Biochem Flashcards

1
Q

Type 1 Fibers

A

Slow, oxidative
Red fibers, slow to fatigue
Maintain prolonged low intensity contracture

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2
Q

Type 2A Fibers

A

Fast oxidative glycolytic

Red fibers that produce ATP by both aerobic and anaerobic metabolism

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3
Q

Type 2B Fibers

A

Fast glycolytic
White fibers, fast to fatigue
ATP produced mainly by anaerobic

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4
Q

Cardiac Muscle Metabolism

A

Red fibers with aerobic metabolism

High mitochondria and myoglobin

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5
Q

Preferred Substrate for Cardiac Muscle

A

Fatty Acids

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6
Q

Smooth Muscle Metabolism

A

Most energy is from glycolysis
Less oxidative capacity then cardiac muscle
Can also use lactate as substrate

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7
Q

What is the immediate source of ATP in muscles?

A

Myosin ATPase

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8
Q

What enzymes maintain ATP equilibrium?

A

Creatine kinase and Adenylate kinase (2 ADP create ATP and AMP)

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9
Q

How can we measure kidney function using creatine?

A

The spontaneous breakdown of phosphocreatine into creatine is normally at a constant level so excretion in the kidneys is at regular rate

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10
Q

Role of AMP in ATP replenishment during contraction

A

Rising levels of AMP causes activation of glycogen phosphorylase b that stimulates glycogenolysis to make more glucose available for ATP production, It also activates phosphofructokinase-1 to stimulate glycolysis

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11
Q

Three methods of that stimulate glycogenolysis pathway

A

1) High AMP from adenylate cyclase
2) Nerve impluse release of Ca
3) Epinephrine stimulating cAMP to turn on PKA

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12
Q

McArdle’s Disease

A

Glycogen storage disease where glycogen phosphorylase is deficient. Increased lactate production for energy during exercise

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13
Q

Carb Metabolism in FED State of Skeletal Muscle

A

BLood glucose rises causing increased insulin which leads to increased GLUT-4 transporters membrane.
Glycogen synthesis in Type 2B fibers if stores depleted

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14
Q

Fat Metabolism in Skeletal Muscle

A

FA released from chylomicra and VLDL, fat oxidation less important process until glucose levels fall

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15
Q

Metabolism of BCAA in Skeletal Muscle

A

Amino acids produced via protein synthesis as required

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16
Q

Advantages of carbs over fat

A

Catabolism switches on faster, maxium rate of ATP formation greater, and yeild slightly more ATP per oxygen molecule

17
Q

Disadvantage of carbs

A

Produce about 7 times less energy per gram because it is stored hydrated

18
Q

Oxygen Dept

A

The continued consumption of oxygen after vigorous sustained exercise is over

19
Q

Cori Cycle

A

RBC lack mitochondria and use anaerobic glycolysis solely for ATP production and waste product is lactate that is converter back to glucose in liver

20
Q

Causes of Muscular Fatigue

A

Increase in Pi and fall in pH

21
Q

Glucose-Fatty Acid Cycle

A

When glucose is high insulin is high too and inhibits release of FA, when glucose/insulin are low FA is not inhibited and released

22
Q

What amino acids largely released by muscle during starvation?

A

Alanine and Glutamine

23
Q

Starvation

A

Glucose reserved for brain
Muscle uses FA and ketone bodies
Muscles provide C-skeleton for liver to make glucose

24
Q

Cardiac Muscle in FED State

A

Oxidative catabolism mostly of FA, very little glycogen stored

25
Q

Cardiac Muscle in Fasting State

A

Oxidize FA and ketone bodies

26
Q

Metabolism during Myocardial Infarction

A

ATP levels fall and AMP levels increase and anaerobic glycolysis stimulated

27
Q

X-Linked Muscular Dystorphies

A

Duchenne Muscular Dystrophy

Becker Muscular Dystrophy

28
Q

Duchenne MD

A

Dystropin virtually absent
Frameshift mutation
Cower’s Sign

29
Q

Becker’s MD

A

Reduced or modified dystrophin

Non-frameshift mutation

30
Q

Myotonic MD

A
Autosomal Dominant
Expansion Repeat Mutation
Most common form of MD
Anticipation more likely in female offspring
Myotonia (difficulty relaxing muscles)
31
Q

Limb-girdle MD

A

Mutation in genes encoding sarcoglycans

Dystrophy in extremities/girdles

32
Q

Oculopharyngeal MD

A

Expansion Repeat Mutation

Drooping eyelids, weakness in facial and pharyngeal muscles

33
Q

Congenital MD

A

Autosomal Recessive

Deficiency usually in laminin-2

34
Q

Bethlem Myopathy

A

Autosomal dominant

Mutation affecting Type 4 collagen

35
Q

Malignant Hyperthermia

A

Pathogenic release of Ca in response to anesthesia, hypermetabolic state with muscular rigidity