), Na+/K+ (to give fluids)

stool viral culture (RARE)- identify virus

Imaging:

  • AXR- exclude bowel obstruction
161
Q

risk factors for viral gastroenteritis

A
  • close contact with infected people
  • poor hygiene
  • contaminated food/water
  • extreme ages (younger kids/elderly)
162
Q

Management for viral gastroenteritis

A
  1. oral rehydration or IV fluids crystalloid soloution (for SEVERE DEHYDRATION)

consider if can’t tolerate oral hydration: anti-emetics (neurological side effects)/ anti-diarrhoeal drugs (not for inflammatory causes)

163
Q

define infectious diarrhoea

A

diarrhoea caused by infectious agents (bacteria, virus, protozoa)

164
Q

Define Mallory-weiss tear

A

tear of mucous membranes in oesophagus near gastro-oesophageal junction => bleeding

*rare

165
Q

causes of Mallory-weiss

A
  • violent vomiting/ coughing
  • alcohol => vomiting
  • bulimia
  • childbirth
  • hiatus hernia - increase abdomen pressure
166
Q

presenting symptoms of mallory-weiss syndrome

A
  • can be asymptomatic
  • abdominal pain
  • involuntary retching
  • severe vomiting
  • melaena (black stools)
  • haematemesis (blood in stool)
167
Q

examination findings of mallory-weiss syndrome

A
  • melaena (PR exam)
  • signs of hypovolemia (tachycardia, low bp)
168
Q

investigations for mallory-weiss syndrome

A
  • Bloods- FBC - check for anaemia
  • OGD (oesophago-gastro-duodenoscopy) - look for tear
169
Q

Management of mallory-weiss syndrome

A
  • usually self-resolving
  • if bleeding doesn’t stop => surgery, coagulation therapy, arteriography, injection sclerotherapy
  • transfusion if XS blood loss
170
Q

Complications of mallory-weiss syndrome

A
  • Borrhaeeve’s syndrome - transmural oesophageal perforation
171
Q

causes of infectious diarrhoea

A

Viral

  • Norovirus- food-borne gastroenteritis
  • Rotavirus - most common cause of diarrhoea in children
  • Adenovirus
  • Astrovirus- common diarrhoea cause in children, elderly, compromised immune system

Bacteria (=> dysenteric disease- BLOODY diarrhoea)

  • Salmonella enteritidis- contaminated food/drink
  • Esherichia coli- contaminated food/dairy
  • Shigella- BLOODY diarrhoea
  • Campylobacter- food-borne, BLOODY diarrhoea
  • Vibrio infection- raw seafood/sushi
  • Staph aureus- EXPLOSIVE diarrhoea (toxins released by bacteria)
  • C. difficile - antibiotic overuse

Protozoa (parasite)

  • giardia lamblia- contaminated food/person-person EXPLOSIVE diarrhoea
  • entamoeba histolytica- faecal-oral transmission, BLOODY diarrhoea
  • Cryptosporidium- WATERY stool (GI/resp illness)
172
Q

What mechanisms cause infectious diarrhoea?

A
  1. Increased intestinal secretion of fluid/electrolytes usally due to SECRETORY ENDOTOXINS (E.coli)
  2. Impaired intestinal absorption of fluids/electrolytes (E.coli, Cryptosporidium, shigella, salmonella, rotavirus)
173
Q

Presenting symptoms of infectious diarrhoea

A

DIARRHOEA

  • Acute watery diarrhoea (resolves within 10days)
  • Bloody diarrhoea (dysentry) - usually invasive enteropathogen
  • Perisistent diarrhoea (>14 days) +/- weight loss and signs of nutrient deficiency
  • fever
  • nausea/vomiting
  • abdominal pain

History

  • Recent travel history
  • Recent oral intake (contaminated food/water)
  • anyone else with diarrhoea
174
Q

What groups are at increased risk of infectious diarrhoea?

A
  • age: infants, young children, elderly
  • immunocompromised (HIV/AIDS/ chemotherapy)
  • exposure to enteropathogens (recent travel/ contaminated food/water)
  • antibiotic use + elderly/cancer patients
175
Q

Examination findings of infectious diarrhoea

A
  • check for signs of dehydration (raised HR, low bp, high RR, reduced skin turgor, dry mucous membranes)
  • +/- painful swollen joints (reiter’s syndrome)
  • guillan-barre syndrome- autoimmune nerve damage (C. jejuni infection)
176
Q

Investigations for infectious diarrhoea

A

Bedside

  • Urine dip
  • Stool MC&S (FIRST LINE)

Bloods

  • FBC - check for anaemia, high WCC (infection)
  • CRP/ESR- inflammation marker

Imaging

  • Abdo ultrasound (for unwell patients => check bowel obstruction/ severity of infectious colitis)
  • Endoscopy + biopsy (for perisitant diarrhoea - shows atrophy of cells/ protozoal cysts or exclude IBD/infectious colitis

Other

  • Biopsy- mucosal oedema (sign of infection)
  • PCR test on stool - check for viral infections
177
Q

Management of infectious diarrhoea

A
  • Oral rehydration therapy
  • Supportive treatment = IV fluids (in severe dehydration for fluid + electrolyte replacement
  • anti-diarrhoeal medications
  1. antimotility = Ioperamide
  2. antisecretory agents
  • Treat cause => antibiotics (cholera/dysentry, not always needed)/ anti-virals
  • analgesia/ anti-pyretics (for fever/pain)
    *
178
Q

define malabsorption

A
  • difficulty digesting nutrients
  • difficulty absorbing nutrients
179
Q

Causes of malabsorption

A

Difficulty digesting

  • lactose intolerance (missing lactase enzyme)
  • Whipple disease (bacterial infection effects digestion + absorption)

Difficulty absorbing nutrients

  • Crohn’s- damage to intestine
  • cystic fibrosis (affects pancreas => reduced enzyme secretion- less proteins/fats/vit A,D,E,K absorbed)
  • Chronic pancreatitis
  • Zollinger-Ellison - pancreatic insufficiency
  • Coeliac disease (autoantibodies attack villi of small bowel)
  • Pernicious anaemia (attacks parietal cells => less IF=> less B12 absorption)
  • parasites (giardia lamblia)
    *
180
Q

Presenting symptoms of malabsorption

A
  • avoiding specific foods
  • bloating/gas
  • chronic diarrhoea
  • steatorrhoea (Coeliac)
  • growth failure
  • weight loss
  • +/- oligoamenorrhoea (stop menstruating)
  • +/- bleeding (low Vit K)
  • +/- oedema (protein/calorie malnutrition)

Ask about

  • Family Hx (coeliac, Crohn’s, CF, lactose intolerance)
181
Q

Investigations for malabsorption

A

Bedside

  • Stool MC&S

Bloods

  • FBC- anaemia (low Hb)
  • ESR/CRP
  • Vitamin B12
  • Iron studies (ferritin)
  • Clotting screen (Vit K deficiency)
  • serum albumin
  • Calcium
  • LFTs
  • coeliac screen (autoantibodies)

Imaging

  • abdominal US (check gallbladder/liver/pancreas)

Breath hydrogen test - check for intestinal bacterial overgrowth

182
Q

Management of malabsorption

A
  • Nutritional support

Depends on cause

  • Coeliac - gluten-free diet
  • Pancreatic insufficiency => oral replacement of enzymes
  • crohn’s => steroids
  • blockage of bile => SURGERY
  • pernicious anaemia => B12/ folate injections
183
Q

Complications of malabsorption

A
  • coeliac => infertility, small bowel adenoma
  • anaemia
  • stunted growth
  • rickets/osteomalacia/osteoporosis (low Ca2+)
184
Q

define malnutrition

A

state resulting from lack of uptake/intake of nutrition leading to changed body composition + body cell mass leading to low physical/mental function and clinical outcome from disease

  • undernutrition- not getting enough nutrients
  • overnutrition- getting too many nutrients
185
Q

causes of malnutrition

A
  • disease related anorexia- reduced appetite (feeling sick/diarrhoea)=> cancer, liver disease, COPD
  • malabsorption - Crohn’s/ UC
  • mental health problems- depression, schizophrenia=> low desire to eat
  • eating disorders - anorexia, bulliemia
  • dementia- can forget to eat
  • increased energy requirement => healing after surgery/burns, tremors
  • medicine side effects reducing appetite
  • elderly -poor dentition/ disabilities
  • swallowing difficulty (dysphagia)
186
Q

symptoms of malnutrition

A
  • unintentional weight loss (5-10%)
  • low BM1 (<18.5)
  • lack of intrest in eating/drinking
  • feeling tired
  • feeling weakness
  • getting ill more often/ longer recovery time
  • stunted growth in children
187
Q

What’s is used in hospital to diagnose malnutirition?

A

MUST (malnutrition universal screening tool)

  • based on BMI/ unplanned weight loss
  • assessed within 6hrs
  • if diagnosed => refer to dietician
188
Q

Investigations for malnutrition

A

Bedside

  • BMI
  • stool culture (check for parasites => malnutrition)
  • mid upper arm diameter

Bloods

  • FBC- check for anaemia/ infection
  • blood glucose
  • U&Es- dehydration
  • B12/folate levels
  • iron studies - ferritin
  • TFTs
  • Ca2+/ zinc/ vitamin levels
  • cholesterol (low)
  • albumin - BUT is reduced by inflammation
189
Q

management for malnutrition

A
  • Lifestyle => balanced diet, increase snacking,
  1. Nutritional supplements (oral nutrition)
  2. Enteral feeding (NGT, NJT, NDT)
  3. Parental feeding (IV -nutrients into venous blood) - only if dysfunctional GIT (Crohn’s, short bowel syndrome, ischaemic bowel disease, cancer)
190
Q

Problems with enteral feeding (NGT)

A
  • refeeding syndrome (too many nutritents too quickly)
  • metabolic- deranged electrolyte, hyperglycaemia
  • mechanical - tube displacement, tube blockage
  • aspiration
  • nausea/vomiting/diarrhoea
  • tube infection
191
Q

problems with parenteral nutrition

A
  • mechanical - arrhythmias, thrombosis
  • catheter related infections
  • metabolic- deranged electrolytes
192
Q

What is refeeding syndrome and it’s pathogenesis?

A
  • when starved individual is fed nutrients too quickly

When starved

  • less insulin release
  • gluconeogenesis/ glycogenolysis

when fed

  • increased insulin => glycogenensis
  • Na+/water retention => oedema
  • hypokalemia/ low Mg2+/ phosphate
  • used up thiamine (co-enzyme in carb metabolism) => WERNIKE’S ENCEPHALOPATHY

Consequences:

  • wernicke’s encephalopathy
  • respiratory depression
  • arrythmias/ tachycardia/ HF => cardiac arrest/ DEATH
193
Q

How is refeeding syndrome managed?

A
  • micronutrients
  • monitor electrolytes
  • thiamine supplements
  • monitor fluid output (Na+/K+)
194
Q

define Hepatitis A & E viruses

A

hepatitis caused by hepatits A virus (HAV) or Hepatitis E virus (HEV)

  • HAV = picornavirus
  • HEV= calicivirus
  • small non-enveloping single stranded RNA virus
  • (common in developing countries- poorer sanitation)
  • 3-6 week recovery
195
Q

Describe how HAV/HEV are transmitted?

A

via faecal-oral route

  1. replicate in hepatocytes and are secreted into bile
  2. Immune response causes liver inflammation/ hepatocyte necrosis
  3. Infected cells killed by CD8+ / NK cells

*Incubation of virus = 3-6 weeks

196
Q

Presenting symptoms of HAV/HEV

A

Early

  • fever, malaise
  • anorexia
  • nausea/ vomiting

Late- signs of hepatitis

  • dark urine
  • pale stools
  • jaundice
  • itching

*Incubation of virus = 3-6 weeks

197
Q

Examination findings of HAV/HEV

A
  • pyrexia
  • tender hepatomegaly
  • jaundice
  • palpable spleen
  • absence of chronic liver disease signs
198
Q

Investigations for HAV/HEV

A

Bedside - urinalysis

  • +ve biliubin
  • raised urobilinogen

Bloods

  • LFTs - raised ALT, AST, ALP
  • high ESR
  • low albumin

Viral serology

  • anti-HAV IgM- acute illness phase (disappears >5 months)
  • anti-HAV IgG- recovery phase/ lifelong
  • anti-HEV IgM (1-4 weeks after)
  • anti-HEV IgG
199
Q

Management of HAV/HEV

A
  • Bed rest + Treat symptoms
  • anti-pyretics
  • anti-emetic
  • cholecystyramine (for severe pruitus)

Prevention (NOTIFIABLE DISEASE)

  • clean water/sanitation/ good hygiene
  • passive immunisation (IM antibody) for short term protection
  • active immunisation with attenuated HAV virus when travelling to endemic countries

*IMMUNISATION only for HAV virus

200
Q

Complications of HAV/HEV

A
  • fulminant hepatic failure (>80% mortality)
  • post-hepatic syndrome
  • cholestatic hepatitis => prolonged jaundice/itching
201
Q

define Hepatitis B and D viruses

A

Hepatitis B

  • Hepatitis caused by infection of HBV (Hep B virus)
  • acute or chronic (viraemia + hepatic inflammation >6months)
  • Double stranded DNA virus

Hepatitis D

  • Hepatitis caused by infection of HDV (Hep D virus) is a defective virus
  • can only co-infect with Hep B/ with a carrier of HBV
  • single stranded RNA virus
202
Q

Transmission of HBV

A
  • Sexual contact
  • bloodborne
  • vertical transmission (mother => baby)
203
Q

Risk factors for HDV

A
  • IV drug user
  • sexual contact with HBV carriers
  • unscreened blood/blood products in haemodialysis
  • infants of HBeAg/HBsAg positive mothers
204
Q

What viral proteins are produced by HBV?

A
  • HBcAg- core antigen
  • HBsAg- surface antigen
  • HBeAg- e antigen

*HDV has HBsAg antigen

205
Q

Presenting symptoms of HBV/HDV

A

Early

  • fever, malaise
  • anorexia
  • nausea, vomiting
  • diarrhoea
  • RUQ pain
  • serum sickness type illness (fever, arthralgia, polyarthritis, urticaria, maculopapular rashes)

Later

  • jaundice
  • pale stools
206
Q

Examination findings of HBV/HDV

A

Acute

  • jaundice
  • pyrexia
  • tender hepatomegaly
  • splenomegaly
  • cervical lymphadenopathy
  • sometimes urticaria/ maculopapular rash

Chronic

  • usually no findings
  • some signs of chronic liver disease
207
Q

Investigations for HBV/HDV

A

Bloods

  • LFTs- high ALT,AST, ALP, bilirubin
  • clotting screen (high PT- in severe disease)

Viral serology (GOLD-STANDARD)

  • Acute HBV => +ve HBsAg, IgM anti-HBcAg +/- HBeAg
  • Chronic HBV => +ve HBsAg, IgG anti-HBcAg +/- HBeAg
  • HDV infection => IgM/IgG against HDV

*HBV vaccinated => +ve anti-HBsAg antibody

Other

Liver biopsy (if ascites present/ clotting affected)

208
Q

Management for HBV

A

Acute HBV

  • bed rest + symptom treatment (anti-pyretics, anti-emetics, cholestyramine- for pruitus)
  • NOTIFIABLE DISEASE

Chronic HBV

  • anti-viral treatment (if +ve HbeAg, detectable HBV by PCR, decompensated cirrhosis)
  • interferon alpha (augments anti-viral mechanism)
  • nuceloside analogues
  • On medication for life
209
Q

Prevention of HBV

A
  • Safe sex
  • blood screening
  • sterilise instruments
  • passive immunisation=> Hep B antobodies for infants with +ve HBeAg mothers
  • active immunisation => recombinant HBsAg vaccine for at risk pp/ have +ve HBV mothers
210
Q

Complications of HBV

A
  • Fulminant hepatic failure
  • Chronic HBV (10%)
  • Cirrhosis
  • Hepatic cellular carcinoma
    • HDV => acute liver failure/ rapid disease progression
211
Q

Define Hepatitis C virus

A

hepatitis caused by infection with Hepatitis C virus (HCV) often chronic

  • single stranded RNA virus
  • Has multiple genotypes
  • Can take up to 12 months to recover
212
Q

How is HCV transmitted?

A

PARENTERAL

  • Sexual
  • vertical
213
Q

What patients are at risk of HCV?

A
  • IV drug user
  • haemodilaysis
  • recipients of unscreened blood products
  • tattoing
  • non-sterile acupuncture
  • health care workers
214
Q

Presenting symptoms of HCV

A
  • 90% ASYMPTOMATIC
  • 10% jaundice + mild-flu
215
Q

Examination findings of HCV

A
  • NO SIGNS usually
  • some signs of chronic liver disease
  • can have extrahepatic (rashes/ renal dysfunction)
216
Q

Investigations for HCV

A

Bloods

  • LFTs- acute (high ALT,AST,ALP,bilirubin), chronic (x8 higher AST+ALT)
  • Reverse transcriptase PCR => detects + genotypes HCV
  • Viral serology
  1. IgM anti-HCV antibodies (acute)
  2. IgG anti-HCV antibodies (chronic)

Other

Liver biopsy (check degree of liver inflammation)

features:

  • chronic hepatitis
  • lymphoid follicles in portal tracts
  • fatty change
  • cirrhosis
217
Q

Management of HCV

A

Acute => symptomatic (anti-pyretics, anti-emetics, cholecystyramine) + BED REST

Chronic

  • pegylated interferon alpha
  • nucleoside analogue (ribavirin)
  • Monitor HCV viral load for treatment efficacy
218
Q

Prevention of HCV

A
  • safe sex
  • needle exchange schemes for drug users
  • instrument sterilisation
219
Q

Which viral hepatitis doesn’t have a vaccine?

A

Hepatitis C

220
Q

Complications of HCV

A
  • fulminant hepatic failure
  • chronic HCV (80%) => CIRRHOSIS (20%)
  • hepatocellular carcinoma
221
Q

Define autoimmune hepatitis

A

chronic hepatitis with autoimmune features with circulating autoantibodies and hyperglobulinanaemia

222
Q

Pathogenesis of autoimmune hepatitis

A

environmental agent (virus/drugs) triggers hepatocyte expression of HLA antigens which are attacked by T cells

Inflammatory changes (similar to chronic viral hepatitis)= lymphoid infiltration to portal tracts and hepatocyte necrosis

223
Q

Types of autoimmune hepatitis

A
  • Type 1 classic
  • ANA, Anti-smooth muscle antibodies (ASMA), Anti-actin antibodies, Anti-soluble liver antigen

Type 2

  • Antibodies to liver/kidney microsomes (ALKM-1)
  • antibodies to liver cytosol antigen (ACL-1)
224
Q

Presenting symptoms of autoimmune hepatitis

A
  • can be asymptomatic and discovered through abnormal LFT finding
  • Check FHx for autoimmune diseases
  • rule out alcoholic/ viral hepatitis

Insidious symptoms:

  • Malaise
  • fatigue
  • anorexia
  • weight loss
  • nausea
  • jaundice
  • amennorrhoea
  • epistaxis

Acute hepatitis (25%)

  • fever
  • anorexia
  • nausea/vomiting/ diarrhoea
  • RUQ pain
  • serum sickness (arthralgia, polyarthritis, maculopapular rash)
225
Q

Examination signs of autoimmune hepatitis

A
  • chronic liver disease signs (spider naevi)

Late signs:

  • ascites
  • oedema
  • hepatic encephalopathy

Cushingoid features (round face, acne, hirsutism)

226
Q

Investigations for autoimmune hepatitis

A

Bloods

  • LFTs- high ALT/AST, ALP, GGT, bilirubin, LOW albumin
  • FBC- low Hb, WCC, platelets (hyposplenism from portal hypertension)
  • Clotting- high PT (severe disease)
  • Hypergammaglobulinanaemia - ANA, ASMA, Anti-LKM antibodies

Liver biopsy- check for hepatitis/ cirrhosis

To exclde other causes:

  • Viral serology - rule out viral hepatitis
  • urinary copper (Wilson’s)
  • ferritin/transferrrin saturation (haemochromatosis)
  • a-1 antitrypsin
  • anti-microbial antibodies (PBC)
  • ERCP - rule out PSC
227
Q

Management of autoimmune hepatitis

A

Immunosuppressants

  • steroids (prednisilone)
  • maintenance phase (azothioprine/ 6-mercaptopurine (steroid-sparing agents)
  • Test for TPMT1 activing before starting azothioprine

Monitor

  • Ultrasound/ alpha-fetoprotein every 6-12 months to detect hepatocellular carcinoma in cirrhosis patients
  • Hep A/B vaccines
  • Liver transplant - if patient intolerant to immunosuppression
228
Q

Complications of autoimmune hepatitis

A
  • Fulminant hepatic failure
  • cirrhosis
  • complicatios of portal hypertension => ascites, varices
  • Hepatocellular carcinoma (HCC)
  • Corticosteroid side effects => thin skin, Cushings, impaired wound healing
229
Q

Prognosis of autoimmune hepatits

A
  • 5yr survival with treatment = 85%
  • 5yr surival without = 50%
  • 5yr survival with transplant= >80%
230
Q

Define alcoholic hepatitis

A

liver inflammation due to chronic alcohol use (>15yrs)

231
Q

Presenting symptoms of alcoholic hepatitis

A

mild

  • Epigastric/ RUQ pain
  • low grade fever
  • nausea

Severe

  • jaundice
  • abdominal discomfort/ swelling
  • swollen ankles
  • GI bleeding
232
Q

Examination findings of alcoholic hepatitis

A

mild

  • hands (palmar erythema, dupyutrens contracture)
  • face (facial telangiectasia- red lines)
  • chest (spider naevi, gynaecomastia)
  • hepatomegaly
  • easy bruising

severe

  • jaundice
  • tachycardia
  • fever
  • hepatomegaly
  • ascites
  • encephalopathy (liver flap, drowsy, disorientation - XS ammonia crosses blood-brain barrier)
  • bruising
233
Q

Investigations for alcoholic hepatitis

A

Bloods

  • FBC (low Hb + platelets, high MCV + WCC)
  • LFTs (high AST:ALT, high GGT +ALP, high bilirubin, low albumin)
  • U&Es- low urea + K+
  • clotting - low PT

Imaging

  • USS - check for malignancy/ stones
  • CT/MRI liver

Other

  • GI endoscopy
  • liver biopsy- exclude other types of hepatitis
  • EEG - encephalopathy
234
Q

Management of alcoholic hepatitis

A

acute:

  • thiamine + vitamins (NG tube)
  • correct K+/ Mg/ glucose
  • oral lactulase for encephalopthy (reduce ammonia)
  • monitor urine output + diuretics (for ascites)
  • steroids - FOR INFLAMMATION reduce mortality

*Hepatorenal syndrome => n-acetylcysteine/ glypressin

235
Q

Complications of alcoholic hepatitis

A
  • cirrhosis
  • acute liver decompensation
  • hepatorenal syndrome= cirrhosis + ascites + renal failure
236
Q

Pathophysiology of hepatorenal syndrome

A
  1. splanchnic vessels to intestines VASODILATE (NO, prostaglandins released by liver damage)
  2. reduced blood volume detected by JGA => activates RAAS
  3. VASOCONSTRICTION of renal vessels
  4. KIDNEY failure
237
Q

define Liver cirrhosis

A

scarring of the liver due to previous liver damage (hepatitis, alcohol)

Architectural changes to hepatocytes = more fibrosis, nodular regeneration

238
Q

Causes of liver cirrhosis

A
  • chronic alcohol misuse
  • hepatitis (viral/ autoimmune)
  • Drugs (methotrexate, hepatotoxic drugs)
  • Inherited (a1-antitrypsin deficiency, haematochromatosis, CF, Wilson’s)
  • Primary billiary cholangitis = autoimmune => bile ducts destroy liver
  • Vascular - Budd-chiari syndrome (occlusion of hepatic veins)
  • Non-alcoholic steatohepatitis
239
Q

Presenting symptoms of liver cirrhosis

A
  1. early non-specific (anorexia, weight loss, fatigue, nausea, weakness)
  2. reduced function (bruising, ascites, leg swelling - slowed blood flow through liver so increased pressure in hepatic portal vein)
  3. reduced detoxification (jaundice, galactorrhea, amenorrhoea)
  4. portal hypertension (ascites)
240
Q

examination findings of liver cirrhosis (A=>N)

A
  • Ascites
  • Bruises
  • Clubbing + Caput medusa
  • Duputrens contracture
  • palmar Erythema
  • Fat spleen
  • Gynaecomastia
  • Hepatomegaly, hair loss
  • Itching (bile deposits on skin)
  • Jaundice
  • Leukonycia (hypoalbuminanaemia)
  • Mini testes
  • Spider Nevi
  • Other (steroids, pregancy)
  • Parotid enlargement
  • Terrys nails (distal white, proximal is red)
  • Xanthelesma

hands (palmar erythema, clubbing, leuconykia, terry’s nails)

face (xanthelesma, jaundice, hair loss)

chest (gynaecomastia, spider nevi)

abdomen (ascites, hepatomegaly, splenomegaly, caput medusa, bruising)

241
Q

Investigations for liver cirrhosis

A

Bloods

  • FBC - low Hb, platelets
  • LFTs- raised ALP/ GGT/ AST/ALT/bilirubin, low albumin
  • serum alpha-fetoprotein (marker of liver cancer raised in chronic liver disease)
  • Prolonged PT (clotting)

Identify cause:

  • viral serology (Hep B/C)
  • Iron studies (Haematochromatosis)
  • a-1 antitrypsin levels
  • caeruloplasmin (Wilson’s)
  • Anti-mitochondrial antibody (PBC)
  • ANA, AMSA (autoimmune hepatitis)

Ascitic Tap

  • MC&S- check for infection
  • biochemistry (low glucose, protein, amylase, albumin)
  • >250mm/L neutrophils = bacterial peritonitis

Liver biopsy

  • histology (nodular appearance, fibrosis)
  • grading (inflammation)
  • staging (arhcitectural distortion)

Imaging

  • US - biliary obstruction, ascites
  • CT/MRI - hepatocellular carcinoma

Endosocpy (look at varices)

242
Q

Management of liver cirrhosis

A
  1. Treat CAUSE
  2. Avoid alcohol, NSAIDs, opiates, sedatives, hepatotoxic drugs
  3. Enteral feeding, NGT
  4. Treat complications:

Ascites

  • diuretics
  • Na+ restrict => Fluid restrict if Na+ too high
  • monitor weight

Encephalopathy

  • lactulose (reduces gut absorption of ammonia)
  • phosphate enemas

Spontaneous bacterial peritonitis

  • Antibiotics (metronidazole, cefuroxime)
  • Prophylaxis for reccurent infection- Ciprofloxacin

Surgery

  1. TIPS (transjugular intrahepatic portosystemic shunt => reduces portal hypertension)
  2. Liver transplant (CURATIVE)
243
Q

Complications of liver cirrhosis

A
  • Pulmonary hypertension + Ascites
  • Variceal Bleeding/ haemorrhage
  • Encephalopathy (ammonia not broken down by liver => passes thorugh BBB => brain)
  • Spontaneous bacterial peritonitis
  • Hepatocellular carcinoma
  • Renal failure (hepatorenal syndrome)
  • Pulmonary hypertension (hepatopumonary syndrome)
244
Q

How is the prognosis of liver cirrhosis graded?

A

Child-pugh score

Based on albumin, PT, bilirubin, ascites, encephalopathy

245
Q

Define liver failure

A

liver dysfunction of healthy liver (acute liver failure) or acute deterioration of chronic liver disease (acute-on-chronic liver failure) leading to

  • jaundice (elevated unconjugated bilirubin)
  • encephalopathy (reduced ammonia breakdown => BBB to brain)
  • coagulapathy (reduced clotting factors/platlets)
246
Q

How to classify liver failure?

A

by onset from jaundice to development of encephalopathy

  • hyperacute = <7 days
  • acute= 1-4 weeks
  • subacute = 5+ weeks
247
Q

Causes of liver failure

A
  • paracetomol overdose
  • Viral Hepatitias (A=>E)
  • malignancy
  • Other: autoimmune hepatitis, Budd-chiari, Wilson’s, Haematochromatosis, poisonous mushrooms, pregnancy
248
Q

Presenting symptoms of liver failure

A
  • asymptomatic
  • non-specific (nausea, jaundice, fever)
249
Q

Examination findings of liver failure

A
  • ascites
  • bruising/ bleeding
  • splenomegaly
  • pyrexia (infection)
  • asterix
  • encephalopathy (ataxia, confusion, opthalmoplegia)
  • smell of pear drops
  • Kaiser-flaeisher rings (Wilson’s)
250
Q

Investigations for liver failure

A

Bloods

  • FBC- Hb (anaemia), WCC (infection)
  • glucose
  • LFTs (raised bilirubin/ CCT/ALP/AST/ALT, low albumin)
  • U&Es- hepatorenal failure
  • ESR/CRP
  • Coagulation screen
  • ABG
  • group and save

Identify cause

  • viral serology- hepatitis
  • iron studies/Ferritin- Haemotochromatosis
  • caeruloplasmin -Wilson’s
  • paracetomol levels
  • autoantibodies (ANA, AMSA)

Ascitic tap

  • Spontaneous bacterial peritonitis (neutrophil >250mmol/L)
  • MC&S
  • biochemisty (glucose, amylase, albumin)

Imaging

  • Liver US/ CT
  • Doppler ultrasound - Budd-chiari

EEG- monitor encephalopathy

251
Q

haemolytic jaundice LFT results

A

unconjugated bilirubin = increased

conjugated bilirubin = normal

urine urobilinogen = increased

ALT/AST = normal

ALP = normal

252
Q

hepatic jaundice LFT results

A

unconjugated bilirubin = increased

conjugated bilirubin = increased

urine urobilinogen = increased

ALT/AST = increased

ALP = normal/mild increase

253
Q

cholestatic jaundice LFT results

A

unconjugated bilirubin = normal

conjugated bilirubin = increased

urine urobilinogen = decreased

ALT/AST = normal/mild increase

ALP = increased

254
Q

Management of liver failure

A
  1. RESUS (ABC)- oxygen, fluids, cannula, transfusion?
  2. Treat cause
  • N-acetylsteine for paracetomol overdose
  • anti-virals for viral Hepatitis

Treat/ prevent complications

  • monitor vitals (vitals, PT, creatinine, pH, urine output)
  • encephalopathy (lactulose, phosphate enemas)
  • coagulopathy (IV vitamin K, FFP, platelet infusion)
  • antibiotic and antifungal prophylaxis
  • renal failure (haemodialysis, nutition)
  • protect gastric mucosa (PPIs)
  • cerebral oedema (mannitol)
  • hypoglycaemia treatment

Surgery- Liver transplant

255
Q

Why do patients with liver failure get cerebral oedema?

A
  1. liver doesn’t clear nitrogenous compunds, so astrocytes in clear it which reqiures convert glutamate => glutamine
  2. Glutamine changes osmotic balance in cells and causes fluid shift to brain cells
  3. Cerebral oedema (rasied ICP)
256
Q

What drugs to avoid in liver failure?

A
  • sedatives
  • NSAIDs
  • opiates
  • other drugs metabolised in liver
257
Q

what is gastrointestinal perforation?

A

perforation of wall of GIT with spillage of bowel contents into blood

258
Q

common causes for gastrointestinal perforation

A

large bowel: diverticultis, colorectal cancer, appendicitis
gastroduodenal: perforated ulcer
small bowel (RARE):trauma, infection, crohn’s
oseophagus: borrhaeve’s perforation

259
Q

what drugs can increase risk of gastrointestinal perforation?

A

NSAIDs
steroids
bisphosphonates

260
Q

presenting symptoms of GI perforation

A

very UNWELL
shock signs
pyrexia
pallor
dehydration

261
Q

examination findings of GI perforation

A

loss of liver dullness (overlying gas)
peritonitis signs:
- guarding
- rigidity
- rebound tenderness
- absent bowel sounds

262
Q

investigations + findings for GI perforation

A
  1. Bloods- FBCs, U&Es (high urea after GI bleed), LFTs
  2. CXR - air under diaphragm
  3. AXR- abdominal gas shadowing
  4. Gatrograffin swallow- if oesophageal perforation
263
Q

management plan for GI perforation (large bowel/ gastroduodenal/ oesophageal)

A

immediate:
- IV fluids + electrolytes
- antibiotics (cefuroxime, metronidazole)

surgical:
- for large bowel=> peritoneal lavage + resect perforated section (Hartmann’s procedure)
- for gastroduodenal =>laparotomy, peritoneal lavage and closed with omental patch
- for oesophageal => pleural lavage, repair oesophagus

264
Q

what is Hartmann’s procedure?

A

removing the affected section of the bowel and creating an alternative path for faeces to be passed

265
Q

why are gastric ulcers biopsied?

A

check for malignancy

266
Q

prognosis for GI perforation

  1. large bowel
  2. gastroduodenal
A
  1. high risk of faecal peritonitis if untreated => SEPSIS (death)
  2. perforated gastric carcinomas have poor prognosis
267
Q

complications of GI perforation

A
  • peritonitis (large/small bowel)
  • shock, sepsis, mediastinitis (oesophagus)
268
Q

common side effects of metronidazole (antibiotic)

A
  • nausea
  • diarrhoea
  • metallic taste in mouth

Year 3 (27 decks)

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