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Biochemistry/Physiology > Quiz 5 - Renal Physiology, Enzymes, Glucose Regulation and Formation > Flashcards

Quiz 5 - Renal Physiology, Enzymes, Glucose Regulation and Formation Flashcards

1
Q

Body fluid compartments

A
  1. Plasma - 3 L
  2. Interstitial fluid - 11 L
  3. Intracellular fluid - 28 L
    TOTAL - 42 L
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2
Q

Blood volume

A

5 L, 3 in plasma, 2 intracellular in RBCs

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3
Q

How much volume can kidneys dispose of per day?

A

0.5 - 20 L

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4
Q

How is fluid lost other than kidneys?

A

Insensible loss (passive) from skin - 700ml/day
Sweat from heavy exercise - 100ml/day
Feces - 100ml/day

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5
Q

How do kidneys control blood volume?

A

Controlling urine volume can rapidly shed, or preserve pressure.
Controlling electrolyte balances regulate tonicity of cells by retention or excretion of ions.

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6
Q

Metabolic wastes excreted in urine

A

Urea - protein metabolism
Uric acid - nucleic acid metabolism
Creatinine - muscle metabolism
Bilirubin - hemoglobin metabolism

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7
Q

Foreign substances excreted in urine

A

Pesticieds, food additives, toxins, drugs (penicillin)

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8
Q

Renal regulation of pH

A

Excrete or retain H+, HCO3-

Generation of HCO3- and NH4+ from breakdown of glutamine

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9
Q

What hematopoetic cytokine is produced by the kidneys?

A

Erythropoietin (EPO)

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10
Q

Gluconeogenesis

A

Anabolic generation of glucose, performed in the liver and kidneys

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11
Q

Renal cortex

A

Outermost part of kidney

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12
Q

Renal medulla

A

Innermost part of kidney, contain renal pyramids and nephrons

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13
Q

Renal papilla

A

tube that connects pyramids to renal pelvis

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14
Q

Renal pelvis

A

Duct that collects urine and carries it to the ureter

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15
Q

Path of blood through kidneys

A

Renal Artery > Afferent arterioles > Glomerular Capillaries > Efferent Arterioles > Peritubular capillaries (Vasa Recta) > Renal vein

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16
Q

Glomerulus

A

Small cluster of glomerular capillaries, surrounded by a Bowman’s Capsule

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17
Q

Bowman’s Capsule

A

Surrounds glomerulus, collects filtrate and passes it to the proximal tubule

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18
Q

Path of filtration

A

Glomerulus/Bowman’s Capsule > Proximal Tubule > Loop of Henle > Distal Tubule > Collecting Duct > Papilla > Renal Pelvis > Ureter

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19
Q

Cortical nephrons

A

70% of nephrons, located in cortex, loop of Henle penetrates medulla

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20
Q

Juxtamedullary nephrons

A

30% of nephrons, located in medulla, long loop of Henle that penetrates deep into medulla

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21
Q

Vasa Recta

A

Peritubular capillaries that come from efferent arterioles and surround the loop of Henle

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22
Q

Urinary Excretion Rate

A

= (Filtration rate - reabsorption) + secretion

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23
Q

Filtration

A

Contents exit blood, are excreted

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24
Q

Reabsorption

A

Some or all of filtered materials are taken back into the blood

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25
Q

Secretion

A

After filtration, further materials are removed from blood and excreted

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26
Q

Glomerular Filtration Rate (GFR)

A

= Kf X Net Filtration pressure, Kf - glomerular capillary filtration coefficient
Net filtration pressure = sum of colloid and hydrostatic pressures across capillary
Around 180L/day, total plasma volume cycled through filtration 60 times/day

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27
Q

Reabsorption amount

A

Around 179L/day

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28
Q

What happens to glucose and creatinine in the kidneys

A

Glucose - 100% reabsorbed

Creatinine - 100% excreted

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29
Q

Glomerular capillaries

A

Endothelium - fenestrated, (-) charged
Basement membrane - collagen/proteoglycan mesh, (-) charged
Epithelium - podocytes (form slit pores) (-) charged

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30
Q

Pro filtration pressures

A

Glomerular hydrostatic pressure, around 60mmHg

Bowman’s capsule colloid pressure = 0

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31
Q

Anti filtration pressures

A

Bowman’s capsule hydrostatic pressure, around 18 mmHg

Glomerular Colloid presssure, around 32 mmHg

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32
Q

Diabetes and GFR

A

Retained glucose creates colloid osmotic pressure in bowman’s capsule, causing increased urine output.

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33
Q

Alterations to GFR

A

Constriction of afferent arterioles will decrease GFR
Dilation of afferent arterioles will increase GFR
Constriction of efferent arterioles will increase GFR
Dilation of efferent arterioles will decrease GFR

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34
Q

Neural and hormonal control of GFR

A

Sympathetic Nervous system and Norepinephrine (chatecholamines) reduce GFR
Angiotensin II doesn’t effect GFR but lowers RBF
Prostaglandins and Endothelial-derived Nitric Oxide increase GFR

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35
Q

Macula Densa

A

Sensory region in on distal tubule forms juxtaglomerular complex with afferent and efferent arterioles, monitors a decrease in NaCl in distal tubule, indicating a decreased GFR, causes secretion of Renin to increase GFR

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36
Q

Diabetic Neuropathy

A

Increased flow out because increased glucose filtered, therefore increased water and Na+ excretion
Leads to damage of nephron, decreased function.

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37
Q

Filtration summary

A

Bowman’s capsule - 100% filtrate produced
Proximal tubule - 80% filtrate reabsorbed (active and passive)
Loop of Henle - 6% filtrate reabsorbed, H20 and salt conservation
Distal tubule - 9% of filtrate reabsorbed, variable reabsorption and active secretion
Collecting tubule - 4% filtrate reabsorbed, variable salt and H2O reabsorption
Urine volume - 1% of total filtrate

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38
Q

Na/K ATPase in the tubules

A

Primary active transporter sets up gradient for secondary active transport. Na+ reabsorption highly linked to the reabsorption of many other things

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39
Q

Cotransport

A

Na+ brings in Glucose and amino acids

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40
Q

Counter-transport

A

Na+ in pushes H+ out

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41
Q

What happens in the proximal tubule?

A

65% of water reabsorbed, Na+, Cl-, glucose, amino acids and HCO3- reabsorbed.
Na+ amount decreases but concentration does not because water follows it.

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42
Q

What happens in the loop of Henle?

A

Thin descending segment - permeable to water, but not ions (20% H20 reabsorbed)
Thick ascending segment - not permeable to water, lots of active transporters for Na+, Cl- and K+ and other ions

43
Q

Countercurrent Exchange

A

The extraction of ions in the ascending thick segment creates a concentration gradient that pulls water out of the thin descending cycle, further concentrating the fluid in the tubes. This positive feedback cycle leads to the high concentration gradient within the loop of Henle and allows the minimum amount of water to be excreted with the maximum amount of waste.

44
Q

What does the distal tubule do?

A

Proximal part is impermeable to water, reabsorbes ions.
Distal half contains Principal Cells (for reabsorbing Na+ and water and secreting K+) and Intercalated cells (that reabsorb K+ and HCO3- and secrete H+)
Late distal tubule is permeable to water, controlled by ADH. Less permeable = more water excretion

45
Q

What do the collecting ducts do?

A

Reabsorb 10% of filtered water and Na+, regulated by ADH. Pump H+ into lumen to regulate pH
Permeable to urea, allowing some back into medulla

46
Q

What does urea do?

A

Maintains hyperosmotic state in interstitial fluid of renal medulla. Urea is removed from tubule in collecting ducts, and secreted back into tubule in the lower parts of the loop of Henle.

47
Q

What do enzymes do?

A

Increase chemical reaction rate
Reduce free energy needed to drive reactions
Increase probability of reaction occurrance

48
Q

Globular proteins

A

Almost all proteins are globular in shape with a specific binding site or pocket

49
Q

Substrate selective

A

Proteins bind to specific parts, of specific subtrates. Functional group, charge, region, etc.

50
Q

Coenzymes

A

Other proteins or organic components that bind to enzymes to compliment their function

51
Q

Cofactors

A

Inorganic ions that bind to enzymes to compliment their function. Ex.) Cu2+, Mn2+, Zn2+, Fe2+

52
Q

Holoenzyme

A

Complete catalytically active enzyme with coenzymes and cofactors bound.

53
Q

Weak interactions

A

Enzymes generally bind to their substrates with weak interactions

54
Q

Oxidoreductase

A

Transfer of electrons

55
Q

Transferase

A

Group transfer

56
Q

Hydrolase

A

Hydrolysis reactions

57
Q

Lyase

A

Cleavage of C-C, C-O, C-N or other bonds leaving double bonds or rings

58
Q

Isomerases

A

Transfer groups to yield isomeric forms

59
Q

Ligases

A

Formation of C-C, C-S, C-O, C-N bonds by condensation. Requires ATP or other cofactor

60
Q

Lock and Key model

A

Untrue. Substrate does not fit perfectly into enzyme or activation energy would increase because bound substrate would be in lower energy state

61
Q

Induced Fit model

A

Enzyme is complimentary to transition state rather than substrate or product, lowers activation energy by decreasing energy needed to meet transition state.

62
Q

Activation Barriers

A
  1. Entropy of molecules in solution
  2. Solvation shell - water molecules surrounding substrate
  3. Substrate conformation
  4. Substrate orientation
63
Q

Enzyme solutions to activation barriers

A
  1. Organize substrates, reduce entropy
  2. Weak bonds desolvate substrates
  3. Weak bonds alter conformation
  4. Enzymes induce fit
64
Q

Enolase reaction

A

Glycolysis reaction. 2 Mg2+ cofactors stabilize the transition state while the enzyme shifts charges and electrons to form the product

65
Q

Kinetics

A

Rate at which enzymes create products

66
Q

Velocity

A

Measure of reaction rate. Affected by enzyme, substrate, cofactors and coenzymes, enzyme modifications, pH, temperature

67
Q

Michaelis-Menten Equation

A

V = (Vmax[S])/(Km+[S]) Plots Velocity over Substrate concentration. Involves only single substrate reactions

68
Q

Michaelis-Menten Constant

A

Km. Substrate concentration at which the initial reaction velocity (Vo) equals one-half the maximum reaction velocity (Vmax)

69
Q

Ternary Complex

A

An enzyme bound to 2 substrates to create products.

Can bind in a random or order

70
Q

Irreversible inhibition

A

Inhibitor binds covalently to the tenzyme, preventing function and leading to degradation.

71
Q

Reversible Inhibition

A

Inhibitor binds to enzyme or substrate to temporarily affect catalysis. Can be competitive, uncompetitive, mixed, noncompetitive

72
Q

Competitive Inhibition

A

Inhibitor binds in substrate binding site.

Shifts Km to right, but Vmax unchanged

73
Q

Uncompetitive Inhibition

A

Inhibitor binds to enzyme in place other than substrate binding site. Km either unchanged or shifted left, Vmax decreased

74
Q

Mixed Inhibition

A

Separate binding site from substrate, may bind to substrate or enzyme. Km shifted right and Vmax reduced.

75
Q

Noncompetitive

A

Rare, Vmax reduced, but not Km

76
Q

Allosteric Enzymes

A

Function of enzyme regulated by modifications
Enzyme conformation changed by effector binding.
Complex proteins
Do not follow Michaelis-Menten

77
Q

Types of post-translational modifications of enzymes

A 
Phosphorylation - addition of PO3
Methylation - addition of CH3
Myristoylation - addition of myristoyl (long chain ketone)
Acetylation - addition of acetyl group
Ubiquitination - addition of ubiquitin
Adenylation - addition of tyrosine
ADP-ribosylation - addition of NAD
78
Q

Homotropic Regulation

A

The substrate itself is the molecule that modifies activity

Ex.) Hemoglobin binding to O2

79
Q

Heterotropic regulation

A

Involves post-translational modifications

80
Q

4 Functions of Glucose

A
  1. Source of ATP
  2. Energy Storage
  3. Molecular Precursor
  4. Structural Backbone
81
Q

Catabolic Pathways

A

Glycolysis
Citric Acid Cycle
Oxidative Phosphorylation
Glycogenolysis

82
Q

Anabolic Pathways

A

Gluconeogenesis

Glycogenesis

83
Q

How presence regulates metabolic activity

A

Concentration - production or modification of enzymes

Localization - protein complexes, etc.

84
Q

How kinetics regulate metabolic activity

A

Substrates and modification of enzymes change kinetics

85
Q

Where does glucose initially come from

A

Diet. Enzymes digest food into glucose and other small sugars where it is absorbed and distributed to where it is needed.

86
Q

Digestive enzymes

A

Amylase
Lactase
Sucrase
Maltase

87
Q

3 major pathways of glucose metabolism

A
  1. Respiration - forms ATP
  2. Storage - forms glycogen, glucose
  3. Regenerative - forms glucose
88
Q

Key regulators of glucose pathways

A 
Insulin
Glucagon
Epinephrine
Glucose
ATP/AMP
89
Q

Which metabolic pathways are exclusive

A

Glycolysis =/= gluconeogenesis

Glycogenesis =/= glycogenolysis

90
Q

Glycogen

A

Stores intercellular glucose
Branched glucose homopolysaccharide
Primary mechanism for intracellular energy storage
Primarily found in liver (10% of liver weight) and muscle (2% of muscle weight)
Necessary to maintain cellular osmolarity
Forms large molecular complexes
Stored in granule organelles

91
Q

Glycogenolysis pathway

A

Glucose + Hexokinase > Glucose-6-phosphate + Phosphoglucomutase > Glucose-1-phosphate + UDP-glucose pyrophosphorylase > Uracil diphosphate-glucose + Glycogen synthase > Glycogen chain + Glycogen branching enzyme > Glycogen particle

92
Q

Which is the point of regulation in glycogenesis

A

Uracil diphopshate-glucose > Glycogen chain

Glycogen Synthase Enzyme

93
Q

Glycogenin

A

Protein required as anchor point for formation of large glycogen complexes

94
Q

Glycogenolysis pathway

A

Glycogen + Glycogen Phosphorylase + debranching enzyme > Glucose 1-phosphate + Phosphoglucomutase > Glucose 6 phosphate + Glucose 6-phosphatase (in ER) > Glucose

95
Q

Glycogen Synthase regulation

A

Insulin promotes activation and inhibits inactivation of GS
Glucagon/Epinephrine blocks activation
Glucose and Glucose 6-phosphate promote activation

96
Q

Glycogen phosphorylase regulation

A

Glucagon in the liver and epinephrine in the muscles promote conversion of Glycogen Phosphorylase to a more active state
Glucose will inhibit phosphorylase by occupying glycogen binding sites
Insulin inhibits phosphorylase by promoting PP1 to convert phosphorylase to a less active state

97
Q

How does Insulin activate Glycogenesis

A

Insulin binds to TYRK receptor > Self phosphorylates > PI3K activated > PIP2 becomes PIP3 > Series of proteins Phosphorylates GS > PP1 activates GS
Insulin, G6P and Glucose promote PP1 function
Glucagon, epinephrine inhibit PP1 function

98
Q

Glucagon/Epinephrine

A

Glucagon will cause the Liver to increase blood glucose by promoting Glycogen phosphorylase
Epinephrine will increase intracellular glucose of that particular cell
Pathway involves Adenylyl Cyclase, Phosphorylase

99
Q

Gluconeogenesis

A

Synthesis of glucose
Can occur in all cells but occurs primarily in the liver
Converts lactate or pyruvate
Energetically costly

100
Q

PEP formation pathway from lactate

A

Lactate + Lactate dehydrogenase > Pyruvate (enters mitochondria) + Pyruvate Carboxylase > Oxaloacetate + mitochondrial PEP carboxykinase > Phosphoenolpyruvate (PEP) (Leaves mitochondria

101
Q

Gluconeogenesis pathway from PEP

A

PEP + Enolase > 2-phosphoglycerate + phosphoglycerate reductase > 3-phosphoglycerate + phosphoglycerate kinase > 1,3 biphosphoglycerate + glyceraldehyde 3-phosphate dehydrogenase > glyceraldehyde 3-phosphate + triose phosphate isomerase > dihydroxyacetone phosphate + glyceraldehyde 3 phosphate + aldolase > Fructose 1,6-bisphosphate + fructose 1,6-bisphosphatase > fructose 6 phosphate + phosphohexoisomerase > glucose 6-phosphate + glucose 6-phosphatase > glucose

102
Q

Which steps in gluconeogenesis are regulated

A

Fructose 1,6-bisphosphate > fructose 6-phosphate
- AMP inhibits FBPase-1
Pyruvate > Oxaloacetate
- Acetyl-CoA promotes pyruvate carboxylase
Insulin causes generation of Glucose 6-phosphatase and PEP carboxylase by activating PKB and FOX01

103
Q

Challenge of Metabolic System

A

Organism-wide metabolic homeostasis
Cellular energetics change rapidly
Global metabolic demands change rapidly
Intracellular states drive physiologic changes that influence energetics
Intracellular ATP/AMP content regulates metabolic function

104
Q

Does the body recognize changes in ATP or AMP faster and why?

A

AMP because the relative change is much greater with AMP over ATP.

Biochemistry/Physiology (10 decks)

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