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Biochemistry > NOT M2P > Flashcards

NOT M2P Flashcards

1
Q

What are the isoprenoids?

A

Steroids, lipid vitamins, terpenes

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2
Q

What are eicosanoids?

A

Prostaglandins, thromboxanes, leukotrienes

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3
Q

What are the glycerophopholipids?

A

Ether phospholipids, platelet activating factor, plasmalogens, phasphatidates, shingomyelins

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4
Q

What are the glycosphingolipids?

A

Cerbrosides, gangliosides, other GSL

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5
Q

What are the phospholipids

A

PE, PC, PS, PI, other PLs

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6
Q

Which FA is 14:0?

A

Myristic acid

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7
Q

Which FA is 16:0?

A

Palmitic acid

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8
Q

Which FA is 16:1?

A

Palmitoleic acid

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9
Q

Which FA is 18:0?

A

Stearic acid

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10
Q

Which FA is 18:1?

A

Oleic acid

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11
Q

Which FA is 18:2?

A

Linoleic acid

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12
Q

Which FA is 18:3?

A

Linolenic acid

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13
Q

Which FA is 20:4?

A

Archidonic acid

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14
Q

What does phospholipase A2 do?

A

Acts on PI releasing arachidonic acid–>prostaglandins

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15
Q

What does phospholipase C do?

A

Activated by PIP2, so is involved with second messengers

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16
Q

What does PGH synthase do?

A

converts Arachidonic acid –> PGH2 (prostaglandin)
COX1 - constitutively-expressed in most tissues
COX2 - induced by cytokines associated with inflammatory response

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17
Q

What is the purpose of aspirin?

A

Inhibition of COX1/2, irreversible inhibitor of COX1, reversible inhibitor of COX2

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18
Q

Which inhibitors are used for asthma?

A

Inhibitors of 5-LOX and antagonists of CysLT1 receptor

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19
Q

Where does cholesterol come from?

A

De novo - 70%

Dietary - 30%

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20
Q

What is the committed, rate limited step of cholesterol de novo synthesis?

A

HMG COA reductase, uses 2NADPH

Target for Statin drugs

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21
Q

What does Farnesyl PP give rise to?

A

Dolichol, Ubiquinone, Prenylated proteins, Squalene

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22
Q

What is 7-dehydrocholesterol?

A

Precursor for Vit. D

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23
Q

How is HMG COA reductase regulated?

A
  • Transcription factor SREBP-2 binding to the sterol regulatory element, SREBP-2 is associated with SCAP, when high [sterol], SCAP binds Insig, causing retention
  • When high [sterol], HMGCoA reductase ubiquitination and proteosomal degredation
  • HMG CoA reductase is -P by AMPK (inactive)
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24
Q

How is HMGCoA reductase upregulated?

A

By decreased cAMP levels by insulin, and increased thyroxine

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25
Q

What is the rate limited step in bile acid production?

A

Introduction of -OH group at C7 by cholesterol-7-alpha-hydroxylase

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26
Q

What is characteristic of 3-beta-hydroxysteroid dehydrogenase deficiency?

A

Virtually no glucocorticoids, mineralocorticoids, active androgens, or estrogens, salt excretion in urine, female-like genitalia

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27
Q

What is characteristic of 17-alpha-hydroxylase deficiency

A

No sex hormones or cortisol, increased production of mineralocortioids causes NA and fluid retention, and hypertension, female-like genitalia

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28
Q

What is characteristic of 21-alpha-hydroxylase deficiency?

A

Mineralocoricoids and glucocorticoids are virtually absent, salt wasting, overproduction of androgens leads to masculinization of external genitalia in females and early virilization in males

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29
Q

What is characteristic of 11-beta1-hydroxylase deficiency?

A

decrease in serum cortisol, aldosterone, and coricosterone, increased production of deoxycortisosterone causes fluid retention, low-renin hypertension, causes masculinization and virilization

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30
Q

Which apolipoproteins is not associated with HDL?

A

Apo B

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31
Q

Which apolipoproteins are associated with LDL-R?

A

ApoE, ApoB100

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32
Q

What is the purpose of chylomicrons?

A

Assembled in intestinal mucosa and carry dietary triglycerides, cholesterol, and cholesteryl esters, fat-soluble vitamins and other lipids to peripheral tissues

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33
Q

Which apolipoprotein is specific for CM?

A

ApoB48

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34
Q

Which protein loads apoB48 with lipid and what is the AR disorder associated with it?

A

Microsomal triacylglycerol transfer protein (MTP), and abetalipoproteinemia is a mutation in MTP leading to steatorrhea and fat-soluble vitamin deficiency

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35
Q

Which enzyme is anchored to the membrane of endothelial cells of capillaries in most tissues? which tissue is the exception?

A

EXCEPT LIVER, Lipoprotein lipase, activated by apo C-II to hydrolyze TAG -> glycerol + FA

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36
Q

What causes hyperlipoproteinemia type I?

A

Defect in Lipoprotein lipase or apo CII leading to accumulation in CM

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37
Q

What is a means of regulation for LDL-R function?

A

Serine protease PCSK9 blocking LDL-R recycling to the cell surface

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38
Q

What is characteristic of familial hypercholesterolemia (FH)?

A

Genetic defects in the LDL pathway leading to the accumulation of LDL in the plasma, including mutated LDL-R, ApoB, PCSK9

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39
Q

What is the friedewald equation to estimate LDL-chol?

A

Total Chol = HDL + TG/5 + LDL-chol

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40
Q

What is the major difference between myoglobin (Mb) and hemoglobin (Hb)?

A

Myoglobin helps diffuse O2 in the cells while Hb is the major transporter of O2 from the lungs to tissues
-Hb participates in Cooperative binding (once 1 binds its easier for the rest to bind)

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41
Q

which molecule is bound to Hb in the ferrous form?

A

Oxygen

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42
Q

Which molecule is bound to Hb in the ferric form?

A

Water

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43
Q

Where is the primary organs where myoglobin is found?

A

Heart and muscle

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44
Q

What is meant by P50?

A

When half of the O2 binding sites within the hemeglobin is full, normally 26 Torr

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45
Q

According to Bohr what increases O2 release?

A

A rightward shift (increase CO2, increase Acid H+, lowering PH) thereby reducing the affinity for O2 and increases likelihood to release O2

46
Q

Binding of what stabilizes the T form of Hb?

A

CO2, a little more than 10% of the body’s CO is expelled via Hb

47
Q

What will an increase in 2,3 BPG cause>

A

A stabilization of the deoxy state (T) and reducing the affinity for O2

48
Q

What would happen if there wasn’t any BPG?

A

The Heme would have a greater affinity for the Oxygen and would not release it in the tissues

49
Q

What happens with increased temperature or increased CO?

A

Increased temp, better release of O2

Increased CO, less release of O2

50
Q

What is characteristic of fetal Hb?

A

HbF has a greater affinity for O2 than HbA. The gamma chain of HbF has a much lower affinity for 2,3BPG leading to a leftward shift to aid in getting O2 from Mom

51
Q

Which hemoglobinopathies are associated with erythrocytosis versus anemia?

A

Rightward shift = anemia (Hb Titusville)

Leftward shift = erythrocytosis (HB helsinki)

52
Q

What is characteristic of methemoglobinemia?

A

Inherited enzyme deficiency of NADH-methemoglobin reductase enzyme that reduces Fe3 (ferric) to the Fe2 (ferrous) form. The patient presents with a blue skin tone and brown blood

53
Q

Where does synthesis of heme occur?

A

In all cells except mature RBC

54
Q

What is the rate controlled enzyme in heme synthesis?

A

ALA synthase, which combines Glycine and succinyl CoA with the coenzyme PLP to become ALA + CO2
OCCURS IN THE MITOCHONDRION

55
Q

What is the main difference between Uroporphyrin I and Uroporphyrin III?

A

The location of propionic acid versus methyl groups coming off of 7/8 on the porphyrin,
UroI - 7 = A, 8=P
Uro III - 7 = P, 8=A

56
Q

What is the main difference between Coproporphyrin I and coproporphyrin III?

A

Copr I - 7 = M, 8=P

Copr III - 7 = P, 8=M

57
Q

How is ALAS-II (erythroid) regulated?

A

Translation of mRNA controlled by iron, as iron availability increases, translation increases

58
Q

How is ALAS-I (hepatic) regulated?

A

Translation of mRNA inhibited when high [heme]

-High [heme] inhibits transport of ALAS-I into mitochrondria, and catalytic activity via feedback inhibition

59
Q

What compounds induce ALAS-I?

A

Barbiturates, xenobiotics, increase P450 in the liver

60
Q

Which enzyme is inhibited by lead?

A
  • Porphobilinogen synthase (replaces Zn)/ALA dehydrogenase

- Ferrochelatase

61
Q

What are porphyrias and where do the different types accumulate?

A
  • Porphyrias - defects in heme synthesis
  • Non-erythropoietic accumulates in liver
  • Erythropoietic - accumulates in bone marrow
62
Q

What is characteristic of acute intermittent porphyria (AIP)?

A
  • non erythropoietic (acute)
  • affects hydroxymethylbilane synthase (decreased) and ALA synthase (increased)
  • Effects the nervous system
63
Q

What is characteristic of porphyria cutanea tarda (PCT)?

A

Non-erythropoietic (chronic)

  • affects uroporphyrinogen decarboxylase (decreased) and ALA synthase (increased)
  • Effects skin; can be induced by liver disease, discolored urine
64
Q

What is characteristic of Lead poisoning?

A
  • Affects all tissues
  • Affects ALA dehydratase (decreased), ferrochelatase (decreased), and ALA synthase (increased)
  • presents in the nervous system; blood (anemia)
65
Q

What is measured in UCB versus CB blood test?

A

UCB measures the “free” bilirubin bound to albumin - Total bilirubin - CB = UCB
-CB measures the Bilirubin diglucuronide (direct)

66
Q

What is hyperbilirubinemia?

A

An increase of bilirubin above 0.1-1.0 mg/dL

67
Q

How does hyperbilirubinemia occur?

A
  1. excessive production of bilirubin (prehepatic)
  2. disturbance in conjucation (hepatic)
  3. Interference in excretion (hepatic or post hepatic
68
Q

What is associated with an excessive production of bilirubin and what would happen to the UCB value?

A

Hemolytic jaundice, sickle cell anemia, G6PD deficiency, PK deficiency, UCB increases in blood

69
Q

What is associated with a decrease or absence of conjugation and what would happen to the UCB value?

A

Physiological jaundice, Crigler-Najjar (I/II), Gilberts disease, liver damage, increase in blood UCB

70
Q

What is associated with inhibition of excretion of CB and what happens to the CB value in blood and UCB?

A

Dubin-johnson syndrome, increase CB in blood, urinary CB will increase and intestinal CB decrease (pale poop, dark urine)

71
Q

How is iron lost?

A

Not excreted from the body in a regulated manner, loss through exfoliation

72
Q

What are the 5 iron binding proteins and where are they found?

A
  1. Apoferritin (most tissues) when bound is ferritin
  2. Transferrin (blood) for transport
  3. Lactoferrin - binds iron for uptake
  4. Mobilferrin (intestinal cells) intracellular transport
  5. Mitoferrin - across inner mito membrane`
73
Q

Why do antiacids affect iron absorption?

A

The iron is transported via a symport H+ from the intestinal lumen to the enterocyte

74
Q

What is the critical control of iron homeostasis?

A

Transport of Fe2+ out of enterocytes by ferroportin controlled by Hepcidin

75
Q

How is hepcidin synthesis controlled?

A

In iron excess, hepcidin synthesis is increased leading to a decrease in ferroportin and decreased release of iron from enterocyte
-In iron deficiency hepcidin synthesis decreased, increased release of iron

76
Q

What is associated with hereditary hemochromatosis?

A

Iron overload in liver, heart, and other organs usually in ferritin and hemosiderin. “Bronze diabetes”
-Defects in high iron gene (HFE)

77
Q

How is [apoferritin] controlled?

A

IRE at the 5’ end, so when low iron, IRP is bound stopping mRNA synthesis
- IRPs are degraded when [iron] is high

78
Q

How is the transferrin receptor controlled?

A

IRE at the 3’ end, so when low [iron] IRPs are available stabilizing mRNA and increases receptor concentration

79
Q

How does iron affect ALAS II?

A

IRE at the 5’ end, when high [iron] mRNA synthesis occurs (IRPs getting degraded)

80
Q

What are the 5 steps of clotting?

A
  1. formation of a fibrin clot
  2. formation of a platelet plug
  3. vasoconstrictions
  4. anticoagulation
  5. clot dissolution
81
Q

How are proteins activated in the various clotting pathways?

A
  1. Proteolytic cleavage (serine proteases)

2. Conformation change (no proteolysis)

82
Q

What post-transcriptional modification is important in clotting? What drug targets this reaction?

A

gamma-carboxylation in the lumen of RER in liver

  • Vit K is coenzyme
  • Dicumarol and Warfarin (Coumadin) targets Vit K epoxide reductase
83
Q

What is the key protein in the extrinsic pathway?

A

Transcription factor (III) which binds VII

84
Q

Which protein is not associated with bleeding when it is deficient?

A

XII

85
Q

Which deficiency is associated with hemophilia A and hemophilia B

A 
A = VIII
B = IX
86
Q

What mutation in which gene leads to increased tendency to clot?

A

G20210A in the prothrombin gene increases expression and increased clotting

87
Q

Which factors are serine proteases?

A

II, VII, IX, X, XI, XII

88
Q

Which factors are Gla-containing proteases?

A

II, VII, IX, X

89
Q

Which factors are accessory proteins?

A

III, V, VIII

90
Q

What is associated with Bernard-soulier syndrome?

A

Deficiency in platelet receptor for VWF

91
Q

What do fibrinogen molecules do?

A

Link activated platelets to one another

92
Q

What is associated with Glanzmann’s thrombasthenia?

A

Defect in platelet receptor for fibrinogen

93
Q

What is most important in limiting clotting?

A

Antithrombin III made by liver, which is a SERPIN, inactivating thrombin, IXa through XIIa, and VIIa-TF, greatly increased by heparin

94
Q

Other than AT3 what limits clotting?

A

Protein C-S complex inactivates VIIIa and Va, and Tissue factor pathway inhibitor

95
Q

What is characteristic of thrombophilia?

A

Deficiencies of proteins C, S, or anti thrombin III, presence of factor V leiden, and excess prothrombin

96
Q

What is a tumor defined as?

A

a tumor is a heritably altered, relatively autonomous growth of tissue

97
Q

What are the 6 characteristics of cancer?

A
  1. Self sufficient GFs
  2. Insensitive to antiGFs
  3. Evasion of Apoptosis
  4. Immortal
  5. Angiogenesis
  6. Tissue invasion and metastasis
98
Q

Which protein is a powerful tumor supressor, how does it perform this function and when inhibited, how is it restored?

A

Retinoblastoma (Rb), sequesters E2F. Cyclin dependent kinase phospohrylates Rb unleashing E2F (^growth), and TFG-beta restores Rb

99
Q

What gene induces apoptosis?

A

p53, more than 50% of human cancers has inactive p53

100
Q

What is the most useful test in detecting carcinogens?

A

Ames Test

101
Q

Which factor in inflammation inhibits apoptosis?

A

Prostaglandin (PGE2)

102
Q

How are viruses carcinogenic?

A

HPV: The early genes E6, E7 sequester p53, and Rb
SV40: Early protein T antigen sequesters p53 and Rb

103
Q

What is an example of an transducing RNA virus?

A

Insert viral oncogenes ex: Src, when transduced v-src. Has a tyrosine kinase activity -P various target genes part of growth/differentiation/migration
From the rous sarcoma virus

104
Q

What is an example of a non-transducing cis-acting RNA virus?

A

Avian Leukosis Virus, ALV

process referred to as promoter insertion

105
Q

What is an example of a non-transducing trans-acting RNA virus?

A

Human t-cell leukemia virus type I (HTLV-I)

trans-regulating protein Tax activates transcription

106
Q

What is associated with common hyperlipidemia IIa?

A

AKA: Familial hypercholesterolemia

High [LDL], high plasma [Chol]

107
Q

What is associated with hyperlipidemia III?

A

AKA Dysbetalipoproteinemia

High “floating” [LDL], high plasma [chol & TG], defect in receptor ApoE

108
Q

What is associated with hyperlipidemiaV?

A

Elevated [VLDL & CM], elevated plasma [TG]

either a LPL deficiency or ApoC-II deficiency

109
Q

What is associated with hyperlipidemia I?

A

Elevated [CM], elevated plasma [TG]

either a LPL deficiency or ApoC-II deficiency

110
Q

what is characteristic of abetalipoproteinemia?

A

Virtual absence of apoB-containing lipoproteins
decreased plasma [TG/TC]
due to molecular abn in MTP involved in lipidating apoB

111
Q

What is characteristic of Tangier disease?

A

Virtual absence of HDL

defect in plasma membrane ABC transporter

Biochemistry (2 decks)

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