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GDAN > Nutrition > Flashcards

Nutrition Flashcards

1
Q

Fat-soluble vitamins

A

ADEK (can be stored)

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2
Q

Water-soluble vitamins

A

B1,2,3,6,9,12, C. Co-enzymes/co-factors.

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3
Q

Vitamin A

A

Retinoic acid. Binds to proteins in the retina so that visual pigments can be formed. Can bind to nuclear DNA and affect gene expression and processed like differentiation e.g. the formation of immune cells.
Deficiency = night blindness (mild) or metaplasia and keratinised conjunctive epithelium so a thicker cornea, and weak immune system.

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4
Q

Vitamin D

A

Active forms are D2, D3. Regulates plasma calcium, calcitonin and parathyroid hormone. Promotes bone turnover and mineralisation.
Deficiency = weak bones, rickets, osteomalacia

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5
Q

Vitamin E

A

Antioxidant and cell signalling. Other antioxidants in the body so deficiency isn’t a problem.

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6
Q

Vitamin K

A

Needed for vitamin K dependent coagulation factors. Modifies proteins after they’ve been made e.g. it carboxylates glutamate.
Deficiency = Haemorraghic diseases. Many drugs e.g. warfarin are vitamin K antagonists.

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7
Q

Vitamin B1

A

Thiamine. Involved in ATP synthesis pathway, Myelin, acetylcholine neurotransmitter, Cl- channels, glycolysis pathway.
Deficiency = weakness and stiffness.

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8
Q

Vitamin B2

A

Riboflavin e.g. FAD. e- /H+ carrier in the electron transport chain/for oxidation and reduction. Synthesised by a bacteria in the body and recycled so deficiency is uncommon.

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9
Q

Vitamin B3

A

Niacin. NAD precursor. Synthesised from a dietary aas so if deficient in this then deficient in B3.

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10
Q

Vitamin B6

A

Involved in transamination and aas regulation.

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11
Q

Vitamin B9 / B12

A

Folate and B12. Carbon carrier co-enzymes, needed for many pathways e.g. making ATP or myelin.
Deficiency = anaemia (macrocytic). Babies v sensitive to B9 deficiency so pregnant women given supplements.

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12
Q

Vitamin C

A

Ascorbic acid. Antioxidant and reducing sugar. Needed for iron uptake and absorption, collagen maintenance and synthesis of neurotransmitters.

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13
Q

Oral signs of vitamin deficiencies

A

Vitamin B2,3,6 = angular chelitis
B2 = magenta tounge
B3,6,9,12 = glottitis
C = spongy, bleeding gums.

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14
Q

Control mechanisms for the GI tracts

A

ANS - parasympathetic
Enteric nervous system
Gut peptide - eteroendocrine cells

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15
Q

ENS

A

a separate nervous system for GI tract, inner is the submucosal plexus and outer is myenteric. Short fibres (local circuits) detect intrinsic stimuli e.g. chyme in the stomach, extrinsic stimuli e.g. smell detected by long fibres (NAS, ENS).

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16
Q

A gut peptide control mechanism for the GI tract

A

Eteroendocrine cells release paracrine hormones and neurotransmitters that are stimulated by internal stimuli e.g. pH, and act via negative feedback mechanisms e.g. are released in response to a stimulus but act to reduce that stimulus and therefore aren’t stimulated as much.

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17
Q

Phases of deglutination

A

oral phase, pharyngeal phase, oesophageal phase

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18
Q

The 4 regions of the stomach and the openings

A 
Openings = oesophageal and duodenum
Regions = cardia, fungus, body, pylorus
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19
Q

Gastric functions

A

Motility - alternative relaxing and tensing of longitudinal and circular muscles. Compartmentalising so processing have time to completely finish. Trituration so food can be broken down and dissolve and mix.
Digest food
Absorb alcohol and fat-soluble drugs
Protect against bacteria via the lining and HCL and mechanisms (lining also protects against self-digestion)

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20
Q

Trituration

A

Motility of the stomach to allow the food to be mixed, ground down and dissolved.

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21
Q

Constituents of gastric juice

A

HCL, water, mucus
Pepsin and pepsinogen to make it (enzyme)
Intrinsic factor and glycoproteins (B12 digestion)

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22
Q

Gastric Glands

A

Cardiac, pyloric, oxyntic.

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23
Q

Cells that release the constituents of gastric juice

A

Duct neck cells = water and mucus
Parietal cells = HCL and intrinsic factor
Chief cells = pepsinogen
Endocrine cells = regulate acid secretion e.g. G cells release gastrin which stimulates acid secretion. D-cells release somatostatin which inhibits acid secretion.

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24
Q

The role of gastrin

A

Stimulates/increases acid secretion.

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25
Q

Somatostatin’s role

A

Inhibits secretion of acid from parietal cells.

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26
Q

How does food move through the stomach

A

Food presence stimulates fungus and body to relax to make more space. Contraction of the middle of body forces chyle down to the atrium and pylorus. Contractions in the atrium (systole) push chyle back up to mix and grind food. Some chyle moves to the duodenum and this inhibits motility in the stomach so that it starts to relax.

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27
Q

Phases of gastric mobility

A

Cephalic phase - Parasympathetic CNS reacts to smell/sight/etc = increased stomach motility and mucus and HCL and enzymes.
Gastric phase - food triggers peristalsis and release of gastrin which increases motility and secretions.
Intestinal phase - chyle in duodenum inhibits motility in the stomach to slow it down.

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28
Q

What is peristalsis

A

Contraction of muscles

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29
Q

Retropulsion in the stomach

A

Atrial systole pushed chyle back into the stomach so it can be broken up more.

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30
Q

Retropulsion in the stomach

A

Atrial systole pushed chyle back into the stomach so it can be broken up more.

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31
Q

Pancreas secretions

A

Acinar cells secrete enzymes that digest lipids, proteins, sugars, etc and then intercalated duct cells add water and ions (carboxylates/alkaline)

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32
Q

Duodenal feedback

A

Nutrients in food –> CCK –> more enzymes secreted
HCL in chyme –> Secretin –> more ions and water
(from pancreas)

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33
Q

Gallbladder functions

A

Concentrate the bile.
Neutralise the alkaline by adding H+ ions.
Store the bile
Secrete it in a controlled way.

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34
Q

The liver synthesises and functions

A

Liver secretions contain bile, bilirubin, proteins to protect against infection and alkaline ions.
Functions are to remove waste e.g. cholesterol, to maintain a pH and aid digestion of lipids via emulsification.

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35
Q

CCK actions

A

Causes more enzymes to be secreted from the pancreas in response to nutrients being detected in the chyme. It contracts the gallbladder and relaxes the sphincter of Oddi so that bile can be secreted.

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36
Q

Secretin actions

A

Makes the pancreas secrete more alkaline ions in response to HCL in the chyme. Stimulates the gallbladder to secrete bile.

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37
Q

How is bile delivery from the gall bladder controlled

A

Secretin stimulates the gallbladder to secrete bile and CCK relaxes the sphincter of Oddi and starts contractions so bile can be secreted.

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38
Q

Gallstones

A

When the balance of components and regulatory systems are off, calcified cholesterol, calcium and bilirubin in the gallbladder. V painful and can cause inflammation and infections.

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39
Q

Regions of the small intestines

A

Duodenum, jejunum, ilium.

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40
Q

What is the unstirred layer

A

Glycocalyx layer, where substances can sit so they can be absorbed.

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41
Q

How are carbs absorbed into the small intestines

A

Glucose and galactose move into the cells by co-transport, carried by a Na+ ion that moves in due to a concentration gradient, created by Na+ ions being actively transported out of the cells. Fructose moves in by facilitated diffusion, and all move into the blood by facilitated diffusion.

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42
Q

How are proteins absorbed into the small intestines

A

Large peptides are broken down by peptidase into aas and small peptides, and then actively transported into the cells. Small peptides get broken down by intracellular protease, into aas. The aas move into the blood by diffusion.

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43
Q

Lipid absorption out of the intestine lumen

A

Lipids are broken down by enzymes and bile salts, then combined with micelles so they can be transported across the glycocalyx/unstirred layer. The monoglycerides diffuse through the cells’ membranes. When in the cell, they combine with proteins, glycoproteins and cholesterol to form chylomicrons and then move into the lymph/lacteal system.

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44
Q

The structure of the larger intestines

A

No microvilli but lots of mucus-secreting goblet cells to compact and help move the chyme.
No carrier-mediated absorption e.g. just diffusion.
Absorption of water, ions, vitamins, sugars and salts remaining.
Pockets allow the chyme to move slower so max absorption of substances (Haustra).
Lymphoid tissue protects the large intestines from bacteria.
Sphincters regulate exits.

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45
Q

The benefits of gut flora

A

Complex carb and fibre fermentation.
Produces some vitamins (B9, K) and helps absorb B12.
Regulates the gut’s immune response.

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46
Q

Benefits of dietary fibre

A

Holds water and slows down the absorption of enzymes and nutrients.
Slows down the emptying of the gut and controls the motility of the chyme by adding bulk.
Prevents and treats constipation and haemorrhage.
Increases motility of the gut.

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47
Q

Types/causes of malabsorption

A

. Infection of the intestines changes the way they react to substances e.g. immune response to gluten caused by coeliacs disease.
. Problems with the digestive system e.g. the enzymes
. Damaged carriers/problems with the absorption of the nutrients.

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48
Q

Causes of diarrhoea

A

. Changes in osmotic gradient - nutrients not digested properly/lots of solute in chyme means more water moves into lumen than out.
. Changes in cells lining the intestines - e.g. cholera makes more Cl- ions move into lumen so water gets moved in too bc of the changes in osmotic gradient.
. More water released than absorbed.
. Infection/inflammation of the epithelium alters absorption/secretion.
. Changes in motility - irritable bowel syndrome mean chyme moves too fast for water absorption.

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49
Q

Colon motility and controls

A

Normally segmented contractions allow the chyme to be mixed and give time to water absorption. When defecating, mass movement into rectum activates stretch receptors which send afferent signals to the spinal cord.
Voluntary control of external anal sphincter.
Parasymp and symp control internal anal sphincter

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50
Q

Control of storage and emptying of the colon

A 
Storage = relaxation of rectum/colon and sphincters closing.  
Emptying = contractions in colon/rectum and raised abdominal pressure. Relaxation/opening of sphincters.  Doesn't work if obstruction or spinal cord damage.
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51
Q

Different stages of toxic detection

A

Pre-ingestion (sight, smell, taste)
Pre-absorption (mechano- and chemoreceptors in lumen detects toxins and chemicals and cause emesis to stop absorption)
Post-absorption (chemoreceptive centre outside blood-brain barrier stimulates vomiting centres to stop chemicals and toxins going through blood-brain barrier)

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52
Q

Nausea function and symptoms

A

To stop further ingestion of food. Causes sweating, salvation, palor, changed breathing and heart rate.

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53
Q

Steps to vomiting

A

Duodenum contracts so food goes into the stomach (which relaxes to accommodate this).
Antral mobility inhibited to stop gastric emptying.
Slow and deep breathing to close the glottis and reduce oesophageal pressure.
Air and saliva are drawn into the oesophagus to protect it and decrease pressure.
Expiration against a closed glottis and abdominal contractions increase abdominal pressure.
External and inner oesophageal sphincters open.
Contraction of stomach and abdomen and diaphragm.

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54
Q

How is the respiratory tract protected during emesis (vomiting)

A
  • Glottis closed
  • Soft palate elevated to close the nasopharynx
  • To protect the respiratory tract from acidic contents.
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55
Q

What triggers emesis

A

. Chemoreceptor centre in the blood-brain barrier - drugs, toxins.
. Chemical and mechanical receptors
. Irritation to back of the throat
. Stimulation of hypothalamus - pain, sight, smell
. Vestibular apparatus
. Distention of the stomach or duodenum

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56
Q

Emetic pathway

A

5-HT molecules released which bind to nerves or via blood go to the chemoreceptive centre and stimulate vomiting centre directly or indirectly.

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57
Q

Chemotherapy’s affect on the emetic pathway

A

Causes release of 5-HT receptors

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58
Q

Anti-emetic drugs

A

Block 5-HT/are antagonists and stop them from acting on the vomiting centre. Anti-histamines can act in the same way to stop travel sickness as histamine stimulates the release of 5-HT too.

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59
Q

Nutritional excess’ effects on oral health and examples

A

Excess fluoride = fluorosis

Some drugs e.g. tetracycline (fibrosis drug) can cause intrinsic enamel staining during enamel formation

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60
Q

Nutritional (Vitamin/mineral) deficiencies that affect oral health

A

Vit K, A, C, D, B9/12
Protein
Calcium and phosphate

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61
Q

How does a deficiency of Vit D affect oral health

A 
Delayed dental development/eruption
Enlarged pulp horns and pulp chambers
Clefts or grooves in the enamel/dentine
Enamel hypoplasia
Spontaneous abscesses and more problems with the teeth.
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62
Q

How does a deficiency of Vit C affect oral health

A

Affects collagen formation so caused inflamed, bleeding gums, and lack of PDL so wobbly teeth.

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63
Q

How does a deficiency of Vit B9/B12 affect oral health

A

Affects DNA synthesis (Carbon Carriers). Leads to glossitis, ulcers, angular chelitits and poor gum health.

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64
Q

How does a deficiency of Calcium/phosphate affect oral health

A

Enamel hypoplasia

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65
Q

How does a deficiency of Vit K affect oral health

A

Bleeding (coagulation problems)

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66
Q

How does a deficiency of protein affect oral health

A

Pale ulcers

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67
Q

Main oral signs of malnutrition

A

Ulcers, glossitis, angular chelitis,

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68
Q

the effects of PEG feeding on oral health

A

No bacteria or sugar = no caries but no saliva stimulation so build up of calculus which can chip off and be inhaled.

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69
Q

Orofacial granulomatitis

A

Hypersensitivity to certain substances e.g. benzoates, some essential oils, cinnamon, preservatives.
Causes inflamed lips and gums, ulcers, angular chelitits in while GI tract.
Treat by having a restricted diet and steroids to dampen the immune response

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70
Q

Triglyceride structure

A

Glycerol attached to 3 fatty acids via ester bonds.

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71
Q

Digestion of lipids

A

Broken down by lipases and micelles into triglycerides and then enter intestine epithelial cells where they are combined with proteins and cholesterol to form chylomicrons which enter the lymphatic system.

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72
Q

Structure of chylomicrons

A

A casing of phospholipids so they can diffuse into cells.
Apoproteins can be detected by receptors.
Cholesterol
Triglycerides in middle

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73
Q

How are chylomicrons digested after they are in blood

A

Broken down into fatty acids and glycerol by lipoprotein lipases, released by cells that need the fatty acids e.g. adipose tissue. This is controlled by insulin which detects the apoproteins. Fatty acids are taken into the cells and glycerol and remnants recycled.

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74
Q

VLDL and digestion

A

Similar structure to chylomicrons. Made by the liver - fatty acid + glycerol and then other lipids and proteins added.

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75
Q

Fatty acid oxidation

A

Beta oxidation. Fatty acids diffuse into cells and stimulate acyl CoA to go to mitochondria (via ATP) where it is converted into acetyl CoA (releases e- for e- transport chain) and enters TCA cycle. Stimulated by high glucagon or low insulin levels.

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76
Q

What is cholesterol needed for and how does the body regulate it

A

Needed for bile (biliary salts), cell membranes, steroids hormones, VLDL, Vit D. Absorbed by gut epithelium but can’t be completed metabolised so some gets returned to the lumen and excreted. Can be synthesised and recycled

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77
Q

How is cholesterol synthesised by the body

A

Synthesised in the liver. Acetyl CoA converted into a precursor via enzyme reductase (target for Statins).

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78
Q

How do bile salts act

A

Negative charge (e-) breaks up the lipids. Get modified by bacteria so can’t always be recycled. Can be converted to cholesterol esters and added to VLDL.

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79
Q

LDL

A

Remnants of VLDL made into LDL. Mostly cholesterol and can go to the liver to be broken down or circulate and be absorbed by cells that need cholesterol e.g. for cell membranes.

80
Q

What is diabetes mellitus

A

When blood glucose stays too high for too long.

81
Q

Symptoms of diabetes

A 
Vasculature problems and changes
Blurry vision
Tiredness
Weight changes
Tingling feet
Itchy dry skin (osmotic changes)
Increased thirst and urination
More infections
Slow wound healing
82
Q

Complications of diabetes

A 
Strokes
Heart Problems
Nerve problems
Kidney and renal damage.
Vasculature changes - micro and periphery and local. Can cause strokes and heart problems.
83
Q

Types of diabetes

A

Type 1, 2, gestational, pre-diabetes

84
Q

Type 1 diabetes and treatment

A

Chronic. Genetic function, viral infection. Cells that produce insulin are attacked or not formed right so high blood glucose. Treat by insulin injections and diet/exercise.

85
Q

Type 2 diabetes and treatment

A

Genetic predisposition. Beta cells affect insulin production + insulin resistance and inadequate glucose uptake. Treat by oral hypoglycaemia meds and diet/exercise.

86
Q

Gestational diabetes

A

Due to pregnancy - hormonal changes affecting tissues so they are less responsive to insulin.

87
Q

Pre-diabetes

A

Blood glucose not regulated but symptoms not that severe yet e.g. impaired fasting diabetes or impaired glucose tolerance.

88
Q

Impaired fasting diabetes

A

Blood glucose high - can lead to type 2 diabetes but lifestyle changes can reduce risk.

89
Q

Impaired glucose tolerance.

A

Blood glucose not reduced quickly after a meal. Can cause CVD

90
Q

How to diagnose diabetes

A

Fasting plasma glucose test - measure after fasting for a set time
Glucose tolerance test - Measure increase and drop in blood glucose after eating glucose.
Hb glycated test
Fructose-amine test

91
Q

Glycated Hb test

A

More glucose coating Hb = higher blood glucose. Monitors the effects from last 8-12 weeks

92
Q

Fructose-amine test

A

Same as glycated Hb but broken down faster so measured over 1-2 weeks.

93
Q

What increases hyperglycaemia

A

Steroids, diuretics

94
Q

What increases hypoglycaemia

A

Alcohol, antibacterial, hormone deficiency

95
Q

Drugs for treatment of diabetes

A

Oral hypoglycaemic agents stop glucose production by the liver (gluconeogenesis).
Sulfonylureas - increase the amount of insulin made by the pancreas.

96
Q

How does diabetes affect oral health

A 
Ulcers
Inflamed bleeding /gum disease.
Slower healing
Dry mouth
More infections e.g. oral thrush
97
Q

How does diet/nutrition change in adulthood/older age

A

Need less sugar bc less active and slower metabolism but need same nutrients so need more nutrient dense food.

98
Q

Things that increase cancer risk

A

Diet, environment, drugs, age, gender, genes, lifestyle, host factors e.g. inflammation

99
Q

How does diet and exercise affect cells.

A

Affects cell turnover, epigenetics, cell differentiation, DNA replication, cell cycle, DNA repair, carcinogen metabolism, inflammation and immunity, hormone regulation.

100
Q

Diet/nutrition habits that increase risk of cancer

A

Red meats, processed food, added sugar, gaining weight in adulthood, sedimentary behaviour,

101
Q

Diet/nutrition habits that decrease risk of cancer

A

Fibres, fruit and veg, active, low sugars/nutrient dense food

102
Q

Breastfeeding importance and limitation

A

Provides all the nutrients baby needs and Ig and reduced mum’s chance of breast cancer and the baby’s chance of childhood diabetes and infections. Limitations if cleft palate or metabolism problems or untreated HIV.

103
Q

Changes in nutrition for babies as they grow up

A

Need more energy but less sugar and more nutrients and proteins (girls) and calcium (boys bones)

104
Q

Campaigns to improve diet/nutrition in children

A 
PHE
NHS 5x fruit/veg a day
Sugar tax
British nutritional foundation
Government standards - Ofsted
National healthy school's programme
105
Q

Nutrition definition

A

Sum of the processes of an organism that take and use materials from the environment to sustain it.

106
Q

Non-starch polysaccharides

A

In cell walls of plants. Not broken down by body/not digested but bulks out the food, creates a full feeling, slows down the motility of the chyme, stops constipation and colon cancer. But combines with minerals so can lead to mineral deficiency and gas.

107
Q

Glycaemic index

A

How fast a carb enters the blood as glucose. Low means slow breakdown and gradual release of energy.

108
Q

Types of fats and uses

A

Saturated and unsaturated, transfatty acids (frying, baking) Needed for cell walls, hormones, fat-soluble vitamins.

109
Q

Water importance (general)

A

Needed in most body processes and reactions, lubricant and temperature control. Made by the breakdown of food but too much can cause swelling of organs (change is osmosis)

110
Q

Dimensions of age

A 
Chronological
Biological
Social
Personal
Subjective
111
Q

Age strata vs cohort

A

Cohort is a group born at a set time and grows old together. Strata is people who share similar social rights and duties by age.

112
Q

Theories of ageing

A 
Disengagent theory
Structural dependancy (how they're treated by the system/society)
Cultural gerontology (3rd age after kids and employment)
113
Q

Influences on ageing

A

Genes, environment, diet, lifestyle, mentaility, drugs, illness, level of independence.

114
Q

Common oral health problems caused by ageing

A

Loss of teeth, TSL, breakdown of teeth, gum disease, atrophy of bone and muscles and joints, dry mouth due to meds.

115
Q

Shortened dental arch

A 
20-50yrs = 12
40-80yrs = 10
70+ = 8
116
Q

National care standards 2003

A

Before going into a care facility, members need an assessment of needs. Dental care must be provided and the hygiene and health of the member must be maintained.

117
Q

Uses of cephalogram

A

Assess treatment, diagnosis, treatment planning, measure/predict growth.

118
Q

Aluminium wedge in a cephalogram

A

Collimates the beam so only the bits we need to see are radiated. Allows soft and hard tissues to be seen.

119
Q

Limits of a cephalogram

A

Distortion, magnification and movement during imaging make it not reproducible. 2D

120
Q

Points to identify on a cephalogram

A

Nasopalatal line (anterior and posterior nasal spine)
The most concave bit on anterior of the maxilla and mandible
Incisal point and root point on upper and lower incisors
The lowest point on mandible
The intersection between verticle line of ramus and line of the mandible (at the angle of the mandible)
Pituitary fossa midpoint.
Frontonasal suture

121
Q

Angles to measure on a cephalogram

A

the angle of mandible and maxilla from the base of the cranium.
the angle of incisal teeth from the maxilla /mandible.
Relationship bw maxilla and mandible.

122
Q

How to check mean height on a age:growth chart

A

50th centile

123
Q

Why is there a dip after infancy on the height: age growth chart

A

Start being measured stood up so some compression

124
Q

What is infantile growth dependent on

A

Size and health of the mother
Any chronic illnesses
Genes
The efficiency of feeding via the placenta.

125
Q

Limitations to growth charts

A

Need separate graphs for ethnic minorities
Don’t take into account changes in height per generation
Need to be updated regularly

126
Q

Steps to determining growth problems when treating patients

A

History
Clinical exam
Special/additional tests

127
Q

Details in a growth history when checking for growth problems

A

Social history/parenting
Birth/pregnancy details
Family growth/size details
Any chronic illness

128
Q

Details in a clinical assessment for growth problems

A 
Hanging angle of arms from side
Finger size and spread and crease pattern
Weight
Height
Sexual development
129
Q

Additional tests to check for growth problems

A

Sitting height
Head circumference
Skinfold thickness
Wrist radiograph

130
Q

Velocity growth:age chart vs height:age

A

Better at diagnosing/can do it earlier
More accurate
2 measurements taken 6 months apart

131
Q

Parenting styles

A

Authoritarian (bad)
Authoritative
Permissive
Neglectful/rejecting

132
Q

How is gross status assessed

A 
Measuring change in height
Sexual maturity
Hand-wrist radiographs
Radiographic assessment of cervical spine maturation
Growth velocity
133
Q

Peak height velocity

A

The highest point on growth velocity graph

134
Q

Scammonds curves

A

General (height:age)
Lymphoid (max at ~10yrs)
Genitals
Neural

135
Q

Benefits of measuring standing height and instrument used

A

Non-invasive and easy
Good at measuring current growth state but can predict peak height velocity +/- 6 months.
Uses a stadiometer

136
Q

Hormones that control growth

A 
GH
GHSH
IGH-1
Oestrogen
Androgen
Glucocorticoids
Thyroid hormones
137
Q

Excessive growth disorders

A

Gigantism - excessive GH before growth plate closure
Acromegaly - excessive GH after growth plate closure so no increase in height but bones and other parts can grow and can cause CVD bc enlarged vessels.

138
Q

Growth hormones details

A

Hypothalamus produced GHSH which stimulates the pituitary gland to stimulate GH which stimulates the liver to produce IGF-1. GH and IGF-1 act on bone e.g. chondrocytes differentiation and proliferation.
IGF-1 causes systemic growth and can regulate this system (inhibits hypothalamus secretion of GHSH)

139
Q

Oestrogen’s actions on growth

A

Increases GH secretion. Can play a role in epiphyseal plate closure (height)

140
Q

Androgen’s actions on growth

A

E.g. testosterone. Can be converted into oestrogen and stimulate GH

141
Q

Glucocorticoids

A

Increase GH secretion and affect GHSH. Released when stressed but long-term exposure reduced GH release. In adults can cause osteoporosis and diabetes.

142
Q

GH’s effects on insulin

A

GH causes the release of glucose and breakdown of fat so more Insulin released. But over-time can cause resistance to insulin and diabetes.

143
Q

Thyroid hormones

A

Mostly released pre-puberty and drives IGF-1 synthesis and growth. After puberty, GH takes over and less TH hormone.
Affects chondrocytes and Ob and causes liner growth/height.

144
Q

GH on muscle growth

A

GH acts via IGF-1 = the proliferation of myofibrils. But doesn’t cause hypertrophy so not a performance enhancer.

145
Q

What happens if too much or too little glucose in blood

A

To much = more water moves into blood bc of osmosis so dehydration and death of tissues,
Too little = not enough ATP or glucose for the brain (coma). RBC don’t have enough ATP then can’t carry O2 to cells so cell death.

146
Q

Hormones that regulate blood glucose

A

Insulin (increased if glucose increased)
Glucagon (increased if glucose decreased)
Adrenaline a bit (causes more gluconeogenesis)

147
Q

Main sources of glucose

A

Diet, glycogen and gluconeogenesis. Fatty acid oxidation makes energy but not glucose.

148
Q

Digestion of glucose

A

A-amylase in the mouth breaks down polysaccharides, Amylase from the pancreas breaks down further. Maltase, sucrase, etc break down the disaccharides. Co-transported into epithelial cells and facilitated diffusion into blood.

149
Q

Glycogen

A

Stored in the liver and muscles. Broken down if glucose in the blood is low (stimulated by glucagon)

150
Q

Liver’s role in blood glucose

A

The liver breaks down glycogen into glucose and circulates it into the blood. Controlled by low glucose in blood and hormones

151
Q

Muscle’s roles in blood glucose

A

Stores glycogen and then breaks it down into ATP by anaerobic glycolysis or through TCA cycle. Regulated by ATP or energy demand or adrenaline.

152
Q

Gluoneogenesis

A

Normally only in the liver. Making glucose from non-carb sources using proteins. Lactate, glycerol, ass are a precursor.
Promoted by low blood glucose levels bc low insulin causes aas and glycerol release, and exercise causes lactate and adrenaline.

153
Q

Ketone bodies

A

Made from fatty acids or acetyl CoA in the liver and can be converted into acetyl CoA and enter the TCA cycle. Can also be used to fuel the brain bc cross blood-brain barrier.

154
Q

Where is calcium stored/found in the body

A

99% in bones. In kidneys and blood plasma and ECF

155
Q

Methods of dietary absorption of calcium

A 
Paracellular = through the gap junctions. Most Ca2+ absorbed this way but need a high conc gradient.
Transcellular = through the cell's membranes, active. and needs lots of proteins and only has a low intake.
156
Q

Hormones/molecules involved in calcium homeostasis

A

Parathyroid hormone - chief cells
Calcitonin - parafollicular cells
Vitamin D

157
Q

Parathyroid hormone in calcium homeostasis

A

Made by chief cells. Low calcium in the blood stimulates it and it causes osteolytic osteolysis by targeting Oc which demineralise the bone and release Calcium.
Activates vitamin D

158
Q

Calcitonin in calcium homeostasis

A

Secreted by parafollicular cells in the thyroid. Stimulated by a high conc of calcium in the blood. Increases bone mineralisation so calcium moves out of plasma and into the bones.

159
Q

Vitamin D in calcium homeostasis

A

Activated by parathyroid hormone.
Binds to a DNA transcription molecule and regulates expression of a gene/upregulates genes.
Increases Ca absorption from the lumen by upregulating carrier proteins and making channels/gap junctions more permeable to calcium.
May stimulate Ob and regulate bone turnover and other non-bone functions e.g. in the immune system.

160
Q

Lack of vitamin D’s effects on bones/calcium homeostasis

A

Rickets

Osteomalacia (in bones that have formed) = More radiolucent bones on a radiograph, Psuedo fractures of bones bc of the unmineralised matrix, poor deposition of cementum so PDL doesn’t attach and causes periodontitis.

Weaker, less dense trabeculae - osteoporosis.

On developing teeth = large pulp chamber, enamel hypoplasia.

161
Q

T-score (bones)

A

The density of bones, can be seen on a radiograph. 2 = healthy bones, -4 = osteoporosis.

162
Q

Bone pathogenisis in old people

A

Osteoporosis
Lack of oestrogen (so more activated Oc), lack of vitamin D from sun and Ca2+ from diet = imbalance of bone turnover.
Treat by giving Oc inhibitor and calcium and Vit D.

163
Q

How does exercise affect bone health

A

Increases bone strength in children and reduces the chances of bone pathology when older.

164
Q

Bone function

A

Support and protect organs
Store calcium/calcium homeostasis
Bone marrow where stem cells and blood cells made
Allows movement by attaching to ligaments and muscles.

165
Q

Bone types

A

Trabecular (from lamellar)
Cortical - irregular overlapping Haversions systems.
Woven bone - formed quickly during rapid growth/repair.

166
Q

Cells in bone and their function

A

Ob for bone matrix formation/mineralisation
Trapped Ob in mineralised bone matrix = osteocytes. Channels made to communicate w each other and blood vessels and allow nutrients in.
Oc to breakdown matrix
Bone lining cells
Osteoprogenitor/stromal cells.

167
Q

How is bone remodeled and the stages

A

Resorption stage = 3 weeks. Bone lining cells breakdown and expose some of the ECM. Oc breakdown and demineralise the ECM using enzymes and create resorption pits and then die after 3 weeks.
Bone formation = 3-4 months. Ob comes in and secrete ECM and then it gets mineralised and trapped Ob become osteocytes. Bone lining cells line it.

168
Q

Types of bone formation methods

A

Intramembranous ossification

Endochondral ossification

169
Q

Intramembranous ossification mechanism

A

Stem cells/ectomesenchyme/mesenchyme differentiate into Ob cells.
Ob lay down ECM (osteoid) in fibres and then minerals put down on it. Mineralised strands = trabecula. Layers of the osteoid = lamella. Trabecula joins together to make woven bone or fill in completely to make compact/cortical bone.

170
Q

IMO bone examples

A

Bones of head and face and clavicle.

171
Q

Defects of IMO example

A

Cleidocranial Dysostosis = Small or no clavicle
Malocclusion severe
Missing or deformed teeth
Cleft palate/high arched palate

Defect in the gene needed for stem cells to differentiate into Ob.

172
Q

Endochondral ossification mechanisms

A

Stem cells/ectomesenchyme/mesenchyme differentiate into chondroblasts and then chondrocytes.
Make the cartilage precursor of bone (hyaline). Chondrocytes undergo hypertrophy and signal released into the matrix to allow blood vessels to grow into collagen, bringing Ob and Oc.
Mineralisation and more vascular and hyaline cartilage remodelled into the woven bone.

173
Q

ECO bone examples and defects

A

All other bones apart from head and face and clavicle.

174
Q

Epiphyseal growth plate

A

Chrondocytes proliferate and get more ECM. Cells become hypertrophic and dissolve the matrix and begin to mineralise it and produce signals for blood vessels to grow. Cartilage matrix is mineralised and chondrocytes die by apoptosis and new bone produced on mineralised cartilage.

175
Q

Mechanisms of bone healing

A

Inflammation at site of impact. Dead bone material is removed by Oc. IMO at periosteum to make lamellar bone and ECO to reform the cartilage.

176
Q

Defects of ECO

A

Dwarfism/achondroplasia = (small limbs) and class 3 malocclusion.

177
Q

Mechanisms of tissue growth

A

Interstitial growth

Appositional/direct growth

178
Q

Interstitial growth

A

Cells proliferating or growing e.g. hyperplasia or hypertrophy. For soft tissues, cartilages, synchondroses, sutures.

179
Q

Direct growth/apposition growth

A

In layers - bone added to the surface by Ob or removed from the surface by Oc.

180
Q

In fully formed bones, how can they grow

A

Only by appositional growth at the periosteum = periosteal apposition (inc sutural deposition)

181
Q

Theories for the mechanisms of tissue growth

A

Sutural directed growth
Cartilage directed growth
Functional matrix theory

182
Q

Sutural directed growth

A

Disproven - sutures aren’t centres of growth but lots of growth can happen here, induced by soft tissue growth.

183
Q

Cartilage directed growth

A

E.g. at synchondroses. Growing cartilage can be replaced by bone ECO. Evidence e.g. transplanted cartilages can grow.

184
Q

Functional matrix theory

A

Bone growth is in response to surrounding tissue growth.

185
Q

What is a synchondrose and examples

A

An immovable joint between 2 bones, surrounded by cartilage, e.g. spheno-occipital (posterior, lengthens the skull) and sphenoethmoidal - at the base of the cranium.

186
Q

How does the maxilla grow

A

Surface and sutural deposition (inc at tuberosity) and growth translation and modelling (drift) - the surface is remodelling in the opposite direction to where the bone is being translated. Moves down and forwards and some rotation.

187
Q

How does the mandible grow

A

In length by cartilage replacement (resorption and apposition).

188
Q

How does the angular relationship bw the maxilla and mandible change w age.

A

Some structures don’t change e.g. retromolar region where ID canal is. Changes are due to surface apposition.

189
Q

Soft tissue growth

A

Forward and downward face growth. The nose grows down and forwards (independent of skeletal classification). Lips grow in length.

190
Q

Eating disorders can be predisposed by ..?

A

Genetics, other mental health conditions e.g. anxiety, depression, OCD, substance abuse, social and family life, bullying.

191
Q

Types of eating disorders

A

Orthorexia Nervosa, Anorexia Nervosa, Bulimia Nervosa, BED

192
Q

Orthorexia Nervosa

A

Obsession w eating healthy/clean foods and pressuring other people. Clinical signs = malnutrition e.g. angular cheilitis, weak immune system, fatigue.

193
Q

Anorexia Nervosa

A

Body image problem. Rapid weight loss, withdrawal, clinical signs = malnourished, dehydrated, weak immune system (gum disease), fatigue and can lead to cardiac problems and affects puberty and fertility.
Management = watch out for clinical emergencies, pear drops for halitosis, saliva substitutes.

194
Q

Bulimia Nervosa

A

Binge eating and purging. Clinical signs = malnourished, dehydrated, cardiac problems, colon problems bc of laxatives, acid in oesophagus and mouth (erosion, ulcers), caries, swollen parotid, acne. Manage by prevention (F-, fissure sealant) and prepare for medical emergencies.

195
Q

Binge-eating disorder

A

Binge-eating without the purging. Can lead to obesity and diabetes, signs of weight gain, bad skin, caries.

196
Q

Models of disability

A

Medical model - what they can’t do/what’s wrong w them.
Individual model - similar to medical.
Social model - society is disabling, stops them doing stuff.
Biopsychosocial model - WHO definition of disability.

GDAN (3 decks)

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