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Semester 3 > GI Session 7 > Flashcards

GI Session 7 Flashcards

1
Q

What are the innate physical defences against toxins?

A 
Sight
Smell
Memory
Saliva
Gastric acid
Small intestinal secretions
Colonic mucus
Anaerobic conditions in small bowel and colon
Peristalsis and segmentation
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2
Q

What components of saliva allow it to be an effective defence when dealing with toxins?

A 
Lysozymes for G+ve
Lactoperoxidase for G-ve
Complement
IgA
Polymorphs
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3
Q

What are the innate cellular defences against toxins in the GI tract?

A 
Neutrophils
Eosinophils
Basophils
Macrophages
Natural killer cells
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4
Q

When is eosinophilia seen?

A

Asthma
Hay fever
Parasitic infection

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5
Q

What are the captive immune defences against toxin insult in the GI tract?

A

B lymphocytes release IgA and IgE for extracellular microbes

T lymphocytes act against intracellular microbes in MALT

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6
Q

What is xerostomia?

A

Decreased salivary flow due to severe illness and/or dehydration

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7
Q

How does xerostomia lead to parotitis?

A

S.aureus overgrowth in mouth –> dental caries –> microbes up Warton’s duct –> parotitis

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8
Q

What does xerostomia predispose to in the mouth?

A

Candida albicans (thrush) and lingua villosa nigra (black hairy tongue) due to fungal overgrowth

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9
Q

What defences does the oesophagus have against toxins?

A

Flow of liquids

Peristalsis

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10
Q

What defences does the stomach have against toxins?

A

2.5 l of gastric juice with pH as low as 0.87

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11
Q

Does the gastric juice in the stomach kill all bacteria and viruses?

A

No

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12
Q

What defences does the small intestine have against toxins?

A 
Bile acting as a detergent so normally sterile
Proteolytic emzymes
Anaerobic environment
Shedding of epithelial cells
Peristalsis
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13
Q

What defences does the colon have against toxins?

A

Anaerobic environment for water recovery –> faeces 40% bacteria
Mucous layer

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14
Q

Why are early morning gastric washings used to diagnose TB?

A

M.tuberculosis is resistant to gastric acid

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15
Q

What viruses are resistant to gastric acid?

A

Enteroviruses e.g. Hep A, polio, coxsackie and norovirus

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16
Q

What effect does achlorhydia have on susceptibility to infection?

A

Increases

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17
Q

What can cause achlorhydia?

A

Pernicious anaemia
H2 antagonists
PPIs

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18
Q

What infections can achlorhydia lead to?

A

Shigellosis
Cholera
Salmonella

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19
Q

What causes pseudomembranous colitis in hospital pts taking PPIs?

A

C.diff

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20
Q

What can lead to loss of mucosa and other colonic defences causing overwhelming sepsis and rapid death?

A

Intestinal or hepatic ischaemia due to arterial disease, systemic hypotension or intestinal venous thrombosis

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21
Q

What toxins can the GI tract be exposed to?

A 
Chemical
Bacterial
Viruses
Protozoa
Nematodes (roundworms)
Cestodes (tapeworms)
Trematodes (flukes)
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22
Q

What is a portal blood system?

A

2 capillary systems in series

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23
Q

What are the two capillary systems involved in the hepatic portal system?

A

Feedin arteriole and draining venule of a villus

Hepatic lobule capillary system

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24
Q

What is the purpose of the hepatic lobule capillary system?

A

Provides bloodflow for highly active cells surrounding bile canaliculi to transport waste materials out of hepatic sinusoids

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25
Q

What can cause liver failure?

A 
Viral hepatitis
Alcohol
Drugs
Industrial solvents
Mushroom poisoning
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26
Q

What are the consequences of liver failure?

A

Increased susceptibility to infections, esp bacterial but also fungal
Increased susceptibility to toxins, drugs and hormones
Increased blood ammonia

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27
Q

Why do blood ammonia levels rise in liver failure?

A

Production by colonic bacteria and deamination of a.a. not cleared

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28
Q

What is cirrhosis?

A

Hepatic fibrosis

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29
Q

What are the consequences of portosystemic shunting due to portal venous hypertension?

A

Toxin shunting
Oesophageal Varices
Haemorrhoids
Caput medusae

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30
Q

What movement of veins occurs at the oesophogastric and anorectal junctions?

A

Cross from siting in the serosa to below mucosa

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31
Q

What is Caput medusa?

A

Pressure changes in portal venous hypertension –> bloodflow into obliterated L umbilical vein as the porta hepatis drains into it

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32
Q

What does the bloodflow of the tortuous veins in Caput medusa indicate?

A

Whether they are due to SVC obstruction, IVC obstruction or portal venous hypertension

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33
Q

What is Harvey’s test?

A

Assess cause of Caput medusa
Empty veins by applying pressure and observe refill speed: travelling upwards is faster than travelling downwards
Repeat in opposite direction to check

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34
Q

Where is GALT found?

A

Diffusely distributed and nodular in tonsils, Peyer’s patches and appendix

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35
Q

What are the three sets of tonsils?

A

Palatine
Lingual
Nasopharyngeal (adenoids)

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36
Q

Where do the tonsils drain?

A

Cervical LN associated with deep jugular vein

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37
Q

What is the purpose of iliocaecal lymphatic tissue?

A

Protect against bacterial reflux from the colon as mucosa here is not sufficient

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38
Q

What can cause appendicitis?

A

Lymphoid hyperplasia at appendix base
Faecolith
Chicken pox –> purulent appendicitis in children

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39
Q

What is the pathogenesis of typhoid fever?

A

Causes inflammation of Peyer’s patches in terminal ileum –> perforation –> death

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40
Q

What is the pathogenesis of mesenteric adenitis?

A

RIF pain in children due to adenovirus/coxsackie virus invading LN at terminal ileum

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41
Q

Why do chemical toxins such as metals/metaloids/solvents/drugs lead to multi organ failure?

A

They have developed quicker than our defences to them

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42
Q

Which enzyme conjugates bilirubin in the liver?

A

Glucuronyltransferase

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43
Q

Why does urobilinogen not colour urine?

A

It is soluble

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44
Q

What is prehepatic jaundice?

A

Excessive haemolysis and the liver cannot cope with the excess bilirubin

45
Q

What can cause inherited prehepatic jaundice?

A 
RBC membrane defects
Hb abnormalities
Metabolic defects
Congenital hyperbilirubinaemia
Gilbert's syndrome
Dublin-Johnson syndrome (affected transporter protein)
46
Q

What can cause acquired prehepatic jaundice?

A

Immune disease
Infection
Drugs
Burns

47
Q

Why are the lab findings in prehepatic jaundice?

A 
Unconjugated hyperbilirubinaemia 
Reticulocytosis
Anaemia
Increased LDH
Decreased haptoglobin
48
Q

What causes decreased haptoglobin in prehepatic jaundice?

A

Binding with Hb

49
Q

What is hepatic jaundice?

A

Deranged hepatocytes function and swelling of hepatocytes

50
Q

What are congenital causes of hepatic jaundice?

A

Gilbert’s or Crigler-Najjor syndromes

51
Q

What are acquired causes of hepatic jaundice?

A 
Hep viruses
EBV
Autoimmune disease
Alcohol
Haemachromatosis
Wilson's disease
Drugs
Cirrhosis
Widespread hepatic tumours
52
Q

What are the lab findings in hepatic jaundice?

A

Mixed unconjugated/conjugated hyperbilirubinaemia
Raised AST/ALT
Normal or raised ALP
Abnormal clotting: raised INR and decreased platelets

53
Q

Why might ALP be raised in hepatic jaundice?

A

Due to cholestasis from swollen cells

54
Q

What is post-hepatic jaundice?

A

Intra/extrahepatic obstruction of the biliary system blocking passage of conjugate bilirubin

55
Q

What can cause post-healthcare jaundice?

A

Intrahepatic: hepatitis, drugs, cirrhosis, primary biliary cirrhosis
Extrahepatic (distal to bile canaliculi): gallstones, biliary stricture, carcinoma, pancreatitis, sclerosing cholangitis

56
Q

What are the lab findings in post-hepatic jaundice?

A 
Conjugated hyperbilirubinaemia 
Dark urine
Lack of urobilinogen
Raised canalicular enzymes
Normal or increased AST and ALT
57
Q

Why is there no urobilinogen in post-hepatic jaundice?

A

No bilirubin in bowel so none formed

58
Q

Why might AST and ALT be raised in post-hepatic jaundice?

A

Mild hepatocyte damage due to build up of pressure

59
Q

What LFTs indicate hepatocellular damage?

A 
Raised aminotransferases (AST and ALT)
Increased gamma-glutamyl transpeptide
60
Q

What LFTs indicate cholestasis?

A

Raised bilirubin

Raised alkaline phosphatase (ALP)

61
Q

What LFTs indicate impaired synthetic function of the liver?

A 
Decreased albumin
Increased prothrombin (raised INF and decreased platelets)
62
Q

What is the pathogenesis of acute/chronic hepatitis?

A

Virus, autoimmune, drug or herditary cause –> acute hepatocyte breakdown –> increased aminotransferases and jaundice –> decreased albumin and clotting factors

63
Q

What is alpha-1-antitrypsin disease?

A

Autosomal recessive condition causing hepatitis and emphysema in bases of lungs

64
Q

What is the Tx for hepatitis caused by alpha-1-antitrypsin deficiency?

A

Transplant

65
Q

What is Wilson’s disease?

A

Autosomal recessive condition causing copper deposition in liver, basal ganglia, kidney and eyes

66
Q

What is the Tx for hepatitis caused by Wilson’s disease?

A

Penecillamine (chelating agent)

67
Q

What is the pathogenesis of alcoholic liver disease?

A

Alcohol consumption and probable genetic factors –> fatty change –> alcoholi helatitis –> cirrhosis

68
Q

What are the consequence of alcoholic cirrhosis?

A 
Epilepsy
Hepatocellular carcinoma
Liver failure
Wernicke-Korsakoff syndrome
Encephalopathy 
Cerebral atrophy --> dementia
69
Q

What is the pathogenesis of liver cirrhosis?

A

Chronic inflammation –> liver cell necrosis –> nodular regeneration and fibrosis –> increased bloodflow resistance and deranged liver function

70
Q

What is the pathogenesis of biliary cirrhosis?

A

Autoimmune chronic destruction of bile ducts –> jaundice, pruritis, xanthelasma and hepatosplenomegaly

71
Q

What is Haemachromatosis?

A

Autosomal recessive condition causing deposition of iron in heart, pancreas, pituitary, liver and skin

72
Q

What is the Tx haemachromatosis?

A

Venesection

73
Q

What are the consequences of liver cirrhosis?

A 
Spontaneous bacterial peritonitis
Jaundice
Anaemia
Brushing
Palmar erythema
Dupuytren's contracture
Portal hypertension
74
Q

What can cause obstruction of the portal vein leading to portal hypertension?

A

Congenital
Thrombosis
Extrinsic compression

75
Q

What can cause obstruction of bloodflow in the liver leading to portal hypertension?

A

Cirrhosis
Hepatoportal sclerosis
Schistosomiasis
Sarcoidosis

76
Q

What are the consequences of portal hypertension?

A 
Splenomegaly
Ascites
Spider naevi
Caput medusa
Oesophageal/rectal Varices
77
Q

What causes spider naevi in portal hypertension?

A

Resp ducked oestrogen removal by the liver

78
Q

What is fulminant hepatic failure?

A

An acute and/or severe decompensation of hepatic function with onset of hepatic encephalopathy within 2 months of liver disease diagnosis

79
Q

What is seen in fulminant hepatic failure before supportive treatment +/- transplant?

A 
Jaundice
Encephalopathy
Decreased level of consciousness
Hypoglycaemia
Decreased K+/Ca2+
Haemorrhage
80
Q

What indicates urgent transplant in fulminant hepatic failure?

A

Hypoglycaemia

81
Q

What can cause fulminant hepatic failure?

A 
Hep A,D,E
Drugs
Reye's syndrome
Alcohol
Pregnancy
82
Q

What is hepatic encephalopathy?

A

Reversible neuropsychiatric deficit caused by raised toxin levels in the blood

83
Q

Why does ammonia especially cause hepatic encephalopathy?

A

Urea cycle function impaired –> small ammonia can pass through the BBB causing toxicity and brain swelling

84
Q

What are the S/S of hepatic encephalopathy?

A 
Flapping tremor
Decreased level of consciousness
Personality changes
Constructional apraxia
Slow, slurred speech
85
Q

What can a liver failure pt experience that leads to development of hepatic encephalopathy?

A 
Sepsis
Infection
Constipation
Diuretic Tx
Alcohol withdrawal
86
Q

What are the majority of liver metastases due to?

A

50% from colorectal tumours metastasising via portal venous drainage

87
Q

How does the incidence of primary liver tumours compare to the incidence of liver metastases?

A

20x more metastases

88
Q

What type of benign tumour can develop in the liver?

A

Haemangioma
Focal nodular hyperplasia
Polycystic liver disease

89
Q

How does the gallbladder change depending on how long it takes a gallstone to form?

A

Long time –> shrunken, fibrotic gallbladder

Short time –> large gallbladder

90
Q

What can prevent passage of bile from the liver to the duodenum?

A 
Gallstones
Gallbladder structures
Gallbladder atresia in neonates
Infection
Inflammation
Neoplasia
91
Q

What are the risk factors for developing cholelithiasis (gallstones)?

A 
Female
Age
Obesity with rapid weight loss
Diet
Multiparity
Ileal disease
Resection --> interruption of enterohepatic circulation
Haemolytic disease
92
Q

What three type of gallstones can develop?

A

Mixed
Pure cholesterol
Pigment stones

93
Q

What is the most common type of gallstone?

A

Mixed

94
Q

What is found in mixed gallstones?

A

Cholesterol
Calcium
Pigment

95
Q

What is the pathogenesis of biliary colic?

A

Impaction of stone in Hartman’s pouch –> gallbladder contraction–> post prandial pain

96
Q

What is the pathogenesis of cholecystitis?

A

Stones –> localised oedema –> mucosa ulceration –> fibropurulent exudate –> pain, SIRS, pyrexia, sepsis

97
Q

What is ascending cholangitis?

A

Where stone blocks common bile duct and causes inflammation proximal to blockage

98
Q

What is Charcot’s triad?

A

RUQ pain + jaundice + fever

Indicates life threatening condition requiring urgent Abx

99
Q

How do gallstones lead to biliary enteric fistula and gallstone ileus?

A

Fistula eroded between gallbladder and duodenum –> large stone obstructs ileum

100
Q

What are 90% of pancreatic cancers?

A

Ductal adenocarcinoma

101
Q

What are the causes of acute pancreatitis?

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion bite (Trinidad)
Hyperlipidaemia
ERCP/iatrogenic
Drugs
102
Q

What happens in acute pancreatitis?

A 
Duct obstruction --> juice and bile reflux
Acinar damage --> reflux
Protease--> tissue destruction
Lipase--> fat necrosis
Elastase--> BV destruction
103
Q

What are the S/S of acute pancreatitis?

A 
Severe pain
Vomiting
Dehydration
Shock
Ecchymosis
Raised amylase, ALP, bilirubin and reduced calcium
Glycaemia
104
Q

What is the pathogenesis of chronic pancreatitis?

A

Chronic alcoholism/CF/inherited/biliary disease –> chronic inflammatory condition –> parenchymal destruction, fibrosis, loss of acini, duct stenosis

105
Q

What are the S/S of chronic pancreatitis?

A 
Pain
Malabsorption--> steatorrhoea
Decreased albumin
Weight loss
DM
Jaundice
106
Q

What Tx can be used in acute pancreatitis?

A

Supportive: ITU, fluids ?Abx

107
Q

What Tx can be used in chronic pancreatitis?

A

Lifestyle changes
Steroids
Supportive

108
Q

What is a Whipple procedure?

A

Surgical procedure which removes gallbladder and uses Y loop to reroute small intestine around pancreas to treat S/S of pancreatic disease

109
Q

What S/S indicate use of Whipple procedure?

A 
Palpable gallbladder
Pain due to coeliac trunk compression
Vomiting
Carcinomatosis
Malabsorption
DM

Semester 3 (50 decks)

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