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AdvAnced PAthoPhysiology hesi FinAl exAm 2026||||questions And Answers with rAtionAles/grAded A+/2026 uPdAte/100% correct /instAnt downloAd

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AdvAnced PAthoPhysiology hesi

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AdvAnced PAthoPhysiology hesi FinAl exAm 2026||||questions
And Answers with rAtionAles/grAded A+/2026 uPdAte/100%
correct /instAnt downloAd



SECTION 1: CELLULAR AND MOLECULAR FOUNDATIONS (Questions 1-8)




**Question 1**



What organelle produces hydrogen peroxide (H₂O₂) by using oxygen to remove hydrogen atoms
from specific substrates in an oxidative reaction?



A) Lysosomes

B) Peroxisomes

C) Ribosomes

D) Mitochondria



**Answer:** B) Peroxisomes


**Rationale:** Peroxisomes contain oxidative enzymes that remove hydrogen atoms and
combine them with oxygen to produce hydrogen peroxide. This organelle is also involved in the
breakdown of very-long-chain fatty acids and the synthesis of plasmalogens .



---



**Question 2**



In a normal, nonmutant state, an oncogene is referred to as what?



A) Basal cell

B) Target cell

,C) Caretaker gene

D) Proto-oncogene



**Answer:** D) Proto-oncogene


**Rationale:** In its normal state, an oncogene is called a proto-oncogene. Proto-oncogenes are
normal genes that regulate cell growth and differentiation. When mutated or overexpressed, they
become oncogenes that drive uncontrolled cell proliferation. Basal cells are in epithelial tissue;
target cells receive mutations or substances; caretaker genes maintain genomic integrity .



---



**Question 3**



Two "hits" are required to inactivate tumor-suppressor genes because:



A) Each allele must be altered, and each person has two copies of each gene, one from each
parent

B) The first hit stops tissue growth, and the second hit is needed to cause abnormal tissue growth

C) Tumor-suppressor genes are larger than proto-oncogenes, requiring two hits to affect
carcinogenesis

D) The first hit is insufficient to cause enough damage to cause a mutation



**Answer:** A) Each allele must be altered, and each person has two copies of each gene, one
from each parent



**Rationale:** A single genetic event can activate an oncogene (acting dominantly). However,
each person has two copies (alleles) of each tumor-suppressor gene. Both alleles must be
inactivated for the tumor-suppressor function to be lost, following the Knudson two-hit
hypothesis. This explains why hereditary cancer syndromes often involve a germline mutation
(first hit) followed by a somatic mutation (second hit) .



---



**Question 4**

, How do cancer cells use the enzyme telomerase?



A) To repair telomeres to restore somatic cell growth

B) As an intracellular signaling chemical to stimulate cell division

C) To switch off telomerase to enable cells to divide indefinitely

D) To switch on telomerase to enable cells to divide indefinitely



**Answer:** D) To switch on telomerase to enable cells to divide indefinitely


**Rationale:** Cancer cells activate telomerase to restore and maintain their telomeres, allowing
cells to divide indefinitely (immortalization). Normal somatic cells have limited telomerase activity
and undergo replicative senescence after a finite number of divisions. Telomerase activation is a
hallmark of cancer .



---



**Question 5**



What is a consequence of plasma membrane damage to the mitochondria?



A) Enzymatic digestion halts DNA synthesis

B) Influx of calcium ions halts adenosine triphosphate (ATP) production

C) Edema from an influx in sodium causes a reduction in ATP production

D) Potassium shifts out of the mitochondria, which destroys the infrastructure



**Answer:** B) Influx of calcium ions halts adenosine triphosphate (ATP) production


**Rationale:** Mitochondrial membrane damage allows calcium ions to enter the mitochondria,
which impairs oxidative phosphorylation and halts ATP production. This leads to cellular energy
failure and can trigger apoptosis. Calcium overload also opens the mitochondrial permeability
transition pore, releasing pro-apoptotic factors .



---

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