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Liver > Liver PTS > Flashcards

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

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2
Q

Liver: what happens if estrogen regulation goes wrong?

A

Gynecomastia
Spider naevi
Palmar erythema

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3
Q

Liver: what happens if detoxification goes wrong?

A

Hepatic encephalopathy (changes to the brain due to liver disease)

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4
Q

Liver: what happens if carbohydrate metabolism goes wrong?

A

Hypoglycaemia

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5
Q

Liver: what happens if clotting factor production goes wrong?

A

Easy bruising
Easy bleeding

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6
Q

Liver: what happens if bilirubin regulation goes wrong?

A

Jaundice-stool and urine changes
Pruritis (itchy skin)

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7
Q

Liver: what happens if immunity from the Kupffer cells in RE system doesn’t work?

A

Spontaneous bacterial infections

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8
Q

Describe the presentation of a patient with acute liver failure

A

Malaise
Nausea
Anorexia
Jaundice
Rarer: confusion, bleeding, pain, hypoglycaemia

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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

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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

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11
Q

Name the causes of chronic liver failure

A

Alcohol
Viral: Hep B/C
Autoimmune
Metabolic: iron/copper

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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

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13
Q

What are the LFT’s?

A

Serum bilirubin
Serum albumin
Prothrombin time: INR

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14
Q

What are the liver hepatic enzymes?

A

Aminotransferases: AST and ALT
ALP-alkaline phosphatase
GGT

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15
Q

What happens to aminotransferases when hepatocytes are damages?

A

Leak into blood

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16
Q

Which is more specific in hepatocellular disease: AST or ALT?

A

ALT

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17
Q

When is ALP raised?

A

Raised in intra/extra hepatic cholestatic disease of any cause
Biliary tree

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18
Q

Define liver failure

A

Liver loses its ability to repair and regenerate leading to decompensation

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19
Q

Name the categories that cause liver failure

A

Infection
Metabolic
Autoimmune
Neoplastic
Vascular
Toxins

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20
Q

Give some examples of common infections that cause liver failure

A

Viral hepatitis

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21
Q

Give some examples of metabolic conditions that can cause liver failure

A

Wilson’s
Alpha 1 antitrypsin

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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

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23
Q

Name some vascular causes of liver failure

A

Budd Chiari: occlusion of hepatic veins
Ischaemia

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24
Q

Name some common toxins that cause liver failure

A

Paracetamol
Alcohol

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25
Q

Name the signs of liver failure

A

Jaundice
Coagulopathy
Hepatic encephalopathy: altered mood/dyspraxia
Liver flap/asterixis
Fetor hepaticus: sweet and must breath/urine

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26
Q

How is liver failure diagnosed?

A

Clinical examination
Bloods: Increased PT, increased AST/ALT, toxicology screen, U&E, FBC
If ascites present: peritoneal tap with microscopy and culture

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27
Q

What test might you do to assess liver failure in a patient with ascites?

A

Peritoneal tap with microscopy and culture

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28
Q

Describe the conservative management of liver failure

A

Fluids
Analgesia

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29
Q

Describe the medical management of liver failure

A

Treat complications:
Ascites: diuretics
Cerebral edema: mannitol
Bleeding: vitamin K
Encephalopathy: lactulose
Sepsis: sepsis 6, antibiotics
Hypoglycaemia-dextrose

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30
Q

How would you treat ascites from liver failure?

A

Diuretics

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31
Q

How would you treat cerebral oedema from liver failure?

A

Mannitol

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32
Q

How would you treat bleeding form liver failure?

A

Vitamin K

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33
Q

How would you treat encephalopathy from liver failure?

A

Lactulose

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34
Q

How would you treat hypoglycemia from liver failure?

A

dextrose

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35
Q

How would you surgically treat liver failure?

A

Transplant

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36
Q

How is hepatitis A spread?

A

Faeco-oral

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37
Q

What kind of virus is hep a?

A

RNA

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38
Q

What tests could you do to look for hep A?

A

Bloods:
AST/ALT raised
Raised IgG and IgM

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39
Q

Describe the management of hep a

A

Generally supportive
Vaccine available

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40
Q

Describe the infection form hep a

A

Acute and mild

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41
Q

How is hep B spread?

A

blood products and bodily fluids

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42
Q

What kind of virus is hep B?

A

DNA

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43
Q

Describe the kind of infection from hep b

A

Can be severe

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44
Q

How would you test for hep B

A

HBV ‘assay’:
-HBs-ag
HBe-ag
Anti-HBs
Anti-HBc

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45
Q

Describe the management of hep B

A

Vaccination
Pegylated interferon alpha 2a
Tenofivor-inhibits viral replication

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46
Q

What complications can arise from hep b

A

Cirrhosis
HCC: hepatocellular carcinoma

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47
Q

How is Hep C spread?

A

Blood products and bodily fluids

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48
Q

What kind of virus is Hep C?

A

RNA

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49
Q

How would you test for Hep C?

A

HCV RNA
Anti-HCV serology

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50
Q

What kind of infection is Hep C?

A

Very slow progressing

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51
Q

Describe the management of Hep C

A

Direct acting anti-virals
Ribavarin
Sofusbuvir

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52
Q

What complications can arise from Hep C?

A

Cirrhosis
HCC

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53
Q

How is Hep D spread?

A

Blood products and bodily fluids

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54
Q

What kind of virus is Hep D?

A

RNA-requires hep B

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55
Q

What kind of infection does Hep D cause?

A

Makes HBV worse-more likely to progress onto cirrhosis or HCC

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56
Q

What tests are there for Hep D?

A

HDV-RNA
Anti-HDV

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57
Q

Describe the management of Hep D

A

Treat HBV

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58
Q

What complications can arise form Hep D

A

Cirrhosis
HCC

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59
Q

How is hepatitis E spread?

A

Faeco=oral route

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60
Q

What kind of virus is hep E

A

RNA

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61
Q

What kind of infection does Hep E cause?

A

Normally mild

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62
Q

What tests can be used to diagnose Hep E

A

HVE RNA
Anti HVE

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63
Q

Describe the management of hepatitis E

A

Supportive treatment

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64
Q

What complications can arise from hepatitis E?

A

Cirrhosis
HCC

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65
Q

What would the Hep B core antibody be in someone who has never had HBV?

A

Negative

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66
Q

What would the Hep B core antibody be in someone who has been vaccinated against hep b

A

Negative

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67
Q

What would the Hep B core antibody be in someone who has had a previous hep b infection

A

positive

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68
Q

What would the Hep B core antibody be in someone with chronic hep b?

A

positive

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69
Q

What would the hep b surface antibody be in someone who has never had HBV?

A

negative

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70
Q

What would the hep b surface antibody be in someone who has been vaccinated against hep b

A

positive

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71
Q

What would the hep b surface antibody be in someone who has had a previous hep b infection?

A

positive

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72
Q

What would the hep b surface antibody be in someone who has chronic HBV

A

negative

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73
Q

What would the HB surface antigen be in someone who has never had hep B

A

negative

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74
Q

What would the HB surface antigen be in someone who has been vaccinated against hep b?

A

negative

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75
Q

What would the HB surface antigen be in someone with a previous HBV infection

A

negative

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76
Q

What would the HB surface antigen be in someone who has chronic HBV?

A

positive

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77
Q

Describe the normal metabolism of paracetamol in the liver

A

3 pathways:
1)Glucuronidation pathway p(gluc)
2)Sulfatinon pathway p(sulf)
3)p450 pathway->NAPQI +gluthalione->NAPQI glutathione

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78
Q

Describe how the liver becomes damaged in a paracetamol overdose

A

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

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79
Q

Describe what happens in a paracetamol overdose

A

Not enough glutathione stores in the liver so toxic NAPQI builds up and leads to liver damage

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80
Q

Describe the clinical presentation of a paracetemol overdose

A

Nausea
Vomiting
Anorexia
Right upper quadrant pain

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81
Q

Describe the treatment for a paracetamol overdose

A

Activated charcoal: within 1 hour of ingestion
N-acetylcysteine

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82
Q

Describe the stages of non-alcoholic liver disease

A

Healthy-steatosis-steatohepatitis-fibrosis-cirrhosis

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83
Q

What is steatosis?

A

Build up of fat in the liver cells

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84
Q

Describe the clinical presentation of someone with non-alcoholic fatty liver disease

A

Asymptomatic
Nausea, vomiting, diarrhoea, hepatomegaly

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85
Q

How is non-alcoholic fatty liver disease diagnosed?

A

Imaging
Biopsy (diagnostic)

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86
Q

What is the main treatment for non-alcoholic liver disease

A

Reduce weight

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87
Q

Describe the progression of alcoholic liver disease

A

Fatty liver->alcoholic hepatitis->cirrhosis

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88
Q

What is the equation used to determine the number of units of alcohol?

A

Strength (ABV) x volume (ml) /1000

89
Q

What investigations should be carried out to look for alcoholic liver disease?

A

GGT: very raised
AST, ALT: mildly raised
FBC: macrocytic anaemia

90
Q

What are the main complications of alcoholic liver disease?

A

Wernicke-Korsakoff encephalopathy-caused by lack of vitamin B1
Acute/chronic pancreatitis
Mallory Weiss tear

91
Q

Describe the signs and symptoms of Wernicke-Korsakoff encephalopathy

A

Ataxia
Confusion
Nystagmus
Memory impairment

92
Q

What is the treatment for Wernicke-Korsakoff encephalopathy?

A

Treat with IV thiamine

93
Q

What is Mallory-Weiss Syndrome?

A

Tear of the tissue of your lower oesophagus

94
Q

Define cirrhosis

A

Loss of normal hepatic architecture with fibrosis-liver injury causes necrosis and apoptosis

95
Q

Name some causes of cirrhosis

A

Common: alcohol abuse, non-alcoholic fatty liver disease, hepatitis
Others: Haemochromatosis, Wilson’s disease, ATA1 deficiency

96
Q

Describe the clinical presentation of someone with cirrhosis

A

Ascites
Clubbing
Palmar erythema
Xanthelasma
Spider naevi
Hepatomegaly
Peripheral oedema

97
Q

Describe the investigations you can use to assess for cirrhosis

A

Low platelets, high INR, low albumin
US and CT: hepatomegaly
Liver biopsy

98
Q

Describe the treatment for liver cirrhosis

A

Alcohol abstinence and good nutrition
Liver transplantation

99
Q

What screening should be carried out in patients with cirrhosis?

A

Screening for hepatocellular carcinoma every 6 months

100
Q

What is portal hypertension?

A

High pressure in your portal venous system

101
Q

Describe the causes of prehepatic portal hypertension

A

Portal vein thrombosis

102
Q

Describe the causes of intrahepatic portal hypertension

A

Schistosomiasis(parasitic worm)
Cirrhosis
Budd Chiari syndrome

103
Q

What are the causes of post hepatic portal hypertension

A

RH failure
IVC obstruction

104
Q

Describe the clinical presentation of someone with portal hypertension

A

Usually asymptomatic

105
Q

What is portal vein circulation

A

Circulation of nutrient-rich blood between gut and liver: drained by portal vein

106
Q

What are oesophageal varices?

A

Abnormally enlarged vessels in the esophagus that often occur in patients with serious liver disease

107
Q

Why are oesophagela varices dangerous?

A

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
Q

Describe the investigations carried out to look for oesophageal varices

A

Investigate using upper GI endoscopy

109
Q

Describe the medical treatment for oesophageal varices

A

Beta-blockers to reduce cardiac output and partial pressure
Nitrates to reduce portal pressure

110
Q

Describe the surgical treatment for oesophageal varices

A

Band ligation
Trans jugular intrahepatic portosystemic shunt (TIPSS)

111
Q

What is a TIPS procedure?

A

Inserting a stent to connect the portal veins to adjacent vessels with lower pressure: relieves pressure of blood flowing through the diseased liver

112
Q

Describe the process of bilirubin conjugation

A

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
Q

Describe the pathophysiology of pre hepatic jaundice

A

Increased haemolysis
Increased unconjugated bilirubin as liver can’t conjugate bilirubin fast enough

114
Q

Name some common causes of pre hepatic jaundice

A

Malaria, sickle cells, haemolytic anaemia

115
Q

Describe the pathophysiology of intra hepatic jaundice

A

Liver damage results in increased conjugated and unconjugated bilirubin in blood

116
Q

Describe some causes of intra hepatic jaundice

A

Viral hepatitis, hepatotoxic drugs like paracetemol and alcohol

117
Q

Describe the pathophysiology of post hepatic jaundice

A

Blockage of bile ducts results in backflow of conjugated bilirubin into the blood

118
Q

Describe the causes of post-hepatic jaundice

A

Gallstones, hepatic tumours, pancreatic tumours

119
Q

What are the 3 main biliary tract diseases?

A

Gallstones-biliary colic
Cholecystitis
Cholangitis

120
Q

Which biliary tract disease will present with right upper quadrant pain but no fever or jaundice?

A

Biliary colic

121
Q

Which biliary tract disease will present with RUQ pain, and fever but no jaundice?

A

Acute cholecystitis

122
Q

Which biliary tract disease will present with RUQ pain, fever and jaundice?

A

Cholangitis

123
Q

Describe the pathophysiology of biliary colic

A

Gallstone blocking the cystic or common bile duct without signs of cystic inflammation

124
Q

What is bile made of?

A

Cholesterol
Pigments
Phospholipids

125
Q

What can gallstones be made from?

A

1) Cholesterol-extra production: obesity and fatty diets
2) Pigment-seen in hemolytic anaemia
3)Mixed-made of both cholesterol and pigment

126
Q

Describe the clinical presentation of a patient with biliary colic

A

‘Colicky’ RUQ pain that is worse after eating large fatty meals
Might also radiate to epigastrium and back

127
Q

Why is biliary colic pain worse after eating large or fatty meals?

A

Triggers gallbladder to contract against the blockage

128
Q

What are the risk factors for biliary colic?

A

5F’s
Fat
Fertile
Forty
Female
Family history

129
Q

What investigations would you carry out in someone you suspect to have biliary colic?

A

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
Q

What findings would you look for when doing an US on a patient with biliary colic?

A
  1. Stones
  2. Gallbladder wall thickens (inflammation)
  3. Duct dilation (suggests distal blockage)
131
Q

What are the differential diagnoses for biliary colic?

A

Other causes of RUQ pain:
Cholecystitis and cholangitis (often from untreated gallstones anyway)
IBD
Pancreatitis
GORD
Peptic ulcers

132
Q

What is the treatment for biliary colic

A

NSAIDs/analgesia
Optional cholecystectomy as gallstones often occur

133
Q

Describe the pathophysiology of cholecystitis

A

Stone is blocking the ducts
Bile builds up causing gallbladder distention
Distention may reduce vascular supply
Retained bile causes inflammation of the gallbladder

134
Q

Describe the presentation of a patient with cholecystitis

A

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
Q

What is Murphy’s sign?

A

Severe pain on deep inhalation with examiners hand pressed into RUQ

136
Q

What investigations can be used to diagnose cholecystitis?

A

Positive Murphy’s sign
Inflammatory markers: FBC, CRP
Ultrasound: thick gallstone walls form inflammation

137
Q

Describe the treatment for cholecystitis

A

IV antibiotics
Heavy analgesia
IV fluids
Eventual cholecystectomy if needed

138
Q

Describe the pathophysiology of cholangitis

A

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
Q

Describe the clinical presentation of someone with cholangitis

A

Severe RUQ pain
Fever and jaundice
May be septic and/or have some pancreatitis

140
Q

Describe the investigations carried out to diagnose cholangitis

A

FBC, LFT’s, CRP: leukocytosis, raised ALP and bilirubin, raised CRP
Blood cultures: work out pathogen to treat with appropriate antibiotics
Ultrasound+/-ERCP

141
Q

What is ERCP?

A

Endoscopic retrograde cholangiopancreatography-biliary tree contrast x-ray

142
Q

Describe the treatment for cholangitis

A

Treat sepsis
ERCP and stenting to mechanically clear the blockage
Surgery/cholecystectomy

143
Q

Describe the pathophysiology of acute pancreatitis

A

Self-perpetuating inflammation of the pancreas causes leakage of enzymes and autodigestion
Pancrease can heal after acute episodes but is still bad

144
Q

What are the causes of acute pancreatitis?

A

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
Q

What are the 2 main causes of acute pancreatitis

A

Gallstones
Alcohol

146
Q

Describe the pathophysiology of acute pancreatitis caused by gallstones

A

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
Q

Describe the pathophysiology of acute pancreatitis caused by alcohol

A

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
Q

What is Grey Tuner’s sign and how does acute pancreatitis cause it?

A

Abdominal skin discoloration from retroperitoneal bleeding
Leaky and damaged pancreas autodigest nearby structures causing haemorrhage

149
Q

How can acute pancreatitis cause hyperglycaemia?

A

Deranges pancreatic function so can cause reduction of insulin production

150
Q

Describe the clinical presentation of someone with acute pancreatitis

A

Severe epigastric pain radiating to the back
Anorexia, fever, jaundice, Grey-Turner’s sign, nausea and vomiting, tachycardia

151
Q

Describe the investigations for acute pancreatitis

A

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
Q

Describe the acute pancreatitis scoring

A

APACHE 2: assess severity within 24 hours
Glasgow & Ranson score: prediction of severe attack only after 48 hours

153
Q

Describe the treatment for acute pancreatitis

A

Nil by mouth
Analgesics
Prophylactic antibiotics
Assess severity
If gallstones are cause: treat them

154
Q

Describe the pathophysiology of chronic pancreatitis

A

Obstruction of bicarbonate secretion in the pancreatic lumen causes early activation of trypsinogen and autodigestion which is replaced by fibrosis

155
Q

Describe the common causes of chronic pancreatitis

A

Hereditary: CF
Autoimmune
CKD

156
Q

Describe the presentation of someone with chronic pancreatitis

A

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
Q

What investigations are done to diagnose chronic pancreatitis

A

Serum amylase and lipase: may be raised if enough cells left to make them
Abdominal US, CT, MRI

158
Q

Describe the treatment for chronic pancreatitis

A

Stop drinking
Pancreatic enzyme supplements and PPI to help digestion
Insulin for DM
Duct drainage

159
Q

What is infective diarrhea

A

Increased stool frequency and volume, decreased consistency

160
Q

Describe the causes of infective diarrhoes

A

Viral-rotavirus, norovirus, adenovirus
Bacterial-Ecoli, salmonella, C difficile
Parasites like giardia
Antibiotics
Anxiety, food allergy
Chronic-IBS, IBD, coeliac, bowel cancer

161
Q

What are the risk factors for developing chronic diarrhea

A

Foreign travel
Crowded areas
Poor hygiene

162
Q

Describe the clinical presentation of a patient with infective diarrhoea

A

Loose stools, vomiting, abdominal cramping
Viral-fever, fatigue, headache, myalgia

163
Q

What are the red flag symptoms when assessing infective diarrhea?

A

Bloodrecent hospital treatment
antibiotic treatment
persistent vomiting
weight loss
painless watery diarrhoea

164
Q

What investigations should be carried out when assessing infective diarrhoes

A

H/E-look for dehydration
Stool culture

165
Q

Describe the management for infective diarrhoea

A

Treat cause
Oral rehydration
Anti-motility like loperamide, codeine
Antibiotics for gastroenteritis
Anti-emetics

166
Q

What is hemochromatosis?

A

Too much iron

167
Q

Describe the pathophysiology of hemochromatosis

A

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
Q

Describe the clinical presentation of someone with hemochromatosis

A

Fatigue, arthralgia, weakness
Hypogonadism, like erectile dysfunction
Slate-grey skin (brownish/bronze)
Chronic liver disease, heart failure, arrhythmias

169
Q

Describe the investigations carried out to assess hemochromatosis

A

Bloods: iron study, LFT’s
Genetic testing
Liver biopsy-gold standard
MRI-detects iron overload

170
Q

Describe the management for hemochromatosis

A

Venesection: Removal of blood and RBC’s
Chelation: -desferrioxamine
Liver transplant

171
Q

What is Wilson’s disease?

A

Too much copper in liver and CNS

172
Q

Describe the pathophysiology of Wilson’s disease

A

Error of copper metabolism->copper deposition in organs like liver, basal ganglia, cornea

173
Q

Describe the clinical presentation of someone with Wilson’s disease

A

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
Q

Describe the investigations for Wilson’s disease

A

Serum copper and ceruloplasmin reduced(not always)
24hr urinary copper excretion: high
Liver biopsy-diagnostic

175
Q

Describe the management of Wilson’s disease

A

Avoid high copper foods-liver chocolate, mushrooms, shellfish
Chelating agent: penicillamine
Liver transplant

176
Q

What is A1AT defieincy?

A

Alpha 1 antitrypsin deficiency
Autosomal recessive genetic disorder, may result in liver/lung disease

177
Q

Describe the pathophysiology of A1AT deficiency

A

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
Q

Describe the presentation of someone with alpha 1 antitrypsin deficiency

A

Lung: like COPD, SOB, emphysema
Liver: cirrhosis, hepatitis, neonatal jaundice

179
Q

Describe the investigations carried out to diagnose ATA1 deficiency

A

Bloods: serum A1AT levels low
CXR, PFT’s, LFT’s, liver biopsy

180
Q

Describe the management of A1AT deficiency

A

No treatment
Treat complications of liver disease
Stop smoking, manage emphysema
Liver transplant

181
Q

What is ascites?

A

Excessive buildup of fluid in peritoneal cavity

182
Q

Describe the pathophysiology of ascites

A

Poor liver function->low albumin->low blood oncotic pressure->fluid loss to the peritoneal cavity

183
Q

Describe the causes of ascites

A

Main cause: liver cirrhosis
Also: late stage cancers, CHF, nephrotic syndromes, pancreatitis etc

184
Q

Describe the presentation of someone with ascites

A

Large distended abdomen
Shifting dullness

185
Q

What is shifting dullness?

A

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
Q

Describe the treatment of ascites

A

Low sodium diet (<2000mg/day)
Conbination of spironolactone and furosemide (diuretics) to drain fluid
Identify and treat cause

187
Q

What is peritonitis?

A

Inflammation from infection or irritation of peritoneum

188
Q

Describe the pathophysiology of peritonitis

A

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
Q

Which pathogens most commonly cause peritonitis?

A

S. aureus
Klebsiella
E.Coli

190
Q

Describe the clinical presentation of someone with peritonitis

A

-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
Q

Describe the investigations carried out to diagnose peritonitis

A

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
Q

Describe the treatment for peritonitis

A

ABCDE
Treat underlying cause,e.g. surgery for perforated bowels
IV fluids
IV antibiotics-broad spec then pathogen specific
Peritoneal lavage(surgically clean)

193
Q

What is a hernia?

A

Protrusion of an organ through a defect in the wall of its containing cavity

194
Q

Describe the classification of hernias

A
  1. Reducible-can be pushed back in
  2. Irreducible
  3. Obstructed-intestinal flow stopped
  4. Strangulated-blood supply cut off-ischaemia +/-gangrene
195
Q

What is an inguinal hernia?

A

Protrusion of abdo contents through inguinal canal

196
Q

Describe the pathophysiology of inguinal hernias

A

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
Q

What are the risk factors for an inguinal hernia

A

Male
Chronic cough
Heavy lifting
Past abdominal surgery

198
Q

Describe the clinical presentation of someone with an inguinal hernia

A

Swelling in groin/scrotum
Maybe painful
Impulse
Maybe reducible

199
Q

Describe the investigations for an inguinal hernia

A

Clinical diangosis
US/CT/MRI

200
Q

Describe the management for inguinal hernias

A

If small: reassure
Surgery
Truss: supportive undergarment to hold tissue in place

201
Q

What is a femoral hernia?

A

Bowel comes through femoral canal

202
Q

Describe the pathophysiology of a femoral hernia

A

Likely to be irreducible and strangulate (due to rigidity of canal’s borders)

203
Q

Describe the clinical presentation of someone with a femoral hernia

A

Mass in upper medial thigh
Neck of hernia is inferior and material to pubic tubercle
May be cough impulse

204
Q

Describe the diagnosis for a femoral hernia

A

Clinical diagnosis
US/CT.MRI

205
Q

Describe the management for a femoral hernia

A

Surgery

206
Q

What is a hiatus hernia?

A

Herniation of stomach through oesophageal aperture of diaphragm

207
Q

Describe the pathophysiology of a hiatus hernia

A

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
Q

What are the risk factors for a hiatus hernia?

A

Obesity
Female
Pregnancy
Ascites
Advanced age
Skeletal deformities

209
Q

Describe the clinical presentation of someone with a hiatus hernia

A

Heartburn/GORD
Dysphagia

210
Q

What investigations should be carried out to diagnose hiatus hernia?

A

CXR
Barium swallow
Endoscopy
Oesophageal manometry

211
Q

Describe the management fro hiatus hernia

A

Lose weight
PPI
Surgery

212
Q

What is an incisional hernia?

A

Through surgical scar

213
Q

What is an epigastric hernia?

A

Through linea alba above umbilicus

214
Q

What is an umbilical hernia?

A

At umbilicus

215
Q

Describe the management for incisional, epigastric and umbilical hernias

A

Surgery

216
Q

What is Wernicke Korsakoff syndrome?

A

Combined B1 deficiency (alcohol causes B1 deficiency) and alcohol withdrawal symptoms

217
Q

What are the symptoms of Wernicke Korsakoff syndrome?

A

Ataxia, nystagmus, encephalopathy
Patients may be ‘confabulational’-make up stories to fill in the gaps in their memory-disproportionate memory loss

218
Q

What is the treatment for Wernicke Korsakoff syndrome?

A

IV thaimine

Liver (1 decks)

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