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Physiology > Oxygen - friend or foe? > Flashcards

Oxygen - friend or foe? Flashcards

1
Q

what are the functions of ATP?

A

Transport substances across cell membranes
muscle contraction
energy for the cells

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2
Q

which organ uses the most energy?

A

liver

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3
Q

what oxidation?

A

addition of oxygen or removal of electrons

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4
Q

what is reduction?

A

removal of oxygen or addition of electrons

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5
Q

what is respiration?

A

the process of breaking down organic molecules to harvest chemical energy

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6
Q

breaking down of sucrose

A

requires sucrase

produces D-fructose and D-glucose

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7
Q

breaking down of lactose

A

requires lactase

produces D-galactose and D-glucose

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8
Q

what happens in glycolysis?

A

storage as glycogen
conversion to nucleotides and fatty acids
generation of ATP energy

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9
Q

anaerobic respiration

A

produces lactate

generates less ATP

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10
Q

Glycolytic enzyme

A

mutation-associated demonstrated or possible defects

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11
Q

Hexokinase 1

A

nonspherocytic hemolytic anemia

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12
Q

Hexokinase 2

A

nonspherocytic hemolytic anemia
insulin resistance
possible cause of increased glycolysis in cancer cells

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13
Q

Glucokinase

A

gestational diabetes, hyperinsulinism of the newborn

maturity-onset diabetes of the young

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14
Q

phosphoglucose isomerase

A

nonspherocytic hemolytic anemia

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15
Q

Phosphofructokinase

A

exercise intolerance and compensated hemolysis - tarui disease

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16
Q

Aldolase B

A

hereditary fructose intolerance

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17
Q

triosephosphate isomerase

A

multisystem disease

lethality in early childhood

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18
Q

glyceraldehyde 3-phosphate dehydrogenase

A

diverse nonglycolytic functions, could be involved in prostate cancer, age-related neurodegenerative disease

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19
Q

phosphoglycerokinase

A

chronic hemolytic anemia

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20
Q

phosphoglycerate mutase

A

exercise intolerance

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21
Q

enolase 1

A

deregulation of c-myc oncogene

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22
Q

pyruvate kinase

A

alpha-hereditary hemolytic anemia

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23
Q

Tarui’s disease

A

phosphofructokinase deficiency
affects skeletal muscle
autosomal recessive

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24
Q

symptoms of Tarui’s disease

A

muscle pain
fatigue on everyday activity
fixed contractures with rhabdomyolysis
risk of acute renal failure

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25
Q

what is the treatment for taruis disease?

A

no specific treatment
maintain healthy diet
control weight
take regular gentle aerobic exercise

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26
Q

fumarase deficiency

A

very rare
causes micocephaly
frontal bossing
micrognathia

27
Q

examples of mitochondrial disease

A 
mitochondrial myopathy
diabetes mellitus at early age
deafness at early age
leber's hereditary optic neuropathy
leigh syndrome
neuropathy, ataxia, retinitis pigmentosa and ptosis
dementia
myoclonic epilepsy with ragged red fibres
mitochondrial DNA depletion syndrome
28
Q

Leber’s hereditary optic neuropathy

A

visual loss in young adulthood

degeneration of the optic nerves and retina

29
Q

Leigh syndrome

A

seizures
altered states of consciousness
dementia
ventilatory failure

30
Q

myoclonic epilepsy with ragged red fibres

A 
progressive myoclonic epilepsy
short stature
hearing loss
lactic acidosis
exercise intolerance
31
Q

oxygen cascade

A

the process of declining oxygen tension from atmosphere to mitochondria

32
Q

disruption of oxygen cascade

A

at any point of the cascade will lead to insufficient availability of oxygen to meet energetic demands = hypoxia

33
Q

what is in the oxygen cascade?

A

air - alveoli - end capillary - arterial blood - tissue capillary - cell - mitochondira

34
Q

what are the different types of hypoxia?

A

hypoxic
anaemic
circulatory
histotoxic

35
Q

hypoxic hypoxia

A

low pp O2
inadequate haemoglobin sats
pulmonary diseases
high altitude

36
Q

anaemic hypoxia

A

decreased O2 carrying capacity of blood
anaemia
CO poisoning

37
Q

circulatory hypoxia

A

decreased O2 delivery to tissues
cardiac failure
hypotension
shock

38
Q

histotoxic hypoxia

A

inability to use oxygen
normal O2 delivery
cyanide poisoning
mitochondrial disease

39
Q

cellular effects of hypoxia

A

early/ reversible and late/ irreversible

40
Q

what are the early/ reversible effects of hypoxia?

A 
mitochondrial ATP production stops
anaerobic glycolysis begins
cellular ATP depletion
sodium pump fails
protein synthesis fails
accumulation of sodium ions
water enters the cells and causes swelling
41
Q

what are the late/ irreversible effects of hypoxia?

A

cell and organelles swell
membrane integrity fails
mitochondrial pores open > apoptosis
leakage of cell proteins > necrosis

42
Q

How are reactive oxygen species formed?

A

O2 is a strong oxidising agent

partial reduction of oxygen yields reactive oxygen species

43
Q

ROS - the players

A

partial reduction of oxygen yields:
superoxide anion radical
hydrogen peroxide
ROS species can react together to form further ROS - hydroxyl radicals

44
Q

Exception

A

singlet oxygen is a ROS but not a radical or from other ROS species

45
Q

where do ROS come from?

A

mitochondria

46
Q

what are some other sources of ROS?

A

Endogenous and exogenous

47
Q

what are endogenous sources of ROS?

A 
mitochondrial respiratory chain
respiratory burst and NADH oxidase
xanthine oxidase
lipoxygenases
glucose oxidase
myeloperoxidase
nitric oxide synthase
cyclo-oxygenase
transition metas
48
Q

what are exogenous sources of ROS?

A 
pollutants
radiation
cigarette smoking
food and nutrients
drugs
xenobiotics
49
Q

what do ROS do?

A

damage cells by causes free radial substitution chain reactions
cause cancer

50
Q

cellular antioxidant defences

A

antioxidant enzyme systems

located in organelles and cytosol - isoforms

51
Q

what are the antioxidant enzyme systems?

A

superoxide dismutase
catalase
glutathione peroxidase

52
Q

oxidative stress

A

to prevent this there needs to be a balance between ROS production and ROS removal

53
Q

what can oxidative stress do?

A

cause a whole host of diseases - asthma, vasospasm, atherosclerosis. cancer, inflammatory diseases, alzheimer’s and parkinson’s, rheumatoid arthritis, dermatitis, ischemic bowel

54
Q

immune cells and ROS

A

immune cells kill pathogens with ROS

55
Q

hyperbaric oxygen

A

patient inhales 100% oxygen at higher atmospheric pressure

15 times more oxygen received

56
Q

how does hyperbaric oxygen work?

A

under pressure more oxygen is forced into the tissues so new blood vessels grow
plasma can carry 100% oxygen under pressure
red blood cells flow into new blood cells
extra oxygen is diffused to the tissues from the new blood vessels

57
Q

what can be hyperbaric oxygen be used for?

A

wound healing- diabetic ulcers and other ulcers/ infected wounds
the bends - decompression sickness

58
Q

what is photodynamic therapy?

A

uses photosensitiser which becomes activated when red light or daylight is shone onto the skin where it is applied. Causes changes in the oxygen molecules - oxidisation forming ROS in abnormal skin cells. The ROS kill abnormal cells.
There is minimal damage to normal cells

59
Q

what is decompression sickness?

A

dissolved gases coming out of solution and forming bubbles inside the body on depressurisation
causes joint pain, rashes , paralysis and death.

60
Q

when are ROS useful?

A

used as signalling molecules

61
Q

what does nitric oxide do?

A

vasodilation

62
Q

what can ROS damage?

A

DNA
lipids
proteins

63
Q

what does carbon monoxide poisoning cause?

A

cherry red colour to skin

64
Q

what is basal metabolic rate?

A

metabolic rate at rest

Physiology (46 decks)

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