Hard stuff for the exam

Question 1

Why is it important to have different concentrations of ions in the ICF and ECF?

Answer 1

Setting the membrane potential

Generating electrical activity

Muscle contraction

Nutrient uptake via secondary active transport

Generation of intracellular signaling cascades

Question 2

How is the corticopapillary osmotic gradient established in the kidney’s interstitial fluid?

Answer 2

Initially, no osmotic gradient; interstitial fluid and nephron tubule fluid have uniform osmolarity (~300 mOsm/L).

Sodium is transported out of the thin descending and thick ascending limbs of the loop of Henle.
The thick ascending limb is impermeable to water, causing sodium to increase interstitial osmolarity.

This creates a 200 mOsm/L osmolarity difference between the tubular fluid and interstitial fluid.
Sodium equilibrates between the descending limb and interstitium, maintaining fluid osmolarity at 300 mOsm/L.

Continuous cycles of sodium transport and fluid movement create a corticopapillary gradient, reaching up to 1200 mOsm/L from cortex to inner medulla.

Question 3

What is the renin-angiotensin system and its effects on blood pressure and sodium reabsorption?

Answer 3

Renin: Secreted by the kidneys’ granular cells, it converts angiotensinogen to angiotensin I.

Rate-Limiting Factor: More renin means more angiotensin I.

ACE: Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) in the lungs.
Receptors: Angiotensin II binds to AT1 (vasoconstriction) and AT2 (sodium and water reabsorption) receptors.

Sodium Reabsorption:
Activates sodium-hydrogen exchanger (apical membrane) and sodium-potassium ATPase (basolateral membrane).

Sodium is reabsorbed from the tubular lumen to interstitial space and then to capillaries, water follows.

Receptor Distribution: ~95% AT1 and ~5% AT2, so AT1 effects (vasoconstriction) dominate.

Blood Pressure: Injection of renin or angiotensin II increases blood pressure.

Aldosterone: Angiotensin II induces

aldosterone production in the adrenal medulla.

Aldosterone Effect: Binds to mineralocorticoid receptors (MR), causing ENaC channels insertion and sodium reabsorption into the interstitial fluid.

Question 4

How does sodium reabsorption affect osmolarity, ADH secretion, and blood volume?

Answer 4

Osmolarity Increase: Sodium reabsorption increases osmolarity.

Osmoreceptors: Hypothalamic osmoreceptors detect increased osmolarity and secrete ADH.

ADH Effect: ADH increases water retention by signaling aquaporins, balancing osmolality.

Blood Volume: Increased water retention raises blood volume.

Cardiopulmonary Receptors: Sense increased heart stretch from higher blood volume, decrease sympathetic drive to kidneys, leading to sodium and water excretion (reflex pathway).

Pressure Response: Significant blood volume increase raises blood pressure, sensed by carotid and aortic baroreceptors.

Question 5

How does decreased blood volume affect blood pressure and what are the body’s responses?

Answer 5

Decreased Blood Volume: Leads to decreased blood pressure.

Sensors: Atrial volume receptors and aortic/carotid baroreceptors detect the change.

Cardiovascular Response: Increases cardiac output and causes vasoconstriction to raise blood pressure.

Fluid Intake: Increases extracellular and intracellular fluid volumes, raising blood pressure.

Kidney Response:
Conserves water via increased sympathetic nerve activity.
Causes vasoconstriction of the afferent arteriole.
Activates the renin-angiotensin-aldosterone system, promoting sodium and water retention.

Question 6

How is ADH release triggered and what are its effects on water reabsorption?

Answer 6

Triggers:
Increased Osmolarity: Detected by osmoreceptors in the posterior pituitary of the hypothalamus.
Decreased Blood Volume: Detected by atrial stretch receptors.
Decreased Blood Pressure: Detected by carotid and aortic baroreceptors.
ADH Release:
Released in response to increased osmolarity or decreased blood volume/pressure.
Binds to V2 receptors in the kidney.
Effects:
Inserts aquaporins on the tubular lumen side.
Facilitates water reabsorption along its concentration gradient into the capillaries.

Question 7

What is the arterial baroreceptor reflex and how does it function?

Answer 7

Location and Structure:

Carotid Baroreceptors: Located in the carotid sinus with nerve endings in the adventitia.
Carotid Sinus Nerve: Connects to the glossopharyngeal nerve, which relays information to the nucleus tractus solitarius (NTS) in the brain.
Function:

Sensing Stretch: Baroreceptors detect stretch in the arterial walls.
Response to Changes: Respond primarily to sudden changes in arterial pressure, not gradual changes. Gradual changes may result in baroreceptors resetting to a new mean pressure.
Mechanism:

Increased Arterial Pressure: Causes increased stretch in the arteries, leading to increased baroreceptor firing.
Neural Pathways:
Parasympathetic Nervous System (PNS): Increased baroreceptor firing stimulates the PNS, decreasing heart rate (HR) and cardiac output (CO).

Sympathetic Nervous System (SNS): Inhibited by the cardiovascular medullary (CVLM) inhibition of the rostral ventrolateral medulla (RVLM), resulting in decreased HR and vasodilation.
Outcome:

Decreased Cardiac Output: Due to reduced heart rate.
Decreased Vascular Resistance: Due to vasodilation.
Result: Decreased arterial pressure.

Question 8

What do the components of the PQRST complex represent in an ECG?

Answer 8

P Wave: Atrial depolarization (contraction of the atria).
PR Interval: Measures time from the start of atrial depolarization to the start of ventricular depolarization; indicates the conduction time from atria to ventricles through the AV node (0.12 to 0.20 seconds).
QRS Complex: Ventricular depolarization (contraction of the ventricles).
ST Segment: Time when the ventricles are depolarized and electrically neutral; significant for indicating ischemia or infarction if altered.
T Wave: Ventricular repolarization (ventricles preparing for the next contraction).
QT Interval: Measures total time of ventricular depolarization and repolarization; important for assessing risk of arrhythmias.

Question 9

List of energy output processes

Answer 9

Mechanical work
Synthetic reactions
Membrane transport
Signal generation and conduction
Heat product
Detoxification and degradation

Question 10

Peripheral fatigue is caused by

Answer 10

Neuro-muscular transmission
Muscle fibre action potential
Excitation-contraction coupling
Depletion of substrates for metabolism
Accumulation of waste-products

Question 11

Neuromuscular Transmission

Answer 11

a. Neurotransmitter Depletion:

Acetylcholine (ACh) Depletion: During prolonged or intense muscle activity, the availability of ACh at the neuromuscular junction may decrease. ACh is essential for transmitting the nerve impulse to the muscle fiber, and its depletion can impair muscle activation.
b. Receptor Desensitization:

ACh Receptor Desensitization: Repeated stimulation can lead to desensitization of ACh receptors on the muscle fiber membrane. This reduces the efficacy of neurotransmission, leading to a decline in muscle force production.
c. Synaptic Failure:

Impaired Synaptic Function: Prolonged activity can lead to synaptic fatigue, where the ability of the nerve terminal to release ACh diminishes, thus weakening the signal transmission to the muscle fiber.

Question 12

Muscle Fiber Action Potential

Answer 12

Ion Imbalance:

Potassium Accumulation: During repeated muscle contractions, potassium ions accumulate in the extracellular space, altering the membrane potential and impairing the generation and propagation of action potentials.
Sodium-Potassium Pump Inefficiency: Prolonged activity can overwhelm the sodium-potassium pump, leading to an inability to restore the resting membrane potential effectively.
b. Membrane Fatigue:

Reduced Excitability: Continuous stimulation can reduce the excitability of the muscle membrane, making it harder to initiate action potentials and propagate them along the muscle fiber.

Question 13

Excitation-Contraction Coupling

Answer 13

a. Calcium Handling:

Sarcoplasmic Reticulum (SR) Function: The ability of the SR to release and reuptake calcium can become compromised with prolonged activity. Calcium is crucial for muscle contraction, and any impairment in its handling can reduce force production.
Calcium Sensitivity: Changes in the sensitivity of the myofibrils to calcium can also contribute to fatigue. If the myofilaments become less responsive to calcium, the force of contraction will diminish.

Question 14

Depletion of Substrates for Metabolism

Answer 14

a. Glycogen Depletion:

Muscle Glycogen Stores: Prolonged or intense exercise depletes muscle glycogen, a primary energy source. Glycogen depletion reduces ATP availability, impairing muscle contraction and leading to fatigue.
b. Creatine Phosphate Depletion:

Phosphocreatine System: The phosphocreatine system provides immediate ATP for short bursts of activity. Depletion of creatine phosphate stores limits ATP regeneration, contributing to fatigue in high-intensity activities.
c. Blood Glucose and Fatty Acids:

Substrate Availability: Reduced availability of blood glucose and fatty acids also limits ATP production through aerobic and anaerobic pathways, leading to decreased muscle performance.

Question 15

Accumulation of Waste Products

Answer 15

Lactic Acid:

Lactate and Hydrogen Ions: Anaerobic metabolism produces lactic acid, which dissociates into lactate and hydrogen ions. The accumulation of hydrogen ions lowers pH (acidosis), impairing enzyme function and muscle contraction.
b. Inorganic Phosphate:

Pi Accumulation: During ATP breakdown, inorganic phosphate (Pi) accumulates within the muscle. High Pi levels can interfere with calcium release from the SR and the interaction between actin and myosin, reducing force production.
c. Reactive Oxygen Species (ROS):

Oxidative Stress: Exercise-induced ROS can damage cellular structures, including proteins, lipids, and DNA, impairing muscle function and contributing to fatigue.

Question 16

How does increased H+ affect muscle enzyme function?

Answer 16

Lower pH (acidosis) impairs the activity of key metabolic enzymes, reducing ATP production.

Question 17

What effect does increased H+ have on contractile proteins?

Answer 17

Acidosis reduces the sensitivity of actin and myosin to calcium, impairing cross-bridge cycling and muscle contraction.

Question 18

How does acidosis impact calcium handling in muscle cells?

Answer 18

It affects calcium release from the sarcoplasmic reticulum (SR) and reduces calcium binding to troponin, weakening muscle contractions.

Question 19

What role does increased H+ play in neuromuscular transmission?

Answer 19

Acidosis can affect the propagation of action potentials along the muscle membrane, impairing muscle activation and contraction.

Question 20

How does increased Pi affect cross-bridge cycling?

Answer 20

Pi interferes with myosin-ATP interaction and slows down the cross-bridge detachment phase, reducing the efficiency of muscle contractions.

Question 21

How does increased Pi impact calcium release in muscles?

Answer 21

Pi can precipitate with calcium in the SR, reducing the amount of free calcium available for muscle contraction.

Question 22

What effect does increased Pi have on mitochondrial function?

Answer 22

Elevated Pi levels can reduce the efficiency of oxidative phosphorylation, impairing ATP production during prolonged exercise.

Question 23

How do increased H+ and Pi together contribute to muscle fatigue?

Answer 23

Both metabolites reduce force production by impairing enzyme activity, calcium handling, and cross-bridge cycling, leading to decreased muscle performance during intense or prolonged exercise.

Question 24

What are the 3 main pumps?

Answer 24

Na+/K+ ATPase
Serca Pump
Mysoin ATPase

Question 25

Na+/K+ - ATPase:

Answer 25

Role: Maintains membrane potential and restores ionic gradients.
Energy Use: Consumes ATP to transport Na+ out and K+ in.
Fatigue Impact: Ionic imbalances and reduced excitability due to ATP depletion contribute to fatigue.

Question 26

SERCA Pump:

Answer 26

Role: Reuptakes calcium into the SR, enabling muscle relaxation.
Energy Use: Consumes ATP to transport Ca2+ against its gradient.
Fatigue Impact: Impaired calcium reuptake due to ATP depletion leads to prolonged contraction and reduced relaxation efficiency, contributing to fatigue.

Question 27

Myosin ATPase:

Answer 27

Role: Powers cross-bridge cycling for muscle contraction.
Energy Use: Hydrolyzes ATP for actin-myosin interactions.
Fatigue Impact: Reduced ATP availability and Pi accumulation impair force generation and contraction efficiency, leading to fatigue.

Question 28

What is the role of Myosin Light Chain Kinase (MLCK) in muscle contraction and how does it relate to muscle fatigue?

Answer 28

MLCK phosphorylates myosin light chains in response to Ca2+ -calmodulin, enabling cross-bridge cycling and contraction in smooth muscle. During fatigue, impaired calcium handling and ATP depletion reduce MLCK activation and phosphorylation efficiency, leading to decreased muscle performance and increased fatigue.

Question 29

How does a decrease in Gibbs free energy relate to muscle fatigue?

Answer 29

A decrease in Gibbs free energy (Δ𝐺) in muscle cells signifies less available energy for biochemical reactions, including ATP hydrolysis, which is crucial for muscle contraction. During prolonged or intense exercise, ATP depletion and accumulation of metabolic byproducts like H+ and Pi reduce ΔG, impairing ATP production and usage. This energy deficit contributes to reduced muscle force, slower contractions, and overall fatigue.

Question 30

What is the function of the descending limb of the loop of Henle?

Answer 30

The descending limb is permeable to water but not to solutes, allowing water to exit into the hyperosmotic medullary interstitium, which concentrates the filtrate.

Question 31

What is the function of the ascending limb of the loop of Henle?

Answer 31

he ascending limb is impermeable to water but actively transports solutes (Na+, K+, Cl-) out, making the filtrate more dilute while increasing the osmolarity of the surrounding interstitial fluid

Question 32

How is the osmotic gradient in the kidney’s medulla created and maintained?

Answer 32

The gradient is created by the opposing functions of the descending and ascending limbs of the loop of Henle and is maintained by the active transport of solutes in the ascending limb.

Question 33

What role does the vasa recta play in the kidney’s counter-current mechanism?

Answer 33

The vasa recta preserve the osmotic gradient by allowing slow exchange of water and solutes, minimizing the washout of the gradient through counter-current exchange.

Question 34

What is the effect of high levels of ADH on urine concentration in human kidneys?

Answer 34

High levels of ADH lead to increased water reabsorption in the collecting ducts by promoting the insertion of more aquaporin-2 channels into the duct cells. This results in more water being reabsorbed into the bloodstream, significantly increasing urine concentration and reducing urine volume.

Question 35

How do increased transport proteins in the ascending limb of the loop of Henle affect urine concentration?

Answer 35

Increased activity or numbers of Na+/K+/2Cl- co-transporters and other ion pumps in the ascending limb enhance the removal of solutes from the filtrate. This enhances the medullary osmotic gradient, facilitating greater water reabsorption in the collecting ducts and leading to higher urine concentration.

Question 36

What is the impact of a high density of aquaporins in the collecting ducts on urine concentration?

Answer 36

A high density of aquaporins in the collecting ducts, especially aquaporin-2, which is regulated by ADH, allows for increased water reabsorption back into the bloodstream. This results in highly concentrated urine as more water is extracted from the filtrate.

Question 37

What is the effect of an enhanced vasa recta function on urine concentration?

Answer 37

Enhanced function of the vasa recta, with even slower blood flow and more efficient solute exchange, better preserves the medullary osmotic gradient. This increased efficiency helps to extract more water from the collecting duct, leading to more concentrated urine.

Question 38

How does increased sensitivity to hormonal signals like aldosterone affect urine concentration?

Answer 38

Increased sensitivity to aldosterone leads to greater sodium reabsorption in the distal convoluted tubule and collecting duct, which enhances water reabsorption due to osmotic balance. This results in a more concentrated urine as more water is reclaimed under the influence of this hormone.

Question 39

Wolff-parkinson-white syndrome

Answer 39

Pre-excitation
Short PR
Wide QRS
Delta Wave

Question 40

Normal PR interval

Answer 40

0.12-0.20s

Question 41

Normal QRS interval

Answer 41

0.08-0.11s

Question 42

Some p waves going up and some p waves going down

Answer 42

Means firing is happening at different places in the atria. Happening from 2 pacemaker spots

Question 43

What are the key ECG characteristics of atrial fibrillation (AF)?

Answer 43

Atrial fibrillation is characterized by the absence of P waves on the ECG. Instead, there are irregular, erratic oscillations known as fibrillatory waves. The R-R intervals are irregularly irregular, with no consistent pattern. The ventricular response may vary depending on how many impulses travel from the atria to the ventricles through the AV node.

Question 44

What are the distinctive ECG features of ventricular fibrillation (VF)?

Answer 44

Ventricular fibrillation presents as chaotic and erratic electrical activity on the ECG, with no discernible P waves, QRS complexes, or T waves. Instead, the ECG line appears as irregular, erratic spikes, with varying amplitudes and frequencies. This pattern signifies ineffective ventricular contractions and is a medical emergency requiring immediate intervention.

Question 45

Which part of the heart does each lead (V1-V6) primarily detect?

Answer 45

V1-2 - Right ventricle
V3-4 - Septum
V5-6 - Left ventricle

Question 46

What characterizes an ectopic ECG?

Answer 46

Appearance: On the ECG tracing, an ectopic beat appears as a premature, abnormal waveform occurring before the expected QRS complex.
Origin: Ectopic beats originate from an abnormal focus within the heart, such as the atria (atrial ectopic beat) or the ventricles (ventricular ectopic beat).
Timing: Ectopic beats disrupt the normal cardiac rhythm, occurring earlier than expected in the cardiac cycle.
Shape: The ectopic beat’s waveform may differ from the normal sinus rhythm, exhibiting variations in amplitude, duration, and morphology.
Compensation: Following an ectopic beat, there may be a compensatory pause as the heart’s conduction system resets before the next normal beat.

Question 47

What are the advantages of including precordial leads in a standard ECG?

Answer 47

Enhanced View of Ventricular Activity: Precordial leads (V1-V6) are positioned on the chest to directly record electrical activity from different regions of the ventricles, providing a detailed view of ventricular depolarization.

Improved Detection of Anterior Wall Abnormalities: Leads V1-V4 are specifically oriented to detect abnormalities in the anterior wall of the left ventricle, such as myocardial infarction or ischemia. This improves sensitivity for diagnosing anterior wall pathologies.

Detection of Ventricular Hypertrophy: Precordial leads are useful for detecting ventricular hypertrophy, as changes in the QRS complex amplitude and duration can indicate hypertrophy of the ventricular walls.

Assessment of Ventricular Conduction Delays: Precordial leads help assess ventricular conduction delays, such as bundle branch blocks, by observing changes in the QRS complex morphology and duration across different leads.

Localization of Arrhythmias: Precordial leads aid in localizing the origin of certain arrhythmias, such as ventricular tachycardia, by identifying the specific region of the ventricles where abnormal electrical activity originates.

Comprehensive Evaluation of Cardiac Electrical Activity: By complementing the standard limb leads (I, II, III, aVL, aVF, and aVR), precordial leads provide a more complete assessment of cardiac electrical activity from various perspectives, improving diagnostic accuracy and clinical decision-making.

Question 48

What are the sequential events in the renal response to eating salt?

Answer 48

Stimulation of RAAS: Increased sodium levels in the blood stimulate the release of renin, initiating the renin-angiotensin-aldosterone system (RAAS).

Release of Aldosterone: Activation of RAAS leads to the release of aldosterone, a hormone produced by the adrenal glands.

Aldosterone Action: Aldosterone promotes sodium reabsorption in the kidneys, enhancing the retention of sodium within the body.

Increased Sodium Reabsorption: As a result of aldosterone action, the kidneys respond by increasing sodium reabsorption in the renal tubules, primarily in the distal tubules and collecting ducts.

Passive Water Retention: As sodium is reabsorbed, water follows passively through osmosis, leading to increased water retention in the body.

Blood Pressure Regulation: The renal response to salt intake influences blood pressure by adjusting blood volume and vascular tone through sodium retention or excretion.

Question 49

How does sodium enter the bloodstream

Answer 49

Dietary Intake: Sodium enters the bloodstream primarily through dietary intake, as it is a common component of many foods, particularly processed and packaged foods, as well as table salt (sodium chloride).

Absorption in the Small Intestine: In the small intestine, sodium is actively transported across the intestinal epithelial cells, primarily in the duodenum and jejunum. This absorption process is facilitated by sodium-dependent transporters such as the sodium-glucose co-transporter (SGLT) and sodium-hydrogen exchanger (NHE).

Role of Sodium Channels: Sodium channels located on the apical (luminal) membrane of intestinal epithelial cells facilitate the entry of sodium ions into the cells from the intestinal lumen. These channels play a crucial role in sodium absorption from the gut.

Transport Across the Cell: Once inside the intestinal epithelial cells, sodium ions are actively transported across the basolateral membrane into the interstitial fluid. This transport is mediated by sodium-potassium ATPase pumps, which maintain the sodium gradient and drive sodium uptake into the bloodstream.

Systemic Circulation: Sodium enters the systemic circulation via capillaries in the intestinal villi, where it is transported throughout the body by the bloodstream, contributing to overall sodium balance and electrolyte homeostasis.

Question 50

How do the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone (RAA) system interact to regulate blood pressure?

Answer 50

SNS Activation:
Response to Low Blood Pressure: The SNS is activated in response to low blood pressure or volume, detected by baroreceptors in the aorta and carotid arteries.

Effects on Heart and Blood Vessels: SNS activation leads to increased heart rate (positive chronotropic effect) and increased force of contraction (positive inotropic effect). It also causes vasoconstriction, which increases peripheral resistance and raises blood pressure.

Stimulation of Renin Release: Sympathetic nerve fibers innervate the juxtaglomerular cells in the kidneys. Activation of these fibers triggers the release of renin into the bloodstream.

Renin-Angiotensin-Aldosterone System (RAAS):
Renin Release: Renin is an enzyme that converts angiotensinogen, produced by the liver, into angiotensin I.

Formation of Angiotensin II: Angiotensin I is then converted to angiotensin II by the angiotensin-converting enzyme (ACE) primarily in the lungs.

Actions of Angiotensin II: Angiotensin II is a potent vasoconstrictor, which increases blood pressure. It also stimulates the adrenal cortex to release aldosterone and promotes the release of antidiuretic hormone (ADH) from the pituitary gland.

Aldosterone Effects: Aldosterone increases sodium reabsorption and potassium excretion in the kidneys, leading to increased water retention, expanded blood volume, and higher blood pressure.

Question 51

What changes occur in the kidneys when drinking a hyperosmotic solution?

Answer 51

Increased Plasma Osmolarity:

Initial Effect: Ingesting a hyperosmotic solution increases the osmolarity of the blood.
Detection by Osmoreceptors: Osmoreceptors in the hypothalamus detect the increase in plasma osmolarity and trigger a series of responses to restore balance.
Antidiuretic Hormone (ADH) Release:

Stimulation of ADH: The increased plasma osmolarity stimulates the posterior pituitary gland to release ADH (vasopressin).
Effect on Kidneys: ADH acts on the kidneys, specifically on the collecting ducts, making them more permeable to water. This leads to increased water reabsorption back into the bloodstream, which helps to dilute the plasma and reduce osmolarity.
Decreased Urine Output:

Concentrated Urine: With increased water reabsorption due to ADH, the kidneys produce a smaller volume of more concentrated urine.
Water Conservation: This mechanism helps to conserve water in the body and mitigate the effects of the hyperosmotic solution on plasma osmolarity.
Renin-Angiotensin-Aldosterone

System (RAAS) Activation:
Potential Activation: If the ingestion of the hyperosmotic solution also leads to a decrease in blood volume or blood pressure, the RAAS may be activated.

Aldosterone Release: Aldosterone promotes sodium reabsorption in the distal tubules and collecting ducts of the kidneys. Since water follows sodium, this also aids in water retention, further contributing to increased blood volume and pressure.

Natriuresis:
Excretion of Excess Sodium: The kidneys may also respond by excreting excess sodium to balance the increased solute load. This process, known as natriuresis, involves the excretion of sodium in the urine.

Balance Restoration: Natriuresis helps to restore osmotic balance by eliminating the excess sodium introduced by the hyperosmotic solution.
Feedback Mechanisms:

Negative Feedback: Once plasma osmolarity and blood volume are normalized, negative feedback mechanisms reduce the release of ADH and other hormones to prevent overcorrection.

Homeostasis: The kidneys continuously adjust the excretion or reabsorption of water and solutes to maintain homeostasis.

Question 52

What changes occur in the body’s fluid compartments when drinking a hyperosmotic drink?

Answer 52

Initial Increase in ECF Osmolarity:

Hyperosmotic Solution: The hyperosmotic drink has a higher solute concentration than body fluids.
Osmolarity Rise: Upon ingestion and absorption into the bloodstream, the osmolarity of the extracellular fluid (ECF) increases due to the higher concentration of solutes.
Water Movement from ICF to ECF:

Osmotic Gradient: The increased osmolarity in the ECF creates an osmotic gradient between the ECF and the intracellular fluid (ICF).
Cellular Dehydration: Water moves out of the cells (ICF) into the ECF to balance the osmotic pressure. This movement results in a decrease in ICF volume and an increase in ECF volume.
Expansion of ECF Volume:

Volume Increase: The ECF volume expands due to the influx of water from the ICF, increasing the overall volume of the ECF.
Dilution of Solutes: This movement of water helps to dilute the solutes in the ECF, partially counteracting the initial increase in osmolarity.
Stimulation of ADH Release:

Osmoreceptors Activation: Osmoreceptors in the hypothalamus detect the increased ECF osmolarity.
ADH Release: In response, the posterior pituitary gland releases antidiuretic hormone (ADH), which acts on the kidneys to promote water reabsorption in the collecting ducts.
Increased Water Reabsorption:

Effect of ADH: ADH increases the permeability of the renal collecting ducts to water, allowing more water to be reabsorbed back into the bloodstream.
Concentrated Urine: This results in the production of a smaller volume of concentrated urine, conserving water and helping to reduce ECF osmolarity.
Normalization of ECF Osmolarity:

Restoring Balance: The reabsorbed water helps to lower the osmolarity of the ECF, bringing it closer to normal levels.
Steady-State: Eventually, the osmotic balance between the ECF and ICF is restored, stabilizing fluid compartments.

Question 53

What changes occur in the body’s fluid compartments when drinking a hypoosmotic drink?

Answer 53

Initial Decrease in ECF Osmolarity:

Hypoosmotic Solution: The hypoosmotic drink has a lower solute concentration than body fluids.
Osmolarity Drop: Upon ingestion and absorption into the bloodstream, the osmolarity of the extracellular fluid (ECF) decreases due to the dilution of solutes.
Water Movement from ECF to ICF:

Osmotic Gradient: The decreased osmolarity in the ECF creates an osmotic gradient between the ECF and the intracellular fluid (ICF).
Cellular Hydration: Water moves into the cells (ICF) from the ECF to balance the osmotic pressure. This movement results in an increase in ICF volume and a decrease in ECF volume.
Expansion of ICF Volume:

Volume Increase: The ICF volume expands due to the influx of water from the ECF, increasing the overall volume of the ICF.
Dilution of Solutes: This movement of water dilutes the solutes in the ICF, partially counteracting the initial decrease in osmolarity.
Inhibition of ADH Release:

Osmoreceptors Activation: Osmoreceptors in the hypothalamus detect the decreased ECF osmolarity.
ADH Inhibition: In response, the posterior pituitary gland reduces the release of antidiuretic hormone (ADH), decreasing its action on the kidneys.
Decreased Water Reabsorption:

Effect of Reduced ADH: With lower levels of ADH, the permeability of the renal collecting ducts to water decreases, resulting in less water being reabsorbed back into the bloodstream.
Dilute Urine: This leads to the production of a larger volume of dilute urine, helping to eliminate the excess water and increase ECF osmolarity.
Normalization of ECF Osmolarity:

Restoring Balance: The excretion of excess water helps to increase the osmolarity of the ECF, bringing it closer to normal levels.
Steady-State: Eventually, the osmotic balance between the ECF and ICF is restored, stabilizing fluid compartments.

Question 54

What changes occur in the kidneys when drinking a hypoosmotic solution

Answer 54

Decreased Plasma Osmolarity:

Initial Effect: Ingesting a hypoosmotic solution decreases the osmolarity of the blood.
Detection by Osmoreceptors: Osmoreceptors in the hypothalamus detect the decrease in plasma osmolarity and trigger a series of responses to restore balance.
Inhibition of ADH Release:

Reduced ADH: The decreased plasma osmolarity inhibits the posterior pituitary gland from releasing ADH (vasopressin).
Effect on Kidneys: Lower levels of ADH decrease the permeability of the collecting ducts in the kidneys to water, reducing water reabsorption.
Increased Urine Output:

Dilute Urine: With decreased water reabsorption due to lower ADH levels, the kidneys produce a larger volume of more dilute urine.
Water Elimination: This mechanism helps to eliminate excess water from the body and increase plasma osmolarity.
Feedback Mechanisms:

Negative Feedback: Once plasma osmolarity and blood volume are normalized, negative feedback mechanisms ensure that ADH release and kidney function are adjusted to maintain homeostasis.
Homeostasis: The kidneys continuously adjust the excretion or reabsorption of water and solutes to maintain homeostasis.

Question 55

What effect does a selective β1 adrenergic antagonist have on cardiac output and venous return?

Answer 55

Selective β1 Adrenergic Antagonist:
Mechanism: Selective β1 adrenergic antagonists (such as metoprolol) block the β1 receptors primarily found in the heart.
Heart Rate Reduction: Blocking β1 receptors decreases heart rate (negative chronotropic effect) and reduces the force of cardiac contraction (negative inotropic effect).
Cardiac Output: As a result, cardiac output (CO) is reduced because CO = heart rate (HR) × stroke volume (SV), and both HR and SV are decreased.
Venous Return: The β1 adrenergic antagonist primarily affects the heart, so direct effects on venous return are minimal. However, decreased cardiac output can indirectly reduce venous return due to a decrease in the driving force for blood circulation.

Question 56

Why might a man taking a selective β1 adrenergic antagonist and furosemide be at increased risk of orthostatic hypotension?

Answer 56

Baroreceptor Reflex Impairment:

Normal Mechanism: Normally, when a person stands up, gravity causes blood to pool in the lower extremities, leading to a temporary drop in venous return and blood pressure. The baroreceptors in the carotid sinuses and aortic arch detect this drop and trigger a reflex that increases heart rate and vasoconstriction to maintain blood pressure.
Effect of β1 Adrenergic Antagonist: A β1 adrenergic antagonist (e.g., metoprolol) blocks the sympathetic stimulation of the heart, reducing its ability to increase heart rate and contractility in response to the baroreceptor reflex. This impairs the body’s ability to compensate for the sudden drop in blood pressure when standing.
Reduced Blood Volume:

Effect of Furosemide: Furosemide is a potent diuretic that reduces blood volume by increasing urine output. Lower blood volume means there is less venous return to the heart, resulting in reduced preload (the initial stretching of cardiac myocytes before contraction).
Impact on Cardiac Output: Reduced blood volume decreases stroke volume and, consequently, cardiac output. When standing, the reduced venous return exacerbates the drop in blood pressure, as the heart has less blood to pump.
Combined Effects on Arterial Pressure:

Impaired Compensation: Normally, the body compensates for the drop in venous return and blood pressure upon standing by increasing heart rate and vasoconstriction. However, the β1 adrenergic antagonist limits the increase in heart rate and contractility, while the reduced blood volume from furosemide limits the amount of blood available for circulation.
Decreased Vascular Resistance: The β1 antagonist may also indirectly reduce vascular resistance by diminishing sympathetic tone, further impairing the body’s ability to maintain blood pressure upon standing.

Question 57

What are the renal excretory responses to ingestion of 500ml of water in a normal human?

Answer 57

Decreased Plasma Osmolarity:
Water Absorption: Ingested water is absorbed from the gastrointestinal tract into the bloodstream, diluting the plasma and decreasing plasma osmolarity.
Detection by Osmoreceptors:
Hypothalamus: Osmoreceptors in the hypothalamus detect the decrease in plasma osmolarity.
Reduced ADH Secretion:
Posterior Pituitary: In response to lower plasma osmolarity, the posterior pituitary gland reduces the secretion of antidiuretic hormone (ADH).
Effects on Kidneys:
Collecting Ducts: Lower levels of ADH decrease the permeability of the collecting ducts in the kidneys to water.
Increased Urine Output: Less water is reabsorbed, resulting in increased urine volume and decreased urine osmolarity (more dilute urine).
Restoration of Osmolarity:
Normalization: The increased excretion of water helps to restore plasma osmolarity to normal levels.

Question 58

What are the renal excretory responses to ingestion of 500ml of water in a patient with untreated central diabetes insipidus?

Answer 58

Lack of ADH:
Central Diabetes Insipidus: The posterior pituitary gland does not secrete sufficient ADH (or any at all), regardless of plasma osmolarity changes.
Effects on Kidneys:
Collecting Ducts: The absence of ADH means the collecting ducts remain impermeable to water.
Increased Urine Output: As a result, large volumes of very dilute urine are excreted (even more so after ingesting water).
Continued Polyuria:
Persistent Symptom: The patient continues to experience polyuria (excessive urination) and cannot concentrate their urine, leading to persistent dehydration risks

Question 59

Similarities between normal patient and one with central diabetes insipidus

Answer 59

Initial Response to Ingested Water:
In both normal individuals and patients with untreated central diabetes insipidus, ingestion of 500ml of water initially decreases plasma osmolarity.
Differences:
ADH Secretion:

Normal Human: Reduced plasma osmolarity inhibits ADH secretion from the posterior pituitary, decreasing water reabsorption in the kidneys.
Central Diabetes Insipidus: ADH is not adequately secreted regardless of plasma osmolarity, so the kidneys do not reabsorb water effectively.
Kidney Response:

Normal Human: Decreased ADH levels result in reduced water reabsorption in the collecting ducts, leading to increased urine volume and decreased urine osmolarity.
Central Diabetes Insipidus: Absence of ADH means that the collecting ducts remain impermeable to water, resulting in excessive urine output and persistently low urine osmolarity.
Urine Volume and Composition:

Normal Human: Increased urine volume but within normal limits, with urine becoming more dilute (low osmolarity).
Central Diabetes Insipidus: Very high urine volume (polyuria) with extremely dilute urine (very low osmolarity).
Regulation of Plasma Osmolarity:

Normal Human: Plasma osmolarity is restored to normal levels through the excretion of excess water.
Central Diabetes Insipidus: Plasma osmolarity remains higher than normal due to the continued inability to retain water, leading to ongoing thirst and risk of dehydration.

Question 60

How does lowering total peripheral resistance (TPR) reduce the workload on the heart?

Answer 60

Reduced Afterload:

Decreased Resistance: By lowering TPR, these medications decrease the resistance against which the heart must pump blood.
Reduced Cardiac Workload: With less resistance, the heart requires less energy and force to eject blood, reducing myocardial oxygen demand and workload.
Cardiac Output:

Improved Efficiency: Reduced afterload can improve cardiac output, as the heart can pump more blood with less effort.
Ejection Fraction: Improved ejection fraction due to decreased afterload means better overall cardiac efficiency and performance.

Question 61

How does reducing fluid retention help to reduce the workload on the heart?

Answer 61

How does reducing fluid retention help to reduce the workload on the heart?

Fluid Retention:

Preload: Fluid retention increases blood volume, leading to higher venous return and increased preload (the volume of blood in the ventricles at the end of diastole).
Medications Reducing Fluid Retention:

Diuretics: Drugs like furosemide and thiazides increase urine output, reducing blood volume.
Aldosterone Antagonists: Medications like spironolactone reduce sodium and water retention.
Reduced Preload:

Lower Blood Volume: By reducing blood volume, these medications decrease venous return and preload.
Reduced Cardiac Workload: Lower preload reduces the stretch and filling pressure on the heart, decreasing the work required during diastole.
Cardiac Efficiency:

Optimal Filling Pressure: Reduced preload helps maintain optimal ventricular filling pressure, preventing excessive stretching and improving cardiac efficiency.
Reduced Risk of Edema: Lower fluid retention decreases the risk of pulmonary and peripheral edema, common in heart failure, further reducing stress on the heart.

Question 62

α1 Adrenoceptors

Answer 62

Mediate vasoconstriction, smooth muscle contraction (including bladder and prostate), and pupil dilation.

Theses receptors are linked to G-protein receptors that activate smooth muscle contraction through the IP3 signal transduction pathway and ultimately vasoconstriction

Question 63

β2 Adrenoceptors

Answer 63

Mediate vasodilation, bronchodilation, glycogenolysis, gluconeogenesis, and relaxation of smooth muscle in the uterus and gastrointestinal tract.

Act via cAMP to inhibit myosin light chain kinase, and thus inhibit contraction

Question 64

What is the role of fast conducting sodium channels in ventricular depolarization?

Answer 64

Initiation of Action Potential:

Resting Membrane Potential: Ventricular myocytes (heart muscle cells) have a resting membrane potential of around -90 mV.
Depolarization Trigger: When an action potential from the sinoatrial (SA) node or atrioventricular (AV) node reaches the ventricular myocytes, it depolarizes the membrane to a threshold potential.
Activation of Fast Sodium Channels:

Threshold Potential: Upon reaching approximately -70 mV, voltage-gated fast sodium channels (Na⁺ channels) in the ventricular myocytes open rapidly.
Rapid Sodium Influx: The opening of these channels allows a rapid influx of sodium ions (Na⁺) into the cell due to the concentration gradient and electrochemical gradient.
Rapid Depolarization Phase:

Phase 0 of Action Potential: The rapid influx of Na⁺ causes the membrane potential to spike from -70 mV to approximately +30 mV. This phase is known as Phase 0 of the cardiac action potential.
Depolarization Wave: This rapid depolarization propagates quickly through the ventricular myocardium, ensuring that the ventricular myocytes contract almost simultaneously.
Propagation of the Action Potential:

Conducting System: The fast sodium channels ensure the rapid propagation of the action potential through the His-Purkinje system and the ventricular muscle, facilitating a coordinated contraction.
Efficient Contraction: This synchronized depolarization is crucial for efficient ventricular contraction, allowing the ventricles to pump blood effectively into the pulmonary artery and aorta.
Repolarization and Inactivation:

Inactivation of Sodium Channels: After a few milliseconds, the fast sodium channels close and become inactivated.
Subsequent Phases: This is followed by other ionic currents (like potassium efflux) that contribute to the repolarization (Phases 1-3) and return to the resting membrane potential (Phase 4).

Question 65

Describe the changes in venous return and cardiac output that occur in heart failure.

Answer 65

Changes in Venous Return
Increased Venous Pressure:

Heart’s Reduced Pumping Ability: In heart failure, the weakened heart cannot effectively pump blood out of the ventricles, leading to blood backing up in the venous system.
Venous Congestion: This backup increases venous pressure, causing congestion in systemic veins (right-sided heart failure) or pulmonary veins (left-sided heart failure).
Fluid Retention:

RAAS Activation: The body compensates for reduced cardiac output by activating the renin-angiotensin-aldosterone system (RAAS), leading to sodium and water retention.
Increased Blood Volume: Fluid retention increases blood volume, which in turn increases venous return to the heart.
Venoconstriction:

Sympathetic Nervous System Activation: Increased sympathetic activity causes venoconstriction, which increases venous return by reducing venous capacitance and pushing more blood towards the heart.
Changes in Cardiac Output
Reduced Stroke Volume:

Impaired Contractility: The weakened myocardium in heart failure cannot contract forcefully, leading to a reduced stroke volume (the amount of blood ejected with each heartbeat).
Increased End-Diastolic Volume: The ventricle is often overfilled due to the increased venous return and impaired ejection, leading to higher end-diastolic volume and pressure.
Decreased Cardiac Output:

Overall Reduction: Cardiac output (CO = stroke volume × heart rate) decreases because the reduction in stroke volume is not fully compensated by any increase in heart rate.
Ineffective Compensation: Although the heart may attempt to beat faster (tachycardia) to maintain cardiac output, this is often insufficient and can exacerbate heart failure symptoms.
Compensatory Mechanisms:

Sympathetic Nervous System: Increases heart rate and contractility initially, but chronic activation leads to further heart damage and reduced cardiac efficiency.
Frank-Starling Mechanism: Initially, increased venous return may help increase stroke volume slightly, but in heart failure, the overstretched myocardium loses efficiency, leading to a plateau or decrease in stroke volume despite higher filling pressures.
Pathophysiological Consequences
Pulmonary Congestion:

Left-Sided Heart Failure: Blood backs up into the pulmonary veins, leading to increased pressure and fluid leakage into the lungs (pulmonary edema).
Peripheral Edema:

Right-Sided Heart Failure: Blood backs up into the systemic venous system, causing fluid accumulation in tissues (peripheral edema) and organs (e.g., hepatomegaly, ascites).
Reduced Tissue Perfusion:

Insufficient Blood Flow: Decreased cardiac output leads to inadequate blood flow to tissues and organs, resulting in fatigue, reduced exercise tolerance, and organ dysfunction.

Question 66

How do pressure-volume loops explain why lying down with the legs elevated can immediately help restore cardiac output and relieve symptoms of atrial fibrillation?

Answer 66

Pressure-Volume Loop Basics:

Axes: The x-axis represents volume (mL) in the left ventricle, and the y-axis represents pressure (mmHg).
Phases: The loop consists of four phases: filling (diastole), isovolumetric contraction, ejection (systole), and isovolumetric relaxation.
Normal Pressure-Volume Loop:

End-Diastolic Volume (EDV): The volume of blood in the ventricle at the end of filling.
End-Systolic Volume (ESV): The volume of blood remaining in the ventricle after contraction.
Stroke Volume (SV): The difference between EDV and ESV, representing the amount of blood ejected during each beat.
Effects of Atrial Fibrillation on Cardiac Function
Impaired Atrial Contraction:

Loss of Atrial Kick: Atrial fibrillation (AF) causes the atria to quiver instead of contracting effectively, reducing the “atrial kick” that contributes to ventricular filling.
Reduced Preload: This results in lower EDV and decreased stroke volume.
Pressure-Volume Loop in AF:

Shift in EDV: Without the atrial kick, the pressure-volume loop shifts to the left, indicating reduced preload and stroke volume.
Effects of Leg Elevation
Increase in Venous Return:

Mechanism: Elevating the legs uses gravity to promote the return of blood from the lower extremities to the heart, increasing venous return.
Increased Preload: Increased venous return raises the EDV, enhancing ventricular filling.
Restoring Cardiac Output:

Pressure-Volume Loop Adjustment: With increased preload, the pressure-volume loop shifts to the right, indicating higher EDV.
Enhanced Stroke Volume: The increased EDV results in a greater stroke volume, thereby improving cardiac output.
Symptom Relief:

Improved Hemodynamics: The increased stroke volume and cardiac output improve overall blood flow and perfusion, alleviating symptoms such as dizziness, fatigue, and shortness of breath associated with atrial fibrillation.
Immediate Effect: This position provides an immediate increase in venous return and preload, offering quick relief from the hemodynamic instability caused by AF.

Question 67

What is the effect of vasoconstriction of the afferent arteriole on blood volume?

Answer 67

Decreased Glomerular Filtration Rate (GFR):

Reduced Blood Flow: Vasoconstriction narrows the afferent arteriole, limiting the amount of blood entering the glomerulus.
Decreased Filtration: With reduced blood flow into the glomerulus, there is a decrease in the rate at which plasma is filtered into the renal tubules, leading to a lower GFR.
Increased Blood Volume:

Renin-Angiotensin-Aldosterone System (RAAS) Activation: Decreased renal blood flow and GFR trigger the release of renin from the juxtaglomerular cells of the kidney.
Angiotensin II Production: Renin converts angiotensinogen into angiotensin I, which is then converted into angiotensin II by angiotensin-converting enzyme (ACE).
Aldosterone Release: Angiotensin II stimulates aldosterone secretion from the adrenal cortex.
Sodium and Water Retention: Aldosterone promotes sodium and water reabsorption in the distal convoluted tubule and collecting ducts of the kidney, leading to increased blood volume.

Question 68

What are the different types of homeostatic receptors and their functions?

Answer 68

Osmoreceptors:

Location: Hypothalamus (specifically in the supraoptic and paraventricular nuclei).
Function: Detect changes in the osmolarity of blood plasma.
Response:
When plasma osmolarity increases (indicating dehydration), osmoreceptors stimulate the release of antidiuretic hormone (ADH) from the posterior pituitary, which increases water reabsorption in the kidneys to dilute the plasma.
When plasma osmolarity decreases, ADH release is inhibited, reducing water reabsorption.
Baroreceptors:

Location: Carotid sinus and aortic arch.
Function: Detect changes in blood pressure by sensing the stretch of blood vessel walls.
Response:
High blood pressure stretches the vessel walls more, increasing baroreceptor firing, which decreases sympathetic nervous system activity and increases parasympathetic activity to lower heart rate and dilate blood vessels, reducing blood pressure.
Low blood pressure results in less stretch, decreasing baroreceptor firing, which increases sympathetic activity to raise heart rate, constrict blood vessels, and increase blood pressure.
Chemoreceptors:

Peripheral Chemoreceptors:
Location: Carotid bodies and aortic bodies.
Function: Detect changes in blood levels of oxygen (O₂), carbon dioxide (CO₂), and pH.
Response:
Low O₂, high CO₂, or low pH (acidosis) increase chemoreceptor activity, stimulating respiratory centers in the brainstem to increase ventilation, enhancing O₂ uptake and CO₂ expulsion.
Central Chemoreceptors:
Location: Medulla oblongata (near the respiratory center).
Function: Detect changes in the pH of cerebrospinal fluid, which reflects CO₂ levels in the blood.
Response:
High CO₂ (causing acidosis) triggers an increase in breathing rate to expel CO₂ and restore pH balance.

Question 69

What are the compensatory mechanisms for metabolic acidosis?

Answer 69

Compensatory Mechanisms for Metabolic Acidosis
Overview:

The body employs both respiratory and renal compensations to counteract metabolic acidosis.
Respiratory Compensation:

Detection: Chemoreceptors in the brain and carotid bodies detect decreased blood pH.
Hyperventilation: The respiratory center increases the rate and depth of breathing to expel CO₂ more rapidly.
Effect: Reducing CO₂ levels lowers the concentration of carbonic acid in the blood, helping to increase pH back toward normal. This is a rapid response mechanism.
Renal Compensation:

Bicarbonate Reabsorption: The kidneys increase the reabsorption of bicarbonate (HCO₃⁻) from the filtrate back into the blood to buffer excess hydrogen ions.
Hydrogen Ion Excretion: The kidneys enhance the secretion of hydrogen ions (H⁺) into the urine.
Ammonium Production: The kidneys increase the production and excretion of ammonium (NH₄⁺), which binds to hydrogen ions in the urine, allowing more H⁺ to be excreted.
Phosphate Buffering: The kidneys also use phosphate buffers in the urine to excrete additional hydrogen ions.
Effect: These renal adjustments help to restore acid-base balance by increasing blood pH. This is a slower but more sustainable response compared to respiratory compensation.

Question 70

What are the compensatory mechanisms for metabolic alkalosis?

Answer 70

The body employs both respiratory and renal compensations to counteract metabolic alkalosis.
Respiratory Compensation:

Detection: Chemoreceptors in the brain and carotid bodies detect increased blood pH.
Hypoventilation: The respiratory center decreases the rate and depth of breathing to retain CO₂.
Effect: Increasing CO₂ levels raises the concentration of carbonic acid in the blood, helping to decrease pH back toward normal. This is a rapid response mechanism.
Renal Compensation:

Bicarbonate Excretion: The kidneys decrease reabsorption of bicarbonate (HCO₃⁻), increasing its excretion in the urine.
Hydrogen Ion Retention: The kidneys retain more hydrogen ions (H⁺) by reducing their secretion into the urine.
Decreased Ammonium Production: The kidneys reduce the production and excretion of ammonium (NH₄⁺), leading to less trapping of hydrogen ions in the urine.
Phosphate Buffering: There is decreased utilization of phosphate buffers for hydrogen ion excretion in the urine.
Effect: These renal adjustments help to decrease blood pH. This is a slower but more sustainable response compared to respiratory compensation.

Question 71

PNS and HR

Answer 71

Slows HR by acetylcholine release. Acetylcholine increases K+, resulting in a hyperpolarized and decreased pacemaker slope

Question 72

SNS and HR

Answer 72

HR increases by norepinephrine at SA node increasing slope of pacemaker depolarisation

Question 73

Ways to make urine more concentrated

Answer 73

Increase ADH (Antidiuretic Hormone) release.

Enhance aldosterone secretion.
Activate the Renin-Angiotensin-Aldosterone System (RAAS).
Increase medullary osmolarity through the counter-current multiplication system.
Reduce Glomerular Filtration Rate (GFR).
Enhance urea recycling in the kidney.
Increase activity or number of sodium transport proteins.
Ensure proper hydration and dietary balance.

Question 74

To increase Na+ reabsorption

Answer 74

increased RAA
Increases SNS
Increased ADH

Question 75

To decrease Na+ reabsorption

Answer 75

Increased ANP
Increase RAA & SNS activity
Dopamine
Prostaglandins

Question 76

Describe the creatine phosphokinase reaction/shuttle.

Answer 76

Fast Acting, Low Yield Metabolic Process

Provides quick bursts of energy.
Most effective for activities lasting 1-5 seconds (e.g., powerlifting, sprints).
ATP Production and Diffusion

ATP produced at the mitochondria cannot quickly diffuse across membranes.
Creatine acts as a shuttle to rapidly deliver ATP to required tissues.
Creatine Kinase Mechanism

Creatine is combined with a phosphate from ATP via creatine kinase, producing creatine phosphate (CrP).
CrP can quickly move to the required tissue.
In the tissue, creatine kinase detaches the phosphate from CrP and attaches it to ADP, regenerating ATP.
System Characteristics

Fast Kinetics: Effective for rapid energy delivery.
Low Yield: Provides energy for a short duration.
Ideal Usage

Suitable for explosive movements.
Example: Powerlifting (e.g., clean and jerk) where rapid energy is needed for a short duration.

Question 77

Describe lactic anaerobic glycolysis.

Answer 77

Medium Kinetics, Moderate Energy Production

Effective for activities lasting 10 seconds to just over 2 minutes (e.g., 400m sprint).
Glycolytic Pathway from Glucose

Glucose enters the cell and is phosphorylated by hexokinase to G6P using 1 ATP.
G6P enters the glycolytic pathway; another ATP is consumed at the phosphofructokinase step.
Yields 4 ATP, with a net gain of 2 ATP without using oxygen.
Overall reaction: 1 Glucose + 2 ADP → 2 ATP + 1 Lactate.
Glycolytic Pathway from Glycogen

G6P can be produced from glycogen (intracellular glucose store).
Glycogen is broken down by phosphorylase into glucose-1-phosphate, then converted to G6P.
Does not use ATP, resulting in a net gain of 3 ATP.
Overall reaction: 1 G6P + 3 ADP + 3 Pi → 3 ATP + 1 Lactate.
End Product Limitation: Lactate

Lactate accumulates in the absence of oxygen, increasing intracellular H⁺ concentration.
High H⁺ concentration inhibits Ca²⁺ release from the sarcoplasmic reticulum (SR) and competes for binding sites in the crossbridge cycle, inhibiting muscle contraction.
System Characteristics

Medium Kinetics: Provides energy at a moderate rate.
Moderate Yield: Produces medium levels of ATP.
Ideal Usage

Suitable for medium-duration, high-intensity activities.
Example: 400m sprint, where energy is needed quickly but for a longer duration than explosive movements.

Question 78

Describe oxidative phosphorylation.

Answer 78

Oxidative Phosphorylation
Slow Kinetics, Very High Yield Energy Production

Effective for long-duration activities (e.g., marathon running).
Metabolic Pathway

Uses glucose, fats, and proteins as starting points.
These substrates are broken down to enter the Krebs cycle (Citric Acid Cycle) within the mitochondria.
The Krebs cycle works alongside the electron transport chain (ETC).
ATP Production

ADP is phosphorylated into ATP during the electron transport chain.
Generates 30-32 ATP per glucose molecule, depending on the shuttle system used for transporting electrons from the cytosol to the mitochondria.
Reaction: Glucose + O₂ + ADP → CO₂ + H₂O + 30-32 ATP.
Sustainability

The process can continue indefinitely as long as oxygen and fuel substrates (glucose, fats, proteins) are available.
System Characteristics

Slow Kinetics: Provides energy at a slower rate.
Very High Yield: Produces a large amount of ATP.
Ideal Usage

Suitable for long-duration, steady-state activities.
Example: Marathon running, where a constant and sustained energy supply is needed for prolonged periods.