Pathophysiology Exam 1 Learning Objectives
Distinguish exocytosis, endocrine signaling, paracrine signaling, and autocrine signaling - ANSWER
Exocytosis - intracellular trafficking of proteins for secretion
Endocrine signaling - intercellular signaling for DISTANT signaling with release of hormones into
bloodstream for downstream targets
Paracrine signaling - intercellular signaling for LOCAL signaling on nearby cells common in
inflammatory reactions with release of cytokines and others
Autocrine signaling - intercellular signaling for LOCAL signaling within SAME cell with release of
cytokines and others
Distinguish the terms etiology, pathogenesis, morphological outcome and clinical significance -
ANSWER Etiology - WHY a disease arises including genetic and environmental components
Pathogenesis - HOW a disease arises
Morphological outcome - structural changes in a cell/tissue leading to disease outcome
Clinical significance - clinical relevance and how much a new finding will affect how provider treats a
patient's condition
Distinguished atrophy, hypertrophy, hyperplasia, dysplasia and metaplasia. - ANSWER all cellular
adaptations to stress but result in cell survival with some decrease in function
atrophy - decrease in cell size usually due to decreased nutrient supply or disuse
hypertrophy - increased size of cell or organ, organelle number
hyperplasia - increased number in cells
metaplasia - conversion of cell type
,physiological hypertrophy - ANSWER due to increased WORKLOAD
non-dividing striated muscle in exercise - increase in size in individual muscle fibers to meet
increased demand
uterine smooth muscle in response to hormonal stimulation - non pregnant v pregnant
pathological hypertrophy - ANSWER workload imbalance - increased systemic resistance causing HTN
or increase in venous return
response to injury/infection - cardiac valve disease causing hypertrophic left ventricle
genetic - hypertrophic cardiomyopathy
pathological hyperplasia - ANSWER seen in prostate
increase in cell number and size of prostate - may lead to prostate cancer
dysplasia - ANSWER abnormal change in size and shape of cells, disorganized replacement and
increased risk for neoplastic event
Distinguish the concepts of homeostasis and cellular adaptation - ANSWER homeostasis - cell
constantly adjusting structure and function to accommodate changing demands and extracellular
stress in order to maintain a steady state
cellular adaptation - when cells are exposed to physiological stress or injurious stimuli - achieve NEW
steady state to preserve viability and function
if too much external stress -- cell injury may occur
within certain limits, injury can be REVERSIBLE and homeostasis restored
,if stress too severe or persistent - IRREVERSIBLE injury and cell death
Distinguished necrosis and apoptosis by causes in morphological features - ANSWER Necrosis - rapid
and uncontrollable form of cell death, indication of pathological process
morphology - coagulative, liquefactive, gangrenous, caseous, fat
Apoptosis - choreographed set of molecular pathways activated that result in cell death, may not be
indication of pathological process (occurs in healthy cells too)
morphology - intrinsic and extrinsic pathways, cell size decreases, condensation of chromatin with
fragmentation of nuclear DNA, formation of membrane bound apoptotic bodies, phagocytosis
Distinguish ischemia from hypoxia. Identify their common feature - ANSWER Ischemia - reduced
blood supply, oxygen deficiency and supply of nutrients
hypoxia - oxygen deficiency
common feature - oxygen deficiency to cells and tissue
Distinguish oxidative stress from oxidative phosphorylation - ANSWER oxidative stress - cellular
damage induced by accumulation of ROS
oxidative phosphorylation - process of production of ATP from redox reaction in the ETC in order for
cells to perform their normal metabolic functions
Explain how excess free radical production can cause deleterious effects on the mitochondria and
plasma membrane - ANSWER PEROXIDATION of the membrane - chain reaction where production of
free radicals causes more free radical production
Mitochondria - decreased ATP production, decreased energy dependent functions leading to cellular
injury and necrosis
, Membranes - damage to lysosomal membranes (leakage of enzymes), damage to plasma membrane
(impaired transport functions, leakage of cellular contents) both leading to necrosis
free radical - ANSWER A species with an unpaired electron causing them to be unstable and readily
interact with nucleic acids, proteins, and lipids
Identify and explain 4 distinct causes of cellular injury - ANSWER ischemia, toxins, infections,
immunologic reactions, genetic, nutritional imbalances, aging
ISCHEMIA/HYPOXIA - ATP depletion, loss of cellular homeostasis as enzymes and pumps cannot
function
FREE RADICAL PRODUCTION - attacking nucleic acids, proteins, and lipids via peroxidation
CALCIUM DISRUPTION - calcium levels kept low intracellularly by pumps in plasma membrane and
mitochondria/ER within cell - INFLUX or EFLUX into cytoplasm causes enzyme activation (ATPase,
phospholipases, proteases, endonucleases)
MEMBRANE PERMEABILITY - ATP depletion, Na/K pumps leading to OSMOTIC IMBALANCE - cellular
swelling
Identify four types of enzymes affected by disruption of calcium homeostasis - ANSWER ATPase - ATP
degradation
phospholipase - membrane damage at bilayer
proteases - membrane damage and cytoskeletal damage
endonucleases - nuclear damage and cleaving DNA
What are the two sources of increased cytoplasmic calcium that lead to intercellular injury - ANSWER
Intracellular stores - mitochondria or ER
Extracellular stores into cytoplasm - from increased membrane permeability/injury to membrane
Identify 3 enzymes that promote free radical production and three agents that scavenge free
radicals or decrease their production - ANSWER PROMOTE - phagocyte oxidase, myeloperoxidase,
superoxide dismutase
Distinguish exocytosis, endocrine signaling, paracrine signaling, and autocrine signaling - ANSWER
Exocytosis - intracellular trafficking of proteins for secretion
Endocrine signaling - intercellular signaling for DISTANT signaling with release of hormones into
bloodstream for downstream targets
Paracrine signaling - intercellular signaling for LOCAL signaling on nearby cells common in
inflammatory reactions with release of cytokines and others
Autocrine signaling - intercellular signaling for LOCAL signaling within SAME cell with release of
cytokines and others
Distinguish the terms etiology, pathogenesis, morphological outcome and clinical significance -
ANSWER Etiology - WHY a disease arises including genetic and environmental components
Pathogenesis - HOW a disease arises
Morphological outcome - structural changes in a cell/tissue leading to disease outcome
Clinical significance - clinical relevance and how much a new finding will affect how provider treats a
patient's condition
Distinguished atrophy, hypertrophy, hyperplasia, dysplasia and metaplasia. - ANSWER all cellular
adaptations to stress but result in cell survival with some decrease in function
atrophy - decrease in cell size usually due to decreased nutrient supply or disuse
hypertrophy - increased size of cell or organ, organelle number
hyperplasia - increased number in cells
metaplasia - conversion of cell type
,physiological hypertrophy - ANSWER due to increased WORKLOAD
non-dividing striated muscle in exercise - increase in size in individual muscle fibers to meet
increased demand
uterine smooth muscle in response to hormonal stimulation - non pregnant v pregnant
pathological hypertrophy - ANSWER workload imbalance - increased systemic resistance causing HTN
or increase in venous return
response to injury/infection - cardiac valve disease causing hypertrophic left ventricle
genetic - hypertrophic cardiomyopathy
pathological hyperplasia - ANSWER seen in prostate
increase in cell number and size of prostate - may lead to prostate cancer
dysplasia - ANSWER abnormal change in size and shape of cells, disorganized replacement and
increased risk for neoplastic event
Distinguish the concepts of homeostasis and cellular adaptation - ANSWER homeostasis - cell
constantly adjusting structure and function to accommodate changing demands and extracellular
stress in order to maintain a steady state
cellular adaptation - when cells are exposed to physiological stress or injurious stimuli - achieve NEW
steady state to preserve viability and function
if too much external stress -- cell injury may occur
within certain limits, injury can be REVERSIBLE and homeostasis restored
,if stress too severe or persistent - IRREVERSIBLE injury and cell death
Distinguished necrosis and apoptosis by causes in morphological features - ANSWER Necrosis - rapid
and uncontrollable form of cell death, indication of pathological process
morphology - coagulative, liquefactive, gangrenous, caseous, fat
Apoptosis - choreographed set of molecular pathways activated that result in cell death, may not be
indication of pathological process (occurs in healthy cells too)
morphology - intrinsic and extrinsic pathways, cell size decreases, condensation of chromatin with
fragmentation of nuclear DNA, formation of membrane bound apoptotic bodies, phagocytosis
Distinguish ischemia from hypoxia. Identify their common feature - ANSWER Ischemia - reduced
blood supply, oxygen deficiency and supply of nutrients
hypoxia - oxygen deficiency
common feature - oxygen deficiency to cells and tissue
Distinguish oxidative stress from oxidative phosphorylation - ANSWER oxidative stress - cellular
damage induced by accumulation of ROS
oxidative phosphorylation - process of production of ATP from redox reaction in the ETC in order for
cells to perform their normal metabolic functions
Explain how excess free radical production can cause deleterious effects on the mitochondria and
plasma membrane - ANSWER PEROXIDATION of the membrane - chain reaction where production of
free radicals causes more free radical production
Mitochondria - decreased ATP production, decreased energy dependent functions leading to cellular
injury and necrosis
, Membranes - damage to lysosomal membranes (leakage of enzymes), damage to plasma membrane
(impaired transport functions, leakage of cellular contents) both leading to necrosis
free radical - ANSWER A species with an unpaired electron causing them to be unstable and readily
interact with nucleic acids, proteins, and lipids
Identify and explain 4 distinct causes of cellular injury - ANSWER ischemia, toxins, infections,
immunologic reactions, genetic, nutritional imbalances, aging
ISCHEMIA/HYPOXIA - ATP depletion, loss of cellular homeostasis as enzymes and pumps cannot
function
FREE RADICAL PRODUCTION - attacking nucleic acids, proteins, and lipids via peroxidation
CALCIUM DISRUPTION - calcium levels kept low intracellularly by pumps in plasma membrane and
mitochondria/ER within cell - INFLUX or EFLUX into cytoplasm causes enzyme activation (ATPase,
phospholipases, proteases, endonucleases)
MEMBRANE PERMEABILITY - ATP depletion, Na/K pumps leading to OSMOTIC IMBALANCE - cellular
swelling
Identify four types of enzymes affected by disruption of calcium homeostasis - ANSWER ATPase - ATP
degradation
phospholipase - membrane damage at bilayer
proteases - membrane damage and cytoskeletal damage
endonucleases - nuclear damage and cleaving DNA
What are the two sources of increased cytoplasmic calcium that lead to intercellular injury - ANSWER
Intracellular stores - mitochondria or ER
Extracellular stores into cytoplasm - from increased membrane permeability/injury to membrane
Identify 3 enzymes that promote free radical production and three agents that scavenge free
radicals or decrease their production - ANSWER PROMOTE - phagocyte oxidase, myeloperoxidase,
superoxide dismutase
