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Biochem 1502 > Winter Exam 2 > Flashcards

Winter Exam 2 Flashcards

1
Q

What are the 3 types of extracellular molecules in ECM?

A

1) GAGs and proteoglycans 2) fibrous proteins -collagen, elastin 3) adhesive proteins - fibronectine, laminin

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2
Q

What are GAGs?

A

aka mucopolysaccharides, are repeating disaccharides. Neg surface charge that attracts water to create turgor. Bottle brush or fir tree appearance. HA acid backbone

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3
Q

Describe Collagen

A

resistent to shear, make up 25% of protein mass, composed of a triple helix strucutre (a chains). Every third residue is Gly

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4
Q

How is collagen synthesized?

A

translated from mRNA -> pro-a chins -> proline and lysine hydroxylated (VitC) -> hydroxylysine glycosylated -> triple helix secreted into ECM -> propeptides cleaved -> tropocollagens -> crossling to form collagen fibrils ->allysine (lysil oxidase) -> mature fibrils

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5
Q

What happens when there is not enough Vit C (Scurvy)?

A

no stable triple helix is formed and there are defective pro-a chains. Immediate degradation. Only newly produced collagen is effected.
Tissues w rapid collagen turnover are effected most - vessels, bruising, wounds, teeth

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6
Q

What is Osteogenesis Imperfecta?

A

abnormal collagen type 1 production, aka brittle bone disease, never have normal collagen, mostly autosomal dominant.
Type 1: low concentration of collagen of normal structure
Type 2: abnormal collagen; severe

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7
Q

What is Ehlers-Danlos syndrome?

A

defect in fibrillar collagen, joint and skin effected

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8
Q

Describe the structure of Elastin

A

non-polar amino acids: gly, ala, val. Also rich in pro and lys.

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9
Q

Describe elastin synthesis

A

secreted tropoelastin interact with fibrillin-1 -> 4 (3 allysines and 1 lysine sidechains) elastins form desmosine that can stretch and recoil

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10
Q

What is Marfan syndrome?

A

Fibrillin-1 mutation, improper elastin structure. Effects aorta, eye, lungs, dura, abnormally long people

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11
Q

What is a1-antitrypsin deficiency?

A

a1-antitrypsin keeps destructive neutrophil elastase in check so it does not cause too much inflammation. A deficiency tho, has a reduced ability of this. Lung tissue cannot regenerate and predesposed to emphysema.

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12
Q

Where are the adhesive glycoproteins fibronectin and laminin found?

A

Fibronectin: CT
Laminin: Epithelium

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13
Q

What are the 3 binding domains of fibronectin and laminin?

A

1) cells (via integrins)
2) collagen
3) proteoglycans

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14
Q

What is the purpose of fibronectin and laminin?

A

To link ECM to cells (as well as the actin/cytoskeleton within the cell)

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15
Q

Describe Cadherins

A

transmembrane Ca-dependent cell to cell adhesion. Cadherins bind to each other (P,E,N-Cadherins). Hold cells together and tissue integrity

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16
Q

Describe Selectins

A

Cell surface, carb binding proteins that join cells. Selectin on one cell binds to glycoprotein/lipid on other (P,E,L-selectins). For blood stream and WBCs

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17
Q

Immunoglobulin Superfamily

A

Ca-INDEPENDENT cell-cell adhesino. Ligands for integrins. (ICAMs, MadCAM). During development

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18
Q

Describe Integrins

A

a/b transmembrane chains, b2 on leukocytes

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19
Q

What is the principal receptor for cell binding to ECM components?

A

integrins (weak affinity)

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20
Q

What is inside out signaling?

A

When changes within a cell results in alterations of inegrin properties.

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21
Q

What are examples of adhesion diseases?

A

cancer, Leukocyte adhesion deficiency, pemphigus, Asthma, RA, infections

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22
Q

An adhesion molecule binds to collagen. This adhesion molecule most likely belongs to which family?

A

Integrins

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23
Q

What is primary hemostasis?

A

Formation of platelet plugs, initiated in response to a vascular injury

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24
Q

What are platelets derived from?

A

Megakaryocytes.

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25
Q

Normal concentration of platelets?

A

150,000-3000,000 /microL blood

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26
Q

What is thrombocytopenia dn thrombocytosis?

A

thrombocytopenia: 400,000 platelets

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27
Q

What is Platelt Derived Growth Factor PDGF?

A

produced by platelets. They activate tyrosine kinase that promotes cell proliferation and wound healing

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28
Q

Why does normal epithelium not interact with blood components?

A

1) endothelial cells and platelets both have neg. charges

2) Endothelial cells produce factors (PGI2) that inhibit hemostasis and platelet aggregation

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29
Q

What happens to a vessel wall when there is injury?

A

1) physical barrier lost
2) No PGI2 synthesized
3) platelets interact with subendothelium

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30
Q

What are the different platelet receptors and what do they bind to?

A

Gp Ia-IIa : collagen in subendothelium
Gp Ib-IX : von Willebrand factor in subendo
Gp IIb-IIIa : fibrinogen in blood

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31
Q

What is a platelet disorder that has an absence of the receptor Gp Ib-Ix?

A

Bernard - Soulier disease

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32
Q

What is a platelet disorder with the absence of Gp-IIb-IIIa?

A

Glanzman thrombasthenia

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33
Q

What is von Willebrand disease?

A

defect in vWf. Excess bleeding but no spontaneous bleeding. Most common. Equally common in males and females

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34
Q

What do activated platelets release?

A

ADP and Thromboxane A2 (TXA2) - a required potent inducer of platelet aggregation

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35
Q

How is TXA2 produced?

A

arachidonic acid metabolism: platelet membrane -> arachidonic acid -> TXA2 (through cyclooxygenase pathway)

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36
Q

How does aspiring work?

A

It is an anti-platelet agent. It inhibits the cyclooxygenase (COX) pathway by acetylating COX-1. This inhibits TXA2 production

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37
Q

How does platelet activation effect platelet receptors?

A

induces conformation of Gp IIb-IIIa (integrin) so platelets can bind to fibrinogen with high affinity. Binding of fibrinogen mediates platelet-platelet interactions

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38
Q

What is secondary hemostasis?

A

Formation of fibrin to stablilize the platelet plug

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39
Q

What is the intrinsic pathway for coagulation?

A

all components are in plasma to form fibrin

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40
Q

What is the extrinsic pathway for coag?

A

require external factors (tissue factor) to form fibrin

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41
Q

What is the current understanding of the balance bw intrinsic and extrinsic hemostasis pathways?

A

the extrinsic pathway initiates coagulation while the intrinsic pathway continues the process

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42
Q

What is another name for Factor 2 and 2a?

A

Prothrombin and thrombin

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43
Q

Which factors are considered coenzymes as well?

A

Factor 5a and 8a

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44
Q

Which cofactor is required for the formation of zymogen forms of serine proteases?

A

Vit K

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45
Q

Which factor initiates the extrinsic pathway?

A

Factor 7

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46
Q

Which factor is produced in both the intrinsic and extrinsic pathway?

A

Factors 7 and 10a

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47
Q

Which factor converts prothrombin to thrombin?

A

Factor 10a

also Ca, Factor Va, and phospholipds are needed

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48
Q

What does thrombin do?

A

Converts fibrinogen to fibrin

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49
Q

What causes Hemophila A and B?

A

Deficiencies in Factor 8 and 9 repectively. They are both lcinically identical - X-lined recessive, same reaction effected.

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50
Q

What is the Tissue Factor Pathway Inhibitor TFPI?

A

protease inhibiting F7 and F10a.
associates with surface endothelium.
1) first binds to F10a and once there is excess
2) Then binds to F7 so neither component works in hemostasis

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51
Q

What is Antithrombin?

A

protease inhibiting thrombin and F10a.
Major inactivator of Thrombin, F10a, F9a
Much faster in presence of heparan sulfate and heparin (drug)

52
Q

What is antirhthrombin deficiency a risk factor for?

A

thrombosis

53
Q

Describe the difference bw low and high molecular weight heparin.

A

LMWH activates antithrombin to inhibit F10a only, while HMW inhibits F10a AND thrombin

54
Q

What is the Protein C/S Pathway

A

Thrombin binds to thrombomodulin, so now thrombin is able to cleave Protein C to Ca. Protein Ca associates with S and destroys cofactors, F5a, F8a

55
Q

What are risk factors form thrombosis?

A

Protein Ca def, Protein S def, Factor V Leiden, Antithrombin def., Factor Vleid:ProteinCa resistence (Arg->Gln), Elevated homocysteine

56
Q

Describe the fibrinolysis pathway

A

plasminogen is converted to plasmin by PAs (serine protease). Then plasmin degrades fibrin into D-dimers.

57
Q

What are some inhibitors of fibrinolysis?

A

a2-antitrypsin which inhibits plasmin

PAI-2 and PAI-2 inhibit tPA and uPA

58
Q

Name some conditions where venous thromboisis is a frequent problem

A

MI, CHF, chronic lung disease, stroke

59
Q

How do platelet receptor inhibitors work?

A

They bind to platelet receptors, which inhibits platelet adhesion and aggregation
EX: plavix, GpIIb-IIIa inhibitors

60
Q

How does heparin therapy work and what are some complicaitons?

A

Activates antithrombin

Bleeding, thrombocytopenia

61
Q

How does Warfarin work?

A

inhibts VitK-dependent gamma-carboxylase in liver.

62
Q

How is Vitamin K involved in coagulation pathway?

A

Vit K is a coenzyme for gamma-carboxylase. Helps form factors 2, 7, 9, 10 so that it can bind to calcium

63
Q

What is prothrombin time PT and what is the normal range?

A

time required to form a clot after tisue factor is added to plasma. 11-12 sec

64
Q

What is INR?

A

International normalized ratio. Normal = 1. If INR>7, risk of bleeding. Therapeutic range is 2-3

65
Q

Name a few clot busters

A

t-PA, u-PA, streptokinase. They activate plasminogen

66
Q

What is the final product of the porphyrin senthetic pathway?

A

heme

67
Q

Where are the major sites of heme biosynth?

A

1) liver

2) erythroid cells of bone marrow (majority)

68
Q

What are the mian porphyrins and their corresponding sidechains?

A

1) uroporpyrin - acetate and propionate
2) Coporporphyrin - methyl and propionate
3) Protoporphyrin IX - vinyl and propionate

69
Q

Which distribtion of porphyrin side chains is found in humans and what is the structre?

A

Type III - alternating A and Ps except for the D ring (bottom left ring)

70
Q

What is heme consisted of

A

one ferous ion in the center of a protoporphyrin IX

71
Q

When cellular requirements of heme are met, what happens?

A

Heme is converted to hemin by ferrous oxidation. Hemin inhibits hepatic ALA synthase activity by decreasing mRNA stability of ALAS

72
Q

What is derepression?

A

It is the upregulation of ALA synthase (and therefore heme) after drug exposure enhances heme utilization (lowering [heme])

73
Q

How does Lead inhibit heme formation?

A

Lead replaces Zn containing enzymes such as ALA dehydratase and ferrochelestase.
Non-competitive inhibition

74
Q

What is observed in lead poisoning?

A

Elevated ALA and anemia

75
Q

What is porphyria?

A

inherited (usually autosomal dominant) defect in heme synthesis. Results in low heme. Leads to an increase in ALA synthase via derepression. Erythropoietic or Hepatic (chronic or acute hepatic)

76
Q

Describe porphyria cutanea tarda

A

most common. chronic.

Def of unrporphyrinogen decarb. So accumulation of U3

77
Q

Describe ALA dehratase deficiency

A

IDK

78
Q

How much bilirubin can the liver excrete and how much does it actually excrete?

A

3000mg vs 300 mg

79
Q

Where is conjugated bilirubin normally found?

A

In hepatocytes. NOT in blood.

80
Q

What is Gilbet Syndrome>

A

gluconyltransferase deficiency. benign

81
Q

What test is indicative of alcohol abuse?

A

If AST:ALT is 2:1 or greater

82
Q

What is indicative of hepatocellular disease?

A

Disproportinately high AST, ALT levels compared to ALP levels

83
Q

What do low and normal levels of albuin indicate?

A

low: chronic disease (cirrhosis/cancer)
normal: acute (viral hepatitis)

84
Q

Which LDH isozyme is specific to liver?

A

LDH5

85
Q

What is cholestasis?

A

obstructino of bile duct perhaps to tumor or bile stone

86
Q

What test levels are associated with cholestasis?

A

elevated: ALP, ALT, AST, 5NT, GGT

87
Q

What is jaunice?

A

Deposition of bilirubin due to increased bilirubin levels i nblood

88
Q

What is hemolytic jaundice?

A

massive lysis of RBCs leads to production of more bilirubin. Liver cant conjugate it. High unconjugated bilirubin. Urine is dark yellow.
INCREASED INDIRECT BILIRUBIN

89
Q

What is hepatocelluar jaunice?

A

damage to lieer cells so high AST and ALT. Excess urobilinogen in blood. red/orange urine. Insufficeitn secretion ofbile from liver to bile (leaks into blood) -> INCREASED conjugated/DIRECT bilirubin

90
Q

What is obstructive jaunice?

A

Bile duct obstructed. Liver regurgitates conjugated bilirubin into blod. red/orange urine.
INCREASED DIRECT BILIRUBIN

91
Q

Why are some newborns jauniced?

A

low activity of Glucuronyl transferase so bilirubin accumulates

92
Q

Which LFT is most likely to be high in sickle cell anemia?

A

Unconjugated bilirubin (hemolytic jaunice

93
Q

What are the 3 domains for receptros with tyrosine kinase activity?

A

1) ligand binding N terminus
2) alpha helical domain across bilayer
3) effector region

94
Q

Explain the mechanism of steroid signaling

A

1) GF binds
2) tyrosine kinase of receptor activate each other
3) tyrosine residues phophorylated
4) SH2 adaptor proteins dock

95
Q

How does Ras work?

A

GTP binding protein. binds to SH2 that binds to tyrosine receptors. Ras activates a Ser/Thr cascade called MAP kinase cascade. Longer lived. MAPK activates trancription factors

96
Q

What are STATs?

A

Signal, Transducers, and activators of transcription. Contain SH2. STATs form dimers, go to nucleus and then bind to DNA

97
Q

Describe the PI3 pathway

A

PI3 binds to phosphoryltaed tyrosines. PIP2 gets phosphrylated. Akt phophorylates Bad (cell survival). PTEN dephosphrotayles PIP3 to inactivate pathway.

98
Q

Where are the IRS proteins found?

A

IRS 1 and 2: widely expressed
IRS3: adipose
IRS4: thymus, brain, kidney

99
Q

What are examples of PI3 kinase pathway?

A

glucose transport, protein synth, glycogen synth, cell prolif, cell survivial

100
Q

MISS vs NISS

A

membrane initiated vs nuclear initiated sterioid signaling. MISS is faster

101
Q

Which cells are permanently in G0 phase?

A

Neurons

102
Q

waht is quiescence and senescence

A

Quiescence: cells that can be activated reversibly
Senescence: when proliferative capacity irreversibly decreases w age

103
Q

How are antimetabolites involved with anticancer drugs?

A

interfere w purin or pyrimideine by inhibiting synthesis. S phase specific

104
Q

How are anticancer antibiotics involved in cancer treatmtent?

A

specific and non specific. interruption with DNA

105
Q

Mitotic Spindle Poisons

A

M phase specific, Vinca plants. Binds to tubulin causes depolymerizaiton.

106
Q

Through what does the degradation of cyclins occure?

A

protesomal pathway (ubiquitin is added for degredation)

107
Q

Which CDKs drive cell through M and S phases, repsectively?

A

CDK1 and CDK2. Present in constant amount but activity fluctuatesd

108
Q

What are the targets for CDK1?

A

mitotic specific - mitosis machinery, microtubules…

109
Q

What are the targets for CDK2?

A

DNA specific enzymes

110
Q

Name the cyclins and CDKs that associate w each other

A

Clyclin D with CDK 4/6 - through R point
Cyclin E/A with CDK 2 - DNA synth init
Cyclin B with CDK1 - M transition

111
Q

What does the retinoblastoma protein do/

A

prevents advacne of cell cycle into s phase by holding tranx factors. . Underphosphorylated RB is active.

112
Q

function of p53

A

1) regulates genes
2) arrests cycle
3) apoptosis

113
Q

Apoptosis process?

A

1) cells shrin from lamin cleavage
2) chromatin breaks down.condenses
3) fragmentation. macrophages
4) Phosphotidyl sering translocation

114
Q

Which 3 amino acids can be phosphoylated?

A

Ser, Thr, Tyr

115
Q

What do Ser Thr kinases associate with?

A

Smad

116
Q

What are some ligands for SerThr kinases

A

TGF-B, BMPs

117
Q

What do SH2 and SH3 interact w?

A

SH2-phosphorylated tyrosines

SH3- other intracellular signaling molecules

118
Q

Describe Ras

A

momomeric GTPase. active when GTP is bound

119
Q

What is neurofibrin?

A

a type of GTPase, that inactivates Ras

120
Q

Which post translational mod is needed for Ras functiom?

A

farneslation

121
Q

Mutations in KRAS can cause carcinomas in which parts ofb body?

A

lung, pancreas, colon

122
Q

What is Burkitts lymphoma?

A

translocation of 8 to 14. Overproduces c-myc gene. No mutation tho!

123
Q

What factor is overproduced in RA?

A

Tumor Necrosis Factor -alpha TNF-a

124
Q

Do tumor repressors act dominantly or recessively?

A

recessively

125
Q

What is Bcl2

A

a pro survivor facor. activation mutation tho will cause cancer

126
Q

What is Warburgs phenomenon?

A

Cancer shifts to glysoclysis even in aerobic conditions

127
Q

How does APC and inactivating mutations fo APC work?

A

Inactivating mutations disregulates beta-catenin, which then moves to the nucleus and activates genes. in proliferation.

Biochem 1502 (3 decks)

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