GastroIntestinal Flashcards

(457 cards)

1
Q

what are the 4 lines that divid the nine regions of the abdomen?

A

two midclavicular
one lower part of costal margin
one through the tubercles of the pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the names of the nine regions of the abdomen?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the three parts of the developing gut?

A

foregut, midgut, hindgut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where does the foregut end?

A

1/2 way duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where does the midgut end?

A

2/3 along transverse colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

where does the hind gut end?

A

upper anal canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

the parietal peritoneum is innervated by…?

A

somatic nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the visceral peritoneum is innervated by….

A

visceral sensory nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is secreted by the stomach that allows for vit b12 absorbtion?

A

intrinsic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what cells in the stomach produce intrinsic factor and gastric acid?

A

parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

in the Cephalic phase, what neurotransmitter triggers the release of gastrin and histamine?

A

acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what peptide hormone acts directly on parietal cells to priduce gastric acid.

how else does it trugger the secretion of gastric acid?

A

Gastrin acts directly on parietal cells to produce Gastric Acid
Gastrin also acts directly on histamine, which acts on parietal cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what peptide inhibits the activity of the stomach?

A

somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In the gastric phase, what condition will inhibit gastrin (and therefore indirectly, histamine) and stiumlate somatostatin?

A

low luminal pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

in the intestinal phase, which enterogastrones are released to inhibit gastric acid secretion?

A

secretin and cholecystokinin (CCK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what conditions in the duodenum trigger the release of enterogastrones that inhibit gastric acid secretion?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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 =

A

1 (parasympathetic) neurotransmitter = (ACh +) cephalic
1 hormone = (gastrin +) gastric/cephalic
2 paracrine factors = (histamine +, somatostatin -) - gastric’cephalic
2 key enterogastrones = (secretin -, CCK -) intestinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is an ulcer?

A

a breach in a mucosal surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

name FOUR ways the gastric mucosa defends itself

A
  1. alkaline bicarb rich mucus -
  2. tight junctions between epithelial cells prevent gasttic acid or enzymes passing between cells
  3. replace amaged cells
  4. negative feedback loops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how do NSAIDs cause peptic ulcers?

A

NSAIDS inhibit cyclo-oxygenase 1.

Cyclooxgenase 1 = prostaglandin = mucus secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how do Helicobacter pylori cause ulcers?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do you treat helicobacter pylori?

A

Eradicate the organism!
Triple therapy: 1 proton pump inhibitor
2 antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how do you treat peptic ulcer disease caused by NSAIDs?

A

Prostaglandin analogues – misoprostol = increases mucus production

Reduce acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

which cells in the stomach produce pepsinogen?
which produce pepsin?

A

cheif cells

NO cells produce pepsin (active protease would digest body)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what stiumulates the initiation of the Cephalic phase?
sight/smell/thought/taste/chewing of food =vagus nerve
26
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 ## Footnote this stimulates release of gastrin, (and histamine = parietal) = parietal plus decrease somatostatin
27
what turns it off in the gastric phase?
- Excess acidity (no food in stomach) - emotional distress (sympathetic override: f/f>r/d) ## Footnote inhibits gastrin (indirectly inhibits histamine) stiumlates somatostatin
28
whatt stimulates the start of the intestinal phase?
- partially digested food presnt (Chyme) ## Footnote more acid secretion
29
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
30
pepsin activation is an example of what?
positive feedback loop
31
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
32
pepsin is responsible for what % of protein digestion?
20%
33
Empty stomach has a volume of ? it can accomidate ? this shows its ?
50ml 1.5L Receptive relaxation
34
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
35
Perisaltic waves move towards the ?
antrum
36
peristaltic waves are initially... they are most powerful in the ... ... closes as the wave reaches it
weak gastric antrum Pylorus
37
# av the pacemaker cells of the stomach are
interstitial cells of Cajal
38
the strength of peristaltic contraction increases with what?
-Gastrin -Gastric distenion (mediated by Mechanoreceptors)
39
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
40
overfilling of duodenum results in?
dumping syndrome
41
what is gastroparesis
delayed gastric emptying
42
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
43
name some symptoms of gastroparesis
Nausea Early satiety Vomiting undigested food - Feculent vomiting (rotted food) GORD Abdo pain/bloating Anorexia
44
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
45
on a whiteboards, label this.
46
Label this!
47
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
48
what artery supplies the foregut?
celiac trunk
49
what artery supplies the midgut?
SMA | superior mesenteric artery
50
what artery supplies that hindgut?
IMA | inferior mesenteric artery
51
nerve supply of foregut?
S: greater splachnic (T5-T9) P: Vagus
52
nerve supply of midgut?
S: Lesser Splanchnic (T10-T11) P: Vagus
53
nerve supply of hindgut?
S: Least splanchnic (T12-L1) P: Pelvic splanchnics
54
where is visceral pain from foregut felt?
epigastric region
55
where is visceral pain from the midgut felt?
umbilical region
56
where is visceral pain from the hindgut felt?
suprapubic region
57
what tissue is the primitive gut tube formed from?
Endoderm. (visceral mesoderm froms the connection = dorsal mesentry)
58
what is happening in B and what can its failure lead to?
closure of the ventral body wall. Faulure of closure:
59
label the red boxes (connections). what type of tissue do they derive from?
60
aside from gene expressions, what helps the gut tibe to differentiate into its different componentst?
the concentration of retinoic acid
61
two mesenteries of the foregut?
dorsal mesentery and ventral mesentery
62
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
63
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)
64
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
65
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
66
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
67
the ventral mesentry is split into the:
lesser omentum and falciform ligament
68
Name 3 defences of the Oral Cavity
1. mucosa 2. Saliva (wash away particles and viruses, plue lymphatics around glands 3. Palatine tonsile (surveillance for immune system)
69
how many teeth in children/adults
children = 20, adults 32
70
Two types of Intralobular Ducts? | saliva
Intercalated and Striated
71
salivary Ducts secrete {a] and {b} and reabsorb {c} and {d}
[a] K+ and [b] HCO3 [c] Na+ and [d] Cl-
72
5 functions of saliva
1. Lubricant (chewing swallowing speech) 2. Oral Hygiene 3. Maintain pH 4. amylase 5. aqueous solvent necessary for taste
73
2 types of salivary secretion
serous (amylase) mucous (lubrication)
74
3 salivary glands and their secretions..
1. Parotid 25% (serous only) 2. Submandibular 70% (mucous and serous) 3. Sublingular 5% (mainly **mucous** ) 4. Minor (mainly mucous)
75
how much saliva do we produce a day?
800-1500ml
76
what factors can affect compostion and amount of saliva?
flow rate circadian rhythm type/size gland stimulation diet sex age
77
what % of salivary flow are the major salivary glands responsible for, the rest?
80% parotid, submandibular, sublingual 20% minor glands
78
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)
79
three structures around the parotid gland?
* External carotid artery * Retromandibular vein * Facial nerve (supplying the muscles of facial expression)
80
parotid gland innervated by:
parasympathetic: Glossopharyngeal (CNIX) sympathetic: Auriculotemporal (CNV3)
81
innervation of the sublingual gland
Para: chorda tympani (VII) Symp: lingual nerve (VII)
82
submandibular innervation
Para: chorda tympani (VII) Symp: lingual (VII)
83
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.
84
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
85
where is insulin produced?
pancreas
86
what promotes the uptake of glucose into cells for storage in the liver?
insulin
87
what is glucose stores as in muscle? what promotes this?
88
how does the brain get energy?
89
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
90
How to adipocytes get energy?
* Glucose taken up, promoted by insulin * Used to make ATP or stored as triglycerides
91
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)
92
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
93
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
94
what is glycogenolysis? what facilipromtoesates it?
break down of glycogen into glucose promotes by: glucagon
95
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
96
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 ## Footnote alanin-glutanine shuttle, pyruvate/lactate shuttle, B-oxidation
97
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
98
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
99
what is the main anabolic hormone? what is meant by this?
insulin anabolic = storgae -promotes glycogen and fat storage and protein synthesis
100
what is the main catabolic hormone? what is meant by this?
glucagon catabolic = energy release (glycogenolysis, gluconeogenesis, ketogenesis)
101
How does Cortisol affect fuel metabolism?
cortisol = stress hormone: prepares body for stress repsponse: * lypolysis * gluconeogenisis * glycogen storage * protein breakdown
102
how does adrenaline affect fuel metabolism?
fight or flight gets energy in the blood stream ready to be utilised (glycogenolysis, gluconeogenesis, lipolysis)
103
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
104
how does growth hormone affect fuel metabolism?
Growth hormone; (gluconeogenesis, glycogen synthesis lipolysis, protein synthesis, decreased glucose use)
105
whoat hormone increases appetite?
Ghrelin
106
what hormone decreases appetite?
leptin
107
what happens with leptin in obesity
high leptin levels, develop leptin resistance
108
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
109
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
110
what is secreted by cheif cells?
pepsinogen
111
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
112
what do D cells in the stomach secrete?
Somatostatin
113
how many layers of muscle cells are in stomach tissue?
3 longitudinal, circular, oblique
114
what cells produce intrinsic factor and what is its function?
parietal cells. Allows absorption of Vitamin B12 in the terminal ileum
115
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
116
what does the common bile duct drain into?
duodenum
117
what substance is secreted by G cells in the stomach?
Gastrin
118
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
119
2what cells in the stomach secrete Histamine?
Enterochromaffin-like (ECL) Cells
120
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
121
what type of cell line the oesopphagus?
stratified squamous epithelial
122
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
123
what is ferritin and where can it be found
protein that stores iron. found in cytoplasm of cells and sometimes serum.
124
what can cause ferritin excess?
1. Excess iron storage disorders (e.g. hereditary haemochromatosis, multiple blood transfusions, iron replacement therapy) 2. Non-iron related (ege. liver disease, malignancies, tissue distructions, inflammation, infection, autoimmune)
125
what can cause ferritin deficiency?
ONLY Iron Deficiency
126
what are the water soluble vitamins?
B, C and folate
127
what are the fat soulble vitamins?
ADEK
128
Vitamin A functions
vision, spermatogenesis, prevention of fetal reabsorbtion Growth
129
clinical features of vitamin A deficiency
night blindness, xeropthalmia, blindness | rare in affluent countries
130
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)
131
Funtions of Vitamin D
* increase intestineal absorbtion of calcium * resorbtion and formation of bone * reduced renal excretion of calcium
132
what can a vitamin D deficiency lead to?
demineralisation of bone: rickets in children, osteomalacia in adults
133
where is vitamin E stored within the body?
liver, plasma and adipose cells
134
what are the daily vitamin E requirements?
4mg/day in men, 3mg/day in women
135
same some sources of vitamin E
nuts, oils, spinach, avocado
136
what can a vitamin E deficiency cause?
fat malabsorbtion, premature infants
137
which vitamin is key in the activation of some blood clotting factors? bonus: which factors?
vitamin K VII, IX, X, II(prothrombin)
138
how can you assess vitamin K levels?
prothrombin time | how long a blood clot takes to form
139
sources of vitamin k?
leafy greens
140
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
141
what can a vitamin K deficiency lead to?
haemorrhagic disease of the newborn (rare in adults)
142
how much vitamin C do adults need a day?
40mg
143
what is the function of vitamin C?
collagen synthasism antioxidant iron absorbtion
144
what can a vitamin C deficiency lead to?
scurvy, easy bruising and bleeding, teeth and gum disease, hair loss
145
what are the two active forms of vitamin B12?
methyl**cobalamin** 5-deoxyadenosyl**cobalamin**
146
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
147
sourced of vitamin B12?
meat, fish, eggs, milk
148
what can cause a vitamin B12 deficiency?
* pernicious anaemia - autoimmune destruction of parietal cells * malabsorbtion * veganism
149
symptoms of B12 deficiency?
macrocytic anaemia peripheral neuropathy
150
when might someoe need more folate?
pregnancy
151
what are the functions of folate?
DNA synthesis
152
in which food might you find folate acid?
folate fortified cereals
153
symptoms of folate defeciency
macrocytic anaemia foetal development abnormalities (spina bifida)
154
what can cause a folate deficiency?
malabsorbtion leukemia, haemolytic anaemia
155
156
how much background radiation in an Xray?
4 months
157
how much background radiation in a CT?
4.5 years
158
label the arrows on this abdominal CT
159
label the arrows on this abdominal CT
160
label this CT
161
162
what are these lines in these bowl obstructions. where are each of the obstructions?
163
what is the red arrow pointing to? what is the likely cause?
free air under the diaphram. perforation
164
Label the: * liver * gall bladder * ascending colon * bladder
165
label the: * Kidney * Aorta * Stomach * Liver * IVC * Aorta
166
label the arrows
167
label the arrows
168
what is a normal diameter ofL small intestine, large intestine, caecum
3cm, 6cm, 9cm
169
what is a xenobiotic?
foreign substance which have no nutritional valur so need to be excereted. can be toxic if not excreted in time.
170
how do xenobiotics enter the body?
mostly ingested - eg DRUGS can be inhaled
171
what do xenobiotic damage if they enter the body?
proetins, lipid and can bind to DNA (carcinogen)
172
compounds need to be hydophillic/hydrophobic to be excreted in the urine.
hydorphillic
173
which enzymes are important for phase 1 reactions in liver detox?
Cytochome P450 (CYP)
174
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
175
phase I of drug metabolsim results in small/large increase in hydophilicity phase II?
phase i = small increase phase ii = large increase
176
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
177
what enzyme facilitates phase ii or drug metabolism (detox)
transferase | there are many. UGT important. ## Footnote Uridine 5'-diphospho-glucuronosyltransferase (UDP-glucuronosyltransferase, UGT)
178
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
179
where does biotransformation occur in the hepatocyte?
smooth ER
180
where can CYPs be found?
smooth ER (sometimes called microsomal enzymes)
181
what is the function of CYPs?
oxidise substrate (via oxidation, reduction or hydrolysis)
182
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
183
aside from the liver, whereelse does xenobiotic metabolism occur?
gut mucosa. (many CYP450 enzymes present in gut)
184
which enzyme metabolises ethanol?
CYP2E1
185
give an outline of the mechanism of CYPs and Reductase in xenobiotic metabolism
Oxygen binds to Haem in CYP450 Reductase uses NADH to become more active. Addition of OH group = **more soluble**
186
how does factors such as smoking, grilled meat and cabbage affect xenobiotic metabolism?
it INDUCES a CYP enzyme = more breakdwon = higher conc of some medications (eg Clozapine) therefore must reduce the durg to avoid toxicity.
187
how does grapefruit juice affect drug metabolism?
Grapefruit juci inhibits some CYPs CYPs metabolise statins. If on Statins, grapfruit juice will reduce the breakdown therefore build up.
188
what are the 5 ways xenobiotic metabolism can occur?
1. inactivation and elimination 2. fromation of different active compound 3. activation of pro drugs 4. Toxification of less toxic xenobiotics 5. active drug to reactive intermediates
189
what phases of metabolism does "inactivation" use in xrnobiotic metabolism?
phase I and Phase II
190
why is "inactivation" a slow metabolism process?
it is mostly distributed in fat and small proportion freely dissolved in blood plasma
191
Give an example of "formation of another active compund" metabolism
codeine -->morphine usesCYP2D6 | structurally similar
192
give an example of "Activation of Pro Drugs" xenobiotic metabolism
Loratadine ---> desloratadine (antihistamines) | inactive --> active in liver
193
Give an example of "active drug to Reactive Intermediate" xenobiotic metabolism
Paracetamol (inoquous) --> NAPQI (toxic)
194
what is Phase III of Xenobiotic metabolism?
removal of drugs/metabolites via urine, plasma, bile
195
By what procceses is paracetamol usually metabolised by?
Glucuronidation (50%) and Sulfation (40%)
196
what is the harmful intermediate of Paracetamol metabolism? By what enzyme?
NAPQI by CYP2E1 (10%) build up
197
What happens during a paractemol overdose? (or with ethanol and paracetamol)
Normal routes of metabolisation overwhelmed (gulcuronidation and suphation), CYP2E1 = more = more NAPQI (too much to be excreted) =hepatocyte damage (high levels of CYP2E1)
198
what does CYP2E1 metabolise?
paracetamol and ethanol
199
what happens if someone take ethanol and then paracetamol?
already high CYP2E1 from alcohol. Metabolism more likely to use 10% harmful route = more toxic NAPQI
200
what are the 3 types of phase I biotransfromation reactions?
oxidation, reduction, hydrolysis | expose functional group
201
give some exapmles of phase II biotransformation reactions
Conjugation reactions (add polar group): * glucuronidation * sulphation (paracetamol) * methylation * acylation | use transferase enzymes
202
what are the 4 phases of pharmokinetics?
A = Absorbtion D = Distribution M = Metabolism E = Elimination
203
What are CYPs, where are they found and what do they do?
Cytochrome P450s Microsomal enzymes Phase 1 xenobiotic metabolism (biformation) (andalso involved in Glucuronidation (phase II))
204
where are non microsomal enzymes found? e.g.
mitochondira and cytoplasm Conjugases/transferases conjugation (phase II)
205
why isnt ethanol commonly excreted? (only 2-10% excreted in urine)
small molecule. and used as fuel
206
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
207
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
208
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
209
treatment of paracetamol overdose?
acetylcysteine
210
3 funtions of the colon
1.absorb water and electrolytes (osmosis) 2.excretion of waste (motility) 3.production of vitamins/regulation of immune system (microbiome)
211
212
213
what are the three layers that make up the muscularis propria?
1. Inner circular muscle (segmentation) 2. Auerbach Nerve Plexus 3. Longitudinal Muscle (mass peristalsis)
214
this is a sample from colon. Lable the two layer of muscle that can be seen
215
Explain the Intrinsic nerve supply to the colon
Myenteric Plexus (Auerbach's) and submucosla plexus
216
in the colon, which nerves are responsible for motility?
myenteric plexus
217
in the colon, which nerves are responsible for absorbtion?
submucosa plexus
218
which anal sphincter, the internal or external, has voluntary control?
the external sphincter has voluntary control. the internall sphincter has involuntary control
219
which anal sphincter, the internal or external, is responsible for giving us the urge to push? which nerves enable this?
the external sphincter. mechanoreceptor nerves give us the urge
220
what is stool sampling, and which part of the anal canal is responsible for it?
The internal Canal: relaxes 7-8x and hour to test whether solid/gas/liquid
221
aside from the internal and external sphincter, what mechanism in the lower rectum promotes continence?
The Puborectalis muscle sling which creates the Anorectal Angle
222
what are the four phases of defection?
1. basal 2. pre-expulsive 3. expulsive 4. termination
223
in what phase of defecation foes segmental mixing in the colon happen. during this phase, what is happening with the puborectalis and anorectal angle?
Basal phase: - rectum empty - puborectallis contracted = 90° anorectal angle
224
during the **pre-expulsive** phase of defecation, the rectum is filling causing distension (but also adaptive relaxation). Explain which muscles in the anal sphincter are contracted/relaxed during this phase
External AS = still contracted Internal AS = relaxes - for stool sampling Puborectalis = contracted (AR Angle still 90°)
225
which phase of defecation is this? what manouver facilitates this
expulsive phase (everything relaxed) Valsalva manouevre and posture aids emptying
226
name four factors that can contribute to constipation/obstructive defecation
1. consistency of stool (diet) 2. bowel motility (diabetes) 3. physical blockage to bowel (tumour) 4. pelvic floor disorders (Anatomical - rectal prolapse)
226
what facilitates the termination phase of defecation?
Traction loss causes sudden contraction of EAS = closing Valsalva ceases Change in posture (to standing)
227
what factors can lead to faecal incontinence?
1. consistency of stool 2. diseased bowel mucosa 3. reduced rectal capacity 4. pelvic floor disorder
228
what is a triglyceride?
an ester derived from glycerol and three fatty acids. Triglycerides are the main constituents of body fat in humans
229
what is the difference between a saturated and unsaturated fatty acid?
saturated = lined up sunsaturated = double bond = kink
230
Name 4 functions of Fat
1. energy reserve 2. hormone metabolism (vit D and sex hormones) 3. Cell membrane and structure 4. inflammatory cascade
231
where is cholesterol esterified? by what?
in lipoprotein. by acyl-CoA or Lecithin (cholesterol acyltransferase)
232
where is cholesterol processed?
the liver
233
how is cholesterol excreted?
bile exclusively
234
how is cholesterol carried through the circulatory system?
Lipoproteins
235
energy value of fats?
9 kcal/g
236
decribe the makeup of lipoproteins
TG and cholesterol core phosopholipis, cholesterol, protein surface ## Footnote protein:lipid detrmines density
237
what determines the densisty of a lipoprotein?
protein:lipid little protein -------------------->high protein low density------------------------>high density chylomicron < VLDL < LDL < HDL
238
where is Apoprotein B (lipid carrier)synthesised?
RER
239
where are lipid components (TG, Cholesterol esters) synthesised?
sER
240
what protein adds lipid components (sER) to ApoB (RER)?
microsomal TAG transfer Proteins
241
What happens to the ApoB in the gogi apparatus?
glycosylated
242
what is denovo lipogenisis in the liver dependent on?
insulin concentration and sensitivity
243
Most body fat is stored in [a] Some is stored in the [b] Liver oxidizes [c] when necessary
[a] adipocytes [b] hepatocytes [c] triglycerides
244
what % of energy is stored in: triglycerides proteins carbohydrates
Triglycerides – 78% Protein – 21% Carbohydrate – 1%
245
where are LDL formed and what is there function?
Formed in plasma Main cholesterol carrier Delivers cholesterol to all cells in body Essential for cell membrane and steroid hormone production
246
what can happen with high levels of LDL?
High level of LDL-> will be taken up by cells via endocytosis and deposition will increase risk factors for heart attacks
247
what is "good" Cholesterol, where is it formed and what is its function?
High density lipoproteins (HDL) Formed in liver Removes excess cholesterol from blood and tissues delivering it to the liver to be secreted into bile
248
where are VLDL formed and what is its function?
Synthesised in hepatocytes Deliver triglycerides from liver to adipocytes
249
by what mechanism are fats mainly broken down by? how does this produce energy? where does it occur?
Fats broken down via Fatty acid beta oxidation: It is the catabolism of fatty acids to produce energy Occurs in mitochondria of hepatocytes
250
what three things regulate mitochondiral B oxidation?
CPT Carnitine Maolonyl-CoA
251
name 3 types of protein and what they are used for
3 types of protein: Plasma protein: - E.g. Albumin, fibrinogen, globulin Clotting Proteins - Required for coagulation Complement proteins - Part of innate immune response
252
the body can produce all clotting factors except for?
Clotting factors: Produces ALL factors EXCEPT: calcium (IV) and von Willebrand factor (VIII) Liver facilitates vitamin K absorption Vitamin K= 1972 (10,9,7,2)
253
vitamin K is essential for the synthesis of which clotting factors?
X, IX VII, II (1972)
254
what is the purpose of the glucose-alanine cycle?
The purpose of this cycle is to move proteins from muscles to the liver when glycogen stores are low
255
what enzyme in the glucose-alanine cycle can be used to measure liver function?
alanine aminotransferase (ALT)
255
what is the main source of nitrogen? where is it mainly lost?
dietary protein. loss through gut and kidneys as urea
256
when an amino acid can't be produced de novo, what will it be called?
essential - must be found in the diet
257
how can amino acids be used for glucose synthesis?
lose amino group, leaving carbon backbone for glucose synthesis and energy metabolism
258
how to amino acids bond toeachother?
peptide bond (dipeptide) (polypeptide eg insulin) protein = >50 AAs
259
how much nitrogen lost per day via renal excretion?
70g/day
260
how much nitrogen lost a day via faeces?
10g/day
261
we can/cannot store amino acids
cannot
262
what are the three main fates of AA's?
1. Form other biomolecules (eg nucleotides 2. form into proteins 3. remove nitrogenous amino acid group removed and have carbon backbone used to make glucose
263
who might have a positive Nitrogen Balance?
Pregnant/Lactating women (need more protien) intake>excretion of Nitrogen
264
who might have a nigeative nitrogen balance?
protein malnutrition severe illness essential AA deficiency (intake
265
how does Kwashiorkor disease differ from Marasmus?
In Kwashiorkor, there is sufficient calorie intake but inadequate protein. In Marasmus, both portein and calories insifficient
266
how are proteins digested in the stomach and small intestine?
Stomach: HCl, Pepsin Small intestine: Trypsin(ogen)
267
what facilitates the absorbtion of AAs into the bloodsteam?
eneterocytes
268
give an example of a conditionally essential amino acid
Tyrosine
268
what is an alphaketoacid derived from and what is their purpose?
acceptthe amino group from AA during transamination when you remove the amino group from AA, you are left with a carbon backbone. these are important metabollic intermediates (TCA cycle) eg Alanine ---> Pyruvate
269
describe what happens in transamination.
an amino acid transfers its amino group to an accepting alphaketoacid. turn into eachother
270
what is transamination catalysed by?
alanine amino transferase (ALT)
271
what is this reaction an example of?
transamination
272
in the fasting state, what happens to amino acids? which is the most importans AA
1. AA --->TCA for ATP 2. To liver for gluconeogenesis Alanine: can be turned into Pyrivate in the liver for utilisation in gluconeogenesis
273
what are the two main means of protein degredation?
1. Proteasome - ubiquitin dependent 2. Lysosome - ball of death
274
Proteasome is [a] dependent
ubiquitin
275
what is ubiquitin?
the mark of death (for a protein) more ubiquitin = more degredation signalling (>4 a lot)
276
what is proteasome?
the executioner of the protein. (has caps either end that regulate which proteins han enter for destruction)
277
# ``` ``` where do lysosomes occur? How does Lysosomal protein degredation occur?
within the cell autophagy - eats itself: can be selective/nonselective/extracellular
278
what is it called when lysosomal protein degredation goes wrong?
cystinosis * genetic, recessive * cystine not transported out and crystallises * eye and kidney problems
279
Liver synthesises most proteins except for?
immunoglobins
280
how much albumin is produced by the liver a day?
10-15g
281
two functions of albumin
Oncotic Pressure of Blood vessels - INTO capilliaries Carrier protein (hormones, vitamins, electrolytes, drugs)
282
what can happen if the urea cycle goes wrong?
ammonia toxicity (dolls eyes)
283
how should ammonia toxicity be treated?
avoid catabolism induce anabolism INSULIN
284
name 6 causes of hypoalbuminaemia
1. Inflammation 2. Liver disease 3. Renal Disease 4. Trauma 5. Sepsis
285
What might cause high albumin levels?
dehydration
286
do you know the urea cycle?
Old Colourful Cats Always Ask For Awesome Umbrellas
287
do you know the glucose alanine cycle
288
how much fluid does the small intestine absorb?
7.5L a day
289
how much fluid does the large intestine absorb?
<1.5L/day
290
how much salvia doe we swallow a day?
1.5L
291
How many L of Gastric Secretions do we produce a day?
2L
292
How many L of pancreatic juices do we produce a day?
1.5L
293
Bow much Bile do we produce a day?
0.5L
294
how many L of intestinal secretions do we produce a day?
1.5L
295
how much liquid is excreted (feacally) a day?
<200ml
296
where is iron absorbed?
Duodenum
297
Where is vitamin B12 absorbed?
terminal ileum
298
where is folic acid absorbed
duodenum
299
where does secretion/absorbtion occur: villi/crypt
villi = absorbtion crypt = secretion
300
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 ## Footnote water follows sodium
301
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
302
name some factors that influence absorbtion/secretion in the intestine
Absorbtion: number of enterocytes blood and lymph flow nutrient intake GI motility Secretion: Irritants Bile Bacterial toxins
303
what is the name of the cell of intestinal lining?
enterocytes
304
what has happened to the villi here? when might you see villi like this?
Villi atrophy. coeliac disease - cant absorb = malnutrition and diarrohea
305
how does cholera lead to diarrhoea? how can it be treated?
bacteria stimulate adeny;ate cyclase to produce cAMP dramatic efflux of Cl- therefore Na+ therefore water treat with rehydration: sodium and glucose : creates a gradient that pushes fluid back into cell
306
define digestion
breakdown of large comlex organic molecules to molecules that can be used by the body
307
carbohydrates are broken down into? protein into fats into
monosaccharodes amino acids fatty acids/glycerol
308
name two places histologically in the GI where digestion occurs
in GI lumen by secreted enzymes on surface of enterocytes by membrain bound enzymes
309
Absorbtion im GI tract occurs by what mechanisms? (5)
1. simple diffusion 2. facilitated diffusion 3. active transport 4. endocytosis 5. paracellular transport
310
surface are of small intestine is greatly increased by:
extensive folding, villi and microvillia
311
what breaksstarch and glycogen into disaccharides?
amylase
312
by what process are glucose and galactose absorbed by? whayt about fructose?
Na- dependednt secondary active transport system fructose absoribed by facilitated transport
313
by what process are amino acids absorbed into the process?
facilitated diffusion and cotransport
314
what breaks proteins into polypeptides? where? what breaks polypepties into short peptides and AAs? where? what breaks these into AAs? where?
315
what is needed for fat absorbtion?
bile
316
where does bile go after its been used for fat absorbtion?
reabsorbed in terminal ileum and go back to liver to be recycled (7-8x a day) if no, and goes into the large intestine = irritant = diarhoea
317
fat is tranported in [?] system via [?]
lymphatic system (then blood) via Chylomicrons
318
What do amylases breakdown? where are they made?
starch salviary glands and pancreas =mouth, stomach and SI
319
what enzyme breaks down triglycerides? where are they found?
lipase salivary glands and stomach and pancreas (SI)
320
where is pepsin found and what does it break down?
proteins. stomach
321
what enzymes are found in the pancreas?
Amylase Lipase and Colipase Phospholipase Trypsin Chymotrypisin
322
what enzyme breaks down peptides?
trypsin and Chymotrypsin Pancreas
323
What does Enterokinase do and where is it found?
activated Trypsinogen--> Trypsin. intestine
324
what do diasaccharidases target and where are they found?
complex sugars. intestine
325
where are peptidases found?
intestine.
326
what controls the excretion of saliva? what is this stimulated by? what is the effect of stimulation?
Controlled by: Salivary centre in medulla Stimulated by: pressure and chemoreceptors in mouth Effect: Autonomic nerves stimulate salivary glands to secrete
327
Substances of the stomach: FUNCTION
328
Substances of stomach: SOURCE
329
what cells in the pancreas secrete digestive enzymes?
acinar cells
330
what cells in the pancrease secrete hormones?
Pancreatic Islet Cells
331
what is the endocrine function of the pancreas?
secrete insulin and glucagon from islet cells of langerhans
332
what stimulates the release of secretin? what does secretin stiumlate the release of?
acid in duodenum stimulates secretin. secretin stimulates Bicarbonate secretions by pancreas
333
what stimulates the release of Cholecystokinin? what does this stimulate the release of?
HCl, protein and Fats in the duodenum stimulate the release of CCK. CCK stimulates the release of Enzymes in pancreas
334
Three main functions of the liver
**1) Metabolic regulation** Store absorbed nutrients, vitamins Release nutrients as needed **2) Haematological regulation** Plasma protein production Remove old RBCs ** 3) Production of bile** Required for fat digestion and absorption
335
What is the pancreases main function? what %
99% exocrine = digestion: bicarb and enzyme
336
what nerve stimulates the pancreas to produce chemicals?
vagus = "hungry+
337
what is PEI?
Pancreatic Enzyme Insufficiency: reduction in pancreatic enzyme activity in intestinal lumen below threshold required to maintain normal digestion ## Footnote symptoms: malnutrition
338
causes of PEI?
**Parenchymal**: Cancers; pancreatitis; CF **Extra Pancreatic:** Coeliac, IBS (no CCK) **Post Surgical:** Short Bowel, Whipple
339
treatment of PEI?
PERT pancreatic enzyme replacement therapy
340
how to test for PEI
(used to be multiple poo samples) Faecal Pancreatic Elastase
341
where is CCK produced, by what cells?
I cells of duodenum and jejunum
342
name a stucture in right hypochomndrium
liver
343
name some structures in each of the 9 regions of the abdomen
344
name some structures in the transpyloric plane
* pylorus of stomach * neck of pancreas * first part of duodenum * SMA
345
where is McBurney's point? what is it?
2/3 of the way **from** umbilicus and Anterior Superior Iliac Spine. Where the appendix is.
346
name the muscles of the abdomen
347
name the muscles in the anterior wall muscles
* Transverse abdominis * Internal Oblique (up) * External Oblique (down) * Rectus abdominus
348
what runs down the middle of the rectus abdominis
linea alba
349
of the visceral and pariteal peritoneum, which gives generalised pain and which gives more specific?
visceral = generalised parieteal = specific
350
Which organs are Retroperitoneal? (Not surrounded by mesentry)
SADPUCKER!! S: suprarenal (adrenal) gland A: aorta/IVC D: duodenum (second and third part) P: pancreas (except tail) U: ureters C: colon (ascending and descending) K: kidneys E: Esophagus R: rectum
351
what is the lesser omentum made from?
ventral mesentery
352
what is the greater omentum made from?
dorsal mesentery
353
what is the blood supply of the greater omentum? what is the blood supply of the lesser omentum?
both = gastro-omental artery (branch of gastroduodenal)
354
what connects the greater and lesser sacs?
epiploic foramen (foramen of Winslow)
355
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
356
function of the spleen?
-Filtering blood by removing waste and filtering out old/damaged cells: these old cells can get their components recycled -Can store blood for future use -also filters blood for microorganisms (eg encapsulated bacteria) and produces lymphocytes
357
# ``` ``` Gastrin: Source? Action? Regulation?
358
Somatostatin. Source? Action? Regulation?
359
Cholecytokinin. Source? Action? Regulation?
360
Secretin Source? Action? Regulation?
361
Glucose- Dependent Insulinotropic Peptide (GIP). Source? Action? Regulation?
INHIBITS gastric acid
362
Ghrelin. Source? Action? Regulation?
363
what do ECL (enterochromaffin Like Cells) cells do? where are they found
These cells secrete histamine when gastrin stimulates them. Histamine binds to receptors on the parietal cells and increases hydrochloric acid secretion. These cells exist mainly in the fundus of the stomach.
364
what do enterochromaffin cells do?
These cells secrete serotonin. Serotonin is involved in regulating gastrointestinal motility and fluid secretion.
365
Gastric Acid. Source? Action? Regulation?
366
Intrinsic Factor Source? Action? Regulation?
367
Pepsin. Source? Action? Regulation? Zymogen?
368
Bicarbonate. Source? Action? Regulation?
369
in the parietal cell, what is it that combines H2O and CO2 to get H2CO3
Carbonic Anhydrase
370
What is gastric motility, peristalsis and emptying regulated by?
interstitial cells of cajal
371
Water distribution in the body. again lol - learn it.
372
give two ways that sodium ions are transported in intestines. what us this enhanced by?
1. sodium-hydrogen antiporter on luminal membrane 2. epithelial sodium channels - enhanced by absorption of short-chain fatty acids in colon through specialised symporters
373
explain how chloride ions are transported in intestines.
follows sodium due to electrochemical gradient to allow absorption of chloride Chloride is exchanged for bicarbonate
374
explain how water is tranported in intestines
due to electrolyte absorption there is an osmotic gradient to allow water absorption
375
explain how potassium is transported in intestines
can be excreted or absorbed based on lumen concentration due to water absorption and sodium absorption
376
where is iron, folate, vitamin B12 and Bile salts absorbed?
Dude Is Just Feeling Ill Bro Duodenum:Iron Jejunum:Folate Ileum:B12, Bile Salts (terminal ileum)
377
what are the water soluble vitamins? where are they absorbed>
B12, C small intestine
378
what are the fat soluble vitamins and where are they absorbed?
ADEK small intestine - duo and jej
379
what is BMR?
number of calories you burn as your body performs basic (basal) life-sustaining function
380
what can increase BMR?
Factors that can increase BMR include: having a higher muscle-to-body fat ratio, being male, pregnancy, growing children, stress, and having a fever
381
Vitman A deficiency? sources:
night blindness] sources: Liver, carrots, eggs, tomaroes
382
vitamin D deficiency? | vi
rickets source: fish oils, fortified milk, sunlight
383
vitamin B3 deficiency?
pellagra
384
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
385
only monosaccharides are absorbed by enterocytes. Name three monosaccharides.
glucose galactose fructose
386
how is fructose absorbed in the gut?
by facilitated diffusion by GLUT5
387
what transports catbohydrates into the blood?
GLUT2
388
summarise protein digestion
1. starts in stomach with **pepsin** → preliminary breakdown of protein 2. continued through pancreatic enzymes -**chymotrypsinogen, trypsinogen, elastase, carboxypeptidase** 3. finally through border enzymes split into amino acids, dipeptides and tripeptides
389
how are proteins absorbed into the blood?
AAs = thorugh sodium cotransporter = facilitated diffusion dipeptides and tripeptides = through H+ cotransporter = bcome AAs
390
summarise lipid absorbtion
They get absorbed into **enterocyte** where they become a **chylomicron** and then the process of lipid distribution begins.
391
what are the three stages of swallowing?
**1. VOLUNTARY (ORAL PHASE)** -BOLUS MOVES FROM ORAL CAVITY INTO OROPHARYNX (activation of CN IX) **2. INVOLUNTARY (PHARYNGEAL)** -elevation of soft palate seals of nasopharynx. glottis closes, epiglottis covers. -BOLUS MOVES FROM THE OROPHARYNX INTO THE OESOPHAGUS **3. INVOLUNTARY (OESOPHAGEAL PHASE)** BOLUS MOVES THROUGH THE OESOPHAGUS INTO THE STOMACH
392
what is a gag reflex?
REFLEX ELEVATION OF PHARYNX STIMULATED BY OROPHARYNX IRRITATION (often accompanied by vomiting as well) AFFERENT LIMB: GLOSSOPHARYNGEAL NERVE (CN IX), EFFERENT LIMB: VAGUS NERVE (CN X)
393
where does the foregut end?
1/2 way along duodenum (insertion of common bile duct and pancreatic duct)
394
what are the five stages of development of the midgut?
1. elongation 2. physological herniation (week 6) 3. rotation (around SMA) 4. retration (week 10) 5. 5fixation
395
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.
396
what will the cephalic limb of the primary intestinal loop give rise to? | head end
disatl duodenum, jejunum, part of the ileum
397
what will the caudal limb of the primary intestinal loop give rise to?
distal ileum ceacum and appendix ascending colon proximal 2/3 transverse colon
398
what week does the physiological herniation stage of midgut embryological dvelopment occur? what happens? why does this happen?
week 6. intestinal loop herniates out of abdominal cavity into the umbilical cord. Rotation starts (90° anticlockwise around SMA) because the abdominal cavity is too small for both the gut loops and the liver which are both rapidly growing.
399
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
400
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.)
401
what happeens during phase 5 of embryological development of midgut?
Fixation. some mesenteries contact the posterior abdominal wall and become retroperitoneal. A fascial layer -Toldt fascia - develops bewteen parietal and visceral peritoneum
402
how much in total does the midgut rotate during embryologcal developoment?
270° anticlockwise 90° in herniation 180° post herniation
403
what are the three branches of the celiac trunk?
left gastric splenic common hepatic
404
two sphincters of the stomach?
oeophageal sphincter pyloric sphincter
405
innervation of the stomach?
Parasympathetic: X Sympathetic: coeliac plexus (T5 - T12)
406
four for main anatomical divisions of the stomach?
cardia, fundus, body, pyloric antrum canal and sphincter
407
four layers of the stomach?
MSMS Mucosa Submucosa Muscilaris (OCL) Serosa
408
three layers of the muscularis externa of the stomach?
OCL oblique, Cicular, Longitudinal
409
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)
410
where can epiploic appendages be found? small or large intestine?
large
411
motor, sensory and taste innervation of the tongue?
412
where are each othe the 4 types of tastebuds found? which ones are the most numerous? which ones dont contribute to taste?
413
layers of the GI tract
414
what types of cell are usually found in the oesphagus? what can happen if you get persistent reflux? what is this called?
non-keratinising stratified squamous Barrett's metaplasia will become simple columnar (more resistant to acid) = increase risk of cancer
415
what is the blood supply to the foregut?
coeliac trunk
416
which one of these structures are not retroperitoneal? Kidneys Oesophagus Transverse colon Ureters Rectum
transverse colon
417
which artery does the right gastric artery arise from?
proper hepatic artery
418
which artery does the left gastroepiploic/gastroomental artey arise from?
splenic artery
419
What provides taste sensation to the anterior ⅔ of the tongue?
facial nerve
420
Which muscle fibre(s) run anterior to rectus abdominis
internal and external oblique (not transversus abdominis)
421
What connects the greater and lesser sac?
foramen of winslow
422
Which enzyme combines H2O and CO2 in parietal cells?
carbonic anhydrase
423
What does bile help break down fats into? Chylomicrons LDL HDL Micelles Lipases
micelles
424
What type of epithelium would you find in the oral cavity?
Non Keratinising stratified squamous epithelium
425
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
426
What are the layers of muscle in the oesophagus?
Longitudinal & circular
427
What type of epithelium does the oesophagus have?
Stratified squamous
428
Bilirubin is the by-product of Haemoglobin breakdown. Bacterial enzyme hydrolysis in the gut produces this compound which is excreted in faeces.
stercobillinogen
429
What are the three types of jaunice and how can you tell the difference?
1. Pre Hepatic - excess RBC breakdown overwhelms liver. Lots of UCB = can’t be filtered by kidneys so none in urine 2. Hepatocellular - 3. Post Hepatic (obstructive) - normal UCB, no faecal urobilinogen
430
What is the cause of physiological jaundice of the newborn?
Excess breakdown of foetal haemoglobin
431
name some causes of obstructive jaunice.
cirrhosis, gallstones, hepatitis, pancreatic carcinoma
432
Gilbert's syndome means you cant produce what?
B-UGT enzyme - required for glucuronidation od UCB into CB
433
What structure is situated within the duodenal loop?
pancreas
434
What is the structure in the middle of the hepatic lobule?
Central vein
435
what makes up the portal triad?
436
the liver converts T4 into?
the liiver converts thyroxine (T4) into triiodothyronine (T3)
437
CCK is released in repsonse to?
presence of amino acids in the gut (by the gall bladder)
438
what enzyme catalyses the formation of Conjugated billirubin?
UGT uridine diphosphoglucoronosyl transferase (glucuronyl transferase) | catalyses glucuronidation of UCB
439
heamoglobin is broken down into what two components? what is the fate of these two components?
heam and globin. ## Footnote globin and Fe+ recylced for erthythropoeisis
440
in the macrophage, what is haem broken down into? what enzyme catalyses this?
biliverdin (by haem oxygenease)
441
what enzyme catalyses the reduction of biliverdin into billirubin (UCB)?
biliverdin reductase
442
what protein allows UCB (lipid soluble) to move along blood stream?
albumin
443
Obstructive jaundice is commonly caused by gall stones within what structure?
common bile duct
444
what is glucagon secreted by what cells?
alpha islet cells in pancreas
445
insulin is secreted by what cells?
beta islet cells in pancreas
446
somatostatin is secreted by what cells?
Delta Islet cells
447
pancreatic polypeptide is secreted by what cells?
F islet cells
448
Bilirubin is the by-product of Haemoglobin breakdown. Which compound is returned to the liver by the enterohepatic circulation?
urobilinogen
449
the hepatic blood supply is ?% of the CO?
25%
450
how many segments does the liver have?
8
451
what is the functional unit of the liver?
lobule
452
which cells are important in the reticuloendothelial system?
Kupffer cells
453
what do ito cells do?
Hepatic stellate cells = fat storage cells
454