cell injury, death and adaptation dr heyam awad frcpath
TRANSCRIPT
Cell injury, death and adaptation
Dr Heyam AwadFRCPath
Pathology 1 for dentistry
Coordinator : Dr Heyam Awad• Email: [email protected]
• Lectures will be available on my university website on the day they are given.
• Office hours: Monday and Wednesday 10-12 .. Office in hospital 3rd floor.
Course structureCELL DAMAGE 4 LECTURES Dr HEYAM AWAD
INFLAMMATION 4 LECTURES DR MAHA SHOMAF
AMYLOIDOSIS I LECTURE DR FATIMA OBAIDAT
HEALING AND REPAIR 2 LECTURES DR TAREK AL ODALY
NEOPLASIA 5 LECTURES DR MAHA SHOMAF
RESPIRATORY SYSTEM 5 LECTURES DR FATIMA OBEIDAT
CIRCULATORY SYSTEM 3 LECTURES DR NISREEN ABU SHAHIN
BLOOD VESSELES 3 LECTURES DR MAHA SHOMAF
HEART 2 LECTURES DR MAHA SHOMAF
BLOOD 4 LECTURES DR MAHA SHOMAF
EVALUATION
• 2 EXAMS: 40 MARKS FOR THE MIDTERM AND 60 FOR THE FINAL.
• THEORY AND PRACTICAL.
• MIDTERM IN THE WEEK STARTING 8/11• 8/11 – 12/11 NO LECTURES.. MIDTERM WEEK
• LAST LECTURE 22/12
What is pathology?
• Patho… disease• Logy… study
• Pathology = study of disease involves: causes of disease.. Etiology : mechanisms.. pathogenesis :morphological changes.
• Etiology: Origin of disease , underlying causes.
• Pathogenesis: steps in the development of disease…… cellular and molecular changes .• Morphology: macroscopic and
microscopic changes.
Why to study pathology???
Cellular adaptations and cell injury
• Cells maintain a steady state.. Homeostasis.• Stresses .. Adaptation….. New homeostatic state
with preservation of function.• Stress beyond capability of adaptation.. Cell
injury.• Cell injury… reversible within certain limits• Then .. Irreversible…. Ends in cell death.• Two types of cell death: necrosis and apoptosis.
Adaptation
• Hyertrophy• Hyperplasia• Atrophy• metaplasia
Adaptation
• Adaptive changes are reversible.
• Can be physiologic or pathologic.
• Hypertrophy: Increased cell size.• Hyperplasia: increased number of cells.. Cell
division.• Metaplasia: change from one adult cell type
to another• Atrophy: decreased size.
Hypertrophy versus hyperplasia
Hypertrophy
• Increased cell size.• Due to increased organelles and proteins.• Increased intracellular synthesis..
Caused by: increased demands, hormones or growth factors.
Physiologic hypertrophy
• Uterus during pregnancy… due to estrogen• Skeletal muscle… due to increased demand
Physiologic hypertrophy
Pathologic hypertrophy
• Cardiac.. Hypertensive heart disease• Pathogenesis.. Two types of signals:
mechanical: stretch and trophic: growth factors and androgenic hormones
Pathologic hypertrophy
Pathologic hypertrophy
hyperplasia
• Only in tissues that can replicate.• Can be physiologic or pathologic.
Physiologic hyperplasia
• Hormonal: uterus, breast.• Compensatory: after removal or loss of part of
tissue.
Gingival hyperplasia
Pathologic hyperplasia
• Due to excess in hormones or growth factors.• E:g endometrial hyperplasia.• Controlled.. Responds to decreased
stimulation. This differentiates it from cancer
Normal endometrium
Endometrial hyperplasia
atrophy
• Shrinkage in cell size due to loss of cell substance.
Causes • decreased work load.• Loss of innervation• Loss of endocrine stimulation.• Aging
Muscle atrophy
Brain atrophy
Atrophy
• Physiologic: endometrial atrophy during menopause
• Pathologic: loss of innervation.
atrophy
Mechanisms:• Decreased protein synthesis.• Degradation of cellular proteins.• Autophagy…. Literally means self eating.
metaplasia
• Adult cell type replaced by another adult cell type.
• Arise in reprogrammed stem cells to differentiate along a new pathway.
Epithelial metaplasia
• Respiratory epithelium to squamous.• Barrett's mucosa.. Esophegeal squamous to
columnar
Barrett’s mucosa
Normal esophegeal mucosa
Metaplastic, Barrett’s mucosa
Metaplasia in mesenchymal tissue
• Usually pathologic• Ossification of soft tissue due to injury.