Liver PTS Flashcards
1
Q
What are the functions of the liver?
A
1)Oestrogen regulation
2)Detoxification
3)Metabolises carbs
4)Albumin production
5)Clotting factor production
6)Bilirubin regulation
7)Immunity-Kupffer cells in reticuloendothelial system
2
Q
Liver: what happens if estrogen regulation goes wrong?
A
Gynecomastia
Spider naevi
Palmar erythema
3
Q
Liver: what happens if detoxification goes wrong?
A
Hepatic encephalopathy (changes to the brain due to liver disease)
4
Q
Liver: what happens if carbohydrate metabolism goes wrong?
A
Hypoglycaemia
5
Q
Liver: what happens if clotting factor production goes wrong?
A
Easy bruising
Easy bleeding
6
Q
Liver: what happens if bilirubin regulation goes wrong?
A
Jaundice-stool and urine changes
Pruritis (itchy skin)
7
Q
Liver: what happens if immunity from the Kupffer cells in RE system doesn’t work?
A
Spontaneous bacterial infections
8
Q
Describe the presentation of a patient with acute liver failure
A
Malaise
Nausea
Anorexia
Jaundice
Rarer: confusion, bleeding, pain, hypoglycaemia
9
Q
Describe the presentation of a patient with chronic liver failure
A
Ascites
Oedema
Malaise
Anorexia
Pruritis
Clubbing
Palmar erythema
Xanthelasma(yellow growths near eyelids)
Spider naevi
Bleeding: easy bruising
10
Q
Name the causes of acute liver failure
A
Viral: Hep A/B/EBV
Drugs
Alcohol
Vascular
Obstruction: e.g. gallstones
Congestion: e.g. heart failure
11
Q
Name the causes of chronic liver failure
A
Alcohol
Viral: Hep B/C
Autoimmune
Metabolic: iron/copper
12
Q
Describe the progression of chronic liver disease
A
Chronic liver condition->liver damage->liver symptoms->liver cirrhosis of prolonged->liver failure and higher risk of hepatocellular carcinoma
13
Q
What are the LFT’s?
A
Serum bilirubin
Serum albumin
Prothrombin time: INR
14
Q
What are the liver hepatic enzymes?
A
Aminotransferases: AST and ALT
ALP-alkaline phosphatase
GGT
15
Q
What happens to aminotransferases when hepatocytes are damages?
A
Leak into blood
16
Q
Which is more specific in hepatocellular disease: AST or ALT?
A
ALT
17
Q
When is ALP raised?
A
Raised in intra/extra hepatic cholestatic disease of any cause
Biliary tree
18
Q
Define liver failure
A
Liver loses its ability to repair and regenerate leading to decompensation
19
Q
Name the categories that cause liver failure
A
Infection
Metabolic
Autoimmune
Neoplastic
Vascular
Toxins
20
Q
Give some examples of common infections that cause liver failure
A
Viral hepatitis
21
Q
Give some examples of metabolic conditions that can cause liver failure
A
Wilson’s
Alpha 1 antitrypsin
22
Q
Give some examples of autoimmune conditions that can cause liver failure
A
PBC: primary biliary cholangitis: interlobular ducts
PSC: primary sclerosing cholangitis: intra and extra hepatic
23
Q
Name some vascular causes of liver failure
A
Budd Chiari: occlusion of hepatic veins
Ischaemia
24
Q
Name some common toxins that cause liver failure
A
Paracetamol
Alcohol
25
Name the signs of liver failure
Jaundice
Coagulopathy
Hepatic encephalopathy: altered mood/dyspraxia
Liver flap/asterixis
Fetor hepaticus: sweet and must breath/urine
26
How is liver failure diagnosed?
Clinical examination
Bloods: Increased PT, increased AST/ALT, toxicology screen, U&E, FBC
If ascites present: peritoneal tap with microscopy and culture
27
What test might you do to assess liver failure in a patient with ascites?
Peritoneal tap with microscopy and culture
28
Describe the conservative management of liver failure
Fluids
Analgesia
29
Describe the medical management of liver failure
Treat complications:
Ascites: diuretics
Cerebral edema: mannitol
Bleeding: vitamin K
Encephalopathy: lactulose
Sepsis: sepsis 6, antibiotics
Hypoglycaemia-dextrose
30
How would you treat ascites from liver failure?
Diuretics
31
How would you treat cerebral oedema from liver failure?
Mannitol
32
How would you treat bleeding form liver failure?
Vitamin K
33
How would you treat encephalopathy from liver failure?
Lactulose
34
How would you treat hypoglycemia from liver failure?
dextrose
35
How would you surgically treat liver failure?
Transplant
36
How is hepatitis A spread?
Faeco-oral
37
What kind of virus is hep a?
RNA
38
What tests could you do to look for hep A?
Bloods:
AST/ALT raised
Raised IgG and IgM
39
Describe the management of hep a
Generally supportive
Vaccine available
40
Describe the infection form hep a
Acute and mild
41
How is hep B spread?
blood products and bodily fluids
42
What kind of virus is hep B?
DNA
43
Describe the kind of infection from hep b
Can be severe
44
How would you test for hep B
HBV 'assay':
-HBs-ag
HBe-ag
Anti-HBs
Anti-HBc
45
Describe the management of hep B
Vaccination
Pegylated interferon alpha 2a
Tenofivor-inhibits viral replication
46
What complications can arise from hep b
Cirrhosis
HCC: hepatocellular carcinoma
47
How is Hep C spread?
Blood products and bodily fluids
48
What kind of virus is Hep C?
RNA
49
How would you test for Hep C?
HCV RNA
Anti-HCV serology
50
What kind of infection is Hep C?
Very slow progressing
51
Describe the management of Hep C
Direct acting anti-virals
Ribavarin
Sofusbuvir
52
What complications can arise from Hep C?
Cirrhosis
HCC
53
How is Hep D spread?
Blood products and bodily fluids
54
What kind of virus is Hep D?
RNA-requires hep B
55
What kind of infection does Hep D cause?
Makes HBV worse-more likely to progress onto cirrhosis or HCC
56
What tests are there for Hep D?
HDV-RNA
Anti-HDV
57
Describe the management of Hep D
Treat HBV
58
What complications can arise form Hep D
Cirrhosis
HCC
59
How is hepatitis E spread?
Faeco=oral route
60
What kind of virus is hep E
RNA
61
What kind of infection does Hep E cause?
Normally mild
62
What tests can be used to diagnose Hep E
HVE RNA
Anti HVE
63
Describe the management of hepatitis E
Supportive treatment
64
What complications can arise from hepatitis E?
Cirrhosis
HCC
65
What would the Hep B core antibody be in someone who has never had HBV?
Negative
66
What would the Hep B core antibody be in someone who has been vaccinated against hep b
Negative
67
What would the Hep B core antibody be in someone who has had a previous hep b infection
positive
68
What would the Hep B core antibody be in someone with chronic hep b?
positive
69
What would the hep b surface antibody be in someone who has never had HBV?
negative
70
What would the hep b surface antibody be in someone who has been vaccinated against hep b
positive
71
What would the hep b surface antibody be in someone who has had a previous hep b infection?
positive
72
What would the hep b surface antibody be in someone who has chronic HBV
negative
73
What would the HB surface antigen be in someone who has never had hep B
negative
74
What would the HB surface antigen be in someone who has been vaccinated against hep b?
negative
75
What would the HB surface antigen be in someone with a previous HBV infection
negative
76
What would the HB surface antigen be in someone who has chronic HBV?
positive
77
Describe the normal metabolism of paracetamol in the liver
3 pathways:
1)Glucuronidation pathway p(gluc)
2)Sulfatinon pathway p(sulf)
3)p450 pathway->NAPQI +gluthalione->NAPQI glutathione
78
Describe how the liver becomes damaged in a paracetamol overdose
Glucuronide and sulfate pathways become saturated so more paracetamol is metabolized by the p450 pathway which results in increased NAPQ1 production and not enough glutathione so NAPQ1 accumulates in hepatocytes and causes liver damage
79
Describe what happens in a paracetamol overdose
Not enough glutathione stores in the liver so toxic NAPQI builds up and leads to liver damage
80
Describe the clinical presentation of a paracetemol overdose
Nausea
Vomiting
Anorexia
Right upper quadrant pain
81
Describe the treatment for a paracetamol overdose
Activated charcoal: within 1 hour of ingestion
N-acetylcysteine
82
Describe the stages of non-alcoholic liver disease
Healthy-steatosis-steatohepatitis-fibrosis-cirrhosis
83
What is steatosis?
Build up of fat in the liver cells
84
Describe the clinical presentation of someone with non-alcoholic fatty liver disease
Asymptomatic
Nausea, vomiting, diarrhoea, hepatomegaly
85
How is non-alcoholic fatty liver disease diagnosed?
Imaging
Biopsy (diagnostic)
86
What is the main treatment for non-alcoholic liver disease
Reduce weight
87
Describe the progression of alcoholic liver disease
Fatty liver->alcoholic hepatitis->cirrhosis
88
What is the equation used to determine the number of units of alcohol?
Strength (ABV) x volume (ml) /1000
89
What investigations should be carried out to look for alcoholic liver disease?
GGT: very raised
AST, ALT: mildly raised
FBC: macrocytic anaemia
90
What are the main complications of alcoholic liver disease?
Wernicke-Korsakoff encephalopathy-caused by lack of vitamin B1
Acute/chronic pancreatitis
Mallory Weiss tear
91
Describe the signs and symptoms of Wernicke-Korsakoff encephalopathy
Ataxia
Confusion
Nystagmus
Memory impairment
92
What is the treatment for Wernicke-Korsakoff encephalopathy?
Treat with IV thiamine
93
What is Mallory-Weiss Syndrome?
Tear of the tissue of your lower oesophagus
94
Define cirrhosis
Loss of normal hepatic architecture with fibrosis-liver injury causes necrosis and apoptosis
95
Name some causes of cirrhosis
Common: alcohol abuse, non-alcoholic fatty liver disease, hepatitis
Others: Haemochromatosis, Wilson's disease, ATA1 deficiency
96
Describe the clinical presentation of someone with cirrhosis
Ascites
Clubbing
Palmar erythema
Xanthelasma
Spider naevi
Hepatomegaly
Peripheral oedema
97
Describe the investigations you can use to assess for cirrhosis
Low platelets, high INR, low albumin
US and CT: hepatomegaly
Liver biopsy
98
Describe the treatment for liver cirrhosis
Alcohol abstinence and good nutrition
Liver transplantation
99
What screening should be carried out in patients with cirrhosis?
Screening for hepatocellular carcinoma every 6 months
100
What is portal hypertension?
High pressure in your portal venous system
101
Describe the causes of prehepatic portal hypertension
Portal vein thrombosis
102
Describe the causes of intrahepatic portal hypertension
Schistosomiasis(parasitic worm)
Cirrhosis
Budd Chiari syndrome
103
What are the causes of post hepatic portal hypertension
RH failure
IVC obstruction
104
Describe the clinical presentation of someone with portal hypertension
Usually asymptomatic
105
What is portal vein circulation
Circulation of nutrient-rich blood between gut and liver: drained by portal vein
106
What are oesophageal varices?
Abnormally enlarged vessels in the esophagus that often occur in patients with serious liver disease
107
Why are oesophagela varices dangerous?
Vessels are thin and not meant to transport higher BP so can easily rupture.
Rupture->heamatemesis->blood digested->melaena(black stools from GI bleeding)
108
Describe the investigations carried out to look for oesophageal varices
Investigate using upper GI endoscopy
109
Describe the medical treatment for oesophageal varices
Beta-blockers to reduce cardiac output and partial pressure
Nitrates to reduce portal pressure
110
Describe the surgical treatment for oesophageal varices
Band ligation
Trans jugular intrahepatic portosystemic shunt (TIPSS)
111
What is a TIPS procedure?
Inserting a stent to connect the portal veins to adjacent vessels with lower pressure: relieves pressure of blood flowing through the diseased liver
112
Describe the process of bilirubin conjugation
Hamoglobin broken down into haem and globin
Haem broken down into iron and biliverdin
Biliverdin converted into unconjugated bilirubin
Unconjugated bilirubin binds to albumin and is transported to the liver
Unconjugated bilirubin + glucuronic acid=conjugated bilirubin which is transported to the duodenum in bile
113
Describe the pathophysiology of pre hepatic jaundice
Increased haemolysis
Increased unconjugated bilirubin as liver can't conjugate bilirubin fast enough
114
Name some common causes of pre hepatic jaundice
Malaria, sickle cells, haemolytic anaemia
115
Describe the pathophysiology of intra hepatic jaundice
Liver damage results in increased conjugated and unconjugated bilirubin in blood
116
Describe some causes of intra hepatic jaundice
Viral hepatitis, hepatotoxic drugs like paracetemol and alcohol
117
Describe the pathophysiology of post hepatic jaundice
Blockage of bile ducts results in backflow of conjugated bilirubin into the blood
118
Describe the causes of post-hepatic jaundice
Gallstones, hepatic tumours, pancreatic tumours
119
What are the 3 main biliary tract diseases?
Gallstones-biliary colic
Cholecystitis
Cholangitis
120
Which biliary tract disease will present with right upper quadrant pain but no fever or jaundice?
Biliary colic
121
Which biliary tract disease will present with RUQ pain, and fever but no jaundice?
Acute cholecystitis
122
Which biliary tract disease will present with RUQ pain, fever and jaundice?
Cholangitis
123
Describe the pathophysiology of biliary colic
Gallstone blocking the cystic or common bile duct without signs of cystic inflammation
124
What is bile made of?
Cholesterol
Pigments
Phospholipids
125
What can gallstones be made from?
1) Cholesterol-extra production: obesity and fatty diets
2) Pigment-seen in hemolytic anaemia
3)Mixed-made of both cholesterol and pigment
126
Describe the clinical presentation of a patient with biliary colic
'Colicky' RUQ pain that is worse after eating large fatty meals
Might also radiate to epigastrium and back
127
Why is biliary colic pain worse after eating large or fatty meals?
Triggers gallbladder to contract against the blockage
128
What are the risk factors for biliary colic?
5F's
Fat
Fertile
Forty
Female
Family history
129
What investigations would you carry out in someone you suspect to have biliary colic?
FBC and CRP: signs of inflammatory response so cholecystitis
LFT'sL raised ALP-biliary pathology. Bilirubin and ALT usually normal
Amylase: rule out pancreatitis
Ultrasound: diagnostic test
130
What findings would you look for when doing an US on a patient with biliary colic?
1. Stones
2. Gallbladder wall thickens (inflammation)
3. Duct dilation (suggests distal blockage)
131
What are the differential diagnoses for biliary colic?
Other causes of RUQ pain:
Cholecystitis and cholangitis (often from untreated gallstones anyway)
IBD
Pancreatitis
GORD
Peptic ulcers
132
What is the treatment for biliary colic
NSAIDs/analgesia
Optional cholecystectomy as gallstones often occur
133
Describe the pathophysiology of cholecystitis
Stone is blocking the ducts
Bile builds up causing gallbladder distention
Distention may reduce vascular supply
Retained bile causes inflammation of the gallbladder
134
Describe the presentation of a patient with cholecystitis
Generalized epigastric pain migrating to severe RUQ pain
Signs of inflammation like fever/fatigue
Pain associated with tenderness and guarding from inflamed gallbladder and local peritonitis
135
What is Murphy's sign?
Severe pain on deep inhalation with examiners hand pressed into RUQ
136
What investigations can be used to diagnose cholecystitis?
Positive Murphy's sign
Inflammatory markers: FBC, CRP
Ultrasound: thick gallstone walls form inflammation
137
Describe the treatment for cholecystitis
IV antibiotics
Heavy analgesia
IV fluids
Eventual cholecystectomy if needed
138
Describe the pathophysiology of cholangitis
Due to prolonged bile duct blockage
Bile isn't 'flushing' out the tubes so bacteria can climb up for the GI tract and cause biliary tree infection and consolidation
Prevents bile entering the GI tract so causes jaundice
5-10% mortality and infection can affect the pancreas too as it shares duct with the gallbladder
139
Describe the clinical presentation of someone with cholangitis
Severe RUQ pain
Fever and jaundice
May be septic and/or have some pancreatitis
140
Describe the investigations carried out to diagnose cholangitis
FBC, LFT's, CRP: leukocytosis, raised ALP and bilirubin, raised CRP
Blood cultures: work out pathogen to treat with appropriate antibiotics
Ultrasound+/-ERCP
141
What is ERCP?
Endoscopic retrograde cholangiopancreatography-biliary tree contrast x-ray
142
Describe the treatment for cholangitis
Treat sepsis
ERCP and stenting to mechanically clear the blockage
Surgery/cholecystectomy
143
Describe the pathophysiology of acute pancreatitis
Self-perpetuating inflammation of the pancreas causes leakage of enzymes and autodigestion
Pancrease can heal after acute episodes but is still bad
144
What are the causes of acute pancreatitis?
I GET SMASHED:
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune-especially in Japan
Scorpion venom
Hyperlipidaemia
ERCP-mechanical injury
Drugs: NSAIDs, corticosteroids, ACEi's
145
What are the 2 main causes of acute pancreatitis
Gallstones
Alcohol
146
Describe the pathophysiology of acute pancreatitis caused by gallstones
Blockage of the bile duct->backup of pancreatic juices
Change in luminal concentration causes Ca2+ release inside pancreatic cells and causes then to activate trypsinogen early-> digests the pancreas
147
Describe the pathophysiology of acute pancreatitis caused by alcohol
Contracts the ampulla of Vater obstructing the bile clearance and also affects Ca2+ homeostasis causing release in pancreatic cells and early actuation of trypsinogen
148
What is Grey Tuner's sign and how does acute pancreatitis cause it?
Abdominal skin discoloration from retroperitoneal bleeding
Leaky and damaged pancreas autodigest nearby structures causing haemorrhage
149
How can acute pancreatitis cause hyperglycaemia?
Deranges pancreatic function so can cause reduction of insulin production
150
Describe the clinical presentation of someone with acute pancreatitis
Severe epigastric pain radiating to the back
Anorexia, fever, jaundice, Grey-Turner's sign, nausea and vomiting, tachycardia
151
Describe the investigations for acute pancreatitis
Serum amylase: raised
Urinalysis: raised urinary amylase
Serum lipase: raised and more specific than amylase
Raised CRP
Erect CXR: exclude gastroduodenal rupture, abdominal us, CT, mri
152
Describe the acute pancreatitis scoring
APACHE 2: assess severity within 24 hours
Glasgow & Ranson score: prediction of severe attack only after 48 hours
153
Describe the treatment for acute pancreatitis
Nil by mouth
Analgesics
Prophylactic antibiotics
Assess severity
If gallstones are cause: treat them
154
Describe the pathophysiology of chronic pancreatitis
Obstruction of bicarbonate secretion in the pancreatic lumen causes early activation of trypsinogen and autodigestion which is replaced by fibrosis
155
Describe the common causes of chronic pancreatitis
Hereditary: CF
Autoimmune
CKD
156
Describe the presentation of someone with chronic pancreatitis
Epigastric pain through back. Worse after alcohol and better leaning forward
Nausea and vomiting, malabsorption, painless weight loss, DM
Typically 50 yr old male
157
What investigations are done to diagnose chronic pancreatitis
Serum amylase and lipase: may be raised if enough cells left to make them
Abdominal US, CT, MRI
158
Describe the treatment for chronic pancreatitis
Stop drinking
Pancreatic enzyme supplements and PPI to help digestion
Insulin for DM
Duct drainage
159
What is infective diarrhea
Increased stool frequency and volume, decreased consistency
160
Describe the causes of infective diarrhoes
Viral-rotavirus, norovirus, adenovirus
Bacterial-Ecoli, salmonella, C difficile
Parasites like giardia
Antibiotics
Anxiety, food allergy
Chronic-IBS, IBD, coeliac, bowel cancer
161
What are the risk factors for developing chronic diarrhea
Foreign travel
Crowded areas
Poor hygiene
162
Describe the clinical presentation of a patient with infective diarrhoea
Loose stools, vomiting, abdominal cramping
Viral-fever, fatigue, headache, myalgia
163
What are the red flag symptoms when assessing infective diarrhea?
Bloodrecent hospital treatment
antibiotic treatment
persistent vomiting
weight loss
painless watery diarrhoea
164
What investigations should be carried out when assessing infective diarrhoes
H/E-look for dehydration
Stool culture
165
Describe the management for infective diarrhoea
Treat cause
Oral rehydration
Anti-motility like loperamide, codeine
Antibiotics for gastroenteritis
Anti-emetics
166
What is hemochromatosis?
Too much iron
167
Describe the pathophysiology of hemochromatosis
Mutation in autosomal recessive HFE gene (chromosome 6)
Increased intestinal iron absorption
Iron accumulates in liver, joints, pancreas, heart, skin, gonads and leads to organ damage: liver fibrosis, cirrhosis, HCC
168
Describe the clinical presentation of someone with hemochromatosis
Fatigue, arthralgia, weakness
Hypogonadism, like erectile dysfunction
Slate-grey skin (brownish/bronze)
Chronic liver disease, heart failure, arrhythmias
169
Describe the investigations carried out to assess hemochromatosis
Bloods: iron study, LFT's
Genetic testing
Liver biopsy-gold standard
MRI-detects iron overload
170
Describe the management for hemochromatosis
Venesection: Removal of blood and RBC's
Chelation: -desferrioxamine
Liver transplant
171
What is Wilson's disease?
Too much copper in liver and CNS
172
Describe the pathophysiology of Wilson's disease
Error of copper metabolism->copper deposition in organs like liver, basal ganglia, cornea
173
Describe the clinical presentation of someone with Wilson's disease
Psychiatric: depression, neurotic behavioural patterns
CNS problems: tremor, dysarthria, involuntary movements, dysphagia, reduced memory, eventual dementia
Liver disease-hepatitis, cirrhosis
Kayser-Fleischer ring-copper in cornea, green/brown pigment at outer edge
174
Describe the investigations for Wilson's disease
Serum copper and ceruloplasmin reduced(not always)
24hr urinary copper excretion: high
Liver biopsy-diagnostic
175
Describe the management of Wilson's disease
Avoid high copper foods-liver chocolate, mushrooms, shellfish
Chelating agent: penicillamine
Liver transplant
176
What is A1AT defieincy?
Alpha 1 antitrypsin deficiency
Autosomal recessive genetic disorder, may result in liver/lung disease
177
Describe the pathophysiology of A1AT deficiency
A1AT gene on chromosome 14
Produced in liver
Inhibits neutrophil elastase-proteolytic enzyme produced by neutrophils with inflammation, infection, smoking
With A1AT deficiency, elastase breaks down elastin unchecked
Affects lungs (alveolar wall destruction) and liver
178
Describe the presentation of someone with alpha 1 antitrypsin deficiency
Lung: like COPD, SOB, emphysema
Liver: cirrhosis, hepatitis, neonatal jaundice
179
Describe the investigations carried out to diagnose ATA1 deficiency
Bloods: serum A1AT levels low
CXR, PFT's, LFT's, liver biopsy
180
Describe the management of A1AT deficiency
No treatment
Treat complications of liver disease
Stop smoking, manage emphysema
Liver transplant
181
What is ascites?
Excessive buildup of fluid in peritoneal cavity
182
Describe the pathophysiology of ascites
Poor liver function->low albumin->low blood oncotic pressure->fluid loss to the peritoneal cavity
183
Describe the causes of ascites
Main cause: liver cirrhosis
Also: late stage cancers, CHF, nephrotic syndromes, pancreatitis etc
184
Describe the presentation of someone with ascites
Large distended abdomen
Shifting dullness
185
What is shifting dullness?
Percuss abdomen and observe dullness over fluid versus resonance over air.
Ask patient to roll onto one side, wait a few seconds for fluid to settle at a new level then repercus on the side and observe if the dullness has shifted
186
Describe the treatment of ascites
Low sodium diet (<2000mg/day)
Conbination of spironolactone and furosemide (diuretics) to drain fluid
Identify and treat cause
187
What is peritonitis?
Inflammation from infection or irritation of peritoneum
188
Describe the pathophysiology of peritonitis
Primary: spontaneous bacterial infection and ascites
Secondary: perforation of bowel or appendix, or following infection from tubes breaking the skin
Perforation irritates through the leaked chemicals like bile acids and old clotted blood
189
Which pathogens most commonly cause peritonitis?
S. aureus
Klebsiella
E.Coli
190
Describe the clinical presentation of someone with peritonitis
-Perforations: sudden onset severe abdo pain with generalised shock and collapse
Secondary peritonitis: gradual onset, generalised abdo pain to localised sever pain(inflammation moves from visceral to parietal layers)
Patient will lie still, rigid abdomen, pain relieved by laying hands on abdomen
Pyrexia, tachycardia, potential confusion, nausea and vomiting
191
Describe the investigations carried out to diagnose peritonitis
Bloods: FBC and CRP: amylase(pancreatitis), hCG (ruptured ectopci pregnancy)
Erect CXR for air below diaphragm, AXR to exclude bowel obstruction, CT for abdominal ischaemia
Ascitic tap and blood cultures: look for pathogen
192
Describe the treatment for peritonitis
ABCDE
Treat underlying cause,e.g. surgery for perforated bowels
IV fluids
IV antibiotics-broad spec then pathogen specific
Peritoneal lavage(surgically clean)
193
What is a hernia?
Protrusion of an organ through a defect in the wall of its containing cavity
194
Describe the classification of hernias
1. Reducible-can be pushed back in
2. Irreducible
3. Obstructed-intestinal flow stopped
4. Strangulated-blood supply cut off-ischaemia +/-gangrene
195
What is an inguinal hernia?
Protrusion of abdo contents through inguinal canal
196
Describe the pathophysiology of inguinal hernias
Presents superior +medial to pubic tubercle
Direct-20% medial to inferior epigastric artery, enters inguinal canal through weakness in posterior wall
Indirect – 80%, lateral to inferior epigastric artery, enters inguinal canal through deep inguinal ring
197
What are the risk factors for an inguinal hernia
Male
Chronic cough
Heavy lifting
Past abdominal surgery
198
Describe the clinical presentation of someone with an inguinal hernia
Swelling in groin/scrotum
Maybe painful
Impulse
Maybe reducible
199
Describe the investigations for an inguinal hernia
Clinical diangosis
US/CT/MRI
200
Describe the management for inguinal hernias
If small: reassure
Surgery
Truss: supportive undergarment to hold tissue in place
201
What is a femoral hernia?
Bowel comes through femoral canal
202
Describe the pathophysiology of a femoral hernia
Likely to be irreducible and strangulate (due to rigidity of canal's borders)
203
Describe the clinical presentation of someone with a femoral hernia
Mass in upper medial thigh
Neck of hernia is inferior and material to pubic tubercle
May be cough impulse
204
Describe the diagnosis for a femoral hernia
Clinical diagnosis
US/CT.MRI
205
Describe the management for a femoral hernia
Surgery
206
What is a hiatus hernia?
Herniation of stomach through oesophageal aperture of diaphragm
207
Describe the pathophysiology of a hiatus hernia
Rolling: 20% gastro-oesophageal junction remains in abdomen, part of fundus rolls up through hiatus, LOS intact
Sliding – 80%, GOJ and part of stomach slides up into chest, LOS less competent
208
What are the risk factors for a hiatus hernia?
Obesity
Female
Pregnancy
Ascites
Advanced age
Skeletal deformities
209
Describe the clinical presentation of someone with a hiatus hernia
Heartburn/GORD
Dysphagia
210
What investigations should be carried out to diagnose hiatus hernia?
CXR
Barium swallow
Endoscopy
Oesophageal manometry
211
Describe the management fro hiatus hernia
Lose weight
PPI
Surgery
212
What is an incisional hernia?
Through surgical scar
213
What is an epigastric hernia?
Through linea alba above umbilicus
214
What is an umbilical hernia?
At umbilicus
215
Describe the management for incisional, epigastric and umbilical hernias
Surgery
216
What is Wernicke Korsakoff syndrome?
Combined B1 deficiency (alcohol causes B1 deficiency) and alcohol withdrawal symptoms
217
What are the symptoms of Wernicke Korsakoff syndrome?
Ataxia, nystagmus, encephalopathy
Patients may be 'confabulational'-make up stories to fill in the gaps in their memory-disproportionate memory loss
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What is the treatment for Wernicke Korsakoff syndrome?
IV thaimine
