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Pathophysiology Final Cumulative Exam
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Multifactorial, Idiopathic, Iatrogenic, Congenital, Degenerative, Immunologic, Infectious, Inherited, metabolic, neoplastic, Nutritional, Physical Agent Induced, Psychogenic Etiology Asymptomatic Period of time between exposure and appearance of signs and symptoms Latent Period First signs and symptoms appear Prodromal Period Disease process is established Patient functions normally due to compensatory mechanisms Subclinical Stage Peak Severity of Signs and symptoms Acute Phase Sudden increase in severity of signs/symptoms/disease Exacerbation
Decline in severity. Considered permanent if more than 5 years Remission Stage of recovery after injury/disease/surgery Convalescence Subsequent pathological condition associated with a disease Sequela New, separate process resulting from a pathological change caused by the original disease Complication The study of patterns of disease involving sample populations Epidemiology Native to a local region Endemic disease Spreads to many individuals at the same time Epidemic Spreads to large geographic areas
Increased cell mass and functional capacity in response to excess stimulation Hypertrophy Increased cell number causing an increase in functional capacity Hyperplasia Conversion of one differentiated cell type to another, in order to better tolerate an injurious stimulus Metaplasia Disorderly cell growth: abnormal variations in size, shape, arrangement Referred to as "Pre-neoplastic lesions" Dysplasia Characterized by shrunken (pyknotic) nucleus that is later degraded (karyolysis), swollen cell volume, disrupted plasma and organelle membranes, and spilling of contents into ECF Necrosis Most common type of necrosis Process triggered by ischemia and resulting in plasma membrane and nuclear structure degradation Coagulative (A) Necrosis
Rapid dissolution of dead cells forms a liquefied area composed of lysosomal enzymes and dissolved tissue, resulting in an abscess or cyst Liquefactive (B) Necrosis Release of excess digestive enzymes triggers a process resulting in the death of adipose tissue General causes: trauma, pancreatitis Macroscopic: chalky, white area (saponification) Fat Necrosis (C) Partially degraded dead cells walled off from surrounding tissue by inflammatory white blood cells General causes: tuberculosis Macroscopic: white, soft, friable (cottage cheese) Caseous Necrosis (D) Cellular necrosis affecting a large area. Due to interruption of major blood supply Gangrene Form of coagulative necrosis; Blackened, wrinkles tissue; Clearly demarcated from healthy tissue; extremities Dry Gangrene Form of liquefactive necrosis;
interrupts tissue perfusion, causing disruption in oxygen and nutrient supply, as well as accumulation of waste products causes more injury than hypoxia alone At the cellular level ischemia reduces ATP needed for Na-K pump, causing compensatory increase in anaerobic glycolysis which leads to lactic acidosis Ischemia is reversible in initial stages, until disruption of plasma, mitochondrial and lysosomal membrane damage cause cell death Ischemia Caused by: ischemia*, heart/lung disease and RBC disorders Hypoxia two identical linear chromosome units which separate during meiosis Chromatids point at the centre of X where 2 sister chromatids fuse Centromere human chromosomes exist in homologous pairs with unique DNA sequences, one chromosome from each parent Diploid no clear dominant/recessive alleles, traits combine Codominant
interaction of single gene locus Monogenic interaction of multiple gene loci, heritable, unpredictable, affected by environmental factors Polygenic single base pair substitution, results in affected codon to code an abnormal amino acid Point mutation addition/removal of 1 or more bases, change reading frame (all codons change downstream of mutation), dramatic change to amino acid sequence Frameshift mutation DNA mutation coding for particular protein Mendelian single-gene disorders segment loss/gain/translocation advanced maternal or paternal age, abnormalities in parental chromosome structure Chromosomal abberations ...
No lost genetic material, increased risk of producing abnormal gametes Reciprocal Translocation Exchange one long chromatid arm for a short one Robertsonian Translocation sister chromatids separate incorrectly at centromere Isochromosomes Deleted Fragments- No centromere Cancer forming Deletions Forms a ring; Fragments left over Ring Chromosomes Genetic material swapped on the same side of the centromere Paracentric Inversion Genetic material swapped on opposite sides of the centromere Pericentric Inversion
Duplicated genetic material Duplications Trisomy 21 Down Syndrome Extra chromosome 21 Most common monochromosomal disorder Leading cause of mental retardation Majority of fetuses are either stillborn or aborted Down Syndrome Patau Syndrome Trisomy 13 Edwards Syndrome Trisomy 18 Cri du Chat Syndrome Chromosome 5 1 or more extra X chromosomes: XXY,XXXY
gain-of-function mutation Proto-oncogene overactive proto-oncogene Oncogenes loss-of-function mutation Rb gene, p53, BRCA-1/BRCA- 2 Tumor Suppressor gene inappropriately activate proto-oncogenes and inactivate tumor suppressor genes Proliferation Carcinogens Initiation Mutant cell proliferation Results from: activation of other oncogenes, inactivation of tumor suppressor genes Promoters: nutritional factors, infections, hormones Promotion Proliferating, mutant cells begin to exhibit malignant behavior Cells whose phenotype gives them a growth advantage proliferate more readily
Most malignant cells synthesize telomerase to repair chromosomal telomere, thereby achieving immortality Progression Process whereby cancer cells migrate from tissue of origin to form new malignant cell colonies in distant sites Enzymes digest basement membranes to allow movement through the membranes Metastasis Advanced malignant tumors form new blood vessels to maintain oxygen and nutrient supply for continual growth Angiogenesis B cells - > Plasma Cells, T cells, NK cells Lymphocytes Basophils, Eosinophils, Neutrophils, Mast cells, Monocytes, Macrophages, Dendritic cells Phagocytes Transport O2 & CO Erythrocytes RBC Initiate Blood Clotting
Antimicrobial/antiviral Acute phase reactants Complement cascades and components TNF (tumor necrosis factor), IFN (interferon), opsonins Plasma proteins Rubor (Red) Dolor (Pain) Calor (Heat) Tumor (Swelling) Functio Laesa (Loss of Function) Cardinal Signs of Inflammation Tissue ischemia (as what type of cause of inflammation) Endogenous Causes of Inflammation Physical agents: burns, radiation Chemical agents: acids, corrosives Microbial: most common, gram negative bacteria endotoxins/LPS, exotoxins Exogenous Causes of Inflammation Short duraion: less than 2 weeks Discrete set of events Acute Inflammation
Longer duration Diffuse Can result in scar tissue and deformity Chronic Substance capable of eliciting a humoral or cellular immune response Immunogen Protein that stimulates antibody production Binds to produced antibody: Ag-Ab complex Epitope: specific site on Ag where antibody/T cell receptor bind Antigen Major immunoglobulin in blood 4 subclasses IgG Largest Immunoglobulin IgM Secretory Present in Body Fluids (Tears, Saliva, etc) 2 subclasses
From bone marrow stem cell, migrate to thymus and become immature T cells Immature T cells undergo positive and negative selection T cells encounter specific antigen and become activated Cell Mediated Immune Response IgM antibody appears upon first exposure to antigen, then IgG Primary Immune Response Follows re-exposure to the same antigen Larger quantity of IgG Shorter response time, and longer lasting due to memory cells Secondary Immune Response Damage to a single organ (Hashimoto thyroiditis) Organ Specific Autoimmune Disease Auto-Ab damage multiple organ systems (Lupus) Systemic Autoimmune DIsease Present at birth Genetic: Spontaneous mutation or inherited Most defects are minor or subclinical Congenital (Primary) Immunodeficiency Disorder
HIV/AIDS
Acquired (Primary) Immunodeficiency Disorder Severe Combined Immunodeficiency (SCID) B and T cell Combined (Primary) Immunodeficiency Disorder DiGeorge syndrome T Cell (Primary) Immunodeficiency Disorders IgA Deficiency B Cell ( Primary) Immunodeficiency Disorders Disorders of Phagocytes and Complement Defiencies (Primary) Immunodeficiency Disorders Etiological Factors: Physical, Psychosocial, Nutritional, Environmental, Pharmacological Usually Transient Not present at birth (Secondary) Immunodeficiency Disorders HIV: Retrovirus, Gains access to infect CD4 lymphocytes, result in cell death, STD, Causes AIDS
