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rubin_s_pathology__clinicopathologic_foundations_of_medicine_7th_edition

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Unlock the complexities of human disease with the comprehensive test bank for "Rubin's Pathology: Clinicopathologic Foundations of Medicine, 7th Edition" by David S. Strayer and Emanuel Rubin. This invaluable resource is meticulously designed to help medical students and professionals deepen their understanding of pathophysiology. Imagine having a trusted study companion that not only reinforces key concepts from the textbook but also challenges you with a variety of question types, including multiple-choice, short-answer, and essay questions. Each question is thoughtfully crafted to reflect real-world clinical scenarios, ensuring that your learning experience is both practical and engaging. Whether you're preparing for exams or honing your diagnostic skills, this test bank is your go-to tool for mastering the mechanisms of disease. With chapters covering everything from cellular adaptations to systemic disorders, this test bank is a must-have for anyone committed to excelling in the field of medicine. Embrace the opportunity to transform your theoretical knowledge into practical expertise with every question you tackle.

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Institución
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Pathology

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Subido en
4 de octubre de 2025
Número de páginas
228
Escrito en
2025/2026
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,Chapter |1: |Cell |Adaptation, |Injury |and |Death
Ischemia |and |other |toxic |injuries |increase |the |accumulation |of |intracellular |calcium |as |a |result |of:
1.
A) release |of |stored |calcium |from |the |mitochondria.
B) improved |intracellular |volume |regulation.
C) decreased |influx |across |the |cell |membrane.
D) attraction |of |calcium |to |fatty |infiltrates.
The |patient |is |found |to |have |liver |disease, |resulting |in |the |removal |of |a |lobe |of |his |liver.
2. |Adaptation |to |the |reduced |size |of |the |liver |leads |to | of |the |remaining |liver |cells.
A) metaplasia
B) organ |atrophy
C) compensatory |hyperplasia
| | D) physiologic |hypertrophy
A |person |eating |peanuts |starts |choking |and |collapses. |His |airway |obstruction |is |partially
|cleared, |but |he |remains |hypoxic |until |he |reaches |the |hospital. |The |prolonged |cell |hypoxia

3. |caused |a |cerebral |infarction |and |resulting | in |the |brain.
A) caspase |activation
B) coagulation |necrosis
C) rapid |phagocytosis
D) protein |p53 |deficiency
Bacteria |and |viruses |cause |cell |damage |by | , |which |is |unique |from |the |intracellular
4. |damage |caused |by |other |injurious |agents.


A) disrupting |the |sodium/potassium |ATPase |pump
B) interrupting |oxidative |metabolism |processes
| | C) replicating |and |producing |continued |injury
D) decreasing |protein |synthesis |and |function
The |patient |has |a |prolonged |interruption |in |arterial |blood |flow |to |his |left |kidney, |causing |hypoxic
5. |cell |injury |and |the |release |of |free |radicals. |Free |radicals |damage |cells |by:



A) destroying |phospholipids |in |the |cell |membrane.
B) altering |the |immune |response |of |the |cell.
C) disrupting |calcium |storage |in |the |cell.
D) inactivation |of |enzymes |and |mitochondria.
6. Injured |cells |have |impaired |flow |of |substances |through |the |cell |membrane |as |a |result |of:
A) increased |fat |load.

, B) altered |permeability.
C) altered |glucose |utilization.
D) increased |surface |receptors.
7. Reversible |adaptive |intracellular |responses |are |initiated |by:
A) stimulus |overload.
B) genetic |mutations.
C) chemical |messengers.
D) mitochondrial |DNA.
8. Injured |cells |become |very |swollen |as |a |result |of:
A) increased |cell |protein |synthesis.
B) altered |cell |volume |regulation.
C) passive |entry |of |potassium |into |the |cell.
D) bleb |formation |in |the |plasma |membrane.
A |diabetic |patient |has |impaired |sensation, |circulation, |and |oxygenation |of |his |feet. |He |steps |on |a
|piece |of |glass, |the |wound |does |not |heal, |and |the |area |tissue |becomes |necrotic. |The |necrotic |cell

9. |death |is |characterized |by:


A) rapid |apoptosis.
B) cellular |rupture.
C) shrinkage |and |collapse.
D) chronic |inflammation.
A |99-year-old |woman |has |experienced |the |decline |of |cell |function |associated |with |age. |A |group
10. |of |theories |of |cellular |aging |focus |on |programmed:


A) changes |with |genetic |influences.
B) elimination |of |cell |receptor |sites.
C) insufficient |telomerase |enzyme.
| | D) DNA |mutation |or |faulty |repair.
An |89-year-old |female |patient |has |experienced |significant |decreases |in |her |mobility |and
|stamina |during |a |3-week |hospital |stay |for |the |treatment |of |a |femoral |head |fracture. |Which |of

the |following |phenomena |most |likely |accounts |for |the |patients |decrease |in |muscle |function |that
11. |underlies |her |reduced |mobility?



A) Impaired |muscle |cell |metabolism |resulting |from |metaplasia
B) Dysplasia |as |a |consequence |of |inflammation |during |bone |remodeling
C) Disuse |atrophy |of |muscle |cells |during |a |prolonged |period |of |immobility
D) Ischemic |atrophy |resulting |from |vascular |changes |while |on |bedrest

, A |20-year-old |college |student |has |presented |to |her |campus |medical |clinic |for |a |scheduled
|Papanicolaou |(Pap) |smear. |The |clinician |who |will |interpret |the |smear |will |examine |cell |samples

12. |for |evidence |of:


A) changes |in |cell |shape, |size, |and |organization.
B) the |presence |of |unexpected |cell |types.
| | C) ischemic |changes |in |cell |samples.
D) abnormally |high |numbers |of |cells |in |a |specified |field.
Which |of |the |following |pathophysiologic |processes |is |most |likely |to |result |in |metastatic
| | 13. |calcification?



A) Benign |prostatic |hyperplasia
B) Liver |cirrhosis
C) Impaired |glycogen |metabolism
D) Hyperparathyroidism
Despite |the |low |levels |of |radiation |used |in |contemporary |radiologic |imaging, |a |radiology
|technician |is |aware |of |the |need |to |minimize |her |exposure |to |ionizing |radiation. |What |is |the

14. |primary |rationale |for |the |technicians |precautions?


A) Radiation |stimulates |pathologic |cell |hypertrophy |and |hyperplasia.
B) Radiation |results |in |the |accumulation |of |endogenous |waste |products |in |the |cytoplasm.
C) Radiation |interferes |with |DNA |synthesis |and |mitosis.
D) Radiation |decreases |the |action |potential |of |rapidly |dividing |cells.
The |parents |of |a |4-year-old |girl |have |sought |care |because |their |daughter |has |admitted |to |chewing
|and |swallowing |imported |toy |figurines |that |have |been |determined |to |be |made |of |lead. |Which |of

15. |the |following |blood |tests |should |the |care |team |prioritize?


| | A) White |blood |cell |levels |with |differential
B) Red |blood |cell |levels |and |morphology
C) Urea |and |creatinine |levels
D) Liver |function |panel
A |70-year-old |male |patient |has |been |admitted |to |a |hospital |for |the |treatment |of |a |recent
hemorrhagic |stroke |that |has |left |him |with |numerous |motor |and |sensory|deficits. |These |deficits |are
16. |most |likely |the |result |of |which |of |the |following |mechanisms |of |cell |injury?



A) Free |radical |injury
B) Hypoxia |and |ATP |depletion
C) Interference |with |DNA |synthesis
D) Impaired |calcium |homeostasis
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