Integration of Cells and Tissues Flashcards

1
Q

What carries action potentials so that neurons can communicate with each other?

A

Axons

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2
Q

What percentage of basal metabolism is devoted to the brain?

A

25% since it contains lots of neurons which require energy to maintain their ion concentrations

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3
Q

What is basal metabolism?

A

The number of calories required to keep your body functioning at rest.

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4
Q

What in neurons is responsible for the ion concentration differences between intracellular and extracellular parts of the neuron?

A

Ion pumps, voltage-gated ion channels and ligand-gated ion channel

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5
Q

Which proteins are largely found in skeletal muscle and are responsible for muscle movement?

A

Actin and myosin

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6
Q

What reactions are the main source of energy for muscle for the movement of myosin heads?

A

Oxidation of fats and carbohydrates that produce ATP

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7
Q

How is energy stored in white adipose tissue?

A

In the form of fatty acids which are converted into triacylglycerols

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8
Q

What proteins carry triacylglycerol cells from the liver to adipose tissue?

A

Very low density lipoproteins (VLDL) in the blood

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9
Q

How is triacylglycerol transferred from VLDL to white adipose tissue?

A

Lipoprotein lipase (LPL) removes it from the VLDL and stores it in the adipose tissue

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10
Q

What is GLUT 4?

A

An insulin-stimulated glucose transporter which ensures that when there is excess glucose, this is made into fatty acid and triacylglycerols

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11
Q

What are the 2 main enzymes required for fatty acid synthesis and what are their general roles?

A

Acetyl-CoA carboxylase: Adds a CO2 onto acetyl-CoA to form malonyl-CoA
Fatty acid synthase: Grows the chain of carbons to form the fatty acid

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12
Q

Where is Acetyl-CoA carboxylase and fatty acid synthase found?

A

In the cytoplasm of the cells in adipose tissue

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13
Q

What is the enzyme that can breakdown triacylglycerols into fatty acids in adipose tissue?

A

HSL: hormone sensitive lipase

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14
Q

What organ is the largest in the body besides skin?

A

Liver

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15
Q

Describe the general structure of the liver

A

2 major lobes and 2 smaller lobes which are separated by the falciform ligament
Each lobe is made up of many lobules (the functional units)

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16
Q

Describe the structure of the lobules that make up the liver

A

They are hexagonal in structure and are made from cells called hepatocytes, these are arranged irregularly as channels around a central vein

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17
Q

What are the 2 major vessels in which the liver gets its blood supply from?

A

The hepatic artery (carries oxygenated blood)

The hepatic portal vein (carries nutrients and drugs from the GI tract)

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18
Q

What are sinusoids?

A

The spaces in between the hepatocytes where the blood from the vessels can flow through, bathing the hepatocytes in nutrient and drug rich blood

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19
Q

Why do hepatocytes contain high levels of metabolic enzymes?

A

So they can process the nutrients from the blood (glucose and fatty acids from the diet), as well as metabolising drugs

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20
Q

What vessel does blood drain out from the liver?

A

The hepatic vein

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21
Q

What is the benefit of the liver containing high amounts of glucokinase vs hexokinase?

A

Glucokinase has a greater capacity of phosphorylating glucose and therefore can deal better with increased glucose intake

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22
Q

What is the role of gluconeogenesis and ketogenesis and where are they found?

A

Glucogenesis makes glucose from amino acids
Ketogenesis makes ketones from fatty acids
They are both found in the liver

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23
Q

What are the 2 pathways that fatty acid can follow in the liver?

A

Esterification to triacylglycerols and packaged as VLDL or beta-oxidation to glucose

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24
Q

Where does esterification and beta-oxidation of fatty acids happen in the liver?

A
Esterification = in the cytosol
Beta-oxidation = in the mitochondria
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25
Q

What enzyme in the liver is responsible for controlling how much fatty acid is esterified or oxidised?

A

CAT I: Carnitine acyl transferase

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26
Q

When is CAT I active and when is it inactive?

A

Active when in the starved state and glucose is required

Inactive in the fed state when there is plenty of glucose

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27
Q

What are the Islets of Langerhans?

A

The are found in the pancreas and secrete insulin when in the fed state as glucose passes through the intestines and glucagon in the starved state

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28
Q

What is the role of insulin?

A

To convert glucose into glycogen and triacylglycerol

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29
Q

What happens to glucose in the fed state in adipose tissue?

A

It is converted into fatty acids and triacylglycerols

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30
Q

What happens to glucose in the fed state in the liver?

A

It is converted into glycogen. It is also converted into fatty acids and triacylglycerols and secreted as VLDL which is then transported to adipose tissue

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31
Q

What happens to glucose in the fed state in muscle?

A

It is converted into glycogen

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32
Q

What happens to the secretion of insulin and glucagon in the starved state?

A

Insulin decreases and glucagon increases

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33
Q

What does glucagon stimulate in the liver?

A

The break down of glycogen to glucose which is then released into the blood

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34
Q

What does glucagon stimulate in adipose tissue?

A

The break down of triacylglycerols to fatty acids through lipolysis which are released into the blood and used as energy sources of acetyl-CoA

35
Q

Why does gluconeogenesis and ketogenesis need to occur?

A

The brain cannot use fatty acids and so the liver needs to make glucose from amino acids and ketones from acetyl-CoA (from oxidation of fatty acids)

36
Q

What is the important of glucogenesis?

A

The brain cannot oxidise fatty acids and glucagon is not a large enough energy store, therefore the liver needs to be able to make glucose from other precursors such as amino acids

37
Q

What are the 2 major precursors for glucogenesis?

A

Glycerol (from adipose tissue lipolysis) and gluconeogenic amino acids (pyruvate)

38
Q

Why can glucogenesis be the reverse process of glycolysis?

A

There are 3 irreversible steps of glycolysis and so a different route needs to be taken

39
Q

What is the major precursor for ketogenesis?

A

Acetyl-CoA

40
Q

Where does the acetyl-CoA for ketogenesis come from?

A

Triacylglycerol in adipose tissue undergoes lipolysis and is broken down into fatty acids, these are then beta-oxidised by the liver

41
Q

What are the 2 ketone bodies that can be made from acetyl-CoA from ketogenesis?

A

Acetoacetate and 3-hydroxybutyrate, they are made from the condensation of acetyl-CoA in the mitochondria

42
Q

What happens to the ketone bodies made by ketogenesis in the liver?

A

They are released into the blood where they cross the blood-brain barrier

43
Q

Once in the brain how are the ketone bodies converted into energy?

A

They are broken down into acetyl-CoA which can be fed into the Krebs cycle

44
Q

What is the Cori Cycle?

A

The cycling of glucose and lactate between the muscle and liver that occurs under anaerobic respiration when there is not enough oxygen for the ETC to function during muscle activity

45
Q

What happens to pyruvate under anaerobic conditions?

A

It is reduced by lactate dehydrogenase to form lactate and used NADH

46
Q

What happens when there is a build up of lactate in muscles?

A

It can cause muscle cramps and pain

47
Q

What happens to lactate to prevent muscle cramps when it begins to build up?

A

It diffuses out of the muscle into the blood where it is taken to the liver

48
Q

What happens in the Cori Cycle when lactate enters the liver?

A

It is converted into pyruvate which is then converted into glucose through glucogenesis, the glucose then re-enters into the blood

49
Q

Why can the Cori Cycle not function for long?

A

It requires a lot of ATP

50
Q

What can the liver synthesise from excess glucose?

A

Triacylglycerol and cholesterol

51
Q

Give 4 functions of cholesterol

A

Helps with membrane structure
Precursor for steroid hormones
Precursor for vitamin D
Bile salts

52
Q

What is used to transfer cholesterol ester and triacylglycerols from the liver and why?

A

VLDL as cholesterol and triacylglycerols are insoluble in blood

53
Q

What is used to transport dietary triacylglycerols and cholesterol from the intestine?

A

A lipoprotein called chylomicron

54
Q

Describe the structure of VLDL

A

Triacylglycerols and cholesterol ester form the core which is then covered by a single layer phospholipid with the hydrophilic head groups pointing outward and the hydrophobic tails pointing inward.
The phospholipid also contains cholesterol molecules (not cholesterol ester)
The structure is held together by a large protein called apoprotein B

55
Q

What is the storage form of cholesterol?

A

Cholesterol ester

56
Q

What is apoprotein B?

A

A very large protein that holds together VLDL

57
Q

What happens after the triacylglycerols from VLDL have been removed and stored in adipose tissue?

A

VLDL then becomes LDL and is cholesterol rich, it either returns to the liver or supplied cholesterol to other tissues

58
Q

Give an example of a tissue requiring cholesterol

A

The adrenal cortex for steroid hormone synthesis

59
Q

What can cause high levels of LDL in the blood?

A

Increases in age, excess or imbalanced diet and genetic disorders

60
Q

What happens when there is high levels of LDL in the blood (how does it increase blood clot formation)?

A

It infiltrates wounds in the arteries causing the artery walls to become cholesterol-filled. The artery wall then heals over this cholesterol producing an atherosclerotic plaque which narrows the blood vessel and increases the risk of blood clot formation

61
Q

What is atherosclerosis?

A

When the arteries are narrowed as a result of high LDL

62
Q

What causes coronary heart disease?

A

The blocking of the coronary artery which supplied the heart muscles with oxygen

63
Q

Give a class of drugs that lower cholesterol levels and how

A

Statins, they inhibit the synthesis of cholesterol in the liver resulting in liver increasing LDL uptake from the blood

64
Q

What is the ratio of cells in the Islets of Langerhans that secrete insulin:glucagon

A

3:1

65
Q

What is Type 1 (acute onset) diabetes mellitus?

A

Insulin dependent diabetes, it usually develops by 10 years old and is when there is an insulin deficiency caused by an autoimmune response where there is the destruction of the beta cell

66
Q

What is Type 2 (maturity onset) diabetes mellitus?

A

Non-insulin dependent diabetes, usually develops in middle to old ae and is where tissues don’t respond to insulin (insulin-resistance), also sometimes impaired secretion of insulin by the beta cells

67
Q

What is common about both types of diabetes?

A

The effective concentration of insulin is less than of glucagon

68
Q

Describe the glucose tolerance test

A

The patient fasts overnight and then consumes 50g of glucose. Their blood glucose levels are measured for a few hours to see how their body responds to the glucose

69
Q

Give some metabolic consequences of diabetes that relate to glucose

A
Glucose uptake decreases
Glycogen store decreases
Glucose to fatty acid to triacylglycerol decreases
Glycogen to glucose increases
Gluconeogenesis increases
70
Q

What does high blood glucose levels lead to

A

Modifications of protein structure which impair their functions

71
Q

What is glycosuria?

A

When there is glucose in the urea when blood glucose levels are severely high

72
Q

How does diabetes affect lipolysis (lipids to fatty acids)

A

It increases in order to get an alternative energy source

73
Q

Why does the blood ketone body concentration increase in diabetic patients?

A

The liver takes up fatty acids and converts them into acetyl-CoA via beta-oxidation which makes ketone bodies

74
Q

What is ketoacidosis?

A

When there is high blood ketone levels which causes a decrease in blood pH and therefore coma and death

75
Q

Why can diabetes cause dehydration?

A

Due to water loss during glucose excretion

76
Q

Why does diabetes lead to increased membrane thickness?

A

Glucose can bind to the side chains of the membranes

77
Q

Diabetes can cause capillary closure, what can this lead to?

A

Blindness (retinopathy), renal failure (nephropathy) and severe nerve damage (neuropathy)

78
Q

What is protein glycosylation and when can it occur?

A

Diabetic patients, it is when high blood glucose reacts to form haemoglobin AIC which lowers the capacity for oxygen carrying haemoglobin

79
Q

How does diabetes increase the risk of cardiovascular diseases?

A

Glucose can bind to the apo B of LDL which increases VLDL levels

80
Q

What is the treatment for Type 1 diabetes?

A

injection with replacement insulin

81
Q

How do biguanides such as metformin help treat type 2 diabetes?

A

They increase the glucose uptake and reduce the glucose output by the liver, they also reduce glucose resistance

82
Q

What 2 classes of drugs help reduce insulin resistance in type 2 diabetics?

A

Biguanides and thiazolidinediones

83
Q

What 3 classes of drugs help improve insulin scretion?

A

Sulfonylureas, meglitinides and incretins

84
Q

What do sodium glucose transporter inhibitors do?

A

Increase glucose loss in urine