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Biochemistry Block 1 > Biological Membranes > Flashcards

Biological Membranes Flashcards

1
Q

What is the purpose of integral transmembrane proteins?

A

The control the access of inorganic ions, vitamins and nutrients. Also exit of drugs and the exit of waste products.

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2
Q

What is the concentration levels of K,Na,and Ca in the cytoplasm?

A

The concentration of K=140, Na= 10 and Ca= 10^-4 mmol/L.

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3
Q

What is the concentration levels of K,Na,and Ca outside the cell?

A

The concentration of K=5, Na= 145 and Ca= 1-2 mmol/L.

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4
Q

what is the driving force (indirectly or directly) for transport of ions?

A

ATP

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5
Q

Small non polar and uncharged molecules pas through the membrane via?

A

simple difussion

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6
Q

The term downhill refers to movement of?

A

Molecules moving along the concentration gradient from high to low concentration

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7
Q

The interior of the phospolipid bilayer is?

A

Hydrophobic

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8
Q

The term partition coeficcient refers to?

A

Transport of molecules between oil and water

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9
Q

what kind of proteins control movement of water across the membrane ?

A

Channel proteins.

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10
Q

what is the name of the channel protein gene in water?

A

Aquaporin -2

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11
Q

Neprogenic diabetes insipidus is characterized by?

A

excessive urination. Without the hyperglycemia characteristics of diabetes mellitus.

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12
Q

mutation in which gene gives as result NEPHROGENIC DIABITIS INSIPIDUS?

A

Aquaporin-2

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13
Q

Antibiotics act as what kind of carrier?

A

Ionophores

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14
Q

Ionophores carriers are?

A

Carriers that are bound to an ion to pass across the membrane. only down their electrochemical gradient.

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15
Q

Mention a typical example of mobile ion carrier?

A

VALINOMYCIN

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16
Q

The carrier type NIGERICIN and MONENSIN exchange what kind of ions respectively?

A

K, Na AND H

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17
Q

IONOMYCIN and A23187 are what kind of ionophores?

A

Ca^2+ Only

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18
Q

B-helical Gramicidin A makes transmembrane channel that allows movement of?

A

monovalent cations ( H, Na and K)

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19
Q

Polyene antibiotics AMPHOTERICIN B and NYSTATIN are active againts?

A

YEAST. Use for treatment of topical infections of fungal origin

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20
Q

What are other names for transporters?

A

Porters, permeases, translocases or carrier proteins

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21
Q

what are the two transport system mechanism?

A

facilitated diffusion and active transport

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22
Q

what is facilitated diffusion?

A

Movement down concentration gradient and does not required energy

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23
Q

what is active transport?

A

Movement uphill, against their concentration gradient

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24
Q

T/F The rate of facilitated diffusion is lower than that of simple diffusion ?

A

FALSE

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25
Q

Which type fo diffusion has a maximun transport rate Tmax?

A

facilitated diffusion

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26
Q

which equation can be use to describe facilitated diffusion kinetics?

A

Michaelis-Menten and Lineweaver-Burk type equations

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27
Q

rate is slower and directly proportional to substrate concentration in ?

A

SIMPLE DIFFUSION

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28
Q

Clinical: child with polyuria,failure to thirve and an episode of severe dehydration.
Lab: Urine dipstick shows= Glucosuria and Proteinuria
Bichemical analysis: Aminoaciduria and phosphaturia

The possible diagnosis is ?

A

INFANTILE CYSTINOSIS

- accumulation of cystine in lysosomes , due to defect in lysosomal transport protein

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29
Q

Clinical :
Symptoms: Pellagra-like skin changes on face ,neck,forearms and dorsal aspects of hands and legs
Skin: scaly , rough and hyperpigmented
Complains: Headaches and wekness
urinalysis: hyperaminoaciduria of neutral monoamino-monocarboxylic acids( alanine,serine,threonine,asparagine,glutamine,valine,leucine,
isoleucine,
phenylalanine,tyrosine,tryptophan,histidine and citrulline)

The possible diagnosis is?

A

HARTNUP DISEASE

  • Aminoacids share a common transporter only expressed in luminal border of epithelial cells of renal tubules and intestinal epithelium.
  • pellagra dermatitis and neurological involvement : nutritional niacin deficiency
  • reduced tryptophan intake results in reduced nicotinamide production
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30
Q

what is the treatment for cystinosis?

A

Intake of cysteamine to increase transport of cystine

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31
Q

HARNUP DISEASE is treated with?

A

Oral nicotinamide and application sunblock in affected areas

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32
Q

Glucose transporters difussed via ?

A

FACILITATED DIFFUSION

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33
Q

Glucose transporters are uniport, symport or antiport?

A

UNIPORT

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34
Q

Substrates for GLUT1 are?

A

Glucose, Galactose and mannose

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35
Q

Major sites of expression for GLUT1 ?

A

Erythrocytes , blood tissue barriers(ubiquitous)

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36
Q

Substrates for GLUT2 are?

A

glucose and fructose

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37
Q

Substrates for GLUT3 are?

A

glucose

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38
Q

Substrates for GLUT4 are?

A

glucose

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39
Q

Substrates for GLUT5 are?

A

fructose

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40
Q

Major sites of expression for GLUT2 ?

A

liver,pancreatic islets and intestines

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41
Q

Major sites of expression for GLUT3?

A

brain, testis

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42
Q

Major sites of expression for GLUT4 ?

A

muscle,fat,heart

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43
Q

Major sites of expression for GLUT5?

A

intestine(primarily),testis and kidneys

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44
Q

Major sites of expression for GLUT6?

A

spleen. leukocytes and brain

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45
Q

Major sites of expression for GLUT7 ?

A

small intestine, colon

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46
Q

Major sites of expression for GLUT8 ?

A

testis

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47
Q

Major sites of expression for GLUT9 ?

A

liver.kidney

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48
Q

Major sites of expression for GLUT10 ?

A

heart,lung,brain,liver,muscle,pancreas,kidney

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49
Q

Major sites of expression for GLUT11 ?

A

heart,skeletal muscle,kidney

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50
Q

Major sites of expression for GLUT12?

A

skeletal muscle,heart,prostate, small intestine

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51
Q

Major sites of expression for GLUT13 ?

A

HMIT, primarily expressed in brain

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52
Q

Major sites of expression for GLUT1 4?

A

testis

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53
Q

what is voltage or ligand gating?

A

Ability of transporter to open and close by conformational changes induced for volatge changes or ligand binding.

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54
Q

Clinical:
-Infant
-recurring seizures
-CSF glucose low
CSF lactose low 0.3-0.4 mmol/L;3-4mg/dL(normal values <2.2 mmol/L; <20 mg/dL)
-Ratio ranging from 0.19-0.33(normal value is 0.65)

Possible condition is?

A

Defective glucose transport across the blood brain barrier as a cause of seizures and developmental delay

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55
Q

what are the potential causes for low CSF glucose concentrations?

A

Bacterial meningitis, subarachnoid hemorrhage and hypoglycemia.

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56
Q

CSF LACTATE values are usually found in what conditions?

A

Bacterial meningitis, subarachnoid hemorrhage

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57
Q

Defective glucose transport across the blood brain barrier can be treated with?

A 
KETOGENIC DIET (high fats, low protein , low carbohydrate)
- Brain can use  ketone bodies as oxidizable fuel sources and the entry is not glucose transporter system dependent.
58
Q

GAP JUNCTIONS are located where?

A

betwen endothelial,muscle and neuronal cells cluster of small pores

59
Q

how are pores form?

A

2 cylinders of six CONNEXIN subunits in the plasma membrane join each other

60
Q

what causes deafness and Charcot Marie-Tooth disease?

A

mutations in genes Connexin 26 and Connexin 32

61
Q

larger proteins and nucleic acids enter and leave nucleus via?

A

Nuclear Pores

62
Q

Primary active transport systems use ?

A

ATP

63
Q

Secundary active transport systems use?

A

Electrochemical gradient of Na or H ions

64
Q

pump ATpases are classified into?

A

F-ATpase(coupling factor), V-ATpase(vacuolar), P-ATpase(phosphorylation), ABC( ATP-Binding cassette) transporter.

65
Q

F-ATpases are located in?

A

mitochondrial,chloroplast and bacterial membranes

66
Q

substrate for F-ATpases are?

A

H ions

67
Q

function of ATpases is?

A

ATP synthesis driven by electrochemical gradeint of H ions

68
Q

ATP is transported to the cytoplasm via?

A

ATP-ADP TRANSLOCASE in the mitochondrial inner membrane

69
Q

ATP-ADP TRANSLOCASE is an _______ system?

A

ANTIPORT

70
Q

what is the location of V-type(vacuolar) ATPase?

A

lysosomes,endosomes, and secretory granules and plasma membranes(ruffled border of osteoclast,kidney ephitelial cell)

71
Q

defects in V-ATpase results in ?

A

OSTEOPETROSIS

- increased bone density

72
Q

mutation in ATPase collecting ducts on the kidney causes?

A

Renal tubular acidosis

73
Q

what are the functions of V-ATPases

A

activation of lysosomal enzymes, accumulation of neurotransmitters, turnover of bone, acidification of urine

74
Q

What are the members of the P-ATPase(phosphorylation)

A

Na/K ATPase, H/K ATPase, Ca^2+ ATPase, Cu^2+ ATPase

75
Q

Mutations of ATPase genes cause?

A

BRODY CARDIOMYOPATHY(Ca^2+ ATPase)
FAMILIAL HEMIPLEGIC MIGRAINE TYPE 2 (Na/K ATPase)
Menke’s and wilsons diseases ( Cu^2+ ATPases)

76
Q

location of Na/K ATPase?

A

plasma membranes(ubiquitous, but abundant in kidney and heart)

77
Q

function of Na/K ATPase?

A

Generation of electrochemical gradient of Na and K

78
Q

location of H/K-ATPase?

A

stomach(parietal cell in gastric gland)

79
Q

function of H/KATPase?

A

acidification of stomcah lumen

80
Q

Location CA2+ ATPase?

A

sarcoplasmic reticulum and endoplasmic reticulum

81
Q

function of Ca2+?

A

Ca2+ sequestration into sarcoplasmic(endoplasmic) reticulum

82
Q

location of #2 Ca2+ ATPase?

A

plasma membrane

83
Q

function of #2 Ca2+ ATPase?

A

Ca2+ excretion to outside of the cell

84
Q

location of Cu2+ ATPase?

A

plasma membrane and cytoplasmic vesicles

85
Q

Function of Cu2+ATPase?

A

Cu2+ absorption from intestine and excretion from liver

86
Q

what are the categories for the ABC(ATP-binding cassette) transporter?

A
  1. P-glycoprotein
  2. MRP
  3. CFTR
  4. TAP
87
Q

location of P-glycoprotein?

A

plasma membrane

88
Q

function of P-glycoprotein

A

excretion of harmful substances, multidrug resistance for anticancer drugs

89
Q

location MRP(MULTI DRUG RESISTANCE ASSOCIATED PROTEIN)

A

plasma membrane

90
Q

function of MRP

A

detoxification , multidrug resistance

91
Q

location of CFTR(CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR)

A

plasma membrane

92
Q

Function of CFTR

A

c-AMP dependent chloride channel, regulation of other channels

93
Q

Location of TAP (TRANSPORTER ASSOCIATED WITH ANTIGEN PROCESSING)

A

Endoplasmic reticulum

94
Q

function of TAP

A

presentation of peptides for immune response

95
Q

examples of secundary active transport?

A

uniport(monoport),symport(cotransport),antiport(countertransport)

96
Q

why copper is toxict in excess?

A

binds to proteins and nucleic acids, enhances generation of free radicals and catalyzes oxidation of lipids and proteins in membranes

97
Q

which disease is characterized by failure to incorporate copper into ceruloplasmin in the liver and failure to excrete copper from the liver , resulting in toxic accumulation of copper in the liver and also in the kidney, brain and cornea

A

WILSON’S DISEASE

98
Q

Treatment for WILSON’S DISEASE?

A

chalating agents

  • PENICILLAMINE
  • oral ZINC
99
Q

in which disease copper enters the intestinal cells, but is not transported further, resulting in severe copper deficiency ?

A

MENKES DISEASE

100
Q

Treatment for MENKES DISEASE?

A

subcutaneous administration of cooper histidine complex

101
Q

what are the cause of Cystic fibrosis?

A

mutations of the CFTR gene. ATP binding to CFTR is required for channel opening , the lack of this activity in the ephitelia of CF patients affects both ion and water secretion

102
Q

the following diseases are caused by defects in which transporter?
- tangier , stargardt,progressice intrahepatic cholestasis, dubin johson syndrome, pseudoxanthomaelasticum,familial persisnte hyperinsulinemic hypoglycemia of infancy (PHHI),adrenoleukodystrophy, zellweger syndrome, sitosterolemia and cystic fribrosis

A

ABC TRANSPORTERS

103
Q

what is the most common potentially lethal autosomal recessive disease of caucasian populations?

A

CYSTIC FIBROSIS

104
Q

VOLTAGE DEPENDENT Ca2+ CHANNELS(VDCCs)

A

change the conformation fo t tubules in skeletal muscle in response to membrane depolarization and directly activate a Ca2+ release channel in the sarcoplasmic reticulum membrane

105
Q

what drives the uptake of glucose into intestinal and renal epithelial cells?

A

Na/K-ATPase

106
Q

what transport glucose into the intestinal epithelial cells?

A

AN Na+ COUPLED GLUCOSE SYMPORTER (SGLT1)

107
Q

What facilitates the downhill movement of glucose into the portal circulation?

A

GLUT 2

108
Q

function of SODIUM GLUCOSE TRANSPORTER 2(SGLT2)?

A

glucose re absorption into the renal proximal tubular epithelial cells.

109
Q

what is use for the treatment of hypertension?

A

DHP
Dihydropyridine
nifedipine
* calcium channel blocker

110
Q

what is RYANODINE ?

A

potent inhibitor of the Ca++ channel in the sarcoplasmic reticulum.

111
Q

which are the common Ca2+ channel blockers that inhibits VDCCs?

A

phenylalkylamine(verapamil), benzothiazepine(diltiazem) and dihydropyridine(DHP,nifedipine)

112
Q

inhibition of Na+ channels represses?

A

transmission of the depolarization signal

113
Q

what is used for treatment of congestive heart failure?

A

cardiac glycosides

  • OUABAIN
  • DIGOXIN
114
Q

alfa-bungarotoxin and tetrodotoxin are?

A

snake vemon and puffer fish

115
Q

alfa-bungarotoxin and tetrodotoxin inhibits?

A

voltage dependent Na+ channels

116
Q

lidocaine is used for ?

A

Na+ channel blocker , local anesthetic and antiarrythmic drug

117
Q

P-ATPase in gastric parietal cells maintains?

A

the low PH of the stomach

118
Q

the lumen in the stomach is highly acidic due to ?

A

Presence of a proton pump H/K-ATPase ,PATPase.

119
Q

why is it called an H+/K+-ATPase?

A

Because the pump antiports two cytoplasmic protons and two extracellular potassium ions, coupled with hydrolysis of a molecule of ATP

120
Q

PHLORIZIN inhibits?

A

SGLT1

121
Q

PHLORETIN inhibits?

A

SGLT2

122
Q

what causes glucose/galactose malabsorption?

A

defect on SGLT1

123
Q

The kidney is a major site for regulation of ?

A

Na+ homeostasis.

-several transport systems participate in Na+ handling in the kidney tubules.

124
Q

most of Na+ reabsorption in the tubules occurs in the?

A

PROXIMAL SEGMENTS

125
Q

Na+ reabsorption in the distal nephron is sensitive to?

A

STEROID HORMONE ALDOSTERONE

126
Q

Where’s the gastric pump localized?

A

intracellular vesicles in the resting state.

127
Q

histamine and gastrin are in charge of ?

A

inducing fusion of the vesicles with the plasma membrane

128
Q

in gastric juice acidification the counter ion CL- is secreted through a Cl- channel producing __________ in the lumen.

A

HYDROCHLORIC ACID(HCl: gastric acid)

129
Q

The Na+/H antiporter (NHE3) mediates ________

A

entry of Na+ in the proximal tubule

130
Q

Furosemide-sensitive Na+-K+-2Cl-(symporter)(NKCC2) and Thiazide-sensitive Na+-Cl-(cotransporter)(NCCT) where are localizated?

A

Thick ascending loop of Henle and distal convoluted tubules

131
Q

Amiloridesensitive epithelial Na+ channel(ENaC) is expressed where?

A

Aldosterone-sensitive distal nephron

132
Q

ionic balance of epithelial cells is regulated by??

A

Renal outer medullary K+channel(ROMK) and the Cl- channel ( ClC)

133
Q

What plays a central role in the regulation of circulating volume, extracellular fluid osmolality and blood pressure?

A

The RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

134
Q

Where is RENIN produced?

A

in the juxtaglomerular apparatus of the kidney

135
Q

Angiotensinogen is converted into?

A

Angiotensin I

136
Q

Angiotensin I is converted into?

A

Angiotensin II

137
Q

Angiotensin converting enzyme (ACE) is in charge of ?

A

converting Angiotensin I into Angiotensin II

138
Q

What promotes the release of aldosterone?

A

Angiotensin II

139
Q

what enzyme promotes the renal Na+ and water retention and elevated blood pressure by increasing Na+ reabsorption in the cortical collecting duct ?

A

ALDOSTERONE

140
Q

What promotes elevations in blood pressure by direct vasoconstriction and increasing Na+ reabsoprtion in the proximal tubule?

A

ANGIOTENSIN II

141
Q

OMEPRAZOLE covalently modifies?

A

Cysteine residues located in the extracytoplasmic domain of the Alfa-subunit and inhibits the proton pump.

Biochemistry Block 1 (6 decks)

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