Pathophysiology — Practice Questions flashcards
6 of 55 questions free to study here · 24 topics · the whole deck is built into Willys
Multiple-choice practice questions, one best answer each, on cell injury, acid–base, inflammation, heart and lung disease, shock, kidney, endocrine, neuro, GI, blood and joint disorders.
Practice deck · part of Pathophysiology · written against: Standard nursing/allied-health pathophysiology course; no dosing. Updated 2026-10-10.
Study the free sample
6 questions from the deck as they are. Flip, rate yourself, filter by topic; your progress stays in this browser.
Tap the card or press Space to flip
The 6 sample questions as a list
-
A 58-year-old man who has smoked for 40 years has a bronchial biopsy showing stratified squamous epithelium where ciliated columnar epithelium normally lines the airway. Which consequence of this change best explains his frequent chest infections?
A) Loss of cilia impairs the clearance of mucus and microbes
B) Squamous cells secrete excess mucus that blocks the airways
C) Squamous cells resist the irritants in smoke less well
D) The metaplastic cells have already become malignantA) Loss of cilia impairs the clearance of mucus and microbesCellular Adaptation
Squamous metaplasia swaps a fragile lining for a tougher one, but squamous cells have no cilia or mucus, so the mucociliary escalator is lost. Metaplasia is an adaptive, potentially reversible change, not cancer, although persistent metaplasia can progress to dysplasia. -
One child develops retinoblastoma in both eyes in infancy, while another develops a single tumor in one eye at an older age. Why does the inherited form appear earlier and often in both eyes?
A) Both RB copies are already lost in every retinal cell from birth
B) Every cell already carries one faulty RB copy, so one more hit suffices
C) One mutated RB copy acts like a stuck accelerator in retinal cells
D) The inherited RB mutation switches on tumor angiogenesis in the retinaB) Every cell already carries one faulty RB copy, so one more hit sufficesNeoplasia
RB is a tumor suppressor, so both copies must be lost (the two-hit hypothesis). An inherited faulty copy supplies the first hit in every cell, so a single somatic mutation in any retinal cell is enough; a single altered copy acting as an accelerator describes an oncogene instead. -
After a high cervical spinal cord injury, a patient has low blood pressure, a heart rate of 48 beats per minute, and warm, dry skin. Which mechanism explains the slow heart rate?
A) Lost sympathetic outflow leaves vagal input to the heart unopposed
B) A Cushing reflex from raised intracranial pressure slows the heart
C) Hidden blood loss lowers preload and slows the sinus node directly
D) Histamine released from mast cells depresses the sinus node directlyA) Lost sympathetic outflow leaves vagal input to the heart unopposedShock
In neurogenic shock, the cord injury interrupts sympathetic outflow, so vessels dilate and the heart cannot speed up, while vagal fibers, which travel outside the cord, keep slowing it. The Cushing reflex also causes bradycardia, but it comes with rising, not falling, blood pressure. -
In early chronic kidney disease, serum creatinine can stay near normal after a large share of kidney function is lost. Which description of the creatinine–GFR relationship explains this?
A) Inverse and curved: early small GFR losses raise creatinine steeply
B) Inverse and curved: early large GFR losses barely raise creatinine
C) Direct and linear: creatinine falls in step as GFR falls
D) Inverse and linear: each loss of GFR raises creatinine equallyB) Inverse and curved: early large GFR losses barely raise creatinineChronic Kidney Disease
Creatinine and GFR are inversely related on a curve, so early on a big fall in GFR raises creatinine only a little, while surviving nephrons hyperfilter and hold total GFR up as nephrons are lost. By the time creatinine is clearly abnormal, much filtering capacity is gone, which is why GFR is estimated rather than judged from creatinine alone. -
A patient with a traumatic brain injury has a mean arterial pressure of 80 mm Hg and an intracranial pressure of 30 mm Hg. What is the cerebral perfusion pressure, and how does it change if ICP rises further while MAP stays the same?
A) 110 mm Hg; perfusion pressure falls as ICP rises
B) 50 mm Hg; perfusion pressure stays constant as ICP rises
C) 110 mm Hg; perfusion pressure rises as ICP rises
D) 50 mm Hg; perfusion pressure falls as ICP risesD) 50 mm Hg; perfusion pressure falls as ICP risesStroke and Intracranial Pressure
CPP = MAP − ICP, so 80 − 30 = 50 mm Hg, and every further rise in ICP lowers perfusion pressure unless arterial pressure rises too. Adding the two pressures is the common slip. -
A man with long-standing high serum urate has sudden, intense pain and swelling of his first metatarsophalangeal joint. Why is this joint so often the first affected?
A) Weight-bearing wears away the cartilage of the big toe first
B) Urate is less soluble at the cooler temperature of the toes
C) Bacteria seed the toe joint because its blood flow is lowest
D) Autoimmune pannus forms first in the small joints of the footB) Urate is less soluble at the cooler temperature of the toesBone and Joint Disorders
When urate stays high, it exceeds its solubility, and it is less soluble at cooler temperatures such as those of peripheral joints like the big toe. Neutrophils and macrophages that engulf the crystals release IL-1, producing intense inflammation.
Unlock the whole deck
You are studying a free 6-question sample. All 55 questions of Pathophysiology — Practice Questions, the other 2 Pathophysiology decks, and spaced-repetition scheduling are built into Willys. 14-day free trial, then $14.99 a year.
In Willys, tap Exam Library at the top of your Decks (or Browse Exam Library… under the + button), find the exam on its shelf or by search, tick it and tap Add.
More Pathophysiology decks
← All Pathophysiology decks, with the study guide and topic outline.
About these cards
Review status: Second-reader reviewed, with corrections applied.
Checked against:
- OpenStax Anatomy and Physiology 2e, consulted as a reference where applicable; no text copied.
- StatPearls (StatPearls Publishing, NCBI Bookshelf), consulted as a reference; no text copied.
- Original questions written for this deck; no official, textbook or question-bank items were copied. Medication amounts are deliberately omitted, and nothing here is treatment advice.
These are independent study notes written for Willys. They are not official exam material, may contain mistakes, and are no substitute for your course, your teacher or the exam owner's own publications. Found an error? Tell us — corrections ship as a new version of the deck.
Not clinical guidance. These cards prepare you for an exam. Never use them to make decisions about a patient's care: follow current guidelines, prescribing information and your institution's policies. The decks contain no doses.
Use of these pages is covered by our Terms of Use.