Studied by 8 people
plasma membrane
protects the cell by creating a barrier that separates the intracellular components from the extracellular environment; arranged in a bilayer of lipids, proteins, and carbs
cytoplasm
everything inside the plasma membrane except the nucleus; a colloidal substance made of water, proteins, fats, electrolytes, glycogen, and pigments
nucleus
contains DNA for cellular reproduction
cytoskeleton
framework of proteins organized into filaments and tubules that help cell shape, movement, and intracellular transport
endoplasmic reticulum
network of tubules producing proteins and fats
golgiapparatus
membranous structure that prepares substances for the ER for secretion
lysosomes
small sac that digests cellular debris with hydroltic enzymes
peroxisomes
tiny sac (smaller than lysosomes) containing oxidases that neutralizes free radicals
proteasome
breaks down proteins
mitochondria
aerobic respiration; produces ATP
common cellular functions
transportation
ingestion
secretion
respiration
communication
reproduction
passive transport
no energy required
includes:
diffusion
osmosis
facilitated diffusion
movement of substances across the plasma membrane aided by transport proteins
ex. glucose
active transport
requires energy when transporting particles across the plasma membrane, against the concentration gradient
endocytosis
the process used to transport large substances into cells
includes:
pinocytosis
phagocytosis
pinocytosis
process of ingesting contents of small vesicles containing liquid; requires ATP
phagocytosis
the process of ingesting large particles (cells, bacteria, and damaged cell components) by phagocytes
secretion
extracellular release of products
includes:
exocytosis
exocytosis
vesicles move from the golgi apparatus, fuse with the plasma membrane, and empty their contents into the extracellular environment
cellular responses to stress
atrophy
hypertrophy
hyperplasia
metaplasia
dysplasia
atrophy
the decrease in individual cell size due to different reasons
reasons for atrophy
decreased functional demand
immobilization
ischemia
nutritional deprivation
aging
removal of hormonal signals
hypertrophy
an increase in cell size
reasons for hypertrophy
increase in trophic/growth signals
increased demand
strength building exercises
hyperplasia
an increase in cell number
reasons for hyperplasia
hormone signaling
increased workload
metaplasia
the changing of one cell type to another
reasons for hyperplasia
persistent stressors
ex.
GERD
smoking
dysplasia
the actual change in cell size, shape, uniformity, arrangement, and structure; can be the first cancer cells cue to mutations
reasons for dysplasia
chronic and persistent stressors
abnormal differentiation of dividing cells
mechanisms of cell death
apoptosis
necrosis
apoptosis
cellular suicide; programmed cell death prompted by genetic signals and is designed to replace old cells with new ones re
reasons for apoptosis
damaged genetic material
mutation
old cell age (ex. RBC)
attempt to decrease the number of cells
enzyme reactions in the cell
necrosis
a disordered process associated with inflammation; death of cells related to cell injury causing damage to cell structures (mitochondria), decreasing required ATP
ex. pressure injuries or gangrene
causes of cell injury
physical injury
mechanical injury
thermal injury
chemical injury
mechanical cell injury
caused by impact of a body part causing direct injury
ex. falling off a bike
thermal cell injury
temperature, as occurs with burns and frostbite
chemical cell injury examples
endogenous:
when a person has an allergic reaction, toxins are released from within the body, which causes cell damage and associated symptoms.
exogenous:
alcohol, which can damage the cells of the liver with prolonged exposure.
cardiac hypertrophy
hypertrophic cardiac myopathy; a decrease of cardiac muscle that results from excessive workload and functional demand
pathophysiology of cardiac hypertrophy
genetically inherited (primary)
OR
underlying condition causing a increase in ventricular workload (secondary)
increased pressure in pulmonary circulation
HTN
aortic stenosis
stiff ventricles
clinical manifestations of cardiac hypertrophy
asymptomatic
severe limit in function
heart murmur
decreased perfusion (ischemia, angina)
decreased cardiac output
pump failure:
SOB
chest pain
syncope (MARKER FOR SUDDEN DEATH)
irregular rate and rhythm
diagnostic criteria of cardia hypertrophy
12 lead EKG to identify defects at rest
ambulatory Holter EKG to identify arrhythmias at rest
exercise stress testing
genetic testing
HTN testing
treatment of cardiac hypertrophy
Angiotensin converting enzyme (ACE) inhibitors
Angiotensin II receptor blockers (ARBs)
calcium channel blockers
beta blockers
activity restrictions
acromegaly
a condition of hyperplasia prompted by excessive growth hormone stimulation; commonly manifests as abnormal growth of the hands and feet
pathophysiology of acromegaly
secretion of excessive growth hormone from the pituitary gland and secondary increase in growth factor 1 causes exaggerated skeletal and organ growth after growth plate closure
or
adenoma/tumor on the pituitary gland
clinical manifestations of acromegaly
soft tissue swelling
enlarged hands and feet
altered facial features
prominent brow, jaw, and nasal bones
enlarged tongue and lips
increased spacing between teeth
pain and numbness in teeth deepening voice
snoring
skin changes
coarse hair growth
oily appearance
sweating
body odor
altered reproductive functioning
menstrual cycle alterations
impotence
breast discharge
clinical manifestations of acromegaly
pressure on brain tissues and nerves
headaches
impaired vision
altered pituitary function
Diagnostic criteria of acromegaly
elevated IGF-1
measurement of growth hormone
glucose tolerance test
MRI to rule out adenoma
hx and physical
pharmacologic treatment of acromegaly
(designed to decrease the overproduction of IGF-1 and growth hormone)
somatostatin analogs
inhibits growth hormone secretion
dopamine agonists
less effective than somatostatin
acts on the pituitary to decrease growth hormone and IGF-1 secretion
growth hormone agonistis
binds to growth hormone receptors to block endogenous growth hormone
nonpharmacologic treatment of acromegaly
radiation
can be the primary treatment to shrink adenoma
surgery
removal of adenoma
cervical metaplasia and dysplasia
cells of the cervix responding to the hormonal environment, promoting adaptive and maladaptive responses
metaplasia
changing of cell types as a response to environmental stressors d
dysplasia
abnormal growth and disordered differentiation in dividing cells
pathophysiology of cervical metaplasia and dysplasia
cellular adaption of the squamous and columnar epithelia cells in the transformation zone of the cervix
high or low estrogen can cause changes from squamous to columnar and vice versa
epithelial cells respond to stressors and cause dysplastic changes
abnormal growth
disordered differentiation
premature sloughing off
is usually asymptomatic
risk factors of cervical metaplasia and dysplasia
early onset of sexual activity
multiple sex partners (>3)
exposure to HPV
smoking
diagnostic criteria for cervical metaplasia and dysplasia
screening tests
physical
cervical sampling
cervical assessment
diagnostic excisional procedure
Pap smears
HPV screening
diagnostic testing
colposcopy (biopsy of cervical tissue)
treatment of cervical metaplasia and dysplasia
ablation (removal of superficial cells)
cryosurgery
CO2 laser ablation
cold coagulation
electrocoagulation diathermy ablation
hysterectomy
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