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ESA3 > Gastrointestinal System > Flashcards

Gastrointestinal System Flashcards

1
Q

What are the functions of the gastrointestinal tract?

A

Mechanical disruption of food, temporary food store, chemical digestion and disruption, kill pathogens, absorption of nutrients, elimination of waste material.

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2
Q

How is fluid balance maintained?

A

Somatic and autonomic neural control, histamine, hormones and vasoactive substances alter blood flow and acid secretion, enzymes produced for chemical digestion.

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3
Q

What is saliva?

A

Hypotonic fluid containing water, mucus and solids such as enzymes, bacterial flora, antibodies and epithelial cells.

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4
Q

What is the function of baseline saliva secretion?

A

Maintenance of hydration, reduces friction, prevents bacterial build up (halitosis) and maintenance of dental hygiene.

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5
Q

Name the main salivary glands and the type of secretion they produce:

A

Sublingual- mixed secretions
Submandibular- mixed secretions, drains via Wharton’s duct
Parotid- serous secretions, drains via Stenson’s duct

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6
Q

What are the functions of saliva?

A

Mineralisation, moistening and lubrication of food, taste perception, initiation of digestion, soft tissue repair, dilution and clearance of oral sugars, detoxification, buffering.

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7
Q

Describe the secretory unit:

A

Isotonic saliva produced in the acinus of secretory cells, travels along secretory duct lined by intercalating cells, ions reabsorbed in striated duct so solution becomes hypotonic. Myoepithelial cells may aid contraction and secretion.

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8
Q

What is swallowing/deglutition?

A

Series of orderly processes by which substances are passed from the mouth to the pharynx and then the oesophagus

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9
Q

What may cause dysphagia?

A

Congenital abnormalities, stroke injury, hypertrophy of pharyngeal tonsils

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10
Q

What are the oesophageal sphincters?

A

UOS- cricopharyngeus muscle

LOS- physiological sphincter at T10 level controlled by vagus nerve

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11
Q

Oral phase of swallowing:

A

Voluntary control
Bolus formed and positioned at back of tongue
Reflex action pushes food back via receptors of palatoglossal arch

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12
Q

Pharyngeal phase of swallowing:

A

Soft palate raises and closes opening between naso and oropharynx
Epiglottis is sealed
Tongue moves food into oesophagus

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13
Q

Oesophageal phase of swallowing:

A

LOS relaxes
UOS constricts
Primary peristaltic wave is initiated, distension of oesophagus initiates a secondary wave if the first is insufficient

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14
Q

What is a hiatus hernia?

A

Insufficient tightness of the diaphragmatic opening allows a part of the stomach to enter the thorax

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15
Q

What is the peritoneal cavity?

A

Potential space between visceral and parietal peritoneum that contains a small amount of fluid.

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16
Q

What is the structure of the primitive gut tube?

A

Foregut and hind gut are blind diverticula
Runs from the stomatodeum to the proctodeum
Opening to the yolk sac at the umbilicus

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17
Q

What is the blood supply to the gut?

A

Foregut from the coeliac trunk
Midgut from the superior mesenteric artery
Hind gut from the inferior mesenteric artery

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18
Q

What is the intraembryonic coelum?

A

Begins as one large cavity and is then subdivided by the future diaphragm

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19
Q

What is a mesentery?

A

Double layer of peritoneum suspending the gut tube from the abdominal wall allowing conduit of blood and nerve supply, formed from condensation of the splanchnic mesoderm.

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20
Q

What are the outcomes of the rotation of the stomach?

A

Greater and lesser curvature lie on the right and left hand side
Cardia and pyloric move horizontally pushing the greater curve inferiorly
Puts vagus nerves anterior and posterior
Moves the lesser sac behind the stomach
Creates greater omentum

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21
Q

How does the foregut develop?

A

Respiratory diverticulum forms in ventral wall at junction with the pharyngeal gut placing the oesophagus dorsally
Liver, pancreas and biliary system are formed in the ventral mesentery (foregut association only)
Liver develops from hepatic bud, falciform ligament attaches to ventral body wall
Duodenal lumen is obliterated and recanalised

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22
Q

What are the muscles of the abdominal wall (superficial to deep)?

A

Rectus abdominis
External oblique
Internal oblique
Transversus abdominis

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23
Q

What is a hernia?

A

Protrusion of abdominal viscera into abdominal wall

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24
Q

What is the difference between a direct and indirect inguinal hernia?

A

Direct hernia exits onto the wall via the weak area ‘Hesselbach’s triangle’
Indirect hernia follows the inguinal canal and passes through the deep inguinal ring

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25
Q

What are the borders of Hesselbach’s triangle?

A

Epigastric vessels, inguinal ligament (base) and rectus abdominis (medially)

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26
Q

What is the path of the inguinal canal?

A

From the deep inguinal ring to the superficial inguinal ring, is the pathway from abdominal wall to external genitalia

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27
Q

What is meant by a Richter’s hernia?

A

Inguinal or femoral, progresses more rapidly to gangrene but obstruction is less frequent and the entire lumen is not compromised

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28
Q

What is divarication of recti?

A

Midline lump that only appears on transition from sitting to standing, is common post-partum

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29
Q

What is the spigellian fascia?

A

Aponeurotic layer between rectus abdominis and linea semilunares

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30
Q

What is the difference between strangulation and incarceration?

A

Strangulation occurs when the blood supply is constricted by sweeping and congestion as to arrest its circulation
Incarceration means that the hernia cannot return to the abdominal cavity when pushed

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31
Q

How is a hernia repaired?

A

Obtain primary closure of muscle layer
Lichtenstein repair
Laparoscopic reinforcements
Use of specialised meshes

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32
Q

What is receptive relaxation?

A

The orad stomach allows entry of food without increasing intragastric pressure to prevent reflux

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33
Q

What is the blood supply to the stomach?

A

Lesser curvature- right gastric artery
Greater curvature- right and left gastroepiploic arteries
Duodenum- gastroduodenal artery

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34
Q

What cells are responsible for control of acid secretion and what are their functions?

A

Parietal cells produce HCl and intrinsic factor
G cells produce gastrin
Enterochromaffin like cells produce histamine
Chief cells produce pepsinogen
D cells produce somatostatin
Mucus cells produce mucus

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35
Q

What hormones increase H+ secretion?

A

Gastrin
Histamine
Acetylcholine (vagal stimulation)

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36
Q

How is acid secretion decreased?

A

Somatostatin release inhibits G cells (D cells stimulated by low pH when stomach empty)
Reduced vagal stimulation

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37
Q

What happens during the cephalic phase of digestion?

A

Preparatory- smelling, tasting, chewing
Direct stimulation of parietal cells by vagus nerve
Stimulation of G cells by vagus nerve via gastrin-releasing peptide

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38
Q

What happens in the gastric phase of digestion?

A

Distension of stomach stimulates vagus nerve
Amino acids and peptides stimulate G cells
Food acts as buffer and removes somatostatin inhibition by increasing pH

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39
Q

What happens in the intestinal phase of digestion?

A

Chyme initially stimulates gastrin

Inhibition of G cells by somatostatin

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40
Q

What are the stomach’s defences?

A

Mucus/bicarbonate layer adheres to epithelium (can be dissolved by alcohol)
High turnover of epithelial cells
Prostaglandins maintain mucosal blood flow (inhibited by NSAIDs)

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41
Q

What pharmacological treatments act on the stomach?

A

H2 blockers e.g. Ranitidine

Proton pump inhibitors e.g. Omeprazole

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42
Q

What is the primary intestinal loop?

A

Elongation of the midgut forms a loop with the SMA as its axis, is connected to the yolk sac by the Vitelline duct

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43
Q

What is physiological herniation?

A

The cavity is too small in the 6th week to accommodate the midgut and the liver, so the midgut herniates into the proximal umbilical cord.
The cranial limb returns to the cavity first, and the Cecal bud descends to form the ascending colon

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44
Q

What is Meckel’s diverticulum?

A

Approximately 2 feet from the ileocecal valve and can contain ectopic gastric/pancreatic tissue. Outpouching of a hollow structure, is the vestigial remnant of the omphalomesenteric (Vitelline) duct

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45
Q

What is pyloric stenosis?

A

Hypertrophy of the pylorus muscle not a failure of recanalisation

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46
Q

Where does recanalisation occur?

A

Oesophagus, bile duct and small intestine

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47
Q

What is gastroschisis and how does it differ from omphalcoele?

A

Gastroschisis is a failure of closure of the abdominal wall during folding of the embryo leaving the gut tube and its derivatives outside the body
Omphalcoele/exampholos is the persistence of physiological herniation and so has a covering of skin and subcutaneous tissue

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48
Q

What is the significance of the pectinate line?

A

Divides anal canal into two histologically distinct superior and inferior parts that have different arterial and nervous supply and venous and lymphatic drainage

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49
Q

What is the cloaca?

A

End of the hind gut separated into urogenital sinus and anorectal canal by the urorectal septum

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50
Q

What is the perineal body?

A

Where the urorectal septum fuses with the proctodeum (anal pit)

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51
Q

What is the arterial, venous and nervous supply above the pectinate line?

A

IMA
Pelvic parasympathetic innervation (S2-4)
Drains to internal iliac nodes
Only has stretch sensation

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52
Q

What are the features of the anus below the pectinate line?

A

Pudendal artery
Somatic pudendal nerves (S2-4)
Drainage to superficial inguinal nodes
Touch, temperature and pain sensitive

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53
Q

Where might gut pain be referred to?

A

Foregut produces epigastric pain
Midgut produces periumbilical pain
Hind gut produces suprapubic pain

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54
Q

What are the derivatives of the dorsal mesentery?

A

Greater omentum
Gastrolineal ligament from stomach to spleen
Leinorenal ligament from spleen to kidney
Mesocolon
Mesentery proper

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55
Q

What are the derivatives of the ventral mesentery?

A

Lesser omentum

Falciform ligament

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56
Q

What is gastroesophageal reflux disease (GORD)?

A

Weakness of the lower oesophageal sphincter causing heartburn, cough, sore throat, dysphagia, raised intragastric pressure, hiatus hernia and Barrett’s oesophagus (metaplasia)

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57
Q

What can cause acute gastritis?

A

NSAIDs
Alcohol
Chemotherapy
Bile reflux

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58
Q

What causes chronic gastritis?

A

Helicobacter pylori infection
Antibodies to parietal cells leading to pernicious anaemia
Chronic alcohol abuse

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59
Q

What is peptic ulcer disease?

A

Extends through muscular is mucosa, is most common in the first part of the duodenum and lesser curve of stomach
Can be caused by excess stomach acid, H. pylori and NSAIDs
Causes bleeding, anaemia, melina, haemetemis, weight loss

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60
Q

What are the features of Helicobacter pylori?

A

Faecal-oral transmission
Gram negative, helix shaped, microaerophilic
Produces urease that produces NH4+ ions to increase local pH
Flagellum allows adherence to epithelia
Releases cytotoxins that cause epithelial injury
Degrades mucus layer
Promotes inflammatory response

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61
Q

What is Zollinger-Ellison syndrome?

A

Non-beta islet cell gastrin secreting tumour of the pancreas that can be a part of multiple endocrine neoplasia causing proliferation of the parietal cells and increased H+ producing leading to severe ulceration of the stomach and small bowel

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62
Q

What can trigger stress ulceration?

A

Severe burns, raised intracranial pressure, sepsis, trauma, multi-organ failure

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63
Q

What is contained in the Porto hepatis?

A

Hepatic portal artery and vein

Bile duct

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64
Q

What stimulates the pancreatic acinus to produce digestive enzymes?

A

Cholecystokinin (CCK)

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65
Q

Where is the sphincter of oddi located?

A

Second part of the duodenum, entry from pancreas

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66
Q

What secretions are produced by the pancreas?

A 
Enzymes as zymogens including proteases, amylase and lipases 
Bicarbonate ions (high flow rate increases secretion)
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67
Q

What are the functions of the liver?

A 
Energy metabolism
Detoxification
Plasma protein production
Secretion of bile 
Phagocytosis 
Vitamin and mineral storage
68
Q

What is the functional cell of the liver?

A

Hepatocytes

69
Q

How is the liver structurally arranged?

A

Lobules with acini
Zones 1-3 getting closer to the central vein
Sinusoids connect the hepatic portal vein, artery and bile ducts to the central vein

70
Q

What are the bile acid dependent parts of bile?

A

Bile acids and pigments secreted into canaliculi by hepatocytes

71
Q

What are the bile acid independent constituents of bile?

A

Alkaline solution secreted by duct cells, stimulated by secretin

72
Q

What is the function of bile salts and how does this relate to their structure?

A

Amphipathic in structure and act at oil/water interfaces and form micelles with fatty products that are crucial for emulsification

73
Q

How are lipids absorbed?

A

Diffuse down concentration gradient then re-esterified and packaged with apoproteins into chylomicrons that enter lacteals

74
Q

What is enterohepatic recirculation?

A

Bile salts remain in gut lumen and are reabsorbed in terminal ileum to return to liver where salts are extracted and recycled

75
Q

What is the role of the gallbladder?

A

Stores and concentrates bile

76
Q

What is steatorrhoea?

A

Bile acids or pancreatic Lipases insufficient so fat appears in faeces making them pale and float

77
Q

Give examples of bile pigments:

A

Bilirubin (soluble due to conjugation)

Haemoglobin converted to urobillinogen and then stercobillin

78
Q

What are the GITs innate physical defences?

A

Sight, smell, memory, saliva, gastric acid, small intestinal secretions, colonic mucus, anaerobic environment, peristalsis

79
Q

What constituents of saliva protect against toxins?

A

Lysozyme (affects gram positive)
Lactoperoxidase (gram negs)
Complement
IgA

80
Q

What is xerostomia?

A

Severe illness/dehydration reducing salivary flow leading to increased microbial growth in the mouth

81
Q

Give examples of organisms resistant to gastric acid?

A

Mycobacterium TB

Enteroviruses e.g. Polio, hep A and coxsackie viruses

82
Q

What innate cellular defences does the GIT have?

A

Neutrophils, eosinophils, basophils, mast cells (produce histamine, vasodilation and capillary permeability) and macrophages

83
Q

What can cause liver failure?

A 
Viral hepatitis
Alcohol
Drugs
Industrial solvents
Mushroom poisoning
84
Q

What is hepatic encephalopathy?

A

Increased blood ammonia due to down regulation of the urea cycle and production by colonic bacteria causes confusion and cognitive impairment

85
Q

What is cirrhosis?

A

Hepatic fibrosis and chronic inflammation leading to portal venous hypertension causing portosystemic shunting and toxin shunting.

86
Q

Where might you find portosystemic shunting?

A

Oesophageal varicies
Haemorrhoids
Caput medusae

87
Q

Where would you find modular GALT?

A

Tonsils
Peyer’s patches
Appendix

88
Q

What causes appendicitis?

A

Lymphoid hyperplasia at base
Purulent appendicitis (common in epidemics of chicken pox)
Faecolith blockage

89
Q

What may cause gut ischaemia?

A

Arterial disease
Systemic hypotension
Intestinal venous thrombosis

90
Q

What liver function tests are available?

A

Hepatocellular damage- AST/ALT
Cholestasis- bilirubin, alkaline phosphatase
Synthetic function- albumin, prothrombin time

91
Q

What is pre hepatic jaundice?

A

Excessive haemolysis causing unconjugated hyperbilirubinaemia, anaemia, reticulocytosis, raised LDH and decreased haptoglobin

92
Q

What causes excessive haemolysis?

A

RBC membrane defects, Hb abnormalities and metabolic defects
Immune, mechanical, infection
Gilbert’s, Crigler-Najjar or Dublin-Johnson syndromes

93
Q

What is hepatic jaundice?

A

Deranged hepatocyte function and cholestasis causing mixed hyperbilirubinaemia, raised AST/ALT/ALP and abnormal clotting

94
Q

What affects hepatocyte function?

A

Hepatic inflammation, alcohol, haemochromatosis, Wilson’s disease, drugs, cirrhosis, tumours

95
Q

What is post-hepatic jaundice?

A

Obstruction of the biliary system (intrahepatic or extrahepatic) leading to conjugated hyperbilirubinaemia, no urobillinogen in urine and raised AST/ALT

96
Q

What causes obstruction of the biliary system?

A

Hepatitis, drugs, cirrhosis, gallstones, carcinoma (head of pancreas), pancreatitis, sclerosing cholangitis

97
Q

What is alcoholic liver disease?

A

Fatty change, with alcoholic hepatitis and associated fibrosis, liver cell necrosis and nodular regeneration.
Predisposes to hepatocellular carcinoma, liver failure, Wernicke-Korsakoff syndrome and encephalopathy

98
Q

Symptoms of liver disease:

A

Jaundice, anaemia, bruising, palmar erythema, Dupuytren’s contracture, decreased albumin causing ascites and oedema, decreas

99
Q

What is hereditary haemochromatosis?

A

Autosomal recessive disorder of iron transport and deposition leading to cardiomyopathy, diabetes, hypogonadism, hepatitis etc.

100
Q

What is Wilson’s disease?

A

Autosomal recessive disorder of copper transport and storage leading to cirrhosis, dementia, kidney damage and Kaysar-Fleischer rings

101
Q

What signs are associated with portal hypertension?

A

Splenomegaly, ascites, spider naavi, caput medusae, oesophageal/rectal varices

102
Q

What is meant by fulminant hepatic failure?

A

Onset of hepatic encephalopathy within 2 months of diagnosis of liver disease, can be caused by hepatitis, drugs, pregnancy, alcohol etc.

103
Q

What is encephalopathy?

A

Reversible neuropsychiatric deficit that causes flapping tremor, constructional apraxia, slow, slurred speech and personality changes

104
Q

What factors can precipitate encephalopathy?

A

Sepsis, constipation, diuretics, GI bleeds, alcohol withdrawal

105
Q

What is cholelithiasis?

A

Stones in the gall bladder, may be mixed, cholesterol or pigment stones

106
Q

What is cholecystitis?

A

Stones lead to oedema, ulceration, fibroprurulent exudate causing pain, SIRS, pyrexia and sepsis

107
Q

What are potential complications of gallstones?

A

Impaction causing biliary colic, empyema, obstructive jaundice, ascending cholangitis, acute pancreatitis, gallbladder carcinoma and perforation

108
Q

What is charcot’s triad?

A

Right upper quadrant pain
Jaundice
Fever

109
Q

What is pancreatitis?

A

Inflammatory process caused by effects of enzymes released from pancreatic acinus

110
Q

What causes acute pancreatitis?

A

Gallstones, alcohol, trauma, steroids, mumps, autoimmune, scorpion bite, Hyperlipidaemia, ERCP/iatrogenic, drugs
GET SMASHED

111
Q

What causes chronic pancreatitis?

A

Chronic alcohol abuse. Cystic fibrosis and biliary disease

112
Q

What are the components of intestinal epithelia?

A

Enterocytes- secrete enzymes into the brush border
Goblet cells
Paneth cells- produce antibacterial/antiviral toxins
Glandular cells

113
Q

What is meant by anoikis?

A

Cell death that occurs as cells are detached from surroundings e.g. Shedding of epithelia in the intestines

114
Q

What enzymes are secreted into the brush border to breakdown carbohydrates?

A

Amylase, isomaltose, maltase, alpha dextrinase, sucrase, lactase

115
Q

How is glucose absorbed?

A

SLGT-1 symporter with sodium ions driven by concentration gradient established by sodium-potassium-ATPase, exits cell by GLUT2 channels (fascilitated diffusion).
Galactose also follows this pathway but fructose uses a GLUT-5 channel to enter the enterocytes.

116
Q

What is the principle of oral rehydration therapy?

A

Glucose uptake stimulates sodium uptake via cotransporters so mixture of glucose and salt will stimulate maximum water uptake

117
Q

What enzymes are used to digest proteins in the small intestine?

A

Pepsinogen from chief cells
Trypsinogen converted to trypsin
Endopeptidases hydrolyse inferior peptide bonds
Exopeptidases hydrolyse from C-terminal ends

118
Q

How are amino acids and small peptides absorbed into the intestines?

A

Na+-amino acids cotransporters

Dipeptides, tripeptides moved by H+-cotransporters and converted to amino acids using cytosolic peptidases

119
Q

How is calcium absorbed?

A

Enters cells via fascilitated diffusion driven by a concentration gradient established by calcium-ATPase on the basolateral membrane. Requires vitamin D and is stimulated by PTH

120
Q

How is iron absorbed and transported?

A

Absorbed across the apical membrane then binds to apoferritin to cross the basolateral membrane, carried in the blood by transferrin

121
Q

How is B12 absorbed?

A

In the terminal ileum bound to intrinsic factor secreted by gastric parietal cells

122
Q

What is the motility of the small intestine?

A

Intestinal gradient between meals
Intestinal pacemakers have increased frequency proximally driving slow caudal progression
Segmentation moves contents back and forth mixing
Peristalsis

123
Q

What is the motility of the large intestine?

A

Segmentation (haustra live shuffling)

Mass movement moves content rapidly from transverse colon to rectum

124
Q

What are haustra?

A

Small pouches formed by sacculation of the large intestine

125
Q

How does defaecation take place?

A

Increased intrabdominal pressure and relaxation of the anal sphincters

126
Q

What are the derivatives of the SMA that supply the colon?

A

Middle colic, ileocolic, appendicular

127
Q

What are the derivatives of the IMA that supply the colon?

A

Left colic

IMA becomes superior rectal as it enters the pelvis

128
Q

What is meant by inflammatory bowel disease?

A

Group of conditions characterised by ideographic inflammation of the GIT, usually Crohn’s disease and ulcerative colitis

129
Q

What are features of Crohn’s disease?

A

Ileum involvement common
Affects anywhere in GIT including mouth
Transmural
Skip lesions

130
Q

What are the features of ulcerative colitis?

A

Begins in rectum
Can extend to the entire colon
Continuous pattern
Limited to the mucosa

131
Q

What are the differences in presentation between Crohn’s and ulcerative colitis?

A

Crohn’s has loose stools that are non-bloody, RLQ pain and perianal inflammation
UC has bloody stools with mucus and lower abdominal pain

132
Q

What pathology distinguished Crohn’s from ulcerative colitis?

A

Crohn’s has fibrosis, granulomas, cobblestone appearance

UC has crypt abscesses and friable mucosa

133
Q

What extra intestinal problems are associated with IBD?

A

Musculoskeletal pain, skin problems e.g. Psoriasis, primary sclerosing cholangitis, eye problems

134
Q

How might you investigate for inflammatory bowel disease?

A

Blood work (anaemia), CT/MRI scans, barium enema, colonoscopy, stool cultures

135
Q

What is meant by inflammatory bowel disease?

A

Group of conditions characterised by ideographic inflammation of the GIT, usually Crohn’s disease and ulcerative colitis

136
Q

What are features of Crohn’s disease?

A

Ileum involvement common
Affects anywhere in GIT including mouth
Transmural
Skip lesions

137
Q

What are the features of ulcerative colitis?

A

Begins in rectum
Can extend to the entire colon
Continuous pattern
Limited to the mucosa

138
Q

What are the differences in presentation between Crohn’s and ulcerative colitis?

A

Crohn’s has loose stools that are non-bloody, RLQ pain and perianal inflammation
UC has bloody stools with mucus and lower abdominal pain

139
Q

What pathology distinguished Crohn’s from ulcerative colitis?

A

Crohn’s has fibrosis, granulomas, cobblestone appearance

UC has crypt abscesses and friable mucosa

140
Q

What extra intestinal problems are associated with IBD?

A

Musculoskeletal pain, skin problems e.g. Psoriasis, primary sclerosing cholangitis, eye problems

141
Q

How might you investigate for inflammatory bowel disease?

A

Blood work (anaemia), CT/MRI scans, barium enema, colonoscopy, stool cultures

142
Q

What treatments are available for inflammatory bowel disease?

A

Aminosalicylates e.g. Sulfasalazine for flares and remission
Corticosteroids e.g. Prednisolone for flares only
Immunomodulators e.g. Azathioprine for fistulas and remission

143
Q

What are the functions of colonic bacteria?

A

Synthesise and excrete vitamins e.g. K and B12
Prevents colonisation by pathogens
Kill non-indigenous bacteria
Stimulate development of MALT
Stimulate production of natural antibodies

144
Q

What bacteria are commonly found in the mouth?

A

Strep/staph
Candida
Lactobacillus
Enterococcus

145
Q

What is noma/cancum oris?

A

Tissue destruction of the mouth

146
Q

What is Ludwig’s angina?

A

Migration of streptococcal bacteria from sore throat to lymph nodes resulting in cellulitis which endangers life by compressing the larynx

147
Q

What is Quinsey?

A

Abscess in tonsil, causing deviated uvula and inspiration stridor

148
Q

What bacteria are found in the colon?

A

Bacterioides fragillus
E. coli
Enterococcus faecalis etc

149
Q

What is the role of lactobacillus acidophilus in the vagina?

A

Commensals that converts glycogen to lactic acid which prevents other bacteria and Candida albicans growing. Broad spectrum antibiotics kill lactobacillus leading to vaginal thrush

150
Q

What commensals commonly cause urinary tract infections?

A

E. Coli, enterococcus

151
Q

What causes wet gangrene?

A

Clostridium perfringens is anaerobic and digests glucose producing ethanol and CO2 and a cardio toxin that causes sudden cardiac arrest

152
Q

What are features of oesophageal carcinoma?

A

Squamous cell carcinoma or adenocarcinoma (Barrett’s oesophagus)
Can spread directly through oesophageal wall
Causes dysphagia, weight loss
Investigation by endoscopy, biopsy, barium swallow

153
Q

What are the features of gastric cancer?

A

Association with gastritis, epigastric pain, vomiting and weight loss
May be fungating, ulcerated. May be intestinal with gland formation or diffuse with signet ring cells full of mucin
Can spread through the wall to peritoneum, liver, lymph nodes

154
Q

What are gastro-intestinal stromal tumours?

A

Derived from pacemaker cells (intestinal cells of cajal), unpredictable behaviour e.g. Pleomorphism

155
Q

What conditions may predispose to adenomas of the large intestines?

A

Familial adenomatous polyposis- autosomal dominant condition (chromosome 5)
Gardner’s syndrome- similar to FAP with bone and soft tissue tumours

156
Q

What is the adenoma-carcinoma sequence?

A

Similar anatomical and geographical distribution of adenomas and carcinomas with synchronous/metasynchronous lesions

157
Q

What is Duke’s staging of colorectal adenocarcinoma?

A

A- confined to bowel wall
B- spread through wall but lymph nodes are clear
C- lymph nodes involved

158
Q

What genetic mutations are associated with colorectal adenocarcinoma?

A

FAP, ras mutations, deleted in colorectal cancer gene, p53 loss or inactivation

159
Q

What is a carcinoid tumour?

A

Rare endocrine tumour found in the appendix

160
Q

What are the features of pancreatic carcinoma?

A

Symptoms- weight loss, jaundice, trousseau’s sign (thrombophlebitis)
Firm pale mass that may be necrotic, cystic or haemorrhagic
Acinar tumours with zymogen granules, ductal adenocarcinomas, carcinoma of ampulla of vater

161
Q

What types of islet cell tumours are there?

A

Insulinoma
Glucagonoma (causes necrotic migratory erythema)
VIPoma
Gastrinoma

162
Q

What tumours of the liver are there?

A

Benign hepatic adenoma, bile duct adenoma, hamartoma, haemangioma
Malignant hepatocellular carcinoma, cholangiocarcinoma, hepatoblastoma

163
Q

What causes small bowel obstruction and how would it present?

A

Vomiting early, mild distension, colicky pain, complete constipation occurs very late
Caused by adhesions, hernias, tumours and inflammation

164
Q

What causes large bowel obstruction and how would it present?

A

Presents with significant distension, dull pain, absolute constipation, vomiting is late and faeculant
Caused by colorectal adenocarcinoma, diverticulum structure, hernia and volvulus

165
Q

What signs of a sigmoid volvulus might you see on an AXR?

A

From left iliac fossa to RUQ coffee bean sign

Dilatation of proximal bowel

166
Q

What is toxic megacolon?

A

Colonic dilatation, oedema and pseudo polyps

ESA3 (5 decks)

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