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Semester 3 > GI disorders > Flashcards

GI disorders Flashcards

1
Q

What innate physical barriers do we have that protect us from food poisoning?

A 
Sight
Smell
Memory
Saliva
Gastric acid
Small intestine secretions
Colonic mucus
Anaerobic environment 
Peristalsis/segmentation
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2
Q

What causes xerostomia and what might it result in?

A

Severe illness and/or dehydration results in reduced salivary flow which then leads to microbial overgrowth in the mouth and dental caries
Can lead to parotitis caused by Staph aureus

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3
Q

What is achlorhydira?

A

Do not produce gastric acid. More suceptible to shigellosis, cholera and salmonella.

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4
Q

What microorganisms are resistant to gastric acid?

A 
STB
Helicobacter pylori
Hep A
Polio
Coxsackie
Norovirus
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5
Q

How does the small intestine maintain a sterile environment?

A 
Secretions - proteolytic enzymes, bile
Lack of nutrients
Anaerobic environment
Shedding epithelial cells
Rapid transit (peristalsis)
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6
Q

What protects the colon?

A

Anaerobic environment

Mucus layer

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7
Q

What is the innate cellular protection in the body?

A 
Neutrophils
Macrophages
Natural killer cells
Tissue mast cells
Eosinophils
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8
Q

What cellular protection does the body have against worms?

A

Eosinophils

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9
Q

When might eosinophilia occur?

A

Asthma
Hay fever
Parasitic infections

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10
Q

How do mast cells cause massive fluid loss?

A

Gut infections can activate complement recruite mast cells which release histamine. This causes vasodilation and increased capillary permeability. In untreated cholera, can lose up to 1 l/hr. 60% mortality if untreated

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11
Q

Where do carbon particles localise if injected intravenously?

A

Lungs
Liver
Spleen

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12
Q

What is a portal system?

A

2 capillary systems in series eg. hepatic portal system, hypothalamo-hypophyseal portal system

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13
Q

Where are the 2 capillary systems in the hepatic portal system?

A

Villus and hepatic lobule

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14
Q

What are kupffer cells?

A

Macrophages in the liver

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15
Q

What might cause liver failure?

A 
Viral hepatitis
Alcohol
Drugs eg paracetomol
Industrial solvents
Mushroom poisoning
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16
Q

What does liver failure increase susceptibility to?

A

Infections
Toxins, drugs, hormones
Increased blood ammonia due to failure to clear

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17
Q

What does high ammonia in the body cause?

A

hepatic encephalopathy

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18
Q

What can result from hepatic fibrosis?

A

Leads to portal venous hypertension -> portosystemic shunting and therefore toxin shunting -> oesophageal varicose, haemorrhoids and caput medusae

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19
Q

What adaptive cellular defences do are bodies have?

A

B lymphocytes

T lymphocytes

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20
Q

Where is GALT usually distributed?

A

Tonsils
Peyer’s patches
Appendix

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21
Q

Why is there a lot of lymph tissue at the ileocaecal valve?

A

Lots of bacteria in large intestine which is harmful to the small intestine (likely if valve incompetent) Lymph there to provide appropriate defence if necessary

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22
Q

What is mesenteric adenitis?

A

Common cause of right iliac fossa pain in children can easily be mistaken for appendicitis. Caused mostly by adenovirus/coxsackie virus

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23
Q

How might typhoid fever kill patients?

A

Causes inflamed Peyer’s patches in terminal ileum which can perforate

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24
Q

How is appendicitis caused?

A

Lymphoid hyperplasia at the appendix base can lead to obstructed outflow - stasis=infection
May also be caused by obstruction by faecolith

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25
Q

When is purulent appendicitis most common?

A

During epidemics of chickenpox in children

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26
Q

What processes are affected by liver disease?

A 
Bile production
Carb, protein and lipid metabolism
Protein synthesis
Vitamin D synthesis
Detoxification
Vitamin and mineral storage 
Phagocytosis
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27
Q

What do liver function tests assess?

A

Hepatocellular damage through aminotransferases and gamma-glutamyl transpeptidase
Cholestasis through bilirubin and alkaline phosphate
Synthetic function though albumin and prothrombin time

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28
Q

What are the 3 classifications of jaundice?

A

prehepatic (haemolytic)
hepatic (parenchymal)
Post hepatic (cholestatic)

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29
Q

What is pre-hepatic jaundice?

A

Excessive haemolysis - liver unable to cope with excess bilirubin

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30
Q

What is found in the blood of a patient with pre-hepatic jaundice?

A 
Unconjugated hyperbilirubinaemia
Reticulocytosis
Anaemia
Increased LDH
Decreased haptoglobin
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31
Q

What causes pre-hepatic jaundice?

A

Genetics - red cell membrane defects, haemoglobin abnormalities, metabolic defects
Congenital hyperbilirubinaemias
Immune, mechanical, acquired defects, infections, drugs, burns

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32
Q

What is hepatocellular jaundice?

A

Deranged hepatocyte function. An element of cholestasis

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33
Q

What are the lab findings of hepatocellular jaundice?

A

Mixed unconjugated and conjugated hyperbilirubinaemia
Increased liver enzymes - reflects liver damage
Abnormal clotting

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34
Q

What causes hepatocellular jaundice?

A 
Congenital - Gilbert's syndrome, Crigler-Najjar syndrome
Hepatic inflammation
Drugs
Cirrhosis
Hepatic tumours
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35
Q

What is post-hepatic/cholestatic jaundice?

A

Obstruction of the biliary system - intra/extahepatic

Passage of conjugated bilirubin blocked

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36
Q

What are the lab findings of post-hepatic/cholestatic jaundice?

A 
Conjugated hyperbilirubinaemia 
Bilirubin in urine
No urobilinogen in urine
Increased canalicular enzymes
Increased liver enzymes (mild hepatocyte damage)
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37
Q

What are the potential causes of intrahepatic post-hepatic jaundice?

A

hepatitis
drugs
Cirrhosis
Primary biliary cirrhosis

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38
Q

What are the potential causes of extrahepatic post-hepatic jaundice?

A 
Gallstones
Biliary stricture
Carcinoma
Pancreatitis
Sclerosing cholangitis
39
Q

What are the stages of damage in hepatitis?

A

Acute -> chronic
Acute hepatocyte breakdown - aminotransferase release, jaundice
Prolonged /chronic damage - synthetic failure, decreased albumin, decreased clotting factors

40
Q

What are the potential causes of hepatitis?

A

Viral
Autoimmune
Drugs
Hereditary

41
Q

What is the pathology of alcoholic liver diseae?

A

Fatty changes
Alcoholic hepatitis
Cirrhosis

42
Q

What are the potential complications of alcoholic liver disease?

A 
Hepatocellular carcinoma
Liver failure
Wernicke-Korsakoff syndrome
Encephalopathy
Dementia
Epilepsy
43
Q

What is liver cirrhosis?

A

Liver cell necrosis followed by nodular regeneration and fibrosis, resulting in increased resistance to blood flow and deranged liver function

44
Q

What are the potential causes of liver cirrhosis?

A 
Alcohol 
Hep B & C
Biliary cirrhosis
Autoimmune hepatitis
Haemochromatosis
Wilson's disease
45
Q

What are the clinical features of liver cirrhosis?

A 
Liver dysfunction:
-Jaundice
-Anaemia
-Bruising
-Palmar erythema
-Dupuytren's contracture
-Portal hypertension
Spontaneous bacterial peritonitis
46
Q

What causes GIt ischaemia?

A

Arterial disease, systemic hypotension or intestinal venous thrombosis

47
Q

What investigation results confirm a diagnosis of liver cirrhosis?

A 
Increase ALT/AST/ALP
Increased bilirubin 
Decreased Albumin
Deranged clotting
Decreased Na+
48
Q

What is the management of liver cirrhosis?

A

Stop drinking
Treat complications
Transplantation

49
Q

What are the specific causes of primary biliary cirrhosis and what are the clinical features and treatment?

A

Chronic obstruction of the bile ducts
Jaundice, pruritis, xanthelasma, hepatosplenomegaly
Supportive treatment then liver transplant

50
Q

What is the genetic inheritance of hereditary haemochromotosis?

A

Autosomal recessive

Abnormal iron transport -> iron depostion

51
Q

What are the clinical features of hereditary haemochromatosis?

A 
Heart - cardiomyopathy
Pancreas - diabetes
Pituitary - hypogonadism
Liver - hepatitis/cirrhosis
Skin - hyper pigmentation

Treat by venesection

52
Q

What is the pattern of inheritance of Wilson’s disease?

A

Autosomal recessive. Dissordered copper transport -> deposition

53
Q

What are the clinical features of Wilson’s disease?

A

Liver - hepatitis -> cirrhosis
Basal ganglia - tremor, dysarthria, dementia
Kidney - tubular degeneration
Eyes - Kayser-Fleischer rings

Treat with penecillamine

54
Q

Describe alph 1 antitrypsin deficiency.

A 
Autosomal recessive
Deficient alpha 1 antitrypsin
Liver cirrhosis
Emphysema
Transplant needed
55
Q

Define portal hypertension

A

Portal venous pressure in excess of 20mmHg, resulting from intrahepatic or extra hepatic portal venous compression or occlusion

56
Q

What are the causes of portal hypertension?

A

Obstruction of portal vein: congenital, thrombosis, extrinsic compression
Obstruction of flow within liver: cirrhosis, hepatoportal sclerosis, schistomiasis, sarcoidosis

57
Q

List 5 porto-systemic anastomoses.

A

Oesophagea branch of left gastric vein (portal) and oesophageal tributaries of azygous system
Superior rectal branch of IMV (portal) and inferior rectal veins (systemic)
Portal tributaries of mesentery and retroperitoneal veins (systemic
Portal veins in liver and veins of anterior abdominal wall (systemic)
Portal branches in liver and diaphragm (bare area of liver)

58
Q

What are the clinical manifestations of portal hypertension?

A 
Splenomegaly
Ascites
Spider naevi
Caput medusae
Oesophageal/rectal varices - venous dilation, protrude into lumen, rupture/ulceration -> haemorrhage
59
Q

Describe fulminant hepatic failure.

A

An acute and/or severe decompensation of hepatic function, defined as ‘… onset of hepatic encephalopathy within 2 months after diagnosis of liver disease’, which may be liked to brain oedema.
Decompensation due to increased metabolic demand

60
Q

What are the causes of fulminant hepatic failure?

A 
Hepatitis A, D, E
Drugs
Wilson's disease
Pregnancy
Reye's syndrome
Alcohol
61
Q

What are the features of fulminant hepatic failure?

A 
Jaundice
Encephalopathy
decrease LOC
Hypoglycaemia
Decreased K+/Ca2+
Haemorrhage
62
Q

What is the management of fulminant hepatic failure?

A

Specialist liver unit
Supportive therapy
Liver transplant

63
Q

What is hepatic encephalopathy?

A

Reversible neurosychiatric deficit

Inability of liver to remove toxic substances (ammonia)

64
Q

What might cause hepatic encephalopathy?

A 
Sepsis/infection
Constipation
Diuretics
GI bleeding
Alcohol withdrawal
65
Q

What are the clinical features of hepatic encephalopathy?

A

Flapping tremor
Decreased LOC
Personality changes
Intellectual deterioration - constructional apraxia, slow, slurred speech

66
Q

Name some benign hepatic tumours.

A 
Haemangioma
Focal nodular hyperplasia
Liver cell adenoma
Liver cysts
Polycystic liver disease
Cystadenoma
67
Q

What is a malignant primary hepatic tumour called?

A

Hepatocellular carcinoma (HCC)

68
Q

Where are secondary/metastases in the liver generally from?

A 
Colorectal (50%)
Neuroendocrine
Pancreas
Breast
Stomach
Lung 
Ovary
Kidney

20 cases of liver metastases per 1 HCC
Majority of mets are due to portal venous drainage

69
Q

What pathological processes might cause diseases of the gallbladder and biliary tree?

A

Obstruction
Infection
Inflammation
Neoplasia

70
Q

What % of the population has cholelithiasis (gallstones)?

A

10-20%

71
Q

What are the risk factors for gallstones?

A 
Female
Increasing age
Obesity (rapid weight loss)
Multiparity
Diet
Developed countries
Drugs (OCP)
Ileal disease/resection
Haemolytic disease
72
Q

What types of stones might cause cholelithiasis?

A

Pigment stones - calcium bilirubinate, multiple, small, black
Pure cholesterol - usually solitary, up to 5cm (10%)
Mixed - cholesterol with calcium and bile pigment (80%)

73
Q

What can cholelithiasis cause?

A

Biliary colic - impaction of stones, gallbladder conract, intermittent pain (post prandial)
Cholecystitis - Stones (maybe acalculus (ischaemia/infection). Oedema -> mucosa, ulceration -> fibropurulent exudate, pain, SIRS, pyrexia, sepsis

74
Q

What are the potential complications of cholelithiasis?

A 
Mucocoele
Empyema
Obstructive jaundice
Ascending cholangitis
Acute pancreatitis
Biliary-enteric fistula/gallstone ileus 
Gallbladder carcinoma - 2% of all cancers, associated with gallstones
Gallbladder perforation
75
Q

How is mucocoele caused?

A 
Impaction of stones,
No superadded infection
Mucus secretion
Painful distension
(Empyema also caused like this, with pus)
76
Q

Describe ascending cholangitis.

A 
Life threatening
Charcot's triad:
-RUQ pain
-Jaundice
-Fever
77
Q

What is the function of the pancreas?

A

Endocrine - Insulin, glucagon, somatostatin

Exocrine - Fluid (HCO3-), Enzymes (proteolytic, amylase, lipolytic

78
Q

What are the close anatomical relations of the pancreas?

A

Duodenum
Common bile duct
Portal vein
Coeliac trunk

79
Q

What is pancreatitis?

A

Inflamatory process caused by effects of enzymes released from pancreatic acini

80
Q

What are the different types of pancreatitis?

A

Acute - oedema, haemorrhage, necrosis

Chronic - fibrosis, calcification

81
Q

What are the potential causes of acute pancreatitis?

A

GET SMASHED
Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpian bite
Hyperlipidaemia
ERCP/Iatrogenic
Drugs
82
Q

What is the pathogenesis of acute pancreatitis?

A 
Duct obstruction - juice and bile reflux
Acinar damage - from reflux or drugs
Protease - tissue damage
Lipase - fat necrosis
Elastase - blood vessel destruction
83
Q

What are the biochemical changes seen in acute pancreatitis?

A

Increased amylase, glycaemia and ALP/bilirubin

Decreased Ca2+

84
Q

WHat are the clinical manifestations of acute pancreatitis?

A 
Severe pain
Vomiting
Dehydration
Shock/SIRS
Ecchymosis
Ileus
85
Q

What is the prognostic classification of acute pancreatitis?

A

Clasgow/Ranson - Mild/severe

86
Q

What is the treatment of acute pancreatitis?

A

Supportive

87
Q

What is the mortality of acute pancreatitis?

A

Overall 10%
Severe = 30%
Haemorrhage = 50%

88
Q

What happens to the pancreas in chronic pancreatitis?

A

Parenchymal destruction, fibrosis, loss of acini and duct stenosis

89
Q

What causes chronic pancreatitis?

A

Chronic alcoholism

CF, inherited, biliary disease

90
Q

What are the clinical manifestations of chronic pancreatitis?

A

Pain
Malabsorption - steatorrhea, decreased albumin, weight loss
DM
Jaundice

91
Q

What % of pancreatic carcinomas are ductal?

A

90%

92
Q

What are the risk factors for pancreatic carcinoma?

A

Smoking
Beta napthylamine
Benzidine
Familial pancreatitis

93
Q

What are the clinical features of pancreatic carcinoma?

A 
Initially symptomless
Obstructive jaundice - palpable gallbladder
Pain
Vomiting
Carcinomatosis
Malabsorption
Diabetes
94
Q

What is the prognosis for pancreatic carcinoma?

A

5th of cancer death in UK (5%)
REsective surgery best current treatment but only 5-15% suitable, risks considerable morbidity and mortality, 15-35% 5 year survival rate

Overall, 1-year survival rate approx 12%

Semester 3 (19 decks)

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