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Block 3 > Claire’s Deck Block 3 > Flashcards

Claire’s Deck Block 3 Flashcards

1
Q

If X is filtered AND secreted, what is kidney clearance (C) equal to?

A

C is equal to the renal plasma flow.

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2
Q

How can GFR be estimated?

A

GFR can be estimated using a substance that is filtered but not reabsorbed or secreted.

Examples of such substances are inulin and creatinine.

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3
Q

What percentage of total body weight does intracellular fluid make up?

A

40%

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4
Q

What percentage of total body weight does interstitial fluid (ISF) make up?

A

15%

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5
Q

What percentage of total body weight does plasma make up?

A

5%

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6
Q

What does ISF contain in contrast to plasma?

A

ISF contains no protein.

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7
Q

How much water does the average body contain?

A

Around 40 L.

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8
Q

What regulates water loss from the body?

A

The kidney.

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9
Q

What occurs when too much water and solute are taken in at the same time?

A

Hypervolemia.

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10
Q

What occurs when too much water and solute are lost at the same time?

A

Hypovolemia.

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11
Q

What occurs when too much water is taken in without solute?

A

Overhydration.

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12
Q

What occurs when water is lost without solute?

A

Dehydration.

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13
Q

What occurs if water is lost without solute?

A

Dehydration or hypovolemia occurs.

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14
Q

What happens when solute follows the water?

A

Hypo or hypervolemia occurs.

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15
Q

What happens when solute does not follow the water?

A

Overhydration or dehydration occurs.

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16
Q

What happens if blood volume falls too low?

A

GFR will stop.

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17
Q

What is water loss through the kidney called?

A

Diuresis.

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18
Q

What type of urine is produced if water excretion increases?

A

Diluted urine.

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19
Q

What type of urine is produced if water excretion decreases?

A

Concentrated urine.

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20
Q

What is the ISF of the cortex in relation to plasma?

A

Isosmotic.

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21
Q

What is the ISF of the medulla in relation to plasma?

A

Hyperosmotic.

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22
Q

What is reabsorbed in the ascending loop of Henle?

A

Only solutes.

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23
Q

What happens to filtrate entering the descending limb?

A

It loses water, becoming more concentrated.

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24
Q

What maintains a hyperosmotic medulla and drives water reabsorption?

A

Countercurrent exchange.

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25
Q

Under normal conditions, what is the ADH concentration?

A

Low, and diuresis is high.

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26
Q

What does ADH do to water permeability in the tubule?

A

Increases it, meaning more water gets reabsorbed and urine becomes more concentrated.

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27
Q

What three things stimulate ADH secretion from the hypothalamus?

A

Increase in ECF osmolarity, decrease in blood volume, decrease in BP.

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28
Q

What happens when ECF osmolarity rises?

A

Water moves out of cells, causing them to shrink.

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29
Q

What does natriuresis refer to?

A

The excretion of sodium in the urine.

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30
Q

What does aldosterone do?

A

Causes more Na+ to be reabsorbed through the distal tubule and collecting duct.

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31
Q

What does ANP cause?

A

Increased sodium excretion in urine (increased natriuresis).

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32
Q

What effect does aldosterone have on Na+ excretion?

A

Decreases it, whereas ANP increases it.

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33
Q

What is ADH secretion dependent on?

A

Pressure receptors in the left atrium.

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34
Q

What does ADH do to blood pressure?

A

Raises it by increasing water reabsorption in the kidney.

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35
Q

What factors can affect ECF volume?

A

Salt loading, transfusion, heart failure, dehydration, bleeding, space flight, posture.

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36
Q

What must the pH of ECF be maintained at?

A

7.35 to 7.45.

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37
Q

How can pH of body fluids be maintained?

A

By chemical buffers, ventilation, and kidneys.

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38
Q

What does ventilation determine in the blood?

A

The PCO2.

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39
Q

What happens during hyperventilation?

A

PCO2 decreases.

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40
Q

What happens during hypoventilation?

A

PCO2 increases.

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41
Q

What compensates for metabolic acidosis/alkalosis?

A

Ventilation.

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42
Q

How can the kidney compensate for pH disturbances?

A

Directly: excretion or reabsorption of H+. Indirectly: excretion or reabsorption of HCO3-.

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43
Q

What do the proximal tubules secrete and reabsorb?

A

Secrete H+ and reabsorb HCO3-.

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44
Q

What controls acid excretion in the kidney?

A

The collecting duct through intercalated cells.

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45
Q

How can HCO3- be produced in the kidney?

A

Using ammonia.

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46
Q

In what state do type A intercalated cells function?

A

In an acidosis state.

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47
Q

In what state do type B intercalated cells function?

A

In an alkalosis state.

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48
Q

What is the arterial pH range compatible with life?

A

6.8 to 8.

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49
Q

What is the normal HCO3- to CO2 ratio?

A

20/1.

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50
Q

What arises from an increase in CO2?

A

Respiratory acidosis.

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51
Q

What arises from a decrease in CO2?

A

Respiratory alkalosis.

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52
Q

What arises from an increase in HCO3-?

A

Metabolic alkalosis.

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53
Q

What arises from a decrease in HCO3-?

A

Metabolic acidosis.

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54
Q

What is the most important compensatory organ in respiratory acidosis?

A

The kidney.

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55
Q

What is Lead I in ECG?

A

Right arm to Left arm (0 degrees).

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56
Q

What is Lead II in ECG?

A

Right arm to Left leg (-60 degrees).

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57
Q

What is Lead III in ECG?

A

Left arm to Left leg (+120 degrees).

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58
Q

What do vector directions point towards?

A

The positive pole.

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59
Q

What is Lead aVR in ECG?

A

Left arm/Left leg to Right arm (-150 degrees).

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60
Q

What is Lead aVL in ECG?

A

Right arm/Left leg to Left arm (-30 degrees).

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61
Q

What is Lead aVF in ECG?

A

Right arm/Left arm to Left Leg (+90 degrees).

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62
Q

What do precordial leads assess?

A

Spread of depolarization from a lateral angle.

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63
Q

How many precordial leads are there?

A

6.

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64
Q

What type of leads are created using Wilson’s Central Terminal?

A

Unipolar leads.

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65
Q

What happens when current flows towards the arrowheads in ECG?

A

Upwards deflection occurs.

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66
Q

What happens when current flows away from the arrowheads in ECG?

A

Downwards deflection occurs.

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67
Q

What happens when current flows perpendicular to the arrowheads in ECG?

A

Biphasic aka equiphasic deflection

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68
Q

What happens when current flows obliquely towards the arrowheads in ECG?

A

A less strong upwards deflection occurs.

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69
Q

What happens when current flows obliquely away from the arrowheads in ECG?

A

A less strong downwards deflection occurs.

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70
Q

What are the phases of cardiac muscle action potential?

A

Phase 0: Na+ channels open, causing depolarization. Phase 1: Na+ channels close, K+ are open, repolarization begins. Phase 2: Ca2+ channels open, K+ channels start to close. Phase 3: Ca2+ channels close, K+ continues to exit the cell. Phase 4: Cells reach resting membrane potential.

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71
Q

What does one square on ECG graph paper represent?

A

0.04 seconds and 1mV in voltage.

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72
Q

What is the first negative component on the ECG graph?

A

The Q wave.

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73
Q

What is the first positive component on the ECG graph?

A

The R wave.

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74
Q

What is the negative component following the R wave?

A

The S wave.

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75
Q

How are large waves indicated on an ECG graph?

A

By capital letters.

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76
Q

How are small waves indicated on an ECG graph?

A

By lowercase letters.

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77
Q

Does ventricular rhythm have a P wave?

A

False. Only the atrial rhythm has a P wave.

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78
Q

What determines the heart axis?

A

The vector of depolarization from all limb leads.

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79
Q

What is the normal axis range?

A

-30 and 90+ degrees.

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80
Q

What is Lead I positive between?

A

-90 and +90 degrees.

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81
Q

What is Lead II positive between?

A

-30 and +150 degrees.

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82
Q

If both Lead I and II are positive, what is likely?

A

The axis is likely normal.

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83
Q

What does the PR interval represent?

A

Depolarization of the atrial and AV node.

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84
Q

How long does the PR interval normally last?

A

0.12 to 0.20 seconds.

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85
Q

How long does depolarization of the ventricles (QRS complex) normally last?

A

0.07 to 0.10 seconds.

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86
Q

What is the QT interval longer in?

A

Women than men and varies with changes in heart rate.

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87
Q

What should you be suspicious of regarding the Q-T interval?

A

When it is greater than half of the R-R interval.

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88
Q

What is the normal duration of the QRS complex?

A

0.07 to 0.10 seconds

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89
Q

How does the QT interval vary between women and men?

A

The QT interval is longer in women than men and varies with changes in heart rate.

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90
Q

What is the QT interval at 60 bpm?

A

0.44 seconds

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91
Q

What is the QT interval at 80 bpm?

A

0.37 seconds

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92
Q

What is the QT interval at 100 bpm?

A

0.30 seconds

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93
Q

When should you be suspicious regarding the QT interval?

A

When the Q-T interval is greater than half of the R-R interval.

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94
Q

What characterizes Atrial Fibrillation?

A

Numerous small depolarizations spread through the atria, electrically neutralizing each other, with no P wave and a normal QRS-T complex.

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95
Q

What are Premature Ventricular Contractions?

A

Contractions that occur before the normal time, caused by ectopic foci emitting abnormal impulses during cardiac rhythm, leading to a prolongation of the QRS complex.

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96
Q

What is Torsades de Pointes?

A

A condition characterized by delayed repolarization of ventricular muscles after action potential, with premature ventricular beats leading to pauses and excessively long Q-T intervals.

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97
Q

What is Atrial Flutter?

A

A rapid rate of atrial contraction, typically 2 to 3 beats of the atria for every 1 beat of the ventricle in ECG (2:1).

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98
Q

What is Supraventricular tachycardia?

A

An aberrant rhythm involving the AV node or the atrium, with an almost normal QRS-T complex and may or may not have a P wave.

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99
Q

What defines First degree block?

A

A delay of conduction from atria to ventricle without blockage, characterized by an increased P-R interval (<0.20 sec).

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100
Q

What is Second degree block?

A

Conduction through the A-V bundle may or may not pass to the ventricles, with an increased P-R interval (up to 0.45 sec) and possibly two P waves for every QRS complex in severe cases.

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101
Q

What is Complete A-V block (third degree block)?

A

A complete block of impulse from the atria to the ventricles, where the ventricles establish their own signal, leading to disassociation of the P wave from the QRS complex.

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102
Q

What is Electrical Alternans?

A

A blockage of impulse conduction in the peripheral ventricular Purkinje system causing alternating QRS amplitudes in ECG.

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103
Q

How do you find the QRS axis?

A

The vector will be away from the most negative QRS complex.

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104
Q

How do you find the QRS axis in relation to the equiphase complex?

A

The vector will be perpendicular to the most equiphase (big positive + big negative) QRS complex.

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105
Q

How do you find the QRS axis in relation to the positive QRS complexes?

A

The vector will be in the general direction of the most and second most positive QRS complex.

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106
Q

What is the symbol for capillary hydrostatic pressure?

A

Pc

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107
Q

What is the symbol for ISF hydrostatic pressure?

A

PISF

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108
Q

What is the symbol for plasma colloid osmotic pressure?

A

πP

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109
Q

What is the symbol for interstitial colloid osmotic pressure?

A

πISF

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110
Q

Describe capillary hydrostatic pressure (PC).

A

Capillary hydrostatic pressure (PC) pushes ISF from capillary into interstitium.

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111
Q

Describe ISF hydrostatic pressure (PISF).

A

ISF hydrostatic pressure (PISF) pushes ISF from interstitium into capillary.

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112
Q

Describe plasma colloid osmotic pressure (πP).

A

Plasma colloid osmotic pressure (πP) draws ISF from interstitium into capillary.

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113
Q

Describe interstitial colloid osmotic pressure (πISF).

A

Interstitial colloid osmotic pressure (πISF) draws fluid from capillary into interstitium.

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114
Q

What is a cardiomyocyte’s resting membrane potential (Vm)?

A

-90mV

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115
Q

Why is the resting membrane potential electronegative?

A

There is a deficit of positive charges in the cytosol compared to the extracellular space.

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116
Q

What are the ion concentrations in extracellular space and in the SR (of cardiac cells) compared to the cytosol?

A

There is WAY more calcium outside the cytosol (20,000x) and in SR (10,000x), more sodium (15x) outside the cell, and more potassium inside the cell (40x). This creates a concentration gradient that allows the action potential to happen.

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117
Q

What maintains the concentration gradients in cell walls?

A

Active transporters.

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118
Q

What informs the resting membrane potential (Vo) aside from concentration gradients?

A

The permeability of the cell to K+ at rest.

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119
Q

What is the threshold potential of a cardiac cell action potential?

A

-70mV (Na+ TP)

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120
Q

What is a voltage-gated channel?

A

A voltage-sensitive protein that modulates membrane permeability to ions.

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121
Q

What happens to Vm and ion channels?

A

Changes in Vm lead to conformational changes in ion channels, causing pores to open and ions to enter.

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122
Q

What are the channel activation thresholds of sodium, calcium, and potassium?

A

Na+ = -70mV, Ca2+ = -40mV, K+ = it depends, but near/above 0mV. This means that Na+ channels open first, followed by Ca2+, followed by K+.

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123
Q

Explain the cycle/mechanism of action of a voltage-gated channel.

A

Vm reaches activation threshold (e.g., -70mV for Na+) → channel opens, Na+ enters cell → channel closes once the membrane potential becomes positive → ions are pumped out eventually → repeat.

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124
Q

What are the 5 steps of the cardiac action potential?

A

Phase 4 = resting state, membrane potential = -90mV; Phase 0 = depolarization above -70mV → Na+ channel opens; Phase 1 = Na+ inside cell eventually causes Na+ channel to close; Phase 2 = at -40mV, Ca2+ channel opens, Ca2+ enters cell; Phase 3 = gradients returned to normal (repolarizing).

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125
Q

What is the refractory period for a cardiomyocyte?

A

It lasts from depolarization to muscle relaxation and is long, allowing for full contraction/relaxation of the heart and preventing tetanus.

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126
Q

Characterize a fast action potential.

A

Stable resting potential (-90mV), threshold potential = -70mV (max = +30mV), needs a trigger, fast Na+ entry.

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127
Q

Characterize a slow action potential.

A

Unstable resting potential (-60mV), threshold potential = -40mV (max = 0-20mV), spontaneous (diastolic) depolarization.

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128
Q

Which neurotransmitter and receptor are associated with SNS modulation of pacemaker activity?

A

Norepinephrine and beta-1 receptors.

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129
Q

How does the SNS increase heart rate?

A

Vo increases (threshold is closer to 0/less electronegative) and IH is sped up.

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130
Q

Which neurotransmitter and receptor are associated with PNS modulation of pacemaker activity?

A

Acetylcholine and muscarinic receptors.

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131
Q

How does the PNS decrease heart rate?

A

Vo decreases (hyperpolarized/becomes more electronegative) and IH is slowed down.

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132
Q

What is vagal tone?

A

It refers to the way the PNS decreases heart rate.

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133
Q

What is the pacemaker current (IH)?

A

It’s the reason the heart can beat on its own, activated by repolarization.

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134
Q

Why is the pacemaker current so slow?

A

It is driven by K+ efflux, a gradual process.

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135
Q

Where does the pacemaker current originate?

A

From the HCN channel superfamily, which conducts Na+ and K+.

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136
Q

What connects cardiomyocytes electrically?

A

Gap junctions.

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137
Q

What determines how fast action potentials will be propagated in cardiac tissue?

A

The type and density of gap junctions.

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138
Q

Which parts of the conduction system have slow conduction/APs?

A

SA node and AV node.

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139
Q

Which parts of the conduction system have fast conduction/APs?

A

Atria, ventricles, and His-Purkinje system.

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140
Q

What allows interatrial conduction of action potentials?

A

Bachmann’s bundle.

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141
Q

What is the significance of the AV node being the only conduction pathway between the atria and ventricles?

A

It allows for full atrial contraction and diastolic filling of ventricles before ventricular contraction.

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142
Q

What are subsidiary pacemakers?

A

Any part of the conduction system that can develop auto-rhythmic activity, such as the AV node and Purkinje fibers.

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143
Q

What is Image Occlusion?

A

Image Occlusion is a technique used to hide parts of an image to test knowledge on the occluded areas.

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144
Q

What 5 things can you find in the upper right quadrant of the abdomen?

A

Liver, Gallbladder, Hepatic flexure (of colon), Head of pancreas, Right kidney

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145
Q

What 5 things can you find in the upper left quadrant of the abdomen?

A

Stomach, Spleen, Splenic flexure of colon, Tail of pancreas, Left kidney

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146
Q

What 2 things are in the lower right quadrant of the abdomen?

A

Cecum, Appendix

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147
Q

What’s in the lower left quadrant of the abdomen?

A

Sigmoid colon

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148
Q

Describe diastole for me real quick.

A

The passive phase of the cardiac cycle. Associated with ventricular relaxation and filling, and low ventricular pressure.

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149
Q

Describe systole for me?

A

The active phase of the cardiac cycle. Associated with excitation (depolarization), contraction, development of pressure, and ejection of blood.

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150
Q

Tell me about how the heart valves keep blood flowing in one direction only.

A

It’s all about pressure gradients! When there’s high pressure coming from behind the valve, it opens. When there’s high pressure against the front of the valve, it closes.

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151
Q

In the Wigger’s diagram, what does the P wave indicate?

A

Atrial depolarization (should result in contraction)

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152
Q

In the Wigger’s diagram, what does the QRS complex indicate?

A

Ventricular depolarization (should result in contraction)

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153
Q

In the Wigger’s diagram, what does the T wave indicate?

A

Ventricular repolarization (should result in relaxation)

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154
Q

What’s stroke volume? How do you calculate it?

A

The volume of blood pumped by the ventricle in one beat. SV = end diastolic volume (EDV) - end systolic volume (ESV)

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155
Q

What determines stroke volume?

A

Contractility, or how forcefully your LV contracts; Afterload, or the load that your LV has to work against.

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156
Q

What’s the ejection fraction? How do you calculate it?

A

The proportion of blood that the LV actually ejects when it contracts. EF = Stroke volume (SV)/End-diastolic volume (EDV)

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157
Q

What’s a normal LV ejection fraction? When should you start worrying?

A

> =55% is normal; <40% is a red flag for LV dysfunction.

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158
Q

What’s cardiac output (CO)? How do you calculate it?

A

How much blood your LV can pump in 1 minute. CO = Stroke volume (SV) x heart rate.

159
Q

What’s a typical cardiac output?

A

~5L/min

160
Q

What’s preload? In cardiac ventricles, what determines preload?

A

Preload = the load imposed at rest. In cardiac ventricles, preload is determined by end diastolic volume.

161
Q

What are 5 factors affecting preload?

A

Filling time (HR), Atrial contraction, Filling pressure, Venous return, LV compliance.

162
Q

What does the ‘intrinsic’ heart rate refer to?

A

Just the fact that if you just turned your SNS and PNS off for a minute, the heart would beat around 100 BPM.

163
Q

What are the two main influences on heart rate?

A

SNS and PNS inputs.

164
Q

What are three other things that affect HR?

A

Body temp, Cardiac pressures (e.g., exercise), Function/dysfunction of conducting system.

165
Q

What might cause an increase in EDV?

A

Decreased HR, Lying down, Fluid loading.

166
Q

What might cause a decrease in EDV?

A

Increased HR, Standing up (too fast), Fluid loss/dehydration, Reduced LV compliance (increased stiffness).

167
Q

What’s afterload?

A

How much resistance cardiomyocytes have to pump against when ejecting blood.

168
Q

Which 3 factors determine afterload?

A

LV pressure during ejection, BP in aorta, Vascular tone.

169
Q

How are afterload and stroke volume related?

A

Inverse relationship: Decreased afterload increases stroke volume; Increased afterload decreases stroke volume.

170
Q

How are contractility and stroke volume related?

A

Direct relationship: Increased contractility = increased stroke volume and vice versa.

171
Q

How do SNS and adrenergic stimulation impact contractility?

A

Contractility is increased by SNS and adrenergic stimulation (e.g., norepinephrine).

172
Q

What’s the Frank-Starling law?

A

Stroke volume rises in proportion to ventricular filling (preload).

173
Q

How will an increase in afterload change the Frank-Starling curve?

A

Increased afterload = downward shift.

174
Q

How will an increase in contractility change the Frank-Starling curve?

A

Increase = curve shifted up.

175
Q

What’s the formula for hydrostatic pressure?

A

P = height of fluid column (fluid density).

176
Q

What’s the relevance of hydrostatic pressure to taking blood pressure?

A

If you don’t take it at the right height (at level of heart), the value will be wrong unless you adjust for the height difference.

177
Q

What are venous pressures like at the heart level?

A

At heart level, typically below 10mmHg; can vary widely above and below the heart (~74mmHg per meter of fluid column).

178
Q

What’s the difference between a static and a flowing system with respect to pressure?

A

In a static system, pressure is consistent everywhere; in a flowing system, pressure decreases due to energy loss (friction → heat).

179
Q

Tell me about the issues associated with inadequate and excessive BP.

A

Inadequate = reduced tissue blood flow and shock; Excessive BP = high microvascular pressures and flows, strains LV function and increases O2 consumption.

180
Q

Tell me about how BP changes as you move from LV back to the right atrium.

A

LV = massive fluctuations; Arteries = rapid fluctuation; Arterioles = pressure falling off; Capillaries, Venules, veins = steady fall in pressure; Right atrium = very low pressure.

181
Q

What’s diastolic BP? When does it occur?

A

Minimum arterial BP; occurs just at the beginning of LV ejection.

182
Q

What’s systolic BP? When does it occur?

A

Peak arterial BP; produced by LV ejection.

183
Q

What’s arterial pulse pressure?

A

The difference between systolic and diastolic BPs.

184
Q

What’s the mean arterial pressure? How do you calculate it?

A

The average of your diastolic and systolic BPs; MAP = diastolic + ⅓ pulse pressure.

185
Q

How do you calculate arterial BP?

A

BParterial - Pvenous ≈ CO(TPR); Pvenous is usually negligible.

186
Q

What’s total peripheral resistance? How do you calculate it?

A

The resistance of the entire systemic vasculature; TPR = BP/CO.

187
Q

What determines TPR?

A

Blood vessel properties (length, radius, tone); TPR tends to remain pretty consistent in the short term.

188
Q

How do you calculate resistance?

A

R = 8Lη/πr^4; L = length, η = viscosity, r = radius.

189
Q

Which factor has the most impact on resistance?

A

Radius; the fastest way to change resistance is to vasodilate/vasoconstrict.

190
Q

How are CO and TPR related to mean BP?

A

Directly related; an increase in CO or TPR will increase BP.

191
Q

What are 3 factors influencing pulse pressure?

A

Intermittency of LV ejection, Size of LV stroke volume, Compliance of central arteries.

192
Q

What might cause long-term BP elevation?

A

Increased CO, Increased TPR (or both); typically linked to increased TPR but normal CO.

193
Q

What are 2 effects of stiffened central arteries?

A

Increased systolic pressure, Increased pulse pressure.

194
Q

What are baroreceptors, and how do they modulate BP?

A

Located in aorta and carotid arteries; sense and respond to BP-induced distension.

195
Q

How do your kidneys regulate BP? (2 processes)

A

Increase salt and water retention = increased fluid volume; Renal renin release = vasoconstriction and sympathetic activation.

196
Q

Is renal regulation of BP short or long term?

A

Long term.

197
Q

Which two things determine blood flow to a tissue?

A

Pressure gradient (drives flow through vasculature); Ease with which blood can actually flow through vessels (resistance or conductance).

198
Q

What do hemodynamics describe?

A

Physical factors that govern blood flow (pressure and resistance) through a vascular system.

199
Q

How do you calculate blood flow (F)?

A

F = ΔP/R or F = ΔP(C).

200
Q

What’s a pressure gradient? How do you calculate it?

A

Refers to the pressure gradient driving flow through a tissue; Pressure gradient = arterial pressure - venous pressure.

201
Q

If the pressure gradient is held constant, what’s the relationship between blood flow and vascular resistance?

A

The two are inversely proportional.

202
Q

What’s conductance?

A

The ease with which blood flows through a vessel; opposite of vascular resistance.

203
Q

If the pressure gradient is held constant, what’s the relationship between blood flow and vascular conductance?

A

Direct relationship.

204
Q

What’s the relationship between conductance and resistance?

A

They’re inverses of one another.

205
Q

What are 5 factors that might induce vasoconstriction?

A

Increased myogenic activity, Increased O2, Decreased CO2, Increased endothelin, SNS activation.

206
Q

What are 5 factors that might induce vasodilation?

A

Decreased myogenic activity, Decreased O2, Increased CO2, Increased nitric oxide, PNS activation.

207
Q

What’s the most effective way to adjust vascular resistance and blood flow?

A

Vasoconstriction/dilation (smooth muscle, especially in arterioles).

208
Q

Assuming pressure gradients are held constant, what determines the distribution of flow across vascular beds?

A

Vascular conductance.

209
Q

What’s the difference between an extrinsic and an intrinsic mechanism of blood flow regulation?

A

Extrinsic = mechanism is external to the tissue; Intrinsic = mechanism is contained within the tissue.

210
Q

What are three extrinsic mechanisms that regulate blood flow?

A

SNS, PNS, Circulating factors.

211
Q

Tell me about how the SNS regulates blood flow.

A

Vasoconstriction in most tissues.

212
Q

What’s the difference between an extrinsic and an intrinsic mechanism of blood flow regulation?

A

Extrinsic = mechanism is external to the tissue or vascular bed. Intrinsic = mechanism is contained within the tissue or vascular bed.

213
Q

Tell me about how the SNS regulates blood flow.

A

Vasoconstriction in most tissues. Epinephrine or norepinephrine and alpha adrenergic receptors. Very fast.

214
Q

Tell me about how the PNS regulates blood flow.

A

Doesn’t do a lot actually. Vasodilation in some tissues (e.g., skin, penis). Mediated by nerves releasing acetylcholine, peptides, and nitric oxide.

215
Q

Tell me about how circulating factors regulate blood flow.

A

Substances circulating in your blood. Vasoconstrictors = noradrenaline, angiotensin II, ADH (antidiuretic hormone/vasopressin), endothelin. Vasodilators = histamine, adenosine, nitric oxide.

216
Q

Which vascular beds are capable of autoregulating blood flow?

A

All of them except the pulmonary vascular bed.

217
Q

What type of regulation is metabolic autoregulation? What does it refer to?

A

Intrinsic regulation. Flow is adjusted to match metabolism (O2 consumption).

218
Q

Tell me about how metabolic autoregulation functions in active tissues.

A

Active tissues produce metabolites that are vasodilators (e.g., adenosine, ATP, K+, CO2, H+, etc.) which can trigger metabolic autoregulation, reactive hyperemia, and pressure autoregulation. Relevant in all tissues.

219
Q

What type of regulation is pressure autoregulation? What does it refer to?

A

Intrinsic regulation. Local mechanisms that act to maintain consistent blood flow despite fluctuations in BP. Don’t work well at extremes of pressure.

220
Q

What does the myogenic response/myogenic tone refer to?

A

Pressure/stretch-induced vasoconstriction. May contribute to pressure autoregulation.

221
Q

What does reactive hyperaemia refer to?

A

When circulation is occluded, it’s followed by a period of increased blood flow.

222
Q

Where is autonomic (extrinsic - SNS/PNS) control most prevalent?

A

In skin (autoregulation present but weak).

223
Q

Where is autoregulation (intrinsic) most prevalent?

A

In CNS (local metabolic needs are defended).

224
Q

Why does the CNS exhibit little/no response to autonomic stimulation?

A

Because it’d be really bad if your brain got shut off every time your SNS started firing.

225
Q

Which system (sympathetic/autoregulatory) dominates in skeletal and cardiac muscle?

A

Trick question, they compete to control blood flow.

226
Q

How do intrinsic and extrinsic systems relate to one another?

A

Intrinsic = adjust blood flow to suit local needs. Extrinsic = Can override autoregulatory dilation to ensure BP meets needs of CNS and other vulnerable tissues. Note: Extrinsic overrides don’t apply to CNS.

227
Q

How do you calculate resistance of compartments (vessels) connected in series?

A

Literally just add ‘em all together. Rtotal = R1 + R2 + R3 etc.

228
Q

How do you calculate resistance of compartments (vessels) connected in parallel?

A

Add the inverse of the sum of the inverses. Rtotal = 1/(1/R1 + 1/R2 + 1/R3 etc).

229
Q

How does the total resistance of a network of parallel vessels compare to the resistance of its constituent vessels?

A

Total resistance parallel arrangement of vessels greatly reduces blood flow.

230
Q

What are standard limb leads?

A

Lead I = RA → LA 0° Lead II = RA → LL 60° Lead III = LA → LL 120°

231
Q

What are augmented limb leads?

A

Lead aVR = LA + LL → RA -150° Lead aVL = RA + LL → LA -30° Lead aVF = RA + LA → LL 90°

232
Q

What are precordial leads and what do they assess?

A

6 standard leads attached to the chest Used to assess depolarization from a lateral angle

233
Q

How is precordial lead placement done?

A

V6 on lateral left at 0°, V1 is sorta on the right side of the sternal border (at 120°? Unclear)

234
Q

What is the relationship between the direction of flow of current (depolarization) and the magnitude of deflection on the EKG?

A

Current flow aligns with axis lead (flows from negative to positive) = strong positive deflection Current flow runs against axis lead = strong negative deflection Current flow runs obliquely to axis lead (at a diagonal) = weak deflection in direction of flow with respect to axis of lead If perpendicular to EKG lead, biphasic/equiphasic deflection seen

235
Q

Describe contraction activity of the heart at each part of a QRS complex.

A

Q wave = depolarization down the interventricular septum/bundle branches R wave = Depolarization has reached the apex, starting to split (second half is when it reaches apex and sorta reverses direction) S wave = Depolarization is pretty much finished, the top part (nearest the atria) of ventricles has contracted

236
Q

What is the grid size of ECG paper and ECG paper speed?

A

1mm^2 grid used Normal speed = 25mm/s 25 blocks/s (each block = 4ms)

237
Q

What are 3 ways to estimate heart rate using an ECG?

A

Determine time between RR intervals 60 000/RR interval (in milliseconds) QRS complexes in 10s timeframe x 6

238
Q

What is the ECG voltage standard?

A

It should be about 20mm/20 blocks high

239
Q

How are the components of the QRS complex named?

A

First negative component = Q wave First positive component = R wave Negative component following R wave = S wave

240
Q

What is the convention used to indicate magnitude when naming a QRS complex?

A

Capital letter = large wave Small letter = small wave

241
Q

What is the J point?

A

Marks where the QRS complex ends and the ST segment begins In heart, marks end of depolarization/start of repolarization

242
Q

How do you determine ST segment elevation or depression?

A

ST segment elevation/depression is relative to the preceding PR segment

243
Q

When the heart has an atrial rhythm, what will you always see?

A

P wave preceding a narrow QRS complex Constant PR interval

244
Q

What does no P wave indicate?

A

Ventricular rhythm (SA node broke)

245
Q

How might you determine the QRS axis?

A

Find the most equiphasic QRS (vector is perpendicular to this direction) Find the most positive QRS complex (vector will be pointing in that general direction)

246
Q

How do you estimate heart axis using the quadrant method?

A

You’re gonna have two leads, determine which half of the circle is significant (and where you divide), then read off the part that overlaps

247
Q

Why is three lead analysis better than the quadrant method?

A

More specific - you’re looking for overlap from 3 things instead of 2.

248
Q

If you can’t remember your ECG lead angles, what’s a useful trick to see if the axis is in normal range?

A

If lead I and II are both positive, there’s a pretty good chance that it’s in normal range.

249
Q

What’s happening in the heart during the PR interval, and what’s a normal range?

A

Depolarization of atria and AV node 120-200ms is normal

250
Q

What’s happening in the heart during the QRS duration, and what’s a normal range?

A

Ventricular depolarization 70-100ms is normal

251
Q

How do you determine whether the QT interval is within normal range?

A

Bazzet’s formula (yuck) Or if QT interval is greater than ½ of RR interval, that’s a red flag

252
Q

What are the two flavours of cardiac arrhythmia?

A

Disorders of impulse formation Disorders of impulse conduction

253
Q

What might cause a disorder of impulse formation?

A

Abnormal rhythmicity of pacemaker Shift of pacemaker from SA node to somewhere else

254
Q

What might cause a disorder of impulse conduction?

A

Blocks at different points through the conduction system Abnormal pathways of conduction False impulses from parts of the heart that have no business generating impulses

255
Q

What is atrial fibrillation and how does it look on an ECG?

A

Numerous small depolarizations across atrial that electrically neutralize each other No P waves Normal QRS-T complex

256
Q

What are premature ventricular contractions, what causes them, and how do they look on an ECG?

A

When contraction occurs before you’d expect it to (incomplete ventricular filling) Caused by [ectopic foci] emitting irregular impulses On ECG QRS complex is longer than it should be

257
Q

What are Torsades de Pointes and how do they look on an ECG?

A

Delayed repolarization after AP Premature ventricular contraction → pauses and prolonged post-pause QT intervals Excessively long QT intervals on ECG

258
Q

What are premature ventricular contractions? What causes them? What do they look like on an ECG?

A

When contraction occurs before you’d expect it to (incomplete ventricular filling). Caused by ectopic foci emitting irregular impulses. On ECG, QRS complex is longer than it should be.

259
Q

What are Torsades de Pointes? What do they look like on an ECG?

A

Delayed repolarization after AP. Premature ventricular contraction → pauses and prolonged post-pause QT intervals. Excessively long QT intervals on ECG.

260
Q

What’s atrial flutter? What do you look for on an ECG?

A

Electrical signals travel as a single wave around the atria → rapid rates of atrial contraction. 2-3 atrial contractions for each ventricular contraction. 2:1 atrial:ventricular rhythm on ECG.

261
Q

What’s supraventricular tachycardia? What does it look like on an ECG?

A

Abnormal rhythm of AV node or atrium. QRS-T complex looks almost normal. P wave might be there, might not be. If present, characteristics might be changed.

262
Q

What’s a first-degree block? What does it look like on an ECG?

A

Delayed conduction from atria → ventricles (no true blockage). PR interval is increased (>20ms).

263
Q

What’s a second-degree block? What does it look like on an ECG?

A

Potential block from AV bundle → ventricles. PR interval increased up to 45ms. If severe, see 2:1 P wave:QRS complex.

264
Q

What’s a third-degree block? What does it look like on an ECG?

A

No conduction between atria and ventricles. Ventricles will establish own signal. P wave and QRS complex are dissociated from one another.

265
Q

What’s electrical alternans? What does it look like on an ECG?

A

Impulses not reaching Purkinje system. Inconsistent QRS complex amplitude.

266
Q

What mediates the response to hypoglycemia? What 3 effects does it have?

A

Epinephrine. Increases hepatic glucose production. Decreases insulin secretion. Increases glucagon secretion.

267
Q

Tell me about fuel sources used by the body during starvation.

A

Brain prefers glucose but will use ketone bodies if no glucose available. Tissues without mitochondria require glucose. Other tissues can use fatty acids.

268
Q

How does the body maintain normal tissue function during periods of fasting/starvation?

A

Conserve protein.

269
Q

How does adipose tissue respond to the drop in insulin associated with fasting/starvation?

A

Decreased glucose uptake (via GLUT-4). Decreased pentose phosphate pathway. Increased glucagon (decreased fatty acid and TAG synthesis, decreased glycolysis, increased fatty acid oxidation). Increased NADPH.

270
Q

Which hormone starts the process of breaking down triglycerides from fat stores? How do these components get used?

A

Hormone-sensitive lipase (HSL). Triglycerides → any tissue with mitochondria for ATP synthesis. Glycerol → liver for gluconeogenesis.

271
Q

How does the liver respond to decreased blood glucose?

A

Glycogenolysis (glycogen → glucose). Can maintain blood glucose levels for <12h.

272
Q

What effect does increased glucagon have on the liver?

A

Decreased glycolysis (decreased glucokinase, PFK-1 and pyruvate kinase). Decreased pentose phosphate pathway. Increased NADPH (not consumed by anabolic processes). Increased gluconeogenesis.

273
Q

Which 2 things inhibit glycolysis but activate gluconeogenesis?

A

Citrate. Glucagon.

274
Q

What’s one thing that inhibits glycolysis but doesn’t activate gluconeogenesis?

A

ATP inhibits glycolysis but doesn’t activate gluconeogenesis.

275
Q

Which 2 things activate glycolysis but inhibit gluconeogenesis?

A

AMP. Fructose 2, 6-bisphosphate.

276
Q

What prevents glycolysis and gluconeogenesis from operating at the same time?

A

Glucagon inhibits production of fructose 2, 6-bisphosphate.

277
Q

What is the effect of glucagon on fat metabolism in the liver?

A

Decreased fatty acid synthesis (TAG and VLDL). Increased fatty acid → mitochondria. Increased beta-oxidation.

278
Q

What happens to acetyl CoA in the liver that isn’t needed for the Krebs cycle?

A

Converted into ketone bodies. Acetoacetate and beta-hydroxybutyrate.

279
Q

Where do ketone bodies come from? How are they used?

A

Come from liver. Used by any extrahepatic tissue with mitochondria. Ketone bodies → acetyl CoA → ATP.

280
Q

When do levels of ketone bodies in the blood peak?

A

2-3 weeks into starvation.

281
Q

How is amino acid metabolism sustained during fasting?

A

Amino acids come from muscle (mostly alanine, glutamine, and glycine). Carbon skeletons → pyruvate or Krebs cycle intermediates → gluconeogenesis substrates (except leucine and lysine). Excess nitrogen → urea → urea cycle.

282
Q

What are the substrates for gluconeogenesis?

A

Amino acid carbon skeletons (except leucine and lysine). Lactate. Glycerol.

283
Q

Where does the brain get its fuel from in early starvation?

A

Glucose from hepatic glycogenolysis and hepatic gluconeogenesis (mostly from muscle protein).

284
Q

Where does the brain get its fuel from in late starvation?

A

Ketogenesis.

285
Q

Why can’t the brain use fatty acids for fuel?

A

Fatty acids can’t pass through the blood-brain barrier (because they’re bound to albumin).

286
Q

What effects do decreased insulin and increased glucagon have on carbohydrate metabolism in muscle?

A

Decreased glucose uptake via GLUT-4. Decreased glucose-6-phosphate. Decreased glycolysis. Decreased glycogenesis.

287
Q

What receptors does adipose tissue have that muscles lack?

A

Glucagon receptors.

288
Q

What stimulates glycogen release in muscle?

A

Physical activity (Ca2+ release, AMP increase).

289
Q

How does muscle use fat for fuel during fasting/starvation?

A

Increased LPL in muscle vasculature → fatty acid uptake from VLDL.

290
Q

What is the main source of fuel for muscle during a prolonged fast?

A

Fatty acids (for beta-oxidation) are the main fuel. Ketones also used.

291
Q

How does protein metabolism compare in early vs late fasting?

A

Early = rapid proteolysis for gluconeogenesis to supply glucose to brain and tissues without mitochondria. Late = Decreased proteolysis because ketone bodies are being produced.

292
Q

What effect does exercise have on metabolism in muscle?

A

Similar effect to insulin in that it stimulates GLUT-4 receptors (i.e., glucose can enter myocytes).

293
Q

What does the kidney do during periods of fasting/starvation?

A

Keeps ripping ammonia off of glutamine and glutamate (glutaminase and glutamate dehydrogenase) to make α-ketoglutarate for ATP production and renal gluconeogenesis.

294
Q

What proportion of glucose does the kidney produce during a prolonged fast?

A

Up to 50% of it.

295
Q

How does the urea/NH4+ balance in the kidney change during prolonged fasting?

A

Urea decreases, NH4+ increases. NH4+ used to facilitate H+ (acid) removal from body to spare Na+ and K+.

296
Q

What is the diameter of a capillary? A red blood cell?

A

Both about 6 microns.

297
Q

How does the velocity of blood in capillaries compare to velocity in veins and arteries?

A

Lower in capillaries.

298
Q

How does total cross-sectional area in capillaries compare to that of veins/arteries?

A

Higher cross-sectional area in capillaries.

299
Q

How does nitric oxide (NO) impact microcirculation?

A

Causes vasodilation (in microcirculation).

300
Q

How thick are capillary walls?

A

Around 1 micron thick.

301
Q

How does most diffusion through capillaries occur?

A

Through gaps between adjacent endothelial cells.

302
Q

What is interstitial space?

A

The space between cells.

303
Q

Through what does solute diffusion between blood and tissue occur?

A

Through the ISF fluid.

304
Q

What is diffusion?

A

The main mode of exchange of solutes between blood, ISF, and cells.

305
Q

What determines bulk flow of ISF?

A

Starling’s forces.

306
Q

What does capillary hydrostatic pressure (PC) do?

A

Pushes ISF from capillary into interstitium.

307
Q

What does interstitial colloid osmotic pressure (IIISF) do?

A

Draws fluid from capillary into interstitium.

308
Q

When is PISF increased?

A

When tissue is swollen with excess ISF (edema).

309
Q

Tell me about Starling’s forces in a healthy patient.

A

Outward = 11 mmHG. Inward = 9 mmHG. This results in a net exchange pressure of 2 mmHg and accounts for the net outward flow of ISF (reabsorbed by lymphatics).

310
Q

Tell me about how lymph is drained back into circulation.

A

Most lymph = thoracic duct. A much smaller area = right lymphatic duct.

311
Q

What is edema?

A

Swelling of tissues that occur when too much ISF accumulates.

312
Q

Describe capillary hydrostatic pressure (PC).

A

Pushes ISF from capillary into interstitium.

313
Q

Describe ISF hydrostatic pressure (PISF).

A

Pushes ISF from interstitium into capillary.

314
Q

Describe plasma colloid osmotic pressure (πP).

A

Draws ISF from interstitium into capillary.

315
Q

Describe interstitial colloid osmotic pressure (πISF).

A

Draws fluid from capillary into interstitium.

316
Q

What are the 4 components of the urinary system?

A

Kidneys, Ureters, Bladder, Urethra

317
Q

Are kidneys intraperitoneal or retroperitoneal?

A

Retroperitoneal

318
Q

The kidneys are (approximately) at the level of which vertebra? Are they at the same level?

A

T12-T13. Not on the same level - right kidney sits lower because of your liver.

319
Q

What is the capsule of the kidney?

A

Outer protective layer

320
Q

Trace the path of vessels from renal artery → nephron.

A

Renal artery → Segmental artery → Interlobar artery → Arcuate artery → Interlobular/cortical radiate artery → Afferent arteriole → nephron

321
Q

Approximately how many nephrons per kidney?

A

1 million

322
Q

Where are the nephrons located/what do they span?

A

Medulla and cortex

323
Q

What are the two components of a renal corpuscle?

A

Bowman’s capsule, Glomerulus

324
Q

What are glomerulus (singular? Plural? idk man)?

A

Vessels in Bowman’s capsule

325
Q

What are the 4 components of a renal tubule?

A

Bowman’s capsule, Proximal (convoluted) tubule, Loop of Henle, Distal (also convoluted) tubule

326
Q

Tell me about how the renal tubule is situated in situ.

A

It’s folded in on itself such that the renal corpuscle is in contact with the distal tubule.

327
Q

Where are the renal corpuscles located within the kidney?

A

All in the cortex

328
Q

What’s the difference between a cortical and a juxtamedullary nephron?

A

Cortical = short loops, Juxtamedullary = long loops, extend deep into the medulla

329
Q

The majority of nephrons are which type? What proportion of filtrate do they produce?

A

90% are cortical (short loops). Produce 90% of filtrate.

330
Q

What are the two arterioles associated with the renal tubule?

A

Afferent and efferent arterioles

331
Q

What are the two sets of capillaries associated with the renal tubule?

A

Glomerular (glomerulus) and peritubular

332
Q

Trace the path of blood through the cortical nephron (from the afferent arteriole).

A

Afferent arteriole → glomerular capillaries → efferent arteriole → peritubular capillary

333
Q

What type of circulation is renal microcirculation?

A

Portal circulation

334
Q

How is juxtamedullary nephron circulation different from cortical nephron circulation?

A

Peritubular capillaries include vasa recta (long, narrow capillaries with thin walls)

335
Q

What are vasa recta?

A

Long, narrow capillaries with thin walls. Associate with long loop of Henle that extends into the medulla.

336
Q

Trace the path from renal artery to renal vein for me.

A

Renal artery → segmental artery → interlobar artery → arcuate artery → cortical radiate artery → afferent arterioles → glomerulus → capillaries → cortical radiate vein → arcuate vein → interlobar vein → segmental vein → renal vein

337
Q

What is filtration? Where does it happen?

A

Blood → tubular filtrate in the renal corpuscle only

338
Q

What is reabsorption? Where does it happen?

A

Filtrate → blood in peritubular capillaries

339
Q

What is secretion?

A

Blood (in peritubular capillaries) → filtrate

340
Q

What’s the difference between secretion and excretion?

A

Secretion = blood (in peritubular capillaries) → filtrate; Excretion = filtrate → bladder and external environment

341
Q

How much plasma entering the glomerulus actually gets filtered? Where does the rest go?

A

20% gets filtered. The rest leaves through the efferent arteriole.

342
Q

What’s the normal filtration fraction?

A

~ 0.2

343
Q

How does the renal corpuscle develop?

A

The (developing) glomerulus sorta wiggles itself into the head of the primitive renal tubule.

344
Q

What are podocytes? What do they make up?

A

Cells in Bowman’s capsule that wrap around capillaries of the glomerulus. Make up the epithelial lining of Bowman’s capsule.

345
Q

What are the two structures associated with the two layers of the glomerular filtration barrier (GFB) that actually allow filtration?

A

In endothelium of glomerular capillary = fenestrations; In podocytes = gaps between the foot processes form filtration slits.

346
Q

What gets filtered into Bowman’s capsule?

A

Water, Small solutes (ions, glucose, amino acids, etc)

347
Q

What doesn’t get filtered into Bowman’s capsule?

A

Large particles (albumin, antibodies, hormones, enzymes, etc), Blood cells

348
Q

What’s the glomerular filtration rate (GFR)?

A

Rate at which ultrafiltrate of plasma moves from glomerular capillaries → Bowman’s capsule

349
Q

What’s a normal GFR (per minute? Per day?)

A

125ml/minute, 180L/day

350
Q

What determines filtration strength and direction?

A

Starling forces (capillary BP, pressure inside Bowman’s capsule, osmotic pressures of plasma and filtrate)

351
Q

What are the two types of starling force?

A

Hydrostatic force (push forces) in capillaries and in Bowman’s capsule; Osmotic/oncotic force (pull forces)

352
Q

What’s the predominant component of Starling forces in the kidney?

A

Blood pressure (pushes substances into renal space)

353
Q

GFR is directly determined by what?

A

Blood pressure

354
Q

Is GFR directly determined by arterial BP?

A

Between 40-80mmHg yes, but between 80-180mmHg (normal BP), no. So functionally, no.

355
Q

Tell me how the myogenic response regulates GFR.

A

Afferent arteriole constricts in response to BP-related stretch of vascular wall to limit excessive BP in glomerulus.

356
Q

Tell me how tubulo-glomerular feedback regulates GFR.

A

Macula densa sense [Na+] increases in filtrate (caused by increase GFR) → secretes paracrine to cause vasoconstriction in afferent arteriole.

357
Q

If GFR decreases, what 2 things happen?

A

Macula densa decreases paracrine production (reduces vasoconstriction of afferent arteriole); Granular cells release renin.

358
Q

What’s the point of reabsorption? What gets reabsorbed?

A

The point: so your body can hang onto stuff it needs. All glucose, most water and sodium (99% and 99.5%) get reabsorbed from filtrate → peritubular blood circulation.

359
Q

What are some other bits and bobs that your body probably doesn’t want to excrete?

A

Other sugars, amino acids, medications, etc.

360
Q

What are two features of the structure of the epithelial cells of the proximal tubule facilitate solute exchange?

A

Large surface areas (microvilli on apical membrane + infoldings of basal membrane); Polarized epithelium.

361
Q

What are the four steps that facilitate reabsorption of solutes and fluid (tubule → ISF)?

A

Na+ reabsorbed via active transport; Anions follow Na+ out; Fluid follows particles (osmosis) from tubule → ISF; Permeable solutes diffuse out.

362
Q

Tell me how BP facilitates reabsorption.

A

BP in glomerular capillaries higher than BP in peritubular capillaries.

363
Q

How are most substances reabsorbed?

A

Specific transport systems (carriers)

364
Q

What’s maximum transport (Tm)? What happens if Tm is exceeded?

A

Tm = rate of transport when all carriers are occupied. When Tm is exceeded, you start seeing filtrate in the urine.

365
Q

What’s the renal threshold?

A

The plasma concentration after which a substance starts appearing in the urine.

366
Q

What’s the purpose of secretion in the kidney?

A

Clears substances from the 80% of blood that’s not filtered by the glomerulus.

367
Q

What’s the main way that substances are cleared from the blood via secretion?

A

Active transports (specific to substances - K+, H+, NH4+, medications and metabolic waste products…)

368
Q

What does renal clearance evaluate? What can it give an estimate of?

A

Evaluates overall renal function. Also gives estimates of GFR and renal blood flow.

369
Q

What are the two principles to keep in mind when looking at renal clearance?

A

Only consider routes in (renal artery) and out (renal vein, ureter); Everything in the urine comes from blood plasma.

370
Q

How does clearance (C) relate to GFR when: X is filtered, but not reabsorbed or excreted?

A

If filtered but not reabsorbed or excreted C = GFR.

371
Q

How does clearance (C) relate to GFR when: X is filtered and excreted?

A

If filtered and excreted C > GFR.

372
Q

How does clearance (C) relate to GFR when: X is filtered and partially reabsorbed?

A

If filtered and partially reabsorbed C < GFR.

373
Q

How does clearance (C) relate to GFR when: X is completely reabsorbed?

A

If completely reabsorbed C = 0.

374
Q

How do you calculate clearance (C)?

A

C = (U*V)/P where: U = [substance] in urine in mg/ml, V = rate of urine production in ml/min, P = [substance] in plasma in mg/ml.

375
Q

How can you use renal clearance to estimate renal plasma flow?

A

If X is filtered and secreted, C > GFR but also C = RPF.

376
Q

If a substance is both filtered and secreted by the kidney, how can you estimate renal blood flow?

A

Recall that C = RPF in this situation; RBF = RPF/Htc (hematocrit). Therefore, just divide C/hematocrit to get renal blood flow.

377
Q

How do you use renal clearance to estimate GFR?

A

If X is filtered but not reabsorbed or secreted, C = GFR.

378
Q

In which tissues is glycolysis found? What are its main functions?

A

Found in all tissues. Main functions: ATP production (aerobic or anaerobic), Produces intermediates for other pathways.

379
Q

In which tissues is the Krebs cycle found? What are its main functions?

A

Any tissue with mitochondria. Main functions: ATP production (aerobic), NADH and FADH2 for electron transport chain and gluconeogenesis.

380
Q

In which tissues is the electron transport chain found? What are its main functions?

A

All tissues with mitochondria. ATP production (requires O2).

381
Q

In which tissues is gluconeogenesis found? What are its main functions?

A

Liver and Kidney. Intermediates of other pathways → glucose (for release during fasting).

382
Q

In which tissues is the Cori cycle found? What are its main functions?

A

Lactate producing tissues (muscle + red blood cells) → Liver. Lactate from anaerobic glycolysis → gluconeogenesis in liver.

383
Q

In which tissues is glycogenolysis found? What are its main functions?

A

Most tissues. Main functions: Substrate for gluconeogenesis (liver and kidney only), Substrate for glycolysis (most tissues).

384
Q

In which tissues is glycogen synthesis found? What are its main functions?

A

Most tissues (important in liver and muscles). For carbohydrate storage.

385
Q

In which tissues is the pentose phosphate pathway found? What are its main functions?

A

Partially active in most tissues. Provides ribose for nucleotide synthesis, Provides NADPH for metabolic reactions.

386
Q

In which tissues is glycogen synthesis found? What are its main functions?

A

Most tissues (important in liver and muscles)

For carbohydrate storage

387
Q

In which tissues is the pentose phosphate pathway found? What are its main functions?

A

Partially active in most tissues

Provides ribose for nucleotide synthesis and NADPH for metabolic reactions (synthesis of fatty acids, steroids and sterols, control of oxidative stress)

388
Q

In which tissues is lipogenesis found? What are its main functions?

A

Liver and adipose tissue

Main functions: Carbs → triglyceride synthesis (mostly liver), Fatty acids → triglycerides

389
Q

In which tissues is lipolysis (via hormone sensitive lipase) found? What are its main functions?

A

Adipose tissues

Mobilize triglyceride stores

390
Q

In which tissues is lipolysis (via lipoprotein lipase and hepatic lipase) found? What are its main functions?

A

Capillaries of many tissues (muscle, adipose, not brain)

Release free fatty acids from circulating VLDL and chylomicrons

391
Q

In which tissues is fatty acid b-oxidation found? What are its main functions?

A

Most tissues with mitochondria

Main functions: ATP production (aerobic)

392
Q

In which tissues is ketogenesis found? What are its main functions?

A

Liver

Fatty acids → ketone bodies for fuel during prolonged fast

393
Q

Which tissues can use ketone bodies? What are ketone bodies used to produce?

A

Most extrahepatic tissues with mitochondria

Used to produce substrates for krebs cycle and electron transport chain for ATP production

394
Q

In which tissues does transamination occur? What are its main functions?

A

Most of ‘em

Main functions: Amino acid synthesis and metabolism, Synthesis of nitrogen-containing compounds

Block 3 (3 decks)

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