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PSMA > PBIO > Flashcards

PBIO Flashcards

1
Q

Type 0:

A. GSD 0
B. Andersen disease
C. Tarui disease

A

A. GSD 0

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2
Q

Type 1:

A. Forbes-Cori disease
B. Hers disease
C. Von Gierke

A

C. Von Gierke

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3
Q

Type 2:

A. Forbes-Cori disease
(rare)
B. Pompe disease
(serios type of GSD)
C. Andersen disease

A

B. Pompe disease
(serios type of GSD)

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4
Q

Type 3:

A. Forbes-Cori disease
(rare)
B. McArdle disease
C. Andersen disease

A

A. Forbes-Cori disease
(rare)

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5
Q

Type 4:

A. Tarui disease
B. McArdle disease
C. Andersen disease

A

C. Andersen disease

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6
Q

Type 5:

A. GSD 0
B. Forbes-Cori disease
(rare)
C. McArdle disease

A

C. McArdle disease

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7
Q

Type 6

A. GSD 0
B. Hers disease
C. McArdle disease

A

B. Hers disease

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8
Q

Type 7

A. Pompe disease
B. Von Glerke
C. Tarui disease

A

C. Tarui disease

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9
Q

Deficiency of GSD 0

A. Glycogen synthase
B. Myophosphorylase
C. Debranching enzyme

A

A. Glycogen synthase

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10
Q

Deficiency of Von Gierke

A. Glycogen synthase
B. Myophosphorylase
C. Glucose 6-phosphate

A

C. Glucose 6-phosphate

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11
Q

Deficiency of Pompe disease

A. Phosphprylase (necessary to
breakdown glycogen)
B. Acid maltase enzyme
C. Transglucosidase (glucosyl
transferase enzyme)

A

B. Acid maltase enzyme

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12
Q

Deficiency of Forbes Cori disease

A. Debranching enzyme
B. Acid maltase enzyme
C. Transglucosidase (glucosyl
transferase enzyme)

A

A. Debranching enzyme

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13
Q

Deficiency of Andersen disease

A. Debranching enzyme
B. Myophosphorylase
C. Transglucosidase (glucosyl
transferase enzyme)

A

C. Transglucosidase (glucosyl
transferase enzyme)

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14
Q

Deficiency of McArdle disease

A. Phosphofructokinase
B. Myophosphorylase
C. Phosphprylase (necessary to
breakdown glycogen)

A

B. Myophosphorylase

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15
Q

Deficiency of Hers diseases

A. Phosphofructokinase
B. Myophosphorylase
C. Phosphprylase (necessary to
breakdown glycogen)

A

C. Phosphprylase (necessary to
breakdown glycogen)

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16
Q

Deficiency of Tarui disease

A. phosphofructokinase
B. Acid maltase enzyme
C. Glycogen synthase

A

A. phosphofructokinase

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17
Q

Clinical features of GSD 0

A. Muscle damage
B. Muscle cramps
D. Liver damage

A

B. Muscle cramps

18
Q

Clinical features of Von Gierke

A. Liver damage
B. Cardiac damage
C. Muscle damage

A

A. Liver damage

19
Q

Clinical features of Pompe disease

A. Muscle cramps
B. Liver damage
C. Cardiac damage

A

C. Cardiac damage

20
Q

Clinical features of Forbes Cori disease

A. Muscle damage
B. Cardiac damage
C. Liver damage

A

C. Liver damage

21
Q

Clinical features of Andersen disease

A. Liver damage
B. Muscle crams
C. SOB

A

A. Liver damage

22
Q

Clinical features of McArdle disease

A. Liver damage
B. Muscle damage
C. Muscle cramps

A

B. Muscle damage

23
Q

Clinical features of Hers disease

A. Muscle cramps
B. Muscle damage
C. Liver damage

A

C. Liver damage

24
Q

Clinical features of Tarui disease

A. Cardiac damage
B. Muscle damage
C. Liver damage

A

B. Muscle damage

25
Q

Manifestation of GSD 0

A. Fasting hypoglycemia
B. Extreme enlargement of liver
(accumulation of glycogen)
C. Muscle fatigue, Muscle pain

A

A. Fasting hypoglycemia

26
Q

Manifestation of Von Gierke

A. Fasting hypoglycemia
B. Exercise induce cramps
C. Hepatomegaly, platelet dysfunction and growth retardation

A

C. Hepatomegaly, platelet dysfunction and growth retardation

27
Q

Manifestation of Pompe disease

A. IIA- infantile form, IIB- juvenile, IIC- adult
B. Lysosomal storage disease (accumulation of glycogen in
lysosome)
C. General: skeletal muscle
weakness
D. All the above

A

D. All the above

28
Q

Manifestation of Forbes Cori disease (rare)

I. Hepatomegaly, hypoglycemia
and myopathy
II. Can lead to death within 5 years
of age
III. Affects liver, heart, skeletal
muscle

A. I only
B. II only
C. I and III

A

C. I and III

29
Q

Manifestation of Andersen Disease

I. Rare inherited condition that
causes severe muscle pain and
cramps
II. Abnormal glycogen in liver and
muscle
III. Can lead to death within 5 years
of age

A. I and II
B. II and III
C. II only

A

B. II and III

30
Q

Manifestation of McArdle disease

I. Rare inherited condition that
causes severe muscle pain and
cramps
II. Exercise induce cramps

III. Rhabdomyolysis

A. I only
B. II and III
C. I, II, and III

A

C. I, II, and III

31
Q

Manifestation of Hers disease

I. Lysosomal storage disease
(accumulation of glycogen in
lysosome)
II. Extreme enlargement of liver
(accumulation of glycogen)
III. Abnormal glycogen in liver and
muscle

A. I only
B. II only
C. I, II, and III

A

B. II only

32
Q

Manifestation of Tarui disease

A. Muscle fatigue and Muscle pain
B. Fasting hypoglycemia
C. Hepatomegaly, hypoglycemia
and myopathy

A

A. Muscle fatigue and Muscle pain

33
Q

Site of Cyanide
A. Cytochrome oxidase
B. ADP phosphorylation
C. NADH-CoQ reductase

A

A. Cytochrome oxidase

34
Q

Effect of Cyanide

A. All intermediates before and including cyt a will be in the reduced state; all intermediates after and including cyt c1 will be oxidized states. Blocks site lll
B. Blocks transfer of electrons to O2. Blocks at site IV
C. Inhibits entry of ADP into mitochondria and ATP export. Stop electron transport because of lack of ADP. Inside, all ADP is converted to ATP

A

B. Blocks transfer of electrons to O2. Blocks at site IV

35
Q

Site of Antimycin

A. ADP phosphorylation
B. ADP-ATP transporter
C. Electron transfer from cyt b to cyt c1

A

C. Electron transfer from cyt b to cyt c1

36
Q

Effect of Antimycin

A. All intermediates before and including cyt a will be in the reduced state; all intermediates after and including cyt c1 will be oxidized

B. Blocks phosphorylation of ADP. Does not inhibit uncouples oxidations

C. Blocks oxidation of NADH (site l). NADH will be reduced; Substrates such as succinate that enter via FADH will still be oxidized and make 2 ATPs/mol

A

A. All intermediates before and including cyt a will be in the reduced state; all intermediates after and including cyt c1 will be oxidized

37
Q

Site of Rotenone

A. Cytochrome oxidase
B. NADH-CoQ Reductase
C. Electron transfer from cyt b to cyt c1

A

B. NADH-Co2 Redutase

38
Q

Effect of Rotenone

A. Blocks transfer of electrons to O2. Blocks at site IV

B. Blocks phosphorylation of ADP. Does not inhibit uncouples oxidations

C. Blocks oxidation of NADH (site l). NADH will be reduced; Substrates such as succinate that enter via FADH will still be oxidized and make 2 ATPs/mol

A

C. Blocks oxidation of NADH (site l). NADH will be reduced; Substrates such as succinate that enter via FADH will still be oxidized and make 2 ATPs/mol

39
Q

Site of Oligomycin

A. ADP Phosphorylation
B. NADH-CoQ Reductase
C. Cytochrome oxidase

A

A. ADP phosphorylation

40
Q

Effect of Oligomycin

A. Blocks transfer of electrons to O2. Blocks at site IV

B. Inhibits entry of ADP into mitochondria and ATP export. Stop electron transport because of lack of ADP. Inside, all ADP is converted to ATP

C. Blocks phosphorylation of ADP. Does not inhibit uncouples oxidations

A

C. Blocks phosphorylation of ADP. Does not inhibit uncouples oxidations

41
Q

Site of Atractyloside and bongkrekate

A. NADH-CoQ Reductase
B. Electron transfer from cyt b to cyt c1
C. ADP-ATP transporter

A

B. ADP-ATP transporter

42
Q

Effect of Atractyloside and bongkrekate

A. Blocks phosphorylation of ADP. Does not inhibit uncouples oxidations

B. Inhibits entry of ADP into mitochondria and ATP export. Stop electron transport because of lack of ADP. Inside, all ADP is converted to ATP

C. All intermediates before and including cyt a will be in the reduced state; all intermediates after and including cyt c1 will be oxidized

A

B. Inhibits entry of ADP into mitochondria and ATP export. Stop electron transport because of lack of ADP. Inside, all ADP is converted to ATP

PSMA (7 decks)

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