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opt module d Flashcards

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1
Q

essential nutrients are grouped into

A

minerals
vitamins
amino acids
fatty acids

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2
Q

what is a nutrient

A

A nutrient is any chemical substance that can be used by the human body

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3
Q

examples of minerals

A

phosphorus, calcium, magnesium, iron.

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4
Q

examples of vitamins

A

A,C,D,K

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5
Q

examples of amino acids

A

histidine, tryptophan and others.

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6
Q

examples of fatty acids

A

certain omega-3 and omega-6 fatty acids

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7
Q

malnutrition can be cauesd by

A

an imbalance
an excess of nutrients

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8
Q

protein deficiency is

A

kwashikor

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9
Q

why do you need omega 3

A

controlling blood clotting and building cell membranes in the brain

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10
Q

why do you need omega 6

A

lower ldl (bad cholesterol) and reduce inflammation. protective against heart disease

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11
Q

omega 3: alpha linolenic acid

A
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12
Q

omega 6: linoleic acid

A
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13
Q

where is omega 3 fatty acids found

A

fatty fish (such as salmon); some vegetable oils, such as soybean, rapeseed, flaxseed; and in Brussels sprouts, kale, spinach, walnuts.

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14
Q

where are omega 6 fatty acids found

A

in safflower, corn, cottonseed, and soybean oils.

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15
Q

living organisms proteins synthesis requires how many different L-aminoa cids

A

20

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16
Q

the nine essential amino acids humans cant synthesise are:

A

phenylalanine, valine, threonine, tryptophan, methionine, leucine, isoleucine, lysine, and histidine.

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17
Q

when can tyrosine be synthesised

A

phenylalanine is present in the diet.

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18
Q

what cant be synthesised by ifnants

A

arginine

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19
Q

what are the two conditionally essential amino acids

A

tyrosine and arginine

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20
Q

roles of aminoa cids

A

behaviour
protein synthesis
pH balance
appetite
lactation
stress response
metabolic regulation
endocrine status
proteins egradation
rna and DNA synthesis
osmoregulation

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21
Q

waht is iodine needed for

A

synthesis of thyroid hormones

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22
Q

thyroid hormones neeed for

A

can increase basal metabolic rate, affect protein synthesis, and help regulate long bone growth (in combination with growth hormone) and maturation of neurones. An iodine deficiency, which is quite common in areas where there is no or very little iodine in the diet, can result in goitre and severe retardation in children

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23
Q

calcium and phosphorus are necessary for what

A

formation of bones and teeth Calcium is also necessary for muscle contraction.

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24
Q

Sodium and potassium are involved in the propagation of the

A

nerve impulse.

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25
Q

vitamins cannot be synthesis and must thergroe be

A

incouded in the diet

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26
Q

vitamins are divided into

A

water and fat soluble

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27
Q

fat solubl evitamins

A

retinol
Cholecalciferol(D3), Ergocalciferol (D2)
tocopherols
phylloquinone

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28
Q

water solbule vitamins

A

thiamine
cyanocobalamin
riboflavin
niacin
pyridoxine
bitoin
folic acid
ascorbic acid

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29
Q

what controls appetite

A

the appetite control centre in the hypthalamus

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30
Q

when the stomach is empty, what is released

A

ghrelin

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31
Q

what does ghrelin do

A

stimulate appetite

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32
Q

what inhibits appetite

A

When food is ingested, the release of peptide PYY3-36 from the small intestine (along with insulin from the pancreas and leptin from adipose tissue) inhibit appetite.

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33
Q

danger of overeating

A

elevated blood sugar levels
obesity
diabetes

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34
Q

bmi formula

A

mass / height squared

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35
Q

type II diabetes

A

In individuals with this condition the beta cells in the pancreas still produce insulin. However, these patients develop insulin resistance, which means that the insulin receptors on the cells are no longer stimulated by insulin.

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36
Q

causes of type II diabetes

A

High levels of fatty acids in the blood as a result of diets high in fat but low in fibre.
Overweight, especially obesity, associated with a lack of exercise.
Genetic makeup that influences fat metabolism.

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37
Q

symptoms of type II diabetes

A

Increased (elevated) glucose levels in the blood and urine.
Frequent need to urinate (may lead to excessive thirst).
Tiredness and fatigue.
Some loss of weight.

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38
Q

what is CHD

A

Coronary heart disease (CHD) is a disease in which a substance called plaque builds up inside the coronary arteries. These arteries supply blood with oxygen to the heart muscle.

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39
Q

waht is catabolysis

A

The loss of muscle and adipose tissue mass is caused by the body’s need for caloric intake and to protect the vital systems such as the nervous system and heart muscle. The body breaks down muscles and lipids to generate energy and amino acids. This process is known as catabolysis.

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40
Q

what does anorexia lead ot

A

electrolyte imbalance, skeletal and heart muscle reduction, reduced blood pressure and a slower heart rate. The body can become covered in a fine growth of thin hair. In female patients it can also lead to reduced or absence of menstrual cycles. Extreme cases can lead to death.

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41
Q

vitamin c is also known as

A

l-ascorbic acid

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42
Q

vitamin c is needed for

A

production of collagen

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43
Q

Vitamin C cannot be synthesised by some animals because

A

they have a mutation in the GLO gene which codes for an enzyme that is needed for the last step in the synthesis of L-Ascorbic acid.

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44
Q

what can vitamin d deficinecy cause

A

scurvy

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45
Q

symptoms of scurvy

A

Bleeding gums, gingivitis or loose teeth. Vitamin C is necessary for the synthesis of collagen, which builds and maintains tissue.
Lack of energy. Loss of weight and extreme fatigue.
Mood swings or depression. Irritability and rapid changes in mood may indicate a severe deficiency. Depression is common.
Chronic joint pain. Bleeding in the joints causes constant pain.
Suppressed immune system. Frequent diseases.
Slow wound healing and bruising. Bruising occurs easily and wounds take a long time to heal.

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46
Q

what falsified earlier theories that scurvy was specific to humans

A

1907 study by two norweigan scientists

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47
Q

rda of vitamin c for humans

A

50mg/day

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48
Q

how does pku come about

A

A gene coding for phenylalanine hydroxylase, an enzyme that catalyses the hydroxylation of phenylalanine to tyrosine, is mutated. This results in the inability to convert phenylalanine into tyrosine. As the enzyme can no longer catalyse the last and rate limiting step, phenylalanine accumulates in the body.

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49
Q

how is pku inherited

A

an autosomal recessive trait

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50
Q

consequencces of pku

A

Intellectual disability
Reduced growth of the head
Lack of skin and hair pigmentation
Seizures

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51
Q

waht does the guthrie test test for

A

pku

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52
Q

when does pku need to be deteted and diagnosed

A

within 24 hours of birth, whilst its phenylalanine and tyrosine levels in the infant are normal as a result of the normal metabolism of its mother.

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53
Q

waht can pku children not eat

A

artificial sweetner aspartame

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54
Q

treatment of pku

A

maintain a diet low in phenylalanine

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55
Q

high phenylalanine foods

A

fish
dairy
meat
wheat

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56
Q

low phenylalanine foods

A

most vegetables
most fruit
special breads

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57
Q

why is vitamin d needed

A

absorption of calcium in the digestive system

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58
Q

calcium deficiency

A

This condition is known as osteomalacia in adults (milder condition) or rickets in children (more serious condition)

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59
Q

Two of the most important roles of vitamin D are to

A

maintain skeletal calcium balance by promoting calcium absorption in the intestines and maintaining calcium and phosphate levels for bone formation. In breastfeeding mothers whose vitamin D intake is low, this can cause problems with the bone mineralisation of their infants.

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60
Q

where is vitamin d found

A

in foods such as oily fish, particularly salmon, herring and tuna; egg yolk; liver; and dairy products including milk, cheese and butter.

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61
Q

what is unique about cvitamin d

A

it can be synthesised by the body when skin is exposed to wavelengths of 290-310

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62
Q

waht is cholesterol the precursor of

A

bile acids, vitamin d and steroid hormones such as progesterone and oestrogen

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63
Q

waht is cholesterol in the blood an indicator of the risk of

A

coronary heart disease

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64
Q

which type of cholesterol is associated with an increased risk of developing chd

A

cholesterol contained in ldl

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65
Q

stains

A

a class of drugs used to lower cholesterol levels

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66
Q

how to calculate energy content in food

A

The energy content in foods can be measured by burning a known mass of the food to test. The burning food is placed under the test tube with water. The heat liberated by the burning food is absorbed by a known volume of water. The rise in temperature is recorded (Figure 4). The energy value is calculated as temperature rise × mass of water × specific heat capacity of water (4.184 joules/gºC or 1 calorie/gºC).

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67
Q

the nervous control is mainly prodvided by

A

the autonomic nervous system

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68
Q

what is the autonomic nervous system divied into

A

sympathetic and parasympathetic nervous systems

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69
Q

what does the sympathetic nervous system control

A

responses to danger

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70
Q

what does teh parasympathetic system control

A

homeostasis and processes related to rest and digestion

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71
Q

when does the parasympathetic and sympathetic system speed up and slow doewn

A

The parasympathetic system speeds up digestion when food is ingested, while the sympathetic slows it down when there is no food available.

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72
Q

what are the hormones involved in the chemical control of digestion

A

gastrin
secretin
cholecystokinin

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73
Q

what produces gastrin

A

g cells in the stomach, duodenum and pancreas, in response to physical stimulation due to the presence of food

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74
Q

what happens when gastrin is released

A

it stimulates the production of gastric juice by the parietal cells in the gastric glands

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75
Q

what does gastric juice contain

A

a mixture of water, hydrochloric acid and other inorganic ions, enzymes (pepsin, rennin), mucus, various polypeptides, and intrinsic factor.

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76
Q

what is intrinisc factor necessary for

A

absorbing vitamin b12

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77
Q

when does secretion mof gastric juice stop

A

when there are 1-5l

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78
Q

what produces secretin

A

produced by special cells in the small intestine in response to the presence of acid fluid.

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79
Q

what does the presence of gastric acid do

A

activates prosecretin into secretin.

it stimulates the production of alkali by the pancreas, neutralising the intestinal components.

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80
Q

when does production of pancreatic juice stop

A

whn the pH of the intestine reaches 8 and it is stopped by negative feedback

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81
Q

what does secretin do

A

plays a role in osmoregulation as it regulates water homeostasis throughout the body by acting on the kidney, hypothalamus and pituitary gland.

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82
Q

what produces cholecystokinin

A

small intestine

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83
Q

what does cholecystokinin do

A

It controls the release of pancreatic juice from the pancreas and bile from the gall bladder (bile is produced in the liver and stored in the gall bladder). It also acts as a hunger suppressor.

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84
Q

what is somatostatin

A

an inhibitory hormone secreted by special cells in the stomach, duodenum and pancreas.

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85
Q

what does somatostain do

A

It also acts indirectly by preventing the release of gastrin, CCK and secretin, thus slowing down the digestive process

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86
Q

how does somatostatin travel

A

This hormone travels through blood to directly inhibit acid producing cells

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87
Q

In addition, a regulatory feedback mechanism exists whereby the presence of acid in the lumen of the stomach stimulates ____________ secretion, which in turn slows down acid secretion.

A

somatostatin

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88
Q

what do exocrine glands have

A

ducts that carry their secretory product to the surface of the body or the lumen of the gut.

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89
Q

what produces the hydrogen and chloride ions for stomach ions

A

epithelial/paritetal cells of the stomach lining

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90
Q

development of exocrine gland

A
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91
Q

what is The release of hydrogen ions through protein carriers is coupled with

A

to the intake of potassium ions (K+) from the lumen of the stomach. This process requires energy in the form of ATP

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92
Q

what does pepsin do

A

hydrolyse proteins to peptides

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93
Q

where is pepsin found

A

in the stomach in an inactive form as the pro enzyme pepsinogen

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94
Q

pepsinogen is released by the ??? in the lining of the stomach and is activated into pepsin by the presence of ????

A

chief cells
acid

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95
Q

what do the acid conditions in the stomach favour

A

the hydrolysis reactions by pepsin. the optimum pH for this enzyme is 2

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96
Q

what protects the stomach from the acid

A

mucus cover

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97
Q

what happens to the mucus cover when stressed or spicy

A

it produces an excess of gastir acid which is damaging and can cause a gastric ulcer

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98
Q

main symptoms of stomach ulcer

A

stomach pain, heartburn, nausea and in some cases presence of blood in the stools

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99
Q

what is another cause of gastric ulcers

A

the presence of the bacterium Helicobacter pylori in the stomach. H. pylori produces toxins that cause continuous gastric inflammation. The inflammatory response by the immune system damages the stomach lining.

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100
Q

treatment for h. pylori

A

Amoxicillin: antibiotic that directly inhibits the synthesis of bacterial cell walls.
Clarithromycin: antibiotic that prevents bacteria from growing by inhibiting the translation of peptides in the ribosome, thus inhibiting their protein synthesis.
Proton Pump Inhibitor (PPI): inhibits acidification of stomach.

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101
Q

what do proton pump inhibitors do

A

block the proton pump (hydrogen-potassium-ATPase pump), responsible for the secretion of hydrogen ions (H+) in the stomach. The decrease of H+ into the lumen of the stomach reduces the amount of hydrochloric acid (HCl) produced, which makes the stomach less acidic (Figure 4), making it a suitable treatment of gastric ulcers.

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102
Q

what are polysacharides digested to

A

monosaccharides

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103
Q

what absorbs monosaccharides

A

small intestine
destination
Villus through hepatic portal vein to liver.

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104
Q

what absorbs proteins/aa

A

stoamch
destination
cells of stomach lining

or

small intestine
destination villus through hepatic portavl vein to liver

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105
Q

what are lipids digested to

A

short chain fatty acids

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106
Q

what asbrobs small short chain fatty acids

A

small intestine
destination
villus through hepatic portal vein to liver

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107
Q

what asbrobs small longer chain fatty acids

A

small intestine
destination
lacteal to lymphatic system

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108
Q

what does each villus have

A

a central lacteal whose function is mainly the absorption of fats, capillaries that carry the test of the absorbed molecules to other organs

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109
Q

main adaptations of the villus

A

Increased surface area due to presence of villi and microvilli.
Many mitochondria to provide energy for active transport.
Presence of capillaries in villi for absorption of digested foods.
Presence of lacteal for absorption of absorbed lipids.
Presence of pinocytotic vesicles aid the uptake of fluids.
Presence of tight junctions to ensure molecules do not escape through the membrane, and to maintain a concentration gradient.
Enzymes (peptidases and disaccharidases) bound to epithelial membranes to complete hydrolysis/digestion.

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110
Q

structure of the villus

A
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111
Q

mucosa

A

contains the epithelium formed by enterocytes, goblet cells and endocrine cells. Enterocytes are cells that have microvilli; they digest and absorb substances. Goblet cells produce mucus and endocrine cells secrete hormones.

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112
Q

submucosa

A

contains blood vessels and connective tissue.

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113
Q

circular muscle layer

A

smooth muscle arranged in a circular manner.

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114
Q

longitudinal muscle layer

A

smooth muscle arranged in a longitudinal manner.

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115
Q

serosa

A

single layer of epithelial cells with connective tissue.

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116
Q

cross section of the wall of the small intestine consists of five layers working otuside

A

mucosa
submucosa
circular muscle layer
longitudinal muscle layer
serosa

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117
Q

describe the co transport of glucose

A

Glucose is co-transported with sodium (Na+) by facilitated diffusion. In order for this to happen, Na+ must first be transported out of the cell by active transport (along the basal membrane). This powers the co-transport of glucose and Na+ into the epithelial cells via the apical membrane. The glucose is then carried along the epithelial cell to a sugar transporter protein that allows its transport into the capillaries, which will carry it to the hepatic portal vein.

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118
Q

describe the co transport of proteins

A

digested by proteases into amino acids, which are transported by co-transport with Na+ into the epithelial cells. Amino acid carrier proteins then carry them by facilitated diffusion into the capillaries.

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119
Q

describe the absorption of fats or lopids

A

Fats (or lipids) are emulsified in the intestines by bile. This transforms them into smaller droplets, allowing lipases to digest them into fatty acids and glycerol. The glycerol will be absorbed and used in carbohydrate metabolism and the fatty acids will diffuse into the small intestine epithelial cells. Long chain fatty acids will combine with proteins to form chylomicrons. The chylomicrons travel to the border of the cell in the smooth endoplasmic reticulum and are expelled by exocytosis to later enter the lacteal, thus entering the lymphatic system.

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120
Q

Diagram showing the absorption of digested foods.

A
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121
Q

why does insoluble fibre haev no nutritional beenfit

A

not digested

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122
Q

fibre function

A

Fibre is important because it increases faecal mass, thus stimulating peristaltic movements.

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123
Q

what is dietary fibre

A

the non-digestible carbohydrates, especially cellulose, and lignin that are intrinsic and intact in plants.

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124
Q

constipation

A

unsatisfactory defecation, characterised by infrequent bowel movement, difficult stool passage, or both.

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125
Q

what causes cholera

A

caused by the ingestion of food or water contaminated with the bacterium Vibrio cholerae. When cholera toxin is released from the bacteria in the infected intestine, it binds to the intestinal epithelial cells (enterocytes), triggering endocytosis of the toxin.The toxin then becomes an active enzyme which activates ions and water to leave the infected enterocytes, leading to watery diarrhea.

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126
Q

signs and symptoms of cholera

A

Increased thirst
Dry mouth
Swelling of brain
Weakness
Dizziness
Palpitations
Seizures
Drop in blood pressure
Fainting
Decreased urine output
Kidney failure
Coma
Death

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127
Q

where does the liver receive deoxygenated blood from

A

the spleen, stomach, pancreas, gall bladder and intestines through the hepatic portal vein

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128
Q

what does the hepatic portal vein mainly carry

A

foods absorbed mainly in the small intestine. It is rich in amino acids, glucose, vitamins, minerals and other foods. The blood supplied by this blood vessel represents the majority of the blood received by the liver (around 75% of the total blood supplied to the liver).

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129
Q

why do we say the liver has dual blood supply

A

As the liver receives oxygenated blood from the hepatic artery and deoxygenated blood from the hepatic portal vein, we say that the liver has a dual blood supply. Because the blood from these two sources is mixed before entering the liver, its cells never receive fully oxygenated blood.

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130
Q

In the liver, blood from the hepatic artery and the hepatic portal vein supply

A

the sinusoids that bathe the hepatocytes and Kupffer cells.

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131
Q

waht do hepatocytes monitor

A

the contents of the blood and remove as many toxic substances such as alcohol and drugs before they can reach the rest of the body. enzymes metabolism these toxins to render them harmless

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132
Q

why does blood warm up through the liver

A

Many metabolic reactions take place in the liver. These reactions liberate heat, therefore when blood passes through the liver it is warmed up. This helps to maintain the body temperature in warm-blooded organisms.

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133
Q

the liver consists of

A

four lobes

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134
Q

each liver lobe has

A

100,000 lobules

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135
Q

each lobule consists of

A

a central venule coming from the hepatic vein surrounded by six venules coming from the hepatic portal vein and six arterioles from the hepatic artery. these blood vessels are connected by sinusoids

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136
Q

what are sinusoids

A

tubes that resemble capillaries but have a discontinuous endothelium

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137
Q

capillary vs sinusoid

A
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138
Q

capillary vs sinusoid pores

A

very small pores vs fenestrations

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139
Q

capillary vs sinusoid membranes

A

continuous basement membrane vs discontinuous basement membrane

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140
Q

capillary vs sinusoid shape

A

cylindrical vs no definite shape

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141
Q

capillary vs sinusoid size

A

smaller vs larger

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142
Q

capillary vs sinusoid intracellular space

A

little vs large

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143
Q

capillary vs sinusoid leakiness

A

only small molecules vs leaky

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144
Q

two types of cell in lobules

A

hepatocytes and kupffer cells

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145
Q

what do hepatocytes do

A

Hepatocytes perform most of the liver functions, especially storage and metabolism.

These cells are large (around 25 μm) and constitute around 80% of the total liver cells. Their nucleus is round and found in the centre of the cell. These cells are capable of regenerating when exposed to toxic substances.

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146
Q

what is liver regeneration

A

Liver regeneration involves the replication of hepatocytes followed by the replication of other liver cells. Once cell proliferation is completed, the newly divided cells undergo restructuring and reformation of the extracellular matrix to complete the process. During regeneration, liver function is only partially affected. Because human liver cells regenerate it has become possible to use partial livers from living donors for transplantation, thereby increasing the number of organs that are available for transplantation.

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147
Q

where are plasma proteins synthesised

A

in hepatocytes mainly in the rough endoplasmic reticulum (rER) and processed in Golgi complexes.

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148
Q

what is the role in hepatocytes and toxins

A

As we have mentioned before, hepatocytes are also involved in the degradation of toxins, such as detoxification of alcohol. Many of the detoxification reactions occur in the smooth endoplasmic reticulum (sER). Hepatocytes also have an exocrine function in the secretion of bile.

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149
Q

what do kupffer cells do

A

Kupffer cells are white blood cells (macrophages) that break down red blood cells. Therefore they are involved in the recycling of erythrocytes

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150
Q

what do lobule canals do

A

In the lobules there are also canals (bile canaliculi) that carry bile to the bile duct that leads to the gall bladder where bile is stored until it is used in the small intestine.

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151
Q

blood enters the liver via

A

hepatic portal vein

152
Q

Hepatocytes in the liver absorb most of the glucose and store it as what?

A

glycogen

153
Q

waht do hepatocytes synthesis

A

fatty acids
triglyceriddes
cholesterol
phospholipids

These lipids can be bound to proteins forming lipoproteins, which are now soluble in blood plasma and can therefore be transported in blood to all the body. Much of the cholesterol produced by hepatocytes gets excreted from the body as a component of bile.

154
Q

amino acids entering the liver are transformed into…

A

other aa or are used in the synthesis of new proteins

155
Q

Endoplasmic reticulum and Golgi apparatus in hepatocytes produce plasma proteins. These plasma proteins include fibrinogen used in ???

and albumin that transports ???

A

blood clotting,

hormones and maintains the blood pH.

156
Q

what is deamination

A

When amino acids are no longer necessary, hepatocytes remove the amine group from the acid group. The acid group of the amino acid is used to produce energy or new glucose molecules while the amine group is converted into ammonia. As ammonia is toxic, it is transformed into urea, which is then eliminated by the kidneys in urine.

157
Q

waht does the liver do if it cant break up toxins

A

If it cannot break them down, it attaches these substances to other organic groups (such a glycine), which allows the kidneys to recognise them as unwanted waste material and are therefore excreted.

158
Q

what is the process of metabolising alcohol

A

Ethanol is oxidised into acetaldehyde, a toxic substance, by the hepatic enzyme alcohol dehydrogenase. Acetylaldehyde is converted into a less toxic substance, acetate, by aldehyde dehydrogenase. Acetate is then broken down to acetyl-CoA that can enter fatty acid metabolism or be used in the Krebs cycle. If acetaldehyde is not broken down immediately, it can combine with proteins that induce liver injury. Excess of alcohol can damage the liver, causing cirrhosis.

159
Q

modificatons of erthrocytes to increase their capacity in the transport of oxygen

A

biconcave shape
no nucleus or organelles
rch in hemoglobin

160
Q

explain the adaptions of erthrocytes

A

The biconcave shape increases their surface area:volume ratio, thus increasing the absorption of oxygen. The lack of nucleus increases the amount of hemoglobin in each cell. But at the same time this means that they cannot reproduce, therefore they must be produced in the bone marrow from undifferentiated cells.

161
Q

when do erythrocytes die

A

after about 120 days circulating in blood

162
Q

what happens to odead erythrocytes

A

engulfed by macrophages in the liver, spleen or bone marrow by phagocytosis. In the liver, these macrophages are Kupffer cells.

163
Q

breakdown of erythrocytes in kupffer cells

A

In the Kupffer cells, the hemoglobin is split into globin chains and heme groups. Globin is re-used in protein synthesis. The heme group is transformed into iron and bilirubin. Iron is carried back to the bone marrow where it is used to produce new red blood cells. Bilirubin is secreted into bile that will be used in the emulsification of fats.

164
Q

globin is

A

reused in protein sysntheiss

165
Q

heme group is

A

transofrmed into iron and bilirubin

iron back to bone marrow
bilirubin secreted into bile

166
Q

cholesterol is the precursor for

A

the bile salts, steroid hormones (such as oestrogen and progesterone), and vitamin D.

167
Q

As most animal cells require cholesterol for membrane synthesis, a small portion is added to the

and the rest is

A

membranes of hepatocytes, and the rest is exported as lipoproteins or bile salts.

168
Q

how is cholesterol synthesis ergulated

A

according to its concentration in cells. This depends on the amount ingested in diet, and the regulation is performed by the hormones glucagon (inactivating its synthesis) and insulin (activating its synthesis).

169
Q

is cholesterol soluble in water

A

no they must be carried as plasma lipoproteins

170
Q

what do hdl and ldls contain more of

A

High-density lipoproteins (HDL) contain more protein, while low-density lipoproteins (LDL) contain more lipids.

171
Q

where are ldls and hdls produced

A

in the plasma, however a small amount is synthesised in the liver

172
Q

function of ldls

A

to transport cholesterol from the liver to the other organs

173
Q

function of hdls

A

to transport cholesterol from tissues to the liver

174
Q

fats can deposit in arteries causing a

A

atheroma or plaque

175
Q

what are atheroma or plaques caused by

A

whti eblood cells and ldl

Molecules of LDL deposit in the blood vessels and can become oxidised. This will cause atherosclerosis of the walls of the arteries

176
Q

waht causes atherosclerosis

A

oxidation of ldls

177
Q

what is atherosclerosis

A

narrowing of arteries due to plaque

178
Q

what is ateriosclerosis

A

hardening of arteries

179
Q

how does atheroscleroiss cause disease and stroke

A

If the artery leading to the heart (coronary artery) is clogged, the cells of the heart will not receive enough oxygen and can therefore die. These cells are replaced by fibres causing coronary heart disease (CHD). If the artery leading to the head (carotid artery) is affected, this can lead to a brain stroke.

180
Q

bile salts have a crucial role in digestion as they

A

emulsify fats

181
Q

bile salts function

A

emulsify fat

182
Q

benefit of emulsification

A

they break fats down into smaller droplets to increase their surface area. This allows enzymes (for example pancreatic lipase) to work better.

183
Q

how much bile is produced a day

A

about a litre

184
Q

where do bile salts come from and where do they go

A

Bile salts are synthesised by the liver from surplus cholesterol, and may be modified by bacteria in the intestines. Bile salts are reabsorbed from the intestines into the liver, but lots are lost in faeces. Approximately 600 mg of bile salts are synthesised daily to replace bile acids lost in egestion. Bile salts aid in the digestion and absorption of dietary lipids and fat-soluble vitamins.

185
Q

pathway of bile from liver to gall bladder

A

This fluid is carried by the bile canaliculi to the bile duct, which carries it to the gall bladder to be stored.

186
Q

composition of bile

A

The composition of bile is mainly water (97%), bile salts, cholesterol and fatty acids, bilirubin (from the breakdown of erythrocytes) and inorganic salts.

187
Q

cause of jaundice

A

presence of bilirubin in extracellular fluid Bilirubin in blood binds reversibly to albumin (a plasma protein), forming conjugated bilirubin that travels to the liver, which removes it from the plasma. When the liver is not able to remove the bilirubin from blood, its level may rise (especially in the unconjugated form) and the skin and eyes may begin to appear jaundiced.

It can also be caused by the use of drugs, genetic factors, malaria or anemia.

188
Q

wehn might jaundice occur

A

Increased destruction of red blood cells.
Immaturity in the conjugation of bilirubin (greater in premature babies).
Genetic diseases (e.g. Gilbert syndrome).
Defects in the secretion of conjugated bilirubin from hepatocytes (in liver damage).
Defects in transit of bilirubin to intestines (e.g. with bile duct obstruction).

189
Q

A high level of bilirubin in the blood is a sign of

A

liver malfunction.

190
Q

consequences of jaundice

A

Depending on the level of exposure, the effects range from clinically unnoticeable to severe brain damage and even death. Jaundice is usually a symptom of hepatitis or liver cancer.

191
Q

high bilirubinlevels in ifnants

A

It is common for a baby’s bilirubin level to be a bit high after birth as it might take some time for the liver to function properly (Figure 1). Some of the causes are a mismatch between the blood type of the mother and the child, lack of certain enzymes, or excess or abnormal blood cells. Special blue lights are used on infants whose bilirubin levels are very high.

192
Q

what is cirrhosis

A

a disease where the damaged liver tissue is replaced by scar tissue, as shown in Figure 2. Not only does this affect the functioning of liver cells, but also interferes with the blood supply to these cells

193
Q

symptoms of cirrhosis

A

weakness, fatigue, jaundice and bruising

194
Q

how to test for cirrhoisis

A

liver biopsy

195
Q

treatment for cirrhosis

A

no treatments, except liver transplant

196
Q

caues of cirrhosis

A

Excessive alcohol or drug consumption may cause liver cirrhosis. Other causes of cirrhosis include chronic viral hepatitis B or C, chronic bile duct obstruction, fatty liver disease, excess of iron, cystic fibrosis and Wilson’s disease.

197
Q

Why should alcoholics be entitled to receive a liver transplant?

A

Everybody has the right to live.
They can change their lifestyle and stop drinking.
They might be the only support for a family.
Many people care for them.

198
Q

Why should they not receive a liver transplant?

A

They caused the liver damage by their own choice of drinking.
They must put up with the consequence of their own reckless attitude.
Other people deserve the transplant more.
They can relapse back into drinking and damage the new liver.

199
Q

what does the structure of cardia cmuscle allow for

A

propagation of stimuli throught he heart wall

200
Q

describe the structure of cardiac muscle

A

This muscle has thick and thin muscle fibres with myofibrils containing myofilaments similar to those found in skeletal muscle
The nucleus of cardiac muscle cells is found in the centre of the cell. The cells are rich in mitochondria and glycogen granules that are found adjacent to the myofibrils. Unlike skeletal muscle, which has multinucleate cells, the cardiac muscle has numerous short, cylindrical cells arranged end-to-end, resulting in long, branched fibres giving a characteristic Y-shape

201
Q

intercalated ddisc

A

the attachment site between cardiac muscle cells. It appears as a linear structure transverse to the muscle fibre.

202
Q

what do intercalated discs allow for

A

communication between cells

203
Q

what are gap junctions

A

arrays of densely packed protein channels that permit intercellular passage of ions and small molecules. Electrical activation of the heart requires cell-cell transfer of current via gap junctions.

204
Q

what is the refractory period

A

where cells cannot contract for a secodn time

205
Q

cells have a all or none effect:

A

once a cell is activated, it produces maximum contraction

206
Q

what does the refractory period ensure

A

the contraction or systole of the heart is separated by a resting period or diastole

207
Q

where does heart contraction start

A

This contraction starts in embryonic tissues by specialised cells forming the pacemaker

208
Q

cardiac conduction

A

sinoatrial node
spreads along atria to the
atrioventriculr node
spreads to the ventricle (av valves are closed)
bundle of his
purkinje fibres

209
Q

what is the purpsoe of the dealay between the arrival and passing on of a stimulus at the av node

A

This delay allows time for atrial systole before the atrioventricular (tricuspid and bicuspid or mitral) valves close. The blood therefore leaves the atria to the ventricles when the atrial systole occurs.

210
Q

the delay between the arrival and passing of a stimulus at the AV node gives time for

A

the atria to contract before the AV valves close.

211
Q

The closing of the atrioventricular valves at the beginning of the ventricular contraction (systole) produces the

A

first sound, the lub

212
Q

the closing of the semilunar valves just after the ventricular systole and beginning of the diastole causes the

A

second sound, the dub sound.

213
Q

stethoscope

A

A stethoscope (Figure 2) is normally used to listen to the heart sounds. This is an acoustic device that has a resonator that is placed on the patient’s chest and two tubes connected to earpieces.

214
Q

Why is there a delay between the arrival and passing on of a stimulus at the atrioventricular node? 


A

Allows time for atrial systole before the atrioventricular valves close.

215
Q

what is an action potential

A

an electrical event associated with different concentrations of ions across membranes.

216
Q

the action potential is much longer or shorter in cardiac then in nerve cells

A

much longer

217
Q

The action potentials are explained by the changes in permeability of the membrane of the cardiac muscle cells to different ions,

A
218
Q

what does pacemakers bein myogenic mean

A

this means the action potential is generated by the pacemaker itself.

219
Q

What is the myogenic coordination of heartbeats?

A

Contraction initiated by cardiac muscle cell.

220
Q

What occurs during the depolarisation phase of an action potential in the atrium?

A

Sodium ions enter the cells, increasing the membrane potential.

221
Q

waht is the heart rate

A

the number of times the heart contracts in one minute (beats per minute). A person’s heart rate can be obtained by taking their pulse.

222
Q

factors that increase heart rate

A

Gender: women have slightly higher heart rate than men because they need more energy for metabolism.
Physical activity: more blood is required in muscles for oxygen supply.
Body size: larger people have higher heart rate than smaller people as blood needs to cover a larger area.
Temperature: vasodilation occurring when it is hot increases beats. If a person is running a fever, the pulse is accelerated.
Altitude: the body requires a greater amount of oxygen, therefore cardiac output must increase.
Posture: when one is standing the heart rate is higher than when lying down. This is related to the effect of gravity, as when standing blood needs to be pumped against this force.
Stress: the body will produce epinephrine, which will accelerate the rate.
Eating: more blood needs to be pumped to the stomach and intestines after eating.
Sodium and calcium ions in blood: blood retains more water to dilute the ions, so it needs to pump more. Patients suffering from dehydration will have a higher heart rate due to increase in concentration of ions in blood.
Drugs: caffeine and nicotine are both stimulants of the nervous system and of the cardiac centres, causing an increased heart rate.

223
Q

factors that decrease heart rate

A

Age: heart muscles cannot pump as efficiently.
Potassium ions: decrease action potentials.

224
Q

waht does a pacemaker consist of

A

a battery-powered generator (that sends out electrical impulses) and wires with electrodes to connect to the heart muscle. If the pacemaker senses that the heartbeat is above a certain rate, it will stop sending signals to the heart. The pacemaker can also sense when the heartbeat slows down too much. It will automatically turn back on and start pacing the heart again.

225
Q

how is a pacemaker placed

A

A small cut is made on the left side of the chest or abdomen and the generator is placed under the skin at this location. The pacemaker can have one lead leading to the right atrium or two leads, one to the right atrium and another to the right ventricular walls (Figure 1). Another type of pacemaker also includes a lead to the left ventricle.

226
Q

who might need a pacemaker

A

Patients that have an altered heart rhythm, for example, the heart beats too slowly (bradycardia) or too quickly (tachycardia) or beats irregularly (arrhythmia), might need an artificial pacemaker.

227
Q

when the heart beats faster than normal, it is

A

tachycardia

228
Q

what does an ecg check

A

electrical activity of the heart

Electrodes that detect electrical changes on the skin are placed on the patient’s body

229
Q

the r-r interval between successive beats on the ecg allows

A

calculation of the heart rate

230
Q

the p-wave represents

A

sa node electrical activity and contraction of the atria

231
Q

the qrs complex corresponds to

A

the excitation of the ventricles

232
Q

the t-wave is the

A

relaxation of the ventricles at the end of the contraction.

233
Q

Cardiac conduction and the heart cycle to explain the recording of an ECG.

A
234
Q

How is the heart rate measured using an ECG?

A

Number of R-waves per minute.

235
Q

blood pressure

A

the pressure of blood on the walls of an artery during a systole (highest value recorded) and a diastole (lowest value). During the heart contraction (systole) blood flows out of the heart at a high pressure through arteries, which support the pressure because their walls are elastic and strong. During heart relaxation (diastole) the pressure of the blood on the arteries is at its lowest.

236
Q

blood pressure is measuerd using a

A

sphygmomanometer

237
Q

how does a sphygmomanometer work

A

It consists of an inflatable cuff and a measuring device. This measuring device can be mechanical or digital. The mechanical device measures the pressure in millimetres of mercury, while the digital device makes oscillometric measurements.

238
Q

In the oscillometric method, the cuff pressure is used to detect

A

the small oscillations in the blood flow caused by the pulse. These oscillations increase in amplitude as the cuff pressure falls between systolic and mean arterial pressure. Therefore the systolic blood pressure corresponds to a specific heartbeat: the beat at which the blood pressure becomes higher than the deflating cuff pressure and the blood is capable of flowing in the brachial artery. The oscillations then decrease in amplitude as cuff pressure falls below mean arterial pressure. The corresponding mean oscillation is calculated to estimate blood pressure.

239
Q

Sphygmomanometer measurements
To measure blood pressure, the following steps are taken:

A

The sphygmomanometer cuff is placed on the antecubital fossa of the arm of the patient. The antecubital fossa or elbow pit is the triangular area on the front view of the elbow of a human.
The cuff is inflated. This will stop the flow of blood through the artery.
The air is slowly released until the pressure inside the artery is equal to the pressure exerted by the cuff. At this moment a hissing sound is heard if one places a stethoscope under the cuff, close to the artery.
A pounding sound can be heard as the cuff deflates. This initial sound denotes the systolic pressure.
The sound stops when the pressure of the cuff is smaller than that of the artery. The moment the pounding cannot be heard is the diastolic pressure recording.

240
Q

causes of hypertension

A

gender
obesity
age
lack of physical activitiy
stress and anxiety
alcohol
cafeeine

241
Q

consequences of hypertension on the human body can be:

A

Stroke
Blindness
Arteriosclerosis
Heart attack and heart failure
Kidney failure.

242
Q

Stroke occurs due to

A

a reduced or interrupted supply of blood to the brain. The brain does not get enough oxygen or nutrients, which causes brain cells to die.

243
Q

Blindness can happen

A

because of the ruptured capillaries in the retina or optic nerve or damage to the area of the brain responsible for processing images.

244
Q

Atherosclerosis is a special kind of

A

arteriosclerosis.

245
Q

arteriosclerosis

A

It is caused by the damage of arteries and subsequent formation of scar tissue. A plaque is formed when cholesterol and other lipids build up on this scar tissue. The plaque makes platelets release factors that cause the formation of a clot over the plaque, forming a thrombus. The thrombus blocks the flow of blood to tissues, causing thrombosis. If a thrombus (or clot) occurs in the coronary artery, the supply of blood and oxygen to the areas of the heart muscle is blocked. This causes irregular heartbeats and can lead to coronary heart disease

246
Q

The optimal systolic pressure is less than ???, the normal pressure is ???.

A

120
120

247
Q

epidemiology

A

investigates all the factors and effects that determine the presence or absence of diseases and disorders in a population.

248
Q

coronary heart disease is

A

the name for decreased blood flow and oxygen to the heart muscle caused by narrowed heart arteries. It is also called cardiac ischemia or ischemic heart disease.

249
Q

what is ventriucalr fibrillation

A

the interruption of the electrical impulses that control heartbeat.

250
Q

what can acause ventricular fibrillation

A

the loss of blood flow to the heart or a heart attack. It often begins with ventricular tachycardia (rapid heart beating) and leads to low blood pressure because the ventricles are not able to pump hard enough.

251
Q

symptoms of ventricular fibrillation

A

The symptoms are chest pain, dizziness, nausea, heartburn, fluttering heartbeat, fainting, coma, nerve function loss, changes in mental function and eventually death.

252
Q

cpr

A

Compress the chest to restore blood circulation.
Clear the airway.
Breathe for the person, blowing into the patient’s mouth.

253
Q

what is the eleectrical impulse of the defib used for

A

is used to depolarise the heart muscle in order to re-establish the function of the natural pacemaker. The electrode is a metal paddle or an adhesive pad that is placed on the patient’s chest. If a patient is having a dangerous heart arrhythmia or is in cardiac arrest, a series of electrical shocks is delivered through the electrodes and usually the patient is monitored through an ECG.

254
Q

what is an icd and how is it different to a defib

A

This ICD monitors heart rhythms and sends out shocks when necessary to increase or decrease heart rhythm. This is different from an implanted pacemaker machine because a pacemaker constantly fires to maintain a regular rhythm.

255
Q

Why is the chest compressed during CPR?

A

It restores blood circulation.

256
Q

endocrine glands

A

secrete hrmones into the blood

257
Q

major endocrine glands

A

the pituitary, pineal, thymus, thyroid, and adrenal glands, and the pancreas.

258
Q

men produce hromones in their

A

testes

259
Q

women produce hromones in their

A

ovaries

260
Q

development of endocrine glands

A
261
Q

the target tissue of a hormone consists of

A

cells that have receptor sites for a given hormone. In some cases, the target tissue is found in a single gland or organ. In other cases, the target tissue is scattered throughout the body so that many areas are affected.

262
Q

hormones definitition

A

chemical messengers secreted by cells or glands of the endocrine system that control and regulate the activity of other cells or glands in other parts of the body.

263
Q

hormones are classified as either

A

proteins or steroids

264
Q

which hormones are steroid

A

oestrogen, progesterone, testosterone (sex)

aldosterone, cortisol and estradiol (adrenal cortex)

265
Q

testosterone

A

Testes, ovary and adrenal cortex

Many organs

Secondary sexual characteristics, anabolic effect.

266
Q

progesterone

A

Ovary

Uterus

Maintain endometrium

267
Q

oestrogen

A

Ovary, placenta, liver, muscle and brain, as well as the fat cells

Many organs

Secondary sexual characteristics, accelerate metabolism, and increase uterine growth and endometrium.

268
Q

cortisol

A

Adrenal cortex

Many organs

Increase blood sugar, suppress the immune system, aid in metabolism; decrease bone formation.

269
Q

follicle stimulating hormone

A

Pituitary gland

Ovary/testes

Maturation of follicle/sperm production.

269
Q

thyroid stimulating hormone

A

Anterior pituitary gland

Thyroid

Stimulate production of thyroxin.

270
Q

ADH

A

Hypothalamus

Kidney

Water reabsorption, homeostasis.

271
Q

Growth hormone (somatotropin)

A

Anterior pituitary gland

Muscle, liver, bones

Growth.

272
Q

prolactin

A

Pituitary

Mammary glands

Milk production, metabolism.

273
Q

oxytocin

A

Hypothalamus

Uterus, mammary glands

Birth and lactation.

274
Q

glucagon

A

Pancreas

Liver

Convert stored glycogen to glucose.

275
Q

insulin

A

Pancreas

Muscle cells and fat cells

Promote absorption of glucose.

276
Q

thyroxin

A

Thyroid gland

Most organs

Accelerate metabolism, growth, development and heart rate.

277
Q

epinephrine

A

Adrenal medulla

Heart, muscles, skin, etc.

Fight-or-flight response.

278
Q

what is negative feedback

A

is seen when the output of a pathway inhibits inputs to the pathway.

279
Q

when can the concentration of hormones be controlled

A

Synthesis: the rate of production can be regulated by positive or negative feedback.
Delivery: in endocrine glands, this is regulated by blood flow.
Elimination: hormones are metabolised and excreted once their half-life is over.

280
Q

why can steroid hormones pass through the phospholipids of the cell membrane

A

theyre fat soluble

281
Q

what happens when a steroid hormone passes through a mambrane

A

Once inside the cell, some steroid hormones bind to a receptor in the cytoplasm and others to a receptor in the nucleus.

When the steroid hormone joins a receptor in the cytoplasm, two receptor subunits join together to form one functional DNA-binding unit that can enter the cell nucleus. Once in the nucleus, the receptor-hormone complex binds to specific DNA sequences and regulates transcription of its target genes.

When the steroid hormone binds to the receptor inside the nucleus, the receptor undergoes a conformational change that renders it activated to recognise and bind to specific nucleotide sequences. When the receptor-hormone complex interacts with DNA it alters the transcriptional level (responses can be either activating or repressing) of the associated gene.


The RNA produced is translated into new proteins, for example, enzymes involved in different metabolic processes. This method of action is relatively slow as it involves synthesis of proteins

282
Q

why cant peptide hormones pass through the plasma membrane of the target cell

A

They cannot enter the cell as they can’t pass through the cell membrane. Binding of hormones to membrane receptors activates a cascade mediated by a second messenger inside the cell. 
The sequence of events that results in hormone action is relatively rapid. Figure 2 shows the differences in action of steroid and peptide hormones.

283
Q

what type pf hormone is epinephrine

A

a peptide hormone

284
Q

action of epinephrine

A

Epinephrine attaches to receptors on the membrane of the heart cell called adrenergic receptors. These receptors are coupled to a G-protein. When the epinephrine joins the adrenergic receptor, the G-protein sends a message to the enzyme adenylyl cyclase. This in turn leads to the activation of the secondary messenger, cyclic adenosine monophosphate (cAMP), which induces smooth muscle relaxation, producing vasodilation and increased contraction of the cardiac tissue.

285
Q

HGH significantly reduces what and increases what

A

It has been proven that HGH significantly reduces body fat mass and increases body cell mass and sprint capacity when administered together with testosterone.

286
Q

anabolic steroid hormone effects

A

Increase in size of testes and ovaries, impaired spermatogenesis, growth of breasts in males.
Psychiatric disturbance.
Toxic to the liver.
Dyslipidemia (raised LDL and triglycerides and reduced HDL).
Hypertension.
Increased coagulation and platelet aggregation.
Exaggerated left ventricle growth.

287
Q

functions of thhypothalamus

A

Control of the release of eight major hormones by the pituitary gland.
Temperature regulation.
Control of food and water intake.
Control of daily cycles in physiological state and behavior (biological clock).
Sexual behavior and reproduction.
Control of emotional responses.

288
Q

how is the pituitary gfland connected to the hypothalamus

A

by a slender stalk

289
Q

The hypothalamus controls hormone secretion by which lobes of the pituitary gland

A

the anterior and posterior

290
Q

Hormones secreted by the pituitary gland control…


A

growth, developmental changes, reproduction and homeostasis.

291
Q

how are adh and oxytocin transported

A

down the axons from cells in hypothalamus to the posterior pituitary (neurohypophysis), where they are released into the bloodstream.

292
Q

adenohypophysis

A

The hypothalamus contains many of the neurons that control the endocrine functions of the anterior pituitary

293
Q

how deos the antieror pituitary release hromnes

A

These neurons do not directly release hormones from their endings but rather secrete releasing or release-inhibiting factors (also termed releasing hormones) that regulate release of hormones by the anterior pituitary. Hormones under control of this system include: growth hormone, ACTH, thyrotropin, the gonadotropins (FSH and LH), and prolactin.

294
Q

waht does adh do

A

The ADH released by the posterior pituitary gland acts on the kidneys, increasing the re-absorption of water, reducing the amount of water lost in urine.

295
Q

what does oxytocin do

A

The oxytocin released acts on the uterus, increasing contraction during childbirth, and breasts, inducing milk discharge in lactation.

296
Q

what produceds prolactin, fsh, acth and lh

A

anteiror pituituary gland

297
Q

what does thyrdroid stimulating hormone do

A

induces the thyroid gland to produce thyroxin and other thyroid hormones

298
Q

what does acth do

A

acts on the adrenal glands, iducing the production of steroid hormones such as cortisol

299
Q

what does somatotropin or growth hromone stimulate

A

growth, cell reproduction and regenreation in bones and soft tissues

300
Q

What hormone is involved in the production of sperm?

FSH

Thyroxin

Somatostatin

Cortisol

A

FSH

301
Q

why do breasts increase in size during preganancy

A

an increase in lobules and alveoli

302
Q

how is breastmilk released

A

Prolactin and oxytocin are two major endocrine hormones involved in the initiation and control of lactation. Infant suckling sends messages to the brain, via nerves, that induce the pituitary gland to release prolactin and oxytocin. Prolactin, a protein hormone (Figure 1) produced by the anterior pituitary gland, induces milk production in the breasts. This occurs by binding to mammary epithelial cell receptors, which stimulates synthesis of mRNA of milk proteins. Oxytocin, produced by the hypothalamus and released by the posterior pituitary gland, induces the release of milk by contraction of muscles around lobules. Milk is ejected into the milk ducts of the breasts. Around 1.5 litres of milk are produced daily.

303
Q

summary of breast milk production

A

pituitary gland messaged to release prolactin and oxytocin
prolactin binds to mammary epithelial cell receptors which stimulates synthesis of mrna of milk proteins
oxytocin induces release of milk by contraction of muscles around lobules

304
Q

oxytocin is waht type ofhormonr

A

peptide formed by nine aminoa cids

305
Q

prolactin is what type of hormone

A

protein

306
Q

where is dopamine produced

A

hyppthalamus

307
Q

dopamine inhibits or promotes production of prolactin in the anterior pituitary fland?

A

Dopamine inhibits the production of prolactin in the anterior pituitary gland. This is why dopamine is sometimes called prolactin-inhibitor factor.

308
Q

When a baby suckles the breasts, mechanoreceptors send messages to the hypothalamus to inhibit the production of dopamine, thus increasing the production of

A

prolactin

309
Q

waht is the effect of oestrogen on prolactin

A

increase the production and secretion of prolactin from the pituitary gland.

310
Q

What is a function of oxytocin?

A

Contraction of muscles in mammary glands.

311
Q

why is iodine necessary

A

for synthesis of thyroid hormones

312
Q

how does accumulation of tsh come about

A

If there is dietary iodine deficiency, the thyroid gland will not be able to produce thyroxin. This will decrease the negative feedback on the pituitary gland, leading to the increased production of thyroid-stimulating hormone (TSH). The accumulation of TSH causes the thyroid gland to enlarge, resulting in a condition called goitre.

313
Q

sympyoms of IDD in preganant women

A

miscarrage
stillbirth

314
Q

symptoms of IDD in adults

A

goitre
hypothyroidism
cretinism

315
Q

symotoms of IDD in children

A

impaired physical development
intellectual disability
cretinism

316
Q

type I pneumocytes

A

flat with a greater surface area. involved in the process of gas exchange between the alveoli and blood

317
Q

type II pneumocytes

A

cubic shape and cover a small fraction of the alveolar surface area

They secrete pulmonary surfactant, a fluid that decreases the surface tension within the alveoli. They are also capable of cellular division, giving rise to more type I pneumocytes when the lung tissue is damaged.

318
Q

the hydrogencarbonate buffering system

A

(The rate at which gaseous exchange occurs depends on the pH of blood. It is regulated to stay within the narrow range of 7.35 to 7.45. 
Within blood plasma and tissue fluids, hydrogencarbonate, proteins and ions (such as phosphate) act as buffers to maintain the pH close to neutral (slightly alkaline). )

Carbon dioxide combines with water producing carbonic acid that lowers the pH. The carbonic acid dissociates into hydrogencarbonate that is alkaline, so it increases the pH, plus a hydrogen ion that acidifies the medium, decreasing the pH.

319
Q

which is larger sa type I or type II pneumocytes

A

type I

320
Q

How does the hydrogencarbonate buffering system maintain the pH of blood within limits?

A

Dissolved carbonic acid dissociates into hydrogencarbonate and hydrogen ions.

321
Q

what is haemolglobin composed of

A

four peptide chains, two alpha and two beta chains, each with a ring-like heme group containing an iron atom (yellow).

322
Q

ohow many oxygen molecules bind to hemoglobin

A

4

323
Q

fetal haemoglobin

A

instead of having two alpha and two beta peptides, the fetal haemoglobin has two alpha and two gamma peptides.

324
Q

why is fetal hemolgobin different

A

During pregnancy, the mother must deliver O2 to the fetus and remove CO2 through the placenta. Mother and fetal blood never mix, so capillaries from both must come in close proximity for exchange to happen. In order to get O2 into fetal blood, the haemoglobin in fetuses is slightly different to the adult haemoglobin.

325
Q

waht is myoglobin

A

the protein used to bind oxygen in muscles

326
Q

what composes myoglobin

A

It consists of only one peptide chain and a heme group containing iron

327
Q

how many moelucles bind to myoglobin

A

Myoglobin can only bind one oxygen molecule, but this binding is stronger than that in haemoglobin. Therefore myoglobin can take the oxygen from haemoglobin in respiring muscle cells.

328
Q

how manypeptides and heme groups does hemoglobin have

A

four peptides and four hemes

329
Q

Once the first heme binds to oxygen, there is a small change in the protein structure of haemoglobin, making the heme of another chain join oxygen more

A

easily

330
Q

Cooperative oxygen binding by haemoglobin causes

A

conformational changes in an individual peptide that are propagated to the other peptides. The joining of the third and fourth oxygen molecules becomes easier due to this allosteric change in the haemoglobin molecule, leading to an S-shape or sigmoid curve.

331
Q

partal pressure

A

the individual pressure exerted independently by a particular gas within a mixture of gases.

332
Q

oxygen will be progressively released as what

A

partial oxygen pressure drops in the different tissues of the body. The release of a second, and even more so the third oxygen molecule, require smaller drops in pressure.

333
Q

how does hemoglbin deliver the largest amount of oxygen in the lungs wehre needed

A

As the blood leaves the heart, the partial pressure of oxygen decreases (to about 40 mmHg in the pulmonary arteries) and the haemoglobin molecule releases one oxygen molecule. This causes an allosteric change in the haemoglobin molecule that makes the further release of the other oxygen molecules easier, as less energy is required. This means that a smaller drop in partial pressure is required to liberate a molecule of oxygen, leading to an S-shape or sigmoid curve.

334
Q

at lower partial presssures, does fetal or adult hemoglobin load O2 easier

A

fetal because it binds O2 with greater affinity

335
Q

why isthere no allosteric affect on myoglobin

A

only one peptide

336
Q

What is the oxygen partial pressure in tissues?

A

10 to 40 mmHg.

337
Q

What determines the difference in shape of the haemoglobin and myoglobin dissociation curves?

A

The cooperative effect of four heme groups in haemoglobin

338
Q

Around 20-25% of the carbon dioxide in the red blood cells binds to haemoglobin, forming

A

carbaminohaemoglobin (HbCO2).

339
Q

what happens to the co2 in red blood cells

A

In the red blood cells the carbon dioxide is converted to carbonic acid (H2CO3) by the enzyme carbonic anhydrase. This carbonic acid then dissociates into hydrogen ions (H+) and hydrogencarbonate (bicarbonate) ions (HCO3-). Most of the carbon dioxide is therefore transported as hydrogencarbonate in blood (70-85%).

340
Q

The H+ joins the haemoglobin molecule to form a weak acid called

A

haemoglobinic acid

341
Q

chloride shift

A

he HCO3- leaves the red blood cells to enter the blood plasma. To balance the electric charge in the red blood cells, chloride ions (Cl-) enter the cells by diffusion. This is called the chloride shift. The opposite occurs in pulmonary capillaries, where the decrease in intracellular HCO3- induces the outward movement of Cl-.

342
Q

What is formed when carbonic acid is catabolysed by carbonic anhydrase?

A

carbond ioxide and water

343
Q

What is the chloride shift?

A

Entrance of chloride ions when hydrogencarbonate leaves the erythrocyte.

344
Q

Bohr effect

A

is the shift of the oxygen dissociation curve to the right with the increase of H+ or CO2, as the oxygen binding affinity is inversely related to acidity and carbon dioxide concentration.

345
Q

what does the bohr shift explain

A

the increased release of oxygen by haemoglobin in respiring tissues.

346
Q

A shift to the right in the sigmoid dissociation curve means

A

a decreased O2 affinity, therefore O2 is released.

347
Q

What causes the oxygen dissociation curve to shift to the right?

A

Increase in acidity or in CO2

If the pH of the blood is more acid, there will be a greater availability of H+. The H+ combines with haemoglobin, causing oxyhaemoglobin dissociation and the liberation of O2. The larger the amount of CO2, the greater the amount of H+ produced. This will allow the greater liberation of oxygen in respiring tissues.

348
Q

How does the CO2 concentration of blood affect the release of O2 in tissues?

A

More CO2 in blood will cause a greater release of O2.

The larger the amount of CO2, the greater the amount of H+ produced. The H+ combines with the haemoglobin, thus O2 is released by haemoglobin to the tissues.

349
Q

where is the repsiratory control center

A

in the medulla oblongata

350
Q

what are the detectors of carbon dioxide level in the blood and where are they

A

chemoreceptors in the aorta and carotid artery

351
Q

how can ventilation rate be measured

A

using a spirometer. this is attahced to a kymograph that measures the volume and speed of air blown out

352
Q

total lung capacity

A

maximum amunt of air in lungs 6 dm cubed

353
Q

residual volume

A

amount of air that remains in the lungs 1.5 dm cubed

354
Q

tidal volume

A

amount of air breathed in adn out in noral breathing 0.5 dm cubed

355
Q

the dorsal group is in charge of

A

inspiration

356
Q

the ventral group is in charge of

A

expiration

357
Q

them edulla repsiratory centres can be divided into

A

ventral and dorsal

358
Q

the fall in atmospheric pressuer at higher altidue increases or decreases the partial pressure of oxugen

A

decreases.

359
Q

Haemoglobin has low affinity for oxygen at low pO2, meaning

A

percentage saturation of hemoglobin is low as partial pressure of oxygen decreases

360
Q

mountains ickeness

A

may occur when a person travels from low to high altitude. The most common symptoms are headache, nausea and dizziness. High blood pressure in mountain sickness leads to body fluid buildup. After several days (or even weeks), the body becomes acclimatised.

361
Q

Acclimatisation includes the following changes

A

Heart pumps faster.
Blood vessels increase in diameter.
Lung ventilation rate increases.
Muscles produce more myoglobin to store more oxygen.
More capillaries develop in alveoli.
Amount of erythrocytes increases.

362
Q

why is there a greater number of erythrocytes in blood at high altitude

A

increased production of the hormone erythropoietin

363
Q

erythropoietin (EPO)

A

This peptide hormone is produced in the kidneys and acts in the bone marrow, on precursors of erythrocyte production. EPO levels in blood are usually low, around 10 mU/ml of blood, but can increase to 10,000 mU/ml in cases of lack of oxygen. The greater amount of EPO will increase the amount of erythrocytes. This means that more oxygen is delivered to the muscles, therefore improving endurance capacity.

364
Q

negative effects of epo

A

Increased viscosity of blood.
Reduced blood flow.
High blood pressure.
Increased risk of coronary heart disease.

365
Q

advantages of acclimisation

A

increased stamina
increased sprint speed
natural increase in epo
more oxygen to muscles
increased mitochondria in muscles cells
increase in erythrocytes

366
Q

disadvantages of acclimitisation

A

altitude sickness
high blood pressure
larger heart
increased risk of stroke
unfair advantage
lowered immunological respones

367
Q

carbon monoxide effeect on human

A

binds irreversibly to haemoglobin; therefore gaseous exchange is diminished, causing the smoker to get breathless when exercising.

368
Q

tar effect on human

A

coats lining of alveoli, increasing the risk of emphysema.

369
Q

smoking on cilia

A

cant move mucus out of airways so common breathing infections

370
Q

irritation on bronchi and bronchioles leads to

A

cough

371
Q

Other health problems derived from smoking are:

A

Increased chances of developing lung, throat or mouth cancer.
Cardiovascular disease due to atherosclerosis.
Nicotine increases heart rate and blood pressure.
Nicotine makes blood platelets stickier, increasing the chance of thrombosis.

372
Q

what is emphysema

A

the condition where the walls of the alveoli break down, so air sacs are fewer and larger.

373
Q

main symptoms of emphysemsa

A

cough
shortness of breath

374
Q

diagnosis of emphysema

A

chest x ray and arterial blood gas analysis

375
Q

causes of emphysema

A

Smoking (most important factor).
Congenital (alpha-1 antitrypsin deficiency).
Exposure to passive cigarette smoke.
Air pollution.
Occupational dust (for example in coal mines).
Inhaled chemicals.

376
Q

treatment of emphysema

A

Treatment consists of the use of bronchodilators that cause dilation of bronchi, corticosteroids to reduce inflammation, oxygen supplementation, and antibiotics if there are signs of infection. This does not halt or cure the damage already done to the alveoli; it just alleviates the symptoms. The most important step is to quit smoking. Surgery or even lung transplant is done in very severe cases.

biology (13 decks)

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