Exam 3 Flashcards
(96 cards)
CO₂ Transport in the Blood:
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A. CO₂ diffuses out of cells into systemic capillaries.
- (Figure 18-14, steps 1–2)
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B. Only 7% of CO₂ remains dissolved in plasma.
- (Figure 18-14, steps 1–3)
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C. Nearly 23% of CO₂ binds to hemoglobin (Hb), forming carbaminohemoglobin (Hb*CO₂).
- (Figure 18-14, steps 1–4)
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D. 70% of the CO₂ load is converted to bicarbonate (HCO₃⁻) and H⁺ inside red blood cells.
- Hemoglobin buffers the H⁺ ions.
- (Figure 18-14, steps 1–6)
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E. Bicarbonate (HCO₃⁻) enters the plasma in exchange for Cl⁻ (chloride shift).
- (Figure 18-14, steps 1–9)
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F. At the lungs, dissolved CO₂ diffuses out of the plasma into the alveoli.
- (Figure 18-14, steps 1–10)
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G. By the law of mass action, CO₂ unbinds from hemoglobin and diffuses out of the red blood cells.
- (Figure 18-14, steps 1–12)
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H. The carbonic acid (H₂CO₃) reaction reverses:
- HCO₃⁻ is pulled back into red blood cells and converted back into CO₂, which then diffuses into the alveoli.
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- HCO₃⁻ is pulled back into red blood cells and converted back into CO₂, which then diffuses into the alveoli.
Aldosterone and Sodium Balance
- Aldosterone is a steroid hormone released from the adrenal cortex.
- Function: Regulates both Na⁺ reabsorption and K⁺ secretion.
Mechanism of Aldosterone Action (Figure 20-12)
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Binding:
- Aldosterone diffuses into renal tubule epithelial cells (distal tubule and collecting duct).
- It combines with a cytoplasmic receptor.
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Transcription Initiation:
- The hormone-receptor complex moves to the nucleus and initiates transcription of specific genes.
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Protein Synthesis:
- Translation occurs, leading to the production of new protein channels and Na⁺/K⁺ pumps.
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Modification of Existing Proteins:
- Aldosterone-induced proteins also modify existing channels and pumps, enhancing their activity.
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Functional Outcome:
- Increased Na⁺ reabsorption from the tubular lumen into the blood.
- Increased K⁺ secretion into the tubular lumen.
- Result: Aldosterone simultaneously enhances Na⁺ reabsorption and K⁺ secretion—it cannot regulate one without affecting the other.
Control of Aldosterone Release
- The renin-angiotensin-aldosterone system (RAAS) is the most important factor regulating aldosterone secretion.
Bladder Control and Micturition (Urination)
(a) Bladder at Rest (Filling State)
- Tonic discharge from motor neurons keeps the external sphincter contracted.
- Internal sphincter (smooth muscle) is also contracted due to sympathetic stimulation.
- Bladder smooth muscle is relaxed, allowing filling.
- Higher CNS input can voluntarily reinforce sphincter closure to delay urination.
(b) Micturition (Urination Process)
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Stretch Receptors Activated:
- As the bladder fills, stretch receptors in the bladder wall fire.
- Sensory neurons carry this signal to the spinal cord.
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Reflex Activation:
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Parasympathetic neurons are activated:
- Bladder smooth muscle contracts (involuntary).
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Motor neurons to the external sphincter stop firing:
- External sphincter relaxes (voluntary control can delay this).
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Sympathetic neurons to the internal sphincter stop firing:
- Internal sphincter relaxes and opens.
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Parasympathetic neurons are activated:
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Urination:
- Bladder contracts.
- Both sphincters open.
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Urine is expelled.
- Higher CNS input can either: - Inhibit the reflex to delay urination (e.g., holding pee).
- Facilitate the reflex to initiate urination.
Hemoglobin (Hb) and Oxygen Binding – Cooperativity Explained:
- Hemoglobin (Hb) is made of four subunits, and each subunit can bind one molecule of oxygen (O₂).
- When no oxygen is bound (in deoxyhemoglobin), the subunits are tightly packed together by electrostatic bonds. In this state, hemoglobin has a low affinity (low “attraction”) for oxygen.
- When one oxygen molecule binds to one subunit, it breaks some of these tight bonds and causes a change in the shape (a conformational change) of the hemoglobin.
- This new shape makes it easier for the next oxygen molecule to bind to another subunit.
- So, each time oxygen binds, it increases the hemoglobin’s affinity for oxygen at the remaining open sites.
- This step-by-step increasing ease of binding oxygen is called cooperativity.
Effects of Changes in Hemoglobin’s Oxygen Affinity:
- When the oxygen dissociation curve shifts to the right:
- Hemoglobin has lower affinity for oxygen.
- It loads (binds) oxygen less easily in the lungs.
- But it unloads (releases) oxygen more easily to the tissues.
- When the curve shifts to the left:
- Hemoglobin has higher affinity for oxygen.
- It loads (binds) oxygen more easily in the lungs.
- But it unloads (releases) oxygen less easily to the tissues.
In short:
- Right shift = “Let go of oxygen more easily.”
- Left shift = “Hold onto oxygen more tightly.”
Hemoglobin Saturation at Different Oxygen Levels:
- Under normal conditions, the oxygen pressure (PO₂) in arteries is about 100 mmHg, and hemoglobin is almost fully (100%) saturated with oxygen.
- Even if the oxygen pressure drops to 60 mmHg (which is lower than normal), hemoglobin is still more than 90% saturated.
- This means that even with moderately reduced oxygen levels in the lungs (like at high altitudes or with some lung problems), the blood can still pick up enough oxygen to function fairly normally.
Hemoglobin is very good at picking up oxygen, even if oxygen levels fall a bit.
What is Alveolar PO₂?
- Alveolar PO₂ = the partial pressure of oxygen (O₂) inside the alveoli (tiny air sacs in the lungs where gas exchange happens).
- It depends on:
- How much oxygen you breathe in (air quality, altitude).
- How much oxygen is getting removed into the blood.
- Factors like ventilation (how well you’re breathing).
Think of alveolar PO₂ as the “supply” of oxygen available for the blood to pick up.
What is Arterial PO₂?
- Arterial PO₂ = the partial pressure of oxygen in the blood after it has passed through the lungs and picked up oxygen.
- It shows how much oxygen actually made it into the blood.
- Arterial PO₂ is measured from blood in the arteries (like in an arterial blood gas test, ABG).
Think of arterial PO₂ as the “result” of gas exchange — how much oxygen your blood actually carries.
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Alveolar PO₂ is always a little higher than arterial PO₂ because:
- Some oxygen is lost before reaching the blood (small “normal” inefficiencies in gas exchange).
- There’s mixing with a little bit of venous blood (called a “physiological shunt”).
- If arterial PO₂ drops more than expected compared to alveolar PO₂, it means there’s a problem with gas exchange (like in pneumonia, pulmonary edema, or lung injury).
In short:
- Alveolar PO₂ = oxygen available in the lungs.
- Arterial PO₂ = oxygen actually picked up by the blood.
Hemoglobin Saturation in Venous Blood:
- After blood delivers oxygen to the tissues, it returns to the heart through the veins.
- In normal mixed venous blood, the oxygen pressure (PO₂) is about 40 mmHg.
- At this PO₂, hemoglobin is still about 75% saturated with oxygen.
- That means only about 25% of the oxygen has been unloaded from the hemoglobin to the tissues during circulation.
In short: - Blood doesn’t dump all its oxygen in one trip.
- Most oxygen stays bound to hemoglobin even after delivering oxygen — like a reserve supply.
- This is important because if tissues suddenly need more oxygen (like during exercise), the blood has extra oxygen ready to release.
How DPG, Temperature, and pH Affect Hemoglobin’s Oxygen Binding:
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Increases in:
- 2,3-DPG (made by red blood cells during glycolysis),
- Temperature (body heat),
- Acidity (lower pH, more H⁺ ions)
- A right shift means:
- Hemoglobin holds onto oxygen less tightly.
- Oxygen unloads more easily into tissues.
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Decreases in:
- DPG,
- Temperature,
- Acidity (higher pH, less H⁺)
- A left shift means:
- Hemoglobin holds onto oxygen more tightly.
- Less oxygen unloading into tissues.
Why is this important?
- When tissues are more metabolically active (exercising, fighting infection, etc.), they:
- Produce more heat,
- Produce more acidity (CO₂ → carbonic acid),
- Increase DPG in the blood.
- These changes help hemoglobin release more oxygen where it’s needed most!
In short:
> Hotter, more acidic, and higher DPG = more oxygen unloading.
What is DPG?
- DPG stands for 2,3-diphosphoglycerate (also sometimes called 2,3-BPG — 2,3-bisphosphoglycerate).
- It’s a molecule made inside red blood cells during glycolysis (the process cells use to break down glucose for energy).
- DPG binds to hemoglobin and makes it easier for hemoglobin to release oxygen.
Why does DPG matter?
- When DPG levels go up:
- Hemoglobin becomes less “sticky” to oxygen.
- Oxygen is released more easily into tissues.
- This is really important in conditions like:
- High altitude (where oxygen in the air is lower).
- Anemia (low red blood cell count).
- Exercise (more oxygen needed in muscles).
Your body increases DPG to help unload more oxygen when tissues need it most!
In short:
DPG = a helper molecule that pushes oxygen off hemoglobin when tissues need more oxygen.
Molecules with Greater Oxygen Affinity:
- Some molecules bind oxygen more tightly than others — meaning they have a higher affinity for oxygen.
- This helps deliver oxygen to where it’s most needed.
Examples:
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Fetal Hemoglobin (HbF):
- Higher affinity for O₂ than adult hemoglobin (HbA).
- This allows the fetus to pull oxygen from the mother’s blood across the placenta.
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Myoglobin (in muscle cells):
- Even higher affinity for O₂ than hemoglobin.
- Stores oxygen in muscles, so muscles have a steady oxygen supply, especially during exercise.
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Hemoglobin and Carbon Monoxide (CO):
- Hemoglobin has a much higher affinity for CO than for O₂ (about 200-250 times stronger!).
- If CO is present (like in smoke or exhaust), it binds hemoglobin and blocks oxygen from attaching.
- This makes carbon monoxide poisoning very dangerous — your blood can’t carry oxygen properly.
In short:
> Molecules with higher oxygen affinity (like fetal Hb and myoglobin) help capture and store oxygen, but CO is dangerous because it hijacks hemoglobin and prevents oxygen transport.
What’s a pacemaker cell?
A pacemaker cell is a special type of heart cell that creates its own electrical signals to control the heartbeat — without needing any outside nerve input.
Here’s the breakdown:
- Pacemaker cells are mainly found in the sinoatrial (SA) node of the heart (sometimes called the heart’s “natural pacemaker”).
- They spontaneously generate action potentials (electrical impulses) at regular intervals.
- These electrical signals tell the heart muscles when to contract, making the heart beat in a coordinated rhythm.
In short:
> Pacemaker cells are the “spark plugs” of the heart — they automatically fire electrical signals to keep the heart beating. ❤️⚡
What are Phrenic Motor Neurons?
- Phrenic motor neurons are nerve cells that control the diaphragm — the big muscle under your lungs that helps you breathe.
- They are located in the spinal cord (specifically in the C3–C5 segments) and send their axons through the phrenic nerve to reach the diaphragm.
- When they fire signals, the diaphragm contracts — causing you to inhale.
How does this relate to the pacemaker cells idea?
- Just like the heart has pacemaker cells to automatically make it beat, breathing is also rhythmically controlled — but by neural “pacemaker” activity in the brain.
- There’s a special region in the brainstem (called the pre-Bötzinger complex) that acts like a breathing pacemaker.
- This brain region sends rhythmic signals to the phrenic motor neurons → they stimulate the diaphragm → you breathe in and out automatically!
In short:
> Pacemaker cells control heartbeat,Phrenic motor neurons, driven by brain “pacemakers,” control breathing.
Key parts inside the medullary respiratory center:
Main points:
- The integrating center for breathing is in the medulla oblongata (part of the brainstem).
- Inside the medulla, there’s an area called the reticular formation, and within that is the medullary respiratory center — the “command center” for breathing.
Key parts inside the medullary respiratory center:
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Pre-Bötzinger complex:
- A small group of pacemaker neurons that fire rhythmically.
- They set the basic breathing rhythm (like an internal metronome for breathing).
- These signals activate phrenic motor neurons, which make the diaphragm contract for inhalation.
- If you cut the connection between the pre-Bötzinger complex and the phrenic motor neurons → breathing stops. 😮💨❌
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Dorsal and Ventral respiratory groups:
- Other clusters of neurons in the medulla.
- Their exact job is a little less clear, but they support the rhythm and strength of breathing.
- Damaging these groups doesn’t completely stop breathing — but it can affect it.
In short:
> The pre-Bötzinger complex is the brain’s main breathing pacemaker, sending rhythmic signals to phrenic motor neurons, which control the diaphragm to make you breathe!
Main idea:
- The medulla and pons control basic, automatic breathing.
- But their activity can be influenced (“modulated”) by:
- The cerebral cortex → when you want voluntary control over your breathing (like when you hold your breath or breathe deeply on purpose).
- Sensory input → like when chemoreceptors or stretch receptors detect changes in oxygen, carbon dioxide, pH, or lung stretch and adjust breathing automatically.
In short:
> You normally breathe without thinking (thanks to the medulla and pons),but you can override it voluntarily with your brain (cortex) oryour body can adjust it automatically based on sensory feedback.
What are Baroreceptors?
- Baroreceptors are pressure sensors in your body.
- They mainly detect changes in blood pressure.
- They are found in places like the carotid sinus (in your neck) and the aortic arch (near your heart).
How do they work?
- If blood pressure rises, baroreceptors stretch more → they send more signals to the brain → the brain responds by lowering heart rate and dilating blood vessels to bring pressure back down.
- If blood pressure drops, baroreceptors stretch less → they send fewer signals → the brain responds by increasing heart rate and constricting vessels to raise pressure.
In short:
> Baroreceptors are like blood pressure alarms — they help the brain detect and quickly fix changes in blood pressure. 🩺🚨
Important note:
Baroreceptors don’t directly control breathing, but changes in blood pressure can influence breathing through other reflexes. (Later you’ll learn about chemoreceptors — those do directly affect breathing.)
Alveolar PO₂
Alveolar PO₂
- Alveolar refers to the air sacs (alveoli) in the lungs.
- Alveolar PO₂ = the partial pressure of oxygen in the air inside the alveoli.
- This is where gas exchange happens — oxygen moves from the alveoli into the blood.
Arterial PO₂
- Arterial refers to the oxygen dissolved in the blood, specifically in the arteries after the lungs.
- Arterial PO₂ = the partial pressure of oxygen in the blood plasma after it picks up oxygen from the alveoli.
So basically:
✅ You need good alveolar PO₂ so that oxygen can diffuse into blood and create good arterial PO₂.
If alveolar PO₂ drops (like at high altitude), arterial PO₂ will eventually drop too.
Term | Where? | What it means |
| — | — | — |
| Alveolar PO₂ | In the air sacs of the lungs | How much oxygen is available to move into blood |
| Arterial PO₂ | In the blood (arteries) | How much oxygen has actually moved into the blood |
The Role of Concomitant H⁺ in Respiratory Drive
First,
Concomitant just means “happening at the same time.”
(It’s just a fancy word for “along with” or “together with”.)
Now for the sentence you gave:
- When arterial PCO₂ (carbon dioxide) increases,
- it causes H⁺ (hydrogen ion) concentration to also increase (because CO₂ + water → carbonic acid → more H⁺).
- The real trigger for faster breathing is the rise in H⁺, not just the CO₂ itself.
- That’s why they say “the concomitant increased H⁺” — meaning the H⁺ increase that happens together with the CO₂ increase.
In super simple words:
> When CO₂ in your blood goes up, it automatically causes acid (H⁺) levels to go up too.The brain and chemoreceptors notice the acid, and that’s what actually triggers you to breathe more, not the CO₂ directly.
How We Breathe Without Thinking: The Medulla, Chemoreceptors, and the Roles of CO₂, H⁺, and O₂
Main ideas:
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What controls involuntary breathing?
- The medulla (specifically, the inspiratory neurons).
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Inputs that tell the medulla how to adjust breathing come from:
- Peripheral chemoreceptors (in carotid and aortic bodies).
- Central chemoreceptors (in the brain, near the medulla).
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How does CO₂ affect breathing?
- When arterial PCO₂ rises even slightly, breathing is reflexively stimulated.
- BUT — the real trigger is the increase in H⁺ (acidity) that comes along with the CO₂ increase.
- (Remember: CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻.)
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What if H⁺ increases for other reasons (not from CO₂)?
- Like in metabolic acidosis (for example, after exercise or certain diseases).
- Peripheral chemoreceptors sense this extra H⁺ and stimulate breathing.
- Breathing faster lowers CO₂, which lowers H⁺ back toward normal — a compensation.
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What about low O₂?
- A big drop in arterial PO₂ (like in severe lung disease or very high altitudes) also triggers breathing.
- This happens mostly through peripheral chemoreceptors (because central chemoreceptors mainly care about CO₂ and H⁺).
- Important: The drop in O₂ must be large before it kicks in — the body is less sensitive to O₂ compared to CO₂ and H⁺.
In short:
Trigger | Sensor | Response |
| — | — | — |
| ↑ CO₂ (and ↑ H⁺) | Peripheral + Central Chemoreceptors | Breathe more |
| ↑ H⁺ (not from CO₂) | Peripheral Chemoreceptors | Breathe more |
| ↓ O₂ (big drop) | Peripheral Chemoreceptors | Breathe more |
The Vasa Recta: Maintaining the Kidney’s Medullary Concentration Gradient
Vasa recta = special blood vessels connected to juxtamedullary nephrons in the kidney.
- After blood passes through the glomerulus, it leaves via the efferent arteriole.
- In juxtamedullary nephrons, the efferent arteriole forms long, looping capillaries called the vasa recta.
- The vasa recta dip deep into the medulla and loop back up to the cortex — like a hairpin shape.
Why is this important?
- The vasa recta help maintain the concentration gradient in the kidney medulla.
- This gradient is critical for making concentrated urine (especially when you need to conserve water).
- Without the vasa recta, your kidneys couldn’t create really salty medullas, and you’d lose way too much water.
Visualize it like this:
- Think of the vasa recta as parallel blood highways that dip down and climb back up next to the nephron loops, keeping the medulla “salty” without washing it away.
Anatomy and Function of the Nephron: The Kidney’s Filtration and Processing Unit
🔹 Each nephron (the functional unit of the kidney) has two main parts:
- Renal corpuscle (the filter)
- Tubule (the processing pipe)
🔹 The renal corpuscle has:
- Glomerulus = a ball of capillaries (tiny blood vessels).
- Bowman’s capsule = a cup-like structure that wraps around the glomerulus and catches the filtered fluid (filtrate).
🔹 The tubule starts at Bowman’s capsule and has 4 parts:
- Proximal tubule – reabsorbs most of the good stuff (like glucose, amino acids, water).
- Loop of Henle – dips into the medulla and helps concentrate urine.
- Distal convoluted tubule – fine-tunes salt and water balance.
- Collecting duct – collects filtrate from many nephrons and brings it toward the renal pelvis ➔ ureter ➔ bladder (where urine is stored).
🔹 Blood flow:
- Blood enters the glomerulus through the afferent arteriole.
- After filtering, blood leaves through the efferent arteriole.
- The efferent arteriole then forms peritubular capillaries, which wrap around the tubules to exchange substances (like giving water or taking waste).
In short:
Nephrons filter blood at the corpuscle ➔ process the filtrate through the tubule ➔ send urine out through the collecting ducts ➔ blood is cleaned and returned by the peritubular capillaries.
Glomerular filtration:
Glomerular filtration:
- Passive process: It doesn’t require energy.
- How it works: Hydrostatic pressure (the pressure from the blood flow) forces fluids and solutes through a special membrane in the glomerulus (a ball of capillaries in the kidney).
Why is the glomerulus so efficient?
Compared to other capillaries in the body, the glomerulus is much better at filtering due to these key factors:
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A. Large surface area & high permeability:
- The filtration membrane in the glomerulus has a large surface area (more space to filter) and is very permeable to water and solutes like glucose, ions, and waste products.
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B. Higher glomerular pressure:
- Glomerular pressure is much higher than in other capillary beds (around 55 mm Hg).
- This higher pressure forces more fluid through, allowing the kidneys to filter 180 liters of fluid per day.
- In contrast, other capillary beds in the body only filter about 3-4 liters per day.
Key points:
- Glomerular filtration is efficient because of the combination of a large surface area and higher pressure compared to other capillaries in the body.
- This allows the kidneys to filter a lot of blood each day (180L), which is key for maintaining fluid and electrolyte balance.
What is the Glomerulus?
- The glomerulus is a ball-shaped cluster of tiny blood vessels (capillaries) located inside the renal corpuscle of each nephron.
- It’s where the filtration of blood begins — filtering out water, solutes, and waste products to form filtrate (which eventually becomes urine).
How does it work?
- Blood enters the glomerulus through the afferent arteriole, which brings oxygen-rich blood from the body.
- Filtration occurs because the blood pressure in the glomerulus is high (around 55 mmHg), which forces fluid and small solutes (like salts, glucose, urea) through the walls of the capillaries into the Bowman’s capsule.
- The blood cells and larger proteins are too big to pass through, so they stay in the blood.
- The filtered fluid, now called filtrate, then moves into the proximal convoluted tubule for further processing.
Why is the Glomerulus Efficient?
- Large Surface Area: The glomerular capillaries are tightly packed in a small area, which gives them a large surface area for filtration.
- Permeability: The walls of the capillaries are very permeable, meaning they allow water and small solutes to pass through easily.
- High Pressure: The high pressure in the glomerulus ensures that large amounts of blood are filtered into the Bowman’s capsule.
Why does this matter?
The glomerulus plays a crucial role in your body’s ability to filter blood. It helps remove waste products, maintain fluid balance, and regulate electrolytes (like sodium and potassium), which are all critical for normal body function.
Opposing Forces to Filtration:
Opposing Forces to Filtration:
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Bowman’s Capsule Hydrostatic Pressure (PBC):
- Pressure: 15 mm Hg
- This is the hydrostatic pressure (pressure due to the volume of fluid) inside the Bowman’s capsule (the space surrounding the glomerulus).
- Why it opposes filtration: The pressure inside Bowman’s capsule is higher than the pressure in the glomerular capillaries, pushing fluid back into the glomerulus. This reduces the amount of fluid that can be filtered out of the glomerular capillaries.
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Glomerular Oncotic Pressure (πGC):
- Pressure: 29 mm Hg
- This is the osmotic pressure exerted by plasma proteins (mainly albumin) in the glomerular capillaries. It pulls fluid back into the glomerular capillaries because plasma proteins cannot pass through the filtration barrier and stay in the blood.
- Why it opposes filtration: This pressure opposes the movement of fluid out of the glomerulus because the presence of plasma proteins in the blood increases the osmotic pull, drawing water back into the capillaries.
Summary of Opposing Forces:
- Bowman’s capsule hydrostatic pressure (PBC) (15 mm Hg) pushes back against filtration.
- Glomerular oncotic pressure (πGC) (29 mm Hg) pulls fluid back into the glomerulus.
These forces work against the pressure generated by the glomerular capillary hydrostatic pressure (which is about 55 mm Hg) that drives filtration.