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Respiratory & Renal Physiology — Step 1 practice questions
106 questions in this area, with an explanation for every answer choice.
Three samples below, free and without an account.
How this shows up on Step 1
Physiology questions in this section combine two things the exam tests separately elsewhere. Physiology questions can be reasoned rather than recalled, which makes them the best return on study time. These two systems are examined together because acid-base links them.
Sample questions
Sample question 1
A 68-year-old man with long-standing diabetes has a normal anion gap metabolic acidosis with HYPERkalemia and a urine pH of 5.2. Plasma renin and aldosterone are low. Which of the following best explains his acidosis?
Explanations
A. Accumulation of unmeasured organic anions
Organic anions would raise the anion gap.
B. Inability of alpha-intercalated cells to secrete hydrogen ions, with alkaline urine
Distal (type 1) RTA causes hypokalemia and an inappropriately HIGH urine pH.
C. Hypoaldosteronism reduces distal sodium reabsorption and potassium secretion; the resulting hyperkalemia impairs renal ammoniagenesis and acid excretion · correct
Type 4 RTA is the most common RTA, typically from hyporeninemic hypoaldosteronism in diabetic nephropathy (also from ACE inhibitors, ARBs, NSAIDs, heparin, and potassium-sparing diuretics). Aldosterone deficiency causes hyperkalemia, and high intracellular potassium in proximal tubular cells suppresses ammonia production, limiting urinary buffering — so acid excretion falls despite the ability to acidify urine (pH <5.5). Treat with fludrocortisone or a low-potassium diet and loop diuretics.
D. Failure of proximal bicarbonate reabsorption
Proximal (type 2) RTA causes HYPOkalemia with a normal ability to acidify urine once bicarbonate is depleted.
E. Gastrointestinal bicarbonate loss from diarrhea
Diarrhea causes hypokalemic normal-gap acidosis with a negative urine anion gap.
Sample question 2
A patient undergoes spirometry before and after bronchodilator administration. Which of the following findings would favor asthma over COPD?
Explanations
A. Significant reversibility of airflow obstruction after bronchodilator (e.g., >12% and 200mL improvement in FEV1) · correct
Significant reversibility of airflow obstruction after bronchodilator administration is more characteristic of asthma, reflecting the more reversible nature of the underlying airway inflammation/bronchoconstriction, compared to COPD, which typically shows more FIXED (less reversible) airflow obstruction.
B. A restrictive pattern on spirometry
Both asthma and COPD are obstructive (not restrictive) patterns; a restrictive pattern would suggest a different category of lung disease.
C. No improvement whatsoever after bronchodilator in any case
COPD, not asthma, more classically shows LESS bronchodilator reversibility; this description does not favor asthma.
D. Normal DLCO in all cases with no diagnostic value
DLCO can actually have some diagnostic value (e.g., reduced in emphysema-predominant COPD, often normal in asthma), so this option incorrectly claims no diagnostic value.
E. Complete absence of any airflow obstruction at baseline
This question specifically concerns patients WITH obstruction; complete absence of obstruction would not be the relevant distinguishing finding here.
Sample question 3
Which of the following best explains the mechanism of hypertension in unilateral renal artery stenosis?
Explanations
A. Direct sympathetic nervous system overactivity with no renal involvement
The kidney's own RAAS response is central to this mechanism, not primarily a directly separate sympathetic overactivity process.
B. Direct mechanical obstruction of the aorta itself
This is a renal ARTERY (not aortic) stenosis, and its mechanism relates to RAAS activation, not direct aortic obstruction.
C. Excess ADH secretion as the sole mechanism
While overall fluid balance is affected, the PRIMARY described mechanism is via RAAS activation from perceived renal hypoperfusion, not primarily ADH.
D. Renal artery stenosis has no relationship to blood pressure
Renal artery stenosis has a well-established, direct causal relationship to hypertension.
E. The affected kidney senses reduced perfusion pressure, activating the renin-angiotensin-aldosterone system, causing systemic hypertension · correct
The stenotic kidney senses reduced perfusion pressure (via the juxtaglomerular apparatus), triggering increased renin release and activation of the renin-angiotensin-aldosterone system, causing systemic vasoconstriction and sodium/water retention, driving hypertension — a classic cause of secondary hypertension.
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