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Physiology > GI > Flashcards

GI Flashcards

1
Q

GI tract contains two things?

A
  • Continuous hollow tube- 8m long.
  • Acessory organs: teeth tongue salivary glands etc.
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2
Q

What does the continuous hollow tube do?

A
  • Mechanical process and moves food thrkifh tract.
  • Chemical process and digests food.
  • Absorbs nutrients and water.
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3
Q

What do the accessory organs do?

A

Control secretions and breakdown food.

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4
Q

Neural control mechanism? ANS.

A

Autonomic nervous system.
Parasympathetic and sympathetic.
- Extrinsic nerves, long reflexes and external stimuli.
Involves CNS.
Causes changes in motility and secretion.

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5
Q

Parassymthetic nerves do what to digestion?

A

Stimulate digestion.

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6
Q

Sympathetic nerves?

A

Inhibit digestion.

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7
Q

Enteric nervous system?

A
  • All elements of nervous system.
  • Intrinsic control, short reflex and internal stimuli.
  • Communicates with para and sympathetic but autonomous.
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8
Q

Enteric nervous system- 2 organised neural plexuses.

A
  • Myentric.
  • Submicosal.
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9
Q

What is a plexus?

A

Branching network of vessels and nerves.

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10
Q

Myenteric plexus (Auerbachs)?

A

Between longitudinal and circular layers of muscle in control of digestive tract motility.

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11
Q

Submucosal (Meissners)

A

Between circular and luminal mucosa.
Senses environment of lumen and regulates gi blood flow and epithelial cell function.

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12
Q

Criteria to meet as a GI hormone?

A
  • Substance must be secreted in response to physiologic stimulus.
  • Function must be independent of any neural activity.
  • Must have been isolated purified.
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13
Q

Gastrin?

A

Found in stomach.
Secreted by G cells.
Stimulates HCL production (stimulated pepsinogen in stomach) stimulates gastric contraction.

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14
Q

Secretin?

A

Found in small intestine.
Produced by S cells.
Stimulates water and bicarbonate secretion in pancreatic juice.

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15
Q

Gastric inhibitory peptide (GIP)?

A

Found in small intestine.
Produced by K cells.

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16
Q

Somatostatin?

A

Founded in small intestine stomach and pancreas.
Produced by D cells.

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17
Q

Motilin ?

A

Found in Small intestine.
Produced by M cells.

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18
Q

Cholecystokinin? CCK,

A

Small intestine.
Produced by I cells.

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19
Q

Enteroendocrine cells (EEC)?

A
  • Single cells scattered through GI tract.
  • Densley packed secretory vesicles.
  • Sness chemical osmotic and ph.
    Release hormones and oaracrines.
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20
Q

Motility= 2 types?

A

Phasic contractions.
Tomic contractions.

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21
Q

Phasic contractions?

A

Short lasting contractions.
Movement of material in small intestine.

  • Peristalsis: Waves of contractions 20cm.
  • Segmented contractions: 10cm.
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22
Q

Tonic contractions?

A

Long lasting contractions.
Closing of sphincter.

  • Controlled movement of material through tract.
  • Maintains ordered sequence of events.
  • Compartmentlaisation ensures processes are complete before moving on to next area.
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23
Q

Peristalsis?

A

Mediated by neurones in myentric plexus.

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24
Q

ICC stands for?

A

Interstitial cells of cajal.
Like pacemakers of gut.
Found in myenteric plexus.
- Electrical activity spread through gap junctions from ICC to muscle.
Produce slow waves.
Differs in regions of GI tract.

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25
Q

Slow waves?

A

Don’t cause contraction until threshold -40 reached.
Activated by:
- Distension- bolus of food stimulates stretch receptors local reflex. Oral contraction and aboral relaxation.
- Parasympathetic nerves. (Acetylcholine).

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26
Q

The colon 99% of the time?

A

Retains material like water and fermentation.
Mixing contents.

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27
Q

Mass movement of material into aboral end of colon?

A

Gastro colic response.
2-3 times a day.

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28
Q

Hirschprungs disease- toxic mega colon?

A

Surgical removal of colon.
All or part of colon has no innervation.
Presents shortly after birth.
Can’t move stool, is blocked. (Without enteric nerve cells stimulating gut).

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29
Q

To start journey with mouth?

A
  • Mastication: Breakdown food.
  • Taste: Inform brain about edibility and duration.
  • Saliva production: Lunrication, protection and digestion.
  • Swallowing: Moveemnt of digested macromolecules to stomach.
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30
Q

Taste?

A

Papillae (taste organs).
Located on tongue- soft hard palate palate epiglottis and larynx.
- Contains taste buds.

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31
Q

Each taste bud has 3 kinds of cells?

A
  1. Epithelial cells.
  2. Support cells.
  3. Gustatory receptor cells (taste cells).
    Unnerved by gustatory affront nerves.
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32
Q

All flavours encoded by 5 taste modalities?

A
  • Sweet, sour, salt, bitter , umami(savor).
    One taste cells responds to one modality .
    Salt- H+.
    Sour- K+.
    Metabotropic: Sweet bitter umami.
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33
Q

Saliva function?

A
  • Hypotonic solution contains more 99% water and 1% dry matter such as proteins.
  • alpha amylase- from parotid gland initiates carb digestion.
  • lipase- secreted within glands of mucosa of tongue (lingual).

Multi functional:
Anti bacterial fungal viral etc.

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34
Q

Swallowing? Phases?

A
  • Oral phase (voluntary).
  • Pharyngeal phase (involuntary).
  • Oesophageal phase.
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35
Q

Oral phase?

A
  • Prep phase: chew and bite.
  • Transfer phase: respiration inhibited and tongue forces bolus(mix of saliva and food) into pharynx.
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36
Q

Pharyngeal phase?

A

Movement of bolus from pharynx into oesophagus.

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37
Q

Oesophageal phase?

A

Delivers bolus to stomach.

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38
Q

Espohagal manometer?

A

Measures oesophageal motility and problems swallowing (dysphagia).

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39
Q

Stomach functions?

A
  1. Motility
    Gastric accommodation
    Trituration (gastric juices)
    Gastric emptying.
  2. Digestion.
  3. Protection.
  4. Absorption.
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40
Q

Gastric juice made of?

A
  • Water and ions.
  • HCL- low ph catalyse pepsiongwn to pepsin.
  • Pepsinogens - pro enzyme of pepsin.
  • Intrinsic factor. Glycoprotein binds to b12 allllwing digestion in ileum.
  • Mucus. Protects gastric mucosa.
  • Gastrin- regulates acid secretion.
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41
Q

Parietal chief and endocrine cells?

A

Parietal- HCl and intrinsic factor.
Chief- Pepsinogen.
Endocrine- G cells (Gastrin stimulate acid secretion).
And D cells (somatostatin to inhibit acid secretion).

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42
Q

HCL secretion?

A

CO2 in parietal cells reacts with oxygen to form bicarbonate then hydrogen ions catalysed by enzyme carbonic anhydrase.

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43
Q

Acid secretion?

A
  • Neuroendocrine (acetylcholine).
  • Endocrine (Gastrin).
  • Paracrine (Histamine).
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44
Q

Motility phases?

A

Cepahlic- 30%
Gastric- 60%
Intestinal- 10%

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45
Q

Gasteic/ peptic ulcers?

A

Mucus entraps alkali.
Break in mucosal barrier.

Bacteria- Helicobacyer pylori.
Symptoms- abdominal pain, bloating, vomitjng bleeding.

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46
Q

Cause of peptic ulcer?

A
  • Excess section of acid and pepsin by gastric mucosa.
  • No ability of gastroduodenal to protect against properties of stomach acid pepsin section.
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47
Q

Duodenum?

A

First loop of small intestine (25-40cm).
Brunner gland- Secrete alkaline fluid.
Received secretions from gall bladder (liver) and pancreas.
Site of metal ion absorption.

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48
Q

Acinus is?

A

Exocrine gland.

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49
Q

Endocrine glands?

A

Islets of langerhans?
Alpha- Glucagon.
Beta- Insukin.

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50
Q

In the duodenum?

A

Secretion of pancreatic juice under hormonal control.
CCK acts as acinar cells causes production of pancreatic juice.
Secretin acts on ducts to cause secretion of alkaline.
Ensure juice is washed to intestine.

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51
Q

Liver structure?

A
  • Hepatic artery: Oxygenated blood.
  • Helatic vein: Deoxygenated blood from liver.
  • Bile: Produced by liver stored in gall bladder. (Biliary system).
  • Portal vein- Nutrint rich blood from liver.
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52
Q

Why do we need to eat?

A
  • Maintenance of body: repair, growth, function.
    There is a need to supply nutrients that cannot be made by the body.
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53
Q

Essential nutrients that need to be part of the diet?

A

Carbs.
Amino acids (proteins).
Fatty acids.
Vitamins.
Minerals and water.

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54
Q

Imbalances may result in?

A

Disease and deficiency disorders.

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55
Q

Macro nutrients?

A

Essential for survival and growth.
- Carbs.
- Proteins.
- Fats.
- Water.

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56
Q

Micro nutrients?

A

Essential for growth and enhance function and usability of macro nutrients.
- Vitamins.
- Minerals.

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57
Q

Around 50% of the diet should be from?

A

Carbs.

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58
Q

35% should be from?

A

Fats.

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59
Q

About 15% from?

A

Proteins.

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60
Q

If our diet has a combination of macronutrients, what does our body do?

A

Metabolism.
- This is chemical reaction in body’s cells that changes food to energy.
- Anabolic or catabolic.

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61
Q

Catabolism?

A

Large to small molecule.
Release ATP.

62
Q

Anabolism?

A

Synthesis molecules.
Use energy.

63
Q

Both reactions release?

A

Heat (role in thermodegukation).

64
Q

Glucose is used in several different ways.

A
65
Q

Catabolism as immediate energy source?

A

Aerobic or anaerobic.

66
Q

Anabolism used as?

A
  • Gycogenesis: Synthesis of glycogen for storage (mainly hepatocytes and muscle).
  • Synthesis of amino acids.
  • Formation of triglycerides.
67
Q

Glycogenolysis and glucagon?

A

Glycogen is broken down into glucose in absence of insulin.

68
Q

Glycogenesis and insulin?

A

Stimulation of heoatocytes and skeletal muscle cells by insulin to convert glucose into glycogen.

69
Q

Gluconeogenesis?

A

Glucose production from protein or fat other than carbs.
Occurs when:
- Starvation.
- Low carbs.
- Endurance exercise.

70
Q

Gkucneogeneis is driven by?

A

Cortisol and pancreatic glucagon.

71
Q

Ketones are?

A

Chemical produced by the body when it burns stored fat.
When on low carb diet or fasting:
- Body uses stored fat as fuel source and converts it into ketones. Called as ketosis.

72
Q

Lipids?

A
  • Diffuse across cell membrane into lymphatic system.
    No energy required.
    Oxidised to produce ATP.
    Acts as structural components (cell walls).
73
Q

If fats are not used immediately?

A

They are stored in adipose tissue.
Triglycerides store more readily that glycogen.

74
Q

Fatty acids are used to?

A

Synthesise triglycerides and phospholipids. Generates ATP.

75
Q

Triglycerides (fats and oils)?

A

Protection.
Insulation.
Energy storage.

76
Q

Phospholipids?

A

Major lipid component.

77
Q

Cholesterol (steroid)?

A

Minor component of all animal cell membranes.

78
Q

Bile salts?

A

Needed for digestion and absorption of dietary lipids.

79
Q

Vitamin D?

A

Helps regulate calcium level in body, needed for bone growth and repair.

80
Q

Adrenocortical hromones?

A

Regulates metabolism, resistance to stress and salt and water balance.

81
Q

Carotene?

A

Needed for synthesis of vitamin A.

82
Q

Vitamin E?

A

Promotes wound healing.

83
Q

Vitamin K?

A

Synthesis of blood clotting proteins.

84
Q

Lipoproteins?

A

Transports lipids in blood.

85
Q

Lipolysis?

A

Triglycerides break down into fatty acid and glycerol.

86
Q

Lipogenesis?

A

Excess carbs proteins etc stored as triglycerides.

87
Q

Amino acids are absorbed from GI by active transport.

A
88
Q

Proteiem metaiblism debuted various biochemical processes responsible and synthesis of proteins and amino acids.

A
89
Q

Anabolism- synthesise new proteins, hormones and enzymes etc.

A
90
Q

Anabolism is stimulated by?

A

Insulin like growth factors.
Oestrogen.
Insulin.

91
Q

Amino acids can’t be stored?

A

So excess proteins are used for ATP production through Krebs cycle.

92
Q

Converted to glucose l, triglycerides or ketone bodies.

A
93
Q

Catabolism is stimulated by?

A

Cortisol.

94
Q

Instant energy?

A

10-15 seconds.
Stored ATP and creatine phosphate.

95
Q

Short term energy?

A

Anaerobic metabolism of glucose.
15- (2-3)mins.

96
Q

Long term energy?

A

Aerobic metabolism.
2-3 minutes beyond.

97
Q

How much energy is required for individual day activities?

A
  • 2000 kcal. Women.
  • 2500 kcal. Men.
98
Q

Proteins are things like fish meat pulses nuts.

A
99
Q

Vitamin A?

A

Essential for light formation.
Deficiency: Night blindness.

100
Q

Vitamin D?

A

Essential for absorbing of calcium and phosphorus form GI tract.
Deficiency: Rickets in children.
Oesteomalacia in adults.

101
Q

Vitamin E?

A

Involved in formation of DNA and RNA and red blood cells.
Deficiency: poor wound healing.

102
Q

Vitamin K?

A

Coenzyme essential for synthesis of several clotting factors by liver including prothrombin.
Deficiency: Delayed clotting time results in excessive bleeding.

103
Q

Thiamine (B1)?

A

Cofactor for glucose and amino acid metabolism.
Essential for pyruvate dehydrogenase.

104
Q

A deference decreases?

A

Advanced glycosykated end products that can lead to endothelial dysfunction and potentially worsen type 2 diabetes.

105
Q

Severe B1 (thiamine) deficiencies can lead to beriberi.

A
106
Q

80-90% of obesity have?

A

Vitamin D deficiency.

107
Q

Vitamin K neonatal injections given at birth.

A
108
Q

Vitamin C scurvy early symptoms, weakness gum disease sore arms and legs.

A
109
Q

Hypervitamonis?

A

Fat soluble vitamins are stored as fat.
Can build up and cause problems.

110
Q

Some women need to avoid?

A

Liver products.

111
Q

Iron deficiency?

A

Anemia.
Weak tired decrease cognitive ability.

112
Q

Calcium?

A

Osteopenia- low bone mass.
Osteoporosis reductions in bone mass.

Fatigue muscle cramp cardiac arrurhnia.

113
Q

Pescatarinism?

A

Someone who doesn’t eat red meat or poultry.
May have problems with B12 vitamin D and iron levels.

114
Q

Vegetarism?

A

Problems with maintaining protein and iron levels.
Need essential amino acids lucine and methionine.

Infertility - lycine.
Absorption of zinc- methionine.

115
Q

Veganism?

A

Protein replacement problems.
Lack of B12.
Dizziness tinnitus lesion.

116
Q

Malnutrition?

A

Too little or too much of certain nutrients.

117
Q

Undernutriiton?

A

Not getting enough protein calories or micronutrients.

118
Q

Over nutrition?

A

Overconsumption of certain nutrients.

119
Q

Marasmus and Kwashikor?

A

Marasmus - Defieciency of all macronutrients with inadequate energy intake.

Kwashirokr- Protein deficiency disorder.
Leads to liver damage and or oedema.

120
Q

In Phenylketorneuria the derive enzyme is?

A

Phenylalanine hydroxylase.

121
Q

Which repository pattern is typically associated with diabetic ketoacidosis?

A

Kussmauls breathing.

Rapid, deep breathing.

122
Q

Food intake in excess energy?

A

Positive energy balance.

123
Q

Food intake less than energy?

A

Negative energy balance.

124
Q

Negative energy balance lead to?

A

Decline in metabolism.

125
Q

It is thought we have centres in hypothalamus that control desire food?

A

Orexigenic.
Anorexigenic.

126
Q

Stretch receptors?

A

Activate pathways in vagus nerve and inhibit food intake.

127
Q

Peptide (PYY) and CCk and insulin?

A

GI hormones released when indigestion food suppress further feeding.

128
Q

Leptin?

A

Inhibits food intake.

129
Q

Ghrelin?

A

Stimulated appetite.

130
Q

Rewards signals?

A

Reduces amount of food eaten.

131
Q

Basic metabolic rate?

A

Energy released at complete rest.

132
Q

Resting metabolic rate?

A

Similar to basal but includes movement of light activities.

133
Q

Factors affecting Bmr?

A
  • Gnestics.
    Height weight.
    Age.
    Body temperature.
    Growth.
134
Q

Most important determinant of BmR is body size.

A
135
Q

Obese have higher BMR because they have fat free mass.

A
136
Q

TEF is energy cost of digestion, absorption.
Comprises about 10% of TEE in sedentary individuals.
Lower TEF seen in obese.

A
137
Q

BMI classify overweight and obesity.

A
138
Q

BMI classify overweight and obesity.

A
139
Q

Obesity can lead to?

A

Cancer.
Cardiovascular disease.
Hypertension.
Type 2.

140
Q

BMI disadvantage?

A

Not suitable for those with high lean body mass.

141
Q

Obesity thought to account for?

A

80-85 for risk developing type 2.

142
Q

Type 2 is insulin resistance impaired insulin secretion l and hyperglycaemia.
Complications associated with kidneys nerves and eyes.
Excess weight can produce insulin resistance.

A
143
Q

Primary attributes of physical activity are?

A

Type.
Frequency.
Duration.
Intensity.

144
Q

5HT3 receptor antagonists?

A
  • Ondansetron.
  • Blocks serotonin (5HT3).
    Used motions sicknes etc.
145
Q

Dopamine D2 antagonist?

A

Metoclopramide.
Blocks D2 receptors.

146
Q

H1 histamine antagonist?

A

Promethazine.
Blocks histamine receptors.

147
Q

NK1 receptor antagonist?

A

Aprepitant.
Blocks NK1 in brain.

148
Q

Proton pump inhibitors PPI?

A

Example Omeprazole.
Irreversibly inhibits H+ K+ ATPasw in gastric parietal cells reducing acid secretion.
GERD, peptic ulcers.

149
Q

H2 receptor antagonist?

A

Ranitide or famitidine.
Blocks H2 receptors in gastric parietal cells reducing acid secretion.
Mild peptic ulcers, GERD.

150
Q

Antacids?

A

Magnesium hydroxide, aluminium hydroxide.
Neutralise stomach acid.
Mild GER and ulcers.

151
Q

Protagladkin analogs analogs?

A

Mistroplol.
Increase mucus and bicarbonate production reduces acid secretion.
Prevent NSAID induced ulcers.

152
Q

Diarrhoea?

A
  • Opiod recept agonist, slows fur motility like lopermaide.

Physiology (2 decks)

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