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Alimentary System > Upper GI Conditions 2 > Flashcards

Upper GI Conditions 2 Flashcards

1
Q

What 2 ducts form the Common Bile duct?

A

Common Hepatic duct + Cystic duct

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2
Q

What 2 ducts form the Ampulla of Vater?

A

Common Bile duct + Pancreatic duct

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3
Q

What is CCK released in response to?

A

Fats, Peptides, AAs in the Duodenum

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4
Q

What does CCK do?

A
  • GB: stimulates GB contraction, relaxation of the Sphincter of Oddi (release of stored bile into the intestine)
  • Pancreas: release of digestive enzymes
  • Stomach: delayed gastric emptying
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5
Q

What is the most common type of Gallstone?

A

Cholesterol stones = 80%

>50% cholesterol, less pigment

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6
Q

What are the risk factors for Cholesterol Gallstones?

A
  • Females
  • Age
  • Obesity
  • Parity
  • OCP
  • Smoking

(4 Fs: Female, 40, Fertile and Fat)

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7
Q

What is the main risk factor for Pigment Gallstones?

A

Haemolytic anaemia

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8
Q

What are the main clinical features of Gallstones?

A
  • Majority asymptomatic (incidental finding)
  • > 90%
  • Biliary Colic
  • > RUQ pain, radiates to back/shoulder, episodes last between 2-6 hours, they resolve spontaneously and occur after eating fatty food, occurs early at night
  • +/- Jaundice
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9
Q

What are the complications of Gallstones?

A

In the GB and Cystic duct:

  • Biliary colic
  • Acute + Chronic Cholecystitis
  • Empyema
  • Perforation
  • Carcinoma
  • Mirizzi’s syndrome (stone in GB obstructing the CBD and causing jaundice)

In the Bile ducts:

  • Obstructive jaundice
  • Cholangitis
  • Pancreatitis

In the gut:

  • Biliary Enteric Fistula (gallstone -> small intestine)
  • Gallstone Ileus (biliary enteric fistula -> GB ruptures -> stone obstructing small intestine)
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10
Q

What are the investigations for pts with suspected gallstone disease?

A
  • Blood tests: LFTs (AST, ALT, ALP)
  • Abdominal USS
  • (MRCP if diagnosis still uncertain)
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11
Q

What is the management of asymptomatic gallstones?

A

No treatment required!

unless they develop symptoms

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12
Q

What is the treatment of symptomatic gallstones?

A
  • Laparoscopic cholecystectomy (!!!)
  • (Open surgery if GB perforation)
  • (if declines non-surgical option: dissolution or lithotripsy)
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13
Q

What are the risk factors for Cholangiocarcinoma?

A
  • PSC (strong association)
  • Congenital cystic disease (ie. choledochal cysts)
  • Biliary-enteric drainage
  • Hepatolithiasis
  • Thorotrast (contrast)
  • Carcinogens: aflatoxins, N-nitroso toxins, etc
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14
Q

What are the clinical features of Cholangiocarcinoma?

A
  • Fever
  • Abdominal pain (± ascites)
  • Malaise
  • Painless Obstructive Jaundice: Increased Bilirubin, Increased ALP, itching
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15
Q

What are the investigations for Cholangiocarcinoma?

A
  • LFTs

- ECRP + Biopsy

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16
Q

What is the management of Cholangiocarcinoma?

A
  • Surgery: Majority unresectable at presentation (70%), and of those that do, majority recur
  • Palliate the Jaundice: Stent (percutaneous vs. ERCP)
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17
Q

What genetic disorder increases risk for Ampullary cancer?

A

FAP !

Familial Adenomatous Polyposis

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18
Q

What us the treatment of choice for Ampullary cancer?

A

Pancreatico-duodenectomy

similar to pancreatic cancer!

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19
Q

What are the causes of Acute Pancreatitis?

A
  • I GET SMASHED *
  • Idiopathic (!!)
  • Gallstones (most common) (!!)
  • Ethanol (!!)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune (PAN)
  • Scorpion venom
  • Hyperlipidaemia, Hypothermia, Hypercalcaemia
  • ERCP and Emboli
  • Drugs
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20
Q

What are the symptoms of Acute Pancreatitis?

A
  • Sudden onset severe Epigastric pain
  • > radiates to back, relieved by sitting forwards
  • Nausea + Vomiting
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21
Q

What are the signs of Acute Pancreatitis?

A
  • In severe disease*
  • Tachycardia, Fever, Shock (hypotension, oliguric)
  • Widespread tenderness with guarding (rigid abdomen)
  • Periumbilical bruising (Cullen’s sign), or Flanks (Grey Turner’s sign)
  • > in severe necrotising pancreatitis due to blood vessel autodigestion + haemorrhage
  • Jaundice, Cholangitis
  • > if caused by gallstones
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22
Q

What investigations would you do for Acute Pancreatitis?

A
  • Bloods: Serum amylase (!!!), serum lipase (more sensitive and specific for pancreatitis), LFTs, inflammatory markers
  • Radiology: Abdominal US (?gallstones!!), contrast-enhanced CT and/or MRI (assesses severity + complications)
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23
Q

Which criteria is used to assess for the severity of Acute Pancreatitis?

A

Modified Glasgow Criteria!

MNEMONIC: PANCREAS

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24
Q

What is the management of Acute Pancreatitis?

A
  • Conservative and Prophylaxis !!*
  • Nasogastric suction
  • > prevents risk of aspiration pneumonia
  • Baseline ABGs
  • Prophylactic abx
  • Analgesia
  • NG tube -> feeding
  • Anticoagulation -> LMWH prophylaxis for DVT
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25
Q

What are the complications of Acute Pancreatitis?

A

Early:

  • Shock
  • ARDS
  • Hypocalcaemia
  • Hyperglycaemia

Late (>1 week):

  • Pancreatic Necrosis + Pseudocyst
  • Pancreatic Abscess
  • Thrombosis
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26
Q

When should you suspect Pancreatic Necrosis development in Acute Pancreatitis?

A
  • Should be suspected in a pt. who has persistent systemic inflammation for 7-10 days after the onset of Pancreatitis
  • Confirmed by CT imaging
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27
Q

When should you suspect Pancreatic Pseudocyst development in Acute Pancreatitis?

A
  • CT imaging: collection of fluid in the lesser sac
  • Fever
  • Mass
  • Persistent raised Amylase or LFTs
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28
Q

What is the management of a Pancreatic Pseudocyst?

A
  • may be found incidentally on CT imaging
  • May resolve spontaneously
  • OR may need drainage (if >6 weeks)
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29
Q

What is the management of Pancreatic Necrosis?

A
  • confirmed by CT imaging
  • if infected (clinical deterioration with raised infection markers): EUS + FNA of necrosis
  • Pancreatic Necrosectomy
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30
Q

What is the definition of Chronic Pancreatitis?

A
  • Continuous inflammatory disease of the Pancreas
  • Characterised by irreversible cellular destruction of the Pancreas
  • Typically causes pain and/or permanent loss of function
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31
Q

What are the aetiology of Chronic Pancreatitis?

A
  • Chronic Alcohol abuse (80%)

Rarely:

  • Cystic Fibrosis
  • Congenital abnormalities: Annular Pancreas, Pancreas Divisum
  • Hereditary Pancreatitis
  • Hypercalcaemia (increased PTH)
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32
Q

What are the clinical features of Chronic Pancreatitis?

A
  • Epigastric pain:
  • > ‘bores’ through to back
  • > relieved by sitting forward or hot water bottles on epigastrium/back
  • Exocrine insufficiency:
  • > weight loss
  • > nutritional deficiencies
  • > steatorrhoea
  • > bloating
  • Endocrine insufficiency
  • > diabetes
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33
Q

What Investigations would you do for Chronic Pancreatitis?

A
  • Imaging: Contrast-enhanced CT (!!!) (pancreatic calcifications confirm the diagnosis) -> MRCP -> EUS
  • Bloods: do NOT check serum Amylase!!, LFTs, HbA1c
  • Faecal Elastase
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34
Q

What is the treatment of Chronic Pancreatitis?

A
  • Drugs: analgesia, lipase (Creon), fat-soluble vitamins
  • Diet: cessation of alcohol/smoking, low-fat diet, well-balanced diet
  • Endoscopic Therapy: ERCP (for stones/strictures of pancreatic duct)
  • Surgery: Pancreatectomy (if all else fails)
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35
Q

What are the clinical features of Pancreatic cancer?

A
  • Epigastric Pain -> radiates to back, relieved by sitting forwards
  • Painless Obstructive Jaundice (head of pancreas)
  • Weight Loss
  • Anorexia, Fatigue, Diarhoea/Steatorrhea, N+V
  • Thrombophlebitis migrans, Portal HT, Ascites
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36
Q

What are the first line investigations for Pancreatic cancer?

A
  • CT Scan (!!!)

- if still unclear: EUS + Biopsy

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37
Q

What is the treatment of Pancreatic cancer?

A

Radical

  • Resection (pancreatico-duodenectomy
  • Whipple’s (head of pancreas)

Palliative:

  • of Jaundice: ERCP or Percutaneous stent insertion +/- RFA
  • Pain: opiates, RT, coeliac plexus infiltration w bupivucaine (nerve block)
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38
Q

What are the most common causes of Chronic Liver Disease?

A
  • Chronic Hepatitis
  • Chronic Cholestasis
  • Fibrosis + Cirrhosis
  • Others: ie. Steatosis
  • Liver Tumours
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39
Q

What are the most common causes of Hepatic Cirrhosis?

A
  • Chronic alcohol abuse (!!!)
  • Chronic HBV or HCV infection (!!!)
  • Genetic disorders: Haemachromatosis, A1AT deficiency, Wilson’s disease
  • Hepatic vein events: Budd-Chiari
  • Non- Alcoholic: Steatohepatitis (NASH)
  • Auto-immunity: PBC, PSC, Autoimmune Hepatitis
  • Drugs: Amiodarone, Methyldopa, Methyltrexate
  • Others: Sarcoidosis, Amyloid, Schistosomiasis
40
Q

What are the clinical examination findings of Chronic Liver Disease?

A
  • Leuconychia
  • Clubbing
  • Palmar erythema
  • Dupuytren’s contracture
  • Spider naevi
  • Xanthelasma
  • Gynaecomastia, loss
    of body hair
  • Hepatomegaly
  • Jaundice
  • Altered mental status
  • Fetor Hepaticus
  • elevated JVP
  • Abdominal veins
41
Q

What are the clinical findings for Compensated Chronic Liver Disease?

A

no symptoms of disease!

Abnormality of LFTs
-> may be routinely detected on screening tests

42
Q

What are the clinical findings for Decompensated Chronic Liver Disease?

A
  • Jaundice
  • Ascites
  • Hepatorenal syndrome
  • Variceal bleeding
  • Hepatic Encephalopathy
43
Q

What are the 3 clinical presentations of Cirrhosis?

A
  • Compensated Chronic Liver Disease
  • Decompensated Chronic Liver Disease
  • Hepatocellular Carcinoma
44
Q

How is the diagnosis of Ascites made?

A
  • Abdominal Distension
  • Dullness in the Flanks
  • Shifting Dullness
  • Umbilical nodule
  • (additional signs of Chronic Liver Disease)
  • Confirmed by US
45
Q

What is the management of Ascites?

A

Diagnostic Paracentesis (!!!) (aka. Ascitic Tap)

  • > test for protein + albumin (SAAG) -> >1.1g/dl = high, <1.1g/dl = low
  • > WCC + differential
46
Q

What does a high SAAG value represent?

A
  • > 1.1g/dl -> transudate*
  • Portal HT
  • CHF
  • Constrictive Pericarditis
  • Budd-Chiarri
  • Myxedema
  • Massive Liver mets
47
Q

What does a low SAAG value represent?

A
  • <1.1g/dl -> exudate*
  • Malignancy
  • TB
  • Chylous Ascites
  • Pancreatitis
  • Biliary Ascites
  • Neprotic Syndrome
  • Serositis
48
Q

What are the treatment options for Ascites?

A
  • Diuretics (!!!) -> 1st line!!
  • Large-volume Paracentesis
  • TIPS (shunt)
  • Aquaretics
  • Liver transplantation (if all else fails)
49
Q

What are the treatment options for Hepatorenal Syndrome?

A
  • Terlipressin (!!!) -> 1st line -> vasoconstricts splanchnic vessels
  • Albumin -> volume expansion -> increases effective blood volume
  • TIPS -> decreases Portal HT
  • Liver transplant -> last resort!
50
Q

What is the pathogenesis of Hepatorenal Syndrome?

A

Portal HT -> NO release -> Splanchnic vasodilation -> decreased effective blood volume -> increased RAAS, Vasopressin release, increased SNS output -> increased renal vasoconstriction -> decreased renal blood flow, decreased GFR and Na+ retention

51
Q

Where is the management of a Variceal Haemorrhage?

A
  • Resuscitate pt.
  • Good IV access
  • Blood transfusion as required
  • Terlipressin (!!)
  • Endoscopic Band Ligation (!!) -> EMERGENCY!!
  • Sengstaken-Blakemore tube (for uncontrolled bleeding)
  • TIPS (if rebleed after banding)
52
Q

What are the precipitants of Hepatic Encephelopathy?

A

• GI bleed
-> proteins in blood get metabolised in the gut -> produces NH3

  • Infection
  • Constipation
  • Dehydration
  • Electrolyte Disturbance
  • Medication esp. sedation

all precipitate an altered mental state -> makes HE worse !!

53
Q

What are the clinical features of Hepatic Encephelopathy?

A
  • Flap -> Asterixis

- Foetor Hepaticus

54
Q

What causes Hepatic Encephelopathy?

A

Build up of toxins due to Chronic Liver Disease -> Liver cannot flush them away so they build up and accumulate in the body -> goes to the brain and causes an altered mental state

55
Q

What are the management of Hepatic Encephelopathy?

A
  • Treat underlying cause (of CLD)
  • Exclude: Infection, Hypoglycaemia, IC Bleed
  • > all contribute to reduced conscious levels
  • Laxatives: Lactulose (!!), Phosphate enemas
  • Broad-spectrum non-absorbed abx.: Rifaximin (!!)
    (-> removes the bacteria which are causing NH3 build-up )
56
Q

What is the most common cause of Hepatocellular Carcinoma?

A
  • Cirrhosis (caused by Chronic Hep B (!!) or Hep C infection)
57
Q

What are the clinical features of Hepatocellular Carcinoma?

A
  • Decompensation of Liver Disease (ie. Ascites, Varices, HRS, HE, etc)
  • Abdominal Mass
  • RUQ pain
  • Fatigue, Anorexia, Weight loss
  • Jaundice
58
Q

What are the investigations of Hepatocellular Carcinoma?

A

AFP (tumour marker) + US!

59
Q

What is the most common cancer in the Lung?

A

Secondary metastases!

Men: CRC
Women: Breast

60
Q

What are the treatment options of Hepatocellular Carcinoma?

A
  • Hepatic resection
  • Liver Transplant
  • Percutaneous Ablation: alcohol, RFA
  • Chemo: TACE (Transcatheter arterial chemo-embolisation, Sorafenib
61
Q

What is the chemical byproduct of alcohol that causes unpleasant symptoms when drinking alcohol?

A

Acetaldehyde = toxic metabolite

62
Q

How does alcohol cause Hypoglycaemia?

A
  • Increases NADH formation
  • > increases NADH/NAD ratio
  • Excess NADH favours the formation of Pyruvate to Lactic Acid
  • This results in less Pyruvate available for Gluconeogenesis -> Hypoglycaemia!
63
Q

How is alcohol metabolised in the Liver?

A
  • Ethanol -> Acetaldehyde (forms NADH)

Excess NADH contributes to…

  • Pyruvate -> Lactic acid formation (-> Lactic acidosis)
  • Lipogenesis (-> excess lipids)
  • It contributes to the Electron Transport Chain where it produces energy
64
Q

What are the screening tests used for Alcoholism?

A

CAGE:
- Have you ever felt the need to Cut down?
- Have you been Annoyed by criticism of your drinking?
- Have you felt Guilty about your drinking?
- Do you need an Eyeopener?
score >2 = problematic drinking

FAST/AUDIT:

  • FAST score of 3 or more is positive
  • If FAST +ve -> complete remaining AUDIT questions to obtain full AUDIT score
65
Q

What is the weekly recommended intake of alcohol for men and women?

A

14 units for both men and women

66
Q

What are the clinical features of Alcoholic Hepatitis?

A
  • Jaundice
  • Hepatic Encephalopathy

• Muscle wasting
-> less eating due to increased alcohol consumption

  • Infection common
  • signs of Decompensated Liver function
67
Q

What are the investigations of Alcohol-related Liver disease?

A
  • Labs: AST>ALT (2:1) (!!!), raised Gamma GT, raised Bilirubin
  • USS Fatty Liver
68
Q

What are the common complications of Alcoholic-related Liver disease?

A
  • Hepatic Encephaloathy
  • Spontaneous Bacterial Peritonitis
  • Alcoholic Hepatitis
  • Steatosis, Steatohepatitis
69
Q

What are the clinical features of Spontaneous Bacterial Peritonitis?

A

Suspect in any pt. with Ascites who deteriorates suddenly

  • Abdominal Pain
  • Fever, Rigors
  • Renal impairment
  • Signs of Sepsis, tachycardia, temperature
70
Q

What is the management of Spontaneous Bacterial Peritonitis?

A
  • Diagnostic Paracentesis (!!!) (aka. Ascitic Tap)

EXUDATE:

  • > high WCC (>0.25 x10^9/L) - esp. Neutrophils
  • > low protein (<25g/L)
71
Q

What is the treatment of Spontaneous Bacterial Peritonitis?

A
  • IV abx
  • Ascitic Fluid Drainage
  • IV Albumin infusion (20% ALBA)
72
Q

What is the treatment of Alcoholic Hepatitis?

A
  • Supportive
  • Treat infection
  • Treat HE
  • Treat alcohol withdrawal
  • Protect against GI bleeding (increased risk)
  • Airway protection/ITU
  • Oral Steroids (!!) -> only if grading severe (only if >9 on Glasgow Alcoholic Hepatitis score)
  • Nutritional (!!): Thiamine (vit B1), frequent feeds, high energy requirements
  • > 100% pts w alcoholic hepatitis are malnourished
73
Q

What are the clinical features of Steatohepatitis (NAFLD)?

A
  • Asymptomatic (25-40% of population -> probably the chief cause of mildly raised
    LFTS in the general population)
  • Raised ALT (ALT > AST)
74
Q

What are the investigations for Steatohepatitis (NAFLD)?

A
  • Diagnosis of exclusion!*
  • Fatty Liver on USS
  • Liver Biopsy (gold-standard!)
75
Q

What are the risk factors for Steatohepatitis (NAFLD)?

A
  • Obesity
  • DM
  • Hypercholesterolaemia
76
Q

What is the treatment of Steatohepatitis (NAFLD)?

A
  • Weight Loss
  • Exercise

no pharmaceutical treatment available!

77
Q

What are the functions of the Liver?

A

• Synthetic Function
-> clotting factors, bile, glucose, albumin, lipids, hormones (IGF-1, angiotensinogen)

• Detoxification
-> of drugs, bilirubin metabolism (conjugation), urea from NH3, breakdown of insulin + hormones

• Immune Function
-> first portal of entry from the gut

• Storage Function
-> stores glycogen, vitamin A, D, B12 and K, copper + iron

78
Q

What would a raised ALP indicate?

A
  • Obstruction of the bile ducts (ie. ?gallstones)
  • Bone disorders (ie. paget’s osetomalacia, fractures, etc)
  • Pregnancy (placenta)
  • Intestinal disorders (ie. PU, bowel perforation, etc)
  • Cancer mets (Liver/bone)
79
Q

What would a raised AST indicate?

A

Alcoholic Liver Disease

AST:ALT ratio -> 2:1

80
Q

What is Gamma GT used for?

A
  • used to confirm Liver source of ALP
    (-> if both Gamma GT + ALP raised then it is confirmed biliary disease)
  • elevated with ALD
  • NSAIDs also raise levels
81
Q

What does low albumin signify?

A
  • Chronic Liver disease
    (-> problem w synthetic function of the Liver)
  • Kidney disorders
  • Malnutrition
82
Q

Why is Prothrombin Time used in LFTs?

A
  • Tells us degree of liver dysfunction
    (-> Liver makes clotting factors)
  • used in scoring systems to decide the stage of Liver disease to decide who needs + gets a Liver transplant
83
Q

Why is Creatinine used in LFTs?

A
  • Marker of Renal function
  • Determines survival from Liver disease
  • Critical marker in determining the need for Liver transplant
84
Q

Why is Platelet count used in LFTs?

A

Platelets low in Cirrhotic pts. due to…

  • Splenomegaly (therefore, an indirect marker of Portal HT), and
  • lack of Thrombopoeitin from the Liver (due to liver damage)
85
Q

At what circulating Bilirubin level is Jaundice detectable?

A

Detectable when total plasma bilirubin levels exceed 34 µmol/L

86
Q

What is Jaundice?

A

Yellowing of the skin, sclerae, and other tissues caused by excess circulating Bilirubin

87
Q

Describe Bilirubin metabolism

A
  • old/damaged RBCs broken down to Haem + Globin in the Spleen (“RBC’s graveyard”)
  • Haem broken down to Bilirubin in the circulation (unconjugated)
  • Bilirubin conjugated in the Liver
  • unconjugated Bilirubin is reabsorbed via Enterohepatic circulation
  • conjugated Bilirubin is metabolised by intestinal lumen bacteria to form stercobilin (excreted in faeces) and urobilin (reabsorbed + excreted in urine)
88
Q

What causes Pre-Hepatic Jaundice?

A

Haemolysis

unconjugated bilirubin

89
Q

What clues in the history would suggest Pre-Hepatic Jaundice?

A
  • History of Anaemia (fatigue, dyspnoea, chest pain)

- Acholuric Jaundice
-> bilirubin is unconjugated and cannot get released into the urine

90
Q

What clues in the history would suggest Hepatic Jaundice?

A
  • Risk factors for Liver disease (ie. IVDU, drug intake)

- Decompensation (ascites, variceal bleed, HE)

91
Q

What clues in the history would suggest Post-Hepatic Jaundice?

A
  • Abdominal pain (RUQ, radiates to back/shoulders)
  • Cholestasis (pruritus, pale stools, high coloured urine)
    (-> due to conjugated bilirubin all coming out in the urine but not able to come out in the stools)
92
Q

What clues in the examination would suggest Pre-Hepatic Jaundice?

A
  • Pallor

- Splenomegaly

93
Q

What clues in the examination would suggest Hepatic Jaundice?

A
  • Stigmata of CLD (spider naevi, gynaecomastia)
  • Ascites (abdominal distension, shifting dullness)
  • Asterixis (Flapping Tremor -> HE!)
94
Q

What clues in the examination would suggest Post-Hepatic Jaundice?

A
  • Palpable GB (RUQ)

Courvoisier’s sign

95
Q

What is the usual cause of painful vs. painless obstructive Jaundice?

A
  • painful = indicates gallstone aetiology

- painless = indicates tumours (nb, cancer!!)

96
Q

What investigations would you do for Jaundice?

A
  • Liver screen: ?type of Liver damage
  • > Hep B, C serology, autoantibody profile, caeruloplasmin + copper (Wilson’s), ferritin + transferrin (haemachromatosis), A1AT, fasting glucose + llipids
  • Abdominal US (!!!)
  • > ?obstruction, ?portal HT, ?cancer
  • CT scan (usually requested in 2ary care)

Alimentary System (11 decks)

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