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Block 1 > CTB > Flashcards

CTB Flashcards

1
Q

List the Macronutrients

A

Carbohydrates
Lipids (fats)
Proteins

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2
Q

What are the Functions of Macronutrients in Health?

A

Provide us with energy

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3
Q

What is Malnutrition?

A

When a person’s diet does not provide enough nutrient (starvation) or the right balance of nutrients for good health

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4
Q

List the Common Micronutrients

A

Vitamins, Minerals

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5
Q

List the Common Vitamins and their Functions in Health

A 
A - Eyesight, Growth, Immunity
B - Carbohydrate, Fatty Acid, Protein metabolism, Nucleic Acid Synthesis
C - Cartilage and bone
D - Calcium and phosphate metabolism
E - Antioxidant
K - Vegetables, fruit
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6
Q

List the Common Minerals and Their Functions in Health

A

Iron - Component of Haemoglobin for O2 transport
Calcium - Bones and Teeth, Nerve, and Muscle Function
Zinc - Enzymes, Immunity
Magnesium - Metabolism, Nerve and Muscle function
Potassium - Fluid Balance, Nerve and Muscle function

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7
Q

What is the Theoretical Energy Content Of the Macronutrients?

A

Carbohydrates - 4kcal
Lipids - 9kcal
Proteins - 5kcal

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8
Q

What percentage energy intake do each of the Macronutrients account for?

A

Carbohydrates - 50 - 75%
Lipids- 15 - 30%
Proteins - 10 - 20%

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9
Q

What is meant by the Thermic Effect of Food?

A

The energy used obtaining energy from food.

  • About 10% for Carbs and Lipids
  • About 20% for Proteins
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10
Q

What is Energy Balance?

A

Difference in energy intake and energy expenditure + Difference in Energy Stores

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11
Q

What is meant by Basal Metabolism?

A

Energy Required to keep your body functioning at rest

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12
Q

Factors affecting Basal Metabolic Rate (BMR)

A

Size (height + weight), Body Composition, Age, Climate, Hormones, illness, Drugs, Malnutrition

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13
Q

Describe Carbohydrate storage

  • Molecule
  • Store Size
  • Storage site
A
  • Gycogen
  • Small
  • Liver, Muscle
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14
Q

Describe Lipid storage

  • Molecule
  • Store Size
  • Storage site
A
  • Triglycerides
  • Moderate - Large (Unlimited)
  • Adipose
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15
Q

Describe Protein storage

  • Molecule
  • Store Size
  • Storage site
A
  • Protein
  • Moderate (Limited)
  • Muscles (plus others)
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16
Q

What Cells is the Oesophagus lined with?

A

Stratified Squamous Epithelial Cells

Protection

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17
Q

What are the major functional differences between cilia and microvilli? 2

A

Cilia are motile and facilitate the transport of substances

Microvilli are non-motile and increase the surface area of the epithelium.

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18
Q

What is the role of tight junctions in cellular transport?

A

Prevent paracellular transport of molecules (water and ions). Also prevent migration of membrane proteins to allow specialised functions of surfaces to be preserved

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19
Q

What are Desmosomes?

A

A type of Cell Junction. Occurs between adjacent cells to provide strong cell-to-cell adhesion.
- Via cadherin attachment to intracellular keratin filaments in cytoskeleton.

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20
Q

What are Gap Junctions made up of?

A

Connexons, Each of which consists 6 connexin proteins

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21
Q

What are Tight Junctions?

What are they made up of?

A

Junctions between adjacent cells to separate the apical from the basolateral membranes.
Made up of Occludins and Claudins - Membrane proteins as well as associated cytoplasmic proteins. Adherens Junctions found below

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22
Q

What is an endocrine gland?

A

A gland which is involved in secreting its products directly into the bloodstream.
E.g. Thyroid gland

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23
Q

What is an exocrine gland?

A

Gland which secretes its secretions into a duct which then empties onto an epithelial surface.
E.g. Salivary glands

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24
Q

Difference between Stereocilia and Cilia

A
  • Stereocilia are non-motile mechanoreceptors. Cilia are motile and facilitate fluid movement across epithelium.
  • Stereocilia found in inner ear
  • Cilia found in Trachea
  • Both contain actin (similarity)
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25
Q

What Cell Types are found in the Kidney?

Where?

A
  • Tubules - Simple Cuboidal

- Glomeruli - Simple Squamous

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26
Q

What is Endocrinology?

A

Science of the structure and function of the endocrine glands, and the diagnosis and treatment of disorders of the endocrine system.

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27
Q

List the Endocrine Organs

A

Hypothalamus, Pituitary gland, Parathyroid glands, Adrenal glands, Thyroid gland, Pancreas, Ovaries, Testes

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28
Q

List Main Hormones

A

Peptides, Amines, Steroids, Thyroid Hormones (Technically peptides)

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29
Q

Describe Synthesis of Peptide Hormones

A

Water-soluble
Transcribed - Translated on rER - Processing rER - Packaging Golgi into Secretory Vesicles - Ready for Exocytosis when stimulated.
Rapid Action - Seconds

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30
Q

Describe Synthesis of Steroid Hormones

A

Derived from Cholesterol, Are synthesised upon stimulation, no store. Lipid Soluble.
- Hydrolysis of esters and release of cholesterol - Conversion of cholesterol to pregnenolone (in the mitochondria) - Processing in smooth ER - Diffusion out of cell.
Hours to Days Action

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31
Q

Describe the Action of Lipid-Soluble Hormones

A
  • Diffuse through bilayer
  • Binds to and activates intracellular receptor
  • Hormone-Receptor Complex Alters Gene expression
  • Transcription and Protein Synthesis
  • Protein alters cell’s activity
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32
Q

Describe the Action of Water-Soluble Hormones

A
  • Binds cell surface Receptor (G-protein coupled receptor/Tyrosine Kinase Receptor)
  • Generate/Inhibit production of signalling molecules e.g. cAMP/IP3.
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33
Q

What is Positive Feedback?

A

Output enhances original stimulus

  • Coagulation cascade
  • Ovulation
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34
Q

What is Negative Feedback?

A

Output reduced the original stimulus

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35
Q

What are the differences between Releasing Hormone, Tropic Hormone, Effector Hormone?

A
  • Releasing Hormone - Released by hypothalamus into portal veins act upon anterior pituitary
  • Tropic Hormone - Affects other endocrine glands
  • Effector Hormone - Affects target cells
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36
Q

What is Addison’s disease (Hypoadrenalism)?

A

Caused by deficiencies of glucocorticoids, mineralocorticoid e.g. aldosterone, and sex hormones.

  • Caused by primary defect
  • Signs + Symptoms - Weight loss, weakness, postural dizziness, confusion, hyperpigmentation
  • Treatment - Lifelong oral steroid replacement.
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37
Q

What is Cushing’s Syndrome

A

Clinical manifestation of excessive glucocorticoid e.g. cortisol production.

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38
Q

Compare Primary + Secondary Endocrine Dysfunction

A
  • Primary - Too much/too little of effector hormone produced by endocrine gland
  • Secondary - Over/Under-Stimulation of endocrine organ by tropic hormones
39
Q

State 5 Functions of Saliva

A
  • Begins Starch Digestion - Alpha-amylase
  • Lubricates food for swallowing
  • Helps Taste
  • Protects oral environment - Cools hot food
  • Washes away bacteria and food particles
  • Destroy bacteria
  • Maintain alkaline environment
40
Q

State Composition of Saliva

A
  • Water
  • High K+, HCO3-, Ca2+ Concentration
  • Low Na+ and Cl- Concentration
  • Mucous
  • Digestive enzymes
  • Antibacterial agents
41
Q

Associated signs and symptoms of Xerostomia (Dry Mouth)

A
  • Dry and painful throat + Tongue roughness
  • Dry cracked lips
  • Difficulty swallowing and speaking
  • Altered taste
  • Burning/scalding sensation in mouth
  • Halitosis
  • Dental caries and periodontal disease
  • Signs of oral infections e.g. candidiasis
42
Q

Causes of Dysphagia

A
  • Oesophageal stricture - Benign
  • Oesophageal stricture - Malignant
  • Foreign Body in oesophagus - Obstruction
  • Oesophageal web
  • External compression of oesophagus, e.g. mediastinal lymph nodes, lung cancer, goitre
43
Q

Patient suffered stroke, Why did Dr make her nil by mouth?

A

Strokes are often associated with dysphagia and patient may therefore be at risk of aspiration.
- NICE recommends must have swallow screened within 4 hours of admission of suspected stroke before being given food, fluid, medication.

44
Q

Outline Functions of the Stomach (5)

A
  • Store food
  • Minimise ingestion of bacteria
  • Dissolve and partially digest food molecules
  • Regulate rate of chyme emptying into small intestine
  • Secrete intrinsic factor
45
Q

What are the main components of Gastric Juice?

A
  • Enzymes
  • Intrinsic Factor
  • Mucous
  • Hydrochloric Acid
46
Q

Where is the Gastric Enzyme Precursor Pepsinogen secreted from?

A

Chief Cell

47
Q

Where is the Gastric HCl secreted from?

A

Parietal Cell

48
Q

Where is Intrinsic Factor secreted from?

What is its function?

A

Parietal Cells in Gastric Glands

- B12 Absorption

49
Q

Where is Gastric Mucus Secreted from?

What is it made up of?

A
  • Surface and Neck Mucus Cells in Gastric Glands
  • Glycoproteins and Glycopolysaccharides
  • Forms Gastric Mucosa
50
Q

What Stimulates Gastric Secretion? 3

A
  • Gastrin
  • Acetylcholine
  • Histamine
51
Q

What inhibits Gastric Secretion?

A
  • Prostaglandins E2 and I2
  • Somatostatin
  • Intestinal Hormones
52
Q

What is the function of Brunner’s glands

A

Branched tubuloalveolar glands. Produce alkaline proteins that help counteract the acid in chyme coming from stomach

53
Q

Which glands are primarily responsible for secreting lingual lipase?

A

Von Ebner’s Glands

54
Q

What vitamin plays a role in blood clotting/bruising

A

Vitamin K

55
Q

What type of epithelium is found in the nasal cavity?

A

Pseudostratified columnar

56
Q

What does the Small Intestine Secrete?

A
  • Mucus
  • Water
  • Intestinal Hormones
57
Q

What is the Role of the Intestinal Hormone Motilin?

A

Stimulates Migrating Motor Complexes (MMCs) via Enteric and Autonomic NS to sweep GI tract of any debris

58
Q

What is the role of Vasoactive Intestinal Peptide?

A

Intestinal Hormone - Increases blood flow to GI Tract

59
Q

What is the Role of Gastric Inhibitory Peptide (GIP)

A

Intestinal Hormone - Inhibits gastric secretion and stimulates insulin secretion

60
Q

What Do Cholecystokinin (CCK) and Secretin Do?

A
  • Inhibit gastric motility and secretion
  • Control Pancreatic and Biliary secretion
    Secretin stimulates pancreas to secrete bicarbonate + stimulates liver to release BILE into gallbladder
    CCK stimulates pancreas to release digestive enzymes and stimulates gallbladder to contract and release bile into hepatopancreatic ampulla/major duodenal papilla
61
Q

What are the Exocrine secretions of the pancreas? What cells are they secreted from

A 
Digestive Enzymes (Trypsin, Chymotrypsin, Carboxypeptidase) - Acinar cells
Alkali (Rich in bicarbonate), Neutralises duodenal contents - Duct cells
62
Q

What are Brunner’s Glands? Found where?

A

Brunner’s glands are found in the Duodenal Mucosal layer and function to secrete alkali/mucus into the duodenal lumen to neutralise chyme

63
Q

What Digestive Enzymes does the Pancreas secrete?

A
  • Trypsin (endopeptidase)
  • Chymotrypsin (endopeptidase)
  • Carboxypeptidase (ectopeptidase)
  • Pancreatic Amylase
  • Lipases
  • Other enzymes
64
Q

Why are Peptidases in Stomach and Small Intestine Lumen Secreted as precursors?

A
  • As they would digest the contents of cells synthesising them if not inactive until they reach the lumen
65
Q

How are Pancreatic Enzyme Precursors activated?

A
  • Membrane-bound Enterokinase in the Duodenum Cleaves Trypsinogen into Trypsin. Trypsin then cleaves the rest of the inactive enzymes to their active state
66
Q

What is the Mechanism of HCO3- From Pancreatic Duct Cells

A

H+ pumped out of duct cells and released into blood.
HCO3- secreted into the duct lumen.
Opposite of stomach Parietal Cells

67
Q

How is Pancreatic ALKALI Secretion Controlled?

A
  • Via Intestinal Hormone Secretin

- Potentiated by CCK / ACh (Can’t alone)

68
Q

How is Pancreatic ENZYME Secretion Controlled?

A

Agonists

  • Intestinal hormone Cholecystokinin
  • Neurotransmitter Acetylcholine (vagus nerve)
69
Q

Describe Fat Emulsification in Small Intestine

A
  • Fats emulsified by bile salts and phospholipids secreted by liver.
    Form emulsion droplets, polar molecules which cluster around polar molecules. Polar ends out Non-polar ends towards lipid product.
    Makes them soluble in order to interact with enzymes in the Small intestine and provides a large surface area.
70
Q

Describe Fat Digestion in the Small Intestine

A

Fats are emulsified by bile salts and phospholipids.

Triglycerides digested by pancreatic lipase to monoglycerides and free fatty acids. Products are held in micelles.

71
Q

What are Micelles?

A

Micelles are small lipid containing molecules. Formed by polar molecules surrounding fatty acids/monoglycerides/fat soluble vitamins/minerals.

72
Q

Describe Fat Absorption

A

Micelles diffuse into an ‘unstirred later’ next to surface of intestinal epithelial cells. Fatty acids and monoglycerides then diffuse across cell membrane. Micelle is not absorbed, breaks down spontaneously. Once in cell are reassembled into triglycerides. Packaged into chylomicrons and exported across basolateral membrane via its lymph vessel. Eventually join circulation via lymphatic system

73
Q

Describe digestion of Starch (2/3 Carbohydrate intake)

A

Starch - Salivary amylase begins process in the mouth.
Pancreatic amylase continues in small intestine; produces maltose and short branched chains of glucose which alpha-glycosidase releases free glucose. / Disaccharide Maltose by Brush border enzyme Maltase

74
Q

Describe digestion of Sucrose and Lactose (1/3 Carbohydrate intake)

A

Digestion of disaccharides: By brush border enzymes: Maltase, Sucrase, Lactase. Products are Glucose, Galactose, Fructose Monosaccharides

75
Q

Describe the Absorption of Carbohydrates / Monosaccharides

A

Across the intestinal epithelial cells (enterocytes) by specific membrane transporters.

  • Fructose enters by facilitated diffusion (GLUT5)
  • Glucose and Fructose enter by secondary active transport via Na+ /Glucose Co-Transporter (SGLT1). Conc gradient maintained by K+/Na+ ATPase on basolateral
  • Then diffuse across cell to basolateral membrane and exit via facilitated diffusion GLUT2 Transporter.
76
Q

Describe Protein Digestion

A

Stomach Pepsin - Polypeptides
Small Intestine Trypsin, Chymotrypsin, and Carboxypeptidase break down into tri/di-peptides
Peptide fragments digested by dipeptidase and amino peptidase on brush border of Small Intestine epithelial cells.
= Tripeptides, dipeptides and free amino acids

77
Q

Describe Protein Absorption

A
  • Absorption of free amino acids - Across intestinal epithelial cell via various specific Na+ co-transporters
  • Absorption of tripeptides and dipeptides, enter via H+ co-transport. Most are hydrolysed by cytosolic peptidase and exit as amino acids via facilitated diffusion. Separate transporters for different types of amino acids
78
Q

Describe Mechanisms of Ca2+ absorption

A

Only small fraction of intake absorbed.
Moves down conc gradient through calcium channel in luminal membrane of small intestine. Inside cytosol is bound reversibly to calbindin (correlates with how much Calcium cell can absorb). Basolateral membrane 2 transporters Calcium ATPase and Sodium/Calcium Exchanger Transporting against conc gradient into blood

79
Q

How does Vitamin D3 regulate Calcium Absorption (2)

A
  • Increasing action of Calcium ATPase

- Increasing levels of calbindin

80
Q

What are the forms of dietary iron?

A

Haem Iron

Free Iron

81
Q

How is Dietary Haem Iron Absorbed?

A

Absorbed by Receptor-mediated endocytosis then digested to release Fe3+
Fe3+ reduced to Fe2+
Portion bound to ferritin (intracellular storage pool)
Rest exits via transmembrane protein Ferroportin 1

82
Q

How is Dietary Free Iron (Fe3+) Absorbed?

A

Fe3+ reduced to Fe2+ by membrane ferrireductase (FR)
Fe2+ crosses membrane via divalent metal transporter 1 (DMT1)
Portion bound to ferritin (intracellular storage pool)
Rest exits via transmembrane protein ferroportin 1

83
Q

Describe Regulation of Iron Absorption

A
  • Portion Iron in enterocyte taken up into intracellular storage pool bound to ferritin, limits amount of iron absorbed into blood.
  • Lost from body in faeces when intestinal mucosa is sloughed into intestine (fast cell turnover).
  • Iron depletion unregulated ferroportin-1 on basolateral membrane. = More uptake into blood
  • Needed during haemorrhages
84
Q

Describe generally Vitamin Absorption, Fat-soluble and Water-soluble

A

Fat soluble vitamins (A, D, E, K) follow pathway for fat absorption
Water soluble vitamins are absorbed by diffusion, facilitated or active transport
B12 absorption by special mediated transport system

85
Q

Describe Vitamin B12 Absorption

A

Released in stomach via Pepsin and acid.
immediately bound to R protein (secreted by salivary glands and stomach). Complex enters duodenum. B12 released and binds Intrinsic Factor. In terminal ileum, Vitamin B12-IF complex absorbed by receptor-mediated endocytosis

86
Q

Name the cell type and location that released intrinsic factor

A

Intrinsic factor released by Parietal Cells of gastric glands of stomach

87
Q

Name of Condition resulting from impaired uptake of Vitamin B12 due to lack of Intrinsic Factor

A

Pernicious Anaemia

88
Q

Why does pernicious anaemia develop?

A

Vitamin B12 is required for the maturation of red blood cells. Deficiency results in deficiency in red blood cells

89
Q

What is Coeliac Disease

A

Defects in absorption of fat and lactose hydrolysis. Lining of intestine becomes sensitive to gluten, resultant damage to mucosa renders unable to absorb especially fats.

90
Q

Explain Lactose Intolerance + Symptoms

A
  • Mild discomfort to severe diarrhoea
  • Lactase deficiency usually as a result of decline over life. Resulting difficulty metabolising lactose.
    Remains in lumen into large intestine. Digested by intestinal bacteria into monosaccharides. No transporter, glucose and galactose digested further (produces gas), fermentation products cause fluid movement across wall into lumen by osmosis causing diarrhoea
91
Q

Symptoms of Malabsorption

A
  • Weight loss
  • Abdominal distension
  • Steatorrhoea (pale, bulky, malodorous stool, float)
  • Diarrhoea
  • Pernicious Anaemia
  • Hypochromic Anaemia
92
Q

How does excessive vomiting affect acid-base balance in the digestive process?

A
  • Leads to large losses of secreted acids from body

- May result in metabolic alkalosis

93
Q

How does diarrhoea affect acid-base balance in the digestive process?

A

Excessive loss of fluid (hence also NaHCO3) in faeces

- May result in metabolic acidosis

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