GI Flashcards
0
Q
Properties of the enteric nervous system and it’s relationship to the autonomic nervous system
A
Post ganglionic plexuses which can work independently to control motility and secretions. Activity is controlled by autonomic innervation with the brain
1
Q
Describe the fluid balance of the gut
A
1l of food
1.5l of saliva
2.5l gastric secretions
9l alkali and water
12.5 small intestine
1.35 large
Deficate 150g
2
Q
Why might a patient have dysphasia?
A
Anaesthetic, neurological defect, oesophageal blockage/ defect in musculature or a tumour tumour
3
Q
Functions of saliva
A
Protection- contains I-, alkaline and Ca to protect teeth, contains lysozyme.
Moistens food to assist swallowing
Digestion- amylase
Prevents xerostomia
4
Q
Components of saliva secreted by each salivary gland
A
Sub maxillary - serous and mucus 70% Parotid - serous 25% Sublingual - mucus 5% Hypotonic. Mucous contains mucins Contains Ca, I, low Cl, K, low Na, hCO3, enzymes, bacteriostats
5
Q
Mechanism of secretion of serous saliva. Different with STIM?
A
Secreted isotonically by acini
Ducts impermeable to h2o and have Na ATPase on Basolateral surface creating conc gradient.
More Na reabsorbed so hypotonic
HCO3 secreted via h+ reabsorption on Basolateral NHX co2 back into cell, HCO3 into lumen via anion exchanger.
Acini secrete I and enzymes. Secretes Cl so ions and h2o follow.
Resting saliva is neutral or slightly acid
Stimulated then
More hco3
Less hypotonic so more Na and less k
More enzymes
6
Q
Control of salivary secretion and effect of atropine
A
Largely nervous control
Sympathetic decreases volume - from the superior cervical ganglion, decreases blood flow
Parasympathetic stimulates acinar secretion, ductal secretion of HCO3 and co-transmitters increase blood flow.
From the medulla - afferent information from nose, mouth and tongue but also conditioned reflexes
7
Q
Describe the process of swallowing
A
Voluntary phase- formation of a bolus, move into pharynx
Pharangeal phase- pressure receptors in palate and anterior pharynx afferent to brain stem swallowing centre. Causes larynx to lift, glottis to close, upper oesophageal sphincter to open and inhibits respiration.
Oesophageal phase- first 1/3 is voluntary. Rapid peristalsis conducted by extrinsic nerve via the swallowing centre. Lower oesophageal sphincter opens.
8
Q
Outline how disordered swallowing may occur
A
Anaesthesia/ surgery may affect the brain stem so that swallowing I not coordinated- risk of aspiration.
Motility problem e.g. Achalasia- smooth muscle does not relax, diffuse oesophageal spasm (DES), scleroderma
Obstruction/ compression e.g. Tumours, squamous cell carcinoma, adenocarcinoma or lymphoma
9
Q
Categorise different types of dysphasia based on pathology
A
Dysphgia - difficulty swallowing solids
Oesophageal dysphagia- difficultly swallowing liquids as they cannot form a bolus so harder to coordinate. Due to problems in lower sphincter or cardia.
Mechanical obstruction often solids then liquids.
Motility then both.
Odynphagia - pain on swallowing
Investigate with barium swallow (especially solids), endoscopy
10
Q
Mechanisms that prevent GORD
A
Lower oesophageal sphincter physiological.
Right Cruz of the diaphragm has a pinch cock effect
horizontal connection of oesophagus to cardia at an acute angle.
Positive intra abdominal pressure closes
Folds in mucosa occlude lumen at the gastro oesophageal junction
Results in Barrett’s oesophagus, cough, hoarseness of voice and asthma.
11
Q
Describe the development of the muscular and fascial layers of the abdominal wall including the inguinal canal
A
Rectus muscles grow within the transversalis fascia
Two sides of developing abdominal wall meet at the linear alba. Develop from somatic mesoderm.
Inguinal canal- oblique through the layers of abdominal wall, testes pushes wall through during development which become the fascial covering of the spermatic cord
12
Q
Explain the developmental basis of umbilical and inguinal herniea
A
Weakness in umbilicus due to malformation after the gut grows outside of the abdominal canal.
Weakness at inguinal rings due to the passage.
13
Q
Describe how the coelomic cavity and peritoneal cavity develop
A
Cephalocaudal folding causes the gut tube to pinch leaving a cranial and caudal section with only he vitaline duct.
Lateral folding creates an endoderm tube. Around this the intra coelomic space gets pinched off to create one cavity or coelom. This later surrounds the viscera and in the abdomen is called the peritoneum.
14
Q
Describe the fate of the embryonic dorsal and ventral mesenteries
A
Ventral in foregut becomes liver, gall bladder and biliary tree and the head of the pancreas and lesser omentum.
Dorsal foregut becomes the tail, neck, body and superior head of the pancreas. Connects stomach to transverse colon.
15
Q
Explain how the omenta and the mesentary of the small intestine form and relate this to their arrangements in the adult
A
Rotation of the stomach so that ventral mesentary lies to the right. Growth of cells on the left is quicker resulting in anteroposterior rotation of the stomach and greater curvature. The greater omentum on the greater curvature fuses with the transverse colon. Mesenteries of small intestine fuse forming a fan shape.
16
Q
Why do some abdominal organs possess mesenteries and some are retro peritoneal
A
Retroperitoneal organs never had a mesentary or had a peritoneum e.g. Kidneys- intermediate mesoderm
Secondary retro peritoneal organs dorsal mesenteries regressed and peritoneum fused so they are attached to the abdominal wall and only have an anterior covering of peritoneum. E.g. Duodenum - posterior peritoneum forms fusion fascia
17
Q
Describe the respiratory primordium development.
A
Respiratory diverticulum forms off the pharyngeal gut. Becomes respiratory primordium. Divided by the trachealoesophageal septum
18
Q
Describe the functions of the stomach
A
Digestion - pepsin and mechanical break down
Kills pathogens- low pH
Storage
19
Q
Describe the components of gastric secretion and their cellular origins
A
HCO3/ mucus - neck cells/ foveolar cells
Pepsin - chief cells
Gastric - G cells/ endocrine cells
HCl- Parietal/oxyntic cells (canaliculi)
20
Q
Explain the mechanism of stomach acid secretion
A
Proton pump into lumen from canaliculi, HCO3 into blood stream. Both produced via mitochondrion
21
Q
Control of gastric acid secretion including phases of control
A
H+ and prostaglandins (neck cells) Controlled by
Gastrin - distension and peptides increase, H+ decreases
ACh/ parasympathetic - stomach distension and CNS
Histamine- gastric and ACh stim, produced by mast cells and act on H2 receptors to stimulate CAM. Sensitive, antagonists are effective.
Phases:
Cephalic phase- CNS stims acid
Gastric phase- neutralisation and peptides and distension stim gastrin
Intestinal phase - hormones inhibit gastrin secretion, pH and peptides fall. Less distension.
22
Q
Outline the ways in which gastric acid secretion may be reduced by drugs
A
Proton pump inhibitors and H2 antagonists
23
Q
Describe the function of the stomach defenses, what can damage these?
A
Unstirred layer of mucus and HCO3 prevents degredation of gastric cells by h+ and pepsin.
NSAIDs inhibit prostaglandins which decreases mucus production.
Alcohol dissolves mucus.
H pylori damages via inflam.
24
Patterns of motility across the stomach
3 squirts a minute.
Rhythmic contraction from fundus to pylorus resulting in contraction of pyloric sphincter so only a squirt into intestine.
Contractions can increase in force not frequency
Decreased by fat, low pH or hypertonicity in duodenum
25
Describe the role of rotation of the midgut loop in the establishment of the disposition of abdominal viscera
Rapid growth of the primitive gut tube and the liver results in the formation of the midgut loop which herniates through the umbilicus. The SMA lies within. There is rotation of 270 degs so that the cranial part lies to the left of the SMA and caudal part. The small intestine begins to develop in the cranial part and the cecal bud develops in the caudal part.
The caudal part becomes the transverse colon, cecum and distal ileium.
The cranial part becomes the duodenum, juju num and proximal ilieum
The cecal bud descends so that the small intestine lies in the middle and the transverse colon superior in the abdominal cavity
The vitelline duct regresses however may remain as a cyst, vitelline fistula or meckle's diverticulum.
Lumen of gut tube - oesophagus, bile duct, small intestine - becomes obliterated due to rapid growth and is recannalised later.
26
Describe the portioning of the cloaca and the development of the anal canal
Urorectal septum divides the cloaca into the urogenital sinus and anorectal canal at the cloacal membrane with the perineal body between. Bottom 1/3 of anal canal has no peritoneum. Pectin ate line where endoderm meets ectoderm.
Superior- columnar, IMA, pelvic parasympathetic nerves S234, stretch only, internal iliac nodes.
Inferior- stat squamous, peudendal artery, peudendal nerve S234, superficial inguinal node, pain and touch
27
Fate of the dorsal and ventral mesenteries
Dorsal- mesocolon, mesentary proper, greater omentum, gastrolienal ligament from stomach to spleen, lienorenal ligament from spleen to kidney
Ventral - letter omentum, falciform ligament
28
Innervation and blood supply to midgut and hindgut
Midgut - SMA, vagus nerve S234 para, sympathetic superior mesenteric ganglion and plexus.
Hindgut- IMA, pelvic S234 and inferior blah
29
Describe the developmental basis for common congenital defects including atresias, stenosis, malrotation, incomplete rotation, omphalocele, exomphalos, imperforate anus and gastroschisis
Atresias e.g. Imperforate anus - failure of anal membrane to rupture. Anal/anorectal agenesis. Hindgut fistulae e.g. Into bladder.
Stenosis- failure of Recanalisation normally in duodenum, vascular accidents may contribute e.g. Volvulus from malrotation. Pylori stenosis due to hyperplaisia without recan. Leads to projectile vomiting,
Malrotation is 90 deg wrong way so duodenum is over TC so volvulus likely/ strangulation or incarceration.
Incomplete rotation- left sided colon only 90 deg
Omphalocele/ examphalos- gut herniates through umbilical chord
Gastroschisis- failure of closure of abdominal wall, rupture through amniotic sac so no covering.
30
Describe the structure and layers of the abdominal wall
```
Peritoneum
Extra peritoneal Fat
Transversalis fascia/ endo abdominal fascia
Transver oblique
Deep fascia
Internal oblique
Middle fascia
External oblique
Scarper fascia
Camper fascia (fatty)
Skin
```
31
Landmarks of the abdominal wall
Arcuate line - 1/3 between umbilicus and pubic crest
Linear alba
Linear semilunaris
McBurney's point 2/3 umbicilus and asis
Tendinosus intersection
Umbilicus- L2
Epigastric fossa- depression in epigastric region just inferior to xiphoid process
32
Describe the musculature of the abdominal wall
External oblique- spinal nerve roots and intercostal nerves T7-11. Flexion of trunk, rotation, compress and support abdominal viscera
Internal oblique - anterior rami T6-12 and first lumbar nerves same function as EO.
Transversus - same inn as IO. Compresses and supports abdominal viscera
RA - IO, flexion, compression, stabalises and tilts pelvis - antilordosis
Pyramidalis in RS
33
Developmental defects and consequences in abdominal wall. Divariation of recti, Rectus sheath Haematoma, ectopia cordis, patent urachus, Urachal cyst, patent vitellointestinal duct, meckle's diverticulum, examphalos, gastroschisis
Di variation of recti- loss of linear alba, e.g. Pregnancy
Rectus sheath haematoma- blood in Rectus sheath may cause abdo pain with or without lump, surgery no normally needed, pregnancy or trauma
Ectopia cordis- failure of maturation of ventral mesoderm, heart outside thoracic cavity, often with other CHD
Meckle's diverticulum- 2 types of mucosa- gastric and pancreatic, 2 feet from ilealceacal valve, 2 inches, 2% of pop, 2:1 men:women
34
Describe visceral and somatic referred pain
Somatic referred pain - damage/ stimuli in proximal part of a sensory neurone where the pain is felt in the more distal structures/ dermatome that the nerve innervates.
Visceral- pain in the region of an afferent nerve is perceived in the region of the efferent sympathetic nerves of the same spinal chord segment
35
Visceral refered pain and development
Foregut - epigastric
Midgut- periumbilical
Hindgut- suprapubic
36
Cardiac refered pain?
Chest (left) neck, left shoulder
37
Oesophageal referred pain
Chest - epigastric
38
Gastric referred pain?
Epi gastric, back
39
Duodenal referred pain
Epi gastric or umbilical
40
9 abdominal division
R and l hypochondriac
Right and left lateral/ lumbar and umbilical
Pubic/ hypogastric and right and left inguinal/iliac
41
Gall bladder
Right hypochondriac/ lumbar and right shoulder
42
Hepatic referred pain
Right hypochondriac/ epigastric, right neck/ shoulder and back (similar to kidney)
43
Splenic referred pain
Left lateral
44
Retro peritoneal referred pain?
Back pain e.g. aorta and pancreas ( also epigastric)
45
Appendix refered pain
Begins in periumbilical. Peritoneum involved then superficial to appendix.
46
Small bowel colic pain
Pain every 40 seconds, periumbilical
47
Large bowel colic pain
Severe pain every 20-30 mins. Suprapubic region
48
Renal/ ureteric colic
Most severe pain.
Ureteric follows inguinal ligaments
Renal found in loin
49
Uterine and bladder pain
Hypogastric
50
Causes of diaphragmatic pain
Spleen, ectopic pregnancy, perforated ulcer
51
Regions the transverse colon is found in
| Also spleen.
Periumbilical and left and right lumbar
52
What landmarks divide the abdomen into 9?
Either sub costal plane or transpyloric or transtubercular (iliac tubercule) or Interspinous plane.
Vertically - mid clavicular to mid inguinal point
53
Describe structure and relationship of supracolic and infra colic compartments
A
54
Common surgical incisions
```
Midline
Transverse
Need strong closure
Appendincpectomy at my burneys point
Gridiron incision
```
55
What is a peritoneal ligament?
A double layer of peritoneum that connects an organ with another organ or to the abdominal wall e.g. Hepatogastric, hepatoduodenal
56
What are the supra/infracolic compartments? Are they connected?
Above and below the transverse mesocolon.
Infra colic divided into left and right by small intestine mesentary. It is also below the greater omentum.
Communication by the parabolic gutters
57
Subphrenic spaces?
Right- under diaphragm and above right side of the live, bounded behind by coronary ligament and on the left the falciform ligament
Left- between diaphragm and anterior superior left liver, anterosuperior aspect of stomach and diaphragmatic surface of spleen. Right is falciform. Behind is anterior layer of left triangular ligament
58
Recto- uterine and vesico uterine pouches?
Rectouterine puch- fold of peritoneum between the posterior vaginal fornix, uterine cervix and rectum.
Vesico- uterine pouch- smaller between fundus of uterus and bladder.
Rectovesicle pouch in males- between rectum and bladder.
59
Developmental defects and consequences in abdominal wall. Divariation of recti, Rectus sheath Haematoma, ectopia cordis, patent urachus, Urachal cyst, patent vitellointestinal duct, meckle's diverticulum, examphalos, gastroschisis
Di variation of recti- loss of linear alba, e.g. Pregnancy
Rectus sheath haematoma- blood in Rectus sheath may cause abdo pain with or without lump, surgery no normally needed, pregnancy or trauma
Ectopia cordis- failure of maturation of ventral mesoderm, heart outside thoracic cavity, often with other CHD
Meckle's diverticulum- 2 types of mucosa- gastric and pancreatic, 2 feet from ilealceacal valve, 2 inches, 2% of pop, 2:1 men:women
60
Mesentary of the small intestine?
Fan shape, divides left and right infracolic, moves inferiorly obliquely to the right. Crosses major structures including the duodenum.
61
Where are the areas of potential weakness in the abdominal wall?
A
62
Describe the areas of potential weakness in the abdominal wall
Myopectineal oriface, epigastric at midline, umbilical, incisional, femoral, direct and indirect inguinal. Hesselbacks triangle
63
Describe the MPO
Divided anteriorly by the inguinal ligament and posteriorly by the iliopubic tract (binds external iliac vessels, thickening of transversalis fascia). Medially by the lateral boarder of the Rectus muscle, superiorly by the arching fibres of the transversus abdominus and internal oblique muscles, laterally by iliopsoas and inferiorly by the Cooper/ Pectineal ligament (extension of lacunar ligament).
Superiorly the spermatic cord perforated and inferiorly, the femoral vessels .
Protected by aponeurosis of transversus abdominus and the transversalis fascia
64
Boarders of Hesselbach's triangle
Lateral inferior epigastric arteries,
Medial Rectus sheath/ linear semilunaris
Inferior - inguinal ligament
65
Structure of the inguinal canal
Anterior- aponeurosis of external oblique and internal oblique (lateral 1/3)
Posterior- transversalis fascia
Inferior- inguinal ligament (rolled by external oblique aponeurosis)
Superior- aponeurosis of internal oblique and transverse abdominus and transversalis fascia.
Deep ring is superior to midpoint of the inguinal ligament and formed by invagination of transversalis fascia
Superficial is just above pubic tubercle formed by invagination of external oblique. Inter rural fibres prevent from opening.
Spermatic cord and round ligament of the uterus. 3 arteries in males, 3 nerves
66
Distinguish direct and indirect hernias and describe their position
Direct Through Hesselbach's triangle
| Indirect inguinal hernia trough deep inguinal ring result of failure of embryonic closure.
67
Describe epigastric, umbilical and femoral hernias
Epigastric- between xiphoid process and umbilicus at linear alba - pregnancy and obesity make it more common
Umbilical- associated with weakness or failure to close, can be acquired- female/ obese.
Femoral hernia - through femoral ring/ canal. May grow- travel t saphenous opening. More likely to strangulated than inguinal. Tender, in femoral triangle. Common in females as they have a wider pelvis. StrangulTion due to rigid boundaries of femoral ring.
Richter's hernia- only one half of lumen
68
Describe the prevalence and incidence of common disorders affecting the stomach
Gastritis common with dyspepsia
Ulcers- 10% of cases
Gastric cancer less than 1%- malt lymphoma or adenocarcinoma
69
Describe the presentation, investigation and outline of the management of common gastric disorders (gastritis)
Presents as GORD
Dyspepsia, epigastric pain, lying down worse, hot drinks
Lifestyle- lose weight, stop smoking, reduce alcohol, aggrevating foods e.g. Fatty
Medication (triple) and antacids e.g. Gaviscom.
Investigate with endoscopy if neccesary.
70
Describe the clinical features and natural history of ulcer disease
Break in epithelium- GU or DU
NSAID which inhibit production of prostaglandins.
Recurrent burning epigastric pain, worse at night, relived with eating, DU when hungry.
Pain in back then posterior perforation
Persistent severe pain then penetration into other organs.
Nausea and vomiting
Weight loss anorexia
Heamatemesis
Asymptomatic
Investigate H pylori
Endoscopy in older patients to exclude cancer
71
H pylori
```
G neg helical urease positive.
Creates ammonia
Colomises gastric epithelium
Triple therapy, PPI, H2 antagonists and clarithromycin/ amoxicillin.
Location effects disease.
Increases gastric acid.
Duodenum if Antrum.
```
72
Describe the macro and microscopic structure of gastric mucosa
```
Macro- rugae
Micro- simple columnar, hexagonal with glands
Cardia- neck
Fundus and body- neck, parietal, chief,
Pylorus- neck g cells
```
73
The attachments of the greater and lesser curvature
Greater - gastro colic ligament, GO
| Lesser- LO, ports hepatis
74
Drainage of greater and lesser curvatures?
Gastric veins into hepatic vein
Short gastric vein and left gastro epiploic into splenic into left renal into hepatic portal
Right gastro epiploic vein into SMV
75
Inflammation of stomach causes
Acute- NSAIDs alcohol
| Chronic- H pylori, atroph and metaplasia
76
Boarders of the epiploic foramen
Anterior - free boarder of the lesser omentum known as the hepatoduodenal
Posterior - peritoneum/ IVC
Superior- caudate lobe
Inferior duodenum, hepatic artery
Left lateral gastro splenic ligament, splenorenal ligament
77
Describe the key properties of chyme leaving the stomach
Hypertonic, acidic, partially digested
78
Describe the digestive functions of the liver and the components of bile
Bile acid dependent:
Secreted by cells lining canaliculi
Contains cholesterol, bile acids e.g. Cholic acid/ chenodeoxycholic acid (emusifies lipids to increase SA for digestion) and pigments.
Bile acid independent:
Secreted by cells lining intra hepatic bile ducts:
Contains alkaline juices
79
Describe how the microscopic structure of the liver relates to its function
Blood:
Flows from portal vein and hepatic artery to periphery of hepatic functional unit (lobule) to the centre of the functional unit which is a vain to the systemic circulation. Lining hepatocytes abosorb nutrients and perform metabolic functions. Through sinusoids
Bile canaliculi run from centre to peripheral bile ducts.
80
Describe the secretions of bile acids and the entero-hepatic circulation of bile acids
Secreted from the gall bladder in response to cholecystokinin (CCK) in response to contraction. Enters duodenum. Reabsorbed in the terminal ileum after being conjugated by bacteria. Returns to liver via portal system and is actively uptaken and secreted again into canaliculi
81
Describe the function of the gall bladder and the formation of gall stones
Storage of bile acids, concentrate by absorbing water, increases changes of precipitation.
Often asymptomatic but can be lodged in biliary tree causing biliary colic, gall bladder infection and cholecystitis. Pain worse after eating due to CCK
82
List the secretions of the endocrine pancreas
Alkaline juice
| Digestive enzymes e.g. Trypsinogen, chymotripsinogen, elastase and carboxypeptidase, amylases and lipases
83
Relate the structure of the endocrine pancreas to its secretions
Acini and ducts
Acini: inactive enzymes packaged into vacuole (zymogen granules) and exocytosed, activated in intestine.
Ducts: secrete alkaline juice
84
Describe mechanisms of secretion of alkaline juice and other secretions
```
Na K ATPase
NHX (ECF side)
Carbonic anhydrase creates H and HCO3
H into ECF and hco3 into lumen
H in ECF creates more cO2/h20 to diffuse
```
85
Describe control of the pancreatic and biliary secretion
Pancreas acini and gall bladder- CCK from duodenal APUD cells in response to hypertonicity and fat
Ducts from secretin from jenjunum in response to low pH
86
Describe the mechanism of digestion of fats
Fats are relatively insoluble in water.
Bile acids enable the fat to be encorporated into micelles so that there is a greater surface area for lipases to work.
They also draw the fat into the Unstirred layer so that the fatty acids can be released slowly into the duodenum.
Inside the epithelial cells they are reconstructed as triacylglycerols and re expelled as chylomicrons transported via lymphatics.
87
Where is the bare area of the liver?
No peritoneum
Between posterior, anterior coronary ligaments and the IVC
Also triangular bare area on left
88
Where is the ligamentum teres
Also known as round ligament.
| Located at the inferior boarder of the liver directly inferior to the falciform ligament.
89
Where does the gall bladder lie on the liver?
Fossa for the gallbladder
90
Parts of the gall bladder
Fundus
Neck
Body
91
Vasculature of gall bladder and biliary tree
Common hepatic - right hepatic - cystic
Commonly arises between the cystic duct, common hepatic duct and visceral surface of liver in the cystohepatic triangle of calot.
Drains through liver directly in hepatic sinusoids or into portal vein, multiple veins
92
Location of pancreas? Vertebral level
L1 and 2( L2= transpyloric plane)
Posterior to stomach, between duodenum on the right and splee. On the left. The transverse mesocolon attaches to its anterior margin.
Head in c shape of duodenum
Neck overlays SMA/ V which joins splenic vein posteriorly
Body left of SMV/A
Tail anterior and left of kidney in splenic hilum and left colic flexure.
93
Arterial supply of pancreas
Arteries from splenic artery all form arches .
Arteries anastomose between gastroduodenal and SMA as anterior and posterior superior and inferior pancreaticoduodenal arteries.
94
Venous drainage of pancreas
Tail into splenic vein
| Head into SMV
95
Arterial supply of spleen
Tortuous splenic artery
96
Defence mechanisms of the GI tract
Innate physical- saliva- lysozyme, lactoperoxidase, complement, IgA, polymorphs, complement- sight smell memory gastric acid, small intestine secretions, mucus, anaerobic, peristalsis
Innate cellular
Adaptive- GALT e.g. Peyers patches, tonsils, IgA and E
97
Describe xerostomia
Dry mouth caused by dehydration, medication, infection and other e.g. Scleroderma. May lead to parotitis (staph aureus)
98
Describe achlorhydria/ pernicious anaemia
Often caused by PIP/H2 antagonists as less H+.
| Salmonella, shigella, cholera infections. b12 deficient
99
Potential results of a GALT infection
Sore through, cervical lymphadenopathy.
Adenovirus/coxsackie. Typhoid can result in perforation.
Lymph nodes can occlude appendix (hyperplasia in chickenpox)
100
The role of the liver in the handling of bile pigments, hormones, drugs, toxins, alcohol
```
Carb, lipid, protein metab
Protein synth
Bile production- conjugates bilirubin and excretes
Phagocytosis
Detoxification e.g. Hormones insulin and alcohol
Vit D production
Vitamin and mineral storage
Albumin for oncotic, clotting factors
```
101
Causes of liver failure
```
Alcohol
Industrial solvents
Infection
Drugs e.g. Isoniazid, methyldopa
Mushrooms
Paracetamol
```
102
Symptoms of liver failure
Susceptible to bacterial and fungal infections
Accumulation of toxins e.g. Hepatic encephalopathy from ammonia
Susceptibility to drugs
Cirrhosis- portal hypertension, shunting, capital medusa, varices, haemorrhoids
103
Symptoms of hepatitis
Raised AST/ALT, jaundice in acute
| Chronic then synthetic failure so low albumin and clotting factors
104
Basic liver function tests
Hepatocellular damage- AST/ALT, y-glutamyl transpeptidase (y-GT)
Cholecystis (bile duct) - bilirubin and alkaline phosphotase
Synthetic function- albumin, prothrombin
105
When is bilirubin clinically detectable
>40umol/l
106
Describe pre hepatic jaundice and causes
Increase in un conjugated bilirubin, pre hepatic cause due to haemolysis
Lab: reticulocytosis, high LDH, anaemia
Causes:
Inherited- membrane defect, haemoglobin abnormalities, metab defect
Congenital - Gilbert's syndrome
Acquired - immune, mechanical, burns, drugs, infection
107
Describe hepatic jaundice
```
Reduce ability of liver to secrete conjugated bilirubin into blood stream
Lad findings: raised AST/ alt, raised conj and unconj bilirubin, abnormal clotting
Causes:
Cirrhosis
Gilbert syndrome
Virus
Alcohol
Paracetamol
Haemochromotosis
Hepatic tumour
```
108
Describe post hepatic jaundice
```
Obstruction in biliary tree causing a back up of bile acids into liver
Lab: conjugated hyperbilirubinaemia, raised canalicular enzymes ALP, raised AST/ALT poss
Causes intrahepatic:
Hepatitis
drugs
Cirrhosis
Primary biliary colic
Extra hepatic:
Gall stone/ biliary stricture
Cancer
Pancreatitis
Sclerosing cholangitis
```
109
Effect of excessive alcohol consumption on the liver
```
Fatty liver- more NADH, more fatty acid synth, more TAG deposits.
Hepatitis - acetylaldehyde
Cirrhosis- loss of function, from cell necrosis with modular regeneration and fibrosis, increased resistance to blood flow.
Complications include
Encephalopathy
Hepatocellular carcinoma
Liver failure
Wernickles korsakoff syndrome
Dementia
Epilepsy
```
110
Causes of cirrhosis
```
Alcohol
Biliary cirrhosis
Haemochromocytosis - Fe
Wilson's disease - cu
Hep B or c
Autoimmune hepatitis
A1 antitrypsink
```
111
Clinical features cirrhosis
```
Jaundice
Portal hypertension
Palmer erythema
Anaemia
Dupuytrens contracture
Bruising
Flapping tremor
```
112
Where are the portal systemic anastomoses?
Oesophageal branch of left gastric vein and azygous vein
Superior rectal (IMV) and inferior rectal
Mesentery and retro peritoneal veins
Veins of anterior abdominal wall (para umbilical to small epigastric of abdo wall)
Portal branches in liver and diaphragm
113
Results of portal hypertension
```
Oesophageal varices
Rectal varices
Caput medusa
Ascites
Splenomegly
Spider naevi
```
114
Risk factors for gallstones
```
Age
Gender female
Obesity and rapid weight loss
Diet
Multiparty
Western world
Drugs- OCP
Ileal disease/ resection
Haemolytic disease
Stones may be mixed pure cholesterol or pigment
```
115
Difference between biliary colic and cholecystitis
Gall bladder contraction vs obstruction/inflammation.
| Cholecystitis results in oedema, infection sepsis, pyrexia, pain, ulceration
116
Complication of cholithiasis
```
Pancreatitis
Ascending cholangitis - life threatening, jaundice, righ UQ pain fever
Obstructive jaundice
Gallbladder carcinoma
Gallbladder perforation
Mucocele
Empyema
Biliary-enteric fistula/gallstone ileus
```
117
Causes of pancreatitis
```
Get smashed
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion
Hyperlipidaemia
Ercp/latrogenic
Drugs
```
118
Clinical signs of pancreatitis
```
High amylase
Low ca
High insulin
High bilirubin alp
Pain
Vomiting
Ecchymosis
Sepsis
Shock
Ileus
```
```
Chronic:
Malabsorption
Weight loss
DM
Jaundice
```
119
Presentation of pancreatic carcinoma
90% ductal
Asymptomatic
Jaundice, pain vomiting, malabsorption, diabetes
120
Microscopic appearance of small intestine
Mucosa folded into villi separated by crypts.
Mitosis occurs in crypts and cells migrate to the villi where they eventually die.
They form a brush boarder with their microvili and with the secretion of enzymes this creates an Unstirred layer.
121
Describe how sugars are absorbed
```
A- amylase in saliva and pancreas yeilds maltose, glucosa, a-limit dextrins by 1-4 bonds.
In brush boarder:
Isomaltase (1-6)
Maltase
Sucrase
Lactase
```
Glucose absorbed via SGLT1 with Na then via GLUT2 into ECF.
Fructose and lactose via facilitated diffusion
Galactose same as glucose.
122
How are amino acids absorbed
Proteins to oligopeptides by pepsin, trypsin, chymotripsin and carboxypeptidase.
Further enzymes in brush boarder.
Aas absorbed via 5 mechanisms mostly Na symporter
Some absorbed as tri/di peptides
123
Describe structure and function of large intestine
The teniae coli (thickened bands of SM) form haustra allowing storage of faeces.
Absorbs water
Absorbs vitamins greater by colonic bacteria e.g. K
124
Absorption of fats
Micelle - Unstirred- diffusion of FA - chylomicrons
125
Absorption of ca
Pumped out of Basolateral membrane. Caatpase
Facilitated diffusion in
Both require vit D
Controlled by PTH
126
Absorption of iron
20mg consumed
Made ferrous by gastric acid and gastro ferrying binds fe and keeps it ferrous
Binds to transferrin secreted by mucosal cells in intestine.
Endocytosed, split and iron is exported to blood
127
Describe oral rehydration
NaCl with glucose and water
| Stim the symporter and add to osmotic gradient.
128
Describe motility across the small intestine
Each short section of bowel has its own pacemaker.
Stomach end is fastest at 8-12 per minute
Circular muscles is not continuous
So causes contents to divide into segments
Mixes and agitates
Segmenting
129
Describe motility of the colon and rectum
Haustral shuttling:
Haustra contract individually pushing contents either side and gradually pushing towards sigmoid colon.
Mass movement - 1-2 times a day
Peristaltic pattern through transverse and descending colon into rectum. Triggers urge to dedicate
Triggered by eating gastro colic reflex
130
Describe the mechanism of defication
After mass movement- pressure receptors in rectum trigger waves of contraction in rectal muscle.
Inner sphincter is parasympathetic activated
External voluntary through sacral reflexes modified by higher process but may be overridden
131
Difference between jenjunum and ileum
```
Jenjunum vs ileum
Dark red vs paler pink
Dense plicae circulares vs sparse/ non
Few arcade loops vs
Dense BV vs
Thick and heavy wall vs thin
Large (2-4 vs 2-3
Less fat vs more
No Peyers patches vs
Liquid vs rlq
```
132
Which part of the duodenum is not retro peritoneal
Duodenal cap/ampulla
133
Pathogenesis of UC
TH2 produces TGF and IL5
Causes ulceration in colon (starts distally at rectum and spreads proximally)
Acutely this can cause the LP to become oedematous forming an abcess and resulting in cryptitis.
Chronicly this can lead to a loss of crypts and atrophy with chronic infiltrate and fibrosis.
134
Pathogenesis of Crohns
TH1 producing Interferon-y and il2
| Widespread non continuous inflammation in any area of bowel. Transmural. Can skip sections
135
Symptoms of UC
Always bleeding
Mucosal friability
Often perianal disease
Distorted vascular pattern
136
Symptoms of crohns
25% bleed
Less chance of perianal disease
Normal vascular pattern
Less common mucosal friability
137
Epidemiology of UC and CD
UC- young female, western adults. smoking helps.
| CD- 15-30 and 60+ smoking worsens
138
Macroscopic changes in UC and CD
CD- cobblestone, thickened, narrowed, fistula and abcessess, ulcers and fissures
UC- inflamed red bleeding, pseudopolyps due to extensive ulceration
139
Microscopic changes UC CD
UC - loss of goblet cells, superficial inflam, crypt abcess, chronic inflam cells in LP
CD- granulomatosis, lymphoid hyperplasia, increase chron inflam cells
140
Investigating Cd and UC
```
Biopsy
Serology anti-neutrophil cytoplasmic antibodies (ANCA) in UC and ASCA in CD
Colonoscopy
Upper GI endoscopy to exclude stuf
Barium follow through
CT with oral contrast
Small bowel ultrasound
MRI (narrowing in CD)- string sign of kantor
```
In UC - colonoscopy and biopsy or AXR to look for dilation
141
Treatment of crohns
Initially - oral glucocorticosteroids, anti TNF a antibodies (infliximab), enteral nutrition
Maintainence- immunosuppressants- methotrexate, azathioprine
Treat perianal disease
142
Treatment of UC
Corticosteroids (can be topical, oral or suppository
Infiximab if extensive
Colectomy
143
Describe the role bacteria play in supporting the normal GI function
```
Synthesise vitamins k b b12 thiamine
Kill non indigenous bacteria
Stimulate growth of malt
Produce antibiotics
Prevent colonisation by pathogenic bacteria
```
144
Describe the broad categorisation of bacteria in the GI tract
Obligate anaerobes e.g. Bacteroides fragilis (g neg bacilli), clostridium but spore forming
Obligate aerobes e.g. Pseudomonas and mycobacterium
Facultative anaerobes e.g. E. coli and staph
Bacilli g pos- clostridium, lactobacillus
Cocci pos- enterococcus faecalis (UTI, meningitis, endocarditis)
145
Cause of gastroenteritis
Campylobacter
Salmonella
Listeria
Possibly staph or clostridium
146
What is noma/ cancrum oris?
Mouth bacteria causing tissue destruction in immunosuppresed patients
147
Cause of dental caries/ gingivitis?
Strep mutans
148
Drugs for bowel surgery?
Metronidazole- anaerobic
Broad spec
Fecal peritonitis has 50% mortality
149
Cause of travellers diarrhoea
Enterotoxinogenic E coli
150
Oesophageal carcinoma features, investigation, pathology, causes, prognosis and treatment
Dysphagia progressive, weight loss, chest pain
Endoscopy, barium swallow, CXR, biopsy
SCC (idiopathic) or AC (dysplasia)
5% 5 year
40% are resectable, gastric tube for feeding
151
Gastric cancer prognosis, risk factors
Women
Geography - Japan
Gastritis - H pylori
Blood group A
152
Clinical features gastric cancer
Epigastric pain
Vague
Vomiting
Weight loss
153
Macro and microscopic features of gastric cancer
Macro:
Fungating
Ulcerative
Infiltrative (leather bottle)
Micro:
Intestinal- variable degree of gland formation
Diffuse - single cells and small groups, signet ring cells
154
Types of gastric cancer, spread, treatment
Early (confined to mucosa) and advanced
Spread - direct, lymph, trams coelomic- liver, peritoneum, ovaries
Treatment- surgery, chemotherapy, Herceptin HER2 receptor
155
Discuss gastric lymphoma
```
Starts as low grade lesion
Strong association with HP
Treat HP may treat cancer
Better prognosis
Commonest lymphoma
```
156
Discuss GI stromal tumours
```
Uncommon
Interstitial cells of cajal
Imatinib specific
Oncogene affected
Unpredictable - necrosis
```
157
Adenoma of large intestine
| Macroscopic, microscopic, behavior, incidence, conditions associated
Sessile or pedunculated
Variable degree of dysplasia
Common with age and western and genetic syndromes
Familial adenomatous polyposis - chromosome 5 AD
Gardners syndrome - also bone and soft tissues
158
Colorectal adenocarcinoma macroscopic, microscopic and spread
60-70 in recto sigmoid
L = stensosing
r= fumigating
Apple core stricture on barium swallow
Variable degree of differntiation, occasionally mucoid or signet ring
Spread direct through bowel, portal to liver or lymph
159
Colorectal adenocarcinoma staging, genetic influence, risk factors and treatment
```
Dukes A-C bowel wall and nodes (highest node clear for 1, involved for 2) or TNM.
Lots of genetic e.g. FAP, DCC, RAS mutation, p53 mutation.
RF:
Low fibre
Slow transit
Polyposis
High fat
UC and CD
Genetics
Treatment:
Suregry for liver
Palliative
Chemo
Radio
```
160
Other bowel cancers
Carcoid- rare endocrine
Lymphoma- primary or secondary
Stromal/ smooth muscle - rare and unpredictable
161
Carcinoma of the pancreas presentation, morphology, histology
Weight loss
Trousseaus sign - bruising
Jaundice
Vague early symptoms,
Most in head, may spread to spleen, firm plae mass when cut is haemorrhagic/ necrotic/ cystic.
80% ductal- adenocarcinoma, well formed glands with poss mucin, granules.
Poor prog
162
Islet cell tumours
Glucagonoma- rash
Insulino,a
VIPoma
Gastrinoma
163
Types of benign liver cancer
Hepatic adenoma
Haemangioma
Bile duct adenoma
164
Malignant liver cancers
Hepatocellular carcinoma
Cholangiocarcinoma
Hepatoblastoma
Secondary
165
Incidence of GI tract cancers
Colorectal 25000
Gastric 11000
Pancreatic 55000
Oesophagus rare
166
Describe the use of AXR for GI
More radiation than CXR
Look for calcification, perforation, has pattern, sort tissue structures and bones - ABC air bowel calcification.
May see mucosal thickening
Not good for inflammation
167
Pros and cons of ultrasound
```
Cheap
Portable
Quick
User dependent
Gall stones
```
168
List common reasons for requesting an AXR
```
Suspected bowel obstruction
Acute exacerbation of IBD
Renal colic (not much now)
Acute abdominal pain
```
169
Compare and contrast the appearance of small and large bowel on an abdominal radiograph and changes with obstruction
Small- central, valvular conniventes, 3cm thick
Large- peripheral, haustra (not all the way across), 6cm, faeces
Caecum 9cm
170
What is an ileus, volvulus, toxic mega colon and lead pipe colon
Ileus is loss of peristalsis e.g. Obstruction or paralysis (K)
Volvulus is twisting of colon around its mesentary resulting in bowel obstruction, ischemia or perforation, sigmoid common, results in coffee bean sign.
Toxic megacolon- acute deterioration of IBS, dilation, oedema, pseudopolyps
Lead pipe colon- severe UC, loss of haustra, featureless
171
CXR in abdo pain
```
Look at zee gas
Perforation in:
Trauma
Iatrogenic
Bowel obstruction
Peptic ulcer
Diverticular
Tumour
```
172
Presentation and causes of small bowel colic
Early vomit
Mid distension
Late absolute constipation
Colic pain2-3 mins
```
Causes
Hernia
Tumour
Inflam
Adhesion
```
173
Presentation and cause large bowel pain
```
Vomit faeculant
Significant distension
Pain
Constipation colic 10-15 mins
Cancer
Diverticula stricture
Hernia
Volvulus
Pseudoobstruction
```
