d human physiology Flashcards

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1
Q

the autonomic nervous system is made up of

A

sympathetic system and parasympathetic system

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2
Q

sympathetic system

A

controls processes involved in responses to danger

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3
Q

parasympathetic system

A

controls homeostasis and processes related to rest and digestion.

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4
Q

which system speeds up digestion adn which slows it down

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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5
Q

gastrin is produced by

A

g cells in the stomach, duodenum and pancreas, in response to physical stimulation due to the presence of food, as well as to chemical stimulation by protein

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6
Q

When gastrin is released, it

A

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

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7
Q

gastric juice contains a mixture of

A

water, hydrochloric acid and other inorganic ions, enzymes (pepsin, rennin), mucus, various polypeptides, and intrinsic factor. Intrinsic factor is necessary for absorbing vitamin B12. Gastric juice changes the pH of the food content from 6.7 to 2, providing acidic conditions that will enhance digestion.

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8
Q

when does production of gastrin stop

A

when there is 1-1.5l of gastric juice

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9
Q

secretin is produced by

A

special cells in the small intestine in response to the presence of acid fluid. The presence of gastric acid activates prosecretin into secretin.

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10
Q

what does secretin do

A

When released, it stimulates the production of alkali by the pancreas, neutralising the intestinal components. When the pH of the intestine reaches 8, the production of pancreatic juice is stopped by negative feedback. Secretin 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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11
Q

Cholecystokinin (CCK) is also produced

A

by the small intestine when food is present in this organ.

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12
Q

waht does cck 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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13
Q

somatostatin

A

an inhibitory hormone secreted by special cells in the stomach, duodenum and pancreas. This hormone travels through blood to directly inhibit acid producing cells. It also acts indirectly by preventing the release of gastrin, CCK and secretin, thus slowing down the digestive process.

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14
Q

exocrine glands have ducts that…

A

carry their secretory product to the surface of the body or the lumen of the gut. These glands include the sweat, sebaceous, and mammary glands and the glands that secrete digestive enzymes.

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15
Q

stomach acid is produced

A

Acid in the stomach is produced by the combination of hydrogen ions (H+) and chloride ions (Cl-) produced by the epithelial cells (known as parietal cells) of the stomach lining. The release of hydrogen ions through protein carriers is coupled 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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16
Q

gastric juice contians

A

HCL and pepsin

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17
Q

what is pepsin

A

a protease that hydrolyses proteins to peptides. Pepsin is found in the stomach in an inactive form as the pro-enzyme pepsinogen.

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18
Q

waht releases pepsinogen

A

he chief cells in the lining of the stomach and is activated into pepsin by the presence of acid.

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19
Q

how is pepsinogen turned into pepsin

A

The hydrochloric acid released by the parietal cells of the stomach removes 44 amino acids from pepsinogen transforming it into pepsin.

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20
Q

how are stomach ulcers formed

A

Acidic conditions help to control pathogens in ingested food. The bacteria present in food cannot survive such acid conditions. 
The mucus cover of the stomach avoids self-damage. In some cases (either because the patient has eaten spicy foods or excess proteins, or is very stressed) the stomach will produce an excess of gastric acid. This can damage the mucus layer, producing gastric problems which might develop into a gastric ulcer. This is when the lining of the stomach is disrupted.

Another cause of gastric ulcers is the presence of the bacterium Helicobacter pylori in the stomach. H. pylori produces toxins that cause continuous gastric inflammation.

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21
Q

Ulcers due to H. pylori are treated with a combination of medications:

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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22
Q

how do proton pump inhibtors work

A

Proton Pump Inhibitors (PPI) 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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23
Q

polysaccharides to monosaccharides

A

absorbed by small intestine
destination the villus through the hepatic portal vein to liver

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24
Q

proteins to amino acids

A

absorbed by stomach
destination cells of stomach lining

small intestine to villus through hepatic portal vein to liver

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25
Q

lipids to short chain fatty acids

A

absorbed by small intestine
destination villus through hepatic portal vein to liver

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26
Q

lipids to longer chain fatty acids

A

small intestine to lacteal to lymphatic system

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27
Q

wall of the small intestine is lined with

A

villi that increase the surface area for the absorption of substances. Each villus has a central lacteal whose function is mainly the absorption of fats, and capillaries that carry the rest of the absorbed molecules to other organs. Most capillaries join to form the hepatic portal vein that carries blood to the liver. The structure of cells in the epithelium of the villus is adapted to the absorption of food

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28
Q

function of the central lacteal

A

absorption of fats

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29
Q

adaptations of the small intestine

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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30
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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31
Q

submucosa

A

contains blood vessels and connective tissue.

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32
Q

circulrar muscle layer

A

smooth muscle arranged in a circular manner

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33
Q

longitudinal muscle layer

A

smooth muscle arranged in a longitudinal manner

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34
Q

serosa

A

single layer of epithelial cells with connective tissue.

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35
Q

polysaccharides are mainly

A

hydrolysed to glucose and absorbed by epithelial cells of the small intestine.

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36
Q

how is glucose absorbed

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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37
Q

how are proteins absorbed

A

These are 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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38
Q

how are fats or lipids absorbed

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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39
Q

lipids are digested by lipases to turn them into

A

fatty acids and glycerol

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40
Q

glycerol will be absorbed an used in

A

carbohydrate metabolism

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41
Q

fatty acids will diffuse into

A

the small itnestien epithelial cells

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42
Q

long chain fatty acids will combine with proteins to form

A

chylomicrons

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43
Q

where do chylomicrons travel

A

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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44
Q

what does the large intenstine absorb

A

water, minerals and vitamin K.

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45
Q

why i s insoluble fibre not digested

A

no nutritional value

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46
Q

what is fibre

A

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

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47
Q

what materials are not absorbed

A

cellulose and lignin from plant matter, bile pigments, the remains of intestinal epithelial cells and bacteria.

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48
Q

what does cholera do

A

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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49
Q

what are essential nutrients grouped into

A

minerals
viamins
amino acids
fatty acids

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50
Q

minerals

A

for example phosphorus, calcium, magnesium, iron.

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51
Q

vitamins

A

for example vitamins A, C, D, K.

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52
Q

amino acids

A

for example histidine, tryptophan and others.
Fatty acids: for example certain omega-3 and omega-6 fatty acids.

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53
Q

Fatty acids

A

for example certain omega-3 and omega-6 fatty acids.

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54
Q

malnutrition can be cause by

A

an imbalance
an excess of nutrients

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55
Q

what is omega 3 needed for

A

controlling body functions lik eblood clotting and building cell membranes in the brain

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56
Q

what is omega 6 needed for

A

lower LDL cholesterol (‘bad’), and reduce inflammation and are protective against heart disease

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57
Q

alpha linolenic acid (omega 3)

A
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58
Q

linoleic acid (omega 6)

A
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59
Q

whre is omega 3 found

A

in fatty fish such as salmon, veg oil, soybean, rapeseed, flaxseed and in brussel sprouts, kale, spinach, walnuts

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60
Q

where is omega 6 found

A

salflower, corn, cottonseed, soybean

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61
Q

what are the nine essential amino acids humans cannot synthesise

A

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

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62
Q

Calcium and phosphorus are necessary for the formation of

A

bones and teeth

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63
Q

Calcium is also necessary

A

for muscle contraction. Sodium and potassium are involved in the propagation of the nerve impulse.

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64
Q

Sodium and potassium are involved in the

A

propagation of the nerve impulse.

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65
Q

retinol

A

fat soluble
found in Liver, leafy vegetables, carrots, fish, soya milk, milk, eggs.

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66
Q

thiamine

A

water soluble
found in Oatmeal, brown rice, vegetables, potatoes, liver, eggs.

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67
Q

cyanocobalamin

A

water soluble
found in Meat and other animal products.

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68
Q

riboflavin

A

water soluble
in Dairy products, bananas, green beans, asparagus.

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69
Q

niacin

A

water soluble
Meat, fish, eggs, many vegetables, mushrooms, tree nuts.

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70
Q

Pantothenic acid

A

water soluble
Meat, broccoli, avocados.

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71
Q

pyridoxine

A

water soluble
Meat, vegetables, tree nuts, bananas.

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72
Q

biotin

A

water soluble
Raw egg yolk, liver, peanuts, leafy green vegetables.

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73
Q

Folic acid

A

water soluble
Leafy vegetables, pasta, bread, cereal, liver.

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74
Q

ascorbic acid

A

water soluble
Many fruits, especially citrus and vegetables, liver.

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75
Q

Cholecalciferol(D3), Ergocalciferol (D2)

A

fat soluble
Fish, eggs, liver, mushrooms

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76
Q

Tocopherols

A

fat soluble
Many fruits and vegetables, nuts and seeds.

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77
Q

Phylloquinone

A

fat soluble
Leafy green vegetables such as spinach, egg yolks, liver.

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78
Q

deficiency

A

a diet lacking in one or more particular nutrients

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79
Q

imbalance

A

a diet that has an inadequate intake of a particular nutrient

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80
Q

excess

A

a diet that has a disproportionate intake of eg carbohydrates, fats or proteins

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81
Q

how is appetite controlled

A

Appetite is controlled by the appetite control centre in the hypothalamus (ACC). The centre regulates our desire to eat. When the stomach is empty, ghrelin is released, stimulating appetite. 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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82
Q

BMI

A

mass/height sq

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83
Q

causes of type 2 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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84
Q

symptoms of type 2 diabetes

A

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

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85
Q

what is chd

A

a disease in which a substance called plaque builds up inside the coronary arteries

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86
Q

what 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.

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87
Q

what dos anorexia lead to

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.
BREAKDOWN OF HEARTMUSCLE

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88
Q

what is vitamin c needed for

A

production of collagen

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89
Q

what is collagen found in

A

skin, connective tissues, tendons and blood vessels

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90
Q

why can vitamin c not be synthesised in some animals

A

because 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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91
Q

what does vitamin c defiencey cause and how can you fix it

A

scurvy. vitamin c found in citrus

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92
Q

symptoms of scurvy

A

bleeding gums, loose teeth
lack of energy
mood swings or depression
chronic joint pain
suppressed immune system
slow wound healing and bruising
suppressed immune system

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93
Q

how is rda calculated

A

A control group (group 0) does not receive any foods containing vitamin C.
Other groups (groups 1 to 10) get increasing levels of a daily supplement of vitamin C in their diet, e.g. group 1 gets 10 mg of vitamin C per day, group 2: 20 mg vitamin C per day, etc.
The control group will start to develop symptoms of scurvy.
Perhaps also groups 1 and 2 may show some symptoms, but above a certain daily supplement of vitamin C, e.g. 30 mg per day, the guinea pigs do not show the common symptoms of scurvy.
The data collected this way can be used to calculate the amount of vitamin C required by a human.

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94
Q

medical consequences of pku

A

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

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95
Q

what is pku

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. PKU is inherited as an autosomal recessive trait which means that patients with PKU have two recessive (mutated) alleles. As the enzyme can no longer catalyse the last and rate limiting step, phenylalanine accumulates in the body.

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96
Q

how is pku diagnosed

A

within 24 hours fobirth via the guthrie test

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97
Q

pku diet

A
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98
Q

why cant pku kids have aspartame

A

The artificial sweetener aspartame contains phenylalanine, so children with PKU cannot eat chewing gum or drink any soft drink that contains this sweetener.

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99
Q

what is vitamin d used for

A

the absorption of calcium in the digestive system. Calcium is needed to build healthy bones,

to maintain skeletal calcium balance by promoting calcium absorption in the intestines and maintaining calcium and phosphate levels for bone formation.

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100
Q

calcium deficiency is

A

a vitamin D deficiency can lead to softening or malformation of the bones. This condition is known as osteomalacia in adults (milder condition) or rickets in children

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101
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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102
Q

what triggers the synthesis of vitamin d

A

xposing the human skin to UV light with a wavelength between 290-310 nm triggers the synthesis of vitamin D in the skin.

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103
Q

what is bile the precursor of

A

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

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104
Q

when are you high risk for cholesterol

A

under 240 in mg dm -3

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105
Q

when are you not at risk for cholesterol

A

under 200

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106
Q

The total cholesterol that is mentioned in the table is the sum of

A

Very Low-Density Lipoprotein (VLDL), Low Density Lipoprotein (LDL) and High Density Lipoprotein (HDL).

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107
Q

which type of cholesterol has been associated with an increased risk of developing chd

A

ldl
low density lipoprotein

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108
Q

statins

A

a class of drugs used to lower cholesterol levels. The drug inhibits the enzyme HMG-CoA reductase, which catalyses the second step in the pathway from Acetyl CoA to cholesterol.

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109
Q

in children, the rd is

A

a) Total calorie intake value (TCV): 120 to 160 kcal/kg of weight.

b) Proteins: 10 to 15% of the total calorie value (TCV), 3g/kg of weight for children.

c) Carbohydrates: 35 to 60% of the TCV.

d) Fats: 35 to 50% of the TCV.

e) Fibre: age in years + 5g (i.e. a four-year-old needs 9g of fibre per day).

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110
Q

rda for adults

A

The accepted values for daily intake (11,300 and 8,800 kJ) for men and women (respectively) between the ages of 31 and 50 are averages. Other factors influence this number such as how active you are, e.g. running three to five times per week, or living a sedentary lifestyle. In the latter case your caloric intake should be less.

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111
Q

What does the structure of the heart cells allow for

A

Propagation of stimuli this rough the heart wall

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112
Q

What does heart muscle contain

A

Thick and thin muscle fibres with myofibrils containing myofilaments similar to those in skeletal muscle

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113
Q

What are the heart cells rich in

A

Mitochondria and glycogen granules that are found adjacent to myofibrils

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114
Q

Describe the types of cells in cardic muscle

A

Numerous short, cyclindrical cells arranged end to end, resulting in long, branched fibres giving a characteristic Y shape.

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115
Q

Intercalated disc

A

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

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116
Q

What do intercalated deists allow for

A

contain adhering junctions between cells that hold cells together and gap junctions, which allows communication between cells.

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117
Q

What are gap junctions

A

Gap junctions are 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.

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118
Q

Refractory period

A

When cells cannot contract. Ensures that the contraction or systole of the heart is separated by a resting period or diastole.

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119
Q

acid in the stomach is produced by

A

by the combination of H+ and CL- produced by the epithelial cells (paritetal cells) of the stomach lining. The release of hydrogen ions through protein carriers is coupled 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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120
Q

what does gastric juice contain

A

hydrochloric acid and pepsin

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121
Q

what is pepsin

A

a protease that hydrolyses proteins to peptides

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122
Q

what releases pepsinogen

A

chief cells in the stomach lining

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123
Q

how is pepsinogen converted into pepsin

A

by the presence of acid

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124
Q

the hcl released by the paretial cells of the stomach removes

A

44 amino acids from pepsinogen transforming it into pepsin

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125
Q

where is pepsin found

A

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

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126
Q

opt pH for pepsin

A

3

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127
Q

acidic condiitons help to

A

control pathogens in ingested food.

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128
Q

what protects the stomach from self damage

A

a mucus cover

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129
Q

when will the stomach produce excess acid

A

spicy food or excess protein or stress

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130
Q

what does excess gastric acid cause

A

gastric ulcer - stomach pain, heartburn, nausea, blood in stool

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131
Q

what can Helicobacter pylori cause and how

A

gastri culcers as H. pylori produces toxins that cause continuous gastric inflammation. The inflammatory response by the immune system damages the stomach lining.

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132
Q

treatment of 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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133
Q

how do PPI’s work

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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134
Q

lipids (short chain fatty acids) are absorbed by

and their destination is

A

small intestine

villus through hepatic portal vein

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135
Q

lipids (long chain fatty acids) absorbed by

A

small intestine

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136
Q

lipids (long chain fatty acids) destination

A

lacteal to lymphatic system

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137
Q

job of the central lacteal found in each villus

A

absorption of fats, and capillaries that carry the rest of the absorbed molecules to other organs

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138
Q

Most capillaries join to form

A

hepatic portal vein

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139
Q

adaptation fo villi

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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140
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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141
Q

submucosa

A

contains blood vessels and connective tissue.

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142
Q

circular muscle layer

A

smooth muscle arranged in a circular manner.

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143
Q

longitudinal muscle laeyr

A

smooth muscle arranged in a longitudinal manner.

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144
Q

serosa

A

single layer of epithelial cells with connective tissue.

145
Q

what are polysaccharides mainly hydrolysed to

A

glucose and absorbed by epithelial cells of the small intestine

146
Q

Polysaccharides are mainly hydrolysed to ??? and absorbed by epithelial cells of the ???

A

glucsoe and absorbed by the small intestine

147
Q

pathway of polyscahharides

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.

148
Q

pathway of proteins

A

These are 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.

149
Q

fats or lipids ar emulsified in th eintesitne by

A

bile

150
Q

fats are emulsified in

A

in the intestine by bile into smalller droplets

151
Q

the emulsification of lipids allows for

A

allowing lipases to digest them into fatty acids and glycerol.

152
Q

pathway of fatty acids

A

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.

153
Q

dietary fibre

A

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

154
Q

what materials are not absorbed

A

celluloe and lignin from plant matter, bile pigments, the remains of intestinal epithelial cells and bacteria

155
Q

what does inflammaiton fothe epithelial cells inside the intestine lead to

A

This will reduce the absorption of water, causing the feces to be loose or liquid (diarrhoea). If the infection persists for several days it can cause dehydration.

156
Q

what i cholera and how does it work

A

Cholera is a disease 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.

157
Q

signs and symptoms fo dehydration

A

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

158
Q

the liver is supplied with oxygenated blood from the heart through the

A

hepatic artery

159
Q

the blood leaves the liver through the

A

hepatic vein which carries deoxygenated blood which joins the vena cava, which returns the blood to the heart

160
Q

whre does the liver recive deoxygenated blood from

A

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

161
Q

what is the hepatic portal vein rich in

A

amino acids, glucose, vitamins, minerals and other foods.

162
Q

why is it said that the liver has a dual blood supply

A

s the liver receives oxygenated blood from the hepatic artery and deoxygenated blood from the hepatic portal vein

163
Q

hepatocytes

A

liver cells

164
Q

macrophages

A

Kupffer cells

165
Q

the hepatocytes monitor

A

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

166
Q

diagram of a lobule in the liver

A
167
Q

each liver lobe has about

A

100 000 lobules, each consisting of 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

168
Q

waht are sinusoids

A

tubes that resemle capillaries but have a discontinuous endothelium

169
Q

capillaris have small pores whilst sinusoids have

A

Fenestrated (with pores of approximately 175 nm diameter)

170
Q

why are hepatocytes ruch in mitochondria

A

Hepatocytes are involved in many metabolic processes, therefore they are rich in mitochondria, Golgi complexes, rER, ribosomes, glycogen granules and lipid droplets.

171
Q

what is liver regeneration

A

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.

172
Q

hepatocytes

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.

173
Q

where are plasma proteins synthesised and processed

A

in hepatocytes in the rough endoplasmic reticulum and processed in golgi complexes

174
Q

kupffer cells are

A

are white blood cells (macrophages) that break down red blood cells. Therefore they are involved in the recycling of erythrocytes, as you will see later in this subtopic.

175
Q

in the lobules there are also canals that carry

A

bile to the bile duct tha tleads to the gall bladder where bile is stored until it is used in the small intestine

176
Q

what in the liver absorbs most of the glucose and stores it as glycogen

A

hepatocytes

177
Q

what happens to fatty acids in the blood passing through the liver

A

absorbed by hepatocytes and metabolised to produce energy in the form of ATP.

178
Q

what syntehsises lipds like triglycerides, cholesterol and phospoholipids

A

hepatocytes 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.

179
Q

amino acids entering the liver are transformed into

A

other amino acids or are used in the synthesis of new proteins. Endoplasmic reticulum and Golgi apparatus in hepatocytes produce plasma proteins. These plasma proteins include fibrinogen used in blood clotting, and albumin that transports hormones and maintains the blood pH.

180
Q

Endoplasmic reticulum and Golgi apparatus in hepatocytes produce

A

plasma proteins. These plasma proteins include fibrinogen used in blood clotting, and albumin that transports hormones and maintains the blood pH.

181
Q

when amino acids are no longer necessary, hepotcytes

A

hepatocytes remove the amine group from the acid group (deamination). 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.

182
Q

detoxification

A

the liver gets rid of drugs, hormones and other toxins. In some cases it breaks down the substances into harmless compounds. 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.

183
Q

how is alochol metabolised

A

The liver is in charge of metabolising alcohol. In Figure 2, it shows the chemical reactions involved in this process. 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.

184
Q

modifications by rbc or erthyocytes

A

EDIT they have a biconcave shape and have lost their nucleus and organelles. These cells are rich in haemoglobin, a protein that binds oxygen (as HL students will see in section haemoglobin and myoglobin). 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.

185
Q

life cycle of erythrocyte

A

produced in the bone marrow and are liberated into the bloodstream. They die after approximately 120 days circulating in blood. Dead erythrocytes are engulfed by macrophages in the liver, spleen or bone marrow by phagocytosis. In the liver, these macrophages are Kupffer cells.

186
Q

how do kupffer cells recyle dead erythrocytes

A

phagocytosis

187
Q

what occurs within kupffer cells

A

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.

188
Q

what is cholesterol the precursor for

A

bile salts, steroid hormones, vitamin D

189
Q

what regulates cholesterol synthesis

A

Cholesterol synthesis is regulated 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)

190
Q

is cholesterol soluble in water

A

no insolube like lipids

191
Q

why must cholesterol be carrid as plasma lipoproteins

A

insoluble in water

192
Q

Different combinations of lipids and proteins produce particles of different densities. High-density lipoproteins (HDL) contain more ???, while low-density lipoproteins (LDL) contain more ???.

A

HDL - protein
LDL - lipids

193
Q

where are LDL and HDL’s produced

A

plasma and a small amount in the liver

194
Q

function of LDL

A

transport cholesterol from the liver to other organs

195
Q

function of HDL

A

to transport cholesterol from tissues to lvier

196
Q

what causes atherosclerosis

A

fats can deposit in arteries causing an atheroma or plaque. This is mainly caused by white blood cells (foam cells) and LDL. Molecules of LDL deposit in the blood vessels and can become oxidised.

197
Q

effect of LDL on blood vessels

A
198
Q

difference between atherosclerosis and arteriosclerosis

A

atherosclerosis (narrowing of arteries due to plaque)
arteriosclerosis (hardening of arteries).

199
Q

which cholesterol is considered ‘good’

A

HDL is considered “good” cholesterol as it removes LDL from blood by transporting it to the liver and helps to maintain the endothelium of the blood vessels, thus avoiding coronary heart problems.

200
Q

bile salts have a crucial role in deigestion as they

A

emulsify fats

201
Q

bile salts

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.

202
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.

203
Q

pathway of bile

A

The liver produces about one litre of bile per day. This fluid is carried by the bile canaliculi to the bile duct, which carries it to the gall bladder to be stored.

204
Q

jandice

A

a condition where the skin and white of the eyes turn yellow. It is caused by the presence of bilirubin in extracellular fluid.

205
Q

bilirubin

A

As you have seen before, bilirubin is produced from haemoglobin breakdown in erythrocyte recycling in the liver. The metabolism of haemoglobin accounts for 65% to 80% of the total bilirubin production. 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.

206
Q

when does 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).

207
Q

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

A

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

208
Q

infants and high bilirubin klevels

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.

209
Q

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. The symptoms are weakness, fatigue, jaundice and bruising. A liver biopsy will confirm the presence of scars. There is no cure for this disease. A liver transplant can be the solution in extreme cases.

210
Q

causes of cirrhosis

A

Excessive alcohol or drug consumption.
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.

211
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.

212
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.

213
Q

cardiac conduction diagram

A
214
Q

the beat of the heart is initaied in

A

the sinoatrial node, a group of specialised cardiac muscle cells found where the superior vena cava joins the right atrium. S

215
Q

after the sinoatrial node, the impulse spreads along the atria to the

A

atrioventricular node

216
Q

after the atrioventricualr node, the impulse spreads to the

A

ventricle

217
Q

There is a delay between the arrival and passing on of a stimulus at the atrioventricular node. This delay allows time for

A

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.

218
Q

why is there a delay in cardiac conduction

A

Remember the delay between the arrival and passing of a stimulus at the AV node gives time for the atria to contract before the AV valves close.

219
Q

The blood is now in the ventricles and the atrioventricular valves are closed. In the interventricular walls there are specialised fibres grouped to form a bundle called

A

bundle of his

220
Q

what happens at the bundle of his anatomically

A

the bundle splits into two branches that go to the left and right ventricles, leading to other specialised cells called Purkinje fibres

221
Q

what do purkinje fibres do

A

carry the impulse at a very high speed. Conducting fibres ensure coordinated contraction of the entire ventricle wall.

222
Q

systole is

A

the ventricular contraction

223
Q

what happens after the systole

A

Blood then flows out of the heart as the semilunar (pulmonary and aortic) valves open and give access to the aorta and pulmonary artery. The heart is now relaxed; this is called the diastole.

224
Q

heart sounds

A

used by the atrioventricular valves and semilunar valves closing causing changes in blood flow.

225
Q

action potential

A

an electrical event associated with differetn concentrations of ions across membranes

226
Q

difference in cardiac muscle contraction

A

The mechanism by which the cardiac muscle contracts is similar to that of the striated skeletal muscle. The membrane action potential leads to an increase in the calcium ions round the myofilaments, activating the myosin-ATPase. This leads to the sliding of the thick and thin filaments. The action potential is much longer (around 300 ms) than in nerve cells (around 2 ms) and skeletal muscle cells (around 4 ms). Do you remember that you studied that cardiac muscle cells have a special disposition forming fibres and have gaps between the cells (gap junctions)? Well, this allows for a more rapid spread of the action potential.

227
Q

role of sodium in cardiac conduction

A

Sodium ions are positive. When the signal reaches the cell, these ions come in, changing the overall membrane potential to positive. The plateau phase is given due to the balance between the potassium ions leaving the cell and the calcium ions coming in. This phase maintains depolarization for a longer time.

228
Q

difference with pacemakers

A

Pacemakers are myogenic, this means the action potential is generated by the pacemaker itself.

229
Q

normal heart rate

A

50 to 100 bpm

230
Q

factors increaseing 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.

231
Q

factors decreasing heart rae

A

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

232
Q

bradcardia

A

heart beats too fast

233
Q

tachycardia

A

heart beats too slowly

234
Q

pacemakers

A

This pacemaker consists of 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.

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.

235
Q

explain ecgs

A

The signals obtained in the ECG are amplified in the ECG machine and displayed on the screen of an oscilloscope or recorded on a moving paper (Figure 2). This gives a graph of voltage variations in time. The R-R interval between successive beats allows the calculation of the heart rate. The P-wave represents the SA node electrical activity and contraction of the atria. The QRS complex corresponds to the excitation of the ventricles. The T-wave is the relaxation of the ventricles at the end of the contraction.

236
Q

blood pressure reading

A

EDIT
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. Blood pressure is measured with a sphygmomanometer (Figure 1). 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.
In the oscillometric method, the cuff pressure is used to detect 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.

237
Q

how do you measure blood pressure

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.

238
Q

severe hypertension vs low

A

Systole Diastole
>180 >110
<90 <50

239
Q

cauess of hyeoroteniosn

A
240
Q

consequences of hypertension

A

Stroke
Blindness
Arteriosclerosis
Heart attack and heart failure
Kidney failure.

241
Q

stroke

A

occurs due to 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.

242
Q

blindnesss

A

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

243
Q

waht is atherosclerosis

A

the hardening of arteries, restricting the flow of oxygen and nutrients to tissues. Atherosclerosis is a special kind of arteriosclerosis. 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 (CHD).

244
Q

epdiemology

A

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

245
Q

what is ischemic heart disease

A

another name for chd

246
Q

classical risk fact ors for CHD

A

smoking
akchol consumption
blood pressure
obesity
cholesterol
diet
genetic predisposition

247
Q

what is ventricular fibrillation

A

the interruption of the electrical impulses that control heartbeat.

248
Q

causes of 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.

249
Q

symptoms of ventricualr fibrillation

A

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

250
Q

what is cpr and it sfunction

A

CPR is a lifesaving technique useful in a heart attack, in which the heartbeat has stopped. CPR can keep oxygenated blood flowing to the brain and other vital organs until more definitive medical treatment can restore a normal heart rhythm. It is quite a simple procedure that can be done by anyone if a doctor is not found in the proximity. To learn CPR properly, you can take an accredited first-aid training course, including CPR and how to use an automated external defibrillator (AED). After calling for emergency medical help, this is what you need to do:

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

251
Q

how to carry out cpr

A

Place the heel of your hand on the breastbone at the centre of the person’s chest. Place your other hand on top of your first hand and interlock your fingers.
Position yourself with your shoulders above your hands.
Using your body weight (not just your arms), press straight down by 5–6cm on their chest.
Repeat this until an ambulance arrives.

If the person has not begun moving after about two minutes of compressions and an automated external defibrillator (AED) is available, apply one shock, then resume compressions for two more minutes before administering a second shock. Continue CPR until there are signs of movement or emergency medical personnel take over.

252
Q

how does a defib help

A

The electrical impulse of the defibrillator 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.
In some cases, an implantable cardioverter-defibrillator (ICD) is used. 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.

253
Q

major endocrine glands

A

pituitary, pineal, thymus, thyroid, adrenal glands, pancreas

254
Q

development of endocrine glands

A
255
Q

what is target tissue

A

consists of cells that have recpetor sites for a given hormone. in some cases it is found on a single gland or organ. in some cases, the target tissues is scattered throughout the body so that many areas are affected

256
Q

hormone def

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.

257
Q

hormones are classified as

A

proteins or steroids

258
Q

epinephrine - PROTEIN
Site of production
Target organs
Main function

A

Adrenal medulla
Heart, muscles, skin, etc.
Fight-or-flight response.

259
Q

thyroxin PROTEIN
Site of production
Target organs
Main function

A

Thyroid gland
Most organs
Accelerate metabolism, growth, development and heart rate.

260
Q

insulin PROTEIN
Site of production
Target organs
Main function

A

Pancreas
Muscle cells and fat cells
Promote absorption of glucose.

261
Q

glucagon PROTEIN
Site of production
Target organs
Main function

A

Pancreas
Liver
Convert stored glycogen to glucose.

262
Q

oxytocin PROTEIN
Site of production
Target organs
Main function

A

Hypothalamus
Uterus, mammary glands
Birth and lactation.

263
Q

prolactin PROTEIN
Site of production
Target organs
Main function

A

Pituitary
Mammary glands
Milk production, metabolism.

264
Q

growth hormone (somatotropin) PROTEIN
Site of production
Target organs
Main function

A

Anterior pituitary gland
Muscle, liver, bones
Growth.

265
Q

ADH (vasopressin) PROTEIN
Site of production
Target organs
Main function

A

Hypothalamus
Kidney
Water reabsorption, homeostasis.

266
Q

thyroid stiumulating homrone PROTEIN
Site of production
Target organs
Main function

A

Anterior pituitary gland
Thyroid
Stimulate production of thyroxin.

267
Q

follicle-stimulating hormone PROTEIN
Site of production
Target organs
Main function

A

Pituitary gland
Ovary/testes
Maturation of follicle/sperm production.

268
Q

cortisol STEROID
Site of production
Target organs
Main function

A

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

269
Q

oestrogen STEROID
Site of production
Target organs
Main function

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.

270
Q

progesterone STEROID
Site of production
Target organs
Main function

A

Ovary
Uterus
Maintain endometrium.

271
Q

tesosterone STEROID
Site of production
Target organs
Main function

A

Testes, ovary and adrenal cortex
Many organs
Secondary sexual characteristics, anabolic effect.

272
Q

negative feedback

A

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

273
Q

how 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.

274
Q

steroid hormones are generally synthesised from

A

cholesterol in the ovaries or testes and in the adrenal glands

275
Q

steroid hormones are what soluble

A

fat soluble

276
Q

what do steroid hormones do

A

they can pass through the phospholipids of the cell membrane. 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 (Figure 2).

277
Q

what do peptide hormones do

A

Peptide hormones bind to receptors in the plasma membrane of the target cell. 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.

278
Q

describe the action of epinephrine

A

Epinephrine is a peptide hormone produced by the adrenal glands in response to stress and during exercise. 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.

279
Q

what is HGH

A

an anbolic steroid hormone. increases body cell mass and sprint capacity when administered together with testosterone.

280
Q

HGH consequences

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.

281
Q

Functions of the hypothalamus

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.

282
Q

Diagram of the hypothalamus and pituitary gland

A
283
Q

Cells in the hypothalamus also secrete

A

ADH
oxytocin

284
Q

Pathway of ADH and oxytocin

A

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

285
Q

What is neurohypophysis

A

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

286
Q

adenohypophysis

A

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

287
Q

Effect of oxytocin

A

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

288
Q

What does the anterior pituitary gland release

A

Prolactin, fsh, lh, gosh, thyroxin ACTH, cortisol, GH

289
Q

Prolactin

A

Milk production

290
Q

FSH and LH

A

Involved in growth of follicles and ovulation, respectively in ovaries in females, and in sperm formation in testes in males

291
Q

Thyroid stimulating hormone

A

hormone that induces the thyroid gland to produce thyroxin and other thyroid hormones.

292
Q

ACTH

A

Stimulates production of steroid hormones like cortisol on adrenal glands

293
Q

Why do breast increase in size in pregnancy

A

due to an increase in lobules and alveoli. The release of oestrogen and progesterone from the placenta and prolactin from the anterior pituitary causes this breast development.

294
Q

How is milk 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.

295
Q

Where is oxytocin produced and released from

A

Hypothalamus and Posterior pituitary gland

296
Q

What type of hormone is oxytocin

A

is a peptide hormone formed by nine amino acids, while prolactin is a protein hormone.

297
Q

Where is dopamine produced

A

Hypothalamus

298
Q

How does dopamine act

A

produced in the hypothalamus, is secreted into the bloodstream and acts as a hormone. Dopamine inhibits the production of prolactin in the anterior pituitary gland. This is why dopamine is sometimes called prolactin-inhibitor factor.

299
Q

Describe the negative feedback loop relating to dopamine and prolactin

A

When a baby suckles the breasts, mechanoreceptors send messages to the hypothalamus to inhibit the production of dopamine, thus increasing the production of prolactin. Prolactin itself enhances the secretion of dopamine, so this creates a negative feedback loop

300
Q

Why is iodine necessary

A

Synthesis of thyroid hormones

301
Q

Sources of iodine

A

Seafood, seaweed, cows milk, table salt

302
Q

How is TSH produced

A

the hypothalamus sends a message to the anterior pituitary to produce TSH, which will stimulate the thyroid gland to produce thyroid hormones. Iodine deficiency affects this hormonal control.

303
Q

If there is an iodine deficiency

A

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. Cretinism occurs when there is a congenital deficiency of thyroid hormones

304
Q

Symptoms Iodine deficiency diseases

A

Miscarriages, stillbirth,
Impaired phys dev, int disability, cretinism
Goitre, hypothyroidism, cretinism

305
Q

the cells froming the alverolus are called

A

pneumocytes

306
Q

type I pneumocytes are

A

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

307
Q

type II pneymocytes

A

have a cubic shape and cover a small fraction of the alveolar surface area (5%). 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.

308
Q

pH of blood

A

regulated to stay in the range of 7.35 to 7.45

309
Q

buffers in teh blood

A

plasma and tissue fluids, hydrogencarbonate, proteins and ions (such as phosphate) act as buffers to maintain the pH close to neutral (slightly alkaline).

310
Q

hydrogencarbonate buffering

A

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.

311
Q

haemoglobin is composed of

A

four peptide chains
two alpha and two beta
each with a ring-like heme group containing an iron atom

312
Q

differences in haemoglobin structure in fetal blood

A

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

313
Q

why is fetal blood different

A

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.

314
Q

myoglobin

A

the protein used ot bind oxygen in muscles.
It consists of only one peptide chain and a heme group containing iron (Figure 4). There is no sequence similarity in haemoglobin and myoglobin chains. 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.

315
Q

wy is the binding of the third and fourth oxygen molecules easier

A

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 easily. Cooperative oxygen binding by haemoglobin causes 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.

316
Q

oxygen dissociation curve

A
317
Q

partial pressure

A

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

318
Q

describe the oxygen dissociation cure

A

If you look at the graph from right to left, blood cells in the capillaries surrounding the alveoli carry 100% of the haemoglobin (shown in purple) as oxyhaemoglobin (with four molecules of oxygen bound, shown in red). These capillaries lead to the pulmonary vein, which carries blood to the heart. 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. In this way, haemoglobin attaches the largest possible amount of oxygen in the lungs, and delivers all of it where and when it is needed.

319
Q

effect of fetal hemoglobin on oxygen dissocaiton curve

A

Fetal haemoglobin binds O2 with a greater affinity, therefore extracting it from the mother’s blood in the placenta. This means that at lower partial pressures of O2, the fetal haemoglobin loads O2 easier than adult haemoglobin. This would cause a shift to the left in the oxygen dissociation curve.

320
Q

is there an allosteric effect for myglobin

A

Myoglobin has a stronger affinity for oxygen than haemoglobin. Because myoglobin is formed by only one peptide, there is no allosteric effect in the molecule

321
Q

carbon dioxide diffuses into ___
some remains dissolved in ____
binds to ___

A

the blood
plasma
haemoglobin

322
Q

waht happens to carbon dioxide in red blood cells

A

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%).
The H+ joins the haemoglobin molecule to form a weak acid called haemoglobinic acid (HbH). The 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-.

323
Q

the affinity of haemoglobin for oxygen is related to the pH of blood and to the partial pressure (or concentration) of CO2 (pCO2). An increase in blood acidity causes a shift of the oxygen dissociation curve to the ???, and a decrease in acidity (a more alkaline pH) will cause a shift to the ???.

A

right
left

324
Q

bohr shift

A

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.

325
Q

bohr shift on oxygen release

A

The Bohr shift explains the increased release of oxygen by haemoglobin in respiring tissues. 
As explained before, inside erythrocytes CO2 reacts with H2O forming H2CO3. The H2CO3 breaks down to H+ and HCO3-. 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. Likewise, if the pH of the blood is more acid, there will be a greater availability of H+ to combine with haemoglobin and more oxygen will be released to the tissues.

326
Q

what is the bohr shift

A

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.

327
Q

what is the medulla oblongata

A

the respiratory control centre

328
Q

where the chemorecpetors

A

aorta and carotid artery

329
Q

what do the chemoreceptros do

A

detect the levels of carbon dioxide in the blood

330
Q

carotid receptors

A

detect changes in the pH of blood. During exercise, the rate of ventilation increases in response to the amount of CO2 in the blood.

331
Q

spirometer

A

ventilation rate can be measured by using this it is attached to a kymograph that measures the volume and speed of air blown out

332
Q

Although the percentage of oxygen in inspired air is constant at different altitudes,

A

the fall in atmospheric pressure at higher altitude decreases the partial pressure of oxygen (pO2)

333
Q

As pO2 decreases, the percentage saturation of haemoglobin decreases rapidly (Figure 1). Haemoglobin has low affinity for oxygen at low pO2, hence it is not fully saturated as it passes through the lungs. This means that the tissues of the body are supplied with less oxygen.

A

edit

334
Q

when does moutnain sickeness coccur

A

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.

335
Q

acclimatisation

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.

336
Q

why is there an increase in the number of erythrocytes

A

increased production of erythropoietin (EPO)

337
Q

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.

338
Q

dangerous effects of EPO

A

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

339
Q

adv of training in high alt

A

increased stamina
natural increase in epo
increase in erythrocytes
more oxygen to muscles
more myoglobin in muscles

340
Q

disadv of training in high alt

A

altitude sickeness
high blood pressure
increased risk of stroke
unfair adv
high blood pressure

341
Q

how does CO affect lung function

A

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

342
Q

how does tar affect lung function

A

Tar coats lining of alveoli, increasing the risk of emphysema.

343
Q

other symtoms of smoking

A

Breathing infections are common due to the fact that cilia do not move mucus out of airways.
Cough due to irritation of bronchi and bronchioles.
Chronic bronchitis.
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.

344
Q

whya re fetuss particularly susceptible to smoking

A

Although smoking increases the amount of fetal haemoglobin, the human fetus does not have a biological capacity to accommodate to maternal cigarette smoking, and therefore the fetus is particularly susceptible to the adverse effects of cigarettes.

345
Q

emphysema

A

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

346
Q

The main symptoms of emphysema are

This condition is detected

A

cough and shortness of breath.

by measuring lung capacity with a spirometer. Diagnosis is confirmed with a chest X-ray and arterial blood gas analysis.

347
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.

348
Q

treatment of emohysema

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. Figure 1 shows the oxygen dissociation curve for a patient with emphysema compared to that of a normal person.

349
Q

where does the cardiac conductions tart

A

embryonic tissues by specilasie dcels forming the pacemaker

350
Q

pathway of cardiac conduction

A

sinoatrial node sends sginals along the atria to the atrioventricular node, to a ventricel. 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. The blood is now in the ventricles and the atrioventricular valves are closed. In the interventricular walls there are specialised fibres grouped to form a bundle called Bundle of His. This bundle splits into two branches that go to the left and right ventricles, leading to other specialised cells called Purkinje fibres. These fibres carry the impulse at a very high speed. Conducting fibres ensure coordinated contraction of the entire ventricle wall. The ventricular contraction is called the systole. Blood then flows out of the heart as the semilunar (pulmonary and aortic) valves open and give access to the aorta and pulmonary artery. The heart is now relaxed; this is called the diast

351
Q

shortneed pathway of cardiac conduction

A

sa node
av note
ventricle
bundle of his
purkinje fivre

352
Q

heart soudns, waht does the dub and lub mean

A

The closing of the atrioventricular valves at the beginning of the ventricular contraction (systole) produces the first sound, the club.
the closing of the semilunar valves just after the ventricular systole and beginning of the diastole causes the second sound, the dub sound.

353
Q

action potential

A

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

354
Q

action potentiall difference inc aradiac and striated cells

A

The action potential is much longer (around 300 ms) than in nerve cells (around 2 ms) and skeletal muscle cells (around 4 ms).

355
Q

why do cardiac muscle cells have a special disposition forming fibres and have gaps between the cells (gap junctions)?

A

allows for a more rapid spread of the action potential.

356
Q

membrane premeability dyring action potetinal in a cardiac cell

A
357
Q

what does myogneic mean

A

actipn potential generated by pacemaker or muscle itself rather than ocmign from neurla origin which wouldne urogenic

358
Q

do pacemakers have gaps in theri action potentials

A

Pacemaker cells have their own intrinsic rhythms of activity; therefore, as one action potential is completed, immediately another action potential is generated in the membrane, even in the absence of nerve impulse.