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MBChB1 Phase 1 > Week 10: Gastrointestinal System > Flashcards

Week 10: Gastrointestinal System Flashcards

1
Q

what is the opening and termination of the alimentary cana/GI system?

A

opening - mouth
termination - anal canal

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2
Q

2 main roles of the digestive system?

A

digestion (processing food)
absorption (transfers nutrients to circultion)

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3
Q

2 groups of organs in the GI system?

A

digestive tract
accessory organs

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4
Q

name accessory organs of the GI system?

A

salivary glands
gallbladder
liver
pancreas

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5
Q

what secretions do the salivary glands produce?

A

serous/watery secretion
mixed seromucous secretion - mixed watery and mucus
mucous secretion

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6
Q

functions of saliva?

A

buffer mouth pH
protects surface of mouth and gut
antimicrobial action
maintains tooth structure
aids with taste
small amount of digestion help

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7
Q

function of gall bladder?

A

stores and concentrates bile

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8
Q

bile function?

A

fat digestion

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9
Q

where is bile produced?

A

liver

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10
Q

name the parts of the GI tract in order?

A

oral cavity
pharynx
oesophagus
stomach
small intestine
large intestine

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11
Q

function of pharynx?

A

food and air passes through

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12
Q

where is the oesophagus found?

A

pharynx to stomach
passes behind heart and trachea

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13
Q

functions of the stomach?

A

churns food/drink
secretes acid and enzymes to begin digestion

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14
Q

what digestion does the saliva do?

A

amylase does starch digestion

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15
Q

3 parts of the small intestine?

A

duodenum
jejunum
ileum

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16
Q

which secretions are present in the duodenum? main function?

A

more digestion, less absorpion
secretions from pancreas
bile

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17
Q

how does the pancreas maintain an alkaline pH?

A

secretes bicarbonate rich fluids

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18
Q

where does undigested material from the ileum move into?

A

large intestine

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19
Q

name parts of the large intestine?

A

caecum
ascending, transverse and descending colon
rectum
anus

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20
Q

name the layers of the GI tract histology.

A

mucosa
submucosa
muscularis propira
adventitia
serosa

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21
Q

how is GI tract stained?

A

Haemotoxylin and eosin

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22
Q

what does the mucosa line?

A

cavities of body and surface of internal organs

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23
Q

what is the lamina propira? function? hat cells does it contain?

A

thin layer of loose connective tissue beneath epithelium
support and provudes nutrients for overlying epithelium
inflammatory cells

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24
Q

structure of muscularis mucosae?

A

smooth muscle

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25
Q

structure of submucosa? what cells does it contain?

A

dense irregular connective tissue
blood vessels, nerves, lymphatic vessels

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26
Q

2 layers of muscularis propira? function?

A

inner circular muscle
outer longitudinal muscle
both smooth muscle
peristalsis - movement of food and products of digestion

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27
Q

what is adventitia?

A

outer layer of fibrous connective tissue surrounding an organ
oral cavity, upper end of oesophagus in chest, ascending/descending colon, rectum

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28
Q

what is serosa?

A

reduces friction in parts of GI tract without adventitia

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29
Q

what epithelia is in the oesophagus?

A

stratified squamous

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30
Q

where are glands found in the oesophagus?

A

submucosa

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31
Q

what epithelia is in the stomach onwards?

A

simple columnar

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32
Q

what glands are in mucosa of stomach?

A

gastric glands for stomach secretions

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33
Q

what are meissners and auerbachs plexus? where are they found?

A

nerve plexuses
m - submucosa
a - between circular and longitudinal muscle

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34
Q

why are villi in small intestine?

A

increase surface area

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35
Q

function of brunners glands in duodenum? where are they found?

A

secrete bicarbinate ions to neutralise acid from stomach
submucosa

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36
Q

function of peyers patches?

A

lymphoid follicles
prevent growth of dangerous bacteria

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37
Q

where are crypts found in small intestine?

A

jejunum

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38
Q

3 parts of pharynx?

A

nasopharynx
oropharynx
laryngopharynx

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39
Q

epiglottis function?

A

elastic cartilage covering trachea preventing food entering lungs

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40
Q

what types of muscle are in each regions of the oesophagus?

A

upper 1/3 - skeletal
middle 1/3 - mixed
lower 1/3 - smooth

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41
Q

what are verticle lines of abdomen called?

A

mid clavicular lines

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42
Q

what is upper horizontal line of abdomen called?

A

subcostal line

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43
Q

what is lower horizontal line of abdomen called?

A

intertubercular line

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44
Q

what is in right hypochondrium of abdomen(1)?

A

liver

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45
Q

what is in the epigastric region of the abdomen (2)?

A

duodenum
liver
gallbladder
pancreas
stomach

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46
Q

what is in the left hypochondrium of the abdomen (3)?

A

spleen and stomach

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47
Q

what is in right lumbar (4) region of abdomen?

A

ascending colon
kidney

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48
Q

what is in umbilical region of abdomen (5)?

A

stomach
pancreas
duodenum
transverse colon
kidneys

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49
Q

what is in left lumbar region of abdomen (6)?

A

descending colon
left kidney

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50
Q

what is in right iliac fossa region of abdomen (7)?

A

caeceum
appensix
ascending colon

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51
Q

what is in hypogastrium region of abdomen (8)?

A

bladder
uterus
ileum

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52
Q

what is in left iliac fossa region of abdomen (9)?

A

sigmoid colon
descending colon

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53
Q

what is fundus of stomach?

A

where air collects

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54
Q

what is cardia in stomach?

A

next to heart

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55
Q

what is anterior and superior to the stomach?

A

lower ribs/diaphragm
liver

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56
Q

what attaches to the greater curvature of the stoach

A

fatty tissue/greater omentum

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57
Q

function of pyloric sphincter?

A

controls entry of secretions from stomach into duodenum

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58
Q

what is pyloric stenosis? what does it present with?

A

thickening/narrowing of pyloric sphincter
prevents chyme passing to duodenum
usually in newborns

projectile vomiting without bile

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59
Q

what breaks down ingestions in the stomach?

A

enzymes and hydrochloric acid

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60
Q

function of rugae in stomach?

A

folds of organ
help increase surface area

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61
Q

what is the 3 muscular layers in the stomach?

A

muscularis propira
oblique muscle layer
muscularis externa

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62
Q

function of muscular layers in stomach?

A

mix chyme together

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63
Q

function of endocrine cells?

A

produce gastrin

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64
Q

function of gastrin?

A

stimulates parietal cells to produce hydrochloric acid

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65
Q

what do chief cells produce?

A

pepsinogen

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66
Q

function of hydrochloric acid?

A

breaks down pepsinogen to pepsin

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67
Q

function of muscus in GI system?

A

protect mucosa

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68
Q

what common bile duct does the duodenum recieve?

A

sphincter of oddi
recieves bile and pancreatic fluid

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69
Q

where does the duodenum end?

A

duodenojejunal junction

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70
Q

what does the serosa hold the small intestine on to? what is it composed of?

A

hold to mesentery
2 layers of mesothelium

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71
Q

what is the mesentery?

A

organ attaching intestines to abdominal wall

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72
Q

what are plica?

A

folds in small intestine similar to rugae

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73
Q

2 broad functions of pancreas?

A

hormonal and digestive

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74
Q

what does the exocrine gland produce in pancreas? how much of pancreas does this make up?

A

99%
digestive enzymes to break down fat/carbs/protein
bicarbonate ions

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75
Q

what is the endocrine portion of pancreas called?

A

islets of langerhans

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76
Q

what 3 hormones does pancreas produce?

A

insulin
glucagon
somastostatin

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77
Q

function of insulin?

A

promotes glucose absorption from blood into liver, skeletal muscle and fat cells
allows conversion to glycogen e.g. storage of glucose

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78
Q

function of glucagon?

A

converts stored glycogen into glucose to help slow down digestive process

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79
Q

function of somastostatin?

A

reduces acid secretion
slows down digestive process

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80
Q

what is the largest gland of the body and heaviest of heart?

A

liver

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81
Q

how many lobes does the liver have?

A

4

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82
Q

what is the liver covered by?

A

lower ribs and costal cartilages

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83
Q

what colour is the liver?

A

red-brown

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84
Q

functions of liver?

A
  • produces bile
  • detoxifies and processes everything absorbed from GI tract
  • regulates glucose in blood
  • synthesises proteins e.g. clotting factors
  • inactivates hormones and drugs and insulin
  • drug metabolism
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85
Q

when can drug metabolism be negative to the liver?

A

when metabolis is more toxic than initial compound

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86
Q

what is the dual supply to the liver?

A

hepatic portal vein from gut and spleen
hepatic arteries

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87
Q

what provides oxygen to liver?

A

hepatic arteries

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88
Q

what carries bile from the liver to the gall bladder?

A

common heptic duct

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89
Q

what forms the extraheptic ducts?

A

intrahepatic ducts

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90
Q

function of caecum? where is it?

A

between ileum and ascending colon
reservoir for chyme

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91
Q

when can the caecum be palpated?

A

faeces
inflammation
pregnancy

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92
Q

what is the ileocaceal valve? where is it?

A

between ileum and caecum
prevents reflux of large bowel contents into ileum during peristalsis

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93
Q

when does the colon become sigmoid colon?

A

when it begins to turn medially

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94
Q

what is the hepatic flexure?

A

when colon meets right lobe of liver and turns 90 degrees - start of transverse colon

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95
Q

what is the splenic flexure?

A

when the colon turns 90 degrees to turn inferiorly

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96
Q

what is the taenia coli?

A

incomplee layers of longitudinal muscle
3 longitudinal bands of smooth muscle outside of colon

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97
Q

what is haustra?

A

ring like circular muscle in inner muscular layer of colon

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98
Q

whar is appendice epiploicae?

A

pouches of peritoneum filled with fat mainly on transverse are sigmoid colon but not rectum

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99
Q

function of goblet cell in GI tract?

A

produce mucus
absorbs fluid from GI tact

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100
Q

3 main vessels of blood supplying GI tract?

A

coeliac trunk/foregut
superior mesenteric artery (midgut)
inferior mesenteric artery/hindgut

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101
Q

what does the foregut/coeliac trunk supply?

A

lower oesophagus
stomach
liver
spleen
first half of duodenum

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102
Q

what does the midgut/superior mesenteric artery supply?

A

last half of duodenum
jejunum
ileum
caecum
appendix
ascending colon
first half transverse colon

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103
Q

what does the hindgut/inferior mesenteric artery supply?

A

last 1/3 transverse colon
descending colon
sigmoid colon
rectum

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104
Q

what is portal venous drainage for?

A

gut and spleen

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105
Q

what drains the lower limb?

A

femoral veins

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106
Q

what drains the pelvis?

A

internal iliac veins

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107
Q

what drains the kidneys?

A

renal veins

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108
Q

what is the main vein draining the liver?

A

hepatic vein

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109
Q

what is dysphagia?

A

difficulty swallowing

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110
Q

what does too little nutrients cause?

A

malnutrition

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111
Q

what is in the eatwell guide?

A

5 portions fruit/veg a day
potatoes bread and carbohydrates
small amounts of oil and spreads
dairy
2 portions fish/week
little red and processed meat
beans and pulses
less often eat sweets/ice cream/chocolate
6-8 glasses water a day

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112
Q

function of carbohydrate in the diet? source?

A

energy source
bread, rice, pasta, cereal

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113
Q

function of protein in the diet? source?

A

repair/growth
meat, fish, dairy, lentils, nuts

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114
Q

function of fat in the diet? source?

A

long term energy store/insulation
meat, cheese, cream, fish, nuts

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115
Q

function of vitamins in the diet? source?

A

A - vision (liver, sweet potato)
B - vegetable
C - antioxidant (citrus)
D - calcium absorption (oily fish)

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116
Q

function of minerals in the diet? source?

A

ca - bone mineralisation (milk)
iron - oxygen transport (red meat)
potassium - banans

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117
Q

function of fibre in the diet? source?

A

effective bowel function
plants

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118
Q

what is triglycerides composed of?

A

glycerol + 3 fatty acids
90% of fat in diet

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119
Q

name 3 dietary fats?

A

triglycerides
phospholipids
cholesterol

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120
Q

function of cholestrol?

A

synthesises estrogen and testosterone and bile salts
present in plasma membreane

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121
Q

structure and function of phospholipids?

A

2 fatty acid chains and glycerol
in plasma membrane

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122
Q

sources of saturated dietary fats?

A

animal foods
meat fat
butter
cheese
cream

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123
Q

sources of unsaturated dietary fats?

A

planst
olive and rapeseed
nuts

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124
Q

sourcesof cholestrol?

A

plants and animals
dairy products
palm and coconut oil

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125
Q

how many essential amino acids are there? what does this mean?

A

9
cant be produced by the body and must be obtained from diet

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126
Q

sources of dietary protein?

A

meat
dairy
eggs
pulses
nuts
seeds

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127
Q

examples of monosaccharides?

A

glucose
fructose
galactose

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128
Q

name 3 disacharides?

A

sucrose
maltose
lactose

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129
Q

what is sucrose made from?

A

glucose and fructose

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130
Q

what is maltose made from?

A

glucose x 2

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131
Q

what is lactose made from?

A

glucose and galactose

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132
Q

what are disaccharides and polysaccharides joined by?

A

glycosidic bonds

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133
Q

name a polyaccharide and its composition?

A

starch
amylose and amylopectin

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134
Q

what is fibre made of?

A

cellulose from plant material

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135
Q

how much calories should men and women eat?

A

men - 2500 cal
women - 2000 cal

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136
Q

how is obesity caused?

A

dietry intake excedds energy expenditure

137
Q

how are carbohydrates (polysaccharides) digested?

A

disaccharide then monosaccharide

138
Q

how are proteins digested?

A

peptide then amino acids

139
Q

how are triglycerides digested?

A

free fatty acid
diacylglycerol
monoacylglycerol
glycerol

140
Q

what is digestion?

A

food is broken down into components simple enough to be absorbed in the inetstine

141
Q

which enzymes carry out digestion?

A

glandular cells (mouth) secrete saliva
chief cells (stomach)
exocrine cells (pancreas)
enzymes bound to apical membrane of enterocytes (in intestine)

142
Q

where is saliva produced?

A

parotid salivary gland
submandibular salivary gland
sublingual salivary gland

143
Q

functions of saliva?

A

moistens food
starts digestion of carbohydrates by a-amylase
produces lingual lipase to start digestion of lipids

144
Q

how does hcl produce pepsin?

A

unfolds pepsinogen and cleaves it to produce pepsin

145
Q

what is a zymogen?

A

an inactive precursor thay are activayed by cleavge of peptide bonds

146
Q

how does bile make fat accessible for enzymes?

A

it emulsifies it

147
Q

how does the liver aid absorption of fats?

A

forms micelles

148
Q

what are bile salts synthesised from? what are they converted to?

A

cholestrol
converted to:
cholic acid
chenodeoxycholic acid

149
Q

what are bile salts conjugated with? what do they then become?

A

amino acid - glycine or taurine
ampipathic , cholestrol hydrophobic, AA is hydrophilic

150
Q

functions of bile?

A

emulsifies liquid aggregates
solubilisation and transport of lipids in aqueous environment

151
Q

outline functions of duodenum, jejunum, ileum

A

duodenum
- mixing secretions from pancreas, liver and duodenum with food
- neutralisation of food
- digestion
- absorption

jejunum
- completes breakdown
- nutrient absorption

ileum
- nutrient absorption

152
Q

function of enterokinase? where is it found?

A

protease activating trypsin from cleaving trypsinogen
duodenum

153
Q

function of trypsin?

A

cleaves zymogens to activate them
procarboxypeptidase to carboxypeptidase
chymotrypsinogen to chymotrypsin

154
Q

name brush border enzymes? where are they found? function?

A

peptidases
lactase
sucrase
maltase
tethered to plasma membrane in small intestine
cleave peptides to amino acids

155
Q

name 3 dietary macromolecules?

A

fats
proteins
carbohydrates

156
Q

why are macromolecules diested as zymogen sometimes?

A

to prevent autodigestion

157
Q

what is mastication? what does the food tyrn into?

A

breaks up food and moistens it
bolus

158
Q

what happens to carbohydrates, proteins and lipids in the mouth?

A

carbs - starch broken down by a-amylase to maltotriose, maltose and a-limit dextrin
proteins - nothing
lipids - lingual lipase present but minor contribution

159
Q

what happens to carbohydrates, proteins and lipids in the stomach?

A

carbs - nothing as a-amylase not activated
proteins - hcl denatures proteins and activates pepsin - endopeptidase cleaving proteins to smaller peptides
lipids - gastric acid present but minor composition

160
Q

what happens to carbohydrates, proteins and lipids in the duodenum?

A

carbs - a-amylase further digests starch, brush border disaccharides - result in monosaccharides
proteins - cleaved by trypsin, chymotrypsin, elastase, carboxypeptidases to produce increasingly smaller peptides, brush border peptidases produce dipeptides/amino acids
lipids - pancreatic lipase digests to monoglycerides and fatty acids
phospholipase digests phospholipids to lysolecithin and fatty acids

161
Q

3 types of absorption?

A

passive (diffusion) - slow, needs conc gradient
facilitated transport - faster, membrane carrier, controllable
active transport - uses atp, fast, uses membrane carrier, controllable

162
Q

draw a micelle

A
163
Q

what are the aims of scientific research in medicine?

A
  • diagnosis of conditions and disease
  • causitave links between lifestyle and disease
  • preventative methods - slowing disease progression or reoccurance
164
Q

what is evidence-based medicine?

A

the integration of best research evidence with clinical expertise and care of individual patients
BEST RESEARCH
PATIENT CONCERNS
CLINICAL EXPERTISE

165
Q

what does qualitative research involve?

A
  • observational studies
  • interview/focus groups/questionnaires
  • e.g. patient experince of living with condition disease, how do patients feel about their care/treatment
166
Q

what does quantitative research involve?

A
  • experimental or observational
  • generating numerical data
  • statistical analysis
  • what is the effect of intervention on comparable groups - does using a nicotine inhaler reduce smoking long term?
167
Q

What are observational studies? When are they used? which type of study is used?

A
  • Collect info about patients without trying to influence their exposure to a treatment/intervention that may prevent disease
  • used when experimentation intervention is unethical to implement or when it is not appropriate to generalise
  • case-control, cohort study
  • may provide evidence of linkage with further investigation required
168
Q

What are experimental studies? what do they compare? which type of study is used?

A
  • assign the exposure or intervention to individuals or groups
  • compare the outcomes in a group of patients with those from a comparable control group
  • randomised controlled trials
169
Q

What is meta-analysis?

A

pooling of data from several randomised controlled trials for statistical analysis to give greater confidence in the conclusions of the review

170
Q

what are randomised controlled trials?

A

number of similar people are randomly assigned to 2 or more groups to test a specific drug, treatment or type of intervention

171
Q

what are systemic review of cohort studies?

A

critical assessment and evaluation of existing cohort or case study

172
Q

what are cohort studies?

A

participants classify whether they have been exposed to something of interest e.g. smoking
- look back at patient records to determine natural history of a condition
- follow participant population over time to observe progression of condition/disease

173
Q

what are case-control studies?

A

participants selected by whether ot not they have condition/disease
may estimate strength of association with a predictor

174
Q

what are case series?

A

most basic type of study
describes medical history of single patient by one or more clinicians

175
Q

what are the strongest and weakest research study types?

A

stongest: meta-analysis
weakest - case series

176
Q

what type of study is a randomised controlled trial?

A

quantitative
measures outcomes after participants recieve intervenion

177
Q

describe what happens in a randomised controlled trial

A
  • experimental group recieves intervention
  • comparison/control group recieves alternative e.g. placebo/standard treatment or nothing
  • groups are followed up to assess effectiveness of intervention
  • difference in response assessed statistically
178
Q

what is a RCT based on?

A

precise question or hypothesis to be tested

179
Q

what should be considered regarding selection criteria in RCT?

A

age
sex
geographical location
social/occupational groups

180
Q

what is eligibility criteria in RCT? what considerations are there?

A

clearly defined inclusion and exclusion criteria

  • potential for effect of intervntion
  • ability to detect effect
  • participant safety
    abilty of patients to give informed consent
181
Q

what is included in estimate of sample size in an RCT?

A
  • enough participants to answer question
  • shouldnt enrol more participants than needed
  • sample size calculated with guidleines
182
Q

how should bias be minimised in an RCT

A

randomise participants and those involved in research are blinded

183
Q

what is random sampling? how can this be ensured?

A

sampling target population where each member of population has an equal chance of being selected
- characteristics of random sample should be similar to population of whole
- target group identified
- random selection of people invited to participate

184
Q

what is random allocation/randomisation?

A

assigning people in a research study to different groups without taking similarities/differences between them into account
- everyone has equal chance of allocation to each group
- uses computer generated random sequence
- cant attribute differences to bias

185
Q

what is a placebo?

A

fake treatment given to patients in control group of clinical trial
indistinguishable from actual treatment

186
Q

what is placebo effect?

A

beneficial effect produced by placebo treatment which cannot be attributed to properties of placebo itself
patient recieve improvement in symptoms from physiological effect of recieving treatment and not actual treatment

187
Q

what is blinding? what does this do?

A

ensures participants/investigators in RCT are unaware of elemnt of study e.g. group allocation
increases validity of trial

188
Q

how is blinding achieved in RCT?

A

use of identical tablets, drug containers, administration methods for interventions and control groups
conceal of group/patient for analysis

189
Q

what is single blinding?

A

patient unaware of type of treatment/intervention they are recieving

190
Q

what is double blinding?

A

patient and investigatiors unaware of treatement/investigation being recieved

191
Q

what is triple blinding?

A

patient, investigator and data analysist are unaware of treatment/intervention being recieved
ensure data analysis is objective
reduces influence of placebo effect

192
Q

what is attrition?

A

participant drop out over time due to death, migration, loss of interest

193
Q

what do positive follow up results of RCT show?

A

benefits of intervention
reduced disease severity/cost to health service in study group

194
Q

what do negative follow up results of RCT show?

A

adverse effects observed - may halt trial early
severity and frequency of abserved side effects

195
Q

2 things RCTs may suffer from?

A

noncompliance
missing outcomes

196
Q

what is noncompliance in RCT?

A

patients not adhering to protocol

197
Q

what is missing outcomes in RCT?

A

participants lost to follow up, outcomes are missed

198
Q

what is intention to treat analysis?

A

solution to noncompliance and missing outcomes in RCT

199
Q

what is intention to treat analysis? what must you always report?

A

ignoring noncompliance/protocol deviation/withdrawal after randomisation
follow up with patients withdrawn from study
include all subjects in groups they were randomly allocated to

once randomised, always analysed

report any deviations or missing responses

200
Q

why do you use confidence intervals in RCT?

A

assess evidence for a difference in outcome between groups

201
Q

what are confidence intervals?

A

range of values that has specified probaility of containing true population parameter
provides confidence level

202
Q

what is number needed to treat?

A

average number of patients who need to recieve treatemnt for one of them to get positive outcome in time specified
closer NNT-1 more effective the trearment

203
Q

what is number needed to harm?

A

measure of chance of experiencing harm in a specified time becase of the treatment or other intervention
should be as large as possible

204
Q

what is a RCT superiority trial?

A

aims to show that a new intervention is more effective than the compartivie treatment - placebo or current best treatment
most clinical trials

205
Q

what is a RCT equivalnce trial?

A

prove that 2 drugs have same clinical benefit
demonstrates that effect of new drug differs from effect of current treatment that is clinically unimportant

206
Q

what is a RCT non-inferiority study?

A

aims to show that effect of new treatment cannot be said to be significantly weaker than current treatment

207
Q

advantages of RCT?

A
  • randomisation produces valid statistical tests
  • gold standard to asses cause and effect
  • produces comparable groups
208
Q

disadvantages of RCT?

A
  • costly and time consuming and difficult to run
  • recruitment may be difficult
  • difficult to administer
  • study may not represent general population
209
Q

what happens if fatty acids are less than 12 carbons long?

A

they go straight to the portal blood

210
Q

what happens if fatty acids are more than 12 carbons long?

A

triglyceride reformed into protein/lipid structyre called chylomicron

211
Q

what is the hepatic portal vein?

A

blood vessel carrying blood from GI tract to the liver

212
Q

what are nutrients essential for?

A

producing energy in the body

213
Q

what is the first law of thermodynamics?

A

energy can neither be created nor destroyed
it is trasnferred from one form to another, or one place to another

214
Q

how is chemical energy derived for humans to maintain a steady state?

A

food

215
Q

what is metabolism?

A

the sum of all chemical reactions in which energy is made available and consumed in the body

216
Q

what is the bodys chemical waste?

A

carbon dioxide
water

217
Q

what are catobolic pathways?

A

complex molecules broken down into smaller ones: energy released

218
Q

what are anabolic pathways?

A

more simple molecule converted into a more complex molecule using energy

219
Q

what is energy used for in the body?

A
  • contraction of muscle and hence all movement (skeletal, cardiac, smooth muscle of the gut and blood vessels etc.)
  • accumulation of ions against concentration gradients e.g. for nerve impulse transmission
  • biosynthesis: building of tissues
  • waste disposal
  • generation of heat
220
Q

when is gibbs free energy positive?

A

product contains more energy than the substrate so energy is required

221
Q

when is gibbs free energy negative?

A

product contains less energy than the substrate so energy is lost

222
Q

how do cells harness lost energy?

A

ATP

223
Q

exergonic vs endergonic reactions?

A

exergonic - energy is lost
endergonic - energy is required

224
Q

how much energy is give out per mole of ATP, and what is this figure within cells?

A

30kj/mole of atp
50kj/mole of atp in cells

225
Q

why must cells have their own capacity to make atp?

A

atp cannot be transferred between cells

226
Q

Name each part of this ATP

A

yellow - phosphate group
pink - ribose
orange - adenine

227
Q

what happens when phosphate bonds are broken in ATP and why?

A

phosphate groups are held together by high energy bonds - they dissipate energy when broken

228
Q

what are the products of ATP hydrolysis?

A

pi + adenosine diphosphate + energy

229
Q

why is atp broken down and when is it remade?

A

broken down - for energy for cellular work
remade - from energy from catabolism

230
Q

what is catabolism?

A

set of metabolic pathways breaking down molecules into smaller units, produces energy

231
Q

how much ATP is turned over every day?

A

80KG

232
Q

what are food macromolecules broken down into?

A

glucose
fatty acids
amino acids

233
Q

how is Acetyl CoA produced from;
- glucose?
- fatty acids?
- amino acids?

A
  1. glycolysis
  2. beta oxidation
  3. transamination, oxidative deamination
234
Q

what does acetyl coa synthesise?

A

metabolites

235
Q

what cycle does acetyl coa contribute to?

A

TCA/krebs cycle

236
Q

why is the TCA cycle called an amphibolic process?

A

has anabolic and catabolic components

237
Q

what 3 macromolecules produce acetyl CoA?

A

carbohydrate
fat
protein

238
Q

2 phases of TCA cycle?

A

decarboxylating
reductive

239
Q

outline how the TCA cycle begins

A

Acetyl CoA enters TCA cycle and condenses with oxaloacetate to form citrate

240
Q

how many carbons does:
- acetyl coa
- oxeloacetate
- citrate
- succinyl coa
have?

A
  1. 2
  2. 4
  3. 6
  4. 4
241
Q

what happens in decarboxylation?

A

citrate metabolised to succinyl coa - loss of 2 carbon molecules forms co2

242
Q

what happens in the reductive phase?

A

succinyl coa metabolised to oxaloacetate which is combined with another acetyl coa so tca cycle can resume

243
Q

how many atp does TCA cycle produce?

A

1 GTP

244
Q

what does TCA cycle produce?

A

1 ATP
3 NADH
1 FADH

245
Q

Which molecules from TCA cycle feed into electron transport chain?

A

nadh and fadh

246
Q

what happens in the electron transport chain?

A

four protein complexes pump protons across the inner mitochondrial membrane
from mitochondrial matrix to intermembrane space

247
Q

how is the differential proton concentration achieved in the mitochondria? where are most protons found?

A

protons pumped across membrane to maintain electrochemical gradient
more protons in intermembrane space as inner membrane is very impermabel

248
Q

how are protons able to be pumped across the membrane?

A

NADH and FADH protons and electrons

249
Q

where does NADH enter the ETC? what does it donate?

A

complex one
donates 2 electrons and 1 proton

250
Q

what happens to electrons donated by NADH in ETC?

A

pass along redox centres in protein complexes

251
Q

what are redox centres?

A

places where reduction and oxidation reactions occur

252
Q

how are electrons passed along redox centres?

A

each protein complex has an increased affinity for electrons

253
Q

how are electrons passed from complex one to three?

A

co enzyme q

254
Q

how are electrons passed to complex four?

A

cytochrome c

255
Q

which protein complexes pump protons into the intermembrane space?

A

1,3,4

256
Q

what is the function of complex 2 in the ETC?

A

where FADH enters
produces atp
encourages oher complexes to pump protons across the membrane

257
Q

what allows protons back into the mitochondrial matrix in the ETC? how?

A

atp synthase
as protons enter the ATP synthase rotates and converts ADP + Pi = ATP

258
Q

What is the main generator of ATP in thw ETC?

A

ATP synthase

259
Q

what happens when electrons reach the end of complex 4 in the ETC?

A

they are donated to molecular oxyegn along with a proton to make water

260
Q

why can RBCs not do the ETC?

A

it requires mitochondria and oxygen

261
Q

what is GTP produced by in the TCA?

A

substrate level phosphorylation: ATP not produced in the ETC/oxiditivate phosphorylation

262
Q

how much atp is produced from 1 NADH oxidised by the ETC? why?

A

2.5
it enters the complex at prtein 1

263
Q

how much atp is produced from 1 FADH oxidised by the ETC?

A

1.5

264
Q

how much ATP altogether produced by 1 Acetyl CoA in TCA cycle?

A

10atp

265
Q

what is the end product of glycolysis?

A

2 pyruvate

266
Q

what is glycolysis?

A

carbohydrate catabolism/breakdown
6 carbon glucose to 2x3 carbon pyruvate molecules

267
Q

where does glycolysis occur? benefit of this?

A

cytosol of all cells
cells without oxygen/mitochondria can produce atp

268
Q

What happens in ATP investment phase of glycolysis?

A

6 carbon glucose molecule broken down to 2x3 carbon glyceraldehyde 3 phosphate molecules
2 ATP required, 2 ADP produced

269
Q

what happens in energy generation stage of glycolysis?

A

4 ADP required to produce 4 ATP
2 pyruvate are produced
2 NAD+ produce 2 NADH

270
Q

what happens under anaerobic conditions after glycolysis?

A

pyruvate converted to lactate
this regenerates NAD+ to keep glycolysis going

271
Q

what happens to NAD+ if pyruvate is made infinitely?

A

NAD+ will run out
glycolysis wont take place
cell death will occur due to lack of energy supply

272
Q

how can NAD+ be regenerated?

A

NADH is oxidised to remove a proton
achieved by fermentation of pyruvate into lactate

273
Q

what is the overall equation for anaerobic glycolysis?

A

glucose + 2ADP + 2pi = 2 lactate + 2 ATP

274
Q

Whta happens to pyruvate from glycolysis under aerobic conditions? how?

A

pyruvate transported to mitochondrion and converted to acetyl-coa by pyruvate dehydrogenase

275
Q

how is acetyl coa formed from pyruvate?

A

3C pyruvate loses a carbon atom which produces CO2

276
Q

What TCA component is formed in aerobic glycolysis?

A

NADH - fed into TCA cycle

277
Q

what is the equation for aerobic glycolysis?

A

pyruvate + NAD+ + pyruvate dehydrogenase = acetyl coa + co2+ NADH

278
Q

How many round of TCA cycle can occur for every glucose molecuke?

A

2

279
Q

What is glucose used for in the body?

A

energy source

280
Q

where is glucose stored in the body?

A

stored as glycogen mainly in liver but also in muscle

281
Q

what happens if you fast for 12-24 hrs?

A

you will run out of glucose stores and the body changes to lipid metabolism

282
Q

how are fats stored in adipose tissue?

A

triglycerides

283
Q

how are triglycerides released from adipose tissue?

A

lipase enzymes

284
Q

what happens when lipase release triglycerides from adipose tissue?

A

broken down to glycerol + fatty acids
transported in the blood via plasma proteins albumin to protect them from water
taken up into cells for oxidation

285
Q

what is oxidation?

A

when an atom, molecule or ion loses one or more electrons in a chemical reaction

286
Q

where are all enzymes required for fatty acid catabolism found?

A

matrix of mitochondria

287
Q

how much atp does modification of fatty acids require?

A

2 atp

288
Q

how is fatty acid modified to cross inner mitochondrial membrane?

A

acetyl coa and 2 atp convert it into fatty acyl coa

289
Q

why is a carnitine shuttle used? what happens?

A

coa on fatty acyl coa is replaced with carnitine
coa cannot cross inner mitochondrial membrane

290
Q

what happens after carnitine shuttle?

A

fatty acyl caritine enters trasnporter protein in inner mitochondrial membrane

291
Q

what happens when fatty acyl carnitine is in the mitochondrial matrix?

A

caritine removed and replaced by coa so fatty acyl coa can be metabolised and undergo fatty acid degregation

292
Q

what is the only fatty acid able to be metabolised?

A

fatty acyl coa

293
Q

how is fatty acyl coa metabolised?

A

beta oxidation

294
Q

how does beta oxidation produce acetyl coa?

A

cleaves carbon backbone of fatty acids between alpha and beta carbons

295
Q

what does each beta oxidation produce?

A

1 NADH and 1 FADH to feed into ETC

296
Q

what is an amine group?

A

NH2

297
Q

what is transamination?

A

removing an amine group from an amino acid and trasnferring it to a keto acid

298
Q

what keto acid is usually involved in transamination?

A

aplha ketoglutarate

299
Q

what does a keto acid do in transamination?

A

transfers ketone group to original amino acid
new amino acid and keto acid are formed

300
Q

what are common amino acids in transamination?

A

glutamate
alanine
asparate

301
Q

what would alanine produce in transamination?

A

pyruvate

302
Q

what would asparate produce in transamination?

A

oxaloacetate

303
Q

what is deamination?

A

catabolism of amino acids where amine group is removed

304
Q

where does deamination take place? what side product is produced when amine group is removed?

A

liver
ammonium - neurotoxic and must be removed by cells

305
Q

what is ammonium converted to?

A

urea - expelled by kidneys

306
Q

why is removal of amine groups important?

A

releases carbon backbone of amino acid and can be regenerated to glucose, fatty acids or krebs cycle intermediates

307
Q

2 classifications of amino acids?

A

glucogenic
ketogenic

308
Q

what breakdown products are produced by glucose?

A

pyruvate
oxaloacetate
intermediated of TCA

309
Q

what breakdown products are produced by ketogenic fatty acids?

A

acetyl coa
acetoacetyl coa

310
Q

what are 2 true ketogenic fatty acids?

A

leucine
lysine

311
Q

what is gluconeogeneiss?

A

production of glucose from non carbohydrate sources

312
Q

where does metabolic fuel come from in prolonged starvation?

A

glucose first and glycogen stores in liver - 16-24hrs
stored fats in adipose tissue - energy reserve for 3 months
protein - 14 days of energy

313
Q

why is protein conserved as an energy source in starvation?

A

so body can move around to forage for food

314
Q

what is the basal metabolic rate?

A

energy required to maintain basic functions when person is lying down and relaxed in normal temperature

315
Q

what are basic functions?

A

blood flow, breathing, digestion, brain activity

316
Q

what additional energy expensiture occurs in females?

A

pregnancy and lactation

317
Q

how much extra calories are required per day in last 3 months of pregnancy and during breast feeding?

A

800
2000

318
Q

how is BMI calculated?

A

weight in kg/height in metres squared

319
Q

when is BMI calculation limited?

A

boxers/rugby/weightlifters have higher muscle mass
would make them obese when they only have extra muscle

320
Q

What symptoms are there of fatigue?

A

tiredness, lack of energy, weakness, exhaustion, sleepiness

321
Q

when can fatigueoccur?

A

when energy being ingested in less than is required

322
Q

what disorders can occur from excess fatigue?

A

chronic fatigue syndrome
endocrine disorders
immune deficiences

323
Q

what is the second law of thermodynamics?

A

when energy is trasnferred from one form to another you lose energy in the form of heat, depleting energy stocks in body

324
Q

what is bulimia nervosa?

A

recurrent episodes of overeating
acompanied with compensatory behaviour aimed at preventing weight gain
preoccupied with body shape or weight influencing self evaluation
not significantly underweight

325
Q

what are compensatory behaviours in EDs?

A

exercise, laxative use, vomiting

326
Q

management of bulimia in children?

A

cognitive behavioural therapy or family based treatment adapted for bulimia
fluoxetine considered with psychological therapy

327
Q

magaemnt of bulimia in adults?

A

cbt adapted for bulimia
antidepressents offered with psychological treatment

328
Q

what is cognitive behavioural therapy?

A

evidence based psychological treatment for mental health problems

329
Q

how to manage binge eating disorder?

A

cbt
antidepressants not recommended

329
Q

what is binge eating disorder?

A

recurrent episodes of binge eating (1x week for 3 months)
not with compensatory behaviours
secretively and ut of control

330
Q

what is anorexia?

A

low body weight - bmi less than 18.5
presistant pattern of behaviours to prevent restoration of normal weight
low body weight central to persons self evaluation
body dysmorphia

331
Q

how to manage anorexia in young people?

A

family based treatment
cbt

332
Q

how to manage anorexia in adults?

A

cbt
olanzapine

333
Q

why should ed treatment be accessed early e.g. first 3 years?

A

anorexia can cause death
neural pathways can form

334
Q

what is arfid?

A

abnormal eating or feeding behaviours
insufficent intake or variety of food
weight loss and nutritional deficiencies

335
Q

what is ofsed?

A

some symptoms of different eating disirders

336
Q

complications of EDs?

A
  • impaired concentration/cognitive performance
  • dry skin, brittle hair, hair loss
  • low BP, arrythmia
  • anaemia
  • impaired renal function
  • constipation
    infertility
337
Q

high risk patients in ED?

A

low bmi and rapid rate of weight loss
low BP and low pulse
electrolyte abnormalities
liver function abnormalities

338
Q

Describe how blood would drain to heart from ileum

A
  • superior mesenteric vein
  • portal vein then liver
  • detoxified then hepatic vein
  • ivc

MBChB1 Phase 1 (12 decks)

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