Cell injury, death and adaptation

Dr Heyam AwadFRCPath

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 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.