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Module 9 > Anaerobic & Aerobic Respiration > Flashcards

Anaerobic & Aerobic Respiration Flashcards

1
Q

what is the structure of mitochondria

A
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2
Q

what is the difference between nuclear vs mitochondrial DNA

A

circular, double stranded

extracellular source of DNA

encodes 37 proteins

nuclear DNA is inherited from all ancestors, mito is inherited from sinle lineage

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3
Q

how are substances transported into the mitochondria

A
  1. outer MM: porins allow passive diffusion of small proteins (CO2, O2, etc)
  2. translocases –> larger proteins need to be transported

TOM: translocator outer membrane

TIML translocator inner membrane

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4
Q

how is mitochondrial fission and fusion

A

fission: increase in mitochondrial number –> splits
fusion: increase in mitochondrial mass –> fused

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5
Q

how are mitochondria highly dynamic

A

cellular migration, fusion, fission, turnover

respond to energetic requirements

exercise, hypoxia

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6
Q

what occurs in exercise training and mitochondria

A
  1. mitochondrial density increased
  2. number of capillaries increased
  3. diffusion index decreased
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7
Q

what is the primary function of mitochondria

A

generate ATP

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8
Q

what is the net production of ATP per glucose

A

38 mol ATP/glucose

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9
Q

how many ATP does glycolysis produce

A

glucose –> 2 pyruvates

+2 ATP

+2 NADH

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10
Q

how many ATP does krebs cycle

A

+2 ATP

+6 NADH

+2 FADH2

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11
Q

how many ATP does ETC

A

+34 ATP

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12
Q

what is glycolysis

A

substrate level phosphorylation

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13
Q

where does gylcolysis occur

A

cytoplasm

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14
Q

does glycolysis require oxygen

A

no

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15
Q

what is anaerobic metabolism

A

reduction of pyruvate to lactate

more rapid than aerobic metabolism

fight or flight –> can’t maintain high levels of lactate, only short periods of time –> muscle damage

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16
Q

what is lactic acidosis and what causes it

A

build up of L-lactate in blood leading to excessively low pH

issue with oxidative metabolism

mitochondrial disease, sepsis, shock, cyanide poisoning, heart failure, propofol, CKD, excessive exercise, high grain diet in ruminants

17
Q

what is ethylene glycocol and how does it cause metabolic acidosis and how is it treated

A

sweet tasting

toxic if even feet/coat contaminated

toxic metabolites: glycolic acid (acidosis), oxalic acid, calcium oxalate crystals (renal failure)

treatment –> ethanol or 4-MP (fomepizole)

18
Q

what is pyruvate dehydrogenase complex

A

converts pyruvate to acetly coA

vitamin B1 (thiamine) needed –> thiamine pyrophosphate (TPP)

thiamine deficiency –> anorexia, cardiac hypertrophy

19
Q

what is the krebs/citric acid cycle

A

pyruvate metabolized to acetly coA –> oxidized in krebs cycle

high energy electron donors –> NADH, FADH2, ETS

20
Q

what is ATP

A

adenosine triphosphate

highly unstable

ADP + Pi ——-> ATP + H2O

converted by ATP synthase

ATP hydrolized to ADP + Pi

21
Q

what is ATP synthase

A

energy powers proton motive force –> protons to intermembrane space –> generates electrical voltage across IMM

last complex in the ETC

22
Q

what is shivering thermogenesis

A

primary motor centre –> activation of antagonistic muscles (contraction but little movement) –> metabolically expensive & inefficient

23
Q

what is non-shivering thermogenesis

A

cold is sensed by brain –> sympathetic nerves are activated –> NE –> brown adipocyte –> cAMP –> protein kinase A –>

acute effects: stimulation of lipolysis, activation of UCP-1 activity

chronic effects: UCP-1 gene transcription, mitochondrial biogenesis, hyperplasia of brown adipose tissue, recruitment of brown adipocyte in white adipose tissue depots

24
Q

what role does UCP1 play in NST

A

makes membrane more permeable –> protons pass thru and bypass ATP synthase –> produces heat in brown adipose tissues

release heat

25
Q

how do animals hibernate

A

abandon euthermia in response to cold/food shortages

reliant on food caches/body reserves over weeks/months

26
Q

how do animals prepare for hibernation

A

increase brown fat depots and UCP1 levels

27
Q

how do neonates use NST

A

at birth –> profound thermolysis

peri/post natal catecholamine surge –> NE, E, dopamine

increased fatty acid levels via hormone sensitive lipase, increase NST

28
Q

what is the role of NST and obesity

A

chronic treatment with B3-AR agonist results in thermogenic and anti-obestity properties (reduction of BW and girth)

stimulates metabolic rate, appearance of BAT deposits

29
Q

how do piglets stay warm

A

lack UCP1 protein –> neonatal hypothermia

UCP-3, SERCA thermogenesis

30
Q

what is the role of mitochondria in ageing

A

produces ROS –> oxidative damage –> functional decline –> ageing

31
Q

what diseases are linked with mitochondria

A

inherited parkinson’s

hypertension

some cancers

alzheimer’s

beta-amyloid localizes to mitochondria

32
Q

what are inherited metabolic disease

A

inborn errors of metabolism

archibald garrod –> mendelian inheritance to phenotypic variation and metabolism –> classic failure to thrive phenotype

33
Q

what is faconi syndrome

A

disorder of proximal kidney tubule

urinary loss of electrolytes and nutrients –> growth retardation, diarrhea, hypokalemia, hyponatraemia, hypochloremia

one is inherited form is mutation in EHHADH –> encodes enzyme involved in fatty acid oxidation

impairs mitochondrial metabolism and functionality of proximal kidney tubule

34
Q

what is metabolic intoxication

A

malignant hyperthermia –> inherited mutation on ryanodine receptor

stress, exercise, heat, volatile anaesthetics

35
Q

what is sensory ataxic neuropathy

A

mutation in mitochondrial gene

clinically presents between 2-8 months of age

lack of muscle coordination, abnormal gait, lack of stregnth/balance in hind limbs

Module 9 (43 decks)

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