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Biochemistry > MCM- Cellular Transport > Flashcards

MCM- Cellular Transport Flashcards

1
Q

The goal of this is to sustain life and capture/harness energy

A

Metabolism

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2
Q

(+) Delta G is what type of reaction

A

Endergonic Reaction

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3
Q

(-) Delta G is what type of reaction

A

Exergonic Reaction

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4
Q

K(eq) = 1

A

Equilibrium

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5
Q

K(eq) > 1

A

Spontaneous; Exergonic

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6
Q

K(eq) < 1

A

Not Spontaneous, Endergonic

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7
Q

What is the most important reaction to sustain life

A

Acid/Base

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8
Q

Bi-Carbonate Ion

A

Increases pH

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9
Q

Acetic Acid Buffer

A

Decreases pH

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10
Q

Kidney Regulation of Blood pH; High

A

Decreases removal of H+; Decrease absorption of HCO3-

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11
Q

Kidney Regulation of Blood pH; Low

A

Increase removal of H+; Increase absorption of HCO3-

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12
Q

Normal Blood pH

A

7.00 +/- 0.03 (7.37-7.43)

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13
Q

Respiratory Acidosis

A

Not breathing enough, retain CO2; increasing H+ in the blood

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14
Q

Hypoventilation effect on blood pH

A

Respiratory Acidosis

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15
Q

Metabolic Acidosis

A

Addition of strong Acid; loss of HCO3-

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16
Q

Respiratory Alkalosis

A

Breathing too much, lose too much CO2, decrease H+ in the blood

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17
Q

Hyperventilation effect on blood pH

A

Respiratory Alkalosis

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18
Q

Metabolic Alkalosis

A

Too many Tums or strong bases added

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19
Q

Enzymes effect on a Rxn

A

Lower Ea (Activation Energy)

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20
Q

3 Parts that determine a reaction

A

Delta G, Ea (Activation Energy), Transition State

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21
Q

6 Classes of Reaction

A

Oxidoreductase, Transferase, Isomerase, Lyases, Ligases, and Hydrolases

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22
Q

Oxidoreductase

A

Transfer e- from donor to acceptor

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23
Q

Transferase

A

Transfer functional group between molecules

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24
Q

Isomerase

A

Transfer functional group internally

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25
Q

Lyases (Synthase)

A

Add or remove atoms to/or from double bonds

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26
Q

Ligases (Synthetase)

A

Form bonds w/ hydrolysis of ATP

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27
Q

Hydrolase

A

Cleave bonds w/ addition of H20

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28
Q

Fit Perfectly into the Active Site

A

Lock and Key

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29
Q

Binds and produces a confirmation change on the active site

A

Induced Fit

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30
Q

Co-Factors

A

Metal ions, non-covalent interactions, stabilize

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31
Q

Co-Enzymes

A

Small Organic Molecules

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32
Q

Copper Co-Factor

A

Cytochrome C Oxidase

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33
Q

Cytochrome C Oxidase

A

Accepts e- form cytochrome-c in the e- transport chain

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34
Q

Iron Co-Factor

A

Heme Proteins (Hemo- and myo- globin)

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35
Q

Magnesium Co-Factor

A

ATPases

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36
Q

ATPases

A

Hydrolyze ATP to ADP and use released energy for mechanical work

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37
Q

Selenium Co-Factor

A

Glutathione Peroxidase

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38
Q

Glutathione Peroxidase

A

anti-oxidant, detoxifies hydrogen peroxide

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39
Q

Zinc Co-Factor

A

Superoxide Dismutase

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40
Q

Superoxide Dismutase

A

anti-oxidant, Binds free radical of molecular oxygen

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41
Q

Co-Enzyme Types

A

Prosthetic group or Co-Substrate

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42
Q

Prosthetic Group

A

Permanent Association; Ex. FAD, FMN, Heme

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43
Q

Co-Suubstrate

A

Temporary Association (Bind and Release); Ex. NAD+

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44
Q

Covalent Modifactions of Enzymess (2)

A

Phosphorylation and Dephosphorylation

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45
Q

Enzyme Kinetic Dependents

A

Substrate Concentration, Km-> Affinity to bind substrate, and Vmax-> max speed at which reaction can occur

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46
Q

Enzyme Inhibitors (3)

A

Non-Competitive

Competitive

Uncompetitive

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47
Q

Competitive Inhibition

A

Can be overcome with increase in [S]

No effect on Vmax

Affinity to bind substrate decrease, so Km Increases

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48
Q

Non-Competitive Inhibition

A

Lowers Vmax because increasing [S] doesnt help

Binds both E and E+S

Km unchanged because it does not bind at active site

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49
Q

Uncompetitive

A

Km and Vmax go down at same factor

Binds E+S only

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50
Q

Inactivation

A

Irreversible loss of function of the enzyme; destruction of key functional groups

Decrease Vmax, Km is unchanged

Vmax goes down because adding [S] does not help

Only overcome by making new enzymes

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51
Q

Chelating co-factors

A

Inhibits the enzyme

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52
Q

What is EDTA used for

A

Chelating out Lead in lead poisoning. EDTA-Ca is introduced and Lead (Pb) binds the EDTA which then is excreted harmlessly through the urine

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53
Q

Allosteric Modification

A

Non-covalent modification; not on the active site

Induces confirmational change in the enzyme

can be positive or negative

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54
Q

Isozymes

A

Same function; different properties depending on the location of the enzyme (i.e. heart, brain, etc.)

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55
Q

What marker is released for an MI

A

Troponin, cTn-1, the specific troponin for cardiac myocytes

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56
Q

Max sensitivity of Troponin after MI

A

10-24 Hours after onset

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57
Q

Why are Pro-Enzymes made in an inactive state

A

So they do not damage the area in which they are made

Mainly digestive enzymes

58
Q

3 Groups of Membrane Lipids

A

Phospholipids

Glycolipids

Cholesterol

59
Q

2 Groups of Phospolipids

A

Glycerophospholipids

and

Sphingolipids

60
Q

Glycerophospholipid Make Up

A

Glycerol backbone, w/ phosphate and 2 fatty acids

61
Q

Sphinogolipid Make Up

A

Sphingosine backbone, long fatty acid chain, and phosphorylcholine

62
Q

Glycolipds Make Up

A

Sphingosine with Carbohydrate residue

63
Q

Where are glycolipids found

A

Outter leaflet of Lipid Bi-Layer

64
Q

Cholesterol Make-up

A

Steroid nucleus with hydroxyl group and hydrocarbon chain

65
Q

Cholesterol Location in Lipid Bi-Layer

A

Embedded in the lipid bi-layer

66
Q

Phosphatidylserine Importance with Apoptosis

A

When Apoptosis is triggered, Phosphatidylserine is put outside the plasme membrane, phagocytes or macrophage recognize this and destroy the cell

67
Q

Niemann-Pick Disease Cause

A

Deficiency of Acid Sphingomyelinase

68
Q

Niemann-Pick Disease Presentation

A

Hallmark is the cherry red spot in the eye, enlargement of the liver and spleen, along with neuro damage

69
Q

Deficiency of Acid Sphingomyelinase

A

Niemann-Pick Disease

70
Q

Acid Sphinogomylenase Job

A

Break down sphingo myelin in the lysosome

71
Q

3 Types of Membrane Proteins

A

Integral

Peripheral

Lipid

72
Q

Integral Membrane Protein location

A

Weave in and out of the bi-layer

73
Q

Integral Membrane Protein Job

A

Act as:

transporters

Ion Channels

Receptors

74
Q

Peripheral Membrane Proteins Location

A

Loosely bound to the membrane, can be removed

75
Q

Lipid-Anchored Membrane Protein Location

A

Tethered to membrane via covalent bond

76
Q

Glycocalyx Functions (3)

A
  1. Protection
  2. Adhesion
  3. Identification
77
Q

Blood Types

A

O

A

B

AB

78
Q

Antigens on the O-Blood Type

A

H-Antigen; Universal Donor

79
Q

Antigen on the A-Blood Type

A

Antigen A

80
Q

Antigen on the B-Blood type

A

Antigen B

81
Q

Antigen on the AB-Blood Type

A

Antigen A

Antigen B

82
Q

Anti-Bodies on O-Blood Type

A

Anti-Bodies:

A & B

83
Q

Anti-Bodies on the A-blood type

A

Antibodies:

B

84
Q

Anti-bodies on the B-Blood Type

A

Antibodies

A

85
Q

Anti-bodies on the AB- Blood type

A

Antibodies

None

Universal Accepter

86
Q

When the Mom and Unborn Child’s Rh factor are different

A

Erthythroblastosis

87
Q

Erythroblastosis

A

When the mom and unborn child’s Rh factor dont match

88
Q

When is Erythroblastosis fatal

A

When the second child is conceived with different Rh

No Anti-bodies the first time

89
Q

3 Factors that affect Membrane Fluidity

A

Temperature

Saturation of Fatty Acids

Cholesterol

90
Q

What Causes Spur Cell Anemia

A

Too much cholesterol in RBC’s

The RBC’s become rigid and lyse in the cappilaries of the spleen

91
Q

When there is too much cholesterol in the RBC’s and they lyse in the capillaries of the Spleen

A

Spur Cell Anemia

92
Q

Types of Transport within the Cell

A

Passive

and

Active

93
Q

Two Types of Active Transport

A

Primary

and Secondary

94
Q

Primary Active Transport

vs.

Secondary Active Transport

A

Primary Active uses ATP directly to move a molecule against its ion gradient

Secondary Active uses the gradient that the Primary Active transport setup to move something against its gradient

95
Q

What type of transport is the Na+/K+ ATPase

A

Active Primary Transport

96
Q

What Type of Transport is the Na+/Ca2+ Exchange

A

Secondary Active Transport

97
Q

Examples of Passive Simple Diffusion

A

H20, O2, Ethanol

98
Q

Examples of Passive Facilitated Diffusion

A

Voltage Gated Na+ channel

Glucose Transporter

99
Q

What does Invokana Inhibit

A

Blocks the re-uptake of glucose; excreting more in the urine

100
Q

Autosomal Recessive Mutation which causes thickened mucos

A

Cystic Fibrosis

101
Q

Which mutation in Cystic Fibrosis causes the symptoms

A

The CFTR gene; a chlorine channel

102
Q

How does the defective Chlorine channel in Cystic Fibrosis lead to the symptoms

A

More negative charge in cell, bring in Na+ to offset the charge, salinity increases, water is brought in to offset salinity, outside of cell is dry. This happens in airway epithileal cells -> thickened mucous

103
Q

What Causes Cystinuria

A

Defect in transport for uptake of cystine and other dibasic amino acids

104
Q

What disease occurs when there is a defect in the transporter of cystine and other dibasic amino acids

A

Cystinuria

105
Q

What does Cystinuria result in

A

Formation of crystals or stones in the kidneys

106
Q

How does Cystinuria Present

A

With renal cholic

107
Q

What kind of genetic defect is present in Hartnup Disease

A

Autosomal recessive,

108
Q

What is defective in Hartnup Disease

A

Transporter for non-polar/neutral Amino Acids.

Most importantly Tryptophan

109
Q

What autosomal recessive disease occurs when there is a defect in the transporter for neutral/non-polar amino acids?

A

Hartnup Disease

110
Q

Hartnup Disease A.K.A.

A

Pellagra

111
Q

Hartnup Disease Presents with

A

Cerebellar ataxia, nystagmus, tremor, photodermatitis, and photosensitivity

112
Q

Name Two Cardiotonic Drugs

A

Digoxin and Ouabain

113
Q

What are Glycosidic Cardiac Drugs

A

Ouabain and Digoxin

114
Q

What do Digoxin and Ouabain inhibit

A

Na+/K+ ATPase in the cardiac myocyte

115
Q

What is the primary target of Ouabain and Digoxin

A

Na+/K+ ATPase

116
Q

What is the clinical target of Digoxin and Ouabain

A

The Na+/Ca2+ Exchanger

117
Q

Effect of inhibition on the Na+/Ca2+ Exchanger on cardiac myocytes

A

Increased Ca2+ in the sarcoplasm, resulting in stronger cardiac contractions

118
Q

Calories in 1 gram of Protein

A

4

119
Q

Calories in 1 gram of Carbohydrate

A

4

120
Q

Calories in 1 gram of Ethanol

A

7

121
Q

Calories in 1 gram of fat

A

9

122
Q

Which is more abundant in Western Diet

Omega-3 or Omega-6

A

Omega-6

123
Q

Essential Amino Acids

A

Phenylalanie
Valine
Tryptophan

Threonine
Isoleucine
Methionine

Histidine
Arginine
Leucine
Lysine

124
Q

Non-Essential Amino Acids

A

Alanine
Asparagine
Aspartic Acid
Cysteine
Glutamic Acid
Glutamine
Glycine
Proline
Serine
Tyrosine

125
Q

Total Energy Expenditure

A

Thermic Effect of Food

Phsyical Activity

Non-exercise induced thermogenesis (twitchiness)

126
Q

Where are most nutrients absorbed?

A

The Duodenum

127
Q

Where are B12 and Fat absorbed

A

Distal Ileum

128
Q

What deficiences are common in Distal Ileum Resections

A

B12 and Fat Soluble Vitamins (D,E,A,K)

129
Q

What disease’s trade marked with excess fat in stool

A

Steatorrhea

130
Q

Steatorrhea symptoms

A

excess fat in stool

fat malabsorption

131
Q

Auto-immune disease of the bowel which causes chronic infalammation

A

Chron’s Disease

132
Q

Chron’s Disease Treatment

A

Distal Ileum Resection

133
Q

What deficiency causes macrocytic megablastic Anemia

A

B9 and B12

134
Q

Rickets

A

Vitamin-D Deficiency

135
Q
A
136
Q
A
137
Q
A
138
Q
A
139
Q
A
140
Q
A
141
Q
A

Biochemistry (7 decks)

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