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BMS > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are the components of a glycerophospholipid?

A

fatty acid tail, glycerol backbone, phosphate head

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2
Q

what is the linkage between the fatty acid tail and glycerol in a glycerophospholipid?

A

ester linkage

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3
Q

type of steroid that intercalates between phospholipids with the -OH closest to the aqueous interface

A

cholesterol

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4
Q

what happens when there are smaller amounts of cholesterol in the membrane

A

“stiffens” the membrane which leads to decrease fluidity

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5
Q

what happens when there are higher amounts of cholesterol in the membrane

A

it interferes with the interactions between lipid tails which leads to increase fluidity

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6
Q

type of lipid with a backbone of sphingosine and when a slightly different shape can decrease the membrane fluidity

A

Sphingolipids

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7
Q

proteins (glycoproteins) and lipids that are bound to carbohydrates that vary in size

A

Glycocalyx

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8
Q

what are the two different formations of membrane lipid called?

A

Micelles and bilayer

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9
Q

which membrane lipid formation is more favourable as the concentration of phospholipids increase?

A

bilayer formation is more favourable over michelles

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10
Q

the ? is key to the survival and normal function of the cell

A

integrity of the plasma membrane

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11
Q

the loss of integrity of the cell membrane leads to ?

A

threatening of cell survival

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12
Q

functions of membrane proteins

A

signaling, protection, structure and movement, transport and general homeostasis

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13
Q

key forces that work across the cell membrane

A

diffusion and osmosis

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14
Q

what is diffusion

A

the movement of molecules from a region of higher concentration to lower concentration

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15
Q

what is osmosis

A

diffusion of water through a semi-permeable membrane

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16
Q

allows water to pass through, but is impermeable to at least one solute

A

semi-permeable

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17
Q

explain Na+/K+ ATPase

A

key plasma membrane transporter, pumps 3 Na+ out of the cytosol into the extracellular fluid (ECF) and pumps 2 K+ into the cytosol (ICF) and uses ATP -> ADP +Pi for hydrolysis. This establishes a gradient of charge across the membrane

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18
Q

A protein moves a substance across a membrane against a concentration gradient using ATP

A

Active transport

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19
Q

A protein forms a channel that allows a substance across the membrane, along its concentration gradient

A

passive transport

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20
Q

a protein carrier binds to a substance and transports it across a membrane, allowing it to follow its concentration gradient

A

facilitated transport

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21
Q

the transport of 2 substances (X and Y) are coupled using the same protein. the concentration gradient of X favours movement into the cell, Y is “pulled” along, even if the gradient for Y does not favour cell entry

A

Co-transport

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22
Q

X and Y move in opposite directions across the cell membrane - the gradient of one of the molecules supplies the energy to drive the transport

A

counter-transport

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23
Q

separate cells into apical and basal compartments, commonly regulates movement across membranes and other epithelial structures

A

tight junctions

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24
Q

types of anchoring junctions

A

Desmosome, Hemi-desmosome, adherens

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25
Q

Parts of Desmosome

A

intracellular component: plaque formed of molecules that are associated with cadherins and intermediate filaments bind to the plaque
extracellular component: cadherins on one cell interact with cadherins on a neighboring cell

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26
Q

difference between hemi-desmosome and desmosome

A

hemi-desmosome’s extracellular component involves integrin instead of cadherins

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27
Q

parts of adherins

A

junction can be either cadherins or integrins, no intermediate filaments, instead have actin filament

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28
Q

functions of the cytoskeleton

A

cellular movement, organization of cellular components/organelles, cellular structure, communication

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29
Q

role of intermediate filaments

A

overall structural integrity of the cell, variety of molecules, variety of molecules

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30
Q

microtubules

A

trafficking of organelles and cell division, organization of overall cellular structure, cellular movement, tubulin

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31
Q

microfilaments

A

cellular movement, structural organization of the plasma membrane, actin

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32
Q

features of the cytoskeleton

A

dynamic, tightly regulated, can generate force

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33
Q

what is the subunit/monomer of actin?

A

G-actin

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34
Q

what is a polymer of actin?

A

F-actin

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35
Q

two forms of F-actin

A

linear arrangement and mesh-like nets

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36
Q

how does F-actin degrade?

A

spontaneously degrades, G-actin hydrolyzes ATP to ADP, which makes it more likely that it will fall off the F-actin strand

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37
Q

factors that affect the stability of F-actin

A
  • concentration of G-actin
  • “caps” that can prevent disassembly
  • proteins that speed up or slow down the rate that G-actin hydrolyzes its ATP
  • nucleating factors or inhibitory factors that modify the formation of F-actin
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38
Q

what is the monomer of microtubules

A

tubulin

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39
Q

what are the two types of tubulin that form dimers

A

alpha and beta tubulin

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40
Q

what type of structure is alpha-beta dimers organized as?

A

helical tube

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41
Q

dynamic instability

A

when the beta monomer of tubulin cleave GTP to GDP +Pi, the dimer tends to “fall off” the microtubule and it falls apart

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42
Q

functions of microtubules

A

cellular organization (MTOC), cellular movement, cell division, signaling

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43
Q

what is the unique shape of centrioles called?

A

tubulin triplet structure ( 9 tubulin triplets, “9X3” structure)

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44
Q

“molecular motors”

A

can move along on F-actin and microtubules which form a network of dynamic filaments and they use ATP to move along it

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45
Q

what kind of protein can walk along microfilaments (F-actin)

A

myosin

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46
Q

what kind of proteins can move along microtubules and cause the “whipping” movements of cilia and flagella

A

dyneins and kinesins

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47
Q

types of intermediate filaments

A

lamins, keratins, vimentin family (vimentin, desmin, GFAP), neurofilaments

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48
Q

what is responsible for the shape of microvilli

A

actin filaments

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49
Q

What are the 2 main classes of lipids structurally?

A

fatty acid and isoprenoid

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50
Q

the 3 components of a phospholipid

A

hydrocarbon chain, backbone, and phosphate-alcohol head group

51
Q

two types of backbone for phospholipids

A

glycerol and ceramide

52
Q

Phospholipids with a glycerol backbone

A

phosphoglycerides

53
Q

phosphatidate

A

if both fatty acids are linked to the glycerol backbone with an esterlinke

54
Q

plasmalogen

A

if one fatty acid is linked to the glycerol backbone with an ester link while the other has an ether link

55
Q

what is the basic structure of a phospholipid called?

A

phosphatidic acid

56
Q

sphingomyelin

A

phospholipid that contains a ceramide backbone, also be classified as a sphingolipid

57
Q

where does phospholipid synthesis occur?

A

primarily on the luminal surface of the smooth ER and the inner mitochondrial membrane

58
Q

what are the steps to phospholipid synthesis

A
  1. synthesis of glycerol backbone
  2. attachment of fatty acids to backbone via ester linkage
  3. addition of head group
  4. exchange/modification of head group
59
Q

flippase

A

special enzyme that moves phospholipids across the ER membrane to the cytosolic side

60
Q

the 5 carbon structural unit of isoprenoids

A

isoprene unit

61
Q

Cholesterol

A

steroids are complex molecules made from 6 isoprene units

62
Q

how many fused rings does cholesterol have?

A

4

63
Q

sterols

A

steroids with a hydroxyl group at C3

64
Q

where does cholesterol synthesis occur?

A

ER

65
Q

what are the steps of cholesterol synthesis?

A
  1. Condensation of 3 acetyl CoA into mevalonate
  2. formation of isopentenyl pyrophosphate
  3. creation of squalene
  4. cyclization of squalene into cholesterol
66
Q

what enzyme is the main regulatory enzyme in cholesterol synthesis pathway and catalyzes the rate limiting step?

A

HMG CoA reductase

67
Q

what promotes the dephosphorylation of HMG-CoA reducatse, activating the enzyme, and in turn promoting cholesterol synthesis

A

insulin

68
Q

what promotes phosphorylation of HMG-CoA reductase, inhibiting the enzyme and in turn inhibit cholesterol synthesis

A

Glucagon

69
Q

what is key in detecting extracellular signals and modifying cell funcation based on those signals?

A

receptors in the cell membrane

70
Q

transduction

A

the intracellular events that transform the extracellular signal into an intracellular signal

71
Q

what is the model of intracellular signalling?

A

the concentration of first messenger increase -> binds to cell membrane receptor -> receptor activates resulting in activation of intracellular protein associated to receptor -> protein activates mechanism to increase activation of second messenger -> second messenger binds to/activates another protein -> protein will activate or inactivate other biochemical signalling cascades

71
Q

what is the largest family of cell membrane receptor?

A

GPCR

72
Q

how many times does the GPCR span through the membrane?

A

7 times

72
Q

what activates G-Protein coupled receptors?

A

when a protein with a guanine nucleotide binds to the receptor

73
Q

what are the 3 protein subunits fo the G protein?

A

alpha, beta, and gamma subunits

74
Q

explain unstimulated alpha subunit in GCPR pathway

A

unstimulated alpha is bound to GDP, and beta-gamma is bound to alpha

75
Q

explain stimulated alpha subunit in GCPR pathway

A

alpha subunit releases GDP, replacing it with GTP and the alpha subunit disengages from the beta-gamma subunits

76
Q

what is the mechanism of Gs GPCR?

A
  1. a ligand binds to a receptor associated with a GS G-protein
  2. Gs releases GDP and binds GTP at the alpha subuniit and the beta-gamma subunit detaches from the G-protein
  3. Gs binds to and activates adenylyl cyclase which is the membrane-bound enzyme that converts ATP to cAMP
  4. cAMP binds to protein kinase A (PKA) - CAMP binds to inhibitors of PKA, whch then detaches, and allows the activates PKA
  5. PKA phosphorylates a multitude of effector proteins
77
Q

what inactivates cAMP and what does it become

A

cyclic AMP phosphodiesterase converts cAMP to 5’-AMP

78
Q

explain Gq GPCR pathway

A
  1. a ligand binds to a receptor assocated with a Gq G protein
  2. Gq-alpha activates phospholipase C
  3. Phospholipase C cleaves a membrane lipid (PIP2) into IP3 and diacylglyceral (DAG)
  4. IP3 activates a Ca2+-release channel in the ER which leads to movements of Ca2+ from ER into the cytosol
  5. Both Ca2+ and DAG work together to activate membrane-bound protein kinase C (PKC)
  6. PKC (the 2nd messenger-activated effector) can modulate the activity of many other effectors and Ca2+ can also bind to other molecules such as calmodulin
79
Q

What inhibits and down regulates the activity of Gs

A

Gi GPCR pathway

80
Q

What does the Gi alpha and bet-gamma subunits do?

A

Gi-alpha inactivates adenylyl cyclase and Gi-beta gamma opens a K+ channel

81
Q

What happens when the Gi beta gamma subunit opens a K+ channel?

A

it brings the cell closer to its nernst potential of K+, this is very negative membrane potential - it tends to cause most cells to be “less” activated

82
Q

What is the Nernst potential for K+?

A

-90 mV

83
Q

Explain the Receptor Tyrosine Kinases (RTKs) pathway

A
  1. ligand binds to receptor monomers
  2. receptor dimerizes and each half phosphorylates the tyrosine residues on the other half
  3. signalling proteins then bind to the phosphorylated receptor and become activated leading to signal cascade
84
Q

Explain the Ras-RTK pathway

A
  1. Ras is a small, intracellular G-protein that is not physically associated with any receptors, whe it encounters an activated RTK, it binds to GTP and gets activated
  2. Ras activates Raf
  3. activated Raf activates MAP kinases which can phosphorylate transcription factors and enzymes
  4. Ras inactivates itself by cleaving GTP -> GDP
85
Q

T or F: Ras has no typical 2nd messengers produced

A

True

86
Q

Which pathway is key to insulin signaling?

A

PI3K -> Akt system

87
Q

Explain the PI3K to Akt system pathway

A
  1. RTK is activated and this causes activation of nearby phosphoinositide-3-kinase (PI3K)
  2. PI3K attaches an additional phosphate to PIP2 to form PIP3
  3. PIP3 accumulates and forms “lipid” rafts in the membrane (PIP 3is the second messenger)
  4. akt and PDK1 accumulate and cluster together at the site of the PIP3 rafts and PDK1 becomes activated by PIP3
  5. when PDK1 is activated, it activates Akt by phosphorylating it
  6. Akt is the effector and it influences a huge range of intracellular targets
88
Q

what is the 2nd messenger in the PI3k pathway?

A

PIP3

89
Q

Explain Nitric oxide-mediated signaling

A
  1. cytosolic calcium increases
  2. increased intracellular calcium activates NOs
  3. NOs produces NO from L-arginine
  4. NO binds to activates guanylyl cyclase (GC) -> production of cGMP from GTP (cGMP is also a second messenger)
  5. elevation in cytosolic cGMP activates a protein kinase (usually PKG) which changes in cellular activtiy
90
Q

define flow

A

movement of a substance from one point in a system (A) to another point in the system (B)

91
Q

how is flow measured

A

amount of substance (volume, moles, charge) that moves over time (seconds, minutes)

92
Q

flow is directly related to what

A

the size of the energy gradient, the greater the gradient the greater the flow

93
Q

which law determines the rate of flow

A

Poiseuille’s law

94
Q

according to the poiseuille’s law, what will increase flow when it increases

A

hydrostatic pressure and radius

95
Q

according to the poiseuille’s law, what will decrease flow when it increases

A

length of the tube, the viscosity of the fluid

96
Q

what is the most important determinant of resistance?

A

radius

97
Q

Which law quantifies how the rate of diffusion is affected by various parameters

A

Fick’s Law

98
Q

Flux

A

the amount of solute moving across a barrier per unit time

99
Q

the rate of flow of charges across a membrane

A

Ohm’s Law

100
Q

Ohm’s law equation

A

I = V/R, I = current, V = voltage, R = resistance

101
Q

According to Ohm’s law, current increases when this increases

A

Voltage

102
Q

according to Ohm’s law, current decreases when this increases

A

Resistance

103
Q

what is the “back of the nose and throat” that leads to the larynx

A

Nasopharynx

104
Q

cartilaginous structure that contains the vocal folds

A

Larynx

105
Q

midline, non-paired conducting airway

A

trachea

106
Q

branching airways that contain variable amounts of cartilage

A

bronchi

107
Q

branching airways that lack cartilage but are surrounded by smooth muscle

A

bronchioles

108
Q

delicate, balloon-like structures that are the main sites of gas exchange

A

alveoli

109
Q

ventilation

A

conducting zone, movement of gas is driven by pressure gradients

110
Q

respiratory or “exchange” zone

A

movement of gas is driven by concentration gradients

111
Q

what is part of the ventilatory apparatus?

A

lungs, chest wall and muscles

112
Q

What happens during inspiration?

A

the external intercostals (ribs move up and out) and diaphragm contract (descends)
- the volume of the thoracic cavity increases -> decrease in the intrathoracic pressure, the drop in intrathoracic pressure leads to drop in pressure of the airspaces of the lungs -> movement of air from atmosphere into lungs

113
Q

what happens during expiration?

A

the diaphragm (rises) and external intercostals (ribs move down and in) relax
- the volume of the thoracic cavity decreases -> an increase in the intrathoracic pressure which leads to airspaces of the lungs increase pressure, movement of air from lungs back to the atmosphere

114
Q

Pleural cavity

A

contains a small amount of fluid and the fluid “connects” the chest wall to the delicate alveoli

115
Q

what happens when you move your thoracic cage and diaphragm?

A

changes in the pleural cavity pressure which in turn will change the alveolar pressure

116
Q

pleural effusion

A

fluid in the pleural space, can be either unilateral or bilateral

117
Q

“gunk” in the airways and alveoli

A

Consolidation

118
Q

when you hear coarse crackles in a patient with consolidation

A

pathological fluid in large airways

119
Q

when you hear fine crackles in a patient with consolidation

A

smaller airways usually

120
Q

wheeze

A

when a small airway is narrowed or constricted, you hear a high-pitched, musical sound on expiration

121
Q

stridor

A

when a large airway is narrowed or constricted, you hear a louder, harsher sound on inspiration and sometimes on expiration

BMS (4 decks)

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