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Phase 1 Notes > GI > Flashcards

GI Flashcards

1
Q

What are some functions of the stomach?

A

Continue digestion
Kill microbes
Secret proteases and intrinsic factors
Lubrication
Mucosal protection

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2
Q

What 4 key cell types are in the stomach?

A

Mucosal cells
Parietal cells
Chief cells
Enteroendocrine cells

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3
Q

What do parietal cells do?

A

(In fungus and body)
Secretes HCL (gastric acid) and intrinsic factors

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4
Q

How much HCL is produced per day?

A

Approx 2L
H+ > 150mM

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5
Q

Describe gastric acid secretion

A

Carbonic anhydride converts CO2 and H2O into H2CO3.
This splits into HCO3- which leaves to the capillaries and so cl- enter cell.
Splits also into H+ which leaves cell into lumen via ATPase as K+ enters cell.
H+ and Cl- in lumen forms acid

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6
Q

Cephalic vs gastric phase

A

Cephalic - Sight, smell, taste of food
Gastric - Presence of peptides, amino acids and gastric distension

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7
Q

When is gastric secretion turned on?

A
  1. Cephalic (parasympathetic) - Acetylcholine is released and directly acts on parietal cells to release gastric and histamine
  2. Gastric - Gastrin released acts on parietal cells and triggers histamine release which acts on parietal cells
  3. Proteins in lumen acts as a buffer and decreases secretion of somatostatin so increases parietal cell activity
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8
Q

When is gastric secretion turned off?

A
  1. low luminal pH directly inhibits gastric and indirectly inhibits histamine secretion. Also stimulates somatostatin secretion
  2. Intestinal phase (duodenal distension) - Release of secretin and Cholecystokinin(CCK) inhibits gastrin, Ach and promotes somatostatin.
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9
Q

Summary of controlling gastric secretion

A

Controlled by brain, stomach and duodenum
1 neurotransmitter- Ach +
1 hormone - gastrin +
2 paracrine factors - histamine +, somatostatin-
2 enterogastrones - secretion -, CCK -

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10
Q

Why is histamine important?

A

Acts directly but also mediates effect of gastrin and acetylcholine (good therapeutic target)

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11
Q

Define a peptic ulcer

A

A breach in a mucosal surface

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12
Q

Causes of peptic ulcers

A

Infection - Helicobacter pylori
Drugs - NSAIDS
Chemical irritants - alcohol, bile salts
Gastrinoma - tumours produce gastrin unregulated

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13
Q

How does gastric mucosa defend itself?

A

Alkaline mucus
Tight junctions between epithelial cells
Replacement of damaged cells
Feedback loop

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14
Q

How does Helicobacter pylori cause peptic ulcers?

A

Lives in gastric mucus and secretes urease - splits urea into CO2 and ammonia (+ H+ = ammonium). Ammonium secretes proteases and damages gastric epithelium, inflammatory response and reduced mucosal defence.

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15
Q

How does NSAIDS cause peptic ulcers?

A

Non Steroidal Anti Inflammatory Drugs
Inhibits cycle-oxygenase 1 needed for prostaglandin synthesis (stimulates mucus secretion)
= reduced mucosal defense

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16
Q

How does Bile salts cause peptic ulcers?

A

Duodenogastric reflex strips away mucus layer

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17
Q

How to treat Helicobacter pylori?

A
  1. Proton pump inhibitors (omeprazole)
  2. Antibiotics (amoxicillin, clarithromycin)
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18
Q

Give an example of a NSAID

A

Misoprostol

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19
Q

What do chief cells release?

A

Pepsinogen (inactive zymogen)

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20
Q

What do mucus cells secrete?

A

Mucus

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21
Q

What do enteroendcrine cells secrete?

A

Gastrin

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22
Q

How is pepsin activated?

A

Pepsinogen to pepsin is pH dependent <2
Pepsin and HCL also activates the conversion
(Only active at low pH and irreversible inactivation by HCO3-)

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23
Q

Why don’t chief cells produce pepsin directly?

A

Don’t want to digest own cells (auto digest)

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24
Q

What does pepsin do?

A

Accelerates protein digestion and accounts for 20% of total protein digestion.
Breaks collagen down in meat and shreads meat for digestion

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25
Q

Volume of stomach while empty vs eating

A

Empty ~50mL
Eating can accommodate ~1.5L

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26
Q

What is receptive relaxation? (Gastric motility)

A

Parasympathetic acting on enteric nerve plexuses
Nitric oxide and serotonin released mediates relaxation.
Coordination - afferent inputs via vagus nerve

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27
Q

Describe peristalsis

A
  1. Waves in gastric body causes weak contractions (little mixing when empty)
  2. More powerful contractions in antrum towards pylorus (pylorus closes to churn food)
  3. Little chyme enters duodenum but a trial contents forced back to body for mixing
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28
Q

How is peristalsis induced?

A

Pacemaker = interstitial cells of Cajal
In muscularis proprietor is constant at 3/minute

Cells undergo slow depolarisation-Repolarisation cycles and transmit waves through gap junctions to adjacent smooth muscle cells.

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29
Q

How is strength of peristaltic contractions increased?

A

By gastrin and gastric distension

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30
Q

How is strength of peristaltic contractions decreased?

A

Duodenal distension

Increased duodenal luminal fat, osmolality, sympathetic NS action

Decreased duodenal luminal pH, parasympathetic NS action

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31
Q

What does overfilling of duodenum cause?

A

Dumping syndrome:
Vomiting, bloating, cramps, dizziness, fatigue

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32
Q

What is gastroparesis?

A

Delayed gastric emptying

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33
Q

What is gastroparesis caused by?

A

Drugs e.g. H2 receptor antagonists, proton pump inhibitors
Abdominal surgery
Parkinson’s
Multiple sclerosis
Etc

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34
Q

Symptoms of gastroparesis

A

Nausea
Early satiety
Vomiting undigested food
GORD
Anorexia

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35
Q

The liver metabolises what 6 substances?

A

Carbohydrate
Fat
Protein
Hormone
Toxin/Drug
Bilirubin

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36
Q

What are some functions of the liver?

A

Storage
Ketogenesis
gluconeogenesis
Vitamins
Blood clotting factors

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37
Q

Describe iron metabolism

A

Dietary iron + reticuloendothelial macrophages form plasma transferrin.

Transferrin used in muscle, stored in liver and used in bone marrow to form haemoglobin.

Iron loss through dead skin cell, menstruation and other blood loss

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38
Q

Describe the structure of ferritin

A

Central core contains 5000 atoms of iron and covered by a large spherical protein of 24 non covalently linked subunits

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39
Q

Concentration of ferritin is directly proportional to?

A

Total iron stores in body

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40
Q

Causes of excess iron storage:

A

Multiple blood transfusions
Haemolytic anaemia
Iron replacement therapy

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41
Q

Causes of non-iron overload:

A

Liver disease
Malignancies
Tissue destruction

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42
Q

Causes of ferritin deficiency

A

Iron deficiency
Ferritin < 20ug/L indicates depletion
Ferritin < 12ug/L indicates absence

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43
Q

What does RDA and AI stand for (vitamins)

A

Recommend Daily Allowance
Adequate Intake

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44
Q

Which vitamins are water vs fat soluble?

A

Water - B, C
Fat - A, D, E, K

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45
Q

Which require more intake? Water or fat soluble vitamins?

A

Water soluble pass more readily so require more regular intake

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46
Q

Sources of vitamin A

A

Retinols - cereal, egg, dairy, red meat
Carotenoids - carrots, spinach, tomatoes

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47
Q

4 functions of vitamin A

A

Vision
Reproduction
Growth
Stabilisation of cellular membrane

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48
Q

Features of vitamin A deficiency or excess

A

Deficiency - night blindness, xerophthalmia
Excess- anorexia, yellowing of skin, joint pain etc

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49
Q

Sources of vitamin D

A

Sunlight + ingested
To the liver.+ hydroxy group
To the kidney = maintain calcium balance

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50
Q

Functions of vitamin D

A

Resorption and formation of bone
Reduced renal excretion of calcium
Increased intestinal absorption of calcium

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51
Q

Deficiency of vitamin D causes:

A

Demineralisation of bone
= rickets in children
= Osteomalacia in adults

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52
Q

Sources of vitamin E

A

Nuts
Oil
Spinach
Carrots
Avocado

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53
Q

Function of vitamin E

A

Important antioxidant
Stores in labels (available) and fixed pools (only used in emergencies)

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54
Q

Vitamin E deficiency caused by:

A

Fat malabsorption
Premature infants

(Excess is relatively safe)

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55
Q

Sources of vitamin K

A

K1 synthesised by plants (food)
K2 synthesised by human intestinal bacteria
K3 + k4 is synthetic

Vitamin K it taken up by liver and transferred to low density lipoprotein which carry it into plasma

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56
Q

Functions of vitamin K

A

Activation of some blood clotting factors
Liver synthesis of plasma clotting factors 2,7,9,10

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57
Q

Deficiency / Excess vitamin K causes:

A

Deficiency- Haemorrhagic disease
Excess - Oxidative damage, red cell fragility

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58
Q

Source of vitamin C

A

Fresh fruit and vegetables

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59
Q

Functions of vitamin C

A

Antioxidant
Iron absorption
Collagen synthesis

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60
Q

What does deficiency / excess of vitamin c cause?

A

Deficiency - scurvy
Excess - GI side effects

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61
Q

Sources of vitamin B12

A

Meat
Fish
Eggs
Milk

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62
Q

Absorption of vitamin B12

A

Binds to R proteins to protect against stomach acid
Released from R protein by pancreatic polypeptide
Intrinsic factor from stomach needed for absorption
Absorbed in terminal ileum and stored in liver.

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63
Q

Causes of vitamin B12 deficiency

A

Malabsorption
Veganism
Pernicious anaemia (autoimmune destruction of IF producing cells)

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64
Q

What is folate?

A

Coenzyme in methylation, DNA synthesis etc
Found in food fortified with folic acid and high requirements in pregnancy

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65
Q

Causes and symptoms of folate deficiency

A

Causes - Malabsorption, drugs
Symptoms - foetal development abnormalities

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66
Q

How can performance of clotting factors be measured?

A

Prothrombin time (PT) - measure extrinsic pathway and long PT may indicate deficiency’s in synthetic capacity of liver.

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67
Q

Intrinsic vs Extrinsic clotting pathways

A

Intrinsic - Activated by internal trauma
12-11-9-8-10
Extrinsic - Activated by external trauma
Tissue factor-7-10

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68
Q

Describe common clotting pathway

A

10 -> Thrombin -> Fibrinogen (1) -> Fibrin clot(13)

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69
Q

Clotting factors produced in the liver

A

1 (Fibrinogen)
2 (Protothrombin)
4
5
6
7

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70
Q

Where is glucose used/ stored?

A

Liver
Muscle
Brain
RBC
Adipocytes

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71
Q

How is glucose used/ stored in the liver?

A

Stored: glycogen
Used: Krebs= ATP or
-> triglycerides -> very low density lipoprotein (VLDL) attached to protein and soluble in blood

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72
Q

What needs constant glucose supply?

A

Brain (can’t store)
RBC (no mitochondria or Krebs cycle - just glycolysis)

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73
Q

How is glucose stored in muscles?

A

Glycogen

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74
Q

How is glucose stored in adipocytes?

A

Triglycerides

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75
Q

How are triglycerides transported?

A

Triglycerides + protein = chylomicrons
Transported in lymphatics

76
Q

What happens during a short fast?

A

Glycogenolysis in liver for brain and RBC

77
Q

What happens in a long fast?

A

Amino acids, lactate and glycerol in gluconeogenesis

78
Q

What happens to fats during fasting?

A

Lipolysis:
Glycerol = Glucose
Fatty acids = ketones for muscle

79
Q

What happens during prolonged fasting?

A

Decreased gluconeogenesis, or glucose available.
So decreased muscle use of ketones and brain uses ketones instead.

80
Q

Hormones regulating fuel metabolism

A

Growth hormone
Somatostatin
Thyroxine
Adrenaline
Noradrenaline
Cortisol
Insulin
Glucagon

81
Q

Insulin vs Glucagon

A

Insulin (anabolic) - glucose + fat storage, protein synthesis

Glucagon (catabolic) - Gluconeogenesis, Glycogenolysis, ketogenesis

82
Q

Effect of adrenaline on fuel metabolism

A

Flight or fight response:
Gluconeogenesis, Glycogenolysis, lipolysis

83
Q

Effect of cortisol on fuel metabolism

A

Preparation for stress response:
Gluconeogenesis, Glycogen storage, Lipolysis,Protein breakdown

84
Q

Effect of thyroxine on fuel metabolism

A

Glycolysis, glucose uptake, protein synthesis, cholesterol synthesis, sensitivity to adrenaline

85
Q

Effect of growth hormone on fuel metabolism

A

Gluconeogenesis, glycogen synthesis, lipolysis, protein synthesis, decreased glucose use

86
Q

3 factors contributing to obesity

A

Genetics
Environment
Energy dysregulation

87
Q

Leptin vs Ghrelin

A

Leptin - Suppresses appetite
(High levels = resistance in obesity)
Ghrelin - Stimulates appetite
(Increases before meals)

88
Q

Some functions of the liver

A

Detoxification of blood
Immune functions
Bile production
Bilirubin breakdown
Energy storage
Fat metabolism
Synthesis of proteins, enzymes, glycogen and fat

89
Q

How are fatty acids transported?

A

Triglycerides or fatty acids bound to albumin
Within lipoproteins
TGs cannot diffuse through cell membrane but FA are released through lipase, facilitated transported into cells and re-esterified to TG

90
Q

Insulin action on lipids

A

Stimulates lipolysis for breakdown of triglycerides to fatty acids,
Reduces Fatty acid exports from adipocytes
(Insulin resistance augments hepatic steatosis)

91
Q

Describe de novo lipogenesis

A

In the liver, Acetyl-CoA undergoes a series of decarboxylate condensation reactions to form a lipoprotein. Dependent on insulin for activation, Acetyl-CoA carboxylate is rate limiting.

92
Q

Describe a lipoprotein

A

Core triglyceride and cholesterol-esters surrounded by phospholipids, cholesterol and specific proteins.
Protein to lipid ratio varies and defined by density.
Chylomicrons carry lipids from gut to muscle and adipose.

93
Q

Describe the pathway of cholesterol

A

Cholesterol is processed in the liver, excreted only through bile, carries by lipoproteins

94
Q

How are fatty acids exported?

A

Apoprotein B synthesised in rER
Lipid components synthesised in sER
Combined and transported in vehicle to gold where ApoB is glycosylated. Vesicles fuses with membrane and VLDL is released.

95
Q

What is bile?

A

Complex lipid-rich micellar solution containing bile acids a, bile pigments, phospholipids, cholesterol etc.
Isomotic with plasma

96
Q

How much bile secreted per day?

A

500-600mls

97
Q

How much of the bile acids secreted, is recycled?

A

95% from enterohepatic circulation

98
Q

How are bile acids synthesised?

A

In pericentral hepatocytes of the acini, cholesterol
-> choline acid and chenodeoxycholic acid (primary bile acids) are conjugated to secondary bile acids which enhances hydrophilicity and acidity.

99
Q

Describe emulsification

A

Fat is hydrophobic so bile salts surround phospholipids (amphipathic = water and lipid soluble). This increases surface area for lipase to release fatty acids from triglycerides.
These diffuse into cells and reform triglycerides to be transported in lymphatics.

100
Q

Function of bile acids

A

Induce bile formation and flow (osmotic)
Increases HCO3 secretion
Lipid digestion with micelles
Cholesterol catabolism
Anti microbial
Prevents calcium gallstones and oxalate renal stones
Excretion of senobiotica, heavy metals etc

101
Q

Describe bile acid circulation

A

Bile travels to gallbladder where it is concentrated. CCK release from duodenal mucosa relaxes sphincter of Oddi and contracts gallbladder = release concentrated mixed micelles.
Bile acids are actively transported to portal circulation in terminal ileum and renters hepatocyte bilary canaliculi.

102
Q

What inhibits bile production?

A

More bile in ileum produces FGF19 = inhibits

103
Q

How much dietary protein do we need?

A

0.75g/kg/day

104
Q

How much protein is excreted per day?

A

Renal = 70g
Faecal = 10g
Skin/hair/sweat loss = unknown

105
Q

Examples of positive nitrogen balance

A

Pregnancy
Lactation
Bodybuilding

106
Q

Examples of negative nitrogen balance

A

Protein malnutrition
Severe illness
Brain injury
Essential amino acid deficiency

107
Q

Describe proteolysis and absorption

A

Dietary protein is denatured in stomach by HCL and pepsin
In small intestine, exo and endopeptidases catalyse breakdown to ogliopeptidws and amino acids
Enterocyte peptidase release amino acids in the bloodstream

108
Q

What is albumin

A

Carrier protein maintains oncotic pressure

109
Q

Types of amino cid degradation

A

TCA (Krebs) cycle
Transamination

110
Q

Describe transamination

A

Alanine + a-ketoglutarate -> pyruvate + glutamate
Catalysed by alanine aminotransferase

(Amino acid 1 + alphaketoacid 2 -> amino acid 2 + alphaketoacid 1)

-> Carbamy, phosphate -> urea cycle

111
Q

Why do some proteins have longer lifespan than others?

A

Faulty/aging/obsolete proteins
Signal transduction
Flexible system to meet protein requirements

(By proteosome or lysosome)

112
Q

What is ubiquitin?

A

A small protein of a carboxyl group and isopeptide bonds with multiple lysine residues. 3 enzymes:
E1 Ubiquitin-activating enzyme
E2 Ubiquitin-conjugating enzyme
E3 - Ubiquitin-protein ligase

Formation of ubiquitin chains = signals death

113
Q

Describe proteosome structure

A

2 caps on either end regulates proteins
Middle proteosome is ATP dependant hydrolase and binds to ubiquitin

114
Q

What is the N-terminal rule?

A

N-terminal residue determines protein half-life

115
Q

What is the main source and loss of nitrogen?

A

Source = dietary protein
Loss = from gut.and kidneys

116
Q

What are essential amino acids?

A

Amino acids only found in diet and cannot be de novo synthesised

117
Q

Why is there an amino acid pool in the blood?

A

In catabolic state there is a constant protein turnover to maintain a free amino acid pool because protein and amino acids are not stored

118
Q

What are pancreatic functions?

A

Endocrine secretion (to blood)
- Alpha cells secrete glucagon
- Beta cells secrete insulin
Exocrine secretion (To pancreatic duct)
- Aqueous HCO3- secretion
- Enzyme secretion (by acini cells)

119
Q

How much HCO3- is produced in a day?

A

1L

120
Q

How is HCO3- secreted?

A

Centroacinar cells continuously produce HCO3- and H2O by exchanging with Cl-

121
Q

Why is bicarbonate secreted?

A

Protects duodenal mucosa and optimises pH for enzyme digestion by neutralising stomach acid.

122
Q

Name pancreatic proteases

A

Trypsin and chymotrypsin are stored as proenzymes trypsinogen and chymotrypsinogen.

Enterokinase activates trypsinogen
Trypsin activates chymotrypsinogen and additional trypsinogen

123
Q

What enzymes do pancreas secrete?

A

Lipase hydrolyse triglycerides to monoglycerides and free fatty acids. (Bile salts aid)

Amylase hydrolysed starch to maltose

Ribonuclease, deoxyribonuclease, gelatinase, elastase

124
Q

What stimulates pancreatic enzyme secretion?

A

Cephalic stage
- Vagal innervation
- gastrin
Intestinal stage
- Secretin (water + bicarb)
- Cholecystokinin (enzyme + bicarb)
- Gastrin (enzyme)

125
Q

Summary of fluids in and out (9L/ day)

A

In
Ingest = 2L
Saliva = 1.5L
Gastric secretion = 2L
Pancreatic juices = 1.5L
Bile = 0.5L
Intestinal secretions = 1.5L

Out
Small intestine = 7.5L
Colon = 1.5L
Excreted = 200ml

126
Q

Factors influencing absorption/secretion

A

Number and structure of enterocytes
Blood and lymph flows
Nutrient intake
GI motility (hormonal /neural)
Bile
Irritants
Bacterial toxins

(Imbalance leads to disease)

127
Q

How are sugars absorbed?

A

Through Na-dependent secondary active transport carriers on microvilli membrane

128
Q

Name the 3 pairs of salivary glands

A

Parotid
Sublingual
Submandibular

(20% saliva from minor mucous salivary glands in lips, cheeks, tongue, hard and soft palate)

129
Q

What are the functions of saliva?

A

Lubricant for mastication, swallowing and speech
Cleans oral cavity and buffer ~ pH 7.2
Dissolves chemicals necessary for taste
Suppresses bacterial growth
Digests starch by amylase

130
Q

Describe regulation of salivary secretion

A

The cerebral cortex and pressure receptors/chemoreceptors in mouth activate salivary centre in medulla. This increases stimulation of autonomic nerves to salivary glands.

131
Q

How much saliva is secreted per day

A

800-1500ml

132
Q

Which glands secrete serous vs mucus

A

Parotid = serous
Submandibular = Both
Sublingual = mucous

133
Q

Define saliva

A

Secretion of proteins and glycoproteins in a buffered electrolyte solution

134
Q

Describe defence of salivary system

A

Mucosa = physical barrier
Palatine tonsils = lymphocyte subset + dendritic
Saliva = Washes away food
Surrounded by lymphatics and immune cells
High blood flow rate

135
Q

Describe the structure of salivary glands

A

2 distinct epithelial tissue:
Acinar cells
- Serous secretes water + a amylase
- Mucous (looks like a flower) secretes water + glycoprotein
Ducts - forms a large duct entering the mouth

136
Q

Describe acinar cell structure

A

Intralobular ducts
- Secretes NaCl rich isotonic fluids
Main excretory ducts
- Intercalated cells connect acini to straiated
- Striated cells for reabsorption of NaCl and secretion of K+ with microvilli for active transport of HCO3- into ducts and mitochondria for energy

137
Q

Where do the salivary glands open to?

A

Parotid - buccinator
Submandibular- sublingual papillae
Sublingual - drains into submandibular

138
Q

What are functions of the colon?

A

Absorb water and electrolytes through osmosis
Excretion of waste (motility)
Production of vitamins (micro biome)
Bacteria ferment fibre (form fatty acid energy store)

139
Q

Midgut vs Hindgut functions

A

Mid = Absorption of water
Hind = motility

140
Q

Describe layers of the colonic wall (lumen out) and

A

Mucosa
Muscularis mucosal (smooth muscle generates high amplitude contractions = mass movement)
Submucosa
Muscularis propria (Inner circular + outer longitudinal)
Subserosa
Serosa

141
Q

Describe histology of the colon

A

Simple columnar epithelium with microvilli for absorption
Goblet cells secret mucous for lubrication
Taeniae coli - 3 ribbons of longitudinal muscle for localised segmental contractions (=haustra)

142
Q

Describe nerve supply of colon

A

Midgut = Vagus
Hindgut = Pelvic splanchnic

Enteric NS (intrinsic)
= Myenteric plexus
= Submucosa plexus

143
Q

Describe the anal sphincter

A

Temporary reservoir for faecal content

Internal anal sphincter = involuntary smooth
External anal sphincter = voluntary striated

144
Q

Describe the 4 stages of defecation

A
  1. Basal
  2. Pre-expulsion
  3. Expulsion
  4. Termination
145
Q

Describe the basal stage of defecation

A

Colon - segmental contractions (mixing)
Rectum - Motor complexes (to keep empty)
Anal sphincter - (contracted)
Puborectalis - contracted at 90 degrees

146
Q

Describe the pre-expulsion phase of defecation

A

Colon - High amplitude contractions mass movement 8x a day and gastro-colic reflex
Rectum - filling causes distension and compliance
Anal sphincter - Contraction of EAS, relaxation of IAS
Puborectalis - remains contracted

147
Q

Describe the expulsion phase of defecation

A

Rectum contracts
IAS, EAS and Pubic Rectalis relaxes
Valsalva posture increases abdominal pressure and opens anorectal angle to aid emptying

148
Q

Describe the termination phase of defecation

A

Traction loss causes sudden contraction of EAS
Valsalva ceases and change in posture to standing

149
Q

What is the parasympathetic defecation reflex?

A

Receptors from the descending/sigmoid colon afferent to spinal chord.
Efferent to internal anal sphincter
Continuous signals from cerebral cortex keeps external sphincter contracted

150
Q

What happens to amino acids in the liver?

A

Form:
NH4+ (toxic so converted to urea) excreted
a-ketoacids undergo citric acid cycle -> gluconeogenesis or respiration

151
Q

What enzyme is predominantly found in muscle and liver?

A

Alanine aminotransferase

152
Q

Describe the transport of glucose and alanine

A

Blood glucose travels from liver to muscle where glycolysis converts it to pyruvate
Muscle protein forms amino acids -> NH4+ -> glutamate
Pyruvate + glutamate -> alanine transported to liver + a-ketoglutarate by alanine aminotransferase
Alanine transferred to liver where opposite reaction occurs to form pyruvate + glutamate -> NH4+ -> Urea via urea cycle

153
Q

Describe the urea cycle

A

Ornithine + ammonia + CO2
-> citrulline + ammonia
-> arginine
-> Anginase releases urea and ornithine

154
Q

What is albumin?

A

A single polypeptide protein
(9-12g produced by liver each day)

155
Q

What is the transcapillary escape route?

A

Rate of albumin leaving the circulation via interstitium, collected by lymphatics and returned by thoracic duct.

156
Q

What is the starlings equation?

A

NDP = Kf x [(Pc-Pi)-rc(pc-pi)]

157
Q

Why is albumin important?

A

Binding and transport
Maintenance of colloid osmotic pressure
Free radicals
Anticoagulant effects

158
Q

Consequences of decreased albumin

A

Decreased colloid Oncotic pressure
Decreased ligand binding

(Associated with malnutrition, liver/renal disease, sepsis, burns/trauma)

159
Q

Small bowel vs Large bowel

A

Small <3cm, contains plicae cicularis
Large <6cm, contains haustral folds

160
Q

Define contrast

A

A dye that is swallowed or injected and forms a contrast on an x-ray

161
Q

Define ultrasound

A

High frequency sound waves bounce off organs
= Real time + non-ionising
= But superficial structures only + not clear

162
Q

Endoscopy vs Colonoscopy vs Laparoscopy

A

A camera through:
Endo - oesophagus
Colon - Anus
Laparo - Abdomen skin

163
Q

What are xenobiotics?

A

Foreign substances with no nutritional value. They serve no purpose so are excreted but may be toxic by damaging cell protein or DNA.

164
Q

Describe the 2 phases of detoxification (Easier to be excreted via urine)

A
  1. Oxidation - Add or expose functional groups to make drugs more polar =increases hydrophilicity
    (Cytochrome P450 enzymes are important here)
  2. Conjugation - Hydrophilic groups added to increase polaricity and hydrophilicity. Conjugation reactions with endogenous molecules and covalent bonds - glucuronidation is the most common. (Transferase enzymes are responsible here)
165
Q

Reactions that also take place in the liver

A

Inactivation and elimination of xenobiotics
Formation of active metabolites
Activation of prodrugs
Toxification of less toxic xenobiotics

Most occur in Endoplasmic reticulum

166
Q

Describe general cytochromes

A

Found in kidney, lungs, liver and intestinal mucosa
10 main groups of cytochrome P450 enzymes encoded for by 55 genes.
All present in sER called microsomal enzymes.

= oxidise substrate and reduce oxygen
= generate free radical compounds
= at least 1 haem group involved in electron transfer
= cytochrome reductase uses NADPH

167
Q

What accounts for 1/3 of all cytochrome enzymes?

A

Cytochrome 3A4 is involved in metabolism of 50% of all clinically prescribed drugs

168
Q

Describe Cytochrome P450 mechanism

A

Bound to phospholipid membrane in smooth ER and attached to cytochrome P450 reductase.
Reaction starts when reductase transfers hydrogen from NADPH to cytochrome P450.
On of the 02 atoms is reduced by H+ to form water,
the other O2 is retained in a highly reactive form to force reactions on a substrate

169
Q

Drug interactions with cytochrome P450 reactions

A

Drugs can compete for binding sites and those with highest affinity are metabolised first
Can by induced and inhibited by different drugs and food

170
Q

Describe non-microsomal enzymes

A

In cytoplasm and mitochondria of hepatocytes and other tissue, non-specific enzymes catalyse few oxidative, reductive, conjugative + hydrolytic reactions.
Not inducible but may have polymorphism

171
Q

Describe metabolism of ethanol

A

Doesn’t fit phase 1 + 2 or need to be conjugated
Only 2-10% excreted as liver uses most for dietary fuel
Can be metabolised by alcohol dehydrogenase to form acetaldehyde then acetate producing NADH by ALDH or through MEOS
Alcohol can induce cytochrome P450 so is metabolised quicker in chronic drinkers

172
Q

Embryology: Describe gut tube differentiation

A

Lateral folding brings the ventral body wall together and concentration gradient of retinoids acid starts to specify lowest levels cranially and highest levels distally.
Differential expression of transcription factors and genes along the tube specify how regions will develop.

173
Q

Name structures of the foregut and it’s derivatives

A

Foregut : oesophagus, stomach, first half of duodenum
Derivatives: liver, pancreas
(Spleen is not a derivative = from mesoderm)

174
Q

What are the 2 mesenteries of the foregut?

A

Dorsal mesentery = spleen develops from

Ventral mesentery = arises from septum transversum and liver grows into it, splitting it into:
- Lesser omentum
- Falciform ligamentum

Pancreas develops from 1 ventral and 1 dorsal bud which fuse

175
Q

Embryology: Describe the formation of the oesophagus

A

Upper 2/3: striated muscle innervated by vagus
Lower 1/3: smooth muscle innervated by splanchnic

Lung bud appears at ventral wall of the foregut week 4 and seperates

176
Q

Embryology: Development of the stomach

A

Gut tube start to dilate at week 4 and rotates 90 degrees clockwise around its long axis = left lies anteriorly and right posteriorly
This also brings duodenum to the right

177
Q

Embryology: development of the liver

A

Liver bud is an outgrowth from the distal foregut around week 3.
Cells proliferate - grow into the septum transversum
Connection between liver bud and foregut narrows = bile duct

178
Q

Embryology: development of the pancreas

A

Dorsal and ventral buds arise from the duodenum
Rotation of the stomach swings the ventral bud posteriorly and buds fuse

179
Q

What is the space behind the stomach called?

A

Lesser sac

180
Q

Name the stages of midgut development

A
  1. Elongation (growth of primary intestinal loop with maintained connection to yolk sac)
  2. Physiological herniation (protrusion into umbilical cord - week 6)
  3. Rotation (90 degrees anti-clockwise around axis of SMA brings caudal limb cranially)
    (Continued elongation and small intestine coils)
  4. Retraction (into abdomen - week 10 and gut loops further 180 degrees anti-clockwise)
  5. Fixation (some mesentery fuse with posterior abdominal wall = retroperitoneal, Toldt fascia forms)
181
Q

What do the Cephalic and caudal limbs of the primary intestinal loop form?

A

Cephalic - Distal duodenum, jejunum, part of ileum
Caudal - Distal ileum, Caecum, Appendix, Ascending colon, Proximal 2/3 transverse colon

182
Q

Embryology: Describe retraction of the gut

A

Jejunum first -> to left
Then ileum -> to right
Last caecum -> to RUQ then descends to right iliac fossa

183
Q

Where does Toldt fascia form?

A

Between parietal and visceral peritoneum

184
Q

When does the appendix form?

A

During the descent of the caecum

185
Q

Where is pain felt during appendicitis?

A

Pain initially felt around umbilicus
= Visceral sensory and lesser splanchnic both return to T10 so brain gets confused (poorly localised)
Pain localises around right iliac fossa
= Parietal peritoneum innervated by somatic nerves is irritated

186
Q

Embryology: Describe development of the Hindgut

A

Last part of Hindgut communicates with cloaca = forms anorectal canal
Boundary between endoderm and surface ectoderm is cloacal membrane.
Urorectal septum grows towards cloacal membrane and seperates allantois (urethra) from the cloaca

187
Q

Embryology: Describe formation of the anorectal canal

A

Ectoderm of cloacal membrane invaginates and forms lower part of anal canal.
Cloacal membrane ruptures so upper and lower parts of anal canal become continuous

Upper + lower parts of anal canal have different blood supply and epithelia (endo/ecto)

Phase 1 Notes (9 decks)

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