McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
1
Reference
Ch. 1 — Prokaryotes and Eukaryotes — Cellular distinctions and
implications for host defense
Stem
A 68-year-old man with a history of chronic obstructive
pulmonary disease presents with fever, productive cough, and
purulent sputum. Gram stain from sputum shows numerous
neutrophils and a high number of small, staining organisms
without clear nuclear structure. The nurse recognizes a likely
organism type and considers host-cell interaction mechanisms.
Which statement best explains how the organism’s cellular
structure affects host immune response?
Options
A. The organism’s lack of membrane-bound organelles allows
rapid phagosome escape, reducing antigen presentation.
B. The organism’s simple cell wall and lack of nucleus trigger
robust innate immune responses via pattern recognition
,receptors.
C. The organism’s mitochondria produce toxins that inhibit
neutrophil chemotaxis.
D. The organism’s nuclear membrane prevents recognition by
toll-like receptors, evading immune detection.
Correct Answer
B
Rationales
Correct (B): Small organisms lacking a true nucleus and
membrane-bound organelles (prokaryotes) possess conserved
pathogen-associated molecular patterns (PAMPs) such as
lipopolysaccharide/peptidoglycan that are recognized by host
pattern recognition receptors (e.g., TLRs). This activates innate
immunity and neutrophil recruitment, matching the clinical
purulence. Mechanistically, McCance highlights prokaryotic
structural features that stimulate innate responses. This
explains the purulent sputum and neutrophil predominance.
Incorrect (A): Escape from the phagosome can occur with some
bacteria, but it is not due to “lack of membrane-bound
organelles”; the statement misattributes mechanism and
overgeneralizes.
Incorrect (C): Prokaryotes do not have mitochondria; attributing
toxin production to bacterial mitochondria is mechanistically
incorrect.
Incorrect (D): Prokaryotes lack a nuclear membrane—this
,option reverses cause/effect and is inconsistent with TLR
biology described in McCance.
Teaching Point
Prokaryotic PAMPs (e.g., LPS, peptidoglycan) activate innate
immunity via TLRs — early purulence signal.
Citation (Simplified APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
2
Reference
Ch. 1 — Cellular Functions — Homeostasis and adaptive
capacity
Stem
A 52-year-old woman presents with progressive fatigue and
pallor. Labs: Hgb 9.8 g/dL, MCV 72 fL. She reports a lifelong
vegetarian diet without B12 supplementation. Which cellular
functional deficit best explains microcytic anemia in this
context?
Options
A. Impaired mitochondrial oxidative phosphorylation reduces
heme synthesis.
B. Decreased DNA replication in erythroid precursors causes
smaller RBCs.
C. Reduced iron absorption at enterocyte apical membrane
, causing decreased hemoglobin synthesis.
D. Loss of cell-to-cell adhesion in bone marrow
microenvironment causes ineffective erythropoiesis.
Correct Answer
C
Rationales
Correct (C): Microcytic anemia with low MCV typically reflects
impaired hemoglobin synthesis; dietary iron deficiency or
reduced iron absorption at enterocytes limits heme availability.
McCance describes how altered nutrient uptake impairs cellular
functions like hemoglobin production, leading to small,
hypochromic RBCs. This best matches the clinical picture.
Incorrect (A): While mitochondria are important for heme
biosynthesis (succinyl-CoA + glycine step), the stem suggests
dietary deficiency; mitochondrial oxidative phosphorylation
impairment would present with multisystem signs, not isolated
microcytosis.
Incorrect (B): Decreased DNA replication causes macrocytosis
(large RBCs), not microcytosis.
Incorrect (D): Loss of marrow adhesion could impair
hematopoiesis but would more often cause pancytopenia or
marrow failure patterns, not isolated microcytic anemia.
Teaching Point
Microcytic anemia = impaired hemoglobin/heme synthesis —
check iron absorption and stores first.
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
1
Reference
Ch. 1 — Prokaryotes and Eukaryotes — Cellular distinctions and
implications for host defense
Stem
A 68-year-old man with a history of chronic obstructive
pulmonary disease presents with fever, productive cough, and
purulent sputum. Gram stain from sputum shows numerous
neutrophils and a high number of small, staining organisms
without clear nuclear structure. The nurse recognizes a likely
organism type and considers host-cell interaction mechanisms.
Which statement best explains how the organism’s cellular
structure affects host immune response?
Options
A. The organism’s lack of membrane-bound organelles allows
rapid phagosome escape, reducing antigen presentation.
B. The organism’s simple cell wall and lack of nucleus trigger
robust innate immune responses via pattern recognition
,receptors.
C. The organism’s mitochondria produce toxins that inhibit
neutrophil chemotaxis.
D. The organism’s nuclear membrane prevents recognition by
toll-like receptors, evading immune detection.
Correct Answer
B
Rationales
Correct (B): Small organisms lacking a true nucleus and
membrane-bound organelles (prokaryotes) possess conserved
pathogen-associated molecular patterns (PAMPs) such as
lipopolysaccharide/peptidoglycan that are recognized by host
pattern recognition receptors (e.g., TLRs). This activates innate
immunity and neutrophil recruitment, matching the clinical
purulence. Mechanistically, McCance highlights prokaryotic
structural features that stimulate innate responses. This
explains the purulent sputum and neutrophil predominance.
Incorrect (A): Escape from the phagosome can occur with some
bacteria, but it is not due to “lack of membrane-bound
organelles”; the statement misattributes mechanism and
overgeneralizes.
Incorrect (C): Prokaryotes do not have mitochondria; attributing
toxin production to bacterial mitochondria is mechanistically
incorrect.
Incorrect (D): Prokaryotes lack a nuclear membrane—this
,option reverses cause/effect and is inconsistent with TLR
biology described in McCance.
Teaching Point
Prokaryotic PAMPs (e.g., LPS, peptidoglycan) activate innate
immunity via TLRs — early purulence signal.
Citation (Simplified APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
2
Reference
Ch. 1 — Cellular Functions — Homeostasis and adaptive
capacity
Stem
A 52-year-old woman presents with progressive fatigue and
pallor. Labs: Hgb 9.8 g/dL, MCV 72 fL. She reports a lifelong
vegetarian diet without B12 supplementation. Which cellular
functional deficit best explains microcytic anemia in this
context?
Options
A. Impaired mitochondrial oxidative phosphorylation reduces
heme synthesis.
B. Decreased DNA replication in erythroid precursors causes
smaller RBCs.
C. Reduced iron absorption at enterocyte apical membrane
, causing decreased hemoglobin synthesis.
D. Loss of cell-to-cell adhesion in bone marrow
microenvironment causes ineffective erythropoiesis.
Correct Answer
C
Rationales
Correct (C): Microcytic anemia with low MCV typically reflects
impaired hemoglobin synthesis; dietary iron deficiency or
reduced iron absorption at enterocytes limits heme availability.
McCance describes how altered nutrient uptake impairs cellular
functions like hemoglobin production, leading to small,
hypochromic RBCs. This best matches the clinical picture.
Incorrect (A): While mitochondria are important for heme
biosynthesis (succinyl-CoA + glycine step), the stem suggests
dietary deficiency; mitochondrial oxidative phosphorylation
impairment would present with multisystem signs, not isolated
microcytosis.
Incorrect (B): Decreased DNA replication causes macrocytosis
(large RBCs), not microcytosis.
Incorrect (D): Loss of marrow adhesion could impair
hematopoiesis but would more often cause pancytopenia or
marrow failure patterns, not isolated microcytic anemia.
Teaching Point
Microcytic anemia = impaired hemoglobin/heme synthesis —
check iron absorption and stores first.
