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Musculoskeletal System > 1 - Biochemistry > Flashcards

1 - Biochemistry Flashcards

1
Q

The immediate source of energy for muscle contraction is?

Which enzyme is involved?

A

ATP—–>ADP + Pi

Myosin ATPase

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2
Q

What does creatine kinase (CK) have to do with muscle contractions?

A

Transformation form ATP + Creatine to Phosphocreatine + ADP, and vice versa

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3
Q

What does adenylate kinase (AK) have to do with muscle contractions?

A

Helps with transforming from 2ADP to ATP +AMP and backwards

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4
Q

What are the energy sources for smooth muscle? major and secondary

A

Most from glycolysis

Can also use lactate

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5
Q

What is the preferred energy substrate used by cardiac muscles? Which others can be used?

A

Metabolism is almost totally aerobic
Preferred: Fatty Acids
Others: Glucose, Ketone Bodies, Lactate

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6
Q

In the replenishment of ATP following muscle contractions, which enzyme is activated by AMP?

A

Glycogen phosphorylase B - glycogenolysis initiated

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7
Q

In the replenishment of ATP following muscle contractions, which enzyme is activated by AMP, Pi, and NH3?

A

Phosphofructokinase-1 - glycolysis initiated

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8
Q

In the replenishment of ATP following muscle contractions, which enzyme is activated by ADP?

A

Isocitrate Dehydrogenase - TCA cycle initiated

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9
Q

In the replenishment of ATP following muscle contractions, which enzyme is activated by Ca++ ions? (4)

A 
Glygogen phosphorylase (glycogenolysis active)
Pyruvate dehydrogenase (glycolysis/TCA active)
Isocitrate dehydrogenase (TCA active)
Oxoglutarate dehydrogenase (TCA active)
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10
Q

Describe McArdle’s Disease

A

A type V glycogen storage disease
Deficiency in muscle glycogen phosphorylase
Myopathy due to defective glycogen breakdown
Painful cramps and fatigue with exercise
*no lactate increase during exercise (abnormal)**
*PRIOR ingestion of sucrose is beneficial

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11
Q

What enzyme releases fatty acids from chylomicrons and VLDL?

A

Lipoprotein lipase

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12
Q

Why are serum fatty acid levels decreased following increased blood glucose levels?

A

Insulin is secreted in raised blood glucose - insulin inhibits lipase responsible for releasing fats

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13
Q

By what mechanism is most energy produced in Type I and IIa fibers?

A

oxidative metabolism

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14
Q

By what mechanism is most energy produced in Type IIb fibers?

A

WHITE FIBERS
glycogen mobilized for rapid release of substrate
lactate via ANEROBIC GLYCOLYSIS

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15
Q

What is the major disadvantage of carbohydrate metabolism?

A

It is stored as hydrated form, so it produces about 7 times less energy per gram

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16
Q

What happens to the lactate produced by white (IIb) muscles metabolism?

A

It goes to the liver to be used in gluconeogenesis (CORI CYCLE)

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17
Q

What is most likely the major contributor to muscle fatigue?

A

Increase in Pi

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18
Q

What are the 2 big theories that try to explain muscle fatigue? Describe them..

A

Increase in Pi – self explanatory (major contributor)

Fall in pH - inhibiting PFK-1 and SR release of Ca+

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19
Q

What is the major pathway of glycogen replenishment?

A

INSULIN activates glycogen synthase (b form to a)

G-6-P presence does the same thing

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20
Q

What are free fatty acids bound to in serum?

A

Albumin?

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21
Q

Red fibers have a higher level of two certain proteins than white? Which has to do with their preference for oxidative metabolism? What proteins are important?

A 
Fatty Acid Binding Protein (FABP)
Lipoprotein Lipase (LPL)
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22
Q

How does increased fat (spare) glucose?

A

Increased free fatty acids (B-oxidation) inhibits PFK-1, so less breakdown of glucose… Refer back to picture slide..

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23
Q

Describe how AMP stimulates the uptake of fatty acids into mitochondria

A

REVIEW PICTURE FOR ANSWER

24
Q

Recall what happens in starvation (4 Points)

A
  1. Glucose is reserved for brain
  2. Muscle uses fatty acids and ketone bodies
  3. Muscles provide amino acid C-skeletons for liver to use in gluconeogenesis
  4. Amino acids largely released as alanine and glutamine
25
Q

Does glucagon activate glycogen phosphorylase in muscle?

A

NO, survival mechanism in early man. Need energy to kill stuff in a starvation situation. So glycogen is saved for movement

26
Q

Major muscle fuel after 4h starvation?

A

Fatty acids

27
Q

Major muscle fuel after 1-2 days?

A

Fatty acids + Ketone Bodies

28
Q

Major muscle fuel after 3 weeks?

A

Fatty acids

29
Q

What hormone stimulates the breakdown of muscle protein to provide C-atoms for liver gluconeogenesis during days 1-2 in starvation?

A

Cortisol

This decreases after day 2 as ketone bodies take over as major fuel source

30
Q

Excess acetyl CoA is converted to _____ (3) by liver mitochondria?

A

Acetoacetate
B-hydroxybutyrate
Acetone

31
Q

How does the muscle utilize ketone bodies as a fuel?

A

Ketone bodies are converted back to 2 molecules of actetyl CoA….. Enzyme? REVIEW Figure near end of lecture

32
Q

Muscle breakdown in starvation yields mainly which 2 amino acids?
What is the major site of metabolism?

A
  1. Alanine and Glutamine

2. Branched-chain amino acids

33
Q

What is the major pathway of catabolism for cardiac muscle in the fed state

A

Oxidative (95%), mostly fatty acids, some glucose

Can oxidize lactate under extreme circumstances

34
Q

Which glucose transporter is important for uptake of glucose into cardiac muscle (response to insulin)

A

GLUT-4

Insulin also stimulates PFK-2 to produce F-2,6- bisphosphate

35
Q

What happens in cardiac muscle metabolism during ischemic conditions?

A

(eg. MI)
ATP levels fall, AMP levels rise
Anerobic glycolysis is stimulated to compensate for the loss of aerobic ATP production via 2 AMP-mediated mechanisms.

36
Q

What are the 2 AMP mediated mechanisms of energy production in ischemic cardiac muscle?

A

Note: goal of both is to activate PFK-1

  1. AMP activates AMPK - AMP-activated protein kinase which phosphorylates PFK-2. PFK-2 increases production of fructose-2,6-bisphosphate —> activeates PFK-1
  2. AMP activates PFK-1 directly (via allosteric binding)

Review picture on slide

37
Q

What are the 2 important X-linked dystophies?

A

Duchenne (DMD)
Becker (BMD)
THE REST ARE AUTOSOMAL

38
Q

What population is Oculopharyngeal Muscular Dystrophy (OPMD) prevalent?

A

French-Canadians

39
Q

Describe the etiology of DMD

A

30% new mutations
Dystrophin gene virtually absent
Cause by frameshift mutations (e.g - deletion/duplication)

40
Q

Describe the etiology of BMD Becker

A

<2% new mutations
Reduced or Modified Dystrophin gene
Caused by point mutations(not frameshift like DMD)

41
Q

Where is the dystrophin gene located?

What is it important for?

A 
X chromasome (dont worry about detail)
Codes for the dystrophin protein which is important for linking cytoskeletal proteins to transmembrane glycoproteins which connect to the ECM.
42
Q

What is used in the diagnosis and carrier detection for MD?

A 
HIstory and Physical 
****SERUM CREATINE KINASE**
Muscle biopsy
Multiplex PCR
SCAIP (useful in prenatal diagnosis, internal primer sequencing)
43
Q

Describe the etiology of myotonic muscular dystrophy (MMD or DM - dystrophia myotonica)?

A

Autosomal dominant
MOST COMMON MD
Affects heart, smooth muscle, CNS, eye, and endocrine system
Caused by a repeat expansion*****
Appears after adolescence, displays anticipation as well (more severe expression generation to generation)

44
Q

Symptoms of MMD?

A 
Myotonia
Muscle Wasting
Cataracts
Diabetes Mellitus
Frontal Balding
Mild Mental Deterioration
Testicular atrophy
*reveiw pic of muscles generally affected (mostly extremities and neck +diaphragm)
45
Q

In MMD, what is the difference between DM1 and DM2?

A

DM1 - is more common (98%), shows anticipation, chromosome 19 (More details??)
DM2 - unlikely, milder in presentation, chromosome 3, no anticipation?

46
Q

Onset/Death in DM1 classic case?

A

Onset: 10-30 yrs
Death: 48-55 yrs

47
Q

Onset/Death in DM1 congenital case?

A

Onset: birth - 10 yrs
Death: 0-45 yrs

Note mild version shows up (20-70yrs) and can live (60yrs-normal)

48
Q

Mechanism of MMD diagnosis?

A

Targeted mutation analysis: PCR to find repeat sequence, Southern blot for larger expansions

49
Q

Describe Facioscapulohumeral Dystrophy (FSHD)

A 
Autosomal dominant
Principally affects upper body 
Defect in long arm of chromosome 4
Onset usually 10-25 yrs old 
Non-symmetrical pattern of weakness, scapular winging, slight scoliosis
50
Q

Describe Limb-girdle Muscular Dystrophies (LGMD)

A

Autosomal dominant AND recessive
Caused by mutations in genes encoding sarcoglycans 4 most common forms
CK levels normal to very high (in some recessive forms)

51
Q

Describe oculopharyngeal musculodystrophy (OPMD)

A

Autosomal dominant
Caused by an expansion of GCN repeat within the gene encoding the poly(A) binding protein (PABPN1)
Characteristic drooping eyelids, weakness in facial and pharyngeal muscles - can extend to limbs
CK levels are usually normal or mildly elevated

52
Q

Describe Congenital Musculodystrophy (CMD)

A

Autosomal recessive, presenting soon after birth
Hypotonia followed by muscle weakness
50% *Due to a deficiency in laminin-2, while others due to defective glycosylation of alpha-dystroglycans (muscle fiber destruction due to impaired binding of laminin)
CK levels usually moderately high

53
Q

Describe Bethlem Myopathy

A

Autosomal dominant, usually onset before 5
Mutation affecting Collagen - VI
Proximal muscle weakness (mild to progressive)
Lifespan not affected

54
Q

Malignant Hyperthermia (MH)

A

Feared (Rare) complication of general anesthesia
DMD, BMD, MMD patients may be particularly susceptible
Pathologic release of Ca++ in response to anesthesia
Hypermetabolic Sate

55
Q

What is the treatment for Malignant hyperthermia (MH)

A

dantrolene sodium

Musculoskeletal System (21 decks)

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