Block 32 Week 7&8 Flashcards
1
Q
history of acute liver failure?
A
- alcohol use
- jaundice and encephalopathy
- meds & herbal meds
- exposures
2
Q
FHx to ask abt in ALF
A
WIlson disease
3
Q
RF for viral hepatitis?
A
- travel
- transfusions
- sexual contacts
- occupation
- body piercing
4
Q
exposure to hepatic toxins?
A
- mushrooms
- organic solvents
- phosphorous contained in fireworks
5
Q
ALF?
A
- characterised by coagulopathy of hepatic origin and altered levels of conciousness due to hepatic encephalopathy
- drug induced liver injury is the most common cause of ALF
6
Q
What is ALF usually accompanied by?
A
- ALF is usually accompanied by transaminitis and hyperbilirubinaemia and usually initated following severe acute liver injury
7
Q
ALF =
A
severe acute liver injury with development of coagulopathy and hepatic encephalopathy within 28 weeks of disease onset
8
Q
Acute liver injury =
A
severe acute liver injury from primary liver aetiology -hepatic encephaolpathy is absent
9
Q
what is the key difference between ALF and ALI?
A
- development of HE is the key differentiating factor between ALF and ALI
10
Q
Secondary liver injury?
A
- secondary liver injury - similar to ALI but no evidence of a primary liver insult
- e.g.s severe sepsis or ischeamic hepatitis
11
Q
classifying ALF?
A
- hyperacute
- acute
- subacute
12
Q
hyperacute ALF?
A
HE within 7 days of noticing jaundice. Best prognosis as much better chance of survival and spontaneous recovery.
13
Q
Acute ALF?
A
HE within 8-28 days of noticing jaundice
14
Q
Subascute ALF?
A
- HE within 5-12 weeks of noticing jaundice (ALF may be defined up to 28 weeks).
- Worst prognosis as usually associated with shrunken liver and limited chance of recovery.
15
Q
CLD?
A
- HE occuring more than 28 weeks after onset of jaundice is categorised as CLD
16
Q
Most common cause of acute liver failure in europe vs rest of the world?
A
- In europe: DILI
- worldwide: viral hepatitis
17
Q
primary causes of ALF?
A
- viruses (A, B, E)
- paracetmol
- toxin induced - death cap mushroom
- pregnancy related e.g fatty liver of pregnancy
18
Q
Conditions causing ALF?
A
- Budd chiari syndrome
- wilson’s disease
19
Q
drugs linked to ALF?
A
- statins, carbamazepine, ecstasy
20
Q
secondary causes of ALF?
A
- ischeamic hepatitis
- severe infection e.g. malaria
- heat stroke
- liver resection e.g. post-hepatectomy liver failure
- malignant infiltration
21
Q
Pathophys of ALF?
A
- Most cases of ALF are associated with a direct insult to the liver leading tomassive hepatocyte necrosisand/orapoptosis, which prevents the liver from carrying out its normal function.
- as it progresses it can lead to hyperdynamic circ state with low systemic vascular resistance
- this can lead to poor peripheral perfusion and multi organ failure
22
Q
How is cerebral autoreg disrupted in ALF?
A
- marked cerebral oedema occurs due to hyperammonaemia causing cytotoxic oedema and increased cerebral blood flow that disrupts cerebral autoregulation.
23
Q
CFs of ALF?
A
- characterised by jaundice, confusion and coagulopathy
- key features are jaundice and HE
24
Q
How does HE present?
A
- HE may manifest as confusion, altered mental status, asterixis (i.e. flapping tremor) and/or coma.
25
features that suggest decompensated cirrhosis rather than ALF?
* in patients w ALI or ALF look for features of CLF e.g. spider naevi, palmar erythema, leuconychia that might suggest first pres of decompensated cirrhosis rather than ALF
26
signs and symptoms of ALF?
* altered mental status, confusion, asterixis, jaundice
* RUQ pain
* hepatomegaly
* ascites
* bruising
* GI bleeding: hamaetemsis, meaena
27
Systemic signs of ALF?
* hypotension and tachycardia from reduced systemic vascular resistance
- raised ICP
28
Raised ICP?
papilloedema, bradycardia, hypertension, low GCS
29
Imaging for ALF?
CT abd pelvis
30
ALI vs ALF?
* The key differentiation between ALI and ALF is the development of HE.
31
contra-indications to liver transplant ?
* previous cirrhosis, which would indicate decompensated cirrhosis rather than ALF, heavy alcohol use, significant co-morbidities (e.g. major cardiac or respiratory disease) or terminal illness (e.g. cancer).
32
ALF management principals - CV, resp, GI, metabolic
33
ALF management principals - renal, coagulopathy, spesis, neurological, liver
34
complications from ALF?
* sepsis due to marked immune dysfunction and progressive multi organ failure - AKI, metabolic disturbance, haemorrhage (GI bleeding) and cerebral dysfunction
* cerebral dysfunction e.g. seizures, irreversible brain injury, cerebral dysfunction is commonly the result of raised intercranial pressure
35
Why are ppl at risk of high output cardiac failure with ALF?
due to slow vascular resistance
36
# Reducing
Alcohol misuse?
* alcohol licensing laws
* taxation
* alcohol control zones
* driving legistation
* gov funded education campagins e.g. 'know your limits'
37
tobacco misuse?
* tobacco licensing laws
* taxation
* smoking in public places bans
* advertising bans
* smoking cessation services
38
illicit substance law?
* misuse of drugs act 2010
39
Risk minimisation w ilicit substances?
* risk minimisation: needle exchange services, maintenance Tx to prevent wider public health problems associated w substance misuse (BBV spread, crime, impact on children)
40
service for illicit substances?
* gov funded internet and phone advice services (FRANK)
41
proactive public health policies?
* Proactive policies attempt to reduce substance misuse related harm prior to initiation, for example by classifying new substancesas they are developed and therefore attempting to limit supply to the market.
42
reactive policies?
* Reactive policies aim to respondquickly to epidemics in substance misuse.
43
e.g. reactive policy
* For example, as new substances or diseases emerge educational campaigns respond to provide early advice to limit potential harms andappropriate interventions have been initiated (e.g. needle exchange services).
44
acute cholangitis?
* infection of the biliary tree which characteristically results in pain, jaundice and fevers
45
acute cholangitis almost always occurs due to
bacterial infection secondary to biliary obstruction.
46
acute cholangitis a.k.a
ascending cholangitis
47
biliary obstruction is often seen secondary to?
choledocholithiasis (gallstones in the biliary tree) or biliary strictures (both benign and malignant).
48
AC epidemiology?
* median presenting age is 50-60 affecting men and women equally
* can occur following ERCP
49
Most common cause of AC?
* choledocholithiasis (stones in bile duct) most common cause
50
Cholelithiasis =
gallstomes
51
acute cholangitis occurs due to?
impaired drainage and bacterial overgrowth
52
AC: benign strictures leading to obstruction can occur due to:
* chronic pancreatitis
* iatrogenic injury
* radio/chemo
53
AC and PSC?
* primary sclerosing cholangitis is associated w UC and is characterised by inflammation and stricturing of bile ducts
* Although the strictures are typically benign, patients are at increased risk of many cancers including cholangiocarcinoma, gallbladder cancer and hepatocellular carcinoma.
54
Malignant stricture?
* can lead to acute cholangitis
* such as cholangiocarcinoma, pancreatic cancer and GB cancer
55
other causes of AC?
* post ERCP
* blocked biliary stent
* extrinsic compression
* parasites - (Ascaris lumbricoides)
56
How does acute cholangitis typically present?
RUQ pain, fever, jaundice - Chracots triad
57
AC - reynolds triad (5)?
- RUQ pain, fever, jaundice, shock, confusion
* shock and confusion tends to be seen in the more serious cases w systemic sepsis
58
symptoms of AC?
* RUQ / epigastric pain
* Fevers
* Malaise
* Nausea/vomiting
59
Signs of AC?
* RUQ/ epigastric tenderness
* pyrexia
* jaundice
* hypotension and confusion in severe cases
60
Ix of acute cholangitis?
* Acute cholangitis is most commonly investigated with USS, CT abdomen/pelvis and MRCP.
* Blood tests reveal elevated inflammatory markers and an obstructive picture (raised bilirubin and ALP, though transaminases may also be elevated) on liver function tests.
61
US?
allows assessment of the gallbladder for gallstones and assessment of the CBD
62
CT?
good visualisation of the biliary tree, including the distal portion, used where USS inconclusive, to evaluate for abnormal lesions/tumours or where other diagnoses are suspected.
63
MRCP?
Magnetic resonance cholangiopancreatography offers excellent visualisation of the biliary tree. Often used where CT/USS are inconclusive.
64
ERCP?
involves endoscopic intubation of the ampulla of Vater. Allows good view of biliary tree whilst allowing therapeutic intervention such as drainage
65
Management of AC?
* ppts w infected obstructed biliary system require urgent drainage - ERCP is first line or PTC if it fails/ unavailable
* antibiotics
* fluids
* analgesia
66
Bile =
* exocrine secretion of the liver
* produced continously by hepatocytes
* contains cholesterol and waste products like bilirubin and bile salts which aid in digestion of fats
67
mechanical causes of biliary obstruction can be divided into
intrahepatic and extrahepatic
68
intrahepatic causes of obst?
* intrahepatIc cholestasis generally occurs at the level of the hepatocyte or biliary canalicular membrane
* causes include viral hepatitis, drug induced hepatitis, drug induced cholestasis, biliary cirrhosis, ALD
69
drugs that cause cholestasis?
* drugs like anabolic steroids and chlorpromazine are known to directly cause cholestasis
* thiazide diuretic use increases risk of gallstones
70
what is a common cause of acute cholestatic injury that can mimic biliary obstruction?
* Amoxicillin/clavulanic acid is one of the most frequent causes of acute cholestatic injury that can mimic biliary obstruction.
71
extrahepatic obstruction?
* Extrahepatic obstruction to the flow of bile can occur within the ducts or secondary to external compression
* overall, gallstones are the most common cause of biliary obstruction
* Other causes of blockage within the ducts include malignancy, infection, and biliary cirrhosis.
72
extrahepatic obstruction causes predominantly?
conjugated bilirubinaemia
73
obst jaundice - Mirrizi syndrome?
* Mirizzi syndrome is the presence of a stone impacted in the cystic duct or the gallbladder neck, causing inflammation and external compression of the common hepatic duct and thus biliary obstruction.
* A fistula may form between the gallbladder and the CBD and the gallstone may then come to lie in the CBD.
74
ALT/ AST are markers of?
* found within liver cells at high concentrations
* marker of hepatocellular injury: hepatitis, liver cirrhosis, drug induced e.g. paracetamol overdose, HCC
75
classical LFT of alcoholic liver disease?
* The AST:ALT ratio can help determine the aetiology of hepatocellular injury, with a >2:1 ratio classical of alcoholic liver disease
76
ALP production?
* ALP is derived from biliary epithelial cells and bones
* Raised ALP levels can therefore be caused by cholestasis or bone disease.
77
cholestasis?
interruption in bile flow from hepatocytes to duodenum
78
ALP rise w normal GGT?
* An ALP rise with normal GGT suggests bone disease (e.g. Paget’s disease, vitamin D deficiency, bony metastases)
79
ALP and GGT rise?
* An ALP rise with associated GGT rise is more suggestive of cholestasis
80
isolated GGT rise?
alcohol excess.
81
bilirubin ?
* breakdown product of hb breakdown
* predominantly metabolised and excreted by the liver
* jaundice usually absent until bilirubin levels exceed 50micromol/L
82
pre-hepatic jaundice?
* increased red blood cell breakdown -> too much bilirubin
* overwhelms the metabolism pathways
* most common cause is haemolysis and patients are often anaemic
83
type of bilirubin that accumulates in pre-hepatoc jaundice?
* Bilirubin is unconjugated in the blood, as the hepatocytes have not yet metabolised it. The remainder of LFTs are generally normal, as the liver is otherwise working well.
84
# Deficiency of
gilberts syndrome?
* congenital disorder
* deficiency of glucosyltransferase - enzyme resp for the conjugation of bilirubin
85
how does gilberts typically present?
* Gilbert’s syndrome classically presents following viral infection with raised bilirubin but normal LFTs/ full blood count.
86
hepatocellular jaundice?
* hepatocyte damage -> inability to metabolise unconjugated bilirubin
* high unconjugated bilirubin levels
* high ALT/AST levels
87
cholestatic/ obstructive jaundice ?
* cholestasis is an interruption in bile flow
* build up of conjugated bilirubin
* high ALP levels associated with high GGT
88
obst jaundice ->
pale stools and dark urine
89
why might stools also be pale in hepatocellular jaundice?
* Stools may also be pale in hepatocellular jaundice, as there is decreased bilirubin metabolism/excretion, however as the bilirubin in the blood is unconjugated, it will not be able to pass into the urine.
* Therefore, the urine should remain a normal colour.
90
causes of cholestasis - intrahep obstruction?
* hepatitis
* cirrhosis
* maligancy
* drugs (e.g. antibiotics, oral contraceptive pills, anabolic steroids)
* pregnancy
91
causes of extrahepatic obstruction ?
* gallstones
* PSC
92
Causes of predominantly unconjugated hyperbilirubinaemia:
* Pre-hepatic jaundice (e.g. haemolysis)
* Gilbert syndrome
93
Causes of predominantly conjugated hyperbilirubinaemia:
* Cholestasis
* Hepatocellular jaundice
94
what suggests a hepatocellular injury?
- greater than 10 fold inc in ALT
- less than 3 fold inc in ALP
95
What suggests cholestasis?
- less than 10 fold inc in ALT
- more than 3 fold inc in ALP
96
what suggests bone pathology?
isolateed ALP rise without GGT -
97
isolated bilirubin rise?
An isolated bilirubin rise without further LFT derangement suggests pre-hepatic jaundice or Gilbert’s disease.
98
summary table for LFTS
99
bilirubin metabolism pathway
100
Acute on chronic liver failure precipitating factors?
* most common precipitating factors for developing ACLF are bacterial infections and alcohol
101
CLD cause?
* Caused by repeated insults to the liver which can result in inflammation, fibrosis and cirrhosis
* variety of aetiological factors including alcohol, toxins, viruses and many others.
102
CLD is defined as?
* CLD is generally defined as progressive liver dysfunction for six months or longer.
* The end result of chronic liver disease is cirrhosis
103
Causes of CLD?
* alc
* viral
* primary biliary cholangitis
* primary scleorsing cholangitis
104
Syndromes linked to CLD?
* inherited e.g. Wilsons disease and alpha-1-antitrypsin deficiency
* budd-chiari syndrome
105
CLD pathophys?
* Chronic liver disease may result from repeated insults that cause inflammation (i.e. chronic hepatitis) or cholestasis (i.e. impairment of bile flow).
* Excess deposition of fat in the liver (i.e. steatosis) can also promote an inflammatory response, which is seen in conditions like non-alcoholic fatty liver disease.
* overtime, fibrosis -> cirrhosis - irreversible liver remodeling
106
compensated cirrhosis?
* patients are typically asymptomatic as a small amount of residual function allows the liver to continue carrying out normal function despite extensive damage.
107
decompensated cirrhosis?
* in this state the liver no longer has the capacity to carry out its normal functions, which results in multiple complications.
* If the insult is removed, the liver may 'recompensate' over time to a state of compensated cirrhosis.
108
features of decomp cirrhosis?
* coagulopathy - bruising and deranged coagulation tests
* jaundice
* encephalopathy - confusion
* ascites - poor albumin synthesis
* GI bleeding from varices
109
Scoring system for cirrhosis?
* classification of decompensated cirrhosis
* child pugh score
110
classical features of CLD?
* spider naevi
* palmar erythema
* jaundice
* hair loss
* leuconychia
* asterixis
* ascites.
111
early features of CLD?
* early clinical features are usually non specific: anorexia, lethargy, weight loss, hepatomegaly, nausea, distrubed sleep pattern
112
stigmata of CLD?
- Caput medusa
- palar erythema
- splenomegaly
- Dupuytrens contracture
- Leuconychia
- Gynaecomastia
- Spider Naevi
113
Caput medusa?
distended and engorged superficial epigastric veins around the umbilicus.
114
Palmar erythema?
red discolouration on the palm of the hand, particularly over the hypothenar eminence.
115
Duputrens contracure?
thickening of the palmar fascia. Causes painless fixed flexion of fingers at the MCP joints (most commonly ring finger).
116
Leuconychia?
appearance of white lines or dots in the nails. Sign of hypoalbuminaemia.
117
gynaecomastia?
Reduced hepatic clearance of androgens leads to peripheral conversion to oestrogen.
118
spider naevi?
due to excess oestrogen, usually found in distribution of SVC
119
encephalopathy?
confusion, often present with a flapping tremor (asterixis)
120
features of decompensation - CAGEJ?
* Encephalopathy
* ascites
* jaundice
* GI bleeding
* coaglopathy
121
Diagnosis of cirrhosis?
* liver biopsy - gold standard diagnostic method for idenfi of cirrhosis
* non invasive liver screen, LFTs, liver biopsy, imaging
- transient elastography
122
transient elastography?
A quick painless test that assesses liver stiffness. It measures sound wave velocity using an ultrasound probe to indicate the ‘degree’ of fibrosis and thus the likelihood of cirrhosis.
123
imaging for cirrhosis?
* US
* CT - more detailed view of the abd viscera and good for secondary findings - e.g. features of portal hypertension
* MRI
124
management of cirrhosis?
* treating underlying cause - alcohol cessation, stopping medications, use of anto-virals in chronic hepatitis
125
encephalopathy - main driver ?
- constipation
- first line = laxatives
126
second line for encephalopathy?
involves the long-term use of antibiotics (i.e. rifaximin) to reduce the proportion of ammonia-producing colonic bacteria.
127
ascites?
* combination of portal hypertension and loss of oncotic pressure
* due to widespread vasodilation and underperfusion of kidneys, RAAS is active leading to excess water and sodium reabsorption that exacerbates ascites.
128
Tx of ascites?
* aldosterone antagonists like spironolactone which can be combined with loop diuretics like furosemide
129
Tx of ascites - paracentesis?
ppts w grade 3 ascites, draianage of ascites w human albumin soltuion
130
GI bleeding?
* development of portal hypertension from cirrhosis
* Cirrhosis leads to the development of portal hypertension because of extensive scarring and increased pressure through the portal system.
* blood is shunted into the systemic circulation at portosystemic sites (i.e. where the portal venous system joins the systemic venous syste
131
how are varices treated?
non selective BBs like propanolol
132
what increases risk of HCC?
* increased risk w cirrhosis or chronic hep B
* 6 monthly survelluence US and AFP blood test
133
A on L liver failure?
* syndrome characterised by acute decompensation of CLD associated w organ failure
* up to half of the cases have no identificable trigger
134
most common causes of AonC liver failure?
* in the remaining patients, sepsis, active alcoholism and relapse of chronic viral hepatitis are the most common reported precipitating factors
135
how is diagnosis of ACLF made?
* The diagnosis of ACLF is made in patients with acute decompensation of liver cirrhosis with organ failure
136
causes of hepatomegaly
137
reducing risk of liver damage?
* stopping alc
* healthy diet
* stopping meds
138
intervention for management of hepatic ascites?
* Refractory ascites may require transjugular intrahepatic portosystemic shunt (TIPSS), which creates a connection between a hepatic vein and an intrahepatic portal vein.
* A PTFE graft is then left between this connectin to allow blood to flow from the portal vein to the inferior vena cava under little resistance.
139
CLD risks?
* alcohol
* blood borne viruses - hep B and C paticularly
* obesity
* diabetes
140
prevention of CLD?
* lifestyle - healthy weight and diet, exercising regularly, avoiding alcohol
* liver disease screeninf
* Tx for conditions that can lead to CLD e.g. diabetes, hep B and hep C, NASH
`
141
Liver function?
* Bilirubin
* ALT - hepatocellular inflammation
* ALP - biliary or bone
* Gamma GGT - biliary disease, alcohol, fatty liver
* Alb - liver synthetic function
142
raised igG?
Autoimmune hepatitis
143
raised IgM?
Primary biliary cirrhosis
144
raised IgA?
Alcoholic liver disease
145
Investigation of patient w LFT abn
146
RF for liver disease?
* blood transfusion
* IV drug use
* surgery
* contacts - sexual
* chemical exposure
147
Wilson disease?
- abn copper deposition in liver, cornea and brain
* Kayser-Fleischer rings in eyes
148
causes of acute liver failure?
- viral hepatitis
- hepatitis due to other viruses: CMV, EBV. herpes viruses 1,2 and 6
149
metabolic cause of acute liver failure?
* Acute fatty liver of pregnancy
* Reye’s syndrome
150
vascular causes of ALF?
* heat stroke
* acute circulatory failure
* veno-occlusive disease
151
Miscellanous causes of ALF?
* wilson disease
* autoimmune hepatitis
* massive tumour infiltration
* liver transplant with primary graft dysfunction
152
Enterically transmitted hepatitis?
A and E
153
Blood borne hepatitis?
B, C, D, G
154
typical biopsy findings in viral hepatitis?
155
hereditary haemochromatosis ?
* increased pigmentation
* typical arthopathy with joint swelling in 2nd aand 3rd MCP joints
156
kayser fleisher rings in wilson disease?
* sunflower cateracts also seen w wilsons disease
157
phase 1 metabolism?
* consist of oxidative and reductive processes.
158
phase 2 reactions?
* products of oxidation, reduction, and hydrolysis are coupled with endogenous substrates such as glucuronic acid, sulfuric acid, and glutathione.
* These processes render polar lipophilic compounds.
159
how are phase 2 products excreted?
bile if the molecules are large or in urine if small
160
phase 3 reactions?
* drugs are actively transported from the cell
161
varices?
* caused by portal hypertension
* varices at the GO junction and pa;osade zone are located more superficially within the wall of the oesophagus so they have a thinner coat and are more likely to bleed
162
what predicts risk of haemorrhage w varices?
* red signs such as red wheal marks - red streaks on varices predict risk of haemorrhage
163
causes of ascites
164
SBP from ascites 2 mechanisms?
- Direct spread: bacterial translocation across the bowel wall
- Haematogenous spread: bacteria enter ascites via the bloodstream in the context of an immunosuppressed state
165
how can SBP present?
SBP may present in a number of ways including peritonitis (i.e. abdominal pain), hepatic encephalopathy, upper gastrointestinal bleeding, acute kidney injury or overt sepsis.
166
intrahepatic cause of biliary disease?
* Primary Biliary Cirrhosis (PBC)
* Primary Sclerosing Cholangitis (PSC)
167
causes of cholestasis?
* Drug induced i.e. Steroids
* Pregnancy
* Infections
* i.e. Cholangitis
168
hepatic causes of jaundice?
* acute on chronic liver disease
* drug induced/ alcohol/viral/autoimmune
169
post hepatic causes of jaundice?
* gallstones/ panc tumours
* always do a clotting screen for jaundice
170
what doe we check for primary biliary cholangitis?
* AMA for primary biliary cholangiting
* more associated w female patients in 40s-50s
171
what do we check for autoimmune hep?
* anti SM antibody - autoimmune hepatitis (usually raised IgG too)
172
what is often raised in PBC?
IgM
173
what is often up in alcoholic liver disease?
IgA
174
primary sclerosing cholangitis?
* PSC - scarring and inflammation of bile ducts, more common in younger male patients
* associated w UC
175
what can you gte w PSC?
raised p-ANCA
176
Which types of hepatitis can cause chronic viral hepatitis?
B and C
177
Wilsons disease presents in which patients?
younger males in their teens-twenties
178
non liver causes of deranged LFTs?
* can occassionally get raised ALT in celiac
* thyrotoxicosis can cause deranged LFTs
179
INR?
* Short history of jaundice
* young lady
* signs of confusion
* no stigmata of CLD
* acute liver failure from paracetamol overdose
180
alf?
* rapidly progressive liver injury occuring in absence of chronic liver disease
* most common in previously healthy adults in their 30s
181
what causes most cases of ALF in the UK?
Paracetamol
182
history taking for liver failure?
* all meds taken in past 6 months: gym supplements (anabolic steroids - usually cholestatic liver injury) , antibiotics, herbal meds
* travel history
* sexual history
183
causes of cirrhosis?
* alcoholic liver disease
* non alcoholic FLD (most don't progress though)
* chronic viral hep - usually hep B and C
* cirrhosis increases risk of hepatocellular carcinoma
184
complications of portal hypertension ?
* GI bleeding - variceal
* encephalopathy
* ascites - spotaneous bacterial peritonitis
* HCC
* hepatorenal syndrome
* hepatic hydrothorax
185
what is often the first presentation of decompensation in cirrhosis?
* most common complication of decompensation in cirrhosis - often the first presentation of decompensated liver disease
* average survival is 9 months
* develop malnutiriton and reduced appetite
186
impacts of ascites on ppts?
* impairs working and social life
* freq leads to hospitalization
187
management of ascites?
* spironolactone +/- furosemude - tends to be better for peripheral oedema
* no salt diet
* fluid restriction
188
what to avoid w ascites?
* NSAIDs and ace inhibitiors
* aminoglycosides - renovascular risks
- iV dextrose
189
dextrose and ascites?
leads to hyponatreamia - bc the diuretics cause hyponatreamia
190
SBP - what is needed in the first 24 hrs?
ascites tap
191
how does SBP present?
* fever, abd pain, hypotension, encephalopathy
* neutrophil count in ascitic fluid of >350/mm3
* usually gram negative bac e.g. E coli
192
Dysentery =
gastroenteritis characterised by diarrhoea with visible blood or mucus. Associated with fever and abdominal pain
193
viruses causing GE?
Rotavirus
Norovirus
Adenovirus
194
Bacterial vs viral GE?
- Watery is more viral
- bloody (inflammatory) - bacterial
195
watery diarrhoea in GE?
- due to predominant small bowel involvement.
- Causes a large volume watery diarrhoea with features of abdominal cramping/bloating and weight loss.
196
Bloody (inflammatory diarrhoea)?
- due to predominant large bowel involvement.
- Causes frequent, smaller-volume bloody or mucoid diarrhoea that is associated with fever and severe abdominal pain.
197
Typical causes of watery diarrhoea:
- Clostridioides (formally Clostridium) difficile
- Clostridium perfringens
- Enterotoxigenic Escherichia coli (ETEC)
198
typical causes od bloody diarrhoea?
- non typhoidal salmonellosis
- campylobacter
- shigella
- EHEC
199
Parasites?
- Parasitic gastroenteritis is commonly associated with foreign travel.
- Giardia spp. is the most commonly identified pathogen in prolonged travellers' diarrhoea.
200
rotavirus?
- most common cause of GE in children
- oral vaccine in the child immunisation programme
201
rotavirus GE?
- Commonly causes a watery diarrhoeal illness with vomiting.
- Vomiting often settles within 1-3 days and diarrhoea within 7 days.
202
203
Norovirus?
- most common cause of GE
- common in winter months
- full recovery usually within 2 days
204
campylobacter?
- undercooked poultry and other contaminated food/water
- C. jejuni is the most commonly implicated species and causes either a watery or bloody diarrhoeal illness 2-5 days after exposure.
205
Campylobacter gastroenteritis has been linked to the development of...
several autoimmune conditions following an acute episode (e.g. reactive arthritis, Guillain-Barré syndrome).
206
bacilus cereus - vomiting illness?
- vomiting illness after reheating starchy foods - 1-5hrs of ingestion and resolution within 6-24 hrs
207
bac cereus - diarrhoeal illness?
Ingestion of contaminated food with the diarrhoeal enterotoxin leads to a watery diarrhoeal illness 8-16 hours following ingestion with quick resolution (i.e. < 24 hours).
208
bacilus vs staphlycoccus?
- Staphylococcus aureus can also produce an enterotoxin that contaminates food and leads to a rapid-onset gastroenteritis illness.
- the vomiting with S. aureus enterotoxin is usually accompanied with diarrhoea.
209
salmonella transmission?
- ingestion of contaminated food such as undercooked poultry (most commonly red and white meat, raw eggs and diary products).
210
Salmonella GE?
- typical watery diarrhoeal illness, but can be bloody, with associated abdominal pain, fever and vomiting.
- The illness typically starts within 3 days of exposure and resolves within a week.
211
Shigella?
- classic cause of dysentery in young children
- bloody/mucoid diarrhoea associated with fever and abdominal pain
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when is shigella most common?
most common in late summer and spread by direct human-to-human transmission because the bacteria only colonises humans and some nonhuman primates.
213
shigella GE?
illness usually begins 1-3 days following exposure and resolves within 7 days.
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Enterohaemorrhagic E. coli ?
- Classically causes a bloody diarrhoeal illness
- the UK, E. coli O157 is the most common serotype of EHEC that commonly infects children < 5 years old.
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EHEC transmission?
- most commonly transmitted by contaminated food (e.g. meat, salad, water) - also seen from direct human-to-human spread, which can be due to contact with infected animals (e.g. petting zoos).
216
EHEC infection?
Infection may be asymptomatic or cause a diarrhoeal illness (classically dysentery-type illness), which begins within 3-4 days of exposure and resolves within 10 days
217
EHEC 0157?
can cause haemolytic uraemic syndrome (HUS) in up to 20% of infected children and accounts for 90% of cases of HUS in children
218
HUS symptoms?
- microangiopathic haemolytic anaemia,
- thrombocytopaenia and
- acute kidney injury
219
ETEC?
Commonly associated with a watery diarrhoeal illness in travellers or resource-limited countries.
220
Entamoeba?
- travellers
- mainly asymptomatic
- presentation ranges from mild diarrhoeal illness to severe dysentery.
221
Giardia?
- commonly implicated in Travellers’ diarrhoea.
- watery diarrhoea
222
GE history taking?
223
symptoms of GE?
- Diarrhoea: may be described as watery, bloody or mucoid
- Nausea & vomiting
- Fever
- Abdominal pain
- General malaise
- Bloating/cramping
- Weight loss
224
Ix of GE?
- stool cultures
- virology
- C diff
- OCP - used to detect parasitic organisms. Usually only performed in Travellers’ diarrhoea or significant travel history
225
Complications of GE?
- Dehydration
- AKI
- HUS
- sepsis
- toxic megacolon
- post infective IBS
226
Inflammatory diseases after GE occur paticularly w?
- reactive arthritis, Guillain-Barré syndrome. - Particularly with Campylobacter spp
227
Ecoli TP?
- Common amongst travellers
- Watery stools
- Abdominal cramps and nausea
228
Giardiasis TP?
- Prolonged,
- non-bloody diarrhoea
229
Cholera TP?
- Profuse, watery diarrhoea
- Severe dehydration resulting in weight loss
- Not common amongst travellers
230
shigella TP?
- Bloody diarrhoea
- Vomiting and abdominal pain
231
Staph aureus TP?
- Severe vomiting
- Short incubation period
232
Campylobacter GE?
- A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody
- May mimic appendicitis
- Complications include Guillain-Barre syndrome
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bac cereus TP?
2 types of illnesses:
- vomiting within 6 hours, stereotypically due to rice
- diarrhoeal illness occurring after 6 hours
234
Amoebiasis TP?
- Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks
235
1 to 6 hr incubation period?
Staphylococcus aureus, Bacillus cereus - vomiting subtype, the diarrhoeal illness has an incubation period of 6-14 hours
236
12 - 48 hrs incubation period?
Salmonella, Escherichia coli
237
48-72 incubation period?
Shigella, Campylobacter
238
> 7 days?
Giardiasis, Amoebiasis
239
PBC?
- The M rule
* IgM
* anti-Mitochondrial antibodies, M2 subtype
* Middle aged females
240
# Antibodies
PSC?
p-anca ab, linked to UC
241
PPIs can cause?
hyponatreamua
242
electrolyte disturbances in refeeding syndrome?
Hypophosphataemia, hypokalaemia and hypomagnesaemia are the characteristic electrolyte disturbances seen in patients with refeeding syndrome
243
what can cause torsades?
hypomag
244
coeliac disease is assoc w ?
iron, folate and vitamin B12 deficiency -> Koilonychia - nail spooning
245
dysphagia is ? unless proven otherwise
oesophageal carcinoma
246
Dysphagia, aspiration pneumonia, halitosis → ?
pharyngeal pouch
247
prophylaxis vs treatment of variceal bleeds?
PROPhylaxis = PROPanolol
Treatment = Terlipressin
248
beta blockers naming?
A-M = Cardio-Selective e.g. Bisoprolol,Metoprolol
N-Z = Non-Selective e.g. Propranolol
249
C diff Infection Tx?
1st: oral vancomycin 10 days
2nd: oral fidaxomicin
3rd: oral vancomycin +/- IV metronidazole
250
Area most likely to be affected by ischaemic colitis?
splenic flexure i
251
presentation of ischaemic colitis?
- RF for IHD like HTN
- the pain gets worse after eating, when the bowel requires more blood flow for its increased energy demands for digestion
252
splenic flexure?
- The splenic flexure marks the point where the majority of blood supplied changes from the superior mesenteric artery (SMA) to the inferior mesenteric artery (IMA) - Watershed area
253
acute mesenteric ischaemia?
- Acute mesenteric ischaemia is typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery.
-Classically patients have a history of atrial fibrillation.
254
pain in acute mesenteric ischaemua?
The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings.
255
chronic mesenteric ischaemia?
- Chronic mesenteric ischaemia is a relatively rare clinical diagnosis due to it's non-specific features and may be thought of as 'intestinal angina'.
- Colickly, intermittent abdominal pain occurs.
256
Common predisposing factors in bowel ischemia?
* increasing age
* atrial fibrillation - particularly for mesenteric ischaemia
* other causes of emboli: endocarditis, malignancy
* cardiovascular disease risk factors: smoking, hypertension, diabetes
257
ischaemic colitis can be seen following ? in young ppts
cocaine use
258
Common features of bowel ischemia?
- abd pain - out of prop in AMI
- rectal bleeding
* diarrhoea
* fever
* bloods typically show an elevated white blood cell count associated with a lactic acidosis
259
most common cause of spont bac pertionitis?
E coli
260
prophylaxis for SBP?
Patients who have had an episode of SBP require antibiotic prophylaxis - ciprofloxacin
261
birds beak appearance?
bird's beak' appearance of the lower oesophagus that is seen in achalasia
262
Causes of liver decompensation?
constipation, infection, electrolyte imbalances, dehydration, upper GI bleeds or increased alcohol intake.
263
Mesenteric ischemia vs IC from 34.2 notes page 8
image
264
Patients with ascites secondary to liver cirrhosis should be given
ald antagonist - spironolactone
265
CD involves inc?
goblet cells
266
which 2 things are seen more freq in UC?
crypt abcseses: UC, UC also causes pseudopolyps more than crohns
267
PPI are a RF for
C diff
268
New onset dysphagia?
New-onset dysphagia is a red flag symptom that requires urgent endoscopy, regardless of age or other symptoms
269
most affected site in crohns?
Terminal ileum
270
Histology of coeliac
Histology of coeliac disease: villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia
271
duodenal vs gastric ulcers?
duodenal ulcers being relieved by food, and gastric ulcer worsening with food.
272
right heart failure assoc w ?
Right heart failure is associated with a firm, smooth, tender and pulsatile liver edge
273
ppts w T1D should be screened for?
Patients with type 1 diabetes or autoimmune thyroid disease should be screened for coeliac disease on diagnosis
274
mild UC flare?
* mild: < 4 stools/day, only a small amount of blood - topical aminosalicyclate , if no improv add oral aminosalicyclaye
275
moderate UC flare?
* moderate: 4-6 stools/day, varying amounts of blood, no systemic upset - topical aminosalicyclate , if no improv add oral aminosalicyclaye
276
severe UC flare?
* severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers) - IV steroids in hosp
277
loss of hausta ->
leadpipe colon -> UC
278
HNPCC is assoc w?
increased risk of pancreatic cancer
279
DKA management - FIG PICK?
F - Fluids
I - Insulin (Fixed rate 0.1u/kg/hr)
G - Monitor glucose
P - Monitor / give potassium
I - Treat any underlying infections / triggers
C - Monitor for signs of cerebral oedema
K - Monitor ketones & pH
280
first-line to maintain remission in patients with Crohn's
azathioprine or mercaptopurine
281
recommended test for H pylori post erad?
urea breath test
282
uc + cholestasis?
(e.g. jaundice, raised ALP) → ? primary sclerosing cholangitis
283
risk of ? w PSC?
Cholangiocarcinoma develops in around 10% of primary sclerosing cholangitis patients
284
what suggests panc cancer?
The presence of painless obstructive jaundice and steatorrhoea is highly suggestive of pancreatic cancer. The presence of a right upper quadrant mass is suggestive of a palpable gallbladder
285
inducing vs remaining remission in CD?
- pred to induce remission
- azathioprine/ mercaptopurine to maintain it
286
C diff ->
C diff -> psuedomembranous colitis
287
high SAAG ascites?
- Ascites: a high SAAG gradient (> 11g/L) indicates portal hypertension
- Causes of this include liver cirrhosis, hepatic failure, venous occlusion (e.g. Budd Chiari syndrome), alcoholic hepatitis, and kwashiorkor malnutrition.
288
low SAAG ascites?
- A low SAAG (<11g/L) suggests the ascitic fluid is an exudate.
- Causes of this include malignancy, infection, pancreatitis and nephrotic syndrome.
289
Budd chiari presentation?
triad of sudden onset abdominal pain, ascites, and tender hepatomegaly
290
alcoholic hep ALT/AST ratio?
The AST/ALT ratio in alcoholic hepatitis is 2:1
291
