Week 3 Term 1

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functions of the liver

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166 Terms

1

functions of the liver

bile production, metabolism, detoxification of blood

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2

where does the coeliac artery lead to

stomach, spleen and hepatic artery

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3

where does the superior mesenteric artery lead to

intestine and pancreas

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4

where does the inferior mesenteric artery lead to

(lower) intestine

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5

where does the liver receive blood from

hepatic artery and portal vein

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6

how much bile does the liver produce daily

250-1500ml

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7

what are the major secretions of hepatocytes

bile salts, phospholipids (lecithin), bile pigment (bilirubin), cholesterol, inorganic ions

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8

why are hepatic sinusoids leaky

allow more contact between blood and hepatocytes

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9

what is the role of bile salts from hepatocytes

used in lipid digestion and absorption

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10

where do bile salts derive from

cholesterol

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11

circulation of bile salts

  • liver synthesises

  • bile salts to gall bladder and duodenum

  • moves through duodenum to ileum

  • bile salt removed from ileum by entering hepatic portal vein or removal in faeces

  • bile salts in hepatic portal vein recycled to liver (where some synthesis occurs again)

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12

where do bile pigments come from

breakdown of haemoglobin conjugates with glucuronic acid

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13

use of glucuronic acid in bile pigment formation

increases polarity and solubility in water

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14

how does bile enter the gall bladder

bile flow to duodenum is prevented by closures of sphincter of oddi so will instead enter gall bladder

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15

why do bile salts and pigments become concentrated in the gall bladder

reabsorption of water and salt in gall bladder

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16

what causes sphincter of oddi relaxation

CCK and neural influences (CCK causes sphincter to relax allowing bile into duodenum as well and pushing some bile out of the gallbladder)

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17

when will bile pass to the duodenum instead of the gall bladder

after a meal

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18

when will bile pass to the gall bladder instead of the duodenum

during relaxation

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19

where are lipoproteins formed

liver

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20

where are plasma proteins and clotting factors synthesised

liver

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21

effect of less albumin in blood

more leakage of water to outside of cells (ascites)

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22

liver endogenous molecules that are controlled

insulin, glucagon, aldosterone, female sex hormones

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23

liver exogenous molecules that are controlled

drugs (some converted to active compound)

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24

mechanisms involved in liver metabolism

oxidation, reduction, methylation, conjugation

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25

describe jaundice

bilirubin accumulation in plasma producing yellowing of skin, sclera and mucous membranes. may produce kernicterus which can lead to nerve degeneration in brain

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26

treatment of jaundice

light (breaks down pigment)

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27

describe haemolytic jaundice

excessive haemolysis of RBC (reaches capacity for excretion of RBC)

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28

describe intrahepatic jaundice

defects in conjugation or secretion of bilirubin by hepatic cells (common in acute)

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29

describe obstructive jaundice

blockage of bile ducts

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30

describe physiological jaundice of newborns

babies have poor capacity for conjugating biluribin

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31

what causes acute hepatitis

hepatitis A, B, C (viral) and drugs (eg paracetamol)

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32

what causes chronic hepatitis

hepatitis B, C (viral)

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33

define cirrhosis

necrosis of liver cells replaced by fibroblasts

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34

causes of cirrhosis

alcohol, hepatitis B and C

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35

treatment for cirrhosis

no treatment, just stop causative effect (or organ transplant)

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36

describe layers of GI tract from lumen to outside

mucosa, submucosa, submucosal plexus, inner circular muscle, myenteric plexus, outer longitudinal muscle

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37

name of GI pacemaker cells

interstitial cells of cajal (ICCs)

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38

what rhythm do ICCs pacemaker cells form

basal electrical rhythm (BER)

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39

what does VIP do to smooth muscle cells in GI tract

relax

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40

what does ACh do to smooth muscle cells in GI tract

contract

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41

direction of food movement in GI tract

unidirectional

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42

what nervous control increases GI motility

parasympathetic nerve activation

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43

what nervous control decreases GI motility

sympathetic nerve activation (NA)

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44

how does sympathetic nerve activation decrease GI motility

directly via beta adrenoceptors and indirectly by decreasing ACh release via alpha-2 adrenoceptors

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45

stages of GI motility

mastication (oropharyngeal) and deglutition (oesophageal)n

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46

what is the role of zones of elevated pressure (ZEP) in the GI tract

prevent transit from one region to another (eg backflow)

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47

how is peristalsis initiated

mechanoreceptors in pharynx detect food bolus which initiates peristaltic wave controlled by vagal nerves (gravity assisted)

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48

what controls GI tract smooth muscle excitability

  • myogenic properties of smooth muscle cells

  • activity of intrinsic nerves

  • activity of extrinsic nerves

  • hormones or locally produced chemicals

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49

when can BER from the GI pacemaker cells cause a peristaltic wave

when underlying smooth muscle is at it's most excitable and is able to reach the threshold potential

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50

why are peristaltic waves weak for the first hour after eating food

to allow gastric contents to mix and make room for the food bolus

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51

how is relaxation in corpus and fundus induced

by vagal relaxation fibres stimulated by oesophageal and gastric distension which is mediated by VIP

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52

stimulatory GI tract motility hormones

gastrin (antrum) and motility (small intestine)

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53

inhibitory GI tract motility hormones

gastrin (proximal stomach), secretin, CCK, NO

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54

how does the meal composition of food eaten affect GI tract motility

  • larger food volume increases rate of gastric emptying

  • size of fragments of food

  • osmolarity (greater or smaller than 200mOsm slows rate of emptying)

  • excess acid slows gastric emptying

  • more fat slows gastric emptying

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55

2 types of contraction in small intestine

segmenting and peristaltic

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56

describe segmenting contraction in the small intestine

occurs in circular muscle and move chyme to and fro to increase exposure to mucosal surface

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57

describe peristaltic contraction in the small intestine

occurs in longitudinal muscle over short distances after a meal

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58

describe migrating motility complex (MMC)

occasional propulsive movement propagating over long distances (peristaltic contractions)

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59

what is the role of ileal-caecal sphincter (ZEP) in the large intestine

prevent retrograde movement of bacteria from the colon during movement of chyme

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60

describe the movement of the large intestine during digestion

slow and non-propulsive (Haustral contractions) to knead contents (similar to segmentation in SI)

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61

describe movement of faeces out of the rectum

  • arrival of faecal material stimulates sensory nerves

  • causes peristaltic wave in colon

  • internal anal sphincter relaxes

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62

how is faeces held in by the anus

external sphincter of anus has voluntary control

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63

how does straining increase defecation volume

increases intra-abdominal pressure on colonic and rectal walls

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64

what will a change in absorption effect (AUC, Tmax, F, V, CL, T1/2)

AUC, Tmax, F (only t1/2 if absorption greatly prolonged)

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65

what will a change in distribution effect (AUC, Tmax, F, V, CL, T1/2)

V, T1/2

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66

what will a change in elimination effect (AUC, Tmax, F, V, CL, T1/2)

AUC, CL, T1/2

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67

what effects rate of passive diffusion

  • concentration gradient across membrane

  • surface area

  • membrane thickness

  • lipid solubility

  • molecule size

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68

why do charged drugs need to become uncharged

only uncharged drugs can cross cell membrane

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69

how do you find the pKa (ionisation constant) of a drug

pH at which drug is 50% charged and 50% uncharged

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70

are weak base drugs more charged or more uncharged in a decreased pH (more acidic)

more charged

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71

are weak acid drugs more or more uncharged in a decreased pH (more acidic)

more uncharged

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72

are weak acid or weak base drugs better for absorption in stomach and intestine and entry into the brain

weak base drugs

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73

do weak acid or weak base drugs have better absorption in the stomach

weak acids

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74

why are weak acid drugs easily absorbed by the stomach

A- + H+ = HA (HA can be absorbed as its uncharged)

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75

why do some drugs need to be taken with food

takes longer for drug to be absorbed

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76

describe acid stable drugs

slower absorption in stomach

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77

describe acid labile drugs

stays in stomach for longer and is more easily broken down

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78

are acid stable or acid labile drugs taken with food normally

acid labile

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79

define human microbiome

all microorganisms that live on or in the body forming a dynamic and interactive microecosystem crucial for maintaining health

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80

main locations on body of human microbiomes

skin, mouth, lungs, GI tract, eye, hair follicles, nasopharyngeal, genital tract (male and female)

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81

normal processes that can be affected by the human microbiome

body weight, mood, cholesterol level, sleep, vitamin absorption, cancer, blood pressure, response to drugs,

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82

factors influencing microbiome diversity

living environment, drugs, birth mode, diet, immune disease, metabolic disease, colorectal cancer, autism, age

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83

factors leading to opportunistic infection

compromised immunity, antibiotic suppression of normal flora, breach of physical barriers, impaired normal clearance mechanisms (smoking impairing cilia)

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84

how can lipid soluble drugs be excreted

metabolised by liver, gut or blood to become a water soluble metabolite which can be excreted by the liver or kidney

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85

how are volatile drugs (eg anaesthetics) excreted

via lungs

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86

examples of drugs inactivated by metabolism

warfarin, phenytoin

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87

examples of drugs activated by metabolism (prodrugs)

clopidogrel, codeine

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88

timeline of paracetamol overdose

  • paracetamol metabolised

  • 10% metabolism by CYP

  • metabolism by these creates NAPQI which is a toxic metabolite

  • metabolite has toxic reactions with proteins and nucleic acids which can lead to liver failure

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89

antidote for paracetamol overdose

N-acetylcysteine

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90

what occurs during phase 1 of drug metabolism

introduction/unmasking of functional group which somewhat increases water solubility using cytochrome P450

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91

what occurs during phase 2 of drug metabolism

conjugation with endogenous chemical at functional centre which gives a great increase in water solubility

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92

Non-viral causes of hepatitis

leptospirosis, brucellosis

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93

preicteric clinical features of acute viral hepatitis

malaise, anorexia, nausea, abdominal discomfort, pyrexia (fever)

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94

interim clinical features of acute viral hepatitis

pale stool, dark urine, jaundice

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95

describe the hepatitis A virus

  • RNA genome

  • positive single strand

  • entry via contaminated food or water

  • excreted in faeces

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96

consequences of hepatitis A

  • asymptomatic infection (worse as adult)

  • acute icteric hepatitis

  • fulminant hepatitis (rare)

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97

prevention of hepatitis A

care with food and water, vaccination (whole killed virus)

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98

describe the DNA of hepatitis B viruses

partially double stranded (one circular DNA and a partial second strand) (hepadnavirus)

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99

envelope of hepatitis A vs B

hepatitis A has no envelope

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100

outcomes of acute hepatitis B infection

  • subclinical infection

  • acute icteric hepatitis

  • fulminant hepatitis

  • chronic infection (10%)

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