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Medicine > GI > Flashcards

GI Flashcards

1
Q

7 functions the liver performs

A

Carbohydrate, fat, protein, hormone and toxin/drug metabolism
Storage
Bilirubin metaoblism and excretion

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2
Q

2 storage spaces of iron in the body?

A

Liver
Reticuloendothelial macrophages

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3
Q

What protein is iron carried by in the plasma?

A

Transferrin

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4
Q

Where is dietary iron absorbed in the GI tract?

A

Duodenum

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5
Q

Where is iron sent to from plasma? What is its role?

A

Muscle cells (plays role in muscle contraction?)
Bone marrow (to form haemoglobin in erythrocytes)

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6
Q

Iron loss from…

A

Menstruation
Other blood loss
Desquamation

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7
Q

Ferritin structure and location

A

Subunits form a shell around a central core which contains up to 5000 iron atoms
Found in cytoplasm of cells and also in serum

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8
Q

Ferritin excess means…
Ferritin deficient means…

A

Could have an excess iron storage disorder
Iron deficiency

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9
Q

Vitamins can act as…(3)

A

Gene activators
Coenzymes/cofactors in metabolism
Free-radical scavengers (protects cell from damage caused by free-radicals)

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10
Q

2 water soluble vitamins

A

B and C

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11
Q

4 fat soluble vitamins

A

A, D, E, K

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12
Q

Why do you require more regular intake of water soluble than fat soluble vitamins?

A

Water soluble pass through the body much more readily so you can become deficient in them quicker.

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13
Q

Sources of carotenoids and how they produce vitamin A

A

Carrots, tomatoes, spinach
Oxidation of carotenoids then produces retinol (vitamin A)

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14
Q

Sources of retinol (vitamin A)

A

cheese, eggs, oily fish

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15
Q

3 functions of vitamin A

A

Vision (used to form rhodopsin)
Reproduction (spermatogenesis)
Growth

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16
Q

Vitamin A deficiency cause and features

A

Due to fat malabsorption
Blindness/Xerophthalmia

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17
Q

Chronic Vit A Excess Symptoms

A

Joint pain, anorexia, hairloss

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18
Q

Acute Vit A Excess Symptoms

A

Abdominal pain, severe headaches

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19
Q

Carotenemia

A

Reversible yellow pigmentation of skin from risen beta-carotene levels in blood

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20
Q

How does sunlight exposure lead to vitamin D production

A

Sunlight stimulates conversion of 7-dehydrocholesterol -> Vitamin D3 which is sent to the liver

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21
Q

Vitamin D dietary sources

A

D3 - Fish and meat
D2 - Supplements

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22
Q

Why is vitamin D3 transported liver->kidneys?

A

To be converted to the active form of vitamin D3 that can be used by the body

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23
Q

3 functions of vitamin D

A

Increased intestinal absorption of calcium
Resorption/formation of bone
Reduces renal calcium excretion

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24
Q

Deficiency of vitamin D causes…

A

Demineralisation of bone:
Rickets in children, osteomalacia in adults

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25
Q

What carries vitamin K from liver to plasma?

A

Low density lipoproteins

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26
Q

Sources of vitamin K

A

Synthesised by plants (K1)
Synthesised by humans in intestinal bacteria (K2)
Synthetic vitamin K (K3, K4)

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27
Q

Vitamin K functions

A

Activation of some clotting factors
Necessary for specific liver synthesis of plasma clotting factors

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28
Q

Vitamin K deficiency causes…

A

Haemorrhagic disease of newborn (bleeding from low clotting factors from low vitamin K levels)

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29
Q

Excess vitamin K causes…

A

Red cell fragility (only in synthetic forms)

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30
Q

Vitamin C source and functions
How much do adults need a day?

A

Fruit and veg
Collagen synthesis
Antioxidant
Iron absorption
40mg/day

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31
Q

Vitamin E storage, function, and amount needed

A

Labile and fixed pools in non-adipose cells
Fixed pool in adipose cells
Important antioxidant (protects body against free radicals)
4mg/day in women
3mg/day in men

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32
Q

Vitamin E deficiency caused by…

A

Fat malabsorption

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33
Q

Result of vitamin C deficiency/excess

A

Deficiency - Scurvy (easy bruising, gum disease, hair loss)
Excess - >1g/day = GI side effects

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34
Q

How is vitamin B12 protected from stomach acid?

A

Binds to R protein (released from R protein by pancreatic polypeptide0

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35
Q

How is vitamin B12 absorbed?

A

Binds to intrinsic factor forming IF-B12 which is absorbed in the terminal ileum and stored in the liver

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36
Q

Vitamin B12 deficiency causes and symptoms

A

Pernicious anaemia (autoimmune destruction of IF producing cells in stomach), malabsorption, veganism
Causes peripheral neuropathy

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36
Q

Vitamin B12 deficiency causes and symptoms

A

Pernicious anaemia (autoimmune destruction of IF producing cells in stomach), malabsorption, veganism
Causes peripheral neuropathy

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37
Q

When do individuals have higher folate requirements?

A

Pregnancy

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38
Q

What are folate functions?

A

Acts as a coenzyme in methylation reactions and DNA synthesis

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39
Q

Folate deficiency causes and symptoms

A

Malabsorption, anticonvulsants (interfere with folic acid metabolism)
Can cause macrocytic anaemia and foetal development abnormalities (neural tube defects)

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40
Q

What activates the extrinsic pathway of the coagulation cascade?

A

Contact between FVII and tissue factor

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41
Q

Clotting factors produced in the liver

A

I (Fibrinogen)
II (Prothrombin)
IV
V
VI
VII

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42
Q

Performance of clotting pathways measured by…

A

Prothrombin time (PT) (extrinsic pathway)
Activated partial thromboplastin time (aPTT) (intrinsic pathway)
(prolonged prothrombin time doesn’t confirm you have liver disease but shows how well your liver can synthesise things)

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43
Q

3 colon functions

A

Absorption of water and electrolytes
Excretion of waste
Producing vitamins

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44
Q

Muscle layers in colon

A

Continuous circular muscle
3 ribbons longitudinal muscle (taeniae coli)

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45
Q

Cells in colon mucosa

A

Simple columnar epithelium (lots of microvilli)
Goblet cells

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46
Q

4 phases of defecation

A

1) Basal
2) Pre-expulsive
3) Expulsive
4) Termination

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47
Q

What occurs in the basal phase of defecation?

A

Segmental mixing in colon
Tonic contraction of anal sphincter
Contraction of puborectalis (maintaining 90degree anorectal angle)

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48
Q

What occurs in the pre-expulsive phase of defecation?

A

High amplitude contractions of colon (gastro-colic reflex)
Rectum fills causing distension
EAS maintains contraction, IAS reflex relaxation
Puborectalis remains contracted

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49
Q

What occurs in the expulsive phase of defecation?

A

Rectum contracts
IAS, EAS, PR relax along with valsalva manoeuvre / posture aids emptying

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50
Q

What occurs in termination phase of defecation?

A

Traction loss due to sudden EAS contraction (closing reflex)

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51
Q

Nerve supply to colon

A

Intrinsic - ENS (Myenteric Plexus, Submucosal Plexus)
Extrinsic - Parasympathetic and Sympathetic

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52
Q

Hard stools caused by…
causing constipation

A

Opioids, low fluid intake, low fibre

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53
Q

How are proteases secreted in stomach?

A

Chief cells produce pepsinogen
Activated in lumen by pepsin and HCl

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54
Q

Where does inactivation of pepsin occur?

A

In small intestine by bicarbonate secretion increasing pH (irreversible inactivation)

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55
Q

Zymogen

A

Inactive protein precursor of an enzyme (pepsinogen)

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56
Q

How is pepsinogen production mediated?

A

Input from ENS (ACh)

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57
Q

Role of pepsin

A

Breaks down collagen in meat into smaller pieces with greater surface area for digestion

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58
Q

Receptive relaxation of body and fundus mediated by…

A

Parasympathetic nervous system acting on enteric nerve plexuses (nitric oxide and serotonin released by enteric nerves mediates relaxation

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59
Q

Any ammonia which evades detoxification as urea can be…

A

Ammonia + Glutamate -> Glutamine (Glutamine Synthetase)

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60
Q

In the glucose alanine cycle, at the muscle, ALT…

A

transaminates the amino group from glutamate forming a-Ketoglutarate. The amino group gets attached to pyruvate making alanine (the opposite occurs at the liver)

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61
Q

Stomach Functions (9)

A

Store/mix food
Dissolve, continue digestion
Regulate emptying into duodenum (due to its larger volume)
Kill microbes
Secrete proteases
Secrete IF (helps in absorption of vit B12 in terminal ileum)
Activate proteases
Lubrication
Mucosal digestion

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62
Q

4 key stomach cell types

A

Mucous cells
Parietal cells (secrete HCl and IF)
Chief cells (secrete pepsinogen)
Enteroendocrine cells (secrete gastrin)

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63
Q

Neural input to stomach supplied primarily by

A

Vagus nerve

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64
Q

How much gastric acid secreted per day in stomach?

A

Approx 2 litres

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65
Q

Arterial supply of foregut, midgut and hindgut

A

Foregut - coeliac trunk
Midgut - SMA
Hindgut - IMA

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66
Q

Symp/Parasymp innervation from ANS of foregut

A

S: Greater splanchnic nerve (T5/6-T9)
P: Vagus

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67
Q

Symp/Parasymp innervation from ANS of midgut

A

S: Lesser splanchnic nerve (T10-11)
P: Vagus

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68
Q

Symp/Parasymp innervation form ANS of hindgut

A

S: Least splanchnic nerve (T12 +/- L1)
P: Pelvic splanchnics

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69
Q

Where is visceral pain felt in foregut?

A

Epigastric region

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70
Q

Where is visceral pain felt in midgut?

A

Umbilical region

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71
Q

Where is visceral pain felt in hindgut?

A

Suprapubic region

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72
Q

Start and end of foregut

A

Start - Distal oesophagus
End - Halfway along duodenum (1st and 2nd parts of duodenum are foregut)

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73
Q

Start and end of midgut

A

Start - Halfway along duodenum (3rd and 4th parts)
End - First 2/3 of transverse colon

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74
Q

Start and end of hindgut

A

Start - Distal 1/3 transverse colon
End - Upper anal canal

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75
Q

Chemical vs Electrical Synapse

A

Chemical - Neurotransmitters (majority)
Electrical - direct flow of ions (less abundant)

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76
Q

Explain chemical synaptic transmission

A

-Axon potential depolarises synaptic terminal membrane
-Opening of voltage-gated Ca channels = Ca influx
-Ca influx triggers neurotransmitter release

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77
Q

Electrical synapse structure

A

Gap junctions
Channel formed by pores in each membrane
Connexon made up of 6 connexins in a ring which form the pore allowing flow of ions

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78
Q

Dendritic spines

A

Tiny protrusions from dendrites which form functional contact with other axons
ER found within them (to make proteins)

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79
Q

Arborisation of neurons

A

Neurons search for appropriate targets by expanding and/or retracting their axons

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80
Q

Oligodendrocytes

A

Myelinating cells of CNS

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81
Q

Myelin sheath formation

A

Wrapping of axons by oligodendrocyte processes (membranes)
Highly compacted - 70% lipid, 30% protein

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82
Q

Microglia

A

Resident immune cells of CNS
Originate from haematopoietic progenitors which migrate to CNS
Resting- Highly ramified, motile processes
Activated - retract processes, motile
Proliferate at sites of injury (phagocytic)

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83
Q

Functions of microglia

A

Immune surveillance
Phagocytosis (debris)
Synaptic plasticity - pruning of spines

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84
Q

Bad microglia

A

Proinflammatory cytokines which cause microgla to increase inflammation in neuro-degenerative diseases

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85
Q

Astrocytes

A

Star-like cells
Most numerous glial cells in CNS

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86
Q

Astrocytes functions

A

-Structural - define brain micro-architecture
-Envelope synapses
-Metabolic support
-Neurovascular coupling - changes in cerebral
blood flow in response to neural activity
-Proliferation in disease (gliosis or astrocytosis)

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87
Q

Define MND

A

Adult onset neurodegenerative disease characterised by loss of upper (motor cortex) and lower (spinal cord) motor neurones

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88
Q

Define MS

A

Autoimmune demyelinating disease where immune cells attack myelin sheath

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89
Q

Tracts of axons that cross midline are called…

A

commissures

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90
Q

Cell bodies located…

A

In ganglia (dorsal root ganglia)

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91
Q

Blood-brain barrier

A

Dyes injected into blood penetrate most tissues, but not the brain (good for disease prevention in brain but problematic for drug delivery)

Formed by endothelial cell tight junctions (few fenestrations), astrocyte end feet and pericytes

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92
Q

Circumventricular organs

A

Permit hormones to leave brain without interrupting BBB
(e.g - pineal body which secretes melatonin into blood or posterior pituitary which secretes hormones into blood)

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93
Q

4 key cell types in gastric epithelium

A

Chief Cells - produce proteases
Mucous Cells - secrete mucous
Parietal Cells - secrete HCl and intrinsic factor
Enteroendocrine Cells - secrete hormones

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94
Q

Gastric Acid Secretion

A

HCl
Approx 2L per day
Neurohumoral regulation (by vagus nerve and variety of hormones)

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95
Q

Pump in gastric parietal cells to decrease lumen pH

A

Pumps H+ into gastric lumen
Pumps K+ into gastric cell
(K+/H+ ATPase pump)

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96
Q

Which 2 ions passively flow out of parietal cell into gastric lumen?

A

K+ and Cl-

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97
Q

Where do H+ ions come from in parietal cells?

A

Cellular respiration
H2O -> OH- + H+

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98
Q

Swapping ions between blood and parietal cells

A

HCO3- enters blood
Cl- enters parietal cell

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99
Q

How are bicarbonate ions produced in parietal cells?

A

CO2 + H2O (catalysed by carbonic anhydrase) -> H2CO3 -> H+ + HCO3-

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100
Q

Turning on gastric acid release (cephalic phase)

A

Parasympathetic nervous system
Sight, smell, taste, chewing stimulates brain to stimulate stomach via vagus nerve
Done through ACh release: acts directly on parietal cells, but also triggers release of gastrin and histamine (which turn on parietal cells)

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101
Q

Turning on gastric acid release (gastric phase)

A

Gastric distension, presence of peptides / amino acids = gastrin release (acts directly on parietal cells)
Gastrin triggers histamine release (acts directly on parietal cells)

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102
Q

Why do proteins in stomach stimulate gastrin release?

A

Proteins act as buffer mopping up H+ ions (=pH rise) and therefore decreased production of somatostatin

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103
Q

Role of somatostatin

A

Inhibit gastric acid release

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104
Q

Turning off gastric acid release (gastric phase)

A

Low luminal pH = inhibited gastrin secretion indirectly inhibiting histamine release
Stimulates somatostatin release

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105
Q

Turning off gastric acid release (intestinal phase)

A

In duodenum: low pH, hypertonic luminal contents, duodenal distension, presence of fatty acids and amino acids

Triggers release of enterogastrones: secretin and cholecystokinin (CCK)

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106
Q

Role of secretin and cholecystokinin (CCK)

A

Inhibit gastrin release, promote somatostatin release

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107
Q

Gastrin, ACh and histamine binding to receptors on parietal cell membranes results in…

A

Upregulation of H+/K+ ATPase pumps

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108
Q

Somatostatin binding to receptors on parietal cell membranes results in…

A

Dwonregulation of H+/K+ ATPase pumps

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109
Q

Autocrine factors

A

Cells releasing a substance that acts on themselves

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110
Q

Paracrine factors

A

Cells releasing a substance that acts on neighbouring cells (histamine and somatostatin)

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111
Q

Hormone

A

Acts on cells at distant sites

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112
Q

Define ulcer

A

Breach in mucosal surface

113
Q

4 peptic ulcer causes

A

Heliobacter pylori infection
Drugs (NSAIDS)
Chemical irritants (alcohol, bile salts)
Gastrinoma

114
Q

4 ways gastric mucosa protects itself from ulcers

A

Alkaline mucus
Tight junctions between cells
Replaces damaged cells
Feedback loops

115
Q

Heliobacter pylori causing peptic ulcers

A

Lives in gastric mucus
Secretes urease splitting urea into CO2 and ammonia
Ammonia + H+ -> Ammonium (toxic to gastric epithelium) = inflammatory response and reduced mucosal defence

116
Q

NSAIDS causing peptic ulcers

A

Lessen inflammatory responses by inhibiting cyclo-oxygenase 1 (needed for prostaglandin synthesis and prostaglandins needed for inflammatory response)
Reduce mucosal defence

117
Q

Bile salts causing peptic ulcers

A

Duodeno-gastric reflex
Regurgitated bile strips away mucus layer
Reduced mucosal defence

118
Q

Proton pump inhibitors which prevent over-secretion of gastric acid

A

Omeprazole, Lansoprazole, Esomeprazole

119
Q

Role of ranitidine

A

Prevents histamine from stimulating parietal cell

120
Q

Mucus secreting cells stimulated by…

A

Prostaglandins

121
Q

Chief cells in gastric mucosa produce…

A

Pepsinogen (which is a zymogen)
Pepsinogen mediated by input from ENS (ACh secretion like HCl secretion from parietal cells)

122
Q

Pepsinogen activation

A

In the gastric lumen, pepsinogen and HCl are present (from chief and parietal cells).
HCl cleaves pepsinogen into pepsin
Pepsin can also digest pepsinogen into pepsin (+ve feedback)
Protein -> Peptides

123
Q

Pepsinogen -> Pepsin most efficient at a pH of…

A

pH less than 2

124
Q

How does the duodenum turn off pepsin production?

A

HCO3- secreted from Brunner’s Glands to increase pH

125
Q

Role of pepsin in protein digestion

A

Not essential but accounts for ~20% total protein digestion
Breaks down collagen in meat

126
Q

Stomach volume variability

A

Empty - 50mL
When eating, up to 1.5L with little increase in luminal pressure

127
Q

Receptive relaxation

A

Relaxation of smooth muscle in body and fundus of stomach to accommodate food
Mediated by Vagus (parasympathetic)

128
Q

Peristalsis in the stomach

A

Waves of contraction begin in gastric body More powerful contraction in antrum Pylorus closes as contraction reaches it to churn/mix food in stomach

129
Q

What are the pacemaker cells of the GI tract?

A

Interstitial cells of Cajal which depolarise and repolarise (stronger contraction when stomach is fuller)
About 3 contractions per minute

130
Q

What hormone stimulates increased strength of peristalsis?

A

Gastrin (due to gastric distension)

131
Q

Strength of peristaltic contractions decreased by…

A

-Increased duodenal fat

-Increased duodenal osmolarity

-Decreased duodenal pH

-Increased sympathetic NS action

-Decreased parasympathetic NS action

132
Q

Overactive stomach results in…

A

Dumping syndrome of chyme into duodenum

133
Q

4 saliva functions

A

-Lubricant for mastication, swallowing and speech

-Oral hygiene (wash, immunity, buffer)

-Digestion

-Remineralisation (Ca(2+) and PO4(3-))

134
Q

Saliva flow rate

A

0.3-7ml per minute

135
Q

Daily saliva secretion in adults from major and minor glands

A

800-1500ml

136
Q

Saliva pH range

A

6.2-7.4

137
Q

2 salivary secretions are…

A

Serous secretion - a amylase (starch digestion)
Mucus secretion - (mucins for lubrication of mucosal surface)

138
Q

Which gland produces the serous saliva secretion?

A

Parotid gland

139
Q

Which glands produce both the serous and mucous secretions?

A

Submandibular and sublingual

140
Q

Minor glands mainly produce what to contribute to saliva?

A

mucus

141
Q

Factors affecting composition and amount of saliva produced

A

Flow rate
Circadian rhythm
Type/size of gland
Duration/type of stimulus
Diet
Drugs
Age
Gender

142
Q

What is saliva?

A

Secretion of proteins and glycoproteins in a buffered electrolyte solution

143
Q

3 defences of oral cavity

A

Mucosa - physical barrier
Palatine tonsils - provide immune cells
Salivary glands - wash away food/bacteria/viruses

144
Q

Activity of glands in oral cavity

A

Submandibular, sublingual and minor glands continuously active

Parotid - usually fairly inactive but stimulated by thought of food or chewing

145
Q

What is whole saliva?

A

salivary gland secretions, blood, oral tissue, microorganisms, food remnants
(can be used for disease diagnosis)

146
Q

2 distinct types of epithelial tissue in salivary glands

A

Acinar cells (make saliva)
Ducts (carry saliva out of glands into mouth)

147
Q

2 types of acini

A

Serous acini (water and a amylase)
Mucous acini (water and glycoproteins)

Differences in their appearance

148
Q

Role of myoepithelial cells in a gland

A

Squeezes the gland pushing saliva out

149
Q

How do cells lining a duct (from a gland) change as they go down the duct?

A

Change from intercalated to striated duct cells
Striated duct cells allow exchange of ions (like Na+/Cl-/HCO3-) to produce the final saliva product

150
Q

Reason for striations in duct lining cells coming from glands

A

Striations increase SA to house more mitochondria so more active transport of bicarbonate can occur)

151
Q

Three pairs of major salivary glands contribute what % of total saliva?

A

Parotid
Submandibular
Sublingual
80%

152
Q

Minor salivary glands contribute what % of total saliva?
What type of acini do they have?

A

20% (situated all of submucosa of oral mucosa)

All mucous glands except for the serous glands of von Ebner

153
Q

What acini are found in the parotid gland?

A

Serous acini

154
Q

What acini are found in the submandibular gland?

A

Mix of serous and mucous acini (referred to as seromucous)

155
Q

What acini are found in the sublingual gland?

A

Mix of serous and mucous acini (but more mucous acini)

156
Q

Stenson’s duct

A

Major duct that connects parotid gland to oral cavity

157
Q

Which nerve runs very close to parotid gland?

A

Facial Nerve

158
Q

Where do submandibular glands lie?

A

Under tongue

159
Q

2 lobes of submandibular glands?
What separates them?

A

Larger superficial lobe
Smaller deep lobe in floor of mouth
Separated by mylohyoid muscle

160
Q

Wharton’s duct

A

Major submandibular duct begins in superior lobe wrapping around posterior border of mylohyoid

Runs along floor of mouth emptying into oral cavity at sublingual papillae

161
Q

Location of sublingual glands

A

Between mylohyoid muscle and oral mucosa of floor of mouth

162
Q

If salivary output falls below 50% of normal flow…

A

Patient experiences xerostomia (dry mouth)

163
Q

Glucose pathway from consumption

A

Absorbed in intestine taken to liver in bloodstream
Distributed to muscle, brain, RBC, adipocytes (storage)

164
Q

Conversion of glucose to glycogen storage in the liver is stimulated by…

A

Insulin

165
Q

What happens to excess glucose in the liver?

A

Converted into Acetyl Co-A and either fed into Kreb’s or makes triglycerides -> very low density lipoproteins

166
Q

2 stores of glycogen

A

Liver and skeletal muscle cells

167
Q

What happens to glucose sent to brain?

A

Converted to Acetyl CoA which enters Kreb’s and forms ATP

168
Q

What happens to glucose sent to RBCs?

A

Converted to pyruvate (then lactate)

169
Q

What happens to glucose sent to adipocytes?

A

Converted to triglycerides (stimulated by insulin)

170
Q

Triglycerides are insoluble in water so are carried around the body bound to a protein forming a…

A

Chylomicron or a VLDL

171
Q

What do chylomicrons travel in back to blood system?

A

Lymphatic system

172
Q

What promotes glycogen in liver to be broken down into glucose?

A

Glucagon (by glycogenolysis)

173
Q

Where does energy come from when glycogen stores are used up?

A

-RBCs release lactate to be used as energy
-Amino acids released from muscle breakdown
-Triglycerides in adipocytes broken down into glycerol
(All sent to liver for gluconeogenesis)

174
Q

During fasting, triglycerides in adipocytes are broken down into…

A

Glycerol (converted to glucose in liver) and fatty acids (used instead of glucose or converted to ketones in the liver)
This process is lipolysis

175
Q

Which hormone stimulates breakdown of triglycerides? in lipolysis?

A

Glucagon

176
Q

After prolonged fasting, gluconeogenesis decreases leading to an increase in…

A

Ketoneogenesis - ketones are used by the brain for energy instead of glucose so therefore there is enough glucose available to be used by RBCs

177
Q

3 hormones released from the adrenal gland?

A

Adrenaline
Noradrenaline
Cortisol

178
Q

2 hormones released form the pancreas?

A

Insulin
Glucagon

179
Q

Hormone released from thyroid gland? What is the hormone’s role?

A

Thyroxine - speeds up metabolism

180
Q

2 hormones released from pituitary gland?

A

Growth hormone
Somatostatin

181
Q

Insulin vs Glucagon?

A

Insulin promotes glycogen and fat storage and protein synthesis (anabolic)

Glucagon promotes glycogenolysis, gluconeogenesis, ketogenesis (catabolic)

182
Q

3 things that use up energy?

A

Activity
BMR
DIT

183
Q

Leptin action in controlling appetite

A

Normal weight - suppresses appetite
In obesity - High leptin levels = leptin resistance = appetite not suppressed

184
Q

Ghrelin role in controlling appetite

A

“Hunger Hormone”
Increases before meals
Stimulates appetite

185
Q

Xenobiotics

A

Foreign substances of no nutritional value (can be harmful if not excreted)
Come form food/drink/breathing

186
Q

Group of enzymes called ….. play major role in process of detoxification

A

Cytochrome P450 enzymes (specifically in phase 1)

187
Q

Xenobiotic biotransformation reaction split into 2 phases…

A

Phase 1 (non-synthetic) - Addition/exposure of small functional groups (amine, hydroxyl etc.) (small increase in hydrophilicity)

Phase 2 (biosynthetic) - Addition of endogenous molecules (large increase in hydrophilicity)

188
Q

Purpose of xenobiotic biotransformation

A

Make compounds less toxic and water soluble so can be excreted

189
Q

Where does detoxification occur?

A

Mostly in liver but also in lungs and small intestine

190
Q

Common features of cytochrome P450 enzymes

A

Present in SER
Oxidise the substrate and reduce oxygen
They’re inducible enzymes
They generate a free radical compound

191
Q

2 exocrine secretions of pancreas

A

Aq bicarbonate
Enzyme

192
Q

2 transport routes of epithelial cells in GI tract

A

Paracellular pathway
Transcellular pathway

193
Q

Pancreas endocrine function

A

Secretes insulin and glucagon from islets of Langerhans

194
Q

Pancreas exocrine function

A

Secretion of pancreatic juice

195
Q

Ethanol metabolism

A

Only 2-10% excreted as it’s used as a fuel

Used to produce NADH (using alcohol dehydrogenase (ADH))

196
Q

Cycle of principal blood flow through liver

A

Heart -> Abdominal Aorta -> Proper Hepatic Artery -> Liver -> Hepatic Veins -> IVC -> Heart

197
Q

Liver microanatomy

A

Organised in lobules with a central (hepatic vein) surrounded by a hexagon of 6 portal triads

198
Q

What constitutes a portal triad

A

Portal Vein
Hepatic Artery
Bile Ducts

199
Q

8 Liver Roles

A

Detoxification - cleans bloods of waste products

Immune Function

Synthesis - clotting factors, glycogen, enzymes

Bile Production

Bilirubin breakdown

Energy storage (glycogen, fats)

Regulating fat metabolism

Ability to regenerate

200
Q

Liver is regulated by 2 things…

A

Endocrine glands (pancreas, adrenal, thyroid)

Nerves

201
Q

Define lipid

A

Esters of fatty acids and glycerol or other compounds (cholesterol)

202
Q

What is the storage form of fat in our body?

A

Triglycerides in adipocytes, hepatocytes, etc.

203
Q

Saturated fatty acids are…
Unsaturated fatty acids are…

A

Solid

Liquid

204
Q

Liver vascular supply

A

Afferent:
75% portal vein
25% hepatic artery

Efferent:
Hepatic veins

205
Q

3 Lipid functions

A

Energy Reserve
Structural (part of cell membranes)
Hormone metabolism

206
Q

Lipids yield how much energy per gram?

A

9-10 kcal

207
Q

How are lipids often transported in blood?

A

As triglycerides

As fatty acids bound to albumin

208
Q

How do lipids enter a cell?

A

TGs can’t diffuse through membrane so FAs are released by lipases to facilitate transport (via several transporter systems like FA binding protein) into cells

In cell, FAs are re-esterified into TGs

209
Q

Breakdown of triglycerides at adipocytes catalysed by…

A

Hormone Sensitive Lipase

210
Q

Breakdown of triglycerides in blood catalysed by…

A

Lipoprotein Lipase

211
Q

Breakdown of triglycerides in hepatocytes catalysed by…

A

Hepatic Lipase

212
Q

Insulin action in fat metabolism

A

Fat storage in adipocytes

Stimulates LPL to breakdown TGs releasing FFAs which can be stored in the form TG in the adipocyte

Reduces activity of HSL reducing FA export from adipocytes

213
Q

Insulin resistance in fat metabolism

A

Increased lipolysis in adipocytes = increased TG in circulation

Increased offer of FA to hepatocytes = greater uptake = increased glucose level and less demand of lipids to be used

214
Q

What constitutes a lipoprotein?

A

A core containing TGs and cholesterol-esters and a surface monolayer of phospholipids, cholesterol and specific protein

215
Q

How are lipoproteins defined?

A

By their density (LDL, HDL, chylomicron)

216
Q

Chylomicrons role

A

Carry lipids from gut to muscle and adipose tissue

217
Q

Chylomicrons fate

A

The remnants taken up by receptor mediated endocytosis

218
Q

How is cholesterol esterified intracellularly?

A

acyl-CoA:cholesterol acyltransferase

219
Q

How is cholesterol esterified in lipoproteins?

A

By lecithin:cholesterol acyltransferase

220
Q

What % of cholesterol is endogenous?

A

90%

221
Q

What is the major organ in which cholesterol is processed?

A

Liver

222
Q

Only method of cholesterol export

A

Through bile (it’s a constituent of bile)

223
Q

What is De novo lipogenesis?

A

Converts excess dietary starch, sugar, protein, and alcohol into specific fatty acids

224
Q

Rate limiting step of De novo lipogenesis

A

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

225
Q

Fatty acid export from liver

A

ApoB 100 synthesised in RER

Lipid components (TG, cholesteorlester) synthesise in SER

These are added by TAG transfer protein to ApoB

Transported to GA where ApoB is gylcosylated

Glycosylated Apo-s with lipid componetns bud off GA and migrate to sinusoidal membrane of hepatocyte

Vesicles fuse with membranes and VLDL released

226
Q

Fatty acid oxidation occurs at 3 locations in the liver… (to produce acetyl co-A)

A

Mitochondrial beta oxidation

Peroxisomal beta oxidation

ER Microsomal omega oxidation

227
Q

Peroxisomal b oxidation

A

Normal ribosomal function

228
Q

Mitochondrial beta oxidation

A

Progressive shortening into acetyl-CoA subunits (condensed into ketone bodies which enter TCA cycle)

229
Q

ER Microsomal omega oxidation

A

CYP4A enzymes oxidise saturated and unsaturated fatty acids

omega-hydroxylation in the ER

Then, decarboxylation of the omega-hydroxy FA in cytosol

This product then enters b-oxidation pathway

230
Q

Main source and loss of nitrogen

A

Source - Dietary protein

Loss - gut and kidneys as urea

231
Q

Amino acid structure

A

H
H2N——-C——-COOH
R

232
Q

Link between 2 amino acids

A

Dipeptide
Peptide bond (C-N)

233
Q

How many amino acids in a polypeptide vs a protein

A

Polypeptide = <50
Protein = >50

234
Q

Nitrogen said to be in balance if…

A

N intake (from dietary protein) is roughly equal to N excretion (+/- 4g/day)

235
Q

Recommended daily dietary protein intake

A

0.75g/kg/day

236
Q

3 sources of N loss

A

Renal excretion (70g/day)

Faecal loss (10g/day)

Skin/hair/sweat loss

237
Q

Essential vs non-essential amino acids

A

Amino acids said to be essential if they can’t be synthesised de novo in vivo

Some amino acids are conditionally essential (so only essential under certain circumstances)

238
Q

Which non-protein molecules are synthesised used N from dietary protein?

A

Neurotransmitters, nitric oxide, nucleotides

239
Q

3 roles of albumin

A

Maintaining appropriate osmotic pressure

Binding and transport of hormones, drugs, etc

Neutralisation of free radicals

240
Q

Transamination of alanine

A

Alanine + a-ketoglutarate <–> Pyruvate + Glutamate
(catalysed by ALT)

241
Q
A
242
Q

Cortisol role in AA catabolism

A

+ proteolysis
- protein synthesis
+ gluconeogenesis

243
Q

Glucagon role in AA catabolism

A

+ glycogenolysis
+ gluconeogenesis
+ AA degradation
+ ureagenesis
+ entry of AAs to liver

244
Q

What is bile?

A

Lipid rich solution containing water, inorganic electrolytes and organic solvents (bile acids, phospholipids, cholesterol, bile pigments)

245
Q

Bile secretion per day from gall bladder

A

500-600ml per day

246
Q

What circulation means the liver doesn’t have to synthesise as much bile?

A

Enterohepatic circulation - Most bile acids secreted by hepatocyte have been previously secreted into intestine

247
Q

3 bile functions

A

Fat digestion/absorption

Cholesterol homeostasis

Excretion of lipid soluble xenobiotics

248
Q

Bile acids (major constituent of bile) are synthesised from… in …

A

Synthesised from cholesterol in hepatocytes

249
Q

What are the primary bile acids formed from cholesterol (lipid soluble)?

A

Cholic Acid (CA)
Chenodeoxycholic Acid (CDCA)
(water soluble)

250
Q

What happens to bile acids before being secreting into bile?

(mechanism to trap them in the lumen of the intestine)

A

CA and CDCA are conjugated making them more hydrophilic and more acidic which makes them stay in the lumen of the intestine

251
Q

Bile acids are amphipathic meaning…

A

Likes water and fat which aids emulsification of lipids (increasing SA) into the aq solution of the lumen

252
Q

Process of digesting fat within a fat globule

A

Amphipathic bile salts and phospholipids surround a TG

Amphipathic protein (colipase) allows lipase to get into close approximation to the emulsion droplet and digest the TG

253
Q

How do FAs and MGs enter the enterocytes?

A

Fatty acids and monoglycerides associate with phospholipids and bile acids allowing aq diffusion through channels into enterocyte (as the bile acids are amphipathic)

254
Q

What happens to FAs and MGs once they are absorbed into the enterocyte?

A

They reform triglycerides and are exocytosed into the blood stream as chylomicrons

255
Q

What happens to FAs and MGs once they are absorbed into the enterocyte?

A

They reform triglycerides and are exocytosed into the blood stream as chylomicrons

256
Q

Fate of bile in fasted vs fed state (enterohepatic circulation part 1)

A

Fasted - bile acids travel down biliary tract from liver -> gallbladder (where they’re concentrated 10x)

Fed - CCK released from duodenal mucosa which relaxes Sphincter of Oddi and contracts gallbladder releasing concentrated solution of mixed micelles (BA, PL, cholesterol)

257
Q

Bile acid reabsorption (enterohepatic circulation part 2)

A

Bile acids conjugated (so remain intraluminal)
Actively transported via apical sodium bile acid transporter (ASBT) into terminal ileum
Re-enters liver via portal circulation
Bile acids taken up by hepatocyte and secreted back towards gall bladder

258
Q

How many enterohepatic cycles per meal

A

2-3 cycles

259
Q

Bile acid negative feedback mechanism in terminal ileum

A

Bile acid binds to Farnesoid X Receptor in terminal ileum triggering synthesis of FGF 19 (hormone)
FGF 19 then inhibits CYP7A1 reducing bile acid production

260
Q

Role of CYP7A1

A

Stimulates conversion of cholesterol into primary bile acids (CA and CDCA) in the liver

261
Q

Na absorption in intestine

A

Glucose/Na (SGLT1) co-transporter on apical membrane brings Na into enterocyte

Na+/K+ATPase transporter then moves 1 Na cell->blood and 1 K blood->cell (on basolateral membrane)

262
Q

Glucose absorption in intestine

A

Glucose/Na (SGLT1) co-transporter on apical membrane brings Glucose into enterocyte

GLUT2 transporter then takes glucose from cell->blood (on basolateral membrane)

263
Q

cAMP effect on intestinal secretion

A

Works to shift Cl- from body into gut lumen

264
Q

4 factors affecting intestinal absorption

A

Number and structure of enterocytes
Blood and lymph flows
Nutrient intake
GI motility

265
Q

What breaks down maltose, sucrose and lactose (disaccharides) into monosaccharides?

A

Maltase, sucrase, lactase

266
Q

Enterocytes absorb glucose and galactose by the Na co-transporter but absorb fructose by…

A

Facilitated transport

267
Q

4 saliva functions

A

Lubricates, cleans oral cavity
Dissolves chemicals
Suppresses bacterial growth
Digest starch by amylase

268
Q

Secretions of the mucous neck cell (in the stomach)

A

Mucus
Bicarbonate

269
Q

Secretions of the parietal cells (in the stomach)

A

Gastric acid (HCl)
Intrinsic factor (complexes with Vit B12 to permit absorption)

270
Q

Secretions of Enterochromaffin-like cells (in the stomach)

A

Histamine

271
Q

Secretions of chief cells (in the stomach)

A

Pepsin(ogen)
Gastric lipase

272
Q

Secretions of D cells (in the stomach)

A

Somatostatin (inhibits gastric acid secretion)

273
Q

Secretions of G cells (in the stomach)

A

Gastrin

274
Q

A lot of gastric acid secretion stimulated by…

A

Parasympathetic pathway of vagus nerve

275
Q

Acidosis vs Acidemia

A

Acidosis - Disorder tending to make blood more acidic than normal

Acidemia - Low blood pH

276
Q

Alkalosis vs Alkalemia

A

Alkalosis - Disorder tending to make blood more alkaline than normal

Alkalemia - High blood pH

277
Q

Transamination reaction between pyruvate and glutamate at the muscle (glucose-alanine cycle)

A

Alanine aminotransferase (ALT) removes the amino group from glutamate forming alpha-ketoglutarate and adds it to pyruvate forming alanine (opposite occurs at liver)

278
Q

Link between Kreb’s and urea cycle

A

Fumarate produced in urea cycle can be fed into Kreb’s

Aspartate produced in Kreb’s can be fed into urea cycle

279
Q

Where does the urea cycle take place?

A

Mitochondria and cytosol

Medicine (14 decks)

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