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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
When is purulent appendicitis most common?
During epidemics of chickenpox in children
26
What processes are affected by liver disease?
``` Bile production Carb, protein and lipid metabolism Protein synthesis Vitamin D synthesis Detoxification Vitamin and mineral storage Phagocytosis ```
27
What do liver function tests assess?
Hepatocellular damage through aminotransferases and gamma-glutamyl transpeptidase Cholestasis through bilirubin and alkaline phosphate Synthetic function though albumin and prothrombin time
28
What are the 3 classifications of jaundice?
prehepatic (haemolytic) hepatic (parenchymal) Post hepatic (cholestatic)
29
What is pre-hepatic jaundice?
Excessive haemolysis - liver unable to cope with excess bilirubin
30
What is found in the blood of a patient with pre-hepatic jaundice?
``` Unconjugated hyperbilirubinaemia Reticulocytosis Anaemia Increased LDH Decreased haptoglobin ```
31
What causes pre-hepatic jaundice?
Genetics - red cell membrane defects, haemoglobin abnormalities, metabolic defects Congenital hyperbilirubinaemias Immune, mechanical, acquired defects, infections, drugs, burns
32
What is hepatocellular jaundice?
Deranged hepatocyte function. An element of cholestasis
33
What are the lab findings of hepatocellular jaundice?
Mixed unconjugated and conjugated hyperbilirubinaemia Increased liver enzymes - reflects liver damage Abnormal clotting
34
What causes hepatocellular jaundice?
``` Congenital - Gilbert's syndrome, Crigler-Najjar syndrome Hepatic inflammation Drugs Cirrhosis Hepatic tumours ```
35
What is post-hepatic/cholestatic jaundice?
Obstruction of the biliary system - intra/extahepatic | Passage of conjugated bilirubin blocked
36
What are the lab findings of post-hepatic/cholestatic jaundice?
``` Conjugated hyperbilirubinaemia Bilirubin in urine No urobilinogen in urine Increased canalicular enzymes Increased liver enzymes (mild hepatocyte damage) ```
37
What are the potential causes of intrahepatic post-hepatic jaundice?
hepatitis drugs Cirrhosis Primary biliary cirrhosis
38
What are the potential causes of extrahepatic post-hepatic jaundice?
``` Gallstones Biliary stricture Carcinoma Pancreatitis Sclerosing cholangitis ```
39
What are the stages of damage in hepatitis?
Acute -> chronic Acute hepatocyte breakdown - aminotransferase release, jaundice Prolonged /chronic damage - synthetic failure, decreased albumin, decreased clotting factors
40
What are the potential causes of hepatitis?
Viral Autoimmune Drugs Hereditary
41
What is the pathology of alcoholic liver diseae?
Fatty changes Alcoholic hepatitis Cirrhosis
42
What are the potential complications of alcoholic liver disease?
``` Hepatocellular carcinoma Liver failure Wernicke-Korsakoff syndrome Encephalopathy Dementia Epilepsy ```
43
What is liver cirrhosis?
Liver cell necrosis followed by nodular regeneration and fibrosis, resulting in increased resistance to blood flow and deranged liver function
44
What are the potential causes of liver cirrhosis?
``` Alcohol Hep B & C Biliary cirrhosis Autoimmune hepatitis Haemochromatosis Wilson's disease ```
45
What are the clinical features of liver cirrhosis?
``` Liver dysfunction: -Jaundice -Anaemia -Bruising -Palmar erythema -Dupuytren's contracture -Portal hypertension Spontaneous bacterial peritonitis ```
46
What causes GIt ischaemia?
Arterial disease, systemic hypotension or intestinal venous thrombosis
47
What investigation results confirm a diagnosis of liver cirrhosis?
``` Increase ALT/AST/ALP Increased bilirubin Decreased Albumin Deranged clotting Decreased Na+ ```
48
What is the management of liver cirrhosis?
Stop drinking Treat complications Transplantation
49
What are the specific causes of primary biliary cirrhosis and what are the clinical features and treatment?
Chronic obstruction of the bile ducts Jaundice, pruritis, xanthelasma, hepatosplenomegaly Supportive treatment then liver transplant
50
What is the genetic inheritance of hereditary haemochromotosis?
Autosomal recessive | Abnormal iron transport -> iron depostion
51
What are the clinical features of hereditary haemochromatosis?
``` Heart - cardiomyopathy Pancreas - diabetes Pituitary - hypogonadism Liver - hepatitis/cirrhosis Skin - hyper pigmentation ``` Treat by venesection
52
What is the pattern of inheritance of Wilson's disease?
Autosomal recessive. Dissordered copper transport -> deposition
53
What are the clinical features of Wilson's disease?
Liver - hepatitis -> cirrhosis Basal ganglia - tremor, dysarthria, dementia Kidney - tubular degeneration Eyes - Kayser-Fleischer rings Treat with penecillamine
54
Describe alph 1 antitrypsin deficiency.
``` Autosomal recessive Deficient alpha 1 antitrypsin Liver cirrhosis Emphysema Transplant needed ```
55
Define portal hypertension
Portal venous pressure in excess of 20mmHg, resulting from intrahepatic or extra hepatic portal venous compression or occlusion
56
What are the causes of portal hypertension?
Obstruction of portal vein: congenital, thrombosis, extrinsic compression Obstruction of flow within liver: cirrhosis, hepatoportal sclerosis, schistomiasis, sarcoidosis
57
List 5 porto-systemic anastomoses.
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
What are the clinical manifestations of portal hypertension?
``` Splenomegaly Ascites Spider naevi Caput medusae Oesophageal/rectal varices - venous dilation, protrude into lumen, rupture/ulceration -> haemorrhage ```
59
Describe fulminant hepatic failure.
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
What are the causes of fulminant hepatic failure?
``` Hepatitis A, D, E Drugs Wilson's disease Pregnancy Reye's syndrome Alcohol ```
61
What are the features of fulminant hepatic failure?
``` Jaundice Encephalopathy decrease LOC Hypoglycaemia Decreased K+/Ca2+ Haemorrhage ```
62
What is the management of fulminant hepatic failure?
Specialist liver unit Supportive therapy Liver transplant
63
What is hepatic encephalopathy?
Reversible neurosychiatric deficit | Inability of liver to remove toxic substances (ammonia)
64
What might cause hepatic encephalopathy?
``` Sepsis/infection Constipation Diuretics GI bleeding Alcohol withdrawal ```
65
What are the clinical features of hepatic encephalopathy?
Flapping tremor Decreased LOC Personality changes Intellectual deterioration - constructional apraxia, slow, slurred speech
66
Name some benign hepatic tumours.
``` Haemangioma Focal nodular hyperplasia Liver cell adenoma Liver cysts Polycystic liver disease Cystadenoma ```
67
What is a malignant primary hepatic tumour called?
Hepatocellular carcinoma (HCC)
68
Where are secondary/metastases in the liver generally from?
``` 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
What pathological processes might cause diseases of the gallbladder and biliary tree?
Obstruction Infection Inflammation Neoplasia
70
What % of the population has cholelithiasis (gallstones)?
10-20%
71
What are the risk factors for gallstones?
``` Female Increasing age Obesity (rapid weight loss) Multiparity Diet Developed countries Drugs (OCP) Ileal disease/resection Haemolytic disease ```
72
What types of stones might cause cholelithiasis?
Pigment stones - calcium bilirubinate, multiple, small, black Pure cholesterol - usually solitary, up to 5cm (10%) Mixed - cholesterol with calcium and bile pigment (80%)
73
What can cholelithiasis cause?
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
What are the potential complications of cholelithiasis?
``` 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
How is mucocoele caused?
``` Impaction of stones, No superadded infection Mucus secretion Painful distension (Empyema also caused like this, with pus) ```
76
Describe ascending cholangitis.
``` Life threatening Charcot's triad: -RUQ pain -Jaundice -Fever ```
77
What is the function of the pancreas?
Endocrine - Insulin, glucagon, somatostatin | Exocrine - Fluid (HCO3-), Enzymes (proteolytic, amylase, lipolytic
78
What are the close anatomical relations of the pancreas?
Duodenum Common bile duct Portal vein Coeliac trunk
79
What is pancreatitis?
Inflamatory process caused by effects of enzymes released from pancreatic acini
80
What are the different types of pancreatitis?
Acute - oedema, haemorrhage, necrosis | Chronic - fibrosis, calcification
81
What are the potential causes of acute pancreatitis?
GET SMASHED Gallstones Ethanol Trauma ``` Steroids Mumps Autoimmune Scorpian bite Hyperlipidaemia ERCP/Iatrogenic Drugs ```
82
What is the pathogenesis of acute pancreatitis?
``` Duct obstruction - juice and bile reflux Acinar damage - from reflux or drugs Protease - tissue damage Lipase - fat necrosis Elastase - blood vessel destruction ```
83
What are the biochemical changes seen in acute pancreatitis?
Increased amylase, glycaemia and ALP/bilirubin | Decreased Ca2+
84
WHat are the clinical manifestations of acute pancreatitis?
``` Severe pain Vomiting Dehydration Shock/SIRS Ecchymosis Ileus ```
85
What is the prognostic classification of acute pancreatitis?
Clasgow/Ranson - Mild/severe
86
What is the treatment of acute pancreatitis?
Supportive
87
What is the mortality of acute pancreatitis?
Overall 10% Severe = 30% Haemorrhage = 50%
88
What happens to the pancreas in chronic pancreatitis?
Parenchymal destruction, fibrosis, loss of acini and duct stenosis
89
What causes chronic pancreatitis?
Chronic alcoholism | CF, inherited, biliary disease
90
What are the clinical manifestations of chronic pancreatitis?
Pain Malabsorption - steatorrhea, decreased albumin, weight loss DM Jaundice
91
What % of pancreatic carcinomas are ductal?
90%
92
What are the risk factors for pancreatic carcinoma?
Smoking Beta napthylamine Benzidine Familial pancreatitis
93
What are the clinical features of pancreatic carcinoma?
``` Initially symptomless Obstructive jaundice - palpable gallbladder Pain Vomiting Carcinomatosis Malabsorption Diabetes ```
94
What is the prognosis for pancreatic carcinoma?
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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