Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 1 Medicine > GI > Flashcards

GI Flashcards

1
Q

Is stage 1 of swallowing voluntary or involuntary?

A

Voluntary.

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

What happens in stage 1 of swallowing?

A

Food is compressed against the roof of the mouth and is pushed to the oropharynx by the tongue.

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

Is stage 2 of swallowing voluntary or involuntary?

A

Involuntary.

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

What happens in stage 2 of swallowing?

A

The nasopharynx closes off due to soft palate elevation. The trachea is closed off by the epiglottis. Elevation of the hyoid bone shortens and widens the pharynx.

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

Is stage 3 of swallowing voluntary or involuntary?

A

Involuntary.

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

What happens in stage 3 of swallowing?

A

The pharyngeal constrictor muscles sequentially contract producing peristaltic waves. This propels the bolus of food down the Oesophagus. This is followed by depression of the hyoid bone.

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

Name 6 muscles/groups of muscles that are involved in swallowing.

A
  1. Buccinator.2. Suprahyoids.3. Muscles of the palate.4. Muscles of the floor of the mouth. 5. Infrahyoids. 6. Pharyngeal constrictor muscles.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which muscle(s) manipulate food in chewing. Elevate the hyoid bone and flatten the floor of the mouth?

A

Buccinator and Suprahyoids.

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

What is the function of the muscles of the soft palate in swallowing?

A

They act to tense and elevate the soft palate.

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

What is the function of the muscles of the floor of the mouth in swallowing?

A

They raise the hyoid bone and larynx.

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

What is the function of the infrahyoids?

A

To depress the hyoid bone and larynx.

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

What is the function of the pharyngeal constrictor muscles?

A

They contract sequentially producing peristaltic waves which drive food into the oesophagus.

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

Do parotid glands have mainly serous or mainly mucous acini?

A

Mainly serous acini.

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

What is serous acini secretion composed of?

A

alpha amylase - this is needed for starch digestion.

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

Do sublingual glands have mainly serous or mainly mucous acini?

A

Mainly mucous acini.

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

What is mucous acini secretion composed of?

A

Mucin - needed for lubrication.

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

Do submandibular glands have mainly serous or mainly mucous acini?

A

They have serous and mucus acini.

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

Which of the main salivary glands is constantly active?

A

Submandibular.

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

What is the function of saliva?

A

It acts as a lubricant for chewing, swallowing and speech. It is important in oral hygiene; has a role in immunity, wash and it can also act as a buffer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the optimum oral pH?

A

7.2

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

What is the pH range of saliva?

A

6.2 - 7.4

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

Name 4 factors that can affect the composition of saliva.

A
  1. Stimulus. 2. Age. 3. Gender. 4. Drugs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Are serous acini dark staining or pale staining on a histological slide?

A

Dark staining. (Mucus acini = pale staining).

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

What is the epithelium lining of intercalated ducts?

A

Simple cuboidal epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the function of intercalated ducts?

A

They connect acini to larger striated ducts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What ions are reabsorbed at striated ducts?

A

Na+ and Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Is saliva hypotonic or hypertonic?

A

Hypotonic - water reabsorption and ion secretion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the importance of the striated duct basal membrane being highly folded?

A

It is folded into microvilli for the active transport of HCO3- against its concentration gradient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What organelle is abundant in striated ducts and why?

A

Mitochondria. For the active transport of ions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Name 2 ions that striated ducts secrete.

A

K+ and HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Name 2 ions that striated ducts reabsorb.

A

Na+ and Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What ducts do striated ducts lead on to?

A

Interlobular (excretory) ducts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the epithelium lining of interlobular ducts?

A

Simple columnar epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the parasympathetic innervation of the Parotid gland?

A

Cn 9 - glossopharyngeal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the parasympathetic innervation of the Sublingual gland?

A

Cn 7 - facial.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the parasympathetic innervation of the Submandibular gland?

A

Cn 7 - facial.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What nerve passes through the parotid gland but does not innervate it?

A

The facial nerve (Cn 7) gives rise to its 5 terminal branches in the parotid gland.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What artery ascends through the parotid gland?

A

The external carotid artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Does parasympathetic innervation stimulate or inhibit salivary secretion?

A

Stimulates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the volume of an empty stomach?

A

50ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the maximum volume of the stomach?

A

1.5L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is receptive relaxation?

A

Smooth muscle in the body and fundus of the stomach relaxes prior to the arrival of food, this allows the stomach volume to increase. There is afferent input from Cn 10. NO and serotonin also influence relaxation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Where do peristaltic waves begin?

A

In the gastric body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Where in the stomach are peristaltic contractions the most powerful?

A

In the gastric antrum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Why is the pyloric sphincter closed as the peristaltic wave reaches it?

A

This prevents chyme entering the duodenum and so the gastric contents are forced back and mixed together in the body of the stomach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

On average, how many peristaltic waves are there a minute?

A

3 (slow repol/depol cycles).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Name 2 factors that can increase the strength of peristaltic contractions.

A
  1. Gastrin.2. Gastric distension.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Name 5 factors that can decrease the strength of peristaltic contractions.

A
  1. Duodenal distension. 2. Low pH in duodenum lumen. 3. Increased duodenal osmolarity. 4. Increased sympathetic action.5. Decreased parasympathetic action.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What do parietal cells secrete?

A

HCl and intrinsic factor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What do chief cells secrete?

A

Pepsinogen and gastric lipase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What cells secrete Gastrin?

A

Enteroendocrine cells / G cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What cells secrete somatostatin?

A

D cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What cells secrete histamine?

A

Enterochromaffin like cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

On average, how much gastric acid do we secrete a day?

A

2L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the hydrogen ion concentration of gastric acid?

A

> 150mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Where does the H+ come from in gastric acid?

A

In parietal cells: H2O + CO2 = HCO3- + H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the mechanism of the H+/K+ ATPase proton pump?

A

It pumps H+ into the stomach lumen and K+ into the parietal cell via primary active transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What ions are exchanged on the side of the parietal cell in contact with the capillaries?

A

Cl- is pumped into the parietal cell and HCO3- moves out of the parietal cell into the capillary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the importance of HCO3- being exchanged for Cl-?

A

HCO3- moving out of the cell increases the rate of the forward reaction and so more H+ are produced. Cl- moving into the cell then moves into the stomach lumen via Cl- channels and combines with H+ to form HCl.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the 4 phases important in regulating gastric acid secretion? Do these phases turn secretion on or off?

A
  1. Cephalic phase - turning ON.2. Gastric phase - turning ON.3. Gastric phase - turning OFF.4. Intestinal phase - turning OFF.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Regulating gastric acid secretion: What stimuli are involved in the cephalic phase?

A

Sight, smell, taste of food. Chewing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Regulating gastric acid secretion: What stimuli are involved in the gastric ON phase?

A

Gastric distension, presence of peptides and amino acids in the stomach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Regulating gastric acid secretion: What stimuli are involved in the gastric OFF phase?

A

Low pH in gastric lumen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Regulating gastric acid secretion: What stimuli are involved in the intestinal phase?

A

Low pH in duodenal lumen, duodenal distension, presence of amino acids and fatty acids in the duodenum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Briefly describe the cephalic phase.

A

The parasympathetic nervous system is triggered by stimuli. This releases Ach. Ach acts on parietal cells and on gastrin and histamine. HCl secretion increases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Briefly describe the gastric ON phase.

A

Gastrin is released in response to the stimuli. This acts on parietal cells and triggers release of histamine (histamine then acts on parietal cells too). HCl secretion increases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Briefly describe the gastric OFF phase.

A

Gastrin is inhibited in response to stimuli and histamine is therefore indirectly inhibited. Somatostatin is also released and this inhibits parietal cells. HCl secretion decreases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Briefly describe the intestinal phase.

A

The enterogastrones secretin and CCK are released in response to stimuli. Secretin inhibits gastrin and stimulates further somatostatin release. HCl secretion decreases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What neurotransmitter is involved in regulating gastric acid secretion?

A

Ach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What hormone is involved in regulating gastric acid secretion?

A

Gastrin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What paracrine factors are involved in regulating gastric acid secretion?

A

Histamine and Somatostatin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What enterogastrones are involved in regulating gastric acid secretion?

A

Secretin and CCK.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Name the 4 main defence mechanisms against gastric acid secretion.

A
  1. Alkaline mucous. 2. Tight junctions between epithelial cells. 3. Replacing damaged cells. 4. Feedback loops.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Define ulcer.

A

A breach in a mucosal surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Name 3 things that can cause peptic ulcers.

A
  1. Helicobacter pylori. 2. NSAIDS.3. Chemical irritants.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Why do NSAIDS cause peptic ulcers?

A

They inhibit cycle-oxygenase 1. Cycle-oxygenase 1 is needed for prostaglandin synthesis, prostaglandins stimulate mucus secretion. Without cycle-oxygenase 1 there is less mucus and so the mucosal defence is reduced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Why does helicobacter pylori cause peptic ulcers?

A

Helicobacter pylori lives in gastric mucus. It secretes urease. Urease breaks into CO2 and NH3. The NH3 combines with H+ to form NH4+. NH4+ damages the gastric epithelium, an inflammatory response is triggered and mucosal defence is reduced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Name 2 drugs that can be used to reduce gastric acid secretion.

A
  1. Proton pump inhibitors. 2. H2 receptor antagonists.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

If water input is 9L, how much is reabsorbed and how much is excreted in the faeces?

A

8.8L is reabsorbed and 0.2L is excreted in the faeces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How does water move across the small intestine?

A

It moves freely by osmosis and also via aquaporins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

How does Na+ move across the small intestine?

A

Na+ is actively transported from the lumen by pumps located in the cell membranes in the ileum and jejunum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

How does K+ move across the small intestine?

A

Via passive diffusion. Movement is determined by the potential difference between lumen and capillaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Where does Cl- and HCO3- reabsorption mainly take place?

A

In the ileum and colon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the mechanism for Cl- and HCO3- reabsorption?

A

Cl- is actively reabsorbed in exchage for HCO3-. The intestinal contents therefore become more alkaline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What enzyme digests starch in the small intestine?

A

Pancreatic amylase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What bonds does pancreatic amylase break?

A

alpha 1-4 linkages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the end products of starch digestion?

A

Maltose!Also maltotriose, glucose polymers and alpha-dextrins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Where in the small intestine are bile salts absorbed?

A

Terminal Ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What enzyme(s) hydrolyse peptide bonds in the stomach?

A

Pepsins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the optimum pH for pepsins?

A

1.6-3.2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Why is pepsin action terminated in the small intestine?

A

The pH in the small intestine is too alkaline and so it denatures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What enzyme(s) further break down peptides in the small intestine?

A

Pancreatic proteases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the precursor molecule for pepsin?

A

Pepsinogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What activates pepsinogen?

A

Low pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What 2 groups can pancreatic proteases be divided into?

A
  1. Endopeptidases e.g. trypsin.2. Exopeptidases e.g. carboxy dipeptidases.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

How do amino acids get absorbed into the blood?

A

Passive diffusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What enzyme(s) hydrolyse cholesterol esters in the intestinal lumen?

A

Pancreatic esterases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What emulsifies lipids?

A

Bile salts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the advantage of emulsifying lipids?

A

It increases the SA for digestion and so digestion is more efficient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What digests lipids in the small intestine?

A

Pancreatic lipases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Are lipids hydrophobic or hydrophilic?

A

Hydrophobic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are the end products of fat digestion?

A

Free fatty acids and monoglycerides.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What triglyceride bonds is pancreatic lipase able to hydrolyse with ease?

A

1 and 3 bonds (the 2 bond is hydrolysed at a slower rate).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What protein binds pancreatic lipase to the surface of the lipid?

A

Co-lipase. This is essential, pancreatic lipase can not work without it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

The end products of fat digestion combine with bile salts and cholesterol to form what?

A

Mixed micelles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is the function of mixed micelles?

A

Lipid transport systems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

How are chylomicrons formed?

A

Triglycerides, phospholipids and cholesterol combine with proteins inside the epithelial cell forming chylomicrons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Is vitamin A fat or water soluble?

A

Fat soluble.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the functions of vitamin A?

A

Vitamin A is needed for cellular growth and differentiation. It is also important for eyesight and lymphocyte production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Name 3 sources of vitamin A.

A
  1. Oily fish.2. Dairy.3. Liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is the recommended daily intake of vitamin A for men and women?

A

Women - 600µg. Men - 700µg.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What are the consequences of vitamin A deficiency?

A

Night blindness, growth retardation, increased susceptibility to infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are the consequences of vitamin A toxicity?

A

Anorexia, vomiting, headache, reduced bone density, conjunctivitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Is vitamin C fat or water soluble?

A

Water soluble (easily lost when boiled).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the functions of vitamin C?

A

Synthesis of collagen, neurotransmitters and carnitine. It has an antioxidant ability and can absorb non-haem iron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Name 4 sources of vitamin C.

A
  1. Citrus fruits. 2. Green leafy veg.3. Potatoes.4. Kidney.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is the recommended daily intake of vitamin C?

A

40mg.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What are the consequences of vitamin C deficiency?

A

Weakness, shortness of breath, aching, bleeding gums, thickening of skin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What are the consequences of vitamin C toxicity?

A

Diarrhoea, nausea, renal stone formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Are B vitamins fat or water soluble?

A

Water soluble.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

How many B vitamins are there?

A

8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What are B vitamins important for?

A

Cell metabolism and energy production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

How long do glycogen stores in a 70Kg adult last?

A

About 12 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

How long do lipid stores in a 70Kg adult last?

A

3 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What percentage of BMR do these organs use?a) Brain.b) Liver.c) Muscle.

A

a) 20%.b) 21%.c) 22%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What fuels does the brain use?

A

Glucose and ketone bodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What fuels does the liver use?

A

Glucose, amino acids, fatty acids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What fuels does muscle use?

A

Glucose, ketone bodies, amino acids and triacylglycerol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What are free sugars and starch associated with effecting?

A

They can cause shifts in blood glucose and insulin due to their rapid absorption. This can strain the pancreas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What type of starch is the most desirable and why?

A

Slowly digestible starch. It is slowly digested and absorbed and so has little influence on blood glucose and insulin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is the cause of lactose intolerance?

A

A deficiency in lactase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Give 3 symptoms of lactose intolerance.

A
  1. Bloating. 2. Diarrhoea. 3. Pain.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Explain the mechanism that produces the symptoms of lactose intolerance.

A

Lactose intolerance has an osmotic effect. H2O and fermentable sugars enter the the large intestine lumen and cause diarrhoea, bloating and pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Why might someone with enterocyte loss be unable to break down lactose?

A

Enterocytes at villi contain lactase. If the enterocytes are lost they may have lactase deficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Define BMR.

A

The energy needed to stay alive at rest, usually 24kcal/kg/day.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Where does the foregut begin and end?

A

Mouth to the major duodenal papilla. (In the embryo - oropharyngeal membrane to the liver bud).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Where does the midgut begin and end?

A

Major duodenal papilla to 2/3 along the TC. (In embryo - liver bud to 2/3 along TC).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Where does the hindgut begin and end?

A

Distal 1/3 of TC to anal canal. (In embryo - distal 1/3 of TC to cloacal membrane).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Why are the foregut, midgut and hindgut divisions different in the adult compared to in the embryo?

A

It changes due to the formation of the ampulla of vater.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Are the pharyngeal clefts formed in the endoderm or ectoderm?

A

Ectoderm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Are the pharyngeal pouches formed in the endoderm or ectoderm?

A

Endoderm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

How many pharyngeal arches are there?

A

5 (4 pharyngeal clefts and pouches).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What does the first pharyngeal arch form?

A

Muscles for mastication. Innervation: Cn 5.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What does the second pharyngeal arch form?

A

Muscles for facial expression. Innervation: Cn 7.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What does the third pharyngeal arch form?

A

Stylopharyngeus muscle. Innervation: Cn 9.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What does the fourth pharyngeal arch form?

A

Cricothyroid muscle. Innervation: External branch of superior laryngeal nerve (Cn 10).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What does the sixth pharyngeal arch form?

A

Intrinsic muscles of the Larynx. Innervation: Recurrent laryngeal nerve (Cn 10).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Why is the stomach the shape it is?

A

Due to differences in growth rates. The greater curvature grows faster than the lesser curvature.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Why does the left vagus nerve become the anterior vagal trunk and the right vagus become the posterior vagal trunk?

A

Due to the 90 degrees clockwise rotation of the stomach in its longitudinal axis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What are the axis of stomach rotation?

A

Longitudinal and anteroposterior.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What does the dorsal mesentery become?

A

The greater omentum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What does the ventral mesentery become?

A

The lesser omentum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What are the 5 stages of midgut development?

A
  1. Elongation. 2. Herniation.3. Rotation. 4. Retraction. 5. Fixation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What connects the midgut to the yolk sac?

A

The Vitelline duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What happens in the elongation stage of midgut development?

A

Rapid elongation forms the primary intestinal loop. The proximal part of the loop forms the small intestine and the distal part forms the large intestine up to 2/3 TC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What happens in the herniation stage of midgut development?

A

The rapid growth of the intestinal loop means it is pushed into the extra embryonic cavity in the umbilical cord.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What happens in the rotation stage of midgut development?

A

The elongated intestinal loop rotates 270 degrees anticlockwise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What happens in the retraction stage of midgut development?

A

In the 10th week the herniated midgut returns into the expanded abdominal cavity. Th jejunum is first to return.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What happens in fixation of midgut organs?

A

This is when some regions of the gut lose their dorsal mesentery. These regions become retroperitoneal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What are the 4 layers of the GI tract?

A
  1. An innermost mucosa.2. A sub-mucosa.3. An external muscle coat (muscularis externa) 4. A serosa.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is the innermost mucosa layer composed of?

A
  • A folded epithelium. - Lamina propria (connective tissue).- Muscularis mucosa (ring of smooth muscle).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What is the submucosa layer composed of?

A

Loose connective tissue containing glands and lymph tissue. Many blood vessels and a rich plexus of nerves that is part of the enteric nervous system (Meissner’s plexus) are also found in the submucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What is the muscular externa composed of? What is its function?

A

Composed of 2 layers of smooth muscle: circular and longitudinal. Nerves that are part of the enteric nerve plexus are also present here (Aurebach’s plexus). Contraction of the muscle helps to break down and food and propel it along the GI tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What is the serous layer composed of?

A

Composed of a simple squamous epithelium that covers the outside surface of the gut tube facing the peritoneal cavity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What enzyme are parietal cells abundant in?

A

Carbonic anhydrase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Give 5 functions of hepatocytes.

A
  1. Creation and storage of energy in the form of glycogen. 2. Synthesise and secrete plasma proteins.3. Remove amino groups from amino acids for the production of urea. (Deamination). 4. Uptake, synthesis and excretion of bilirubin and bile acids. 5. Detoxification and inactivation of drugs and toxins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What are the 2 key stages for fat digestion?

A
  1. Emulsification. 2. Triglyceride hydrolysis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What clinical feature would you see in a patient with fat malabsorption?

A

Pale and smelly faeces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What clinical feature would you see in a patient with vitamin K malabsorption?

A

Bruising.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What clinical feature would you see in a patient with protein malabsorption?

A

Swollen ankles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Where in the layers of the GI tract would Meissner’s plexus be found?

A

In the submucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Where in the layers of the GI tract would Auerbach’s plexus be found?

A

In the muscularis externa between the circular and longitudinal layers of muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Name the abdominal retroperitoneal organs.

A

Supradrenal glands, Aorta, IVC, Duodenum (except cap), Pancreas (except tail), Ureters, Colon (ascending and descending), Kidneys, Oesophagus, Rectum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Name the abdominal intraperitoneal organs.

A

Spleen, Small intestine, Appendix, Liver, Transverse colon, Stomach, Sigmoid colon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What is the arcuate line?

A

The lower limit of the posterior rectus sheath.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What happens to the posterior rectus sheath below the arcuate line?

A

It is absent. The rectus abdominis is in direct contact with the transversalis fascia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What envelopes the rectus abdominis above the arcuate line?

A

It is enveloped by the internal oblique aponeurosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What is the anterior layer of rectus sheath formed from?

A

External oblique aponeurosis and the anterior lamina of the internal oblique aponeurosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What is the posterior layer of the rectus sheath formed from?

A

The posterior lamina of the internal oblique aponeurosis and the transversus abdominis aponeurosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What forms the anterior rectus sheath below the rectus abdominis?

A

The external oblique, internal oblique and transversus abdominis aponeurosis’ all form the anterior rectus sheath. There is no posterior rectus sheath.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What vertebral level does the umbilicus mark when lying down?

A

L3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What abdominal plane would you refer to when carrying out a lumbar puncture?

A

The intercristal plane. It joins the highest points of the pelvis posteriorly and marks the space between L4 and L5.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

Describe 2 ways in which the transpyloric plane can be drawn.

A
  1. The midpoint between the suprasternal notch and the pubic symphysis. 2. Connects the two points marked by the insertion of the rectus sheath into the costal margin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

Name 3 structures that cross the transpyloric plane.

A
  1. The pylorus of the stomach. 2. The gall bladder. 3. The pancreas.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

At what vertebral level is the transpyloric plane?

A

L1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What is the intercristal plane?

A

It connects the highest points of the pelvis at the lower back.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

At what vertebral level is the intercristal plane?

A

L4/5.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What is the intertubercular plane?

A

A line that joins the tubercles of the iliac crests.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

At what vertebral level is the intertubercular plane?

A

L5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What is the subcostal plane?

A

A plane parallel to the lowest points of the costal margins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

At what vertebral level is the subcostal plane?

A

L2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Where is the swallowing centre found?

A

Medulla oblongata.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What molecule is responsible for the activation of pepsinogen into pepsin?

A

HCl.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Give 3 functions of HCl in the stomach.

A
  1. Solubilisation of food particles. 2. Kills microbes. 3. Activates pepsinogen forming pepsin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

Histamine is secreted by enterchromaffin like cells. What are enterochromaffin cells?

A

Enterchromaffin cells are located in the intestine and secrete serotonin, not histamine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

What type of cells are secretin and CCK?

A

Enterogastrones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

Chief cells secrete pepsinogen and and an enzyme. What is the enzyme?

A

Gastric lipase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

Name 3 monosaccharides.

A
  1. Glucose. 2. Fructose. 3. Galactose.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

Name 3 disaccharides.

A
  1. Sucrose (glucose and fructose).2. Lactose (glucose and galactose).3. Maltose (glucose and glucose).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

Name 3 polysaccharides.

A
  1. Starch. 2. Cellulose. 3. Glycogen.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

Where does the majority of complex polysaccharide digestion occur?

A

In the large intestine via gut bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Where is the first site of starch digestion?

A

In the mouth via salivary amylase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

Briefly describe starch digestion.

A

Begins in the mouth via salivary amylase. In the small intestine pancreatic amylases catalyse alpha 1-4 linkages forming maltose. The end products are further broken down by enzymes e.g. maltase on the luminal membrane; this forms monosaccharides. The products diffuse into the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What are proteins digested into?

A

Dipeptides, tripeptides and amino acids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

What enzyme is responsible for protein digestion in the stomach?

A

Pepsin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

What is the optimum pH for pepsin action?

A

1.6 - 3.2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

What does pepsin break proteins into?

A

Peptide fragments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

What enzymes are responsible for protein digestion in the small intestine?

A

Pancreatic proteases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

What are the 2 types of pancreatic proteases?

A
  1. Endopeptidases. 2. Exopeptidases.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

Give 2 examples of an endopeptidase.

A
  1. Trypsin. 2. Chymotrypsin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

Give 2 examples of an exopeptidase.

A
  1. Carboxypeptidases. 2. Aminopeptidases.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

What is the function of endopeptidases?

A

They break peptide bonds between non-terminal amino acids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

What is the function of exopeptidases?

A

They break peptide bonds between terminal amino acids and so form monomers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

Which type of pancreatic protease can form monomers?

A

Exopeptidases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

By what process are the products of protein digestion absorbed into the intestinal epithelial cells?

A

Secondary active transport coupled to H+ or Na+.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

What molecules make up phospholipids?

A

1 glycerol backbone, 2 fatty acids and 1 phosphate group.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

What are triglycerides broken down into?

A

Monoglycerides and free fatty acids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

What enzyme is needed for fat digestion?

A

Pancreatic lipase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

What mechanism speeds up the digestion of fats?

A

Emulsification - the surface area for lipase action is increased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

What substances emulsify lipids?

A

Bile salts and phospholipids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

What enzyme anchors lipase to the surface of an emulsified lipid droplet?

A

Colipase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

Name 4 molecules to make up micelles.

A
  1. Fatty acids. 2. Monoglycerides. 3. Bile salts. 4. Phospholipids.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

What molecule is produced that aids absorption?

A

Micelles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

What is the function of micelles?

A

They are lipid transport systems. They move to the epithelial brush border and release the fatty acids and monoglycerides for absorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

What happens to the fatty acids and monoglycerides inside the intestinal epithelial cells?

A

They are re-synthesised into triglycerides in the smooth ER.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

Why are fatty acids and monoglycerides re-synthesised into triglycerides inside the intestinal epithelial cells?

A

To maintain the concentration gradient for further absorption of fatty acids and monoglycerides.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

Inside the intestinal epithelial cell, triglycerides combine with other lipids e.g. cholesterol to form what molecules?

A

Chylomicrons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

What are the functions of chylomicrons?

A

Chylomicrons move through the lymphatics and the blood stream to tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

How is vitamin B12 absorbed?

A

It binds to a protein, intrinsic factor. It is then absorbed in the terminal ileum via endocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

What can cause pernicious anaemia?

A

If you have low levels of intrinsic factor you will have B12 deficiency. This will mean fewer RBC’s will be formed leading to pernicious anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

What can cause Barrett’s oesophagus?

A

GORD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

Describe Barrett’s oesophagus.

A

When the stratified squamous oesophageal epithelium changes to a simple columnar one at the lower end of the oesophagus. This can be caused by prolonged acid reflux from the stomach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

What is the function of the Vagus nerve in regards to parietal cells?

A

The vagus nerve stimulates the release of Ach which then acts on the parietal cells to increase HCl production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

Give 4 risk factors for GORD.

A
  1. Obesity. 2. Pregnancy. 3. Hiatal hernia. 4. Smoking. (Sedentary lifestyle is not a risk factor).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

Where in the stomach are G cells most numerous?

A

In the antrum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

Name 2 areas of the body with a low pH to combat bacteria.

A

Stomach and vagina.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

Name 3 organs that secrete digestive enzymes.

A
  1. Stomach. 2. Pancreas.3. Salivary glands.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

What structure, visible microscopically, is primarily responsible for absorption?

A

Villi.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

Name 3 physical mechanisms of absorption.

A
  1. Endocytosis. 2. Diffusion/facilitated diffusion. 3. Active transport.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

Name 2 diseases that can cause malabsorption.

A
  1. Crohn’s disease - loss of plicae circulares.2. Coeliac disease - vili atrophy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

Define malnutrition.

A

A lack of nutrition due to not eating enough, being unable to absorb nutrients, eating the wrong things.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

Why might an elderly person be at risk of malnutrition?

A
  1. Immobility - unable to cook and eat.2. Dental problems meaning its difficult to chew foods. 3. Decreased appetite. 4. Not eating the right things.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

Name 3 physical tests for malnutrition.

A
  1. BMI.2. Amount of body fat.3. Height.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

Give 4 complications of malnutrition.

A
  1. Apathy.2. Depression. 3. Increased risk of infection. 4. Anaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

Why is endoscopy preferred to a barium meal?

A

Produces a better image and is more accurate. Also prevents exposure to radiation as a barium meal requires an X-ray.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

What muscles contributes to the upper oesophageal sphincter?

A

Cricopharyngeus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

Where are the stem cells that replace the epithelium located?

A

The base of crypts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

What are the pacemaker cells of the small intestine called?

A

Interstitial cells of Cajal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

Name 2 endocrine secretions from the duodenum?

A
  1. Secretin. 2. CCK.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

Why are fatty acids and monoglycerides re-synthesised into triglycerides inside the epithelial cell?

A

To maintain a diffusion gradient allowing for further reabsorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

Which papillae do not bear taste buds?

A

Filiform papillae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

Does the oesophagus have a serosa layer?

A

No!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
253
Q

What is refeeding syndrome?

A

Metabolic disturbances (hypokalemia, hypomagnesemia etc) that occur due to reinstitution of nutrition to patients who are starved/severley malnourished.

254
Q

What are the functions of the stomach?

A

To store and mix food, dissolve and continue digestion, kill microbes, regulate flow of food, secrete proeases, secrete intrinsic factor, Lubrication.

255
Q

Where is B12 absorbed?

A

Terminal ilium

256
Q

What is chyme?

A

chewed up food that leaves the stomach.

257
Q

What are the areas of the stomach?

A

cardia where the oesophagus joins, fundus at the top, body main top bit, antrum bottom main and pylorus the bit near the sphincter.

258
Q

What are the key cells of the stomach?

A

Mucous cells, parietal cells, chief cells and enteroendocrine cells

259
Q

Where are most of the mucous cells?

A

On the surface of the wall lining.

260
Q

What are gastric pits?

A

The dips in the surface of the stomach. where you get parietal chief and enteroendocrine.

261
Q

Where are you most likely to find parietal cells?

A

In the pits of the fundus and body not antrum

262
Q

Where are you most likely to find chief cells?

A

In the pits of the antrum

263
Q

What is Gastric acid?

A

Hydrochloric acid, about 2 litres a day, more than 150nM H+ concentration

264
Q

Which cells produce gastric acid?

A

Parietal cells

265
Q

How is gastric acid produced?

A

Chloride diffuses into the stomach passively to keep it electrically neutral by having potassium leaving. To increase H+ there is a hydrogen potassium pump ATP is used here. the comes from water. to replenish hydrogen ions carbonic andydrase converts CO2 into carbonic acid and the bicarbonate is released and the let into the blood by swapping with a chloride

266
Q

What is an effect of vomiting ?

A

Low potassium

267
Q

What is the turning on cephalic phase?

A

Initiated by the parasympathetic nervous system. this happens when we see smell or taste food. it causes Acetylcholine to be released onto parietal cells and triggers the release of gastrin and histamine which increases acid production

268
Q

What is the gastric phase turning it on?

A

Gastric distension and the presence of pepties and amino acids stimulates release of gastrin, and this acts on parietal cells. Gastrin triggers the release of histamine which also acts on parietal cells which increase acid production

269
Q

Why is histamine important?

A

It acts directly on parietal cells but also mediates the effects of gastrin and acetylcholine. which make this a good target for drugs

270
Q

Why does protein in the stomach initiate acid release?

A

It is a direct stimulus for gastrin release, the protein acts as a buffer increasing pH by absorbing H+ ions, this leads to decreased somatostatin and more parietal cell activity

271
Q

How is gastric acid secretion reduces in the gastric phase?

A

Low pH directly inhibits gastrin selection, it indirectly inhibits histamine release via gastrin and stimulates somatostatin release which inhibits parietal cell activity

272
Q

How is gastric acid secretion turned off in the intestinal phase?

A

Distension in the duodenum, low luminal pH, hypertonic luminal contents and presenece of amino acids and fatty acids, these lead to enterogastrones being released such as secretin, which inhibits gastrin release and promotes somatostatin, it also releases choecystokinin and reduces ACh release

273
Q

What type of signalling cells are gastrin, acetylcholine, histamine and somato statin?

A

Gastrin is a hormone, Histamin and somatostatin are paracrine chemicals, Acetylcholine is a neurotransmitter

274
Q

How do the chemical act on the parietal cells?

A

Causes the more of the pumps to be put on the surface of the cells

275
Q

What are peptic ulcers?

A

an ulcer is a breach in a mucosal surface.

276
Q

What are the causes of peptic ulcers?

A

Helicobacter pylori infection, Drugs-NSAIDS, Chemical irritants alcohol and bile salts, dietary factors and gastrinoma.

277
Q

What are the mechanisms of peptic ulcers?

A

Too much acid, or weakened mucosal defence

278
Q

How is the stomach lining protected from the acid it produces?

A

Alkaline mucus, tight junctions between epithelial cells, replacement of damaged cells and feedback loops

279
Q

How can helicobacter pylori cause an ulcer?

A

They live in the mucus, secreat urease splitting urea into ammonia and this can bind to hydrogen ions and proteases phospholipases and vacuolating cytotoxin A can damage the gastric epithelium and cause an inflamatory response which reduces mucus production

280
Q

What are NSAIDs responsible for in the stomach?

A

Mucus secretion is stimulated by prostaglandins and Cyclo-oxygenase 1 needed for the synthesis of this, NSAIDS inhibit cyco-oxygenases and this reduces the mucosal defence

281
Q

How can bile salts case ulcers?

A

Duodeno-gastric refux, regurgitated bile strips away mucus layer, reduce mucosal defence

282
Q

How can Helicobacter pylori induced ulcers be treated?

A

Proton pump inhibitor for the acids, and two types of antibiotic to reduce numebrs of bateria

283
Q

How can NSAID ulcers be treated?

A

Give the a proton pump inhibitor or histamine blocker, give them a prostaglandin analogue

284
Q

Which cells secrete intrinsic factor?

A

Parietal cells

285
Q

Which cells produce pepsin?

A

None

286
Q

Which cell produces pepsinogen?

A

The chief cells

287
Q

What is a zymogen?

A

An inactive form of an enzyme

288
Q

What stimulates chief cells?

A

Same as for gastric acid

289
Q

What activates pepsinogen?

A

Hydrochloric acid and pepsin can make it into pepsin

290
Q

How is pepsinogen modified into pepsin?

A

it is cleaved into smaller parts

291
Q

What allows for protease activation?

A

Low pH

292
Q

How can pepsin be inactivated?

A

By reacting with the HCO3 in the small intestine

293
Q

How much of protein digestion is the stomach responsible for?

A

abour 20%

294
Q

What is the role of pepsin?

A

Not essential but accelerates protein digestion. Breaks collagen in meat

295
Q

What is the volume of the stomach?

A

50mL

296
Q

What is the maximum volume of the stomach?

A

1.5L

297
Q

What is receptive relaxation?

A

Passive relaxation of the muscularis propria to increase the volume of the stomach

298
Q

What helps gastric receptive relaxation?

A

Vagus parasympathetic innervation. NO and seretonin and enteric nerve plexuses

299
Q

What is peristalsis?

A

Rhythmic wave like contractions in the walls of the stomach.

300
Q

What are the pacemakers of the stomach?

A

Interstitial cells of khal also in intestines

301
Q

Describe the contraction of the stomach?

A

Weak in fundus and body. forces food to pylorus and it closes the sphincter and squeezes food against it.

302
Q

How is food let out of the stomach?

A

Small letting out of chyme into duodenum

303
Q

How frequent is the basic electrical rhythm?

A

3 times per minute

304
Q

How are gastricdepolarisations transmitted to other cells?

A

through gap junctions

305
Q

How are the pacemakers able to generate action potentials?

A

ACh stimulus and other hormones to stimulate an action potential gastrin can do it and mechano receptors release gastrin

306
Q

What duodenal factors decrease gastric motility?

A

increased duodenal luminal fat duodenal distension, duodenal osmolarity, decreased luminal pH

307
Q

What is the importance of controlling gastric emptying?

A

The capacity of the duodenum is less than the capacity of the stomach

308
Q

What is dumping syndrome?

A

When too much hypertonic solution goes into the duodenum.

309
Q

What are the symptoms of dumping syndrome?

A

Vomiting, bloating, cramps, diarrhoes, dizziness, fatigue, weakness, sweating, dizziness, tachycardia

310
Q

What is gastroparesis and its causes?

A

Delayed gastric emptying, no known cause, can be autonomic neuropathies, drugs, abdominal sugeries, parkinsons, MS scleroderma, amyloidosi, Female gender

311
Q

What drugs can cause gastroparesis?

A

GI agents H2 antagonists, proton pump inhibitors, Anti cholinergic medications, Dephenhydramine, Opiod analgesics, Tricyclic antidepressantsOthers Beta adregenergic agonits, calcium channek blockers, interfereon alpha

312
Q

What are symptoms of gastroparesis?

A

Nausea, early satiety, comiting undigested food, GORD, Abdominal pain, Bloating anorexia

313
Q

What is special about the circulation in the liver?

A

There is the normal blood supply from the hepatic artery and blood returns to the heart by the hepatic veins and the IVC. Blood also comes from the small intestine via the superior and inferior mesenteric vein.

314
Q

What are some of the main functions of the liver?

A

Detoxification- Filters and cleans blood of waste productsImmune functions- fights infections and diseasesSynthesis- of clotting factors proteins enzymes, glycogen and fatsProduction of bile- and breakdown of biirubinEnergy storage- glycogen and fatRegulation of fat metabolism Ability to regenerate

315
Q

Describe the metabolic role of the liver

A

Continuous supply of energy for the body by controlling the metabolism of carbohydrates and fats

316
Q

What regulates the liver metabolic activity?

A

Nerves and endocrine glands like the pancreas thyroid and adrenal glands

317
Q

Where are lipides stored?

A

in adipocytes in hepatocytes and elsewhere

318
Q

Which are more fluid saturated or unsaturated fatty acids?

A

Unsaturaes as they need more space due to their bent shape

319
Q

What are the functions of lipids?

A

Part of cell membranes, Energy reserve, Integral to form cells, can be part of inflamatory cascades(arachadonic acid)Hormone metabolism like sx hormones and vitamin D

320
Q

Where does energy in the body come from?

A

The oxidation of lipids or carbohydrates. 30-40 days of lipid energy lipid reserve 100000kcal

321
Q

Where is the main storage f glycogen?

A

In the liver

322
Q

Where do lipids come from to the liver?

A

The portal vein hepatic artery and lymphatics

323
Q

In what form are lipids brought into the liver?

A

As free fatty acids

324
Q

How can fatty acid storage be increased?

A

Eat more fatty acids.

325
Q

How are lipids transported in the body?

A

As tryglycerides or fatty acids bound to albumin or within lipoproteins. Triglycerides cant pass through membranes by fatty acids can

326
Q

What are the ways that fatty acids can be taken up by the liver?

A

Fatty acid binding proteins, Fatty acid translocase and fatty acid transport polypeptide

327
Q

What is the name of the enzyme that can convert triglycerides into free fatty acids?

A

Lipoprotein lipase

328
Q

What enzyme releases fatty acids from adipocytes?

A

Hormone sensitive lipase

329
Q

What does insulin do in terms of fat storage?

A

Fat storage in adipocytes, stimulates lipoprotein lipase to break down TG to release FFA to be stored in the adipocytes. it reduces the activity of HSL so there is reduced export of lipids from the adipocytes

330
Q

What are the effects of insulin resistance on fats?

A

Increased lipolysis in adipocytes leading to lots of TG in circulation, Increased offer of fatty acids to the liver so their uptake increases. increased glucose levels in blood mean less demand for lipids so used to store energy.

331
Q

What is de novo lipogenesis?

A

Happens in the liver and is the sequential extension of an alkaoic chain starting from Acetyl-CoA via serial decarboxylative condensation reactions.

332
Q

What is the rate limiting step of de novo lipogenesis?

A

Aecetyl-CoA to Malonyl-CoA catalysed by Acetyl-CoA carboxylase

333
Q

What affects the rate of de novo lipogenesis?

A

Rate is related to Fatty acid sythetase which is activated by insulin and inactivated by catecholamines and glucagon, it has negative feedback on itself

334
Q

What are lipoproteins?

A

A core of triglycerides and cholesterol-esters and a surface monolayer of phospholipids colesteral and specific proteins(apoproteins)

335
Q

What determines the type of lipoprotein?

A

the ratio of protein to lipid defined by their density LDL HDL VLDL and chylomicrons

336
Q

What do chylomicrons do?

A

Carry lipids from the gut to muscle and adipose tissue

337
Q

What happens to chylomicron remnants?

A

They are taken up in the liver

338
Q

What percentage of cholesterol comes from food?

A

10%

339
Q

Where is cholesterol processed?

A

In the liver

340
Q

How is cholesterol excreted?

A

Through the bile. it taken by lipoproteins in the circulation to the liver

341
Q

How is fats and cholesterol exported from the liver?

A

As bile acids and VLDL

342
Q

What is the process to export a fatty acid?

A

Apoprotein B100 is synthesised in the rER
the lipid compnent is synthesised in the sER
they are added by TAG proteins to ApoB.
They are sent to the Golgi apparatus where ApoB is glycosylated
and then migrates to the sinusoidal membrane and exocytosed as a VLDL

343
Q

What affects Fatty acid oxidation?

A

Periperal fatty acid availablility increased by glucagon and decreased by insulin.

344
Q

What are the 3 locations for oxidation of fatty acids in the liver?

A

Peroxisomal Beta oxidation
Mitochondrial beta-oxidation
ER Microsomal omega oxidation

345
Q

What is mitochondrial beta-oxidation and what is it regulated by?

A

Oxidation of FAs of various chain lengths.
Progressive shortening of FAs in to acteyl-CoA
Condensed into ketone bodies which can be oxidised and enter the TCA cycle

Regulated by:
CPT (Carnitine Palmitosyl Transferase)
Carnitine concentration
Malonyl-CoA (Inhibits CPT)

346
Q

What is peroxisomal beta oxidation?

A

Main Role in detoxification of:
very long chain FAs
2-methyl branched chain FAs
Dicarbolic acids - very toxic

4 step repeated process to shorten the FAs
By two acyl-CoA oxidases and two Thiolases

347
Q

What is steatosis?

A

Fat gathering in the liver cells

348
Q

What is microsomal omega oxidation?

A

Normally minor but increased pathway in Fat overload.
CYP4A enzymes oxidise saturated and unsaturated fatty acids.
Omega oxidation in the ER
Decarboxylation of omega hydroxyl FAs in cytosol
enter Beta oxidation pathway

349
Q

How are Fatty acids able to regulate actions?

A

Gene expresson by controlling transcription factors. the control metabolic machinary for metabolic machinery for fatty acid metabolism

350
Q

What are PPAR? and what would reduced PPAR sensing lead to?

A

Peroxisome Proliferator-Activated Receptor:

nuclear Receptors important for lipid metabolism
alpha, beta, gamma, delta
all involved in lipid homeostasis, 
gamma is for energy storage
alpha is  for gene transcription

Reduced PPAR sensing leads to steatosis and increased induction of CYP2E1 and proinflammatory cytokines.

351
Q

What happens in defective metabolism of fats?

A

Less oxidation (so fat is overloaded) so microsomal omega oxidation increases
more dicarboxylic acids which inhibit other pathways of oxidation
leads to lipotoxicity and steatohepatitis

352
Q

What are the deaseases reated to fat in the liver?

A

NAFLD non-alcoholic fattty liver diseas and NASH non-alcoholic steatohepatitis.

353
Q

What are the stages of liver damage?

A

Fatty liver (deposits of fat cause enlargement), liver fibrosis (scar tissue forms) and cirrhosis ( growth of connective tissue destroys liver structure .

354
Q

What causes fatty liver?

A

Increased TG in plasma from excess diarary intake and caloric intake. Also increased flux of FA increase releae of FA and uptake by hepatocytes. Decreased FA oxidation which decreased demand for lipids and increases storage.

355
Q

What is steathepatitis?

A

Too much fat in the liver. Leads to large release of TG and FA overload increase Reactive Oxygen species production, It causes inflamation from kupffercells ad ethanol can activate stellate cells for fibrogeneseis. lipidperoxidation products cause inflamation

356
Q

How do you manage fatty liver diseas?

A

Reduce calories, increase demant for consumption. usually will burn the fat off

357
Q

How does alcohol cause fatty liver?

A

The high calorific values cause fat storage.

358
Q

How does alcochol get procesed?

A

Alcohol is metabolised Alcohol dehydrogenase (under normal levels) or by the microsomal ethanol oxidising system using CYP2E1 (in excess) which produces acetaldehyde.

This can be further metabolised to acetate by aldehyde dehydrogenase.
Acetate can be used in the kerbs cycle

In excess, acetaldehyde is produced quicker and in more quantities which is toxic and damages the Hepatocytes from the production of free radicals

359
Q

Which of the layers in the trilamina disk form the mid and hind gut?

A

Endoderm forms the mucosa of the bowl some layers are from mesoderm

360
Q

What types of folding happens in the embryo?

A

Lateral the mesoderm and endoderm come round to make boweltube and is surrunded by the mesoderm to form the mesentry and peritoneal membrane

361
Q

What deos the endoderm give rise to in the GI tract?

A

The endothelium of the bowel the hepatocytes of the liver and exo and endocrine pancreas

362
Q

What does the visceral mesoderm give rise to?

A

The muscular wall connective tissue and cisceral peritonium

363
Q

What is interesting about innervation of parietial peritonium?

A

It is the same as the overlying skin

364
Q

What is interesting about innervation of visceral peritoneum?

A

It is supplied by separate nerves the greater for foregut lesser for mid and least for hind and causes refered pain

365
Q

Where do the lungs develop from?

A

The foregut

366
Q

Where is the boundary of the foregut and midgut?

A

Where the pancreatic duct joins the bowel.

367
Q

What is the first stage of the GI developmen?

A

There is a forward looping supplied by the superior mesenteric artery

368
Q

Where is refered pain for the heart and lungs?

A

T1-T5 inside of forarm and upper arm and on chest

369
Q

Where is referred pain for the Foregut?

A

T5-T9 below nipples and umbilicus

370
Q

Where is referred pain for the midgut?

A

T10-T11 the umbilicus

371
Q

Where is referred pain for the Hindgut?

A

T12 just above hair bearing area

372
Q

Describe the stages of the primitive Gut tube development.

A

Elongation, physiological herniation, rotation, retraction and fixation

373
Q

What happens in elongation and herniation?

A

it elongates and then most of midgut loop passes through the umbilicus. elongates in the cephalic limb close to the head. it has rapid growth while the liver and pancreas grows in week 6

374
Q

Describe the rotation of the tube?

A

the caecum rotates infront of the bowl clockwise from above to put it in the right lower part.

375
Q

Describe retraction?

A

the abdominal area is big enough the mesentry facilitates this as it doesnt extend/ the transverse colon and the duodenum comes in first.

376
Q

Where is the appendix?

A

In a variable position which leads to variable presentation of diseases.

377
Q

What is the fixation stage?

A

on organs that are retroperitoneal the two layers fuse together and fix it to the wall

378
Q

Which parts of the GI tract are fixed?

A

The duodenum apart from very first part. Ascending colon and descending and rectum

379
Q

Where is the mesentry for the transverse colon passing?

A

Above the duodenum and across.

380
Q

Where is the small intestine mesentry running from?

A

The duodena jejunal flecture to the illio cecal valve.

381
Q

How can you look at the bowel?

A

Barium ennema and pump air in to xray it.

382
Q

What embryological faults can happen?

A

rotation- caecum not in right place

retraction- part of bowl in the umbilical cord or can rupture the cord.

383
Q

What is the function of saliva?

A

Lubricant for mastication, swallowing and speechOral hygiene to wash the mouth buffer the acidity, and offer immune defenceAdds digestive enzyme and aids taste and without it can lead to infection and pain

384
Q

What is the flow rate of saliva?

A

0.3-7ml per minute arount 1-1.5L over a day

385
Q

What is the pH of saliva?

A

6.2-7.4

386
Q

What is in the saliva?

A

Water serous secretion of amylase alpha and mucus secretion other enzymes such as water etc

387
Q

Which salivary gland only produces serous secretions?

A

Parotid gland

388
Q

What factors affect the composition of the saliva?

A

Flow rate, circadian rhythm, type and size of gland, duration and type of stimulus, diet, drugs, age ,gender

389
Q

What defenses are there in the mouth?

A

The mucous provides a physical barrier. the palatie tonsils that have lymohocutes and dendritic cells, salivary glands wash away food and bacteria

390
Q

Which glands continuously produce saliva?

A

Submandibular, sublingual and minor glands are continuously producing

391
Q

Which gland only produces secretions when stimulated?

A

The parotid

392
Q

What is the balance between mucous and serous secretions?

A

Unstimulates is mixedstimulated is mainly serous

393
Q

What is whole saliva?

A

Saivary gland secretions, blood, oral tissue, microorganisms and food reminants

394
Q

What are Exosomes?

A

Cell specific lipid microvesicles, can migrate through the vasculature. reside in a number of biofluids eg urin blood breast milk and saliva and we don’t yet know their function but could be to do with immune response and contain DNA

395
Q

What type of tests could the saliva be used for?

A

Diagnostic or prognostic tests

396
Q

What are the structure of the salivary glands?

A

They have two distinct epithelial layers. Acinar cells which surround ducts which form a large duct enterig the mouth. There are many channels and transporters in the apical and basolateral mebranes enabling transport of fluid and electrolytes.

397
Q

What are the two types of acinus?

A

Serous and mucous.

398
Q

Describe the two types of acinar cells histologically

A

serous are dark staining nucleus in basal third and small central ducts secrete water and alpha amylase.

mucous are pale staining nucleus at the base large central duct and secrete water and glycoproteins.

399
Q

What are the types of ducts in the glands?

A

Intralobular ducts and main excretory

400
Q

What are the two divisions of intralobular ducts?

A

Intercalated short and narrow segments with cuboidal cells that connect acini to striated ducts. And striated ducts are major site for sodium chloride reabsorption

401
Q

What is the appearace of striated ducts histologically?

A

Look striated
basal membrane has many microvilli for transport
many mitochondria for transport

402
Q

Other than conduction what are the fuctnios of the ducts?

A

Primary saliver has lots of NaCL and is isotonic but it becomes hypotonic and NaCl also have secretions of potassium and HCO3

403
Q

Which glands are the major salivary glands?

A

Parotid submandibular and sublingual.

404
Q

Where are the parotid glands?

A

just in fron of the ear it has a capusule

405
Q

What structures pass through the parotid gland?

A

The external carotid and termial branches, retromandibular vein, facial nerve.

406
Q

Where is the outlet of the duct for the parotid?

A

above top of the molar on top

407
Q

Where is the submandibular gland?

A

under the manduble bone there are two lobes.

408
Q

What is wharton’s duct?

A

it secretes the saliva from the submandibular and sublingual glands into the mouth. It is positioned in the sublingual papillae

409
Q

Where are the sublingual gland?

A

Between mylohyoid muscle and oral mucosa

410
Q

What does sublingual gland secrete??

A

mixed but mainly mucous

411
Q

What are some of the minor glands?

A

around Buccal labial palatal and lingual regions. at base of tounge von ebner glands that secrete serous. all other minor are mucous producers

412
Q

Which nerve innervates parotid?

A

the 9th cranial nerve does parasympathetic

413
Q

What is Xerostomia?

A

Dry mouth

414
Q

What are the main causes for dry mouth?

A

Radio treatment of cancer, CF sjogrens syndrome and often medications

415
Q

What are other problems with glands?

A

Obstructed glands with stones, infections with them from mumps and parotid has the capsules which causes painDegenerative from radiotherapy.

416
Q

What is Sjogren’s syndrome?

A

An autoimmune condition that affects areas that produce fluids such as the salivary glands and the tear ducts resulting in dryness
Manly post-menopausal females, affects eyes, could be linked to arthritis

417
Q

What is the effects of salivary gland dysfunction?

A

Low lubrication poor hygiene accumulation of plaque and caries gingivitis and periodontal disease and opportunistic infections

418
Q

What is the effects of salivary gland dysfunction?

A

Low lubrication poor hygiene accumulation of plaque and caries gingivitis and periodontal disease and opportunistic infections

419
Q

What is the function of bile?

A

Lipid emulsification and absorption, Cholesterol homeostasis, excretion of lipid soluble xenobiotics drug metabolites and heavy metals

420
Q

What is bile?

A

A complex lipid-rich micellar solution containing water inorganic electrolytes, organic solutes, bile acids, phospholipids, cholesterol, bile pigments)

421
Q

How much bile is produced a day?

A

500-600ml

422
Q

How much of bile acids are lost each time?

A

5%

423
Q

What makes up most of bile?

A

Bile acids then phospholipids cholestrol and protein small bilirubin

424
Q

What are the types of bile acid?

A

Primary: Cholic and Chenodeoxycholic
Secondary: Deoxycholic and lithocholic acids

425
Q

What produces secondary bile acids?

A

Bacterial conversion

426
Q

What is the precursor for bile acids?

A

Cholesterol is used to produce it

427
Q

What is the purpose of bile acid prodction?

A

the primary bile acids are water soluble unlike cholesterol

428
Q

What happens the bile acids before the are secreted?

A

They are conjugated with taurine or glycine to make them lionised at physiological pH and therefore able to produce mixed micelles

429
Q

What is amphipathic?

A

Like water and fat to reduce surface tension and aid emulsification

430
Q

what is the function of emulsofication?

A

gives a large SA for lipolysis enzymes

431
Q

What is colipase?

A

an enzyme that facilitates binding of lipase to the droplet

432
Q

How do the fatty acids and monoglycerides get into the enterocyte?

A

They form micells with bile acids

433
Q

What happens in an enterocyte to the fats?

A

Packaged into the lipoproteins for transport.

434
Q

What are the functions of bile acids?

A

Induce bile flow through osmotic effect.
they are involved in the digestion of dietary fats,
facilitates protein absorption by accelerating hydrolysis,
involved in cholesterol homeostasis
antimicrobial can induce genes
prevents calcium gallstones and renal stones

435
Q

describe the movement of cholesterol from the liver

A

It passes into the duodenum and 50% of all cholesterol including dietary is reabsorbed

436
Q

What do statins do?

A

THey inhibit HMG CoA reductase to prevent cholesterol being formed

437
Q

What does Exetimibe do?

A

Block protein mediated transport of cholesterol across the membrane of the small intestine

438
Q

What happens to bile acids during the fasted state?

A

Bile acids go down the billary tract to gall bladder and get concentrated to 10x

439
Q

What happens to the bile during the fed state?

A

CCK is released from duodenal mucosa which causes the sphincter of oddi to open and contract the gall bladder

440
Q

What happens to bile acids in the small intestine

A

They stay intraluminal, they are reabsorbed in the terminal illium via the apical sodium bile acid transporter. and re enter the liver via portal circulation

441
Q

How often does the circulation happen per meal?

A

2-3 times

442
Q

What is the feedback mechanism for bile acid?

A

bile acids inhibit cholesterol 7 aloha hydroxylase

443
Q

What is farnacoid X receptor?

A

Bile acids are ligands for it. this causes synthesis of Endocrine polypeptide hormen FGF19 to inhibit CYP7A1

444
Q

what can go wrong in the circulation?

A

Inherited defects, deconjugation of bile acids from small bowel bacterial overgrowth, cholecystectomy can cause diarrhoea as it is just stored in duodenum.Ileal resection where absorbed bile acids ebter colon where they inhibit water absorption/ induce secretion resulting in bile salt diarrhoea

445
Q

What happens in biliary obstruction and what are some clinical symptoms?

A

A stone blocks it, pancreatic carcinoma can cause malabsorption of fat soluble vitamins and fat resulting in steatorrhoea

446
Q

What happens in biliary obstruction?

A

A stone blocks it, pancreatic carcinoma can cause malabsorption of fat soluble vitamins and fat resulting in steatorrhoea

447
Q

What is the function of the colon?

A

Production of vitamins, absorption of water and electrolytes and excretion.

448
Q

What makes faeces brown?

A

Stercobilin

449
Q

What are the layers of the colonic wall?

A

Mucosa submucosa, muscularis mucosae and muscularis propria and serosae which encapsulatied

450
Q

What is the muscular layer of the colon like?

A

continuous circular muscle, 3 stripes of longditudinal muscle taeniae coli

451
Q

What are haustrations?

A

bumps in and out of the surface on the large bowel. (the bumps)

452
Q

What is the epithelium in the bowel?

A

Columnar epithelium with goblet cells crypts of leibercoum

453
Q

What is absorbed in the colon?

A

Water by osmosis, sodium is actively transported out of it

454
Q

How are vitamins produced in the colon?

A

By bacteria produce them

455
Q

What is the intrinsic nerve supply in the colon?

A

Meissners and Auerbach’s plexus this contraction continues on its own and is stimulated by faecal matter in the tube.

456
Q

What is the extrinsic innervation to the rectum

A

Parasympathetic - pelvic splanchnic nerves (S2-4)

Sympathetic, Lumbar splanchnic nerves and hypogastric plexus

457
Q

What is the gastro-colic reflex?

A

The stomach stretching and food in the jejunum leading to mass movement of the colon.

458
Q

What is the structure of the anal sphincter?

A

There are many muscles such as levator ani internal and external anal sphincter. The internal is smooth muscle. the external anal sphincter is skeletal muscle

459
Q

What happens when the rectum is empty?

A

both sphincters are contracted puborectalis (a sling that keeps the angle of the rectum acute) muscle is contracted

460
Q

What happens when the rectum fills?

A

the external sphincter is relaxed, puborectalis relaxes, rectum contracts and do a valsalva maneuver (increases abdominal pressure by closing glottis and squeezing muscles

461
Q

How do we know when we need to daefacate?

A

Pressure sensors in the rectum relax the anal sphincter, it is a sampling reflex

462
Q

What could lead to constipation defaecation?

A

Consistency of stool, Bowel motility, physical blockage to the bowel, pelvic floor disorders

463
Q

How can constipation be cured?

A

Drink more water, more dietary fibre, exercise, way sit on the toiletMedical- Laxative,

464
Q

What can cause diarrhoea?

A

Consistency of stool or frequency of movements, diseased bowel mucosa, reduced rectal capacity, pelvic floor disorder

465
Q

What diseases are associated with metabilic problems?

A

Diabetes, obesity, high cholesterol, aorexia.

466
Q

What can happen to proteins in the body?

A

The enter the nitrogen pool and can become tissue protein, enter the urea cycle then citric acid cycle or excreted, or can be put into pyruvate and into the TCA cycle

467
Q

What can happen to carbohydrates?

A

glycolysis to Pyruvate or acetyl CoA and then TCA cycle.

468
Q

What happens to lipds in the body?

A

They undergo beta oxidation to enter TCA cycle

469
Q

What comes from carbohydrates?

A

Glucose

470
Q

What are proteins brokendown into?

A

Amino acids

471
Q

What does fat become?

A

triglycerides

472
Q

Where is glucose absorbed?

A

The intestines

473
Q

Where glucose used?

A

Muscles, Brain, RBC and adipocytes to be stored

474
Q

What happens to glucose in the liver?

A

Insulin promotes the uptake of glucose into cells, here it can be stored as glycogen. or it can be Acetyl CoA for energy production. With excess can be converted into triglycerides can be exported by LDL

475
Q

What happens to glucose in the muscle?

A

Stored as glycogen, or used for respiration

476
Q

How is glucose used in the brain?

A

It is used directly for energy

477
Q

How is glucose used in RBCs?

A

Glucose is converted into pyruvate in glycolysis and then to lactate as cant do aerobic respiration

478
Q

What happens in adipicytes to glucose?

A

Stored as triglycerides in the cells mediated by glucose

479
Q

What happens to amino acids in the bloodstream?

A

They enter cells and are used to construct proteins, they can makehormones or they can feed into the krebs cycle

480
Q

What happens to triglycerides in the body?

A

can be joined to proteins to be transported to the other parts of the body chylomicrons travel in the lymphatics

481
Q

What happens in the fed state?

A

Fuels are oxidesed to energy. excess is stored as triglycerides in adipose tissue, glycogen in the liver and muscle

482
Q

What happens in the body during fasting short term?

A

Energy stores are broken down to produce glucose. glycogen is broken down from the liver glucagon promotes this. the glucose goes to the brain and muscles and RBCs. this is called glycogenolysis

483
Q

What happens in a longer fast initially?

A

All glycogen is used up in stores, amino acids are used preferentially by muscle protein. lactate from RBCs and glycerol can be released from adipocytes. this is all sent to the liver where these molecules produce glucose. Gluconeogenesis

484
Q

What happens in a longer fast to the fats?

A

Triglycerides are split into glycerol that goes to the liver for conversion to glucose, Fatty acids can be used by the kidney and muscle as a source of energy. the fatty acids can produce ketones in an emergency. this is lipolysis and is driven by glucagon

485
Q

What happens in prolonged fasting?

A

cant break down all of the muscles as can’t move. so after a while it preserves muscles. this is when fatty acids are used and ketogenesis often takes place.

486
Q

Which substances can be measured in the blood?

A

Glucose, ketones, insulin, lactate and triglycerides

487
Q

Which hormones that regulate fuel metabolism?

A

Insulin and glucagon, cortisol, Adrenaline and noradrenaline, thyroxine, growth hormone and somatostatin

488
Q

What does insulin do?

A

It is anabolic it promotes glycogen storage, fat storage and protein synthesie?

489
Q

What does glucagon do?

A

It is catabolic it promotes glycogenolysis, gluconeogenesis and ketogenesis

490
Q

What is the effect of cortisol?

A

Lipolysis, protein breakdown, gluconeogenesis and glycogen storage it is a preparation for a stress response

491
Q

What are the effects of adrenaline?

A

Glycogenolysis, gluconeogenesis and lipolysis it is fight or flight hormone

492
Q

What does thyroxine do?

A

It controls glycolysis, cholesterol synthesis, glucose uptake, protein synthesis and sensitises cells to adrenaline

493
Q

What does growth hormone do?

A

Gluconeogenesis glycoge syntheis lipolysis, protein synthesis, decreased glucose use

494
Q

What is Diet induced thermogensis?

A

The heat energy produced from the breakdown of food into its constituent nutrients

495
Q

How is appetite controlled?

A

Ghrelin increases appetite and Leptin decreases hunger. high lipids gives high leptin but in obesity the body becomes desensitised

496
Q

What are the foregut derivatives?

A

oesophagus stomach first half of duodenum pancreas liver, biliary system and dorsal and ventral mesentery ommentum

497
Q

What is the dorsal mesentery?

A

the greater omentum

498
Q

what is the ventral mesentry?

A

the lesser omentum

499
Q

Which artery supplies the foregut?

A

The coealiac axis

500
Q

What is the falciform ligamaent?

A

The free edge of the lesser ommentum that contains the ligamentum teres

501
Q

What is the falciform ligament?

A

The free edge of the lesser ommentum that contains the ligamentum teres

502
Q

Which mesentery does the liver grow in?

A

the lesser omentum/ventral

503
Q

What are the outgrowths of the duodenum?

A

Two into the ventral mesentery( one pancreas the other liver) and one into the dorsal mesentery

504
Q

describe the liver out pouching?

A

The bile ducts grow then some separate to form the liver in the ventral mesntery.it develops to the right of the midline and has overlapping mesentery and there is a bare area.

505
Q

What is the portal triad like?

A

Has peritoneum surrounding it all they are at the edge of the lesser omentum

506
Q

What is the rotation of the pancreas?

A

The dorsal rotates90 degrees to the left side. the ventral rotates to the same position bringing the bile ductwith it to the other pancrease.

507
Q

What areas of the pancreas are formed from the ventral bud and dorsal bud?

A

Ventral bud:
Uncinate process
Head
Main pancreatic duct

Dorsal Bud:
Neck body and tail of the pancreas

508
Q

Whar happen to the superior mesenteric artery and vein?

A

They get sandwiched between the two pancreases

509
Q

Where is the head of the pancreas?

A

right by the duodenum

510
Q

Where is the neck of the pancrease?

A

the bit that overlies the blood vessels

511
Q

Where does the spleen develop?

A

The dorsal mesentry

512
Q

Describe the rotation of the stomach

A

It rotates 90 degrees clockwise so the left side lies anteriorly and the right side lies posteriorly

513
Q

where is the lesser sac?

A

The lesser omentum and greater omentum, posteria of it is the pancreas

514
Q

When does the omentum grow the most?

A

In puberty

515
Q

What happens in iron metabolism?

A

comes in to duodenum put into transferrin and can be made into blood cells muscles or in the liver. it is stored in the liver cells and reticuloendothelal macrophages

516
Q

What is ferritin?

A

Large spherical protein with 24 units, it can contain 50000 atoms of iron an is in the cytoplasm and in the serum, the amout in the serum tells us how much iron in the body.

517
Q

What is ferritin excess?

A

excess iron storage disorder, hereditary haemochromatosis, haemolytic anaemia, multiple blood transfusions, iron suppliments. can be non-iron overload like liver disease

518
Q

What causes ferritin deficiency?

A

Not enough iron

519
Q

What are vitamins used for?

A

Gene activators, free-radical scavengers, coenzymes or cofactors in metabolic reactions

520
Q

Which vitamins are fat soluble?

A

ADEK

521
Q

Which vitamins are water soluble?

A

B and C

522
Q

How long do water soluble vitamin stores last?

A

Not long as easily washed out of body

523
Q

What is vitamin A used for?

A

Used for help in eye function, comes from carrots and meat. it forms rhodopsin in rods of the eye and for spermatogenesis for growth and membranes

524
Q

What is a defficiency in vitamin A?

A

Rare in affluent countries can lead to blindness night blindness can happen in fat malabsorption.

525
Q

What happens with excess vitamin A?

A

Not very very bad but can lead to nausea vomiting headaches, can get yellowing of the skin

526
Q

What is vitamin D used for?

A

increased intestinal absorption of calcium, resorption and formation of bone, reduced renal excretion of calcium.

527
Q

What is the problem with vitamin D deficiency?

A

Rickets in children osteomalacia in adults

528
Q

What is the role of sunlight in vitamin D?

A

sunlight converts it from 7dehydrocholesterol, into cholecalciferol, can come from others and its stored as 25 hydroxyvitamin D then converted to 1,25 dihydroxy to be used

529
Q

What is vitamin E used for?

A

In antioxidants

530
Q

How is vitamin E stored?

A

In adipose as fixed pool, and in licer and plasma as a labile store

531
Q

What is defficiency and excess of vitamin E like?

A

Caused by fat malabsorption CF, premature infants, get haemolytic anaemia, myopathy, retinopathy ataxia and neuropathy in excess its not too harmful

532
Q

What is vitamin K used for?

A

It is stored in licer but then given to LDL. it is used for clotting factors 2,7,9,10 it activates some.

533
Q

What does a defficincy in vitamin K

A

Haemorragic disease of the nowborn not usually a problem in adults.

534
Q

What happens in excess vitamin K?

A

K1 is safe, synthetic forms are more toxic, oxidative damage and red cell fragility

535
Q

What is the use of vitamin C?

A

Collagen synthesis, antioxidant and iron absorption

536
Q

What happens in vitamin C deficiency?

A

Scurvy easy bruising and bleeding teath and gum disease hair loss, quick treatment

537
Q

What happens in excess?

A

Can cause GI side effects

538
Q

What is vitamin B12 deffiecinecy?

A

caused by Pernicious anaemia, autoimmune destruction of IF producing cells in stomach.
malabsorption by lack of acid pancreatic disease or veganism

causes macrocytic anaemia and peripheral neuropathy in prolongued deficiency

539
Q

What are the forms of B12?

A

methylcobalamin and 5-deoxyadenosylcobalamin

540
Q

How is B12 absorbed?

A

Binds to R protein to protect from acid, then binds to intrinsic factor to be absorbed in the terminal ilium

541
Q

What is folate?

A

Found in lots of fortified foods involved in coenzymes for DNA synthesis

542
Q

What is the folate deficiency like?

A

malabsorption taking drugs can cause it, symptoms are high homocystine levels macrocytic anaemia and foetal abnormalites

543
Q

What are the two clotting pathways?

A

intrinsic which is activated by contact, the extrinsic pathway activated by CF7 touching tissue factor.

544
Q

What do the clotting pathways lead to?

A

Common pathway of thrombin turning fibrinogin into fibrin clot

545
Q

What is prothrombin time?

A

The clotting time via extrinsic pathway

546
Q

What is the activated partial thromoplastin time?

A

measures intrinsic pathway measurement

547
Q

What does prolongues PT mean?

A

Prolongued PT may be deficiency in the synthetic capacity of the liver

548
Q

What are the two phase of biotransformations of waste products?

A

Add or expose functional groups to the molecules such as OH SH NH2 or COOH to try and increase hydrophilicity slightly
Phase 2 i biosynthetic where the molecules are conjugated with endogenous molecules like glucoronic acids. it forms covalent bnds and increases hydrophilicity

549
Q

What is glucuronidies?

A

is any substance produced by linking glucuronic acid to another substance via a glycosidic bond which makes substances more water soluble

550
Q

what is the purpose of the drugs being detoxified

A

to make it more hydrophilic so it can be excreted

551
Q

What is Cytochrome P450?

A

There are 10 moan groups encoded by about 60 genes they all are present in sER hence microsomal enzymes, the oxidise substrates and reduce water. they use NADPH they are indicible and can be modified by drigs and generate fre radicals

552
Q

Why is Cytochrom P450 important?

A

It is involved in lots of drug drug reactions one durg can eaffect metabolism of another. they can also be inhibited by food. this can cause overdose

553
Q

What can affect clozapine?

A

Barbituates rafamoicin and smoking can induce it and ciproflaxin are known to inhibit the cytochrome enzyme.

554
Q

What are the clinical uses of this proses of biotransformation?

A

Some drugs are converted into inactive forms quickly, others are changed to another chemical with the same effect, some got from inactive drugs to active drugs, others could cause toxic products during breakdown

555
Q

How are opiates being metabolised?

A

Codine molecule is morphone with OH replaced by methyl, so better distributed around the drug, this is then changed to morphine a useful product also

556
Q

What happens to paracetamol?

A

Paracetamol is glucuronidated or sulohonated to make it more easily excreted but alternatively, some is excreted as NAPQI which can build up in overdose

557
Q

What are some phase two reactions?

A

Glucoronidation sulphation, Glutatione, Methylation, Acylation, Phosphate conjucation

558
Q

What is special about ethanol?

A

It doesn’t fit phase one or phase 2, it is reduced to acetaldehyde, which can be harmful.
this can be done from microsomal systems as well this is worse in frequent drinkers.
it is converted to acetate in the liver but with the liver is overwhelmed it causes a bulid up of acetaldehyde this buildup causes damage

559
Q

What are the parts of an amino acid?

A

Amino group NH2 acid group COOH and a sidechain

560
Q

What is the difference between dipeptides, polypeptides, proteins?

A

Dipeptide is two AA polypeptide is less than 50AA protein is more than 50AA

561
Q

How is nitrogen excreted in the kidney?

A

Not as protein but as urea

562
Q

When might you have a negatice nitrogen balance?

A

Protein malnutrition, severe illness or sepsis, corticosteroids, cancer or deficiency

563
Q

What is Kwashiorkor?

A

Protein-energy malnutrition

564
Q

What happens to amino acid in the fed state?

A

Dietary protein is absorbed as amino acids in the gut. it is take to the liver where it can be conerted into proteins which travel to cells or go as lipoproteins or amino acids in the blood stream.can be converted to glucose

565
Q

How is amino acid absorbed?

A

co transport with sodium and amino acids

566
Q

What are essential amino acids?

A

Ones that the body cannot synthesis on its own

567
Q

What are conditionally essential amino acids?

A

alanine is used to produce tyrosine. so can be produced but only in the presence of others

568
Q

Non essential amino acids?

A

They are substances that are very easily produced by the body

569
Q

What are glucogenic amino acids?

A

Carbon backbone can be used to produce glucose

570
Q

What is a ketogenic amino acid?

A

is one that the backbone can be used for acetyl CoA

571
Q

What are the two ketogenic amino acids?

A

Leucine and lysine

572
Q

What is the way amino acids can be joined with the respitation?

A

They can enter at many stages, becoming pyruvate or CoA

573
Q

What is transamination?

A

conversion of an amino acid and an alpa ketoacid into a different alphaketo acid and producing another amino acid. swappin the amino goup

574
Q

What is the clinical use of transamination?

A

It is a good identifier of liver function

575
Q

What is transamination of alanine?

A

Alanine+ alphaketoglutarate—> pyruvate+ glutamate

576
Q

What is the use of transamination of alanine?

A

it is a shuttle for ammonia to the liver where it can be processed

577
Q

How is ammonia excreted?

A

it is bound with bicarbonate to carbamyl phosphate which enters the urea cycle.

578
Q

What happens to amino acids in the fasting state?

A

protein is broken into AA in the muscle and then put into TCA cycle and sent out to the other organs to be used.

579
Q

Where can the urea cycle happen?

A

In

580
Q

Where can the urea cycle happen?

A

In the liver only

581
Q

Why do some proteins have bigger lifetimes?

A

Degredation factors: faulty ageing or obsolete, signal transduction, flexible system to meet protein/ energy requirements of environment.

582
Q

What are the two main means of protein breakdown?

A

Proteasomes(ubiquitin) and lysosomes

583
Q

What is ubiquitin?

A

A small protein that marks proteins for destructions it uses lysine residues. there are three enzymes that are used.

584
Q

What is a proteasome?

A

Reacts to ubiquiting and contains proteolytic enzymes

585
Q

What is the N-terminal rules?

A

The group at the end of the protein chane determins if it is destroyed. eg PEST or cyclin destruction box

586
Q

What is the alanine glucose cycle?

A

Glucose can be sent to the cells and there it turns into pyruvate that can accept amine group from then the alanine can go to the liver and be turned back into glucose alphaketo-glutamate is made from glutamate

587
Q

What is the aim of the urea cycle?

A

To turn ammonia to urea

588
Q

What is the ornithine cycle?

A

Ammonia is added to citrulline to produce arginine and urea then ornithing has ammonia and CO2 to make citrulline

589
Q

What can the urea cycle be linked to ?

A

the aspartate argininocuccinate shunt of the citric acid cycle

590
Q

Where do the different parts of the urea cycle take place?

A

Ornithine and citruline parts in the mitochondrion. the rest in the cytoplasm.

591
Q

How can you test for inherited metabolic disease?

A

test for bulidup of things in the cycle.

592
Q

What happens to carbamoyl phosphate when it is not removed?

A

It prodcues oratate that can be picked up in urine of patiens with ornithine transcarbamalase problems

593
Q

What is a good test for liver problems?

A

Ammonia testing

594
Q

What is the role of the epithelial cells in the GI tract?

A

To absorb water and ions and secrete them

595
Q

How long is the small intestine?

A

6m aprox

596
Q

What increases the surface area of the small bowel?

A

The vili and the crypts

597
Q

What is the function of the crypts?

A

they secret substances mainly

598
Q

how is the trans cellular process facilitated?

A

The sodium potassium pump pumps sodium into the blood and potassium into the cell. Sodium moves from the intestinal lumen into the cell bringing other substances with it

599
Q

What facilitates secretion in the intestine?

A

Chloride secretion coming into the cell it infuences cAMP which influences the chloride into the lumen and secretion of water.

600
Q

What are the symptoms of digestive system conditions?

A

Diarrhoea, weight loss and failure to thrive

601
Q

What happens in coelia disease?

A

the villi become dammaged?

602
Q

What is prevalence in UK?

A

1 in 100

603
Q

What is gluten?

A

protein is in wheat barley and rye

604
Q

Why are rehydration drinks very salty?

A

The salts are absorbed and draw water into the body

605
Q

Where is carbohydrates broken down first?

A

In the mouth

606
Q

What breaks starch into sugar?

A

amylase to maltose then maltase to glucose

607
Q

What is sucrose made of?

A

Glucose and fructose

608
Q

What is lactose made of?

A

Glucose and galactose

609
Q

How is glucose absorbed?

A

secondary active transport

610
Q

How is fructose absorbed?

A

Facilitated diffusion

611
Q

What molecules are broken down in the mouth?

A

carbohydrates and fats

612
Q

How are amino acids absorbed?

A

They are absorbed by facilitated diffusion.

613
Q

How do fats get absorbed?

A

As free fatty acids through the membrane

614
Q

What enzymes are present in the stomach?

A

Pepsin and Lipase

615
Q

What enzymes are released by the pancreas?

A

Amylase, lipase and colipate, phospholipase, trypsin and chymotrypsin

616
Q

What enzymes are in the small intestine?

A

Disaccaridases enterokinase(activates trypsin) peptidases

617
Q

What do chief cells do?

A

gastric lipases and pepsinogen

618
Q

What are the pancreatic fuctions?

A

Endocrine (insulin glucagon)

Exocrine- bicarbonate and enzymes

619
Q

What is a pancreatic islet?

A

Alpha cells and beta cells and the acini what secrete enzymes into the pancreatic duct.

620
Q

What happens at the different parts of the salivary duct?

A

Acinar Cell: NaCl rich secretions along with main salivary enzymes

Intercalated duct cells: Join acini to larger striated ducts

Striated duct cells: secrete HCO3- and K+ and reabsorb Na and Cl

621
Q

Where is CF involved in the pancreas?

A

It is responsible for chloride and bicarbonate secretion protein

622
Q

What chemicals stimulate the pancreas?

A

Secretin and cholecystokinin

623
Q

Where is CCK produced?

A

In the duodenum and jejunum by the I cells

624
Q

Why is bicarbonate secreted?

A

It buffers the acid from the stomach.

625
Q

What helps activation/production of trypsin?

A

Trypsin and enterokinase

626
Q

What activates chymotripsin?

A

Trypsin

627
Q

How can you divide diseases of the panceas?

A

Intrinsic problems CF Cancer Autoimmune, Not linked directly could be under stimulation of pancreas, post surgical gastric resection whipple’s

628
Q

How do you image it?

A

MRI and CT as ultrasound doesn’t work well externally? Ultrasound through the stomach

629
Q

How can pancreatic insufficiency be treated?

A

Enzyme replacement, bone health assessment stop smoking treat underlying cause

630
Q

What hormone has the strongest effect in inhibiting gastric empyting

A

Cholecystokinin

631
Q

What are the major control mechanisms for gastric emptying?

A

Duodenal gastric feedback
hormones such as CCK
neural control

Year 1 Medicine (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions