GIT Flashcards
1
Q
sites of oesophageal constriction
A
-cervical(C5/6)
-thoracic(T4-T5)
-abdominal(T10/11)
2
Q
order of food
A
oesophagus
stomach
duodenum
jejunum
ilium
caecum
ascending colon
transverse colon
descending colon
sigmoid colon
rectum
anus
3
Q
describe abdominal aortic aneurysm
A
-pulsatile mass above umbilicus
-pain, tenderness, hypotension
4
Q
nutcracker syndrome
A
left renal vein is compressed by SMA leading to impaired flow from the left testicular vein
>can cause varicocele(bag of worms)
5
Q
draw innervation of gut
A
6
Q
label the ligaments in abdomen
A
7
Q
what is part of the lesser omentum
A
-hepatogastric ligament
-hepatoduodenal ligament
8
Q
what does the hepatogastric ligament contain
A
left+right gastric arteries
9
Q
what does the hepatoduodenal ligament contain
A
contains portal triad(hepatic artery+portal vein+common bile duct)
10
Q
what is part of greater omentum
A
-gastrosplenic ligament
-splenorenal ligament
-gastrocolic ligament
11
Q
what does the gastrosplenic ligament contain
A
short gastric arteries
12
Q
what does the splenorenal ligament contain
A
splenic artery, splenic vein, tail of pancreas
13
Q
what does the gastrocolic ligament contain
A
left+right gastroepiploic arteries
14
Q
what epithelium lines the oesophagus
A
stratified squamous epithelium
15
Q
what’s barrett’s oesophagus
A
acid from stomach during chronic reflux changes oesophageal epithelium into simple columnar
16
Q
what epithelium lines the stomach
A
simple columnar epithelium
17
Q
what epithelium lines the small intestine
A
simple columnar epithelium
17
Q
what epithelium lines the large intestine
A
simple columnar
18
Q
3 regions of the gut tube
A
-foregut
-midgut
-hindgut
19
Q
what organs are in the foregut
A
-oesophagus
-stomach
-liver
-gallbadder
-pancreas
-upper duodenum
20
Q
what supplies the foregut in embryological development
A
celiac trunk
21
Q
what is part of the midgut
A
-lower duodenum
-jejunum
-ileum
-cecum
-appendix
-ascending colon
-transverse colon(proximal 2/3)
22
Q
what supplies the midgut in embryological development
A
superior mesenteric artery
23
Q
what is part of the hindgut
A
-transverse colon(distal 1/3)
-descending colon
-sigmoid colon
-rectum
-upper anal canal
-urogenital sinus
24
what supplies the hindgut in embryological development
inferior mesenteric artery
25
26
how does the foregut develop embryological
1.the stomach,liver and spleen(develops later) will all be intraperitoneal organs, as the begin developing and remain within the peritoneum
2.as the stomach rotates, it pulls the other organs attached through the ventral+dorsal mesentery with it
3. The liver fills the right side of the abdomen creating the lesser sax behind the stomach
-ventral mesentery->lesser omentum
-dorsal mesentery->greater omentum
4.pancreas is a secondarily retroperitoneal organ, as it starts developing within the peritoneum but ends up outside in the end
27
midgut embryological development
1.the midgut extends out anteriorly as it grows because there is not enough space in the abdominal cavity at this stage(herniation)
-Meckel's diverticulum=viteline duct fails to obliterate
2.the midgut rotates 90 degrees:
-cranial limb is now on the right side
-caudal limb is now on the left side
3.As the abdominal cavity grows, the contents return inside, and complete another 180 degree rotation(so that the cecum ends up in the right upper quadrant)
4.the colon grows downwards, bringing the appendix into the right iliac fossa
-appendicitis=pain originates in umbilical region and later on appears in right iliac fossa region
28
what is in intraperitoneal
-duodenum(1/2 of first part)
-jejunum+ileum
-cecum+appendix
-transverse colon
-sigmoid colon
-rectum(upper 1/3)
29
what is in retroperitoneum
-duodenum(rest of whats not in intraperitoneum)
-ascending colon
-descending colon
-rectum(middle 1/3)
30
hindgut embryological development process
1.terminal hindgut is called the cloaca(merged with urogenital tract-same hole for urine and faeces)
2.cloaca disintegrates to form the anus-if it doesnt disintegrate you can get an imperforate anus(no hole)
3.if the urorectal septum doesnt form properly there may be a connection between the rectal canal and the urogenital tract
31
Nerves innervating the gut
-sensory nerves-chemoreceptors(pH)+mechanoreceptors(stretch)
-autonomic- glands+smooth muscle
-somatic-skeletal muscle
-enteric- glands+smooth muscle
32
how does sensory nerves work
the sensory nerves detect stretch in mucosa(signal CNS)
33
parasympathetic and sympathetic control of smooth muscle
para=nerves increase gut motility and secretion
symp=decrease gut motility and secretions
34
enteric nervous system
-can function independently from CNS and ANS
-2 intrinsic nerve plexus:>myenteric plexus
>submucosal plexus
35
myenteric plexus
-controls gut motility
-controls sphincters
-located between circular/longitudinal muscles throughout gut
36
submucosal plexus
-controls gut secretions
-located in submucosal layer, in discrete locations of gut
37
describe peristalsis
-propulsion of food through the gut occurs through contraction and lengthening of smooth muscle
-2 layers of smooth muscle:>circular
>longitudina
38
how do circular and longitudinal muscles work together
-circular muscles contract behind food bolus to move it forward
-longitudinal muscles contract ahead of the bolus to widen the tract and allow for easier passage
39
what is a sphincter
a circular muscle that normally is constricted but relaxed to allow passage(prevent backflow of luminal contents)
40
what are the 7 sphincters
-upper oesophageal
-lower oesophageal
-pyloric
-hepatopancreatic
-ileocecal
-internal anal
-external anal
41
which sphincters are controls by somatic innervation(skeletal muscle)
upper oesophageal and external anal
42
bile components
-bile salts (cholesterol derivatives)
-cholesterol
-lecithin
-electrolytes and water
-bile pigments
43
what do bile salts do in bile
-help to emulsify fats in small intestine
44
what does cholesterol do in bile
precursor of bile salts
45
what does lecithin do in bile
combines with bile salt to emulsify fats
46
what do the electrolytes and water do in bile
contains high conc of bicarbonate (HCO3) which neutralises acidic chyme in duodenum
47
what do bile pigments do
-marker for haemolysis
48
how are bile pigments produced
breakdown of haem in haemoglobin or myoglobin
-biliverdin is what gives bile the yellow/green appearance
49
emulsification process
-bile salts+lecithin (in bile) help to emulsify fats in the small intestine
-bile salts + phospholipid lecithin embed themselves around outside of emulsion droplets preventing the from coalescing
-emulsion droplets= net negative charge meaning they repel each other
50
functions of bile
1. help emulsification of fats
2. neutralise acidic gastric juices
3. vehicle to aid excretion of liver productions (e.g bilirubin)
51
ways of regulation of bile secretion
-response to fats (CCK)
-response to acidity (secretin)
52
how does Cholescystokinin (CKK) regulate bile secretion
moderates entry of bile into duodenum by
-contracting gall bladder
-relaxing sphincter of oddi
53
how does secretin regulate bile secretion
-causes alkaline secretions from bile ductal cells
54
types of contractions in the small intestine
-mixing/segmenting contractions
-migrating myoelectric complex (peristaltic)
55
what is mixing/segmenting contraction
-localised constrictions which break down and mix the chyme emptied from the stomach with alkaline secretions and digestive enzymes
-2 steps forward 1 step back
-slow type of contraction allows time for absorption of nutrients
56
how does migrating myoelectric complex work
-when most of the nutrients have been absorbed, mixing contractions are replaced by peristaltic contractions(MMC)
-these contractions flush out the reaining luminal contents to the L intestine, triggered by the hormone motilin.
57
how does the hormone motilin work
-activates MMC when bolus ready to move on to large intestine
-triggered by increased pH(and inhibited by feeding)
58
types of contractions in the large intestine
-mixing/ haustral contractions
-mass movements
59
how does haustral contractions work
-localised activation of myenteric nerves and activation of circular smooth muscle
-very slow, hence allows time for absorption of electrolytes and water
60
how does mass movements work
-simultaneous contraction from teniae coli which move faeces from sigmoid colon to rectum.
-this results in a loss of haustra
-activated by distension of stomach/ duodenum and mediated via ANS
61
what is constipation
-stools <2 times a week
-straning >25% of the time
62
causes of constipation
-pregnancy/ inadequate fibre
-IBS
-spinal cord lesions
-depression, anorexia, nervosa
-intestinal obstruction, colonic disease
-rectal prolapse
-diabetes, hypercalcaemia, hypothyroidism
63
Tx of constipation
laxatives
manual evacuation
increase fibre
64
diarrhoea Sx
cramps
fevers
blood in stool
steatorrhoea(fatty stool)
65
Tx of diarrhoea
fluid replacement
treatment of whatever caused it
66
causes of diarrhoea
IBD
osmotic defects
inflamm defects
abnormal mobility
67
defecation reflex
1. stretch receptors in rectum send signals to the spinal cord
2. parasymp nerves signal rectal contractions + relaxation of internal anal sphincter
3. stools move to anal passage
68
what happens to sphincters if we choose to defecate
external anal sphincter relaxes
69
what happens if we choose not to defecate
retrograde peristalsis occurs meaning cerebral cortex inhibits reflex and External anal sphincter constricts, so stool returns to sigmoid colon
70
composition and function of saliva
-water=speech, drug absorption, taste sensation
-mucin=lubricates food
-amylase/ptyalin=digestion
-immunoglobulins
-ions= e.g calcium phosphate ions prevent demineralisation of teeth
71
what is ptyalism
overproduction of saliva
-Tx= give muscarinic antagonists e.g atropine
72
what is xerostomia
dry mouth, may cause implications such as cavities, gum disease and dysphagia
-Tx= muscarinic agonist e.g pilocarpine
73
excitatory triggers for salivation
-presence of food in mouth
-approach of food
-nausea
74
inhibitory triggers for saliva
-sleep
-fear
75
4 types of gastric gland cells
-mucous cell
-parietal cell
-chief cell
-enteroendocrine cell (G cell or EGL cell)
76
2 types of enteroendocrine cells and functions
G cell-secretes gastrin (increases acid secretion)
EGL cell-secretes histamine (increases acid secretion)
77
function of parietal cell
secretes HCl and intrinsic factor
78
function of chief cell
secretes pepsinogen (protein digestion)
-pepsinogen works as when more HCl is produced, pH decreases which activates pepsinogen to become pepsin which breaks down proteins
79
what does a mucous cell do
secretes mucous (lubrication)
80
what is the stimulus, pathway and response of cephalic phase in the secretion of HCl
-stimulus=approach+ presence of food
-pathway= brainstem activates PSNS+ stimulates Parietal and G cells
-response=increased HCl secretion
81
what is the stimulus, pathway and response of gastric phase in the secretion of HCl
-stimulus=stomach distension+ increased pH+ digested proteins
-pathway= PSNS +enteric NS +stimulates P and G cells
-response=increase HCl secretion
82
what is the stimulus, pathway and response of intestinal phase in the secretion of HCl
-stimulus= duodenal distension+ acidity+ protein digestion products
-pathway= intestinal endocrine secretions+ inhibition of vagal nuclei
-response= decreased HCl secretion
83
what 2 cells are found in exocrine pancreas
acinar
ductal
84
what do acinar cells do
secrete pancreatic enzymes (proteolytic,digestive)
85
what do ductal cells do
secrete alkaline pancreatic fluid with high CO3-
>the high pH helps activate pancreatic enzymes
86
what helps regulate pancreatic secretions
-cholecystokinin(CKK)
-secretin
87
what is CCK released in response to
fats
88
what is secretin released in response to
acidity
89
what is CCK responsible for
-enzyme secretion from pancreatic acinar cells
-inhibiting stomach churning
-constricting pyloric sphincter
90
what is secretin responsible for
causes alkaline secretions from pancreatic ductal cells
91
2 ways cholesterol can be eliminated from the body
-conversion to bile salts
-secretion into the bile
92
what is the rate limiting reaction in bile acid synthesis and what significance does it have
-Rate limiting= from cholesterol to 7a-hydroxycholesterol using the enzyme 7a-hydroxylase.
>bile acid production begins a process to inhibit the enzyme, hence negative feedback and maintaining homeostasis
93
what about bile acids make it less toxic and more soluble
they are conjugated with glycine and taurine
94
percentage of bile salts reabsorbed into the blood
95%
(5% lost in faeces)
95
what is the significance of the hepatic portal vein
-provides 50-70% of oxygen supply to the liver> the rest comes from the hepatic artery
-
96
structure of the hepatic portal vein
formed by union of the Superior mesenteric artery and the splenic vein
97
biliary tree
-breakdown of RBCs produces unconjugated bilirubin(lipid soluble)
-albumin binds to unconjugated bilirubin, transporting in blood and liver
-unconjugated bilirubin gets conjugated in liver(water soluble)
-conjugated bilirubin stored in the gallbladder in bile
-conjugated bilirubin enters the small intestine and exits in the stools(brown colour of stools)
-reabsorbed into blood; some goes into kidneys and exits in urine(yellow colour of urine)
98
what is jaundice and what is it caused by
-yellowing of the skin and sclera
-caused by excessive bilirubin in the bloodstream
99
3 causes of jaundice
pre-hepatic
intra-hepatic
post-hepatic
100
pre-hepatic jaundice
-increased haemolysis of RBC
-increased haem=increased unconjugated bilirubin
-too much for the liver to handle=increased unconjugated bilirubin
101
clinical findings of pre hepatic jaundice
-jaundice
-normal urine(unconj bilirubin is not water soluble)
-normal stool colour
-increased unconj bilirubin in blood
102
intra hepatic jaundice
liver damage= conjugated bilirubin leaks into bloodstream
>also reduced capacity to conjugate bilirubin
103
clinical findings of intrahepatic jaundice
-jaundice
-dark urine(conjugated bilirubin is water soluble)
-normal stool colour
-increased conjugated bilirubin in blood(maybe unconj too)
-increased levels of liver enzymes in blood(bigger increases in trans aminases(AST, ALT))
104
post hepatic jaundice
obstruction within biliary tree preventing bile from entering GIT=backlog of conjugated bilirubin(=increased bilirubin in bloodstream)
105
clinical findings of post hepatic jaundice
-jaundice
-dark urine
-pale stool colour
-increased conjugated bilirubin in blood
-increased levels of cholestatic enzymes in blood(bigger increases in cholestatic enzymes(ALP,GGT))
106
liver enzymes(transaminases)
ALT(alanine aminotransferase)
AST(aspartate transaminases)
107
what does elevated transaminase levels indicate
hepatocellular damage (ALT more specific for liver damage)
108
biliary enzymes(cholestatic enzymes)
ALP(alkaline phosphatase)
GGT(game-glutamyl transferase)
109
what does elevated cholestatic enzyme levels indicate
interrupted bile flow
110
What does elavated AST and ALT mean if ALT=AST
ischaemia (e.g hepatitis)
111
What does elavated AST and ALT mean if ALT>AST
hepatocellular damage
-AST:ALT<1-viral hepatitis, paracetamol overdose
112
What does elavated AST and ALT mean if ALT
alcoholic hepatitis, cirrhosis
-AST:ALT>2=alcoholic hepatitis(specific)
113
ALP,GGT elevated levels meaning
biliary obstruction
114
GGT elevated
excessive alcohol consumption
115
5 liver functions
-transport + conjugation of bilirubin
-protein synthesis
-clotting factor synthesis
-thrombopoietin production
-synthesis of vitamin K dependent clotting factors (2,7,9,10)
116
what are the markers impaired functions for liver
-increased bilirubin levels
-decreased albumin levels
-increased prothrombin time(INR)
-decreased platelet levels
117
what does increased INR caused
increased bleeding time
118
chemoreceptors trigger zone
-key structure in mediating nausea/vomiting
-located in area postrema
-lacks effective BBB-ideal for detecting emetic agents in circulation
-5HT receptors + dopamine receptors
119
vomiting centre role in vomiting
-2nd key structure in mediating nausea/vomiting
-not a discrete brain are
-receives input from CTZ, GIT, CVS, limbic system
-muscarinic receptors
120
4 anti-emetic drug classes
-antimuscarinic-hyoscine
-antihistamines-promethazine
-dopamine(D2) receptor antagonists-metoclopramide, prochlorperazine
-5HT3 antagonists-ondanstetron(gold standard)
121
describe antimuscarinics
-most effective for motion sickness
-both prophylaxis and treatment
-non-selective, competitive antagonist
122
side effects of antimuscarinic anti emetic
-blurry vision
-drowsiness
-dry mouth
-urinary retention
123
describe antihistamines
-most effective for motion or morning sickness
-inhibit H1 receptors in area postrema
124
describe dopamine receptors antagonist
-inhibition of D2 receptors in CTZ
-N.B-stimulates D2 receptors in stomach and duodenum= enhanced gastric emptying without purgation
125
describe 5HT3 antagonists
-main site of action at CTZ
-prevent vomiting in 70-80% of patients on chemotherapy
126
side effects of 5HT3 antagonists
constipation
127
what is used for constipation
purgatives(prokinetic agents)
128
what do purgatives do
increase the transit of food through intestines
129
examples of laxatives
-laxatives
-faecal softeners
-stimulant purgatives
130
types of laxatives
-stimulant laxatives
-osmotic laxatives
-bulk laxatives
131
what do stimulant laxatives do
increase electrolyte/ water secretion by mucosa and increase peristalsis-senna
132
what do osmotic laxatives do
draw water into the gut to accelerate transfer of contents through small intestine-lactulose(movicol), polyethylene glycol
133
what do bulk laxatives do
theyre not digested and form bulky, water-retaining masses in GIT promoting peristalsis( often occurring in natural foods)
-psyllium, metamucil
134
what do faecal softeners
surfactant reduces surface tension of water which produces softer faeces
-coloxyl (docusate)
135
types of anti-diarrhoeal agents
opioids
muscarinic antagonists
136
describe opioids and an example as anti diarrhoeal
-doesnt cross blood brain barrier; no CNS effect
-relatively selective for GIT
-decreases activity of myenteric plexus
-e.g loperamide
137
describe muscarinic antagonists as an anti diarrhoeal
-affects enteric nervous system
-side effects outweigh benefit so not often used
138
what are possible causes of peptic ulcers
H.pylori and NSAIDs.
-usually directly caused by too much acid or not enough protection
139
symptoms of peptic ulcers
-haematemesis
-melena(black, tarry stool due to presence of digested blood)
-abdominal/ epigastric pain
140
when is pain worse with gastric ulcers
pain worsens with eating
141
which type of peptic ulcer pain worsens with eating
gastric
142
when does duodenal ulcer pain worsen
when fasting
143
types of medications for peptic ulcers
-Proton pump inhibitors
-H2 receptor antagonists
-prostaglandin analogues
-sucralfate
-Antibiotics
144
how do protein pump inhibitors work in treating peptic ulcers
-prevents protein pump from inserting into the cell membrane, thus preventing protons from being secreted
-irreversible binding and long acting
145
how are PPIs administered
-as enteric coated granule to prevent degradation, acts as canaliculi
146
example of PPIs
-esomeprazole
=>ends in prazole
147
what type of peptic ulcer treatment work best for excess gastric acid secretion
PPIs
148
Describe how H2 receptor antagonists work for peptic ulcer treatment
-inhibits H2 receptors(histamine)
-reversible competitive inhibitor+shorter acting than PPIs
149
what is H2 receptor antagonists effective at inhibiting
nocturnal acid secretion
150
side effects of H2 receptor antagonists
gynecomastia
151
example of H2 receptor antagonists
ranitidine
=>ends in tidine
152
describe how prostaglandin analogues work for peptic ulcers
-stimulates mucus and bicarbonate secretions
153
when is prostaglandin analogues used vs not used
used in NSAID overload
NOT used in pregnancy
154
example of prastaglandin analogues
misoprostol
155
describe how sucralfate work for peptic ulcers
viscous at gastric pH so it adheres to the surface of ulcers and acts as a barrier
>resistant to acid, pepsin, bile
156
when are antibiotics used for peptic ulcers
in case of H pylori infection
157
how does triple therapy work in peptic ulcers
-start with PPI to make env less hospitable for H pylori, and increase effectiveness of A/Bs
-first A/B e.g amoxicillin to kill H pylori
-second A/B to increase eradication rates e.g clarithromycin
158
what is triple therapy
use of PPIs , and 2 courses of A/Bs
159
what is triple therapy used for
used to treat H pylori caused peptic ulcers, which is the most common type
160
types of salmonella
-typhoidal
-non-typhoidal
161
what is typhoidal salmonella
-no animal reservoir
162
what is non-typhoidal salmonella
-large animal reservoir(transferred to humans through food)
163
symptoms of typhoidal salmonella
typhoid + paratyphoid fever (prolonged)
164
Sx of non-typhoidal salmonella
acute diarrhoea which is self limiting, meaning resolves on its own
165
Dx methods of salmonella
-culture
-blood culture(bactraemia)
-rapid molecular methods
166
Tx of salmonella
-fluid+electrolyte replacement
=>antibiotic us is DISCOURAGED
167
causes of enteric fever
-salmonella typhi
-salmonella paratyphi
168
Sx of enteric fever
-fever, malaise(discomfort), aches
-diarrhoea/constipation(varies for individuals)
-rose spots(occurs in only roughly 30%)
169
Dx methods of enteric fever
stool, blood culture, other body fluid/tissue culture
170
Tx of enteric fever
antibiotic treatment started immediately
e.g ciprofloxacin/ceftriaxone, cefixime
171
causes of shigellosis
-shigella sonnei(mild)
-shigella flexneri/ shigella boydii (more severe)
-shigella dysenteriae(most severe)
172
pathogenesis of shigellosis
invades colonic mucosa causing inflamm+ mucosa ulceration
173
Sx of shigellosis
-gastroenteritis
-diarrhoea (watery first, then contains mucus/blood)
-lower abdominal cramps potentially
174
Dx methods of shigellosis
culture, rapid molecular tests
175
Tx of shigellosis
-rehydration
-in severe cases, antibiotics
176
how is shigellosis primarily spread
faecal oral route
-highly infectious
177
