Cell injury, death and adaptation Dr Heyam Awad FRCPath

Pathology 1 for dentistry Coordinator : Dr Heyam Awad Email: h_awad@ju.edu.jo 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 structure CELL DAMAGE 4 LECTURES Dr HEYAM AWAD INFLAMMATION DR MAHA SHOMAF AMYLOIDOSIS I LECTURE DR FATIMA OBAIDAT HEALING AND REPAIR 2 LECTURES DR TAREK AL ODALY NEOPLASIA 5 LECTURES RESPIRATORY SYSTEM DR FATIMA OBEIDAT CIRCULATORY SYSTEM 3 LECTURES DR NISREEN ABU SHAHIN BLOOD VESSELES HEART BLOOD

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.