Transcript PM2_May2010
Pathophysiology: Introduction to Basic Pathology Lecture 1 Dr. Karen Ronquillo Premed 2 Basic Pathophysiology Basic Pathology Basic Microbiology Bacteriology Virology Mycology Immunology Basic Pharmacology What is Pathology? Pathology Branch of Medicine “suffering’ Studies the underlying causes of diseases “etiology” Mechanisms that result in the signs and symptoms of the patient “pathogenesis” Pathology Bridge between basic science and clinical practice Divisions: General Pathology Systemic Pathology The Cell How do cells react to environmental stress? Hypertrophy Hyperplasia Aplasia Hypoplasia Atrophy Metaplasia Hypertrophy Increase in protein synthesis/ organelles Increase in size of cells Increase in organ/tissue size Hypertrophy Hyperplasia Increase in NUMBER of cells Increase in size of organ/tissue Similar end result as hypertrophy May occur with hypertrophy Hyperplasia Aplasia Failure of cell production Agenesis or absence of an organ:fetus Loss of precursor cells:adults Technetium: scintigraphy Aplasia Hypoplasia Decrease in cell production Atrophy Decrease in mass of preexisting cells Smaller tissue/organ Most common causes: disuse poor nutrition lack of oxygen lack of endocrine stimulation aging injury of the nerves Atrophy Metaplasia Replacement of one tissue by another tissue Several forms: Squamous metaplasia Cartilaginous metaplasia osseous metaplasia myeloid metaplasia Metaplasia Squamous to columnar change in cells Barrett’s esophagus What are the causes of injury/stress? Hypoxic cell injury Free radical injury Chemical cell injury Hypoxic cell injury Complete lack of oxygen/ decreased oxygen Anoxia or hypoxia Causes: ischemia anemia carbon monoxide poisoning decrease tissue perfusion poorly-oxygenated blood Hypoxic cell injury Early stage Hypoxic cell injury Decrease in production of ATP Changes in cell membrane Cellular swelling endoplasmic reticulum mitochondria Ribosomes disaggregate Failure of protein synthesis Clumping of chromatin Late stage Cell membrane damage myelin blebs cell blebs Cell Death Irreversible damage to the cell membranes Calcium influx Mitochondria calcifies Release of cellular enzymes lab exams for AST, ALT, CKMB, LDH Most vulnerable cells: neurons Cardiac enzymes CKMB kit Free radicals: superoxide and hydroxyl radicals Seen in: normal metabolism oxygen toxicity ionizing radiation UV light drugs/chemicals ischemia What will neutralize free radicals? Mechanisms to detoxify free radicals Glutathione Catalase Superoxide dismutase Vitamin A, C, E Cysteine, selenium, ceruloplasmin Spontaneous decay Chemical Injury Carbon tetrachloride and liver damage Morphologic patterns of cell death: NECROSIS AND APOPTOSIS Necrosis sum of all the reactions seen in an injured tissue, leads to cell death autolysis – cell’s enzymes Heterolysis – extrinsic factors Types of necrosis Coagulative necrosis Liquefactive necrosis Caseous necrosis Gangrenous necrosis Fibrinoid necrosis Fat necrosis Coagulative necrosis Interruption of the blood supply Poor collateral circulation heart kidney Characteristic nuclear changes Coagulative necrosis Coagulative Necrosis Liquefactive necrosis Interruption of blood supply Enzymes liquefy the tissue Brain Suppurative infections Bacteria Liquefactive necrosis Caseous necrosis Coagulative + liquefactive “cheese - like” Part of granulomatous inflammation Classic picture: Tuberculosis Caseous necrosis Gangrenous necrosis Interuption of the blood supply to the lower extremities or bowels 2 types: 1. Wet type: complicated by liquefactive necrosis 2. Dry type: complicated by coagulative necrosis Gangrenous necrosis types Fibrinoid necrosis Immune-mediated vascular damage Protein – like material in the blood vessel walls Fat necrosis Traumatic fat necrosis: after injury Breast ENZYMATIC FAT NECROSIS: PANCREAS APOPTOSIS “falling away from” Another cell death pattern “Programmed cell death” Removal of cells Prevents neoplastic transformation Necrosis versus apoptosis Gross irreversible cell injury Passive form of cell death Does not require genes, protein synthesis Marked inflammatory reaction Physiologic programmed cell removal Active form of cell death Requires genes, proteins, energy No inflammatory reaction Genes affecting apoptosis Inhibits: bcl-2 Facilitates: bax p53 Morphological features in apoptosis Involves small clusters of cells only No inflammatory cells Cell membrane blebs Cytoplasmic shrinkage Chromatin condensation Phagocytosis of apoptotic bodies Reversible Cellular changes Fatty change Hyaline change Accumulation of exogenous pigments Accumulation of endogenous pigments Pathologic calcifications Fatty change Liver, heart, kidney Accumulation of intracellular parenchymal triglycerides -increased transport -decrease mobilization -decreased use -overproduction Fatty change: LIVER Hyaline change Accumulation of hyaline HYPERTENSION; DIABETES MELLITUS “glassy” appearance Exogenous pigments Lungs carbon silica iron dust Lead – Plumbism Silver - Argyria Endogenous pigments Bilirubin Hemosiderin Lipofuscin “wear and tear” pigment Elderly patients Liver, heart Brown atrophy Pathologic calcifications Previously damages tissues “dystrophic calcification” scarred heart valves Pathologic calcifications Hypercalcemia “metastatic calcification” Question: A young woman was admitted due to a bacterial infection. CT scan showed an abscess in her brain. What type of necrosis would you expect to see? A.coagulative B.Caseous C.Liquefactive Question: A 15 year old girl was brought into your clinic due to painful menses. She also said that her menstrual blood flow was heavy and had clumps of blood clots and tissues.Menstruation is classified as: A. Apoptosis B. Coagulative Necrosis C. Liquifactive Necrosis