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Term 2: Metabolism > Reddy's Biproduct Metabolism > Flashcards

Reddy's Biproduct Metabolism Flashcards

1
Q

Which of the following tissue / cells obtain energy by
glycolysis as well as by oxidative phosphorylation?

 A.  Brain
 B.  RBCs
 C.  Lens
 D.  Cornea
 E.  Platelets
A

A. Brain

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2
Q

What is Heme made up of?

A
  • Iron

- Porphyrin

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3
Q

What are the initial substrates of Heme?

A
  • Glycine

- Succinyl CoA

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4
Q

What toxin inhibits two steps in the heme synthesis, also lowering sperm count?

A

Lead

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5
Q

What is Porphyrias?

A
  • a disease caused by problems in Heme synthesis
  • skin eruptions. Photosensitivity. Anemia.
  • urine darkens on exposure to light and air
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6
Q

Where is heme synthesized?

A
  • bone marrow

- liver

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7
Q

What enzyme catalyzes the rate-limiting step in Heme synthesis? What inhibits this enzyme?

A
  • ALA Synthase

- inhibited by Heme

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8
Q

Where does conjugation of bilirubin into soluble conjugated bilirubin occur?

A

-the liver

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9
Q

Why does bilirubin need to be conjugated with Glucuronic acid?

A
  • it is only soluble in its conjugated form

- needs to be soluble to be excreted

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10
Q

What does it mean if plasma levels of bilirubin are high?

A

-the liver is unable to conjugate the bilirubin

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11
Q

Where is conjugated bilirubin secreted?

A
  • into the bile then intestine (95% feces)

- Urine (5%)

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12
Q

Detoxification of drugs occurs in which part of the cell?

A.  Mitochondria
B.  Lysosomes
C.  Peroxisomes
D.  Smooth endoplasmic reticulum
E.  Rough endoplasmic reticulum
A

D. Smooth endoplasmic reticulum

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13
Q

What causes neonatal jaundice?

A
  • a deficiency in the conjugating enzyme in the liver (BGT)

- Liver has not matured enough

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14
Q

How does UV light treat premature babies with jaundice?

A

-breaks down insoluble bilirubin into more soluble products, which can be excreted via feces and urine

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15
Q

One of your patients, 60 years old, male
is showing clear signs of jaundice. His
liver function tests (LFTs) show very high total bilirubin and conjugated bilirubin.

These data indicate that jaundice is most likely due to:

A. Liver cirrhosis
B. Obstructive jaundice (aka post-hepatic jaundice)
C. Chronic kidney disease
D. Hemolytic jaundice
E. Neonatal jaundice (conjugating enzyme not being made)

A

B. Obstructive jaundice (aka post-hepatic jaundice)

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16
Q

Photosensitivity, anemia, bright red-colored urine seen in
patients with Porphyria are due to defects in this pathway.

A.  Uric acid formation 
B.  Heme synthesis
C.  Bilirubin conjugation
D.  Hexose monophosphate shunt
E.  Purine salvage pathway
A

B. Heme synthesis

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17
Q

What is creatine phosphate, and what enzyme synthesizes it?

A
  • a form of stored energy in muscle, can make ATP from ADP

- created by creatine phosphokinase (CPK) from Creatine and ATP

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18
Q

What is Creatinine?

A

-a spontaneous degradation product of Creatine and Creatine Phosphate

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19
Q

Aspirin and other NSAIDs inhibit synthesis of:

A. Thromboxanes
B. Prostaglandins
C. Prostaglandins and Leukotrienes
D. Thromboxanes and Prostaglandins
E. Prostaglandins and Phospholipase A2
A

D. Thromboxanes and Prostaglandins

20
Q

Anti-inflammatory effects of Prednisone and
other steroids are largely due to inhibition of:

A. COX-1 and COX-2
B. Epoxygenase (Epox)
C. Lipoxygenase (LOX)
D. Selectively COX-2
E. Phospholipase A2
A

E. Phospholipase A2

21
Q

What happens to dietary porphyrins?

A

-we degrade it (enterocytes), we like to make our own

22
Q

What organ breaks down heme into bilirubin?

A

-the spleen (macrophages)

23
Q

What is the main phospholipid used in prostaglandin, leukotrienes, and thromboxane synthesis?

A

-Arachidonic Acid

24
Q

Anti-inflammatory steroids inhibit production of _________.

A

Arachidonic Acid

25
Q

What is the main waste product of degrading ATP, GTP, and Purines?

A

uric acid

26
Q

What does a folate deficiency lead to?

A

-Megaloblastic anemia

27
Q

Our diet contains many different compounds / substances. In a normal healthy person, which of the following is absorbed nearly 100% in the GI tract and ends up in the portal blood and goes to liver.

A.  Purines / Pyrimidines
B.  Cholesterol
C.  Heme
D.  Epinephrine
E.  Glucose
F.  Insulin
A

E. Glucose

28
Q

Which amino acids are used in the synthesis of purines?

A

GAG

  • glycine
  • aspartate
  • glutamate

*folate

29
Q

What is Lesch-Nyhan syndome?

A
  • purine salvage enzyme HGPRT is missing
  • results in excessive production of uric acid, and increased de novo purine synthesis
  • excess uric acid leads to gout
  • also characterized by motor dysfunction, cognitive deficits, and behavioral disturbances (self-mutilation)
30
Q

What enzyme deficiency causes SCID (only 15% of cases)?

A
  • adenosine deaminase deficiency
  • leads to too much dATP, which inhibits ribonucleotide reductase (RNR), which means cells cannot make DNA (affects rapidly dividing cells, B & T cells)
31
Q

Describe the simplified version of purine disposal.

A

Purines–>Xanthine–>Uric acid

-Uric acid step catalyzed by xanthine oxidase

32
Q

How does allopurinol treat gout?

A

-inhibits xanthine oxidase, so more soluble xanthine is not converted to uric acid

33
Q

Gout is commonly due to accumulation of
uric acid in plasma. Treatment for chronic gout is inhibition of which enzyme?

 A.  Dihydrofolate reductase
 B.  Xanthine oxidase
 C.  HGPRT
 D.  Adenosine deaminase
 E.  Thymidylate synthase
 F. Cyclooxygenase (COX)
 G. Phospholipase A2
A

B. Xanthine oxidase

34
Q

Lesch-Nyhan syndrome is due to defects in:

A. Dihydrofolate reductase
B. Xanthine oxidase
C. Adenosine deaminase
D. HGPRT
E. Lipoxygenase (LOX)
F. Cyclooxygenase (COX)
G. Phospholipase A2
A

D. HGPRT

35
Q

What diseases are associated with pyrimidine degradation?

A

-none

36
Q

Methotrexate is an anti-cancer drug that inhibits multiplication of rapidly dividing cells. Methotrexate works by inhibiting:

 A.  Ribonucleotide reductase
 B.  Xanthine oxidase
 C.  Thymidylate synthase
 D.  Telomerase
 E.  Dihydrofolate reductase (DHFR)
 F.  Cyclooxygenase (COX)
A

E. Dihydrofolate reductase (DHFR)

37
Q

What is folate required for?

A
  • one carbon metabolism (making & transferring methyl groups)
  • formation of purines, pyrimidines, and a bunch of other stuff
38
Q

What cofactors are required for regenerating SAM?

A
  • folate

- B12

39
Q

Why are symptoms of B12 deficiency slow to develop?

A

we have a 6 month supply in our liver

40
Q

What do sulfonamides do?

A
  • specifically inhibit replication of bacteria

- prevents bacterial synthesis of folate

41
Q

What is Methotrexate used for? How does it work?

A
  • used to inhibit replication in rapidly growing cells, such as in psoriasis, cancer, and rheumatoid arthritis
  • it inhibits conversion of folic acid to THF, thus inhibiting pyrimidine synthesis
42
Q

How do we differentiate a folate deficiency from a B12 deficiency?

A
  • both cause macrocytic anemia

- B12 deficiency causes neuropsychiatric sx’s and dementia

43
Q

Vitamin B12 deficiency, but not folate deficiency,
results in neuropsychiatric symptoms.
This may be due to accumulation in cell membranes of:

A. Branched fatty acids
B. Fatty acids with odd number of carbons
C. Trans-fatty acids
D. Oxidized cholesterol
E. S-adenosyl homocysteine
F. Unsaturated fatty acids
G. Saturated fatty acids
A

B. Fatty acids with odd number of carbons

44
Q

One of your patients is diagnosed with Gout.
Needle aspiration of synovial fluid and analysis
confirmed uric acid crystals.

One of the following will NOT be your recommendations.

A. Eat foods low in nucleic acids; list foods to avoid

B. Stay hydrated; drink plenty of water / fluids

C. Stay warm; keep extremities covered

D. Avoid aspirin, diuretics

E. Eat caviar, have a drink and go skiing

A

E. Eat caviar, have a drink and go skiing

45
Q

What is the simple pathway for synthesis of pyrimidines?

A

Amino acids + CO2 –> UMP –> UTP –> CTP

46
Q

Why should patients with gout stay away from aspirin?

A

-Aspirin is acidic, will lower pH of blood thus reducing solubility of uric acid.

Term 2: Metabolism (5 decks)

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