Altered Cell Biology

Pathophysiology
Stephen P. Wood, ACNP, MS
Northeastern University
School of Nursing
2012
 Objectives
Explore and understand cellular adaptation
Explore and understand cellular injury
Explore and understand cell death
Apply this knowledge to the ongoing
understanding of the clinical applications of
pathophysiology
 Cellular Adaptation
Homeostasis optimal conditional for cell to
work.
Greek: hmoios similar, stasis - standing still
Conformers conform to their surrounding.
Regulators
 What are some functions that require
constant adaptation in humans?
Temperature
pH
Heart rate
Blood pressure
Respiratory rate
Vasoconstriction / vasodilation
Metabolism
 Specific Adaptations
Atrophy
Decrease or shrinkage in cell size due to normal
process.
Big thymus gland muscular weakness
Physiologic: Thymus gland
Pathologic: Disuse
 Specific Adaptations
Pathologic decrease protein production and increase protein
catabolism.
Disuse An arm in a cast for 6 weeks
Loss of nourishment.
When this happen, the cells will get tagged for catabolism with a
protein called ubiquitin.
Decrease in ER and mitochondria
Mechanism: production, catabolism
Ubiquitin- proteosome pathway
Tag cell as disfx and this tag will recognize by a proteosome, contain
enzymes proteases, and break down the protein. Then lead to atropy.
Autophagy catabolic process using lysosome (contain enzyme,
tightly regulated)
Breaking down the extra tissues/web between fetal hands and toes
 Special Adaptations
Hypertrophy
Increase in cell size
Increase in the protein constituents
Mechanical Signals increase the size of the contract
protein (body building)
Trophic Signals hormonal signal release of hormone
to increase the uterine size during pregnancy.
Pathological hypertension, heart must contract with
greater force and overtime can lead to ventricular
hypertrophy, increasing the myocyte of the blood cell,
making it less effective.
 Special Adaptations
Hyperplasia
Increased number of cells
Response to injury, chronic inflammation, hormonal signal.
Increase mitosis
Compensatory
Liver can regenerate loss tissues with 2 mechanism using
hyperplasia mitogyn which induce hyperplasia
Hormonal
Indomitual hyperplasia responding to excess estrogen and
causes thicken of the indomituent, lining between the uterus.
Cause pain and trouble with fertility.
Pathologic
Benign prostate hyperplasia.
 Special Adaptations
Dysplasia
Immature cells
Abnormal size, shape or arrangement
Anisocytosis (cells of unequal size)
Poikilocytosis (abnormally shaped cells)
Hyperchromatism (excessive pigmentation)
Presence of mitotic figures (an unusual number of
cells which are currently dividing)
 Special Adaptations
Myelodysplastic disorders
Increased development of ineffective myeloid
(RBC) cells
Hematopoiesis is ineffective
Chem exposure, genetic exposure.
Signs and Symptoms
Pathophysiology
Spleen will take up this ineffective cell anemia
(enlargement of the spleen due to taking up the cell)
Can lead to leukemia.
 Special Adaptations
Metaplasia
Replacing one tissue type with another
Response to physical or pathologic stress
Cigarette smoke
Barrets Esophagitis acid exposure, inflammatory
response activate the the change of cell.
Overview
 Cell Injury
Inability to maintain homeostasis
Reversible recover from the response.
Irreversible
Chemicals cytotoxic, venom.
Hypoxia lack of O2
Angina
MI cell death
Free radicals extra e-, can attack other molecule
Herpes -> disrupt and destroy the cell.
Infectious
Mechanical
Genetic
Metabolic
 Cell Injury: General Mechanisms
Hypoxia
Lack of oxygen
Ischemia
Anoxia
Cascade
 Cell Injury: General Mechanisms
Oxidative stress
Free Radicals (unshared e-, very reactive)
Reactive oxygen species
Target mitochrondria (production of ATP)
Formation
Antioxidants
Target
Example: Acetaminophen Toxicity
 Cell Injury: General Mechanisms
Chemicals
Direct damage Cyanide blocks e- transports.
Exaggerated response Cytokine storm
Citokine signaling molecule induce inflammation.
Metabolites Acetaminophen
Liver usually metabolize it to a non-toxic substrate so
you can urine it out. OD, metobolic pathway will
change, and can lead to damage to liver cell.
Hypersensitivity Bactrim (antibiotic) serum
sickness, joint ache, high fever and rash.
 Cell Injury: Manifestations
Cellular swelling
Lipids and Carbohydrates fatty lipids
Glycogen inability to synthesize glycogen.
Protein synthesis disruption.
Proteins
Pigments hyperpigmentation due to cell
injury or cell death
 Cell Death
Irreversible loss of plasma membrane integrity
Necrosis sum of cellular changes,
ischemia/trauma/infectious process. Mitochrondria
swelling, and lysosome will disrupt.
Apoptosis normal finger and toes apoptosis in fetal.
Signal inhibit apoptosis or signal trigger apoptosis
Mitochrondrai injury, disrupting membrane. Release
smdacs (caspases) from mitochrondral. Smdacs bind to
IAPs (protect the cells, inhibit apoptosis) and deactivate
them and activate apoptosis.
Somatic death
Questions?