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5thyr > GI > Flashcards

GI Flashcards

1
Q

What is mesenteric ishceamia?

A

mesenteric ishceamia

  • reduction in gut perfusion (small bowel)
  • can be acute or chronic (chronic is grumbling pain, like angina in ACS but after food instead of exercise, they loose weight and have food fear)
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2
Q

What are symptoms of mesenteric ishceamia?

A

mesenteric ishceamia

  • central non specific abdo pain
  • vomiting
  • diahroea
  • can lead to peritonitis and systemic sepsis
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3
Q

What investigations would you do for mesenteric ishceamia?

A

mesenteric ishceamia

  • FBC > rasied WCC/CPR
  • blood gas> lactate/acid
  • ECG> look for AF (clot)
  • CT angio to see vessels
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4
Q

What is the treatment for mesenteric ishceamia?

A

mesenteric ishceamia is an EMERGENCY

  1. fluid Ressus
  2. antibiotics (broad spectrum)
  3. laporectomy (WITHIN 60 MINS)
  4. send to ITU
  5. palliate?
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5
Q

Most common causes to consider for upper GI bleed?

What are important things from history that would make you think of these differentials?

A

Upper GI bleed

  • most common cause is peptic ulcer disease (duodenal) NSAIDS (chronic inflammatory conditions) Hpylori
  • mallory-weiss tear (wretching/vomitting)-small amounts of blood
  • variceal tear (alcoholic, malignancy)-large amounts of blood)
  • osphagitis/gastritis (small amounts) (epigastric pain, NSAIDS)
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6
Q

How might someone with an upper GI bleed present?

A

Upper GI bleed

  • Haematemesis – bright red or coffee ground (brown)
  • Melaena – tar black stools, iron smell (if horrific amount in pt. w/ arterial stent, consider chance of arterio-enteric fistula!!)
  • Gastritis – epigastric pain, vomiting
  • Peripherally shut down – Cold, ↓CRT, ↓UO (<0.5ml/kg/hr)
  • Dyspnoea (due to anaemia) – indicates large bleed
  • Hypotensive <90/60 → dizzy and syncope
  • Tachycardic > 100bpm (compensate for ↓BP)
  • ↓GCS
  • Abdo bruising

*Haematochezia – fresh blood or maroon indicates lower GI bleed

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7
Q

How would you manage an upper GI bleed?

(what things in your AtoE?
what imaging?
what scores should you calculate and whats ultimate treatment?

A

AtoE assessment

  1. A
  2. Breathing -give oxygen, ABG and erect chest Xray
  3. Circulation
    -x2 wide bore cannulas
    Bloods
    -Hb (may be normal as takes 30mins to fall)
    -Urea ((prognostic Glasgow Blatchford score and AKI)
    -LFT and coagulation (synthetic function and surgery)
    -Clotting (↓Vit K)
    -ABG
    -Cross-match 4-6 units if Hb < 70 (1 unit for each 10g/L that Hb is less than 140g/L)
    -Monitor urine output with catheter (hourly monitoring)
    -ECG
  • give IV 0.9% Saline or Hartmann’s (whilst waiting for blood)
  • if patient deteriorating despite fluids give O Rh- blood

Disability
Environment-rectal exam -check melaena

Imaging

  • erect chest X ray (pneumoperitonium)
  • CT abdo and pelvis (diagnostic)

Referrals/after care

  • NBM – 24h
  • MUST CALCULATE ROCKALL + BLATCHFORD SCORES!!!
  • REFER for urgent endoscopy (with 24 hrs admission or 2hrs after stabilisation). Not in perforation
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8
Q

What is the treatment for variceal bleeds?

A

Variceal bleeds

  • Prophylactic Abx
  • IV Terlipressin 2mg/6hr QDS 5 d (↓mortality by 34% by ↓portal pressure; CI: IHD) CONSULTANT LED

-Active bleed –URGENT endoscopic band ligation (osophageal) or sclerotherapy (gastric) (both 1st line)

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9
Q

What is the prophylactic treatment of variceal bleeds?

What is the secondary prevention for variceal bleeds (once they’ve bled once)

A

Variceal bleeds (60% will rebleed in 1st year)

  1. Primary prevention – Propanolol or repeat endoscopic banding ligation
  2. Secondary prevention i.e. after bleed – TIPS or endoscopic banding
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10
Q

Complications of variceal bleeds?

A

Variceal bleed complications

  • Variceal bleeds have ↑Risk of SBP (spontaneous bacterial peritonitis)- give prophylactic IV AB
  • Aspiration pneumonia
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11
Q

What is the definitive treatment for active GI bleed (non variceal) ?

A

Depends on endoscopy findings

  • if high risk: achieve endoscopic heamostasis (2 or clips, cautery, adrenaline) start PPI
  • if low risk: no endoscopic heamostasis required. Start PPI

SURGERY – if severe or uncontrollable bleed

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12
Q

What scores are important in upper GI bleeds?

A

Glasgow Blatchford score
-need for admission and endoscopic intervention (0-1 = discharge w/ OP OGD)

Rockall score
-predicts risk of Re-bleeding and mortality post-endoscopy (higher the score, worse the mortality)

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13
Q

When someone is bleeding, when do you transfuse?

when do you give FFP and when do you give platelets?

A

Transfuse
-Cross-match 4-6 units if Hb < 70 (1 unit for each 10g/L that Hb is less than 140g/L)

Giving platelets
-Give platelets if platelet count <50 x109/L.

Giving FFP

  • Give FFP if active bleed and PTT or APT > 1.5x times normal
  • If a patient’s fibrinogen level remains less than 1.5 g/litre despite fresh frozen plasma use, offer cryoprecipitate as well
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14
Q

What do you do if someone is on warfarin with an MAJOR BLEED?

A

Warfarin and ACTIVE MAJOR BLEEDS

  • STOP warfarin
  • IV Vitamin K 5mg
  • Prothrombin complex e.g. Beriplex, Octiplex
  • Re-check INR 24hrs
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15
Q

What do you do about warfarin if MINOR bleed? (INR 5-8 vs INR >8)

A

Warfarin in minor bleeds

  • stop warfarin
  • IV vitamine K 1-3mg (if IRN>8 you can give another dose in 24 hours if not helped)
  • Continue when INR <5
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16
Q

What do you do about raised INR for someone who is NOT bleeding? (INR 5-8 vs INR >8)

A

Warfarin for non bleeds
INR 5-8
-hold warfarin 2 days
-reduce next maintenance dose

INR >8
-stop warfarin
PO vitamin K 1-5mg
Restart when INR < 5.0

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17
Q

What is GORD? What are the causes?

What are the complications of long term GORD?

A

GORD

  • reflux of stomach acid + bile into oesophagus
  • long term GORD can lead to osohagitis/ulcers/strictures and Barrett’s osophagus (squamous to columnar)
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18
Q

Causes of GORD?

RF for GORD?

A

Cause is often physiological:

  • Lower oesophageal sphincter defect hypotension
  • Hiatus hernia
  • Loss of oesophageal peristaltic function or slow Gastric emptying
  • RF: abdominal obesity, over-eating, smoking, alcohol, pregnancy, drugs (TCA, anti-chol, nitrates)
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19
Q

Symptoms of GORD? (oesophageal and extra osophageal)

A

GORD symptoms
-Heart burn (reflux)
>Worse post-meal, lying down
>Relieved by anti-acids (PPI or H2 antag)
-Belching
-Waterbrash – acid causes ↑↑salivation
-Odynophagia – painful swallowing may indicate oesophagitis or ulcers

Extra-osophageal

  • Nocturnal asthma or chronic cough (very common)
  • Laryngitis - hoarseness, throat clearing
  • Sinusitis (acid can get in sinuses>inflammation)
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20
Q

Name some RED FLAGS for people with swallowing/heart burn problems?

A

ALARMS

  • Aneamia
  • Loss of weight
  • Anorexia
  • Recent onset of progressive symptoms (4 weeks)
  • Massess/melena/heamatemasis
  • Swallowing issues (pain or inability)

ANYONE of ANY AGE> 2 week upper GI endoscopy referral

if >55years only need dysphagia

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21
Q

investigations for GORD?

A
  1. Endoscopy (stop PPI 2 weeks before scope)
    - ANYONE of ANY AGE with DYSPHAGIA
    - >55 years with ALARMS
    - or if treatment refractive

If endoscopy is normal:
-24hr pH study ± Manometery – if endoscopy normal

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22
Q

Managment for GORD? (conservative)

A

CONSERVATIVE managment for GORD

  • raise bed head when sleeping
  • weight loss ↓abdo obesity → ↓pressure on stomach
  • stop smoking
  • diet habits (small and regular, avoid hot drinks, alcohol, coffee, eat 3 hours before bed)
  • avoid drugs affecting gastric mobility (nitrates, anticholinergics, CCB-affect sphincter)
  • avoid drugs that damage mucosa – NSAIDs, K+ salts, Bisphosphonates, steroids
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23
Q

Managment for GORD? (medical)

A

MEDICAL managment for GORD
Antacids – Magnesum trisilicate mixture (continuous use not recommended)
Alginates – Gaviscon (continuous use not recommended)

Endoscopy –ve, but symptoms:
1st line: review drugs and lifestyle advice
2nd line: PPI – full dose 1 month and H pylori testing
-If response → low dose PPI PRN
-If no response → H2 antagonist (ranitidine) or pro-kinetic PRN

Endoscopic proven +ve oesophagitis:
1st line: straight to PPI – full dose 1-2 months
If +ve response → carry on with low dose PPI PRN
If no response → H2 antagonist (ranitidine)

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24
Q

Managment for GORD? (surgical)

When would this be appropriate?

A

Managment for GORD (surgical)

  • Nissen Fundoplication or magnetic beadband or radio frequency induced hypertrophy
  • Aims to ↑resting LGOS
  • consider in severe GORD (as confirmed by pH manometry BEFOREHAND) or if refractory to drugs
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25
Q

What is Barrats oesophagus ?

Whats the treatment (for metaplasia and dysplasia) ?

A

Barrats osophagus is where there is Metaplasia (squamous to collumer) >dysplasia>neoplasia

  • metaplasia=endoscopic surveillance with biopsy (3-5 years)
  • dysplasia= endoscopic resection or radiofreq ablation

**High dose PPI to prevent further GORD

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26
Q

Complications of GORD?

A

Complications of GORD

  • Osophageal cancer
  • Plummer vincent syndrome (dysphagia, glossitis, Fe+ defficiency)
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27
Q

What is a hiatus hernia?
How does it happen?
What are risk factors?

A

Hiatus hernia
-Herniation of stomach (typically cardia) through oesophageal aperture of diaphragm

Three possible causative mechanisms:
1 Widening diaphragmatic hiatus (age?/skeletal deformities scoliosis, kyphosis, pectus excarvatum)
2 Oesophageal shortening pulls up the stomach (trauma)
3↑Intra-abdominal pressure Pushes stomach up
(obesity/pregnancy/ascites)

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28
Q

2 types of hiatus hernia?

How do they present differently?

A

Hiatus hernia
1. Sliding (80%) – GOJ slides into thorax
↑↑↑Reflux – common as LOS becomes less competent
-Dysphagia

  1. Rolling (para-oesophageal 20%)
    - GOJ remains in abdo, but part of the stomach (cardia) herniates into thorax
    - Dysphagia
    - Reflux less common
    - Chest pain
    - Epigastric pain/fullness
    - Nausea
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29
Q

Investigations for hiatus hernia?

A

Investigations for hiatus hernia
1. Barium swallow – best diagnostic test ∆

  1. Upper GI endoscopy – in any patient > 55 with new dysphagia, must exclude oesophageal cancer!!
    (stop PPI 2 weeks before scope)
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30
Q

What is treatment of hiatus hernia?

A

Hiatus hernia
1. Lose weight
2. Treat GORD
2. Surgically repair hernia (not done lightly)
only done if risk of strangulation or refractory symptoms despite aggressive medical therapy
-Laparoscopic fundoplication
-Gastropexy – suturing of stomach to abdominal wall

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31
Q

What are the 2 types of oesophageal carcinomas (whats most common)?

What are the risk factors for osophageal carcinomas?

A

Oesophageal carcinoma

  • adenocarcinoma MOST COMMON (lower 1/3rd and Barrett’s)
  • less commonly squamous (upper 2/3rds)

Risk factors

  • MALE>F
  • Diet and alcohol and smoking
  • reflux/osophagitis
  • Barrats
  • Nitrosamine exposure
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32
Q

What are the symptoms of osophageal cancer?

A

Osophageal cancer
- PROGRESSIVE! dysphagia (First solids → soft food → liquids)
-Retrosternal chest pain – reflux
-Painful swallow (dynophagia)
-Regurgitation + Vomiting → Haematemesis or Melaena (small volumes)
-Hiccups, Lymphadenopathy
↓Weight, ↓Appetite, Fatigue (LATE)

If upper oesophageal disease
Hoarseness – pressure on recurrent laryngeal or larynx
Cough – may be paroxysmal if aspiration pneumonia

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33
Q

What are the investigations for osophageal cancer?

A

Osophageal cancer investigations
1st line: Upper GI endoscopy w/ BRUSHINGS+ BIOPSY(∆)
-Urgent (2 wks) – if dysphagia or age ≥ 55 with ALARMS
-Stop PPI 2 weeks before scope

Staging: CT (chest, abdomen and pelvis)
-if no metastatic disease can be found then you can do a local endoscopic US

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34
Q

What is the treatment for osophageal cancer?

A

Osophageal cancer treatment (poor prognosis)

  • Radical Oesophagectomy often Ivor-Lewis (mobilisation of stomach and division of oesophageal hiatus) if T1/2
  • Neo-adjuvant Chemotherapy (cisplatin + 5FU) may be considered

If not suitable: palliative chemo-radiotherapy to restore swallowing

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35
Q

Risk factors for gastric cancer?

A

Risk factors for gastric cancer

  • H.Pylori (two-fold risk)
  • ↑Age (95% cases in pts > 55yo)
  • MALE>F
  • Diet low in fruit + veg
  • Smoking
  • Gastritis
  • Pernicious anaemia (B12)
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36
Q

Symptoms of gastric cancer?

A

Symptoms of gastric cancer

  • Dysphagia + DYSPEPSIA – progressive
  • Nausea + Vomiting → Haematemesis ± Melaena
  • Reflux
  • Upper abdo MASS
  • Epigastric pain/discomfort
ALARMS symptoms  
Anaemia 
Loss of weight  
Anorexia – LoA  
Recent onset, refractory or progressive symptoms  
Melaena or Haematemesis  
Swallowing difficulty (dysphagia)
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37
Q

Investigations for gastric cancer?

What may they show?

A

Gastric cancer
1st line: Upper GI endoscopy w/ BRUSHINGS+ BIOPSY(∆)
-Urgent (2 wks) – if dysphagia or age ≥ 55 with ALARMS
-Stop PPI 2 weeks before scope
(signet ring cells of mucin>poor prognosis)

Bloods – FBC (↓Hb), LFTs

Staging: CT (chest, abdomen and pelvis)
-if no metastatic disease can be found then you can do a local endoscopic US

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38
Q

What is the managment of gastric cancer

A

Managment of gastric cancer
-Gastrectomy (if localised disease)
D1 = excision of tumour + perigastric nodes
D2 = resection extended to include nodes around coeliac axis

Chemo-radiotherapy
Neo-adjuvant 5FU
Adjuvant = 5FU
Palliative

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39
Q

What 2 random signs are associated with gastric cancer?

A

Gastric cancer

  • Troisier’s sign (enlarged left supraclavicular node – Virchow’s node)
  • Acanthosis nigricans
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40
Q

What are the types of pancreatic cancer?

A

Pancreatic cancer
Majority of tumours are EXOCRINE
-ADENOCARCINOMA (95%, poor prog) majority in head>body>tail

Other tumours have better prognosis

  • ampulla of Vater
  • pancreatic islet cells – insulinoma, gastrinoma, glucagonoma
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41
Q

What are the risk factors for pancreatic cancer?

A

Pancreatic cancer

  • KRAS2 mutation (95%)
  • MALES
  • 60 years+
  • smoking
  • DM
  • chronic pancreatitis
  • ↑abdo obesity, ↑fat/processed meat diet
  • hereditary non-polyposis colorectal carcinoma (Lynch)
  • BRCA2 gene
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42
Q

How does pancreatic cancer present?

A

Pancreatic cancer presentation
-PAINLESS JAUNDICE
-Obstructive/cholestatic picture
○pale stools, dark urine, jaundice, pruritus)
-Loss of exocrine function (steatorrhoea)
-Loss of endocrine function (diabetes)
-Epigastric pain/dull backache (worse lying down)
-Nausea + Vomiting (obstructing gastric outlet)

*Courvoisers law (painless, jaundice and palpable gallbladder is NOT gallstones)

Non specific: anorexia/weight loss/epigastric pain

43
Q

Pancreatic cancer investigations/what would you see? (what is diagnostic?)

A

Diagnostic is endoscopic USS ( liver, bile duct, pancreas)
• Pancreatic mass ± dilated biliary tree ± hepatic mets
• If EUS is inconclusive and high suspicion do CT or MRI

Bloods

  • FBC-normochromic anaemia
  • LFTs- ↑Bilirubin, ↑↑ALP, ↑↑GGT (if alcohol) > ↑ALT (mild)
  • ↑Glucose serum
  • Tumour markers – ↑CA19-9

Biopsy – staging prior to surgery

44
Q

Managment of pancreatic cancer

A

Resectable pancreatic cancer (if no mets)

  • less than 20% are suitable
  • Head: Whipples resection with chemo (pancreaticoduodenectomy)
  • Tail:Laparoscopic excision
  • Palliative: can do ERCP with stenting (help with jaundice/anorexia))
45
Q

What cancer does migratory thrombophlebitis (Trousseau sign) most commonly happen in ?

A

Pancreatic cancer commonly causes migratory thrombophlebitis (Trousseau sign)

46
Q

what are you thinking with REALLY elevated ALT?

A
  1. toxins
  2. ischemia
  3. viral
47
Q

What is the most common cause of acute and of chronic viral hepatitis?

A

Hepatitis A = acute

Hepatitis B = chronic

48
Q

What kind of viruses are hepatitis A, B, C?

A 
A = RNA virus
B = dsDNA virus 
C = RNA flavivirus
49
Q

What are some other infective causes of hepatitis?

A 
EBV
CMV 
Malaria 
Syphilis 
Yellow fever 
Adenovirus
50
Q

How is hepatitis A spread?

A

Faeco-oral spread - food sources or anal sex

51
Q

What is the presentation of hepatitis A?

A

Flu-like symptoms e.g. nausea, vomiting, fatigue, anorexia (1-2 weeks)

Icteric phase (jaundice phase)

  • Dark urine and pale stools
  • Jaundice
  • Abdominal phase
  • Can last up to a year (normally couple of weeks)
  • Tender Hepatomegaly
  • Lymphadenopathy
  • Diarrhoea if child
52
Q

What is the incubation period for hepatitis A?

A

14-28 days

53
Q

How do you test for hepatitis A?

A
  • IgM (undetectable after 6 months..acute/recent infection)

- do instead IgG, (detectable for life and determines indicates recovery-no vaccine)

54
Q

Treatment for Hepatitis A?

Is there a vaccine?

A

Hepatitis A

  • Supportive (usually self limiting-fluids antiemetics)
  • Avoid alcohol (until raised liver enzymes normalise)
  • Intereferon-A for Fulminant hepatitis (rare)

Vaccination is ACTIVE-inactivated viral protein

55
Q

How is hepatitis B spread?

A

Transmission is via infected blood or body fluids

  • Sexual route
  • IVDU
  • Vertical transmission - endemic countries (Far East, Africa, Mediterranean)
56
Q

How long is hep B incubation?

A

1-6 months

57
Q

Explain the following antigens/antibodies in Hep B.

HbsAg 
Anti-HBc  (IgG vs IgM)
Anti-HBs
HbeAg
HbeAg
A
  • HbsAg (surface antigen) is present in both natural infection and vaccination 1-6 months after exposure
    (if it is present >6months=chronic infection)
  • Anti-HBc (core antibodies) only present in NATURAL infection - implies past infection. IgG=chonic. IgM=acute
  • Anti-HBs (antibodies to surface antigen-IMMUNITY) either from exposure or immunisation. It is negative in chronic disease-because you’ve never beat the disease
  • HbeAg -INFECTIVITY results from breakdown of core antigen from infected liver cells as is therefore a marker of infectivity
58
Q

What are the symptoms of Hep B

A

Initially systemic flu-like prodrome:

  • Fever (mild)
  • Malaise (profound)
  • Anorexia+ Nausea
  • BONE ACHE AND ITCH Arthralgia + Uticaria (COMMON)

-Jaundice (30-50% adults)
→ dark urine → pale stools
-Fulminant hepatitis (liver failure within 8 wks)
-Might reveal decompensated liver disease – ascites, encephalopathy, GI haemorrhage

59
Q

Treatment for Hepatitis B?

A

Treat if ALT >30 or HBV DNA>2000

Pegylated interferon alfa-2a = first-line (SE:↓WCC, ↓Plt)

Second-line alternatives:

  • Nucleoside analogues (lamivudine, entecavir)
  • Nucleotide analogues (adeofovir, tenofovir)

(aim is prevent cirrhosis and HCC-monitor response with anti-has

60
Q

Is there a vaccine for HepB?

A 
PASSIVE VACCINE (anti-HBV immungogobulin) 
-give to all non immune contacts after high risk exposure
61
Q

How is hepatitis C spread?

A

Blood and bodily fluid spread (most common type in UK)

  • IVDU
  • MSM
  • Contaminated medical equipment
62
Q

How is hepatitis C present?

A

Often asymptomatic or very mild

85% develop silent chronic infection

63
Q

What are the investigations for hepatitis C?

A

Investigations for hepatitis C

  1. Anti-HCV antibodies confirm exposure 3 months after infection (either had or have)
  2. If positive, do reflex testing with PCR
  3. If PCR is positive, it confirms ongoing infection/chronicity so do a liver biopsy to assess damage and need for treatment

(Also, test to determine the HCV genotype)

64
Q

What is the treatment for hepatitis C?

A
  • All patients treated
  • Nucleoside analogues (now generally preferred) e.g. sofosbuvir

(used to have to takepegylated interferon SC weekly and a pill)

65
Q

What is hepatitis D?
How do you test for it?
Whats the treatment?

A
  • Hep D is an incomplete RNA virus (needs Hep B-Hep B vaccination also protects for Hep D)
  • If HBsAg +ve → check Anti-HDV Ab

-Treatment: interferon doesn’t really work=may need transplant

66
Q

How is hepatitis E spread?
Tests?
Treatment?

A

Hep E (similar to hep A)

  • Fecal oral
  • Consumption of pork/shellfish/molluscs

Tests:

  • DIAGNOSTIC is HEV serology (∆)
  • Same as Hep A (↑IgM +ve = acute ↑IgG +ve = life indicates recovery)

Treatment: same as A (supportive, avoid alcohol)

67
Q

What is fulimant liver failure

A

Clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function

68
Q

What happens to the liver in chronic liver disease?

A

Chronic liver disease

  • progressive disease where the liver is replaced by fibrotic tissue and cirrhosis (scarring)
  • Normal liver>fibrosis>cirrhosis
  • 80% of liver parenchyma is destroyed before symptoms arise
69
Q

What are the two types of chronic liver disease?

What can cause the change from one to another?

A

CHRONIC LIVER DISEASE

  • Compensated - this is when the liver can function normally
  • Decompensated - the liver CANNOT function normally

-The liver is sensitive so lots of things can ‘tip’ someone into decompensated. E.g. constipation, HCC, infection, dehydration, bleed, hypotension, thrombosis in protein vein, drugs

70
Q

What are some infectious causes of chronic liver disease?

A 
CHRONIC LIVER DISEASE 
Hepatitis B
Hepatitis C 
CMV 
Yellow fever 
Leptospirosis
71
Q

What drugs can cause chronic liver disease?

A 
CHRONIC LIVER DISEASE 
paracetamol OD
sodium valproate
amiodarone
isoniazid
nitrofurantoin
methotrexate
72
Q

What other conditions can cause chronic liver disease (vascular, autoimmune, metabolic, idiopathic)

A

CHRONIC LIVER DISEASE
Vascular
-Budd chiari syndrome

Autoimmune

  • autoimmune hepatitis
  • PBC
  • PSC (more obstructive)

Metabolic

  • Wilsons disease Chr13 - disorder of hepatic copper deposition
  • Heamachromatosis
  • Alpha1-antitrypsin deficiency

Idiopathic

  • NAFLD
  • Alcohol
73
Q

Signs/symptoms of chronic liver disease? think examination

A

CHRONIC LIVER DISEASE

  • Kayser–Fleischer ring (wilsons diesease)
  • Leukonychia
  • Clubbing
  • Dupytrens contracture
  • Liver flap asterixis
  • Palmar erythema
  • Parotid swelling
  • Spida nevi
  • Gynaecomastia
  • Loss of axillary hair
  • Ascites/swollen ankles
  • Jaundice
  • Caput medusa
  • Period changes
  • Sex drive changes
  • Right hypochondriac pain
  • Confusion
  • Drowsiness
  • Itchy skin
74
Q

What investigations (bloods, imaging, special) would you do for chronic liver disease?

What results would you expect?

A

NON INVASIVE LIVER SCREEN

1)BLOODS
FBC
-↓WCC ↓Platelets (portal HTN>splenomegally)
-anaemia might be present if bleeding
-Blood film – non-megaloblastic macrocytic anaemia suggests alcohol abuse

LFTs and clotting
Initially: ↑Bil ↑AST ↑ALT ↑ALP ↑yGT
Then loss of liver function (↑ INR/PT, ↓Albumin)

U+Es

  • high ammonia
  • low sodium (RAAS affected)
  • high lactate
  • high creatinine
  • low glucose (glycogenolysis/gluconeogenisis impaired)

2) IMAGING
- liver USS with portal dopplers/duplex
- to assess stiffness of liver and vasculature
- every 6 months to check for hepatocellular carcinoma

3 ) SPECIAL TESTS

  • liver biopsy gold standard
  • ascites tap if ascites present
  • Hepatitis serology
  • Alpha-1-antitrypsin defficiency
  • Ferritin (heamachromatisis)
  • Autoimmune antibodies
  • Wisons disease
  • TFT and diabetes (autoimmune link)
75
Q

Managment of decompensated liver disease

A

Decompensated liver disease

1) non invasive liver screen
2) alcohol (pabrinex, chlordiazapoxide)
3) infection screen (sputum, urine)
4) check for AKI (as cause)
5) check for upper GI bleed (as cause and consequence)
6) hepatic encephalopathy (laxatives-however dont anchor-may be head injury>CT scan)
7) other (manage constipation, hydration, clot prevention)

76
Q

Management of chronic liver disease?

A

CHRONIC LIVER DISEASE
- Advise
○ Healthy eating, decrease salt intake
○ Alcohol and smoking advice
○ Med review (stop NSAIDS, sedatives, opiates)
- GIVE VITAMIN K 10mg/d to help with clotting
- Treat underlying cause (cirrhosis is irreversible
- Diuretics for ascites
-Liver transplant– ultimate treatment

  • Can give Colestestyramine for pruritis
77
Q

what is the blood test that would indicate alcoholic hepatitis

A 
Alcoholic liver specific signs 
↑GGT 
↑MCV (macrocytosis) 
↑bilirubin 
AST> ALT
78
Q

What are the 4 signs of liver FAILURE?

What triggers this?

A

1 Jaundice
2 Coagulapathy (↑INR, bruising, ↓factor 9 10 7 2
3 Encephalopathy (Liver flap, Confusion, ↓GCS>give lactulose)
4 Ascites
(variceal rupture)

Can be triggered by infection, GI bleed, constipation, opiates, alcohol, AKI, electrolyte disturbance

if encephalopathy follows jaundice within 2 weeks=acute
if encephalopathy follows jaundice after 2 weeks=chronic

79
Q

What are some other causes of ascites?

A

ASCITES
-Liver cirrhosis most common (75% of patients with ascites have cirrhosis)

Malignancies:

  • GI tract
  • Ovarian (Meig’s)-ascites out of proportion to tumour size
  • Lymphoma
Heart failure 
Nephrotic syndrome 
Pancreatitis (inflammation)
Hypothyroidism 
TB (infection)
80
Q

Symptoms of ascites?

What signs might be found on examination of ascites?

Investigation of choice?

A

ASCITES
Symptoms
-Nausea + LoA – due to pressure on stomach + s.bowel
-Dyspnoea (pressure and reduced venous return)

Examination 
Distention of abdomen
Umbilical/inguinal hernia 
Shifting dullness 
Fluid thrills
Virchows node (left supraclaviclur-upper GI cancer)

USS is Ix of choice

81
Q

How do you manage ascites?

A

ASCITES

  1. Fluid restrict (<1.5L/d) and monitor daily weight
  2. Reduce salt intake
  3. Diuretics 1st line is potassium sparing (SPINOLACTONE) in liver disease (and titrate up)
  4. Therapeutic Paracentesis (neut > 250/mm>SBP)
    - to relieve respiratory distress/ abdo pain
  5. Albumin infusion
82
Q

What score determines severity of liver cirrhosis?

A

CHRONIC LIVER DISEASE

  • Child-pugh score determines severity of cirrhosis (ABC)
  • Based on Albumin, PT, Bilirubin; Ascites, Encephalopathy
83
Q

What infection would you consider in anyone chronic liver patient who suddenly deteriorates?

What organisms commonly cause it?

How can you make diagnosis?

What is the managment?

A 
SBP Spontaneous bacterial peritonitis
-Organisms: commonly  E.coli  
-Diagnosis: ascitic tap: neutrophils>250
-Treatment: IV pip/taxo until sensitivity known 
(give prophylactic AB if at risk)
84
Q

How do you test for hereditary haemochromatosis?

Treatment?

A

Hereditary haemochromatosis

1st line

  • ↑Serum Ferritin
  • ↑increased TRANSFERRIN SATURATION (iron needs a car)
  • low total iron binding capacity (cant bind to anymore-its full)
  • HFE gene (C282Y)

Diagnostic=biopsy

Treatment: regular venesection

(RF for pseudogiut-chostrocalcinosis)

85
Q

Symptoms of Wilsons?
How do you test for Wilsons?
Treatment?

A

Wilson’s
Sx: speech + behaviour problems, Kayser Fleischer)

↑24hr urinary Cu
↓Serum caeruloplasmin (all used up)
↓Serum Cu

Treatment: penicilliamine

86
Q

What is hepatorenal syndrome?

Why is renal failure a complication of liver disease??

A

Hepato-renal syndrome = Cirrhosis + Ascites + Renal failure

Why: ↓Hepatic clearance of immune complex leads to accumulation in kidney → IgA nephropathy and hepatic glomerulosclerosis

If HCV → Mesangiocapillary/membranoproliferative glomerulonephritis

87
Q

What immunoglobulins are assosiated with what conditions? (IgA, IgM, IgG,

A

Immunoglobulins
IgA = alcohol
IgM = PBC
IgG: autoimmune hepatitis (if ANA/SMA/SMA) or PCS (if ANCA)

-all 3: cirrosis

88
Q 
What auto antibodies are assosiated with what conditions?
ANA/SM
LKM
AMA
ANCA
A 
Auto antibodies 
ANA/SM: Autoimmune type 1 (or PSC)
LKM: AI type 2 (only in children)
AMA (M2): PBC 
ANCA: PSC
89
Q

Obstructive picture, ‘beads on a string’ sign and assosiated with IBD?

A

Primary sclerosing cholangitis

  • beads on sting sign found on ERCP
  • assosiated with Ulcerative colitis
  • increased risk of cholangiocarcinoma
90
Q 
Triad of:
1. abdo pain 
2. hepatosplenamegally 
3. ascites 
(painful)

what is it?
investigations?
treatment?
assosiated with?

A

Budd chiari syndrome (acute hepatitis)

  • investigations: urgent USS with doppler
  • treatment: treat as any DVT
  • assosiated with polycythemia vera (too many RBC)

(acute version of portal vein thrombosis)

91
Q

Therapeutic Paracentesis

  • what would make you think SBP?
  • what would make you think underlying malignancy
A

Therapeutic Paracentesis (WCC, RBC, gram stain)

SBP = Neutrophil > 250 cells/mm
high RBC = suspicious of underlying malignancy e.g. HCC

Albumin/protein level

Exudate > 25 g/L; transudate < 25g/l
SAAG (serum ascites-albumin gradient) = serum alb conc – ascetic alb conc
≥ 11 g/L (transudative– cirrhosis, HF, CCF)
<11 g/L (exudative –malignancy, infection, pancreatitis, nephrotic syndrome)

Withdrawal of ≥ 5L may cause post-paracetesis circulatory dysfunction (PPCD) AKI

92
Q

Exudative vs transmutative ascites?
(SAAG high or low)
(causes)

A

Transudate (portal vein pressure)
-high SAAG (>1.1g/dL) (liver cirrhosis/heart failure

Exudate < 25g/l

  • low SAAG (<1.1g/dL)
  • local disease
  • inflammation or malignancy (or pancreatitis/nephrotic syndrome)
93
Q

Why do you get portal HTN in chronic liver disease?

What are some signs of portal HTN? (4)

A

PORTAL HTN
Fibrosis → ↑intrahepatic resistance→ Porto HTN and shunt to other veins

Effect of portal HTN 
-oesophageal varices (haematemesis)
-gastric varices (melena) 
-heamorroids (rectal veins)
-transudative ascites 
-caput medusae – paraumbilical/epigastric veins 
-congestive splenomegaly  
-hypo perfusion of kidneys→ water/salt retention      >transudative pleural effusion
>↑CO
94
Q

Pre hepatic/intrahepatic/post hepatic causes of portal HTN?

A

PORTAL HTN
Prehepatic
• Portal vein thrombosis
• Splenic vein thrombosis

Intrahepatic 
• Cirrhosis 
• Schistosomiasis 
• Hepatic metastases 
• Hepatic sinusoidal obstruction syndrome (aka hepatic veno-occlusive disease)

Post-hepatic
• Budd-Chiari syndrome - hepatic vein obstruction
• Right-sided heart failure
• Constrictive pericarditis

95
Q

1st line treatment for portal HTN?

A

PORTAL HTN
Propanolol (non-cardiac selective beta-blocker) - first-line treatment

Inhibits beta-2-adrenergic receptors in the GI tract>vasoconstriction>decrease portal and collateral blood flow>reduces portal hypertension

96
Q

What is an invasive management option for certain patients with portal hypertension?

A

Trans-jugular intrahepatic portosystemic shunt (TIPSS)

An artificial channel connecting inflow portal vein and the outflow hepatic vein

97
Q

Common indications for TIPSS surgery?

A

Secondary prophylaxis for oesophageal variceal bleeding

Treatment of refractory ascites

Treating portal hypertension in Budd-Chiari syndrome

98
Q

When would you give prophylactic AB for SBP?

A

NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’

also if people have PMH of SBP

99
Q

How long before urea H pylori breath test can you take antibiotics and PPIs?

A

Urea breath test

  • no antibiotics in past 4 weeks
  • no antisecretory drugs (e.g. PPI) in past 2 weekshttps://www.brainscape.com/l/study?classes=16223428-9295674
100
Q

second line treatment for heamatomachrosis if phlebotomy is CI

A

Deferoxame (de iron) if phlebotomy is CI (anemia)

101
Q

best initial test for wilsons disease

A

Kiesher flesher rings

102
Q

What tests can you do

A

Serum copper

  • ceruloplasmin low
  • low total serum copper
  • rasied FREE serum copper

URine copper
-low urine copper

103
Q

Treating od wilsons?

A

Chelating agent

Penicllamine and Triente

104
Q

Drug causes of acute pancreatitis

A 
Steroids 
NSAIDS
thiazides 
azathioprine
sodium val
tetracyclines

5thyr (18 decks)

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