GI Flashcards
(128 cards)
1
Q
what is the large intestine made up of?
A
(from proximal to distal)
caecum
appendix
colon
- ascending colon
- transverse colon
- descending colon
- sigmoid colon
the rectum
anal canal
the anus
2
Q
what is the teniae coli?
A
3 distinct longitudinal bands of smooth muscle, that run from the caecum to the distal end of the sigmoid colon
3
Q
what are haustra?
A
pouches in the colon, formed by tonic contraction of the teniae coli
4
Q
where is the hepatic flexure of the colon?
A
top right side
5
Q
where is the splenic flexure of the colon?
A
top left side
6
Q
where are the 2 paracolic gutters?
A
left and right
between lateral edge of ascending and descending colon and abdominal wall
part of peritonel cavity/greater sac
and potential area for collection of blood or pus
7
Q
where are faeces stored?
A
the rectum
8
Q
which nerves sense the ‘fullness’ of the rectum?
A
normal visceral afferent nerve fibres
9
Q
what muscles control defecation?
A
functioning muscle sphincters
10
Q
where is the pelvic cavity?
A
lies between pelvic inlet and pelvic floor
- rectum is located within here
11
Q
when does the sigmoid colon become the rectum?
A
at level s3
12
Q
where is the rectumsigmod junction?
A
at level s3
13
Q
where is the rectum, anal canal and anus located?
A
rectum - pelvic cavity
anus and anal canal - perineum
14
Q
where does the rectal ampulla lie?
A
superior to the levator ani muscle
15
Q
in males what lies anterior to the superior rectum?
A
rectovesical pouch
16
Q
in females what lies anterior to the superior rectum?
A
rectouterine pouch
17
Q
in males what lies anterior to the inferior rectum?
A
prostate gland
18
Q
in females what lies anterior to the inferior/middle rectum?
A
vagina anf cervix
19
Q
what 3 muscles make up the levator ani muscles?
A
- pubococcygeus
- puborectails
- iliococcygeus
20
Q
where does the breakdown of RBCs happen and what is produced?
A
happens in the spleen
- bilirubin is produced
21
Q
what is used to form bile in the liver?
A
bilirubin
22
Q
why is bile important?
A
it is important for the normal absorption of fats from the small intestine?
23
Q
what ribs protect the liver?
A
ribs 7-11
24
Q
what are the 4 anatomical segments of the liver?
A
right lobe (biggest lobe)
left lobe
caudate lobe
quadrate lobe
25
what is the livers blood supply?
hepatic artery, hepatic portal vein
26
how does blood drain from the liver?
drains blood to the liver via 3 main hepatic veins into the IVC
27
what are the 2 clinically important areas of the peritoneal cavity related to liver?
hepatorenal recess
sub-phrenic recess
(both contained within the greater sac)
28
what is peritonitis?
results in the collection of pus in these recesses (sub- phrenic & hepatorenal) leading to an abscess formation
29
where does the heptal portal vein drain blood from?
foregut. midgut and hindgut to the liver for first pass metabolism (cleaning)
30
where is the portal triad found and what does it contain?
found in the free edge of the lesser omentum
consists of 3 important vessels
- hepatic artery
- hepatic portal vein
- common bile duct
- also contains nerve and lymphatics
31
where is the gallbladder
lies on the posterior aspect of the liver (often firmly affected)
31
what does the gallbladder store?
stores and concentrates biles in between meals
32
how is blood supplied to the gallbladder?
via the cystic artery which is a branch of right hepatic artery (in 75% of people)
33
what does the right and eft hepatic ducts unite to form?
common hepatic duct
34
the common hepatic duct unites with the cystic duct to form?
bile duct
35
where does the bile duct drain into?
2nd part of duodenum
36
what does the bile duct join with and what does it form?
joins with the main pancreatic
and forms the ampulla of vater/hepatopancreatic ampulla
37
what are anatomical sphincters
discrete areas where muscle completely encircles the lumen of the tract
38
where is the pancreas ?
posteriorly lie in the right kidney & adrenal gland, IVC, the bile duct, adnominal aorta, superior mesenteric vessels, left kidney & adrenal gland and part of the portal system
\
- anteriorly lies the stomach
39
where does the blood supply for the pancreas come from?
branches from the splenic artery
- pancreatic branches
close relationship to duodenum so similarities in blood supply
- superior mescentric artery
- gastroduoneal artery
40
what does the small intestines consist of?
- duodenum
- jejunum
- ileum
41
what are the 4 parts of the duodenum?
- superior (duodenal cap) - relatively mobile
- descending
- horizontal
- ascending
41
where does the duodenum begin?
pyloric sphincter
- smooth mucles- autonomic nerves
42
what is the blood supply for the duodenum?
Close relationship to pancreas so similarities in blood supply
- gastroduodenal artery (superior pancreaticoduodenal)
- superior mesenteric artery
( inferior pancreaticoduodenal)
43
where does the jejunum begin?
duodenaljejunal flexure
44
where does the ileum end?
ileocaecal junction
45
whatvare the folds called in the jejunum and ileum called?
plicae circularis
46
what is the blood supply for the jejunum and ileum?
arterial blood from:
- superior mesenteric artery
- via jejunal and ill arteries
venous drainage from:
- jejunal and ill veins
- to superior mesenteric vein
- to hepatic portal vein
47
what is haematemesis?
sign of internal bleeding in the upper GI tract - either coming from the oesophagus, stomach or first portion of your small intestine called your duodenum.
48
what are varices?
- abnormal dilated veins
- thin walled, have potential to rupture - (fill oesophagus with blood)
- formation often due to pathology affecting the portal venous system
49
what is the hepatic portal venous system?
drains blood from absorptive parts pf the GI tract & associated organs for 'cleaning' in the liver
50
what is the systemic venous system?
drains blood fro all other organs and tissues back into the inferior vena cava
51
where does the splenic vein drain blood from and where to?
drains blood from the foregut
drains blood to hepatic portal vein
52
where does the superior mesenteric artery drain blood from and where to?
drains blood from midgut structures to hepatic portal vein
53
where does the inferior mesenteric artery drain blood from and where to?
drain blood from hindgut structures to the splenic vein
54
where are the 3 portal systemic anastomoses?
- distal end of oesophagus
(inferior part drains to portal vein via left gastric vein, superior part drain to the azygous vein)
- skin around umbilicus
(paraumbilical vein drains into the portal vein, inferior epigastric vein into IVC)
- rectum/anal canal
(rectum and superior anal canal drains into inferior mesenteric vein)
55
what is portal hypertension?
clinical term given to increased blood pressures within portal veins
- in the event of portal hypertension, blood will be diverted through the collateral veins back into the systemic venous system
- these collateral veins receive a much larger volume of blood than they are used to = become VARICOSE
- portal hypertension can be a result of liver pathology e.g. cirrhosis
56
what are clinical presentations of portal hypertension?
- oesophageal varices
- caput medusae
- rectal varices
57
what type of transport is the absorption of water? and is driven by the transport of what solutes?
passive transport
- driven by transport of solutes particularly Na+ from the lumen of the intestines to the bloodstream
58
how many litres of water enter the tract per day?
- How much is absorbed by the small intestine
- how much enters the large intestine
9.3L entering the tract per day
- 8.3L absorbed by the small intestine
- 1L enters large intestine of which 90% is absorbed
59
what does the absorption of Na+ provide?
a (local) osmotic force for reabsorption of water
60
what are the principle mechanisms for absorption of water in the GI tract driven by absorption of Na+?
- Na+/glucose co-transport
- Na+/amino acid co-transport
(occurs throughout the small intestine & is most important in the postprandial period, also occurs in the colon in the new born)
- Na+/H+ exchange (occurs in the duodenum & jejunum and is stimulated by luminal HCO3-)
- parallel Na+/H+ and Cl-/HCO3- change (occurs in the ileum and colon and most important in the inter digestive period)
- epithelial Na+ channels (occurs in the colon (distal particularly) and is regulated by aldosterone)
61
explain the Na+ /glucose and Na+ /amino acid co-transport
major mechanisms of postprandial Na+ absorption in the jejunum
- occurs in the colon of new borns
- both examples of secondary active transport
- electrogenic - Na+/K+ ATPase - collectively the overall transport of Na+ generates a transepithelial potential (VTE) in which the lumen is negative and this drive the parallel absorption of Cl-
- neither are regulated by cAMP or Ca2+
62
explain the Na+/H+ exchange in the role of absorption of water in the GI tract driven by Na+
occurs in the jejunum both at the apical (NHE2 & NHE3) and basolateral (NHE1) membranes, but only apical membranes (NHE2 & NHE3) contribute to transepithelial movement of Na+ and the regulation of intracellular pH
- NHE1 is a cellular pH housekeeper
- exchange at the apical membrane, in the jejunum, is stimulated by the alkaline environment of the lumen (i.e high pH = low proton concentration) due to presence of bicarbonate from the pancreas
63
explain the parallel exchange of Na+/H+ and Cl-/HCO3- in the absorption of water in the GI tract driven by Na+
- occurs in the ileum and proximal colon
- primary mechanism of Na+ absorption in the interdigestive period, but does not contribute greatly to postprandial absorption
- Regulated by intracellular cAMP, cGMP and Ca2+, all reduce NaCl absorption
- Reduction in NaCl absorption is a cause of diarrhoea
64
explain what role epithelial Na+ channels (ENaC) play in the absorption of water in the GI tract driven by Na+
- mediate electrogenic Na+ absorption in the distal colon
- Highly efficient and important in Na+ conservation
- increased by aldosterone but NOT regulated by cAMP or cGMP
65
explain the role of aldosterone in the absorption of water driven by Na+
3 actions
1. opens ENaC (seconds)
2. inserts more ENaC into the membrane (minutes)
3. increases synthesis of ENaC and Na+/K+ ATPase (hours)
66
what is the cellular mechanism of Cl- absorption in the small intestine?
driving force provided by lumen negative potential due to electrogenic transport of Na+ (Na+/glucose & Na+/amino acid)
67
what is the cellular mechanism of Cl- absorption in the large intestine?
- driving force provided by lumen negative potential due to electrogenic movement ion Na+ through ENaC
68
explain the cellular mechanisms of Cl- secretion
- occurs at basal rate, but is usually overshadowed by a higher absorption rate
- occurs from crypt cells, rather than villus cells
3 processes are involved on the basal lateral membrane
Na+/K+ ATPase
- Lumen negative potential develops providing voltage-dependent secretion of Na+ through paracellular pathway
Na+/K+/2Cl- co-transporter
- Low intracellular Na+ drives inward movement of Na+, K+ and Cl- via NKCC1
K+ channels
- K+ recycles via K+ channels, but intracellular concentration of Cl- increases providing an electrochemical gradient for Cl- to exit cell via CFTR on the apical membrane
69
explain the role of CFTR
involved in secretion of Cl-
NORMALLY
- Little secretion of Cl- occurs because apical CFTR is either closed, or not present
70
How is CFTR indirectly activated?
- bacterial enterotoxins
- several hormones and neurotrasmitters
- immune cell products
- some laxatives (bile acids)
71
how is CFTR directly activated?
cAMP
cGMP
Ca2+
72
what is the overall effect of the activation of CFTR?
secretory diarrhoea
73
what are the causes of diarrhoea?
- infectious agents – viruses, - bacteria (e.g. traveller’s diarrhoea)
- chronic disease
- toxins
- drugs
- psychological factors
74
what can diarrhoea result in?
- can result in dehydration (Na+ and H20 loss)
- metabolic acidosis (HCO3 LOSS)
- hypokalaemia (low K+)
- MAY BE FATAL IF SEVERE (e.g. CHOLERA)
75
What is the treatment for severe acute diarrhoea?
- maintenance of fluid and electrolyte balance (FIRST PRIORITY)
- use of anti-infective agents (if suitable)
- use of non-antimicrobial antidiarrhoeal agents (symptomatic)
76
what are the major opioids used in the treatment of diarrhoea?
- codeine
- loperamide
- diphenoxylate
76
explain the use of SGLT1 in rehydration therapy?
1. 2 Na+ bind
2. Affinity for glucose increases, glucose binds
3. Na+ and glucose translocate from extracellular to intracellular
4. 2 Na+ dissociate, affinity for glucose falls
5. Glucose dissociates
6. Cycle is repeated
77
what is energy homeostasis?
- physiological process whereby energy intake is matched to energy expenditure over time
- promotes body fuel stability and energy is stored as fat
78
what influences the control of energy intake and body weight?
CNS
1) behaviour - feeding and physical activity
2) ANS activity - regulates energy expenditure
3) Neuroendocrine system - secretion of hormones
the site of interrogation is the BRAIN
- the neural centre responsible is the HYPOTHALAMUS
79
what is satiation?
sensation of fullness generated during meal
80
what is satiety?
- period of time between termination of one meal and the initiation of the next
81
what is adiposity?
the state of being obese
82
describe the role of Cholecystokinin (CCK)
secreted from enteroendocrine cells in
duodenum and jejunum.
Released in proportion to lipids and proteins
in meal. Signals via sensory nerves to hindbrain.
83
describe the role of peptide YY (PYY3-36)
secreted from endocrine mucosal L-cells of G-I tract.
Levels increase rapidly post-prandially.
Inhibits gastric motility, slows emptying and reduces food intake.
84
describe the role of glucagon-like peptide 1 (GLP-1)
product of pro-glucagon
gene.
Also released from L cells in response to food ingestion.
Inhibits gastric emptying and reduces food intake.
Two separate systems – one in gut and one in brain
85
what happens when glutamate, Gaba and opioids are inhered into hypothalamus centres?
INCREASE FOOD INTAKE
- effects are modest/short lasting
86
what happens when monoamines are injected into hypothamlus centres?
act to suppress food intake
87
2 hormones report fat status to brain, what are they?
leptin
- made and released from fat cells
insulin
- made and released from pancreatic beta cells
(level in blood increases, as more fat is stored)
88
what are beta and insulins someone function?
inform brain (hypothalamus) to later energy balance - eat less and increase energy burn
89
what is Gherlin?
peptide, produced and secreted by oxyntic cells in stomach.
levels increase before and decrease after meals
acts to trigger central pathways to prepare body to process in coming nutrients - for store as fats
- helps to control fat metbaloism, increases lipogenesis, and decreases lipid oxidation (liver and adipose)
90
what are the 5 classes of anti-emetic drugs?
- antihistamines (H1 receptor antagonists)
- antimuscarinics (muscarinic acetylcholine receptor antagonists)
- 5-HT3 receptor antagonists
- dopamine receptor antagonists
- neurokinin-1 receptor antagonists
91
name an antimuscarinics (muscarinic acetylcholine receptor antagonists) and what they do
- scopolamine (hyoscine)
- these drugs act primarily as antagonists at muscarinic acetylcholine M1 receptors in the brain
- indicated for motion sickness
91
name 3 antihistamines (H1 receptor antagonists) and what they do
- cyclizine, promethazine, diphenhydramine
- these drugs act on primarily as antagonists at histamine H1 receptors in the brain
- indicated for nausea & vomiting > motion sickness
92
what are the side effects of Antimuscarinics?
Side effects: antimuscarinic side-effects such as dry mouth, tachycardia and constipation
93
What are the side effects of antihistamines?
sedation - because they act at H1 receptors in the brain
94
name 3 5-HT3 receptor antagonists and what they do
- Ondansetron, granisetron and palonosetron
- These drugs act primarily as antagonists at 5-HT3 receptors in the chemoreceptor trigger zone of the medulla in the hindbrain and also the 5-HT3 receptors in the gastrointestinal tract.
95
what are the side effects of 5-HT3 receptor antagonists?
constipation, diarrhoea and headache
96
name some dopamine receptor antagonists and what they do
- Chlorpromazine, droperidol, haloperidol, prochlorperazine, metoclopramide and domperidone
- These drugs act primarily as antagonists at D2 receptors in the chemoreceptor trigger zone of the medulla in the hindbrain (except domperidone) and also the D2 receptors in the gastrointestinal tract
97
what are the side effects of dopamine receptor antagonists?
diarrhoea and extrapyramidal side effects (tremors, muscle rigidity, and involuntary movements) (except domperidone)
98
name 2 neuorokinin-1 receptor antagonists and what they do
- Fosaprepitant and aprepitant
- These drugs act primarily as antagonists at NK1 receptors in the GI tract and the chemoreceptor trigger zone of the medulla in the hindbrain blocking the effects of substance P (which evokes vomiting).
99
what are the side effects of neurokinin-1 receptor antagonists?
constipation and headache
100
what are drugs that affect gastrointestinal motility?
Antidiarrhoeal drugs
(loperamide, diphenoxylate)
drugs that reduce constipation
(naloxegol, prucalopride, lubiprostone)
laxatives
(bulk laxatives, osmotic laxatives, stimulant laxatives)
faecal softeners
(docusate sodium)
101
what are antidiarrhoeal drugs and give some examples of them
electrolyte replacements
- loperamide and diphenoxylate are opiates (bind to µ-opiate receptors)
- sometimes combined with ATROPINE (muscarinic acetylcholine receptor antagonist)
102
what are the side effects of antidiarrhoeal drugs?
constipation, sedation, respiratory depression (common for opiates)
103
what are the 3 types of laxatives?
- bulk laxatives
- osmotic laxatives
- stimulant laxatives
104
what are bulk laxatives?
- Ispaghula husk, methylcellulose
- Bran-bulk formed from polysaccharides that are not digested = bulk leads to a triggering of peristaltic reflexes (involuntary movement that moves food through GI tract)
105
what are osmotic laxatives?
saline purgatives (magnesium sulfate, magnesium hydroxide)
lactulose = osmotic load leads to increased fluid in the bowel promoting movement of the contents in the gut
106
what are stimulant laxatives?
Senna -stimulant purgative - increases electrolyte then water secretion from the rectal mucosa as well as the stimulation of the myenteric plexus = peristaltic reflex (used in bowel obstruction)
- glycerol suppositories - stimulates the rectal mucosa = promotes defecation
107
what do muscus cells secrete?
mucus and bicarbonate
108
what do parietal cells secrete ?
hydrochloric acid
109
what do chief cells secrete?
pepsinogen
110
what do G cells secrete?
gastrin
111
what do D cells secrete?
somatostatin
112
what do enterochromaffin-like cells secrete?
histamine
113
describe the mechanism of histamine
- Histamine is secreted by the enterochromaffin-like cells in the gastric glands in response to stimulation by acetylcholine
- Histamine binds to H2 receptors with subsequent activation of adenylyl cyclase
- The increase in cAMP increases the number of proton pumps, increasing gastric acid secretion from parietal cells
114
describe the mechanism of acetylcholine (ACh)
released by parasympathetic cholinergic neurons
- ACh binds to muscarinic (M3) ACh receptors on parietal cells with subsequent activation of PLC
- The increase in intracellular Ca2+ evokes cell signalling pathways that increase the number of proton pumps, increasing gastric acid secretion from parietal cells
115
describe the mechanism of gastrin
- Gastrin is released by G cells
- Gastrin binds to CCK2 receptors on parietal cells with subsequent activation of PLC
- The increase in intracellular Ca2+ increases the number of proton pumps, increasing gastric acid secretion from parietal cells
116
describe the mechanism of somatostatin?
- Somatostatin is secreted by D cells in the gastric glands
- Somatostatin binds to SST2R receptors, inhibiting adenylyl cyclase
- The decrease in cAMP results in decrease gastric acid secretion from parietal cells
- Somatostatin binding to SST2R receptors on enterochromaffin cells results in reduced histamine release and decreased gastric acid secretion from parietal cells
116
how do antacids reduce symptoms of excessive gastric acid secretion?
by buffering hydrochloric acid
117
how do NSAIDs work?
disrupt hr production of prostaglandins by inhibiting COX-1
-the reduced availability of prostaglandins results in histamine secretion from enterochromaffin-like cells, promoting HCL secretion from parietal cells
118
how does Misoprostol work?
- Misoprostol is an agonist at prostanoid EP3 receptors (greatest affinity) and EP2 and EP4 receptors.
- EP3 receptor activation results in inhibition of gastric acid secretion, mucus secretion, GI smooth muscle contraction and contraction of the uterus during pregnancy.
- EP2 and EP4 receptor activation results in bronchodilation, intestinal fluid secretion and GI smooth muscle relaxation.
119
what can be given for NSAID-induced peptic ulcer?
misoprostol
120
what are the sides effects of misoprostol?
abdominal pain and diarrhoea
121
describe the action of proton pump inhibitors (PPIs) and give examples of THEM?
- Lansoprazole, omeprazole, pantoprazole (INHIBIT H+/K+ ATPase pump) = reduces HCL secretion
- Indicated for benign gastric acid ulceration and NSAID-associated gastric ulceration, gastro-oesophageal reflux disease and Zollinger–Ellison syndrome
122
what are the side effects of proton pump inhibitors?
increases stomach pH reduce defences against infection via the GI tract
123
