GastroIntestinal Flashcards
what are the 4 lines that divid the nine regions of the abdomen?
two midclavicular
one lower part of costal margin
one through the tubercles of the pelvis
what are the names of the nine regions of the abdomen?
what are the three parts of the developing gut?
foregut, midgut, hindgut
where does the foregut end?
1/2 way duodenum
where does the midgut end?
2/3 along transverse colon
where does the hind gut end?
upper anal canal
the parietal peritoneum is innervated by…?
somatic nerves
the visceral peritoneum is innervated by….
visceral sensory nerves
what is secreted by the stomach that allows for vit b12 absorbtion?
intrinsic factor
what cells in the stomach produce intrinsic factor and gastric acid?
parietal cells
in the Cephalic phase, what neurotransmitter triggers the release of gastrin and histamine?
acetylcholine
what peptide hormone acts directly on parietal cells to priduce gastric acid.
how else does it trugger the secretion of gastric acid?
Gastrin acts directly on parietal cells to produce Gastric Acid
Gastrin also acts directly on histamine, which acts on parietal cells.
what peptide inhibits the activity of the stomach?
somatostatin
In the gastric phase, what condition will inhibit gastrin (and therefore indirectly, histamine) and stiumlate somatostatin?
low luminal pH
in the intestinal phase, which enterogastrones are released to inhibit gastric acid secretion?
secretin and cholecystokinin (CCK)
what conditions in the duodenum trigger the release of enterogastrones that inhibit gastric acid secretion?
Duodenal distension
Low luminal pH (2)
Hypertonic luminal contents (higher osmolality than blood)
Presence of amino acids and fatty acids
also reduces vagal/parasymp stim (XAch)
Regulation of gastric acid secretion looks complicated at first but isn’t really!
Controlled by brain, stomach, duodenum
1 (parasympathetic) neurotransmitter =
1 hormone =
2 paracrine factors =
2 key enterogastrones =
1 (parasympathetic) neurotransmitter = (ACh +) cephalic
1 hormone = (gastrin +) gastric/cephalic
2 paracrine factors = (histamine +, somatostatin -) - gastric’cephalic
2 key enterogastrones = (secretin -, CCK -) intestinal
what is an ulcer?
a breach in a mucosal surface
name FOUR ways the gastric mucosa defends itself
- alkaline bicarb rich mucus -
- tight junctions between epithelial cells prevent gasttic acid or enzymes passing between cells
- replace amaged cells
- negative feedback loops
how do NSAIDs cause peptic ulcers?
NSAIDS inhibit cyclo-oxygenase 1.
Cyclooxgenase 1 = prostaglandin = mucus secretion
how do Helicobacter pylori cause ulcers?
Lives in the gastric mucus
Secretes urease, splitting urea into CO2 + ammonia
Ammonia + H+ = Ammonium (DAMAGING)
Ammonium, secreted proteases, phospholipases and vacuolating cytotoxin A damage gastric epithelium
Inflammatory response
Reduced mucosal defence
how do you treat helicobacter pylori?
Eradicate the organism!
Triple therapy: 1 proton pump inhibitor
2 antibiotics
how do you treat peptic ulcer disease caused by NSAIDs?
Prostaglandin analogues – misoprostol = increases mucus production
Reduce acid secretion
which cells in the stomach produce pepsinogen?
which produce pepsin?
cheif cells
NO cells produce pepsin (active protease would digest body)
what stiumulates the initiation of the Cephalic phase?
sight/smell/thought/taste/chewing of food
=vagus nerve
what stimulates thae gastric phase?
gastric distention - acts on stretch receptors to stimulate local and vagovagal reflexes
food chemicals - proteins and amino acids = buffer:mop up H+ causing pH to RISE which decreases Somatostatin
this stimulates release of gastrin, (and histamine = parietal) = parietal
plus decrease somatostatin
what turns it off in the gastric phase?
- Excess acidity
(no food in stomach) - emotional distress (sympathetic override: f/f>r/d)
inhibits gastrin (indirectly inhibits histamine)
stiumlates somatostatin
whatt stimulates the start of the intestinal phase?
- partially digested food presnt (Chyme)
more acid secretion
what turns on the intestinal phase?
- food presence low luminal pH (chyme)
-duodenal distention - hypertonic solution
- amino acids and fatty acids
- SECRETIN
- CCK
- SHORT AND LONG NEURAL PATHWAYS REDUCE PARA = REDUCE ACh
pepsin activation is an example of what?
positive feedback loop
conversion of pepsinogen to pepsin is [a] dependent.
its is an example of a [b] feedback loop in that pepsin also catalyses the reaction
A [c] occurs in the small intestine by HCO3
[a] pH
[b] positive
[c] irreversible inactivation
pepsin is responsible for what % of protein digestion?
20%
Empty stomach has a volume of ?
it can accomidate ?
this shows its ?
50ml
1.5L
Receptive relaxation
Receptive relaxation is mediated by [a]
it is coordinated by the [b]
and is relaxed by [c] and [d] release
[a] parasympathetic Nervous System
[b] Vagus nerve
[c] NO
[d] serotonin
Perisaltic waves move towards the ?
antrum
peristaltic waves are initially…
they are most powerful in the …
… closes as the wave reaches it
weak
gastric antrum
Pylorus
av
the pacemaker cells of the stomach are
interstitial cells of Cajal
the strength of peristaltic contraction increases with what?
-Gastrin
-Gastric distenion (mediated by Mechanoreceptors)
the strength of peristaltic contraction decrease by
same as HCl!!
- high duodenal luminal fat
- high duodenal osmolarity
- high symp NS action
- low para NS action
- low duodenal luminal pH
overfilling of duodenum results in?
dumping syndrome
what is gastroparesis
delayed gastric emptying
what are some causes of gastroparesis?
Idiopathic
Autonomic neuropathies (e.g. in Diabetes mellitus)
Drugs – next slide
Abdominal surgery
Parkinson’s disease
Multiple sclerosis
Scleroderma
Amyloidosis
Female sex
name some symptoms of gastroparesis
Nausea
Early satiety
Vomiting undigested food - Feculent vomiting (rotted food)
GORD
Abdo pain/bloating
Anorexia
name some treatments of gastroparesis
Gastrointestinal agents:
Aluminium hydroxide antacids
H2 receptor antagonists
Proton pump inhibitors
Sucralfate
Anticholinergic medications
Diphenhydramine (Benadryl)
Opioid analgesics
Tricyclic antidepressants
Miscellaneous
Beta-adrenergic receptor agonists
Calcium channel blockers
Interferon alpha
Levodopa
on a whiteboards, label this.
Label this!
The inferior mesenteric vein unites with the [a].
The splenic vein unites with the superior mesenteric vein to form the [b] vein.
The hepatic portal vein enters the liver. Blood is processed, nutrients removed, and the venous blood then enters the hepatic veins, which join the [c].
[a] splenic
[b] portal hepatic
[c] IVC
what artery supplies the foregut?
celiac trunk
what artery supplies the midgut?
SMA
superior mesenteric artery
what artery supplies that hindgut?
IMA
inferior mesenteric artery
nerve supply of foregut?
S: greater splachnic (T5-T9)
P: Vagus
nerve supply of midgut?
S: Lesser Splanchnic (T10-T11)
P: Vagus
nerve supply of hindgut?
S: Least splanchnic (T12-L1)
P: Pelvic splanchnics
where is visceral pain from foregut felt?
epigastric region
where is visceral pain from the midgut felt?
umbilical region
where is visceral pain from the hindgut felt?
suprapubic region
what tissue is the primitive gut tube formed from?
Endoderm.
(visceral mesoderm froms the connection = dorsal mesentry)
what is happening in B and what can its failure lead to?
closure of the ventral body wall.
Faulure of closure:
label the red boxes (connections). what type of tissue do they derive from?
aside from gene expressions, what helps the gut tibe to differentiate into its different componentst?
the concentration of retinoic acid
two mesenteries of the foregut?
dorsal mesentery and
ventral mesentery
when does the lung bud appear on the wall of the foregut?
what then happens (normally) ?
week 4.
they then separate
atresia or fistulas can occur
describe some key aspects of the development of the stomach.
changes shape due to different growth rates of different parts
Rotates 90° clockwise (left–>anteriorly, right–>posteriorly)
Tipping (duodenum—>right oesophagus–>left)
how does the development of the stomach affect the final positions of the foregut?
the rotation of the stomach pulls the mesenteries, omenta and peritoneal ligaments which pull the organs.
some of theses organs (pancreas and duodenum) are pushed into the posterior abdominal wall and become retropeitoneal.
Less sac is formed
The liver bud is an outgrowth of the [a] and appears in week [b]
Cells proliferate into the [S….. T……]
The connection betweem the liver bud and the foregut narrows, this is the [c]
A small outgrowth from the bile duct forms, this is the [d]
The [S….. T…..] becomes membranous and forms to [e] and the [f]
[a] distal foregut
[b] 3
[Septum Transversum]
[c] bile duct
[d] gall bladder
[Septum Transversum]
[e] lesser omentum
[f] falcifom ligament
Development of the Pancreas
[D…] and [V….] buds arise from the duodenum
[D…] develops in the [?]
[V…] swings round due to rotation of stomach
[D] and [V] fuse
Dorsal and Ventral
Dorals develops in the dorsal mesentry
the ventral mesentry is split into the:
lesser omentum
and
falciform ligament
Name 3 defences of the Oral Cavity
- mucosa
- Saliva (wash away particles and viruses, plue lymphatics around glands
- Palatine tonsile (surveillance for immune system)
how many teeth in children/adults
children = 20, adults 32
Two types of Intralobular Ducts?
saliva
Intercalated and Striated
salivary Ducts secrete {a] and {b}
and reabsorb {c} and {d}
[a] K+ and [b] HCO3
[c] Na+ and [d] Cl-
5 functions of saliva
- Lubricant (chewing swallowing speech)
- Oral Hygiene
- Maintain pH
- amylase
- aqueous solvent necessary for taste
2 types of salivary secretion
serous (amylase)
mucous (lubrication)
3 salivary glands and their secretions..
- Parotid 25% (serous only)
- Submandibular 70% (mucous and serous)
- Sublingular 5% (mainly mucous )
- Minor (mainly mucous)
how much saliva do we produce a day?
800-1500ml
what factors can affect compostion and amount of saliva?
flow rate
circadian rhythm
type/size gland
stimulation
diet
sex
age
what % of salivary flow are the major salivary glands responsible for,
the rest?
80% parotid, submandibular, sublingual
20% minor glands
which salivary g;ands are constantly active and which are only active when stimulated
Continuosly active:
-sublingual
-submandibular
-minor
Only when stimulated:
-parotid (thought or smell)
three structures around the parotid gland?
- External carotid artery
- Retromandibular vein
- Facial nerve (supplying the muscles of facial expression)
parotid gland innervated by:
parasympathetic: Glossopharyngeal (CNIX)
sympathetic: Auriculotemporal (CNV3)
innervation of the sublingual gland
Para: chorda tympani (VII)
Symp: lingual nerve (VII)
submandibular innervation
Para: chorda tympani (VII)
Symp: lingual (VII)
Name 4 areas of the body that require glucose.
of these, 4, which require a constant energy supply?
muscle, brain, RBC, adipocytes.
Brain cant store glucose so requires constant flow of glucose from blood,
RBCs have not mitochondria so cant make own energy to require constant gllucose.
what happens to glucose when it enters the liver?
1) converted to glycogen to be stored
or
2) to Acetyl CoA for i. Krebs Cycle = ATP or ii. Trilglycerides = VLDL
where is insulin produced?
pancreas
what promotes the uptake of glucose into cells for storage in the liver?
insulin
what is glucose stores as in muscle?
what promotes this?
how does the brain get energy?
how to erythrocytes get their energy?
- Glucose taken up but cannot be stored
- No mitochondria present
- Glucose gets converted into pyruvate = energy
- This can then diffuse out the cell or be converted into lactate = energy
- Lactate is then released from the cell
How to adipocytes get energy?
- Glucose taken up, promoted by insulin
- Used to make ATP or stored as triglycerides
describe how amino acids are absorbed in the body and what they are use for
absorbed in the jejunum,
converted into proteins and can make hormones
or
feed into Krebs cycle (if glucose stores are low, amino acids and fatty acids can be converted into acetyl coA for Krebs)
Describe how fat is absorbed and transported in the body
Fat broken into triglycerides.
insoluble
therefor transported by lipoproteins
which are carried by chylomicrons which travel into the
lymphatic system and then into the blood
summarise what happens to fuels in the Fed state
fuels are oxidised to energy
any excess is stored:
-triglycerides in adipose tissue
- glycogen in liver and muscle
what is glycogenolysis?
what facilipromtoesates it?
break down of glycogen into glucose
promotes by: glucagon
during a short fast, what will happen in order to maintain glucose supplies to RBCs and brain?
Glucogon will promote glycogenolysis in the liver: break down of glycogen to glucose
during a longer fasting period, when the liver’s store of glycogen is empty, what will the body do to retain glucose supply to the brain and RBCs?
The liver will begin glyconeogenisis:
Amino acids (from muscle), Lactate (from RBCs) and Glycerol (from adipocytes) made into glucose in the liver
alanin-glutanine shuttle, pyruvate/lactate shuttle, B-oxidation
how are fats used as energy during fasting?
Glucogon promotes lipolysis which breaks down triglycerides into glycerol and fatty acids.
glycerol can be converted into glucose in the liver
fatty acids can be converted into ketones in the liver
during prolonger fasting period, what happens to retain energy supplies to blood and brain?
Gluconeogenisis decreases (Cannot break down too much muscle - resp muscle!)
Ketogenesis occurs in the liver (from fatty acids from fats)
ketones supply brain
remaining glucose supplies RBCs
what is the main anabolic hormone?
what is meant by this?
insulin
anabolic = storgae
-promotes glycogen and fat storage and protein synthesis
what is the main catabolic hormone?
what is meant by this?
glucagon
catabolic = energy release
(glycogenolysis, gluconeogenesis, ketogenesis)
How does Cortisol affect fuel metabolism?
cortisol = stress hormone: prepares body for stress repsponse:
* lypolysis
* gluconeogenisis
* glycogen storage
* protein breakdown
how does adrenaline affect fuel metabolism?
fight or flight gets energy in the blood stream ready to be utilised (glycogenolysis, gluconeogenesis, lipolysis)
how does thyroxine affect fuel metabolism?
Thyroxine; generally controls metabolism (glycolysis, cholesterol synthesis, glucose uptake, protein synthesis, sensitises tissues to adrenaline)
too much thyroxine = catabolic
how does growth hormone affect fuel metabolism?
Growth hormone; (gluconeogenesis, glycogen synthesis lipolysis, protein synthesis, decreased glucose use)
whoat hormone increases appetite?
Ghrelin
what hormone decreases appetite?
leptin
what happens with leptin in obesity
high leptin levels, develop leptin resistance
The proton pump is part of the parietal cell.
What is the function of the proton pump with regard to ion exchange across the cell membrane?
K+ into cell, H+ out of cell
Digestion of the different dietary components occurs in different parts of the GI tract.
What is the first location that fat is acted upon by Lipase enzymes when passing through the GI tract?
oral cavity
what is secreted by cheif cells?
pepsinogen
Omeprazole is routinely prescribed for acid reflux.
What is the mechanism of action of Omeprazole on the GI tract?
Inhibition of Proton Pump to reduce acid secretion
what do D cells in the stomach secrete?
Somatostatin
how many layers of muscle cells are in stomach tissue?
3
longitudinal, circular, oblique
what cells produce intrinsic factor and what is its function?
parietal cells.
Allows absorption of Vitamin B12 in the terminal ileum
A 23 year old patient complains of stomach pains after taking a Non-steroidal anti-inflammatory analgesic (NSAID).
How do NSAIDs irritate the stomach?
By inhibition of gastrointestinal mucosal cyclo-oxygenase (COX) activity
what does the common bile duct drain into?
duodenum
what substance is secreted by G cells in the stomach?
Gastrin
Which of the following vessels supplies arterial blood to the Jejunum?
A.
Direct branches from Aorta
B.
Inferior Mesenteric Artery
C.
Right Gastro-Epiploic Artery
D.
Splenic Artery
E.
Superior Mesenteric Artery
E.
Superior Mesenteric Artery
2what cells in the stomach secrete Histamine?
Enterochromaffin-like (ECL) Cells
what structures run through the hepatic portal?
the hepatic artery proper, portal vein, hepatic bile duct, Vagus nerve branches, sympathetics and lymphatics.
It does NOT contain the Hepatic Vein
what type of cell line the oesopphagus?
stratified squamous epithelial
Which of the following statements is correct regarding the function of the Vagus nerve and its action on parietal cells?
A. Vagus nerve is part of the parasympathetic system and releases acetylcholine onto parietal cells
B. Vagus nerve is part of the parasympathetic system and releases histamine onto parietal cells
C. Vagus nerve is part of the parasympathetic system and releases noradrenaline onto parietal cells
D. Vagus nerve is part of the sympathetic system and releases acetylcholine onto parietal cells
E. Vagus nerve is part of the sympathetic system and releases adrenaline onto parietal cells
A. Vagus nerve is part of the parasympathetic system and releases acetylcholine onto parietal cells
what is ferritin and where can it be found
protein that stores iron.
found in cytoplasm of cells and sometimes serum.
what can cause ferritin excess?
- Excess iron storage disorders
(e.g. hereditary haemochromatosis, multiple blood transfusions, iron replacement therapy) - Non-iron related
(ege. liver disease, malignancies, tissue distructions, inflammation, infection, autoimmune)
what can cause ferritin deficiency?
ONLY Iron Deficiency
what are the water soluble vitamins?
B, C and folate
what are the fat soulble vitamins?
ADEK
Vitamin A functions
vision,
spermatogenesis, prevention of fetal reabsorbtion
Growth
clinical features of vitamin A deficiency
night blindness, xeropthalmia, blindness
rare in affluent countries
clinical features of vitamin A excess
abdominal pain, nausea, vomitting, headaches, joint and bome pain, hairloss, sluggishness, weight loss
(Carotenemia: reversible yellowing of skin, non toxic)
Funtions of Vitamin D
- increase intestineal absorbtion of calcium
- resorbtion and formation of bone
- reduced renal excretion of calcium
what can a vitamin D deficiency lead to?
demineralisation of bone:
rickets in children, osteomalacia in adults
where is vitamin E stored within the body?
liver, plasma and adipose cells
what are the daily vitamin E requirements?
4mg/day in men,
3mg/day in women
same some sources of vitamin E
nuts, oils, spinach, avocado
what can a vitamin E deficiency cause?
fat malabsorbtion, premature infants
which vitamin is key in the activation of some blood clotting factors?
bonus: which factors?
vitamin K
VII, IX, X, II(prothrombin)
how can you assess vitamin K levels?
prothrombin time
how long a blood clot takes to form
sources of vitamin k?
leafy greens
where/how is vitamin K stored?
Vitamin K is rapidly taken up by the liver but then is transferred to low density lipoproteins which carry it into the plasma
what can a vitamin K deficiency lead to?
haemorrhagic disease of the newborn
(rare in adults)
how much vitamin C do adults need a day?
40mg
what is the function of vitamin C?
collagen synthasism
antioxidant
iron absorbtion
what can a vitamin C deficiency lead to?
scurvy,
easy bruising and bleeding,
teeth and gum disease,
hair loss
what are the two active forms of vitamin B12?
methylcobalamin
5-deoxyadenosylcobalamin
how is vitamin B12 absoribed?
- released from food by acid and enzymes in the stomach
- binds to R proteins to protect it fro stomach acid
- released from R porteins by pancreatic polypeptide
- Intrinsic Factor (parietal cells) required for absorbtion
- IF-B12 complex absorbed in terminal ileum
- B12 Stored in the liver
sourced of vitamin B12?
meat, fish, eggs, milk
what can cause a vitamin B12 deficiency?
- pernicious anaemia - autoimmune destruction of parietal cells
- malabsorbtion
- veganism
symptoms of B12 deficiency?
macrocytic anaemia
peripheral neuropathy
when might someoe need more folate?
pregnancy
what are the functions of folate?
DNA synthesis
in which food might you find folate acid?
folate fortified cereals
symptoms of folate defeciency
macrocytic anaemia
foetal development abnormalities (spina bifida)
what can cause a folate deficiency?
malabsorbtion
leukemia, haemolytic anaemia
how much background radiation in an Xray?
4 months
how much background radiation in a CT?
4.5 years
label the arrows on this abdominal CT
label the arrows on this abdominal CT
label this CT
what are these lines in these bowl obstructions. where are each of the obstructions?
what is the red arrow pointing to?
what is the likely cause?
free air under the diaphram.
perforation
Label the:
* liver
* gall bladder
* ascending colon
* bladder
label the:
* Kidney
* Aorta
* Stomach
* Liver
* IVC
* Aorta
label the arrows
label the arrows
what is a normal diameter ofL
small intestine, large intestine, caecum
3cm, 6cm, 9cm
what is a xenobiotic?
foreign substance which have no nutritional valur so need to be excereted.
can be toxic if not excreted in time.
how do xenobiotics enter the body?
mostly ingested - eg DRUGS
can be inhaled
what do xenobiotic damage if they enter the body?
proetins, lipid and can bind to DNA (carcinogen)
compounds need to be hydophillic/hydrophobic to be excreted in the urine.
hydorphillic
which enzymes are important for phase 1 reactions in liver detox?
Cytochome P450 (CYP)
what is the purpose of phase 1 in drug metabolism? (detox)
to add or expose a functional group
-oxidation- add electron to make slightly more polar.
uses CYP450
phase I of drug metabolsim results in small/large increase in hydophilicity
phase II?
phase i = small increase
phase ii = large increase
what is the puropse of phase ii drug metabolism (detox)
conjugation
to add a polar substrate.
(covalently bonded)
prodcues (significantly more) hydrophilic metabolite
e.g. glucoronidation, sulfoconjugation, methylation
what enzyme facilitates phase ii or drug metabolism (detox)
transferase
there are many. UGT important.
Uridine 5’-diphospho-glucuronosyltransferase (UDP-glucuronosyltransferase, UGT)
what is the name of the polar body that is added to a substrate during glurcuronidation during phase ii detox to make it more hydophillic?
glucuronide
Conjugation examples = glucuronidation, sulfoconjugation, methylation
where does biotransformation occur in the hepatocyte?
smooth ER
where can CYPs be found?
smooth ER (sometimes called microsomal enzymes)
what is the function of CYPs?
oxidise substrate (via oxidation, reduction or hydrolysis)
What is th most common isoform of CYP450?
what % of drugs is it involved in the metabolism of?
CYP3A4.
50% of all clinically prescribed drugs
90% of Ethanol metabolised via what enzyme?
what does this generate?
why can this become harmful?
Alcohol Dehydrogenase (ADH)
Acetaldehyde (toxic) and NADH (Krebs)
also CYP2E1
10% of Ethanol is metabolised via what?
what does this produce?
Microsomal Ethanol Oxidising System (MEOS)= CYP2E1
acetaldehyde (toxic intermediate) and Reactive Oxygen Species = DNA mutation, Protein damage
chronic alcohol use increases what enzyme? This produces which toxin?
CYP2E1 (5-10x)
Alcohol metabolised quicker
But: Acetaldehyde produced quicker (overwhellms clearing enzymes)
Build up of ROS = liver damage from free radicals and peroxides
this is a sample from colon. Lable the two layer of muscle that can be seen
Explain the Intrinsic nerve supply to the colon
Myenteric Plexus (Auerbach’s) and
submucosla plexus
in the colon, which nerves are responsible for absorbtion?
submucosa plexus
aside from the internal and external sphincter, what mechanism in the lower rectum promotes continence?
The Puborectalis muscle sling
which creates the
Anorectal Angle
which phase of defecation is this?
what manouver facilitates this
expulsive phase
(everything relaxed)
Valsalva manouevre and posture aids emptying
what is the difference between a saturated and unsaturated fatty acid?
saturated = lined up
sunsaturated = double bond = kink
decribe the makeup of lipoproteins
TG and cholesterol core
phosopholipis, cholesterol, protein surface
protein:lipid detrmines density
what determines the densisty of a lipoprotein?
protein:lipid
little protein ——————–>high protein
low density————————>high density
chylomicron < VLDL < LDL < HDL
what protein adds lipid components (sER) to ApoB (RER)?
microsomal TAG transfer Proteins
What happens to the ApoB in the gogi apparatus?
glycosylated
what are the three main fates of AA’s?
- Form other biomolecules (eg nucleotides
- form into proteins
- remove nitrogenous amino acid group removed and have carbon backbone used to make glucose
describe what happens in transamination.
an amino acid transfers its amino group to an accepting alphaketoacid.
turn into eachother
what is this reaction an example of?
transamination
what is it called when lysosomal protein degredation goes wrong?
cystinosis
* genetic, recessive
* cystine not transported out and crystallises
* eye and kidney problems
do you know the urea cycle?
Old Colourful Cats Always Ask For Awesome Umbrellas
do you know the glucose alanine cycle
explain how electrolytes and glucose from the gut enters the blood stream
2 stage transcellular process:
1st stage: membrane transport protein
2nd stage: Na+K+ATPase transporter
water follows sodium
outline how intestinal secretion works.
Cl- enters cell (with Na+ and K+ which are pumped out)
This generates cAMP
this activates CFTR
Chloride secreted into Lumen
Build up of Cl- = negative charge which pulls Na+ into lumen
NaCl secretion
creates osmotic gradient across tight junction and water drawn into lumen
cystic fibrosis transmembrane conductance regulator
what has happened to the villi here?
when might you see villi like this?
Villi atrophy.
coeliac disease - cant absorb = malnutrition and diarrohea
what breaks proteins into polypeptides? where?
what breaks polypepties into short peptides and AAs? where?
what breaks these into AAs? where?
what is needed for fat absorbtion?
bile
Substances of the stomach: FUNCTION
Substances of stomach: SOURCE
name some structures in each of the 9 regions of the abdomen
name the muscles in the anterior wall muscles
- Transverse abdominis
- Internal Oblique (up)
- External Oblique (down)
- Rectus abdominus
what are the two compartments of the greater sac and what do each contain?
supracolic (above transverse mesocolon)
-contains stomach, liver and spleen
infracolic (below transverse mesocolon)
-contains small intestine, ascending and descending colon
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Gastrin:
Source?
Action?
Regulation?
Somatostatin.
Source?
Action?
Regulation?
Cholecytokinin.
Source?
Action?
Regulation?
Secretin
Source?
Action?
Regulation?
Glucose- Dependent Insulinotropic Peptide (GIP).
Source?
Action?
Regulation?
INHIBITS gastric acid
Ghrelin.
Source?
Action?
Regulation?
Gastric Acid.
Source?
Action?
Regulation?
Intrinsic Factor
Source?
Action?
Regulation?
Pepsin.
Source?
Action?
Regulation?
Zymogen?
Bicarbonate.
Source?
Action?
Regulation?
in the parietal cell, what is it that combines H2O and CO2 to get H2CO3
Carbonic Anhydrase
Water distribution in the body.
again lol - learn it.
summarise carbohydrate digestion
starts in mouth with amylase digesting starch
majority of carb digestion in small intestine due to pancreatic amylase
forms disaccharide
the final conversions are done by brush border enzymes
summarise protein digestion
- starts in stomach with pepsin → preliminary breakdown of protein
- continued through pancreatic enzymes
-chymotrypsinogen, trypsinogen, elastase, carboxypeptidase - finally through border enzymes
split into amino acids, dipeptides and tripeptides
explain what happens during elongation phase of embryologcal development of midgut
Rapid formation of primary imtestinal loop.
Vitellin duct narrows
end up with two limbs: caudal and cephalic.
during stage 3 of the embryological development of the mid gut, what happens?
Rotation.
90° anticlockwise around SMA during herniation.
Caudal limb moves cranially.
Elongation.
Caudal elongates but doesnt coil. Cephalic elongates and coils
When does the retraction phase occur in embryological development of midgut?
What happens?
Retraction = week 10
Gut loop returns to abdomen.
Further rotation 180° anticlockwise.
Cephalic returns first to the left of the abdomen (jejunum, ileum)
Followed by the Caudal to the right upper quadrant (causcum descends to right ileac fossa.)
what are the three branches of the celiac trunk?
left gastric
splenic
common hepatic
four for main anatomical divisions of the stomach?
cardia, fundus, body, pyloric antrum canal and sphincter
what are the anatomical differences between the jejunum and ileum
Jejunum: simple arcades + longer vasa recta , ileum: complicated arcades + shorter vasa recta
Jejunum: plicae circulares (circular folds) + numerous villi, ileum: no plicae circulares + less villi
Jejunum: no lymphoid follicles, ileum: many lymphoid follicles (Peyer’s patches)
motor, sensory and taste innervation of the tongue?
where are each othe the 4 types of tastebuds found?
which ones are the most numerous?
which ones dont contribute to taste?
layers of the GI tract
which one of these structures are not retroperitoneal?
Kidneys
Oesophagus
Transverse colon
Ureters
Rectum
transverse colon
which artery does the right gastric artery arise from?
proper hepatic artery
What type of epithelial is this? Where would it be found? What is the black star?
Secretory glandular epithelium (much granular cytoplasm: salivary glands
Star= duct
What type of epithelium does the oesophagus have?
Stratified squamous
Bilirubin is the by-product of Haemoglobin breakdown.
Bacterial enzyme hydrolysis in the gut produces this compound which is excreted in faeces.
stercobillinogen
what makes up the portal triad?
heamoglobin is broken down into what two components?
what is the fate of these two components?
heam and globin.
globin and Fe+ recylced for erthythropoeisis
in the macrophage, what is haem broken down into?
what enzyme catalyses this?
biliverdin (by haem oxygenease)
Obstructive jaundice is commonly caused by gall stones within what structure?
common bile duct
