Gastroenterology Flashcards

1
Q

Achalasia associated with which cancer

A

SCC (10x risk compared to general population)

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2
Q

Achalasia barium swallow findings

A

Bird’s beak

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3
Q

Which subtype of achalasia is most severe?

A

Type 1

Progression from Type 3 to Type 1

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4
Q

Which subtype of achalasia has the best treatment outcome?

A

Type 2

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5
Q

Oral Tx options for achalasia

A

CCB
Isosorbide dinitrate
(effective in 50-60%)

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6
Q

Complication with Botox injection for achalasia

A

Causes submucosal fibrosis and unable to do subsequent definitive surgical treatment

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7
Q

Efficacy of Balloon dilatation in achalasia

A

60-90% effective
Risk of perforation in 1-6%
Recurrence in 2-3 years

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8
Q

Treatment of choice for achalasia

A

POEM (PerOral Endoscopic Myotomy)

  • Success similar to Lap Myotomy, but less recovery ime
  • SE: Reflux ++
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9
Q

Classic endoscopic features of eosinophilic oesophagitis

A
  • Oedema
  • Longitudinal furrows
  • White exudates
  • Concentric rings
  • Strictures and mucosal tearing
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10
Q

Treatment of eosinophilic oesophagitis

A
  • PPI
  • Aerosolised steroids
  • Diet: Elemental; Eliminate milk, wheat, gluten, eggs, nuts, shellfish, soy
  • Dilatations for strictures
  • Esperimental: Budesonide, montelukast
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11
Q

Mucosa change in Barret’s oesophagus

A

Strafed squamous epithelium replaced by cardiac type mucus secreting columnar epithelium +/- intestinal metaplasia

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12
Q

Medical treatment shown to slow/stop progression of Barrett’s to adenocarcinoma

A

PPI and aspirin therapy

  • AspECT trial
  • Surgical therapy is no more effective than PPI
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13
Q

Survival with Oesophageal Adenocarcinoma

A

5 year survival <20%

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14
Q

Mx recommendation for low grade dysplasia in Barrett’s

A

If LGD confirmed on 2 occasions 6 months apart by two pathologists, then endoscopic RFA is recommended OR close surveillence
-Risk of progression to HGD

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15
Q

Risk of HGD in Barrett’s to progress to Adenocarcinoma

A

~10%

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16
Q

Mx of HGD in Barrett’s

A
  • Oesophagectomy vs endoscopic resection
  • Then RFA to rest of Barrett’s due to risk of transformation
  • Annual Gscope annually for 5 years
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17
Q

Risk of recurrence of Barrett’s post surgical excision/RFA

A

~10%

Greatest in first year

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18
Q

Features suggestive of malignant dysphagia

A
Shorter duration
Solids > liquids
Constant and progressive
Older age
Accompanying alarm symptoms
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19
Q

Mx of refractory GORD

A

Failed PPI BD trial for 3 months

  • Check compliance and lifestyle modifcations
  • Trial nocte H2 antagonist
  • Repeat scope and perform pH testing
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20
Q

Location of most gastric ulcers and duodenal ulcers

A

Junction of fundus and antrum along the lesser curvature

DU are usually in the 1st or 2nd part

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21
Q

Evidence of PPI therapy in GI bleeding

A

No mortality benefit

Reduction in need for endoscopic therapy compared to placebo

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22
Q

Forrest Ia

A

Spurter

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23
Q

Forrest IIa

A

Non bleeding visible vessel

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24
Q

Forrest IIb

A

Clot at base

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25
Forrest IIc
Dot
26
Forrest III
Clean Base
27
Evidence for post endoscopy PPI for GI bleeds
Reduces rebleeding significantly | -IB PPI infusion for 72 hours recommended post procedure
28
H pylori genes linked to carcinogenesis
cagA and vacA
29
Cancers associated with H. Pylori
Gastric cancer | MALT lymphoma
30
H pylori associated with a decreased risk of what cancer
Oesophageal adenocarcinoma
31
Treatment of H Pylori
Quad therapy: PPI+Amoxy+Metro+Clarythromycin x 14 days PPI+ Bismuth +Metro+Tetracycline x 14 days
32
Immune cell associated with MALT Lymphoma
Low grade B cell neoplasia
33
H Pylori association with ITP
H pylori eradication improves platelet counts in ~ 50% of ITP
34
When to do post H pylori eradication testing
>4 weeks after completing treatment
35
Duration off ABx and PPI to investigate for H pylori
>4 weeks ABx | >2 weeks PPI
36
Endoscopic features of malignant gastric ulcers
Irregular outline with necrotic or haemorrhagic base Irregular raised margins Prominent and oedematous rugal folds that usually do not extend to the margins
37
What INR is it safe to do a Gscope at
= 2.5
38
When to restart warfarin post UGIB
7-14 days post procedure
39
Histological Features of Coeliac Disease
Intra-epithelial lymphocytes Crypt hyperplasia Villous atrophy
40
Best initial testing for coeliac disease
Anti TTG IgA High sensitivity and specificity -If weakly positive, then do anti endomysial IgA
41
Non Responsive Coeliac Disease
- Compliance! - Alterative associated issues: SIBO, Microscopic colitis, IBS - Diet review - Repeat Histo - Colonic Bx - ?microscopic colitis
42
Refractory Coeliac Disease Type 1
Steroids +/- steroid sparing agent
43
Refractory Coeliac Disease Type 2
Poorer prognosis Oligoclonal T cell expansion High risk of transformation to enteropathy associated T cell lymphoma
44
PAS positive macrophages in sub mucosa on GI biopsies
Whipple's Disease
45
Affect of omeprazole on Gastrin Level
Omeprazole increases Gastrin levels
46
Enterchromaffin cells
Stimulates gastric acid secretion Responds to gastrin Contains Histamine Stains positive with silver
47
Hyperplasia of enterochromaffin cells in the gastric mucosa is associated with
Atrophic gastritis
48
Medication effective in preveting gastric ulceration with NSAID use
Misoprostol
49
Immunosuppressed and small discrete ulcers in the oesophagus - cause?
HSV
50
Immunosuppressed and giant ulcers in the oesophagus - cause?
CMV
51
CD117 (c-KIT)
GIST
52
Main mechanism of reflux in majority of episodes
Transient LOS relaxation due to vagal stimulation in setting of proximal gastric distension
53
Side effect of giving folic acid in B12 deficient patients
Causes severe neuropathy and worsening B12 deficiency because it will stimulate erythropoesis and further worsen B12
54
Side effect of giving glucose prior to thiamine in refeeding syndrome
Acute Beri Beri
55
Refeeding Syndrome - Glucose has what effect on insulin
Hyperinsulinaemia - Which then results in Fluid and salt retention and intracellular K=/PO4 shift - Results in dilutional hypoalbuminaemia
56
Factors which favour intestinal absorption in short bowel syndrome
-Length of remaining bowel (>60-90 cm of SB with colon OR >150 cm small bowel) -Ileum>Jejunum -Ileocecal valve present -Absence of mucosal disease -Presence of colon -
57
Benefit of having a retained ileocecal valve in short bowel syndrome
Reduces risk of Small bowel bacterial overgrowth
58
What renal stones are associated with short gut
Oxalate | -Treat with calcium
59
Role of GLP2 in Short gut syndrome
Provides feedback to the upper intestine to optimise the nutrient and fluid absorption - Mucosal growth - Teduglutide
60
Target Hb for UGIB
70-90 | -Reduces adverse events, further bleeding and improves 6 week survival
61
Evidence for IV PPI for 72 hours post endoscopy for UGIB
-Improved rate of rebleeding, blood transfusion requirement, duration of hospital stay
62
Evidence for Octreotide in variceal bleeding
Reduction in rebleeding and number of patients failing initial haemostasis NO reduction in mortality
63
MOA Terlipressin
Synthetic vasopressin analogue Avoid in significant CAD or PVD
64
Evidence for ABX in vleeding varices
Quinolones/3rd Gen Cephalosporins - REduce all cause and infection mortality - Reduced rebleeding rates
65
Evidence for ABX in vleeding varices
Quinolones/3rd Gen Cephalosporins - REduce all cause and infection mortality - Reduced rebleeding rates
66
Evidence for endoscopic rubber band ligation in acute oesophageal varices
Fewer side effects and more effective than sclerotherapy | Reduced mortality and rebleeding
67
Secondary prophylaxis for oesophageal varices
BB - Propanolol - start at Day 3-5 post acute bleed -Reduce rebleeding and mortality Further banding sessions 2-4 weeks a part until eradication (3-4 sessions)
68
NAFL Definition
Presence of steatosis without liver injury | Minimal risk of disease progression
69
NASH Definition
Hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. Can progress to cirrhosis, liver failure and cancer
70
NASH Cirrhosis Definition
Cirrhosis with current or previous evidence of NASH
71
Cryptogenic Cirrhosis
Cirrhosis with no obvious aetiology. Many have metabolic risk factors and likely to have NASH cirrhosis
72
What percent of Fatty liver progresses to NASH and cirrhosis
20% from fatty liver to NASH | 4-8% NASH to cirrhosis
73
Tests used to screen for advanced liver fibrosis in NAFLD
- Presence of T2DM - Decreased platelets - AST:ALT >1 - NALFD Fibrosis score
74
Fibroscan result that correletes well with portal HTN
>25
75
Most reliable test to rule out advanced hepatic fibrosis (High negative predictive value)
Fibroscan
76
Indications for Liver Bx for NAFLD
Abnormal ALT/GGT AND - >/=3 features of metabolic syndrome (esp T2DM) - NAFLD Fibrosis Score/Fibroscan 8-12
77
Benefits of weight loss in NAFLD
Improves biochemical profile, histo, decreases steatosis, reduces inflammation, decreases fibrosis
78
HCC surveillance in cirrhosis
6 monthly USS in NASH cirrhosis
79
Haemochromatosis Histo
Grade 3 hepatocyte iron accumulation with an acinar distribution pattern Stains with Perl's prussian blue
80
Hereditary Haemachromatosis genetics
Autosomal recessive HFE on chromosome 6 -C282Y mutation
81
TF Saturation in haemachromatosis
>45%
82
Classic triad of haemachromatosis
Bronze skin Cirrhosis Diabetes
83
Most sensitive screening tool for haemachromatosis
Fasting morning transferrin saturation
84
Hepatitis B in pregnancy - Risk with normal delivery and breast milk
No protective effect of C-section | No increased risk with breast milk
85
Hepatitis E Antigen
Correlates with infectivity (marker of active replication) Higher viral load Anti-HbE important sign of serovconversion of eAg and beginning of clearance
86
HbsAg - Anti HBc + Anti HBs -
- Most often: Distant resolved infection wit hloss of HBsAb - Recovering from acute infection before sAb is detected - False positive - PAssive transfer of maternal anti HBc in children up to 3 - Occult Hep B CHECK viral load!
87
Occult Hepatitis B
Presence of HBV DNA without detectable surface antigen | Still at risk of cirrhosis and HCC
88
Hep B Pre core mutant or Basal core promoter mutant
Downregulates HBeAg production: HBeAg negative/Ab positive Increased rates of advanced disease Escaping immune control
89
Risk of death with chronic Hep B
15-25% chance of death associated with virus
90
Chronic Hep B: | Immune Tolerance
High HBV DNA Normal LFTs HBeAg Positive Children usually remain in this phase until 20s to 30s Mx: Monitor 6-12 months
91
Chronic Hep B: | Immune Clearance
Body begins to recognise Hep B and attacks Viral load begins to drop Derranged LFTs Usually HBeAg seroconversion At risk of progression to cirrhosis and HCC at this stage Mx: Medications
92
Chronic Hep B: | Immune Control
Inactive virus Lower HBV DNA Normal LFTs HBeAg negative and Ab positive Mx: Monitor 6-12 months At this stage: 3 things can happen - Clear virus (rare) - Remain in immune control long term - Immune escape
93
Chronic Hep B: | Immune escape
High HBV DNA Derranged LFTs HBeAg negative and Ab positive At risk of cirrhosis and HCC
94
Hep B Surveillance
6 monthly Liver USS and AFP Fibroscan 2 yearly Patient groups: - Cirrhosis - Family or PHx of HCC - HBV Asian men over 40 or women over 50 - HBV africans over 20 - HBV >40 years age with Increased HBV DNA and Increased ALT
95
Treatment of Chronic Hep B: | Polymerase inhibitors
``` TDF Entecavir Lamivudine Adefovir TAF ``` Benefit: - Suppress HBV DNA - HBeAg seroconversion 10-20% - No resistance with Entec and TDF/TAF - Safe in deco,pensated disease Downside: -Indefinite therapy
96
Treatment of Chronic Hep B: | Immunomodulator
Peg Interferon Benefit: - Higher rate of HBeAg loss in 1 year - Finite course - No resistance CI: -Cirrhosis, pregnancy, acute Hep B, immunosuppressed, psych instability
97
What is the normal ULN for ALT
25 in females | 35 in males
98
HBeAg Positive + non cirrhotic | When to treat?
ALT >/= 2xULN HBV DNA >20,000 If HBV DNA <20,000 and persists for 6 months, then treat
99
HBeAg Negative + non cirrhotic
ALT >/= 2xULN | HBV DNA >2,000
100
Choice of Hep B treatment if known previous Lamivudine resistance
TDF/TAF Likely to have Entecavir resistance
101
Choice of Hep B Tx in decompensated cirrhosis
1. Entecavir perferred | 2. TDF/TAF
102
Choice of Hep B Tx in Renal insufficiency
Entecavir preferred
103
Choice of Hep B Tx in Pregnancy/child bearing age
Tenofovir
104
Choice of Hep B Tx in women of child bearing age wishing to eradicate virus prior to pregnancy
Peg Interferon alfa 2a or 2b
105
Choice of Hep B Tx in HIV coinfection
Tenofovir +Emtricitabine or Lamivudine
106
Pregnant woman + Hep B Viral load in 2nd trimester <10^5 -?Mx
Monitor | Infant: HBIG +vaccine at birth w/i 12 hours of birth (efficacy 95%)
107
Pregnant woman + Hep B Viral load in 2nd trimester >10^5
Tenofovir at 28-32 weeks | Infant: HBIG +vaccine at birth within 12 hours of birth
108
Hepatitis D
Most aggressive Hepatitis Needs HBsAg to replicate Treatment Peg interferon for 2 years (30% efficacy) Check for it if ALT not improving with Hep B treatment
109
Commonest cause for liver transplat
Hepatitis C
110
High levels of mutation in Hep C due to what?
RNA polymerase can't proof read
111
Most common genotypes in Australia for Hepatitis C
1 and 3
112
Definition of Quasispecies in Hep C
Different strains within a host | Importnat in viral persistance, lack of response to IFN based therapy and leads to difficulties in vaccine development
113
How to test for Hepatitis C
ELISA Window period of 6 weeks (ranging 2-26 weeks) If indeterminate response - Do HCV RNA
114
Most specific test for Hep C
``` HCV RNA (PCR) -Can pick up active infection earlier with this ``` Qualitative: Diagnosis of infection Quantitative: Viral burden and duration of Tx with IFN
115
Hep C Point of care testing
HCV ab mouth swab or fingerprick HCV viral load in 105 mins Same day result
116
What are the perinatal transmission risks for Hep C
2-8% risk of vertical transmission if RNA + (Higher if HIV +) No increased risk of transmission with breast feeding No evidence for CS Baby: Can only check HCV ab after 15-18 months due to passive transfer from mum
117
Factors related to spontaneous clearance of Hep C
Younger age Female MHC genes, IL28B
118
Extrahepatic Manifestations of Hepatitis C
- Rh Factor postive - T2DM 11x increase risk - Cryo - Membranoproliferative GN 7x risk - PCT - Lichen planus - Lymphoma - Keratoconjunctivitis sicca
119
APRI Test
Used to assess for Fibrosis - AST to Platelet Ratio Index - >1 result is suggestive of cirrhosis Equation: AST/ULN AST all divided by platelet count x100
120
SVR -Sustained virological response in Hep C definition
HCV RNA negative 12 weeks after completion of treatment
121
Direct Acting Antivirals MOA
Target specific non structural proteins of HCV to disrupt viral replication -4 classes
122
Nucleoside NS5B polymerase inhibitors
- Buvirs | - Sofosbuvir
123
Non Nucleoside NS5B polymerase inhibitors
-Dasabuvir
124
NS3/4 Serine protease inhibitors
-Previrs
125
NS5A replication inhibitors
-Asvirs
126
Pangenotypic Hep C treatment
Sofosbuvir/Velpatasvir | -Add ribavirin for Child pugh B and C
127
Hep C treatment duration
Varies with regimes and if cirrhotic - Cirrhosis: 12 weeks - Sometimes less if non cirrhotic
128
Hep C Treatment Adverse effects
Fatigue/Insomnia Headache GI Sx Can Reactivate Hep B!
129
Drug interactions with Hep C treatments
Statins Omeprazole - Reduces absorption Amiodarone (Bradycardia) Potent P-gp inducers (rifampicin, St. Johns wort)
130
MELD scores for HEP C treatment guidance
MELD < 15 -treat MELD 15-20/25 - Treat cautiously MELD >20/25 -Defe Tx until post Transplant - If not a transplant candidate - discuss with patient as may worsen liver failure
131
HCC screening after SVR in Hep C
Mild fibrosis - none | F3-F4 fibrosis: USS and AFP 6 monthly
132
MOA of Cirrhosis
- Primarily due to activation of hepatic stellate cells (liver macrophages) - Involved in healing and repair after biliary or hepatocellular injury - Chronic activation results in increased collagen & extracellular matrix
133
Fibroscan Scores
F0-1: <7.5 = absent/mild disease F2-3: 7.5-13 = unclear F4: >13 = Cirrhosis
134
Factors assessed in Child Pugh Score
- Encephalopathy - Ascites - INR - Albumin - Bilirubin
135
MOA of cirrhotic portal HTN
-Increased vascular resistance due to structure (liver vasc architecture by fibrosis) and Dynamic (increased hepatic vascular tone due to endothelial dysfunction and decreased NO bioavailability
136
Ascites
- Reflects renal Na+ and H2O retention via activation of RAAS - Portal HTN is primary driver, not hypoalbuminaemia
137
SAAG Score
Serum Albumin - Ascites albumin >11 suggestive of portal HTN
138
SBP Leucs and PMN in ascitic fluid
Leucs >500 PMN >250 If significantly higher leucs and polys, may need to consider alternative cause - ?perforation
139
SBP Mx
- 3g Ceftriaxone for 5-7 days (Tazocin if on norflox/bactrim) -IV Conc Albumin load and >2 bottles/day for >3 days -Repeat tap 48 hours post tratment
140
Hepatic Hydrothorax
Ascitic fluid leaking into pleural space, usually right sided
141
Ascites Mx
- Spiro 100mg - Frusemide 20 mg - Aim 1 kg weight loss/day - Restrict salt to 5 g/day (more important than fluid restriction) - AVOID Normal Saline, leads to salt retention and worsening ascites
142
Albumin with paracentesis
20% conc albumin 100 ml over 1/24 for each 2L ascites drained - Colloid osmotic effect 4x that of plasma - Prevents large plasma volume drainage - renal failure/hypotension
143
Ascites refractory to diuretics
- Weekly Albumin infusion shown to improve mortality - TIPS; Terlipressin infusions as outpatient - Transplant consideration
144
Hepatic Encephalopathy | West Haven Criteria
Grade 1: Trivial lack of awareness; euphoria or anxiety; shortened attention span; impaired performance of addition or subtraction Grade 2: Lethargy or apathy; minimal disorientation for time/place; personality change, inappropriate behavior Grade 3: somnloence to semistupor but responsive to verbal stimuli; confusion; gross disorientation Grade 4: Coma
145
Hepatic encephalopathy Mx
Lactulose Rifaximin add on -Reduced recurrence of HE, not mortality
146
Mx of VAriceal bleeding
1. SBP >90 2. Hb >70 3. Blood/ albumin preferable - avoid saline 4. IV thiamine if drinker 5. Blood cultures and empical IV Ceftriaxone 7. Terlipressin 8. Scope
147
TIPS Indications
- Variceal bleeding unable to be treated endoscopically - Diuretic refractory ascites or hepatic hydrothorax - Budd Chiari
148
TIPS Contrindications
Increased Risk of HE! | RHF
149
Type 1 HRS
- Acute deterioration - Poor outcome if untreated (50% survival at 11 days) - Mx: Terlipressin infusion and Albumin, and ultimately need transplant or will ide
150
Type 2 HRS
- Slow progression - A/W refractory ascites - 6 month transplant free survival 40-50%
151
HCC CT Quad phase finding
Arterial enhancement, portal vein washout
152
``` HCC Mx (BCLC Staging) -Single HCC <2 cm, normal Portal pressure ```
Resection
153
``` HCC Mx (BCLC staging) -Single HCC <2 cm, Increased Portal pressure ```
Transplant
154
``` HCC Mx (BCLC staging) -3 nodules <3 cm and no associated diseases ```
Transplant
155
``` HCC Mx (BCLC staging) Early stage -3 nodules <3 cm and no associated diseases ```
RFA
156
``` HCC Mx (BCLC staging) Intermediate -Multinodular and no portal HTN ```
TACE (palliative) - Transarterial chemo embolisation - Can decompensated CLD if portal HTN is present
157
``` HCC Mx (BCLC staging) Advanced -Portal invasion, metastatic disease ```
``` Sorafenib (palliative) -Multi kinase inhibitor (VEGF and platelet derived growth factor receptors), RAF -Only suitable for compensated cirrhosis -ECOG 0-1 ``` SE: Palmar-plantar erythrodysesthesia, Fatigue, fevers, diarrhea, increased bleeding risk (so banding prior) - Lenvatinib (non inferior and also first line) - Can change between the two if there is intolerance
158
``` HCC Mx (BCLC staging) -Child Pugh C ```
Terminal, symptomatic
159
SBP Prophylaxis indication
``` low protein (<10g/L) or Bilirubin >50 with impaired renal function -Norflox 400 mg daily or Bactrim reduces mortality and SBP ```
160
Variceal screening frequency if small varices
annual
161
Variceal screening frequency if no varices
2 yearly
162
Calculating Hepatic Venous Pressure Gradient (HVPG)
HVPG = WHVP - FHVP WHVP = Wedged Hepatic Venous Pressure FHVP = Free Hepatic Venous pressure
163
HVPG suggesting Portal HTN
>5 If >10, then increased likelihood of varices, decompensation and HCC Gives you pressure over the sinusoids
164
MOA of propanolol with varices
Reduction in cardiac output and splanchnic blood flow Allow unopposed alpha-1 adrenergic receptor activity which results in splanchnic vasoconstriction and reduction in portal pressure
165
Kings college criteria for ALF (paracetamol Induced)
- pH <7.3 OR all of the following: - INR >6.5 - Cr >300 micromol/L - Grade 3 or 4 HE
166
Kings college criteria for ALF (non paracetamol induced)
- INR >6.5 OR 3 out of 5 of the following: - Age <11 or >40 - Bilirubin >300 micromol/L - Jaundice to coma time >7 days - INR >3.5 - Drug toxicity
167
MELD Score for Transplantation
>15
168
Early (<3/12) Liver Tx morbidity/mortality
Graft failure (rare) Infection Biliary stricture Renal/diabetes/cosmetic
169
Findings of acute Rejection in Liver Transplant and time period
- Portal Based inflammation (cholestatic LFTs) - Usually at days 7-10 - Occurs in 1/3 - No chronic sequelae - Mx: Bolus steroids
170
Findings of chronic Rejection in Liver Transplant
Rare - Vanishing bile duct syndrome (cholestatic LFTs) - Increase Tacrolimus dose for Mx
171
Milan Criteria for HCC Transplantation
```  Single lesion ≤ 5cm, and/or  Up to 3 separate lesions, all < 3cm  No evidence of gross vascular invasion  No evidence of regional nodal or distal metastases ```
172
UCFS Criteria for HCC Transplantation
 A single nodule ≤ 6.5cm, or  Up to 3 nodules, the largest of which is ≤ 4.5cm  Cumulative tumoursize (sum of all diameters) ≤ 8cm
173
Most specific LFT parameter for liver
ALT
174
LFTs in Pregnancy: | Hyperemesis Gravidarum
1st Trimester Vomiting and weight loss ALT/AST Increase
175
LFTs in Pregnancy: | HELLP
2nd/3rd Trimester/Postpartum HTN, RUQ/epigastric pain, N+V, Headache, visual changes AST >2x ULN; Plt <100,000; LDH >600; Pr:Cr >0.3 mg Mx - Delivery
176
LFTs in Pregnancy: | Preeclampsia
2nd/3rd Trimester/Postpartum HTN, Headache, visual change, RUQ/epigastric pain AST/ALT >2xULN, Plt <100,000 Mx - antihypertensives, MgSO4
177
LFTs in Pregnancy: | Intrahepatic Cholestasis
2nd/3rd trimester Pruritis, steatorrhea, RUQ pain Usually AST/ALT <2xULN Mx - Ursodeoxycholic acid or cholestyramine
178
LFTs in Pregnancy: | Acute Fatty Liver in Pregnancy
3rd Trimester N+V, abdo pain, acute liver failure AST and ALT elevations up to 500 Mx- Delivery
179
Cause of Increased AST:ALT
Alcoholic hepatitis NASH Chronic HCV cirrhosis Wilson's disease
180
Role for Maddrey Score
In Alcoholic Hepatitis Prognostication Uses PT and Bilirubin Score >32 suggests poor prognosis and may benefit from steroids
181
Drug of choice for agitation in patients with hepatic encephalopathy
Haloperidol
182
PBC Histo
shows periportal inflammation, periductal granulomas, and biliary inflammation and necrosis
183
What percent of the liver blood supply is from the hepatic portal vein
75%
184
New Mx in IBS
IBS-D - Ondans - 65% Sx relief - Rifaximin - 40% Sx relief - Eluxadoline IBS - C -Linaclotide - guanylate cyclase c receptor Chronic constipation - Elobixibat - inhibitor of bile acid transporter - Tanapenor - increases intestinal fluid and improves transit
185
Eluxadoline MOA and SE
For IBS-D 29% effective Peripherally acting mixed mu-opioid receptor agonist, gamma opioid receptor antagonist, Kappa opiod receptor agonist SE: Rare sphincter of Oddi Spasm, pancreatitis
186
CAPS - Centrally mediated abdominal pain syndrome
Severe continuous abdominal pain, impacting daily function, chronic, usually associated with psych issues
187
Favorable factor in Hep C treatment
-Genotype 1 (IL-28B polymorphism)
188
USe of amiodarone when starting Hep C Treatment
NEed 3 months off amiodarone as it can precipitate heart block
189
Tx of Hep C genotype 3 and decompensated liver disease
Add riboviran to increase treatment success from 50% to 85%
190
HEp C treatment in pregnacy
Contraindicated in pregnancy | If on ribviran therapy, need to wait 6 months before getting pregnant
191
Sofosbuvir CI
egfr <30
192
Hep C regime for renal impairment
ombitasvir paritaprevir Ritonivir
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Hep C Tx protease inhibitor CI
Child Pugh B or C OR portal HTN
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Ribavirin precautions
PRegnant women Men whose partners are pregnant Haemoglobinopathies Preexisting cardiac disease
195
NAFL Histo
Steatosis with lobular or portal inflammation, with or without hepatocyte ballooning
196
NASH Histo
presence of hepatic steatosis in association with hepatocyte ballooning degeneration and hepatic lobular inflammation
197
Pioglitazone in NAFLD
shown to improve fibrosis, inflammation, and steatosis
198
NAC MOA
replenishing body stores of the antioxidant glutathione. | Glutathione reacts with the toxic NAPQI metabolite so that it does not damage cells and can be safely excreted.
199
Alcoholic Hepatitis Histo
Neutrophil infiltration MAllory Dank bodies (eosinophilic accumulations of intracellular protein aggregates within the cytoplasm of hepatocytes) • Fibrosis with a perivenular, perisinusoidal, and pericellular distribution
200
Liver histo piecemeal necrosis
chronic viral hepatits/AI hepatitis
201
SIBO features
macrocytic anaemia B12 deficiency fecal fat Histopathological findings associated with SIBO include villous blunting, cryptitis, intraepithelial lymphocytosis, and eosinophilia.
202
Diagnosing SIBO
positive carbohydrate breath test or jejunal aspirate culture lactulose/glucose results in an early peak (w/i 90 mins) in breath hydrogen/methane levels due to metabolism by small bowel bacteria.
203
Colonic pseudo-obstruction
appearance of mechanical obstruction without demonstrable evidence of such an obstruction in the intestine in the elderly with serious concurrent medical and surgical/post-operative conditions Risk of perforation if not decompressed
204
UC Histo
``` Mucosal/submucosal Lymphocytic infiltrateGoblet cell depletion Cryptitis Crypt abscesses NO GRANULOMAS ```
205
Crohns histo
``` • Transmural inflammation • Infiltrate of lymphocytes and macrophages • Granulomas in ~ 50% of cases ```
206
NOD1/Card15 in Crohns
Younger onset of disease Small bowel involvement Stricturing phenotype Early initial surgery and surgical recurrence
207
ASCA
Anti saccaromyces cervisiae antibodies Associated with crohns
208
pANCA and IBD
Associatted with UC
209
Extraintestinal IBD manifestations associated with active GI disease
``` • Oral ulcers • Erythema nodosum • Large-joint arthritis • Episcleritis ```
210
IBD Mx: Sulfaslazine and 5 aminosalicylates MOA and SE
Mechanism of action unclear SE Diarrhea (3%), headache (2%), nausea (2%), rash (1%) Main role in UC. - Reduces risk of CRC - Induce and maintain remission in mild-mod UC
211
IBD Mx: Thiopurines MOA
Inhibit purine synthesis Inhibit T and B cell proliferation Induce T-cell apoptosis
212
Low/Absent 6-TGN/ | Low/Absent 6-MMP
Non adherence
213
Low 6-TGN/ | Low 6-MMP
Underdosing
214
High 6-TGN/ | High 6-MMP
Thiopurine refractory | Trial another drug
215
Low 6-TGN/ | High 6-MMP
Thiopurine resistance | Add allopurinol and reduce thiopurine dose
216
IBD Mx: Cyclisporine MOA and SE
Calcineurin antagonist • Potent inhibitor of cell-mediated immunity • Rescue therapy for severe steroid refractory UC SE: Nephrotoxicity, hypertension, neurotoxicity, infections
217
IBD Mx: Vedolizumab MOA
Selectively binds α4β7 integrin on surface of T lymphocytes • Blocks interaction with MAdCAM-1 on intestinal endothelium • Inhibits trafficking of leukocytes to sites of inflammation • Approved for treatment UC and Crohn’s • Excellent safety profile
218
IBD Mx Ustekinumab MOA and indication
Monoclonal antibody to p40 subunit of IL-12 / IL-23 Indications: Crohns
219
Risk for hepatosplenic T cell lymphoma in IBD
Highest risk in men <35 on Infliximab and thiopurine
220
Definition of acute severe colitis in IBD`
``` Bloody stool frequency >6/day plus >1 of: • Pulse >90bpm • Temp >37.8oC • Hb<10.5g/dL • ESR >30mm/hr ```
221
Autoimmune hepatitis histo
predominantly periportal hepatitis Interface hepatitis with lymphoplasmacytic infiltrate Hepatic rosettes
222
Type 1 AIH
Any age Antibodies: ANA, SMA, Anti F-actin
223
Type 2 AIH
Childhood/young adult Antibodies: LKM-1, Anti LC1 USually severe and treatment failure common
224
PRedictor of relapse in AIH at end of therapy and rescue options
End of therapy histo -TAc, Cyc, MMF, Ritux
225
PBC Histo
Non‐suppurative lymphocytic destructive cholangitis on biopsy • Periportal fibrosis
226
Biochemistry findings in PBC
 Serum ALP almost always elevated (typically 3‐4x ULN)  AST, ALT < 200 U/L (unless an overlap syndrome)  Bilirubin ‐ usually rises late  Cholesterol elevated in 85%  IgM ‐ commonly elevated AMA Positive!
227
Mx of PBC
UDCA • Improves liver biochemistries and overall survival ``` Second line: Obeticholic acid (OCA) is a semi‐synthetic analogue of cheno‐deoxycholic acid • Selectively activates the nuclear hormone receptor farnesoid X receptor (FXRagonist) ```
228
Non specific auto antibody that may be present in PSC
pANCA