Uni Week 4 ChatGPT Flashcards
(30 cards)
questions
answers
Discuss the pH buffer system (carbon dioxide-bicarbonate buffer) and the associated Henderson-Hasselbalch equations.
The CO₂/HCO₃⁻ buffer system maintains blood pH. The Henderson-Hasselbalch equation relates pH to the ratio of bicarbonate to carbonic acid, allowing calculation of pH based on respiratory or metabolic changes.
Related video: https://www.osmosis.org/learn/Buffer_systems
Explain why the CO2 and HCO3- buffer pair is physiologically important.
It buffers changes in blood pH rapidly and is regulated via lungs (CO₂) and kidneys (HCO₃⁻), making it ideal for physiological pH control.
Related video: https://www.osmosis.org/learn/Buffer_systems
Describe the renal mechanisms involved in acid base regulation.
The kidneys regulate acid-base balance by reabsorbing filtered HCO₃⁻, secreting H⁺, and generating new bicarbonate via ammonium and phosphate buffering.
Related video: https://www.osmosis.org/learn/Renal_regulation_of_pH
Describe how the kidneys handle ammonium that has been secreted in the proximal tubule.
Ammonium is secreted into the tubule from glutamine metabolism. In the collecting duct, it helps trap H⁺ as NH₄⁺, aiding acid excretion.
Related video: https://www.osmosis.org/learn/Ammonia_buffer_system
Define the four categories of primary acid-base disturbance and the meaning of compensation.
The four are: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Compensation is the body’s attempt to restore pH by altering respiratory or renal function.
Related video: https://www.osmosis.org/learn/Acid-base_imbalances
Describe the renal response to respiratory acid-base disorders.
In respiratory acidosis, kidneys retain HCO₃⁻ and excrete H⁺. In respiratory alkalosis, they excrete more HCO₃⁻ and retain H⁺.
Related video: https://www.osmosis.org/learn/Acid-base_imbalances
Interpret blood gas data to determine acid-base status.
Assess pH, PaCO₂, and HCO₃⁻ to classify the disturbance. Use compensatory rules to distinguish primary vs compensatory changes.
Related video: https://www.osmosis.org/learn/ABG_analysis
Define the anion gap and how it is calculated.
Anion gap = Na⁺ - (Cl⁻ + HCO₃⁻). It helps classify metabolic acidosis into high anion gap or normal anion gap types.
Related video: https://www.osmosis.org/learn/Anion_gap
Describe the aetiology, clinical manifestations and management of metabolic acidosis.
Causes include diarrhea, renal failure, and lactic/ketoacidosis. Symptoms: fatigue, Kussmaul breathing. Treat underlying cause and give bicarbonate if severe.
Related video: https://www.osmosis.org/learn/Metabolic_acidosis
Identify the primary types of renal tubular acidosis (RTA).
Types: Type I (distal), Type II (proximal), Type IV (hypoaldosteronism). Each affects acid handling differently.
Related video: https://www.osmosis.org/learn/Renal_tubular_acidosis
Compare increased vs normal anion gap metabolic acidosis.
Increased gap: due to unmeasured acids (lactate, ketones). Normal gap: due to bicarbonate loss (diarrhea, RTA).
Related video: https://www.osmosis.org/learn/Metabolic_acidosis
Describe the aetiology, manifestations and management of metabolic alkalosis.
Causes include vomiting, diuretics. Symptoms: confusion, muscle cramps. Treat with fluids, correct underlying issue.
Related video: https://www.osmosis.org/learn/Metabolic_alkalosis
Describe the transport processes that maintain sodium balance in the tubules.
Sodium is reabsorbed actively via Na⁺/K⁺ ATPase pumps and transporters throughout the nephron, especially in the proximal tubule.
Related video: https://www.osmosis.org/learn/Sodium_balance
Discuss how hypovolaemia is regulated by the kidneys.
Decreased volume activates RAAS, increases aldosterone, leading to sodium and water retention.
Related video: https://www.osmosis.org/learn/Hypovolemia
Define natriuresis and explain the action of ANP on sodium excretion.
Natriuresis = sodium loss in urine. ANP promotes natriuresis by inhibiting sodium reabsorption in the collecting duct and suppressing RAAS.
Related video: https://www.osmosis.org/learn/Atrial_natriuretic_peptide_(ANP)
Discuss sodium homeostasis dysfunction leading to hyper- and hyponatremia.
Hypernatremia: water loss > sodium loss. Hyponatremia: excess water or sodium loss. Tubular defects or hormone dysregulation may cause both.
Related video: https://www.osmosis.org/learn/Sodium_disorders
Compare and contrast SIADH and DI as causes for sodium concentration disturbances.
SIADH: excess ADH → water retention → hyponatremia. DI: ADH deficiency or resistance → water loss → hypernatremia.
Related video: https://www.osmosis.org/learn/SIADH_vs_DI
Describe how intracellular potassium movement protects the ECF.
Cells buffer K⁺ by taking it up during acute changes, e.g., insulin and β2 agonists promote uptake, stabilizing serum levels.
Related video: https://www.osmosis.org/learn/Potassium_balance
Explain role of principal and intercalated cells in potassium handling.
Principal cells secrete K⁺ in exchange for Na⁺; intercalated cells reabsorb K⁺ during hypokalemia.
Related video: https://www.osmosis.org/learn/Potassium_balance
Describe how plasma K⁺ influences aldosterone secretion.
High K⁺ stimulates aldosterone, increasing K⁺ secretion and Na⁺ reabsorption.
Related video: https://www.osmosis.org/learn/Aldosterone
Describe potassium homeostasis dysfunction leading to hyper-/hypokalaemia.
Hyperkalemia: impaired excretion (renal failure, ACEi). Hypokalemia: GI loss, diuretics. ECG: peaked T (hyper), U wave (hypo).
Related video: https://www.osmosis.org/learn/Potassium_disorders
Describe calcium handling in renal tubules and ECF.
Calcium is filtered and reabsorbed mostly in the proximal tubule; regulated by PTH in DCT.
Related video: https://www.osmosis.org/learn/Calcium_balance
Explain parathyroid hormone action in DCT.
PTH increases Ca²⁺ reabsorption in the distal tubule and stimulates vitamin D activation.
Related video: https://www.osmosis.org/learn/Parathyroid_hormone_(PTH)
