MasterPass PHYSIOLOGY 4

Cholelithiasis and cholecystitis.

Inulin is filtered but not reabsorbed, so its concentration rises.

A sudden shift from fat to carbohydrate metabolism with a sudden rise in insulin secretion.

In health, glucose is completely reabsorbed, so its concentration falls to zero along the length of the PCT.

The nutrition team, comprising a physician, dietician, and pharmacist, reviews patients with nutritional concerns and guides the safe use of parenteral nutrition.

By identifying patients at risk, introducing slow refeeding, and closely monitoring and correcting electrolyte disturbances.

Extracellular fluid (ECF) and intracellular fluid (ICF).

Proximal tubules

A relatively rare but potentially fatal complication characterized by severe hypophosphataemia and other metabolic complications in malnourished patients receiving concentrated calories via TPN.

Sodium is almost completely reabsorbed and is followed by passive diffusion of water, so its concentration remains unchanged.

Within 72 hours of starting the feed.

It surrounds the bile and pancreatic ducts as they emerge into the lumen of the duodenum.

Hydrostatic pressure in Bowman's capsule.

The inferior rectal nerves.

3.5 liters.

It extrudes 3 Na+ into the interstitium in exchange for 2 K+ that are pumped into the cell, creating a Na+ concentration gradient for passive diffusion of sodium into the cell from the lumen.

In adults, TBW is 60% of body weight, while in neonates it is 75–85%.

In neonates, ECF is 30–45% of body weight, while in adults it is 20%.

A closed buffer system is one where the total concentration of buffer within the cell is fixed, such as phosphate and haemoglobin.

They attenuate sympathetic-induced vasoconstriction through vasodilation, thereby increasing RBF.

1/5 of cardiac output, 500 mL/min to each kidney, 500 mL/min/100 g tissue to the cortex, 100 mL/min/100 g tissue to the outer medulla, 20 mL/min/100 g tissue to the inner medulla.

Permeability of capillaries, size of capillary bed (surface area), and hydrostatic and osmotic pressure gradients across the capillary wall (Starling’s forces).

1. Anticipation of undernutrition (<50% of metabolic requirements achieved enterally) for >7 days. 2. Severely undernourished patients unable to ingest large volumes of oral feed prior to surgery, radiation therapy, or chemotherapy. 3. Patients with disorders requiring complete gastrointestinal rest, e.g., ulcerative colitis/pancreatitis. 4. Post-operative patients in whom enteral feeding has either not been possible or has failed after 5 days.

It prevents reflux of colonic material into the ileum.

To store faeces prior to defecation.

A voluntary sphincter made up of an internal and an external ring of muscle at the exit of the rectum.

A buffer consists of a weak acid and its conjugate base (salt).

The pressure exerted by the plasma proteins within the glomerular capillaries (Πgc).

The filtration fraction is the ratio of GFR to renal plasma flow (RPF), approximately 0.16–0.2.

pH = pKa + log [conjugate base]/[acid] or pH = pKa + log [A–]/[HA]

Because plasma proteins become progressively more concentrated as filtration occurs.

It is reduced to zero and filtration ceases.

Pgc: 45, Pb: 10, Πgc: 20, Net: 15

Because creatinine levels remain within the normal range until a significant reduction in renal function occurs, especially in the elderly with reduced muscle mass.

Most of the buffer is in the form of carbon dioxide or carbonic acid.

In the PCT, H+ is secreted in exchange for Na+ and combines with filtered HCO3− to form carbonic acid, which dissociates into H2O and CO2. These move into the tubular cell, where the reaction is reversed, and HCO3− formed enters the interstitium and later the plasma.

The body produces 70 μmol/min or 0.1 mol/day of metabolic acids.

TPN is a form of feeding that supplies all daily nutritional requirements to the patient intravenously.

After the Second World War in Japanese prisoners of war.

The release of bile and pancreatic enzymes into the duodenum.

GFR is a unit of measure of kidney excretory function, defined as the volume of plasma cleared of an ideal substance per unit time, usually expressed as ml/min.

Colloid osmotic pressure in Bowman's capsule.

Pgc (45 mm Hg) and Pb (10 mm Hg).

5–6 liters.

A titration curve is a plot of pH vs. the amount of acid or base added to a buffer solution (titration).

Haemoglobin has six times the buffering capacity of plasma proteins.

179,000 mL

100 mL/min/100 g tissue.

The buffering capacity is maximal when the pH equals the pKa of the buffer system and is significantly reduced when the pH varies by more than 1 from the buffer’s pKa.

The pH increases, and the buffer shifts towards a greater HCO3− concentration.

Peritubular capillaries.

Flow to an organ is equal to the uptake/excretion of a substance by an organ per unit time divided by the arterio-venous (A-V) concentration difference of that substance across that organ (L/min).

Chronic renal failure reduces the production and secretion of ammonia, leading to reduced buffering of urinary H+.

Excess K+ causes intracellular alkalosis, which inhibits H+ secretion.

Transient liver dysfunction, evidenced by increased hepatic transaminases, bilirubin, and alkaline phosphatase.

A condition where arterial pH < 7.35 or [H+] > 45 nmol/L.

A condition where arterial pH > 7.45 or [H+] < 35 nmol/L.

The anion gap (AG) is the difference between measured cations (positively charged ions) and measured anions (negatively charged ions) in serum. It is calculated using the equation: AG = ([Na+] + [K+]) − ([Cl−] + [HCO3−]).

Because TPN solutions are concentrated and have the potential to cause venous thrombosis in peripheral veins.

Because sodium reabsorption is followed by passive water reabsorption, maintaining a constant concentration.

The net filtration rate as a function of the forces favoring filtration and those opposing it.

A buffer is an acid–base buffer solution that resists a change of pH when an acid or base is added to it.

Colloid osmotic pressure in the glomerular capillary.

Voluntary.

RPF represents the total amount of potentially filterable fluid entering the kidneys, approximately 600–700 ml/min.

Ka is the dissociation constant of a buffer, and pKa is the pH at which 50% of the buffer’s acid is dissociated.

Due to its expense, impracticalities, and the need for a bolus followed by an infusion, along with blood and urine sample collection over several hours.

The pH is plotted on the y-axis and the buffer composition on the x-axis.

An open buffer system is one where the total concentration of buffer within a compartment is not fixed, such as the bicarbonate/carbonic acid system.

The pH decreases, and the buffer shifts towards a greater H2CO3 and CO2 concentration.

Renal artery → interlobar arteries → interlobular arteries → afferent arterioles → glomerular capillaries → efferent arterioles.

Due to its fenestrations.

The vasa recta.

RBF can be calculated by plasma clearance of para-aminohippuric acid (PAH), as a modification of the Fick principle.

PAH is used because it has a high extraction ratio (almost completely removed by the kidneys) and is neither utilized nor excreted by any other organ.

Excess acid may be buffered by calcium carbonate in bone, contributing to renal osteodystrophy.

A strong acid fully dissociates in solution (e.g., HCl), while a weak acid does not fully dissociate and acts as a buffer system (e.g., carbonic acid).

pKa is the pH at which an acid is 50% dissociated, indicating the strength of an acid (the lower the pKa, the stronger the acid).

Low in acute setting, as slow renal compensation is incomplete.

Increased PaCO2 in renal tubular cells results in increased secretion of H+ ions, leading to reabsorption of bicarbonate by dissociation of carbonic acid and regeneration of bicarbonate by excretion of H+ with ammonia and phosphate in urine. This process takes 2-3 days.

By decreased acid (H+) secretion and HCO3– retention (reabsorption and regeneration).

Where possible, the enteral route should always be used in preference to parenteral nutrition.

At the junction of the small and large bowels.

Approximately 60% of body weight.

The hypogastric plexus.

Two-thirds of TBW.

Values in women are approximately 10% lower than those in men.

Because afferent arterioles are short and straight, and efferent arterioles have a relatively high resistance.

GFR can be calculated using the plasma clearance of a suitable substance by applying the Fick principle or estimated using prediction formulae based on factors such as age, sex, and serum creatinine level.

Passive diffusion, facilitated diffusion (co-transport and antiport), and active transport.

500–600 mL/min to each kidney.

ECF exceeds ICF.

Pgc: 45, Pb: 10, Πgc: 35, Net: 0

Urinary buffering occurs in the proximal (PCT) and distal (DCT) tubules and collecting ducts.

The buffering capacity increases as the concentration of the non-fixed component (HCO3−) increases.

The area of greatest buffering capacity where a shift in the relative concentrations of bicarbonate and carbon dioxide produces only a small change in pH.

The negative charge repels negatively charged ions, greatly reducing their filtration, while positively charged ions are filtered slightly more than neutral substances.

The ability to maintain a constant RBF over a wide range of mean arterial pressures (MAP) or tissue perfusion pressures (PP) from 90–200 mmHg.

The primary change: alteration of PCO2 indicates respiratory disturbance, while alteration of the bicarbonate buffer system indicates metabolic disturbance.

Carbonic anhydrase, which is present in red blood cells but not in plasma.

An acid is a proton donor, with a pH < 7.0.

pH is calculated as the negative logarithm to the base 10 of the hydrogen ion concentration.

Negative.

A process where there is acid loss or alkali accumulation.

The amount of acid or base required to restore 1 liter of blood to normal pH at a PaCO2 of 5.3 kPa and body temperature. It is negative in acidosis and positive in alkalosis, indicating the severity of the metabolic component of acid-base disturbances.

MUDPILES (Methanol, Uraemia, Diabetic ketoacidosis, Propylene glycol, Iron/isoniazid, Lactic acidosis, Ethylene glycol, Salicylates) or KULT (Ketoacids, Uraemia, Lactic acids, Toxins).

Because glucose is actively reabsorbed in the early part of the PCT.

Acute cardiac failure, confusion, coma, convulsions, and even death.

The glomerular filtration coefficient (permeability × capillary bed surface area).

Hydrostatic pressure in the glomerular capillary.

Approximately 125 ml/min or 180 l/day.

About 180 g/dL or 10 mmol/L

H+ and OH− react to form water, but more HA dissociates to maintain the [H+] constant, therefore the equation shifts to the right.

Πgc rises from 20 mm Hg at the afferent end to 35 mm Hg at the efferent end.

20–25% of cardiac output.

It is useful for determining the pKa of weak acids or bases.

It is mediated by renal sympathetic nerves and affects glomerular capillary pressure.

Because 40-50% of filtered urea may be reabsorbed by the tubules and non-renal factors can affect serum levels.

Nitric oxide causes vasodilation and endothelin causes vasoconstriction, helping to regulate GFR.

45–60 kcal/kg/day

Other sources include lactic acid (strenuous exercise), ketoacids (diabetes, alcohol, starvation), failure of H+ secretion by diseased kidneys (renal failure), and ingestion of acidifying salts (NH4Cl and CaCl2).

Chronic renal failure depletes extracellular buffers and reduces plasma bicarbonate levels.

They have a contractile function that reduces the surface area available for filtration.

Clearance of PAH = urine [PAH] × urine flow / plasma [PAH].

A base is a proton acceptor or hydroxide (OH−) producer, with a pH > 7.0.

Chronic renal failure reduces haemoglobin levels due to depressed production of new red blood cells from diminished erythropoietin secretion.

Respiratory (type 2 respiratory failure).

Intracellular buffering (carbonic acid–bicarbonate buffer system and haemoglobin), occurring within 2 hours.

By increased acid (H+) secretion and HCO3– retention (reabsorption and regeneration).

A primary loss of bicarbonate ions (e.g., due to diarrhea, renal tubular acidosis, Addison’s disease) with a compensatory elevation in chloride concentration.

It indicates that inulin is filtered but not reabsorbed, making it a useful marker for measuring glomerular filtration rate (GFR).

GFR = Kƒ [(P GC − P B) − (Π GC − Π B)]

99.4%

HA (undissociated acid) ↔ H+ (hydrogen ion) + A¯ (conjugate base)

GFR = Kƒ [Pgc − Pb − Πgc]

Hydrostatic pressure in Bowman's capsule (P B) and the osmotic pressure gradient across the glomerular capillaries (Π GC − Π B).

Deoxygenated haemoglobin (pKa 8.2) dissociates more readily than oxygenated haemoglobin (pKa 6.6), making it a better buffer and weaker acid.

The MDRD formula is the most validated for eGFR and does not require weight or height variables because results are normalized to 1.73 m² body surface area.

Plasma proteins are effective buffers because both their carboxyl (COOH) and free amino (NH2) groups dissociate.

They may increase serum creatinine by up to 30%.

30–40 mL/kg/day

Most phosphate buffering occurs in the distal convoluted tubule (DCT) and collecting ducts.

The body produces 200 ml/min or 8 mmol/min, which equals 12 mol/day of respiratory acids.

The pH is equal to the pKa (6.1) for the buffer.

To help mobilize endogenous fat stores and increase insulin sensitivity.

Daily weight, FBC, urea and electrolytes, and liver function tests.

Acidaemia (pH < 7.4).

To restore the pH towards normal by maintaining the ratio PaCO2/[HCO3–].

In chronic respiratory acidosis, renal compensatory mechanisms result in a chronic elevation of plasma bicarbonate, which restores the pH to within the normal range, but typically not to the normal level of 7.40.

A problem with ventilation, diffusion, shunt, or a ventilation-perfusion mismatch.

Intracellular buffering, with a 1–2 mmol/L increase in HCO3– for every 10 mmHg increase in PCO2.

Involuntary; it relaxes in response to stretching.

75% of ECF.

Permeability of capillaries, size of capillary bed (surface area), hydrostatic and osmotic pressure gradients across the capillary wall (Starling’s forces)

Haemoglobin acts as a blood buffer due to the imidazole groups of its histidine residues, which are anionic and accept H+.

The Cockcroft and Gault (C&G) equation and formulas based on the Modification of Diet in Renal Disease (MDRD) study.

93.3%

Inulin is used because it is freely filtered through the glomeruli, not reabsorbed or secreted, not metabolized, not stored in the kidney, has no effect on the filtration rate, is non-toxic, and easy to measure in plasma and urine.

It results in vasoconstriction of afferent arterioles, thereby reducing RBF.

20 mL/min/100 g tissue.

It has wide variation in serum levels and currently has no clinical role in GFR measurement.

1. Sensor: The macula densa in the distal tubular epithelium detects fluid delivery within the tubule. 2. Transmission of signal to the glomerulus. 3. Effector: Vascular smooth muscle in the afferent arteriole adjusts GFR by vasodilatation or vasoconstriction.

2 g/day

Neutral substances of <4 nm diameter are freely filtered, but for substances >8 nm, their filtration approaches zero. Between 4 and 8 nm, filtration is inversely proportional to diameter.

Provision of glucose and oxygen, removal of CO2 and other metabolic products, maintenance of GFR, provision of O2 for active reabsorption of sodium.

Angiotensin II contracts mesangial cells, while PGE2 relaxes them.

Chronic renal failure reduces bicarbonate reabsorption and regeneration.

Volume overload, glucose abnormalities, electrolyte disturbances, metabolic bone disease, and hepatic complications.

Discontinue the TPN temporarily or permanently.

A process where there is acid accumulation or alkali loss.

Through hypoventilation.

Hypoventilation, resulting in a 0.7 mmHg increase in PCO2 for each 1 mmol/L increase in HCO3–.

Renal decreased reabsorption of HCO3– and decreased excretion of ammonium, with a 4–5 mmol/L decrease in HCO3– for every 10 mmHg decrease in PCO2.

The equilibrium shifts to the left, and the H+ ions are ‘neutralised’ by the conjugate base, minimizing an increase in free [H+] and maintaining a constant pH.

Transcellular fluids are secreted fluids separated from plasma by an epithelial layer, found in pleural, peritoneal, gastrointestinal fluids, CSF, intra-ocular fluids, sweat, saliva, and bile.

Not all the filtered glucose is reabsorbed, and glucose starts to appear in the urine.

After O2 has been offloaded, oxyhaemoglobin is reduced to deoxyhaemoglobin, which has a better buffering capacity, explaining why venous pH is only slightly more acidic than arterial pH.

It requires a 24-hour urine collection, is affected by muscle mass, diet, and tubular secretion, and may be inaccurate due to elevated urine [creat] and non-specific chromogens in plasma [creat].

More than 90%.

Phosphate plays a small role in the extracellular fluid but is an important intracellular buffer due to its abundance and dissociation from phosphoric acid to dihydrogen phosphate and then to mono-hydrogen phosphate.

Angiotensin II vasoconstricts the efferent arterioles more than the afferent arterioles, thus maintaining GFR.

30 kcal/kg/day

Ammonia buffering takes place mainly in the PCT and DCT, where H+ combines with secreted NH3 to form NH4+, which is excreted in the urine.

Because at the physiological blood pH of 7.4, small changes in the relative compositions cause a large pH change.

Range of buffer (pH = pKa ± 1) and buffering capacity (ratio of concentrations of weak acid to conjugate base).

Due to the ready excretion of carbonic acid in the form of CO2 by the lungs and the continuous regeneration of bicarbonate by the kidneys.

Likely acute.

Through hyperventilation.

10–20 mmol/L, or 8–16 mmol/L if [K+] is excluded. Modern analyzers predict a normal range of 3–11 mmol/L.

The afferent arteriole vasoconstricts and GFR is reduced.

Essential fatty acids, minerals (e.g., Acetate, Calcium, Chloride, Copper, Magnesium, Potassium, Selenium, Sodium, Zinc), and vitamins (e.g., A, D, E, K, C, Folic acid, Thiamine, Pyridoxine, Niacin)

Using sterile techniques and may be modified based on laboratory results, underlying disorders, hypermetabolism, or other factors.

pH ~ 7.40, PCO2 ~ 5.3 kPa (40 mmHg), HCO3- ~ 24 mmol/L.

Acidosis.

The plasma concentration of bicarbonate when arterial PCO2 is corrected to 5.3 kPa, hemoglobin is fully saturated, and body temperature is 37°C.

Hyperventilation, resulting in a 1.2 mmHg decrease in PCO2 for each 1 mmol/L decrease in HCO3–.

The area of least buffering capacity, where even a small shift in relative concentrations of acid and base produces a large change in pH.

Buffering by bicarbonate results in bicarbonate reabsorption, whereas buffering with phosphate and ammonia results in bicarbonate regeneration.

Between 7.35 and 7.45.

Buffers in tissue and blood, and excretion of acids by kidneys and lungs.

A direct contractile response of the afferent arteriolar smooth muscle to stretch, where an increase in perfusion pressure results in smooth muscle contraction and increased renal vascular resistance, maintaining constant blood flow.

Through a dedicated port of a central venous line with strict asepsis.

RBF can be deduced from RPF if the hematocrit (Hct) is known, using the equation: RBF = RPF / (1 - Hct).

pH = 6.1 + log [HCO3−] / [H2CO3] and since H2CO3 is proportional to PaCO2: pH = 6.1 + log [HCO3−] / 0.225 × PaCO2.

Plasma proteins may be diminished in the presence of increased glomerular permeability in conditions like glomerulonephritis or nephrotic syndrome.

Correction of the acid-base imbalance.

Respiratory acidosis is a consequence of hypoventilation or ventilation-perfusion inequalities, leading to elevated PCO2, which disrupts the ratio of HCO3− to PCO2 and causes a drop in pH.

The presence of acidic unmeasured anions, leading to a secondary loss of bicarbonate ions due to their buffering capacity, while chloride concentration remains unchanged to maintain electroneutrality.

Renal generation of bicarbonate via excretion of ammonium, with a 3–4 mmol/L increase in HCO3– for every 10 mmHg increase in PCO2.

Intracellular buffering, with a 1–2 mmol/L decrease in HCO3– for every 10 mmHg decrease in PCO2.