Liver conditions Flashcards
1
Q
name 7 functions of the liver
A
oestrogen regulation
detoxification
metabolises carbohydrates
albumin production
clotting factor production
bilirubin regulation
immunity (kupffer cells)
2
Q
what are 3 markers of liver function and how would they indicate liver damage
A
bilirubin- increased
albumin- decreased
prothrombin time- increased
3
Q
the presence of which 4 enzymes indicates liver disease
A
ALT
AST
GGT
ALP
4
Q
describe the process of liver cirrhosis
A
cirrhosis= result of chronic inflammation + damage 2 liver cells
when liver cells damaged
-replaced w. scar tissue= fibrosis
-nodules of scar tissue within liver= regenerative nodules
5
Q
common and rarer causes of liver cirrhosis & risk factors
A
mc= ALD, NAFLD, hep B + C
rarer= haemochromatosis, A1AT def, Wilson’s disease
RFs= alcohol misuse, IVDU, unprotected sex, obesity
6
Q
presentations of liver cirrhosis
A
hepatosplenomegaly
jaundice
ascites
HE
palmar erythma
spider naevi
caput medusae
hepatic factor (eggy breath)
xanthelasma (yellow growth on eyelids)
abdo pain
pruritis
n+v
confusion
bleeding
7
Q
1st line + GOLD investigations for liver cirrhosis
A
1st
LFTs=
increased- bilirubin, PT/INR, AST + ALT, ammonia, GGT
decreased- albumin + glucose
FBC= anaemia, thrombocytopenia, leukopenia
U&Es= raised
GOLD= liver biopsy
-destruction of liver parenchyma, regenerative liver nodules
8
Q
complications of liver cirrhosis
A
HCC
spont. bacterial pericarditis
oesophageal varies + portal HTN
HE
hepato-renal syndrome
ascites
bleeding
9
Q
describe general liver failure
A
liver loses ability to regenerate/repair leading 2 decompensation
10
Q
what is the most common cause of acute liver failure
A
paracetamol overdose
11
Q
name 5 causes of acute liver failure
A
DRUGS- paracetamol, alcohol
VIRAL- hep A/B/E, CMV, EBV autoimmune hep
NEOPLASTIC- hepatocellular/metatstic carcinoma
METABOLLIC- Wilson’s disease, alpha 1 anti trypsin, haemochromatosis
VASCULAR- budd chiari
12
Q
presentation of acute liver failure
A
jaundice
abnormal bleeding
hepatic encephalopathy
malaise
n + v
abdo pain
13
Q
describe the west haven 1- 4 criteria for presentation of hepatic encephalopathy
A
- altered mood + sleep issues
- lethargy, mild confusion, asterixis (liver flap)
- marked confusion, quiet
- comatose
14
Q
investigations for acute liver failure:
LFT,FBC,U&Es,imaging. microbiology
A
LFTs: increased- bilirubin, PT, AST + ALT, NH3
decreased- albumin + glucose
FBCs: anaemia, thrombocytopenia, leukopenia
U&Es= raised
imaging= EEG 2 grade HE
USS of abdo 2 check Budd chiari
microbiology 2 rule out infections-blood culture + urine
15
Q
management of acute liver failure
A
ITU, ABCDE, fluids, analgesia- asses 4 liver transplant
treat underlying cause + comps
eg paracetamol overdose- give activated charcoal + N acetyl cysteine within 1hr of overdose
16
Q
name 5 complications of acute liver failure and what you would give to treat them
A
cerebral oedema= IV mannitol
HE= lactulose
ascites= diuretics
bleeding= vit K
sepsis= sepsis 6
17
Q
describe chronic liver failure
A
progressive liver disease over 6+ months, due 2 repeated liver abuse
18
Q
name 3 causes of chronic liver disease
A
progression from acute liver disease
NAFLD
hep C + B
19
Q
list 5 risk factors for chronic liver disease
A
alcohol/drugs
obesity
T2DM
inherited metabolic disease/existing autoimmunity
20
Q
describe the progression to liver failure from hepatitis
A
hepatitis > fibrosis (reversible damage) > cirrhosis (irreversible damage) > either: compensated (some liver function) OR decompensated (end stage liver failure)
21
Q
what is the MELD score used for
A
model for end stage liver disease
- looks at severity for transplant planning
22
Q
what are 5 key presentations of end stage liver failure
A
jaundice
HE
coagulopathy
ascites
oesophageal varices
23
Q
presentation of chronic liver failure (lots)
A
jaundice
ascites
abnormal bleeding
HE (symptoms)
portal hypertension + oesophageal varices
caput medusae
spider naevi
palmar erythema
gynecomastia
fector hepatic
dupuytren’s contracture
24
Q
what is the child Pugh score used for
A
to assess prognosis + extent of treatment required for chronic liver failure
A= 100% 1yr survival
B= 80% 1 yr survival
c= 45% 1 yr survival
25
1st line investigations for chronic liver failure
LFTs= raised - bilirubin, PTT, AST + ALT, NH3, GGT
lowered- albumin + glucose
FBCs= anaemia, thrombocytopenia, leukopenia
U&Es= raised
26
gold standard investigation for chronic liver failure
liver biopsy= 2 determine extent of damage
other = ascites tap + abdo USS
27
management of chronic liver failure
prevent progression- lifestyle mods (no alcohol, lower BMI, low LDL + salt)
liver transplant (MELD score)
manage comps: same as acute
28
name 3 risk factors for alcoholic liver disease
chronic alcohol
obesity
smoking
29
describe the progression to alcoholic liver disease
steatosis (fatty liver) > alcoholic hepatitis > alcoholic cirrhosis
30
presentation of alcoholic liver disease
early stages= asymptomatic
later more severe stages= chronic liver failure symptoms + alcohol dependency
(chronic liver failure symptoms= jaundice, hepatosplenomegaly, spider nave, dupuytren's contracture, palmar erythema, ascites, HE, caput medusae, easy bruising)
31
describe 2 alcohol dependency questionnaires
CAGE=
should you Cut down?
one person Annoyed by your drinking?
feel Guilty about drinking?
do u drink in morning (Eye opener)
- 2+ means dependent
AUDIT- alcohol use disorder ID test
32
1st line investigations for alcoholic liver disease
LFTs= increased- GGT, AST + ALT, ALP, bilirubin
decreased- albumin
AST : ALT ratio = >2
FBC= macrolytic nonmegaloblastic anaemia
33
gold standard investigation for alcoholic liver disease
liver biopsy (2 confirm extent of cirrhosis)
- will see inflammation, steatosis, necrosis, MALLORY CYTOPLASMIC INCLUSION BODIES
34
management of alcoholic liver disease
stop alcohol- give chlordiazepoxide 4 delirium tremors
also= wt. loss, no smoking, steroids for alcoholic hepatitis (prednisolone)
liver transplant if severe- must abstain from alcohol for 3+ months first
35
list 6 complications of alcoholic liver disease and how you would treat them
pancreatitis
HE- lactulose
ascites- diuretics
HCC- chemo, surgery
mallory weiss tear
wernicke Korsakoff syndrome (combined B1 + alcohol withdrawl symptoms)- IV thiamine
36
what would you immediately suspect in anyone that had:
T2DM
obesity
deranged LFTs
non alcoholic fatty liver disease (NAFLD)
37
list 7 risk factors for NAFLD
obesity
hypertension
hyperlipidemia
T2DM
Family history
endocrine disorders
drugs= NSAIDs
38
presentation of NAFLD
typically asymptomatic
- if severe, may present w. signs of liver failure
39
investigations for NAFLD
| and GOLD
imaging= abdo USS, fatty liver (hepatic steatosis) seen as increased echogenicity
bloods-
deranged LFTs: riased ALT= 1st indication of NAFLD
(PT increased, bilirubin increased, decreased albumin)
FBC= thrombocytopenia, hyperglycaemia
Enhanced liver fibrosis (ELF)= 1st line blood test for assessing fibrosis
10.51+, advanced fibrosis
NAFLD fibrosis score
Assess risk of fibrosis w non- invasive scoring system eg Fib-4, >2.67= advanced + refer to hepatology
GOLD= liver biopsy
40
management of NAFLD
wt. loss
control rfs (use statins, metformin etc)
take vit E
41
list 4 complications of NAFLD
HE
ascites
HCC
portal htn + oesophageal varices
42
define viral hepatitis
inflammation of the liver due to viral replication within hepatocytes
43
describe the pathology of viral hepatitis
virus infected cells undergo cytotoxic killing ( causes inflammation in liver) + apoptosis by immune system
hepatocytes undergoing apoptosis= councilman bodies
44
is hep A acute or chronic and how is it spread
acute
-RNA virus spread via faecal- oral route (contaminated food/water)
45
list 3 risk factors for hep A
living/ travelling to endemic area (Africa)
overcrowding
undercooked shellfish
46
presentation of hep A
prodomal phase= 1-2 weeks
- malaise
- n+v
- fever
then:
-jaundice
-dark urine + pale stools
-hepatosplenomegaly
-choleostasis
-fatigue
-headache
-pruritis
-abdo pain
-musc. aches
47
1st line investigations for hep A
bloods= increased- serum AST + ALT, bilirubin, ESR
48
gold standard investigations for hep A
HAV serology:
HAV IgM= active
HAV IgG= recovery/vaccination
49
management of hep A
supportive therapy- resolves by itself
- traveller vaccine available
comps= rapid liver failure
50
how is hep B spread
acute + chronic
enveloped DNA virus transmitted via blood + bodily fluids
50% of chronic hep B cases= under 6 yrs
51
name 4 methods of transmission of hep B
needles
sexual
vertical (mother 2 child)
horizontal (child 2 child)
52
list 5 risk factors for hep B
IVDU
healthcare worker
gay sex
unprotected sex
dialysis patients
53
presentation of hep B
v. similar to hep A
1-2 week prodromal phase:
-malaise
-n+v
-fever
-fatigue
then:
jaundice
dark urine + pale stools
hepatosplenomegaly
URITICARIA
ARTHRALAGIA
54
first line investigations for hep B
LFTs= increased ALT +AST, bilirubin, ALP
55
gold standard investigation for hep B
HBV DNA (direct count of viral load) + serology:
ANTIGENS=
HBsAg (HBV surface antigen)= active infection
HBcAg (core antigen in core of HBV) = active infection
HBeAg (secreted by infected cells)=
HBV replication & infectivity
ANTIBODIES=
Anti-HBc (antibodies against core antigen)- previous or ongoing contact with HBV
IgM anti-HBc= acute or excecerbation of HBV
anti-HBs (antibodies agaistn HBsAg)= recovery + immunity (vax)
anti-Hbe (antibodies against HBeAg)= low HBV replication & remission
56
management of hep B
SC peginterferon alpha 2 or tenofovir injection
prevention = vaccination w. HBV surface antigen (HBsAg)
57
How is hep c transmitted
RNA, transmitted via blood + bodily fluids
acute + chronic
1/4 fight off virus
3/4 become chronic
58
list 5 risk factors for hep c
IVDU
unsafe medical practice
unprotected sex
vertical transmission in childbirth
blood transfusion/organ transplant
59
presentation of hep C
-often asymptomatic in acute
chronic=
jaundice
ascites
hepatosplenomegaly
fever
n+v
malaise
pruritis
abdo pain + musc aches
60
first line investigations for hep C
HCV antibody enzyme immunoassay- HCV IgG
-positive indicates current infection
aminotransferases= elevated
61
gold standard investigation for hep C
PCR (HCV RNA test)- indicates past or current infection
-viral DNA decreasing= recovery
-viral level same= chronic
62
management of hep C
direct acting antivirals (ribavirin, sofosbuvir)
-no vax available
30% of cases progress 2 chronic liver failure (cirrhosis + HCC risk)
63
what does hep D need in order to survive
hep D= an RNA the only survives in patients that also have hep B, hep D attaches itself 2 surface antigen of hep B
spread via blood + bodily fluids
64
presentation of hep D
jaundice
hepatosplenomegaly
dark urine + pale stools
n+v
fever
malaise
ascites
uriticaria
arthralagia
musc aches
abdo pain
65
first line investigations for hep D
LFTs= increased- AST + ALT, bilirubin, ALP
66
gold standard investigation for hep D
serology: HDV IgM or IgG= active infection
HDV RNA in serum
67
management of hep D
no spec treatment
treat hep B- SC pegylated interferon alpha 2a or tenofovir
68
how is hep E spread
RNA spread via faecal oral route (contaminated food + water)
dogs
pigs
undercooked seafood
69
presentation of hep E
fever
malaise
n+v
jaundice
hepatomegaly
dark urine + pale stools
pruritis
abdo pain
70
1st line investigations for hep E
LFTs= increased- AST + ALT, Bilirubin, ESR
71
gold standard investigation for hep E
HEV serology:
HEV IgM antibodies= active infection
HEV IgG antibodies= recovery
HEV RNA= current infection
72
management of hep E
mild illness- no treat
self limiting within a month
73
describe autoimmune hepatitis
inflammation of the liver due to it being attacked by bodies own cells
74
list 4 risk factors for autoimmune hepatitis
female
other autoimmune conditions
viral hepatitis
HLA DR3/DR4 gene mutation
75
who is affected and which antibodies are involved in autoimmune hep type 1
adult women
anti-nuclear antibodies
anti-smooth musc antibodies
anti-soluble liver antigen
76
who is affected and what type of antibodies are involved in autoimmune hep type 2
children
anti-liver kidney microcome antibodies type 1(ALKA-1)
anti-liver cytosol antibodies type 1 (ALCA-1)
77
presentation of autoimmune hepatitis
25%= asymptomatic
jaundice
fatigue
malaise
fever
hepatosplenomegaly
78
1st line investigations for autoimmune hepatitis
LFTs- increased AST + ALT, prolonged PTH
decreased albumin
serology:
T1= ANA, ASMA,ASLA
T2= ALKM-1, ALCA-1
79
gold standard investigation for autoimmune hepatitis
liver biopsy
80
management of autoimmune hepatitis
corticosteroids (prednisolone) + immunosuppressant (azathioprine)
liver transplant if resistant to meds
81
what is hepatic encephalopathy
brain infection due to toxic metabolites (esp ammonia) not removed by liver due 2 liver dysfunction/cirrhosis
82
describe the pathology of hepatic encephalopathy
intestinal bacteria break down proteins into ammonia to be absorbed in gut
liver impairment (cirrhosis) prevents hepatocytes metabolising ammonia into harmless waste products> causing build up of ammonia in blood
>collateral vessels btwn. portal and systemic circulation mean ammonia bypasses liver + enters into systemic circulation directly
83
investigations for hepatic encephalopathy
serum ammonia raised
abnormal LFTs
EEG= decrease in brain wave frequency + amplitude
U&E=(maybe hyponatraemia/kalaemia)
84
management of hepatic encephalopathy
laxatives- LACTULOSE > promotes excretion of ammonia from gut before it is absorbed
ABxs eg rifaximin
reduces no. of intestinal bacteria that produce ammonia
85
describe Wernicke's encephalopathy + Korsakoff syndrome + list 3 causes of it
caused by thiamine deficiency (B1):
alcohol (decreases thiamine levels)
malnutrition
malabsorption (IBD, stomach cancer)
wernickes= acute medical emergency- REVERISBLE stage
-b4 progressing to
Korsakoff syndrome= chronic, irreversible stage
86
pathology of wernickes encephalopathy + Korsakoff syndrome
thiamine def impairs glucose metabolism= decreased cellular energy
brain= vunerable 2 impaired glucose
-alcohol interfers w. conversion of thiamine 2 its active form
87
presentation of wernickes encephalopathy + Korsakoff syndrome
wernickes:
confusion
apathy
difficulty concentrating
opthalmoplegia weakness + paralysis of eye muscles
Korsakoff syndrome:
severe memory impairment
confabulation (makes up stories to fill in gaps)
behavioural changes
88
investigations + management of wernickes encephalopathy & Korsakoff syndrome
clinical diagnosis
low thiamine (B1) levels
deranged LFTs
MRI= degeneration of maxillary bodies
Tx= IV thiamine infusion (pabrinex)
89
define spontaneous bacterial pericarditis & give the m.c cause + 3 risk factors
bacterial infection of ascitic fluid (mc. infection in liver cirrhosis)
mc. caused by E.coli - gram neg
other = staph. aureus - gram pos
RFs= cirrhosis, liver failure, GI bleeding
90
presentation of spontaneous bacterial pericarditis
severe abdo pain w. shock & collapse
fever
ascites
guarding- rigidity helps w. paim
hypotension
n+v
confusion
tachycardia
91
investigations for spontaneous bacterial pericarditis
| inlcudingGOLD
1st:
FBC= leucocytosis, anaemia, raised CRP/ESR
blood cultures + ascitic tap= shows causative microorgansim
hCG test (exclude pregnancy)
abdo x-ray (exclude bowel obstruction)
GOLD= ascitic fluid neutrophil count (ANC) >250 cells/mm3
92
management of spontaneous bacterial pericarditis
IV ABxs= piperacillin/tazobactam
cephalosporins can also be used (cefotaxime)
peritoneal lavage- surgical cleaning of peritoneal cavity
93
define jaundice
also called 'icterus'
yellowing of skin + eyes due to accumulation of conjugated/unconjugated bilirubin
94
describe the pathway of RBC breakdown to excretion of unwanted components
RBCs= broken down by reticuloendothelial macrophages @ spleen
haemoglobin> haem + globin
haem> Fe2+ & biliverdin
biliverdin converted to unconjugated bilirubin by biliverdin reductase
unconjugated bilirubin= insoluble - travels in blood bound to albumin
@liver UGT conjugates bilirubin (now H20 soluble)
conjugated bilirubin stored @ gall bladder + excreted into small intestine as bile
conjugated bilirubin is converted to urobiligen via colonic bacteria
urobiligen converted either:
1. stercobilin (poo)
2. urobilin (oxidised by kidneys, wee)
3. recycled in enterophepatic circulation
95
describe pre-hepatic jaundice
unconjugated hyperbilirubinemia
-due 2 increased RBC breakdown, overwhelming livers ability to conjugate bilirubin
96
causes of pre-hepatic jaundice
HAEMOLYTIC ANAEMIA:
sickle cell anaemia
G6PDH deficiency
autoimmune haemolytic anaemia
thalassemia
malaria
GILBERT'S SYNDROME
CRIGGLER NAJJAR SYNDROME
97
describe intra-hepatic jaundice
dysfunction of hepatic cells- liver loses ability to conjugate bilirubin= mix of conjugated + unconjugated in blood
98
causes of intra-hepatic jaundice
alcoholic liver disease
hepatitis
HCC
hepatotoxic medications
99
describe post-hepatic jaundice
conjugated hyperbilirubinemia
-due to obstruction in biliary drainage
100
list 4 causes of post-hepatic jaundice
gallstones
pancreatic cancer
cholangiocarcinoma
mirizzi syndrome
101
presentation of all 3 types of jaundice
prehepatic= norm urine + stool
intrahepatic= dark urine + norm stool
post-hepatic= dark urine + pale stool
102
what is Courvoisier's sign and what does it indicate
painless jaundice + palpable gallbladder= mc. pancreatic cancer
103
what does jaundice, RUQ pain and fever indicate for Charcot's triad
ascending cholangitis
(can also use Reynold's pentad w. altered mental status & sepsis)
104
what will a LFT show for pre-hepatic jaundice
norm conjugated bilirubin
increased unconjugated bilirubin
increased urobilinogen
norm ASP +ALT +ALP
no conjugated bilirubin in urine
105
what will a LFT show for intra-hepatic jaundice
increased conjugated bilirubin
increased unconjugated bilirubin
decreased urobilinogen
increased ALP, AST + ALT
conjugated bilirubin= present in urine
106
other investigations for jaundice
FBCs
coagulation studies
liver screen
abdo USS
107
describe hepatocellular carcinoma (HCC)
cancer arising from hepatocytes in predominantly cirrhotic liver
90% of all liver cancers
108
risk factors for HCC
chronic hep virus- C+B
Cirrhosis from ALD/NAFLD
109
describe how HCCs metastasise
haematogenous spread- via hepatic/portal veins
spreads 2 lymph nodes, bones & lungs
110
presentation of HCC
signs of decompensated liver failure:
-jaundice
-ascites
-HE
-hepatomegaly
signs of cancer:
unexplained weight loss
tired all the time (TATT)
RUQ pain
111
1st line investigations for HCC
LFT= increased serum AFP (HCC tumour marker)
imaging= abdo USS
112
gold standard investigation for HCC
CT scan
-biopsy usually avoided to prevent tumour spread
113
management of HCCs
surgical resection of tumour
liver transplant
prevention= HBV vax
114
describe cholangiocarcinoma
bile duct cancer- usually adenocarcinomas
10% of liver cancers
poor prognosis
115
list 5 risk factors for cholangiocarcinoma
under 50
parasitic flukeworms
biliary cysts
IBD
primary sclerosing cholangitis
116
presentation of a cholangiocarcinoma
jaundice
weight loss
abdo pain
pruritis
fever
malaise
courvoiser's sign (painless jaundice + palpable gall bladder- also common in pancreatic cancer
117
1st line investigations for a cholangiocarcinoma
increased CA19-9 (tumour marker for cholangiocarcinoma) + increased CEA
LFTs= increased bilirubin, increased ALP
imaging= abdo USS + CT
118
gold standard investigation for a cholangiocarcinoma
ERCP (endoscopic retrograde cholangiopancreatography)- invasive BUT:
- can stent structures in biliary tree (therapeutic)
-can obtain sample for biopsy (diagnostic)
119
management of a cholangiocarcinoma
majority of cases= inoperable bc. patients present v. late- sometimes surgical resection/ ERCP to stent bile duct that cancer is compressing
120
name 2 primary, benign liver tumours
haemangioma (mc. seen on infants as strawberry mark in 1st few weeks of life)
hepatic adenoma
121
where do secondary liver tumour most commonly metastasise from
breasts, GIT, lungs (bronchial)
122
1st line investigations for benign liver tumours
LFT- increased serum ALP
imaging= abdo USS
123
gold standard investigation for benign liver tumours
CT/MRI for staging + primary tumour location
124
management of benign liver tumours
surgical resection of primary/hepatic tumour if possible + chemo
125
what type of tumour is 99% of pancreatic cancer and which part of the pancreas does it normally affect
adenocarcinoma of exocrine pancreas of ductal origin
-usually affects head + neck
126
list 6 risk factors for pancreatic cancer
male, 60+
chronic pancreatitis
smoking
alcohol
diabetes
FHx
127
presentation of pancreatic cancer
Courvoisier's sign (palpable gallbladder + painless jaundice)
pale stool + dark urine
pruritis
weight loss
trousseau sign of malignancy (blood clots felt as small lumps under skin)
128
1st line investigations for pancreatic cancer
abdo USS (pancreatic mass, dilated bile ducts)
129
gold standard investigation for pancreatic cancer
| which tumour marker is present
pancreatic CT protocol
Ca19-9 tumour marker positive
130
management of pancreatic cancer
v. poor prognosis- 5yr survival= 3%
surgical resection + post op chemo if no mets
palliative care
131
describe gallstones
| what is biliary colic pain
cholesterol stones in gallbladder formed from bile (bile= cholesterol + bile pigment + phospholipids)
biliary colic= pain caused by gallstones blocking gallbladder drainage
132
what are 5Fs risk factors for biliary tract diseases (gallstones, cholecystitis, ascending cholangitis)
Fat (BMI +30)
Female
Forty (40+ yrs)
Fertile (preggo/many kids)
Fair
133
presentation of gallstone pain
severe colicky RUQ pain- come & goes (lasts >30mins)-worse after fatty meal
n+v
134
1st line investigations for gallstones
LFTs- increased ALP + bilirubin (If gstone blocking bile duct)
normal FBC + CRP
135
gold standard investigation for gallstones
abdo USS
1. identify stones
2. gb thickness- inflammation
3. duct dilation
136
management of gallstones
1st= NSAIDs + analgesia
then- elective laparoscopic cholecystectomy (removal of gb)
ERCP- bile duct clearance if stones
137
describe cholecystitis
inflammation of gb due 2 blockage of cystic duct- preventing it from draining eg gallstone
bile build up distends gb- can reduce vascular supply- therefore inflammation
138
presentation of cholecystitis
RUQ- may radiate to R shoulder (phrenic)
fever + fatigue
tender Gb/ RUQ tenderness
Murphy's sign positive (press on gb + ask patient to inhale- they will wince + stop inspiring)
139
initial investigations for cholecystitis
positive Murphy's sign
FBC= increased WCC + CRP
LFTs= norm
140
gold standard investigation for cholecystitis
abdo USS
- shows thickened gb wall >3cm + fluid around gb
141
management of cholecystitis
IV fluids + abxs + analgesia
best= cholecystectomy surgery within 24hrs of symptoms
ERCP if gallstones in bileduct
142
describe ascending cholangitis
infection + inflammation of bile ducts
-this is due to prolonged blockage of bile duct by gallstones/bacteria infection from ERCP procedure
- bile isn't 'flushing out ducts'- bacteria migrate from GI tract + cause infection in biliary tree
143
presentation of ascending cholangitis (Charcot's triad)
charcot's triad:
-RUQ pain
-fever
-jaundice
144
1st line investigations for ascending cholangitis
FBC= increased WCC + CRP, leukocytosis
LFT= increased ALP + unconjugated hyperbilirubenia
abdo USS for gb dilation + gallstones
145
gold standard investigation for ascending cholangitis
ERCP
146
management of ascending cholangitis
Iv fluids + Abxs
ERCP then laparoscopic cholecystectomy
gallstone > cholecystitis > cholangitis > sepsis
147
define primary biliary cirrhosis/cholangitis (PBC)
autoimmune disease where T cells attack cells of small bile ducts- causes inflammation
148
list 5 risk factors for PBC
female
40-50 yrs
smoking
other autoimmune conditions
rheumatoid diseases
149
pathology of PBC
1. immune system attacks small intralobular bile ducts in the liver- obstructs bile flow (cholestasis)
2. bile acids (itching + bilirubin (jaundice) + cholesterol (deposits in skin + blood vessels)
3. back pressure of bile obstruction> fibrosis + cirrhosis + liver failure
150
presentation of PBC
-often initially aysmpto
pruritis + fatigue (earlier onset)
jaundice
hepatomegaly + xanthelsma (yellow cholesterol deposits around eyes)
joint pain + abdo pain
signs of cirrhosis
151
1st line investigations for PBC
LFTs- increased- bilirubin, ALP, GGT
decreased albumin
abdo USS (2 exclude extra hepatic cholestasis)
152
gold standard investigation for PBC
serology- AMA (antimicrobial antibodies) present
other= liver biopsy for bile duct lesions + granuloma formation
153
management of PBC
1st= URSODEOXYCHOLIC ACID ( bile analogue, reduces intestinal absorption of cholesterol)
for pruritis- cholestyramine
vit ADEK supplements
consider liver transplant
154
describe primary sclerosing cholangitis (PSC)
inflammation + fibrosis of intra + extra hepatic ducts- results in strictured 'beading' appearance of bile ducts + narrowing of bile ducts
155
list 3 risk factors for PSC
male
40-50 yrs
strong link 2 IBD (esp UC)
156
pathology of PSC
same path as PBC, but affects more ducts
157
presentation of PSC
pruritis + fatigue
jaundice
charcot's triad
hepatosplenomegaly
IBD
158
1st line investigations for PSC
LFTs- increased: bilirubin, AST, ALT, ALP, GGT
decreased albumin
serology;
AMAs positive
HBVsAg/HCVAB positive
pANCA positive in 33-88%
159
gold standard investigation for PSC
imaging- MCRP (magnetic resonance cholangiopancreatography)
-will see bile ducts strictures or lesions
160
management of PSC
treat symptoms (ursodeoxycholic acid doesnt work)
pruritis- cholestyramine
fat soluble ADEK
consider liver transplantation
161
describe acute pancreatitis and its 3 main causes
sudden + rapid onset inflammation of the pancreas
1. gallstones
2. alcohol
3. post ERCP
162
list all the causes of acute pancreatitis using I GET SMASHED
Idiotpathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom/ spider bite
Hypercalcaemia/hyprelipidemia
ERCP
Drugs (azathioprine, NSAIDs, ACE-i)
163
describe the pathology of acute pancreatitis
gallstones obstruct flow of pancreatic secretions into duodenum- causes accumulation of digestive enzymes + reflux of bile= inflammation
host defences= overwhelmed - therefore auto digestion- inflammation + enzymes leak into blood
164
presentation of acute pancreatitis
sudden, severe epigastric pain radiating to back
jaundice
fever
steathorrea
Grey Turner sign (flank bruising)
Cullen sign (periumbilical bruising)
hypocalcaemia
vomiting
signs of hypovolemia + pleural effusion
165
investigations for pancreatitis
bloods= increased serum amylase (x3 times upper level) + increased serum lipase
FBC=
leukocytosis w. L shifts (increase in immature vs mature WBCs)
increased haemocrit, CRP, urea
decreased calcium
imaging= chest x-ray, abdo USS (gallstones, CT scan (inflammation, necrosis, effusions)
166
what does an acute pancreatitis diagnosis require
needs out of 3 of:
1. acute abdo pain
2. increased pancreatic enzymes (amylase/lipase)
3. abnormal imaging
167
list the Glasgow score and what it Is for
assessing severity of acute pancreatitis (after 48hrs)
PANCREAS
PaO2 low
Age 55+
Neutrophils raised
Calcium low
uRea raised
Enzymes raised
Albumin low
Sugar raised
use APACHE 2 - assess severity within 24hrs
168
management of acute pancreatitis
ABCDE
IV fluids
analgesia
nil by mouth
O2
antibiotics
electrolyte replacement
169
define chronic pancreatitis
persistant chronic inflammation (3+ months) = irreversible fibrosis and reduced pancreas function
170
list 5 causes of pancreatitis
alcohol (mc)
trauma
CKD
progression from acute
CF
171
list 6 presentations of pancreatitis
severe epigastric pain radiating to back
jaundice
loss of exocrine function (no lipase secreted in GI tract)
loss of endocrine function (lack of insulin> T2DM)
wt. loss
n + v
172
1st line investigations for pancreatitis
bloods= low/no amylase + lipase
faecal- elastase 1 (low)
faecal fat (high)
pancreatic function tests (decreased function)
ERCP for visualisation of ducts
173
gold standard investigation for pancreatitis
x-ray/CT/MRI= shows calcification of pancreas + dilated bile ducts
174
management of pancreatitis
control risk factors- (no alcohol + smoking + decreased BMI)
control pain (analgesia + NSAIDs)
pancreatic supplements eg lipase
insulin for T2DM
ERCP
surgery 2 drain bile ducts
175
what is portal hypertension a complication of and what does it lead to
portal HTN= comp of cirrhosis
- increases BP in portal vein
176
list the causes of pre-hepatic, intra-hepatic and post-hepatic portal hypertension
pre-hepatic- portal vein obstruction (thrombus)
intra-hepatic- cirrhosis (mc.), sarcoidosis , schistosomiasis (caused by blood flukes aka worms)
post-hepatic= R sided heart failure, constructive pericarditis, budd chiari
177
what is the normal venous pressure in the portal vein
5-8mmHg
178
describe the pathology of portal HTN
cirrhosis> causes venous blood to accumulate in portal system- pressure increases (+8mmHg)
causes formation of portosystemic shunts- blood directed into systemic veins
liver therefore receives less blood- liver function + detoxification decrease
therefore toxic products in blood eg NH3 (can cross BBB + causes HE) increase
increase of portosystemic shunts @ oesophagus- causes oesophageal varices @ cardia + lower oesophagus- these can rupture + cause GI bleed
179
presentation of portal HTN
asymptomatic until comps. occur:
ascites
caput medusae
GI bleeding from oesophageal varices
haemoptysis
malaena
jaundice
HE symptoms
180
1st line investigations for portal HTN (4)
liver USS (nodules= cirrhosis)
CT/MRI (ascites, cirrhosis, splenomegaly)
endoscopy (oesophageal varices)
Labs (FBC, LFT, serology)
181
gold standard investigation for portal HTN
hepatic venous blood pressure against gradient measurement (diff in pressure between IVC & portal vein)
182
management of portal HTN
beta blockers 2 reduce portal venous pressure
treat comps
183
what are oesophageal varices and what are they a direct complication of
enlarged + fragile oesophageal veins that can easily rupture- direct comp of portal HTN + liver cirrhosis
184
what are 4 presentations of oesophageal varices
upper GI bleeding:
-haematemesis
-melaena
-haematochezia (fresh blood in poo)
-splenomegaly
185
1st line and gold standard investigation for oesophageal varices + other tests
oesophagogastroduodenoscopy (presence of varices)
other=
FBC- anaemia, thrombocytopenia
LFTs= increased AST, ALD, ALT, bilirubin
U&Es= hyponatremia
186
how would you stop bleeding when managing oesophageal varices
1. IV trelipressin
2. vatical banding
3. balloon tamponade
4. TiPPS- (trans- jugular intrahepatic portosystemic shunt)> decreases portal pressure by diverting blood 2 other larger veins
187
how would you prevent bleeding when managing oesophageal varices
Beta blockers (non-selective eg propranolol) + nitrates
repeat vatical banding
last resort= liver transplant (decompensated cirrhosis)
188
describe ascites
collection of fluid in peritoneal cavity
poor liver function= decreased albumin> decreased blood oncotic pressure> fluid loss into peritoneal cavity
189
list 3 categories of conditions causing ascites
local inflammation=
peritonitis, TB, abdo cancer
low protein= nephrotic syndrome, hypoalbumenia (liver failure)
flow stasis (build up causes leakage) = cirrhosis, budd chiari, congestive heart failure, constrictive pericarditis
190
presentation of ascites
distended abdo
shifting dullness
may have jaundice + pruritis
191
how would you check for shifting dullness in ascites
1. tap on central abdo when supine
2. tap on flanks- dull due 2 fluid
3. ask patient to lie on side and tap top flank- resonant (fluid has shifted 2 otherside + bowel floated here)
192
1st line investigations for ascites
shifting dullness on examination
ascites tap (peritocentesis of 10-20ml of fluid)
193
describe an ascites tap
peritocentesis of 10-20ml of fluid
1.cytology (WCC)
2. protein measurement:
- Transudate fluid proteins= <25g/L, serum ascites-albumin gradient= <11g/L
clear fluid due to hydrostatic pressure
increase in hydrostatic pressure due 2 cirrhosis, heart failure, portal HTN, budd chiari
-Exudate fluid proteins= >25g/L, serum ascites-albumin gradient= >11g/L
cloudy fluid due to decreased oncotic pressure
decrease in oncotic pressure due to malignancy, peritonitis, TB, nephrotic syndrome
194
gold standard investigation for ascites
abdo USS
195
management of ascites
treat underlying cause
diuretic (spironolactone, furosemide) 2 increase Na+ excretion, therefore more fluid flushed out
lower Na+ in diet
paracentesis
liver transplant
196
what is peritonitis
inflammation of peritoneal cavity
197
name 2 primary causes of peritonitis
ascites
spontaneous bacterial peritonitis (infection)
-
bacterial causes:
gram neg- e.coli, klebsiella
gram pos- staph aureaus
198
what is a secondary cause of peritonitis
underlying cause eg bile, malignancy
199
presentation of peritonitis
sudden onset + severe abdo pain
then> collapse + septic shock
fever
rigidity helps pain (guarding etc)
poorly localised to well localised
usually +/- ascites
200
investigations for ascites
ascites tap- shows neutrophilia
cultures show causative organism
increased ESR + CRP
exclude pregnancy + bowel obstructions as causes
chest x-ray- shows air under diaphragm
201
management of ascites
A-E assessment
treat underlying cause; IV fluids + IV abxs
surgery= peritoneal lavage (cleaning out of peritoneum)
comps= sepsis if not treated early
202
what happens in haemochromatosis
body absorbs too much Fe= increase in total body Fe + Fe deposition in tissues
-can poison tissues (liver, pancreas, heart, pituitary)
203
which mutation causes haemochromatosis and what does it cause
auto recessive mutation of HFE gene on chromosome 6
causes increased iron absorption, xtra iron= Organ damage via free radical production
204
name 3 risk factors for haemochromatosis
male (women lose Fe in menstruation)
50+
family history
205
presentation of haemochromatosis
chronic tiredness
joint pain
pigmentation (bronze/slate discolouration)
hair loss
hypogonadism (due 2 a. pit damage)
liver cirrhosis symptoms
erectile dysfunction
heart failure
cog symptoms- memory + mood disturbance
206
1st line investigations for haemochromatosis
Fe studies:
increased- serum Fe, transferrin saturation, ferritin
decreased- TIBC (total iron binding capacity- don't want to bind more Fe)
LFTs= increased aminotransferases
other= genetic test (HFE)
207
gold standard investigation for haemochromatosis
liver biopsy- Prussian blue stain= brown spots of Fe deposited in hepatocytes
208
management of haemochromatosis
1st= phlebotomy/venesection to decreased serum Fe- done weekly
2nd= iron chelation (desferrioxamine) + lifestyle mods
209
what is Wilson's disease
excessive accumulation of copper in body + tissues- can lead to tissue damage
210
name 2 risk factors for Wilson's diseaes
under 20
family history
211
what mutation occurs in Wilson's disease
auto recessive defecit of ATP7B copper-binding protein- leads to copper build up in hepatocyest + production of free radicals
212
presentations of Wilson's disease for:
liver, neuro, psych, eyes
liver: hepatitis, cirrhosis
neuro:
parkinsonism (tremor, bradykinesia, rigidity)
dysarthria (speech difficulties)
concentration + coord difficulty
dementia
psych: depression, psychosis
eyes: kayser-fleischer rings in cornea (brown rings of copper deposits in Descemet's membrane)
213
1st line investigations for Wilson's disease
serum copper + ceruloplasmin reduced (copper in tissues, not blood)
24hr urinary copper excretion= high
LFTs= abnormal
214
gold standard investigation for Wilson's disease + others
liver biopsy= increased copper + hepatitis
other= silt lamp examination (4 Kayser-fleischer rings)
genetic testing
215
management of Wilson's disease (1st line & second line)
1st line= copper chelation with penicillamine
2nd line= zinc salts, decreased copper diet (less chocolate, nuts, mushrooms, shellfish)
cirrhosis= consider liver transplant
216
describe acute anti trypsin deficiency
genetic abnormality of protein alpha 1 anti trypsin
-alpha 1 antitrypsin= normally inactivates elastase (breaks down elastin)
-therefore A1AT deficiency= elastase breaks down elastin unchecked
217
where is A1AT produced
in the liver
218
what dose A1AT deficiency cause in the lungs
protease enzymes attack connective tissue in lungs > damages alveoli causing emphysema + bronchitis
219
presentations of A1AT in the lungs
young/middle aged with COPD like symptoms
dyspnoea
chronic cough
wheeze
emphysema
220
presentations of A1AT in the liver
jaundice
cirrhosis (+comps)
hepatitis
hepatosplenomegaly
221
investigations for A1AT
decreased serum A1AT
reduced pulmonary function tests (spirometry obstruction FEV:FVC <0.7)
Chest x-ray= barrel chest (hyper inflated lungs)
CT= panacinar emphysema
LFTS= increased- bilirubin, aminotransferase ALP
liver biopsy- cirrhosis + periodic acid schiff staining A1AT mutant globules
genetic test= positive for PI mutation
222
management of A1AT
no treatment= curative
no smoking
manage emphysema eg inhalers
A1AT infusions
consider decompensation patients for liver transplantation
223
how many mg/kg of paracetamol over a 24hr period is considered toxic
>200mg/kg in 24hr period
224
what is the max dose of paracetamol for adults in 24hr
4g
225
what happens in a paracetamol overdose
not enough glutathione stores to inactivate NAPQI
-causes build of toxic NAPQI > damages liver
226
presentation of a paracetamol overdose
acute, severe RUQ pain
severe n+v
227
investigations for a paracetamol overdose
serum paracetamol concentration= increased
LFT= increased ALT + PTT
hypoglycaemia
228
management of a paracetamol overdose
N-acetylcysteine + activated charcoal within 1hr of digestion
N-acetylcysteine increases availability of glutathione
229
describe Gilbert's syndrome
auto recessive condition - mc. of hereditary jaundice- causes mild unconjugated hyperbilirubenia due 2 deficient/abnoraml UGT
230
presentation of Gilbert's and crigier najjar
gilbert's= short episodes of jaundice- asymptomatic in-between
crigier najjar= more severe jaundice- treat w. phototherapy (breaks down unconjugated bilirubin)
231
what is a hernia
protrusion of an organ thru. defect in wall of its cavity- typically bowel
232
name 3 kinds of hernias
reducible- able to 'push back into place'
irreducible
-obstructed (intestinal obstruction)
-strangulated (intestinal ischaemia)
incarcerated- contents are fixed in sac
233
describe rolling and sliding hiatal hernias
hiatal hernia= herniation of stomach thru diaphragm hiatus
rolling= gastroesophageal junction stays in abdo, part of fundus rolls into thorax
sliding= stomach + gastroesophageal junc slide up through diaphragmp
234
presentations and investigations for a hiatal hernia
SXs=
GORD
dysphagia
dyspepsia
Dx=
Chest x-ray
barium swallow (diagnosis)
endoscopy
oesophageal manometry
235
describe an inguinal hernia and its risk factors
protrusion of abdo contents thru inguinal canal
-spermatic cord herniates thru inguinal canal in males
RFs= male, heavy lifting, past abdo surgery, chronic cough
236
describe direct and indirect inguinal hernias
direct= into hesselbach's triangle 2 inferior epigastric arteries
indirect= bowel herniates thru inguinal canal
237
presentation and investigations for inguinal hernias
painful swelling in groin- pointing along groin Margin
+/- reducible
investigations=
usually clinical diagnosis, if unsure use abdo USS/CT/MRI
238
describe a femoral hernia and its risk factors
bowel goes thru femoral cord- v. likely to strangulate due 2 rigid femoral canal borders
RFs= female, mid-old age
239
presentations and investigations for a femoral hernia
swelling in upper thigh- pointing down
investigations= usually clinical, USS of abdo/pelvis if unsure
240
how would you treat all kinds of hernias
surgery
