B05 - Function And Regulation at Medizinische Universität Wien | Flashcards & Summaries

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Lernmaterialien für B05 - Function and Regulation an der Medizinische Universität Wien

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Functions of proteins in the body

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  • Cell groth, repair & maintenance
  • Cellular information
  • Enzymatic function
  • (Peptide)Hormones
  • Mechanical Work
  • pH Balance
  • Immune system
  • Energy Source
  • Transportation
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Give a short overview and the most important facts of renal blood flow

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Renal artery enters the kidney via the hilus → segmental artery → lobar artery → interlobar artry → afferent arteriole → entering glomerulus → efferent arteriol → peritubular capillaries → interlobular vein → renal vein;

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What is the role of vitamin A in rhodopsin formation? 

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Conversion of the all-trans retinol (form of vitamin A) into 11-cis retinol by isomerase --> converted into 11-cis retinal, which combines with scotopsin to form a new rhodopsin; 


Night-Blindness occurs in any person with severe vitamin A deficiency. The reason for this is that without vitamin A, the amounts of retinal and rhodopsin that can be formed are severely depressed (because the amount of light available at night is too little to permit adequate vision).

                                       

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Which hormones should you use, when you want to achieve a fast increase of volume, regardless of osmolarity?

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Increase of Aldosterone to increase volume & increase of ADH

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What are the reference values for water needs?

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  • Water loss: 0,9L due to respiration & sweating, 0,2L in feces & 1,5L due to urine;
  • Water intake: 1.5L drinking, 0.9L food & 0.3L due to metabolic oxidation processes;
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How does aldosterone regulate kidney function? Describe 1. the mechanism of action of aldosterone on kidney function, 2. the consequence of increased or reduced alosterone levels on urinary concentration, electrolyte and water balance, and blood pressure

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  • Mode of Action: Uses an osmole to drag water along the membrane! Aldestorone increases Na-reabsorption into the blood vessel by exchanging for K+ (increased secretion) → this leads to an increased tonicity, which pulls water out of the tubule (= increased H2O reabsorption)

  • Consequences: increases the osmol and thereby increases the volume → osmolarity does not really get affected!


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What is the difference in contractility, excitability, extensability & elasticity?

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  • Contractility = ability of muscle to shorten → generates a pulling force;
  • Excitability = capacity of muscle to respon to a stimulus;
  • Extensibility = muscle can be stretched to its nromal resting length and beyond to a limited degree;
  • Elasitcity = ability of muscle to recoil to originial resting length after stretched;
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How much O2/CO2 is dissolved or bound to hemoglobin?

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  • O2 dissolved: 1,5%; O2 bound to hemoglobin: 98,5%
  • CO2 dissolved: 10%; CO2 bound to hemoglobin: 30%; CO2 as bicarbonate: 60%
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Explain the term “refractory period” and give examples!

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Refractory period is a period immediately following a stimulus during which further stimulation has no effect, unless it is not strong enough.

-> skeletal muscle cells have a really short refractory period, therefore, more contractions can be triggered within a shorter time period -> skeletal muscle is tetanizable!

-> cardiac muscle has due to the long plateau of cardiac AP a longer refractory period -> cardiac muscle is not tetanizable (really important that only the primary pacemaker can trigger AP within the heart);

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Discuss the reasons for a faster sedimentation rate of red blood cells!

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Faster Sedimentation rate = less stability of suspension; this is an indirect marker for inflammation;

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Discuss the differences between skeletal and cardiac muscle excitation-contraction coupling!

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  1. Skeletal muscle excitation-contraction coupling: key principle = direct coupling of the voltage gated calcium channel that acts as a voltage sensor within the sacrolemma to the calcium-release channel within the SR -> when the voltage gated Ca-channel gets activated a plug-like thing is pulled out of the Ca-release channel -> Ca2+ influx into the cell -> Ca2+ binding to troponin complex and thereby moving it away from the actin-binding site -> myosin can bind to actin -> muscle contraction;

  2. Cardiac muscle excitation-contraction coupling: key principle = calcium induced calcium release! The sakrolemma gets depolarized by an cardiac action potential -> voltage gated Ca-Channels are opened & influx of Ca2+ into the cell -> exactly this Ca2+ induces Ca-releasing Channel within the SR to release Ca2+ -> binding to troponin complex and thereby moving it away from the actin-binding site -> myosin can bind to actin -> muscle contraction;

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TESTE DEIN WISSEN

Explain the similarities and differences of skeletal and cardiac muscle action potentials!

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  1. Skeletal Muscle Action Potential: fast influx of Na+ into the cell -> when the threshold is reached depolarization of the membrane + overshoot to about +30mV (= equilibrium potential of Na) -> no more Na+ can enter the cell; now the slower K-Channels open their gates -> Efflux of K+ out of the cell = repolarization starts due to loss of charges inside the cell -> Hyperpolarization and refractive period -> resting membrane potential is reached again;

  2. Cardiac Muscle Action potential: threshold is also reached by a fast influx of Na+ into the cell -> depolarization starts until about +70mV (= equilibrium potential of Na within cardiac muscle cells) -> nor more Na+ can enter the cell & the slower K-Channels open their gates -> PARTIAL (!) repolarization until voltage gated Ca-Channels open their gates -> strong influx of Ca2+ into the cell, which keeps the plateau level alive for about 300ms -> even stronger efflux of K(ir) leads to complete repolarization;

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  • 108262 Karteikarten
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  • 21 Lernmaterialien

Beispielhafte Karteikarten für deinen B05 - Function and Regulation Kurs an der Medizinische Universität Wien - von Kommilitonen auf StudySmarter erstellt!

Q:

Functions of proteins in the body

A:
  • Cell groth, repair & maintenance
  • Cellular information
  • Enzymatic function
  • (Peptide)Hormones
  • Mechanical Work
  • pH Balance
  • Immune system
  • Energy Source
  • Transportation
Q:

Give a short overview and the most important facts of renal blood flow

A:

Renal artery enters the kidney via the hilus → segmental artery → lobar artery → interlobar artry → afferent arteriole → entering glomerulus → efferent arteriol → peritubular capillaries → interlobular vein → renal vein;

Q:

What is the role of vitamin A in rhodopsin formation? 

A:

Conversion of the all-trans retinol (form of vitamin A) into 11-cis retinol by isomerase --> converted into 11-cis retinal, which combines with scotopsin to form a new rhodopsin; 


Night-Blindness occurs in any person with severe vitamin A deficiency. The reason for this is that without vitamin A, the amounts of retinal and rhodopsin that can be formed are severely depressed (because the amount of light available at night is too little to permit adequate vision).

                                       

Q:

Which hormones should you use, when you want to achieve a fast increase of volume, regardless of osmolarity?

A:

Increase of Aldosterone to increase volume & increase of ADH

Q:

What are the reference values for water needs?

A:
  • Water loss: 0,9L due to respiration & sweating, 0,2L in feces & 1,5L due to urine;
  • Water intake: 1.5L drinking, 0.9L food & 0.3L due to metabolic oxidation processes;
Mehr Karteikarten anzeigen
Q:

How does aldosterone regulate kidney function? Describe 1. the mechanism of action of aldosterone on kidney function, 2. the consequence of increased or reduced alosterone levels on urinary concentration, electrolyte and water balance, and blood pressure

A:
  • Mode of Action: Uses an osmole to drag water along the membrane! Aldestorone increases Na-reabsorption into the blood vessel by exchanging for K+ (increased secretion) → this leads to an increased tonicity, which pulls water out of the tubule (= increased H2O reabsorption)

  • Consequences: increases the osmol and thereby increases the volume → osmolarity does not really get affected!


Q:

What is the difference in contractility, excitability, extensability & elasticity?

A:
  • Contractility = ability of muscle to shorten → generates a pulling force;
  • Excitability = capacity of muscle to respon to a stimulus;
  • Extensibility = muscle can be stretched to its nromal resting length and beyond to a limited degree;
  • Elasitcity = ability of muscle to recoil to originial resting length after stretched;
Q:

How much O2/CO2 is dissolved or bound to hemoglobin?

A:
  • O2 dissolved: 1,5%; O2 bound to hemoglobin: 98,5%
  • CO2 dissolved: 10%; CO2 bound to hemoglobin: 30%; CO2 as bicarbonate: 60%
Q:

Explain the term “refractory period” and give examples!

A:

Refractory period is a period immediately following a stimulus during which further stimulation has no effect, unless it is not strong enough.

-> skeletal muscle cells have a really short refractory period, therefore, more contractions can be triggered within a shorter time period -> skeletal muscle is tetanizable!

-> cardiac muscle has due to the long plateau of cardiac AP a longer refractory period -> cardiac muscle is not tetanizable (really important that only the primary pacemaker can trigger AP within the heart);

Q:

Discuss the reasons for a faster sedimentation rate of red blood cells!

A:

Faster Sedimentation rate = less stability of suspension; this is an indirect marker for inflammation;

Q:

Discuss the differences between skeletal and cardiac muscle excitation-contraction coupling!

A:
  1. Skeletal muscle excitation-contraction coupling: key principle = direct coupling of the voltage gated calcium channel that acts as a voltage sensor within the sacrolemma to the calcium-release channel within the SR -> when the voltage gated Ca-channel gets activated a plug-like thing is pulled out of the Ca-release channel -> Ca2+ influx into the cell -> Ca2+ binding to troponin complex and thereby moving it away from the actin-binding site -> myosin can bind to actin -> muscle contraction;

  2. Cardiac muscle excitation-contraction coupling: key principle = calcium induced calcium release! The sakrolemma gets depolarized by an cardiac action potential -> voltage gated Ca-Channels are opened & influx of Ca2+ into the cell -> exactly this Ca2+ induces Ca-releasing Channel within the SR to release Ca2+ -> binding to troponin complex and thereby moving it away from the actin-binding site -> myosin can bind to actin -> muscle contraction;

Q:

Explain the similarities and differences of skeletal and cardiac muscle action potentials!

A:
  1. Skeletal Muscle Action Potential: fast influx of Na+ into the cell -> when the threshold is reached depolarization of the membrane + overshoot to about +30mV (= equilibrium potential of Na) -> no more Na+ can enter the cell; now the slower K-Channels open their gates -> Efflux of K+ out of the cell = repolarization starts due to loss of charges inside the cell -> Hyperpolarization and refractive period -> resting membrane potential is reached again;

  2. Cardiac Muscle Action potential: threshold is also reached by a fast influx of Na+ into the cell -> depolarization starts until about +70mV (= equilibrium potential of Na within cardiac muscle cells) -> nor more Na+ can enter the cell & the slower K-Channels open their gates -> PARTIAL (!) repolarization until voltage gated Ca-Channels open their gates -> strong influx of Ca2+ into the cell, which keeps the plateau level alive for about 300ms -> even stronger efflux of K(ir) leads to complete repolarization;

B05 - Function and Regulation

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