NUR 301 EXAM 1 2026/2027 – COMPREHENSIVE STUDY GUIDE, PRACTICE
QUESTIONS & EXAM REVIEW
How the cell can adapt: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia etc - ANS ✔✔-atrophy:
decreased size of cell from disuse, denervation, decreased hormones, malnutrition, and decreased blood
flow- results in decreased O2 consumption, decreased protein synthesis and increased catabolism
-hypertrophy: cell size increases and so does organs from muscle experiencing increased work,
hypertension, uterus increases in pregnancy
-hyperplasia: increased number of cells, response to injury or cell death, often with hypertrophy
-metaplasia: conversion to a simpler type of cell, less specialized, loses functions, reversible if stressors
removed
-dysplasia: deranged cell growth, abnormal size shape and organization, precursor to malignancy
·Multiple ways a cell can be injured - ANS ✔✔-reversible, irreversible, chemical, infection, genetic,
nutrition, physical agents
·Apply knowledge of how hypoxia is detrimental to the cells of the body- understand the physiological
process of hypoxia - ANS ✔✔-no oxygen=no ATP
-caused from: decreased oxygen in the air, decreased hemoglobin, respiratory or cardiac disease,
decreased blood supply, cells cannot use ATP (ischemia)
·Substances that are manifestations on cellular injury - ANS ✔✔-infiltrates: normal substances produced
in excess or at increased rate- lipids, proteins, carbs, calcium, pigments-builds up in cytoplasm and
accumulates by inhalation, ingestion, and infection
·Types of cellular death (necrosis) - when and where do you see it manifest? What role does ischemia
play in its development? - ANS ✔✔-coagulative: most common, cause ischemia, hypoxic injury, tissue
firm and swollen like cooked egg-ex: kidney and heart d/t increased blood supply
-liquefactive: brain and nerve cell, cells digested by own digestive enzymes, tissue softens and liquefies,
usually walled off by normal tissue is an abscess- bacterial infection
-caseous: coagulation and liquefactive combined, inflammatory response walled off in tubercle (mostly
from TB)
-fat: breast and pancreas, lipase releases free fatty acids, enzymes leak out and dissolve triglycerides,
tissue is opaque and chalky
·Types of gangrene- when and where do you see it manifest? How does gangrene differ from necrosis? -
ANS ✔✔-dry: caused by coagulative necrosis, mostly extremities, skin dry wrinkled and dark brown, line
of demarcation, few systemic symptoms
-wet: liquefaction usually with internal organs, no line of demarcation, severe systemic symptoms, tissue,
moist, black, and swollen pus
-gas: anaerobic organism (clostridium in soil), common after traumas and open fractures, bacteria
produce toxin
Distribution of extracellular & intracellular fluid - ANS ✔✔-Intracellular fluid (within cells) is
approximately 40% of the total body weight.
, -The extracellular (outside the cells) fluid comprises approximately 20% of total body weight and further
subcategorizes as plasma at approximately 5% of body weight and interstitial space which is
approximately 12% of body weight.
What are the roles of antidiuretic hormone (ADH) and aldosterone- when are they activated, what
electrolytes are affected? - ANS ✔✔-ADH: produced in the hypothalamus and is released by the
pituitary, it stimulates the reabsorption of water in kidney tubules (increases plasma osmolarity)
decrease in urinary output
-aldosterone: stimulated by fluid deficit, circulating blood volume, concentration of N+ and K+ (RAAS
system)
Review osmosis and diffusion - these are passive fluid transportation - ANS ✔✔-osmosis: movement of
water across a semi-permeable membrane from lesser to greater concentration of particles
-diffusion: movement of particles from greater to lesser concentration if cell membrane is permeable
Active transport involves the Na/K pump... understand what happens when this breaks down - ANS
✔✔NA/K uses active transport to move molecules from high to low (Na in and K out) powered by ATP- if
broke cell would stop working
Net Filtration Hydrostatic & Oncotic pressure - ANS ✔✔-hydrostatic pressure push fluids and electrolytes
out of vessels to cells (arterial end is higher mm)
-oncotic pressure: balanced by hydrostatic, pressure pulls fluids and electrolytes from cell back into
vessels- plasma proteins
Fluid deficit and overload (Dehydration & overhydration): who is at risk, what are the clinical
manifestations, and lab interpretations - ANS ✔✔-dehydration:
a. causes vommiting, nausea, diarrhea, and fluid intake, gastric suction, and hemorrhage
b. s/s: tachycardia, weak pulse, irritability, restless, thirst, weight loss, dry mucus membranes, oliguria
c. lab tests: increased hemoglobin, hematocrit, sodium, and BUN (serum concentration)
-overhydration:
a. causes: polydipsia, kidney failure, CHF, third spacing fluid, diet high in NA, loss of plasma protein
b. s/s: bounding pulse, hypertension, neck vein distention, polyuria, edema, short of breath, weight gain
c. lab tests: decreased hemoglobin, hematocrit, sodium, BUN
Edema: Causes, clinical manifestations & types - ANS ✔✔-causes increased capillary pressure
(hydrostatic), decreased colloidal osmotic pressure (Oncotic), increased capillary permeability, and
obstructive of loss lymphatic flow
-life threatening in brain, larynx, or lungs
Electrolytes: Na, Cl, K, Ca, Phos & Mg (know function, normal lab values, regulation, clinical
manifestations of being too high or too low) - be able to recognize in scenarios that are provided - ANS
✔✔LOOK AT WORD DOC
Acid/Base Balance: know normal values - ANS ✔✔-ph (7.35-7.45)
-Pa (35 to 45)
-HCO3 (21 to 28)
Acid/Base regulators:
QUESTIONS & EXAM REVIEW
How the cell can adapt: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia etc - ANS ✔✔-atrophy:
decreased size of cell from disuse, denervation, decreased hormones, malnutrition, and decreased blood
flow- results in decreased O2 consumption, decreased protein synthesis and increased catabolism
-hypertrophy: cell size increases and so does organs from muscle experiencing increased work,
hypertension, uterus increases in pregnancy
-hyperplasia: increased number of cells, response to injury or cell death, often with hypertrophy
-metaplasia: conversion to a simpler type of cell, less specialized, loses functions, reversible if stressors
removed
-dysplasia: deranged cell growth, abnormal size shape and organization, precursor to malignancy
·Multiple ways a cell can be injured - ANS ✔✔-reversible, irreversible, chemical, infection, genetic,
nutrition, physical agents
·Apply knowledge of how hypoxia is detrimental to the cells of the body- understand the physiological
process of hypoxia - ANS ✔✔-no oxygen=no ATP
-caused from: decreased oxygen in the air, decreased hemoglobin, respiratory or cardiac disease,
decreased blood supply, cells cannot use ATP (ischemia)
·Substances that are manifestations on cellular injury - ANS ✔✔-infiltrates: normal substances produced
in excess or at increased rate- lipids, proteins, carbs, calcium, pigments-builds up in cytoplasm and
accumulates by inhalation, ingestion, and infection
·Types of cellular death (necrosis) - when and where do you see it manifest? What role does ischemia
play in its development? - ANS ✔✔-coagulative: most common, cause ischemia, hypoxic injury, tissue
firm and swollen like cooked egg-ex: kidney and heart d/t increased blood supply
-liquefactive: brain and nerve cell, cells digested by own digestive enzymes, tissue softens and liquefies,
usually walled off by normal tissue is an abscess- bacterial infection
-caseous: coagulation and liquefactive combined, inflammatory response walled off in tubercle (mostly
from TB)
-fat: breast and pancreas, lipase releases free fatty acids, enzymes leak out and dissolve triglycerides,
tissue is opaque and chalky
·Types of gangrene- when and where do you see it manifest? How does gangrene differ from necrosis? -
ANS ✔✔-dry: caused by coagulative necrosis, mostly extremities, skin dry wrinkled and dark brown, line
of demarcation, few systemic symptoms
-wet: liquefaction usually with internal organs, no line of demarcation, severe systemic symptoms, tissue,
moist, black, and swollen pus
-gas: anaerobic organism (clostridium in soil), common after traumas and open fractures, bacteria
produce toxin
Distribution of extracellular & intracellular fluid - ANS ✔✔-Intracellular fluid (within cells) is
approximately 40% of the total body weight.
, -The extracellular (outside the cells) fluid comprises approximately 20% of total body weight and further
subcategorizes as plasma at approximately 5% of body weight and interstitial space which is
approximately 12% of body weight.
What are the roles of antidiuretic hormone (ADH) and aldosterone- when are they activated, what
electrolytes are affected? - ANS ✔✔-ADH: produced in the hypothalamus and is released by the
pituitary, it stimulates the reabsorption of water in kidney tubules (increases plasma osmolarity)
decrease in urinary output
-aldosterone: stimulated by fluid deficit, circulating blood volume, concentration of N+ and K+ (RAAS
system)
Review osmosis and diffusion - these are passive fluid transportation - ANS ✔✔-osmosis: movement of
water across a semi-permeable membrane from lesser to greater concentration of particles
-diffusion: movement of particles from greater to lesser concentration if cell membrane is permeable
Active transport involves the Na/K pump... understand what happens when this breaks down - ANS
✔✔NA/K uses active transport to move molecules from high to low (Na in and K out) powered by ATP- if
broke cell would stop working
Net Filtration Hydrostatic & Oncotic pressure - ANS ✔✔-hydrostatic pressure push fluids and electrolytes
out of vessels to cells (arterial end is higher mm)
-oncotic pressure: balanced by hydrostatic, pressure pulls fluids and electrolytes from cell back into
vessels- plasma proteins
Fluid deficit and overload (Dehydration & overhydration): who is at risk, what are the clinical
manifestations, and lab interpretations - ANS ✔✔-dehydration:
a. causes vommiting, nausea, diarrhea, and fluid intake, gastric suction, and hemorrhage
b. s/s: tachycardia, weak pulse, irritability, restless, thirst, weight loss, dry mucus membranes, oliguria
c. lab tests: increased hemoglobin, hematocrit, sodium, and BUN (serum concentration)
-overhydration:
a. causes: polydipsia, kidney failure, CHF, third spacing fluid, diet high in NA, loss of plasma protein
b. s/s: bounding pulse, hypertension, neck vein distention, polyuria, edema, short of breath, weight gain
c. lab tests: decreased hemoglobin, hematocrit, sodium, BUN
Edema: Causes, clinical manifestations & types - ANS ✔✔-causes increased capillary pressure
(hydrostatic), decreased colloidal osmotic pressure (Oncotic), increased capillary permeability, and
obstructive of loss lymphatic flow
-life threatening in brain, larynx, or lungs
Electrolytes: Na, Cl, K, Ca, Phos & Mg (know function, normal lab values, regulation, clinical
manifestations of being too high or too low) - be able to recognize in scenarios that are provided - ANS
✔✔LOOK AT WORD DOC
Acid/Base Balance: know normal values - ANS ✔✔-ph (7.35-7.45)
-Pa (35 to 45)
-HCO3 (21 to 28)
Acid/Base regulators:
