Ch. 2 - Altered Cells and TIssues

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