Exam 1: Important Words Flashcards
Etiology
Cause of a disease
infectious disease: etiology is infectious organism
Pathogenesis
Biochemical and molecular mechanisms of disease development
Morphology
Appearance of cells/tissue/organs
Clinical features (manifestations)
Functional consequences of morphological changes
Hypoxia
Not enough oxygen
Modes of Cell Death
Necrosis
Signalling
Unregulated (pathological)
Cell breaks down/explodes and contents are released
Spread/damage neighboring cells
Modes of Cell Death
Apoptosis
Multiple
Regulated (physiological)
Cell disassembles and packages contents for phagocytosis
Avoids damage of surrounding cells
Modes of Cell Death
Necroptosis
Regulated necrosis
Modes of Cell Death
Anoikis
Detachment-induced cell death
Modes of Cell Death
Ferroptosis
Iron based cell death
Necrosis
Necrotic Tissue
Loss of nuclei
Breakdown of membranes
Cells have ruptured
Necrosis
Coagulative
Loss of cell architecture but not tissue architecture
Necrosis
Liquefactive
Digestion of cells results in viscous mass
Cells gone but more liquid
Necrosis
Caseous
Fragmented cells and granular debris surrounded by inflammation
Cells are gone but more solid; Cheese like
Necrosis
Fibrinoid
Immune complexes and fibrin in walls of blood vessels
Fbrin from blood gets into blood vessel wall and attaches to immune complexes
Apoptotic Signaling
Extrinsic
Death receptors on the plasma membrane are activated and transduce a signal through intracellular signalling pathways to activate caspases
Signal initiated from outside cell
Apoptotic Signalling
Intrinsic
Mitochondrial signals induce release of pro-apoptotic proteins that activate caspases
Signal initiated from inside cell
Apoptotic Signalling
Caspases
Specific proteases that disassemble the cell for packaging into apoptotic bodies
Biochemical markers of apoptosis
Inflammatory
Cysteine Aspartases
Caspases
Initiators
Autocatalytic
Caspases
Executioners
Cleavage
Bcl-2 Protein Family
B cell lymphoma 2
Stress and Death
p53-induced cell death
Critical in DNA damage repair
Activates negative regulators of cell cycle progression
Induces apoptosis promoting genes
Stress and Death
ER stress/UPR
Halts protein translation and upregulates chaperone expression to fold proteins properly or activate cell death
Stress and Death
PIDDosome
Formed in response to p53 signaling caused by DNA damage to repair or destroy damaged cells
Stress and Death
ER stress
Accumulation of misfolded proteins
Stress and Death
Unfolded Protein Response (UPR)
Stress response that promotes degradation of extra proteins and increased chaperone production to improve folding
Immune Response: Inflammation
Clinically
redness, swelling, pain
Immune Response: Inflammation
Histologically
Edema, WBC
Edema
Mediated by mast cells (immediate) and eosinophils (later response)
Immune Response: Inflammation
Pyogenic
Pur production
Immune Response: Inflammation
Granuloma
macrophages surrounded by T cells
Mass of immune cells
Immune Response: Inflammation
Tumor Necrosis Factor (TNF)
Important mediator (cytokine)
Immune Response: Inflammation
Acute Inflammation
Dilation of small blood vessels
Increased microvasculature permeability
Migration and activiation of immune cells
Immune Response: Inflammation
Chronic Inflammation
Infiltration by macrophages, lymphocytes, plasma cells
Increased tissue destruction
Attempts at healing
Meningitis
Meninges
Cover for CNS/protectant
1. Dura mater
2. Arachnoid/subarachnoid
3. Pia mater
Meningitis
Immunoglobulin A (IgA)
Produced by plasma cells associated with mucosa
First line of defense
Not inflammatory
Primarily acts thru exclusion
Meningitis
Ciliostasis
Prevents movement of bacteria out of bronchial tubes
Meningitis
Adhesie Pili
Projections from bacteria that can bind non-ciliated mucosal cells
Can cross epithelium once bound
Meningitis
Exotoxins
High antigenic (antitoxin neutralizes)
Highly Toxic (fatal in micorgram quantities)
Ususally do not insuce fever
Usually bind to specific receptors
Excreted by cell
Meningitis
Endotoxins
Weakly immunogenic
Toxic at 10-100s micrograms
Induce fever
No specific receptions
Part of cell wall
Trichinosis
Enteric Phase
Occurs in GI Tract
Strong immune response to larvae
Increased intestinal mobility
Trichinosis
Muscle phase
Larva exit blood vessels and enter skeletal muscle - infects muscle fibers
Integumentary Disorders
Growths
Cyst
Malformation
Benign/malignant neoplasm
Integumentary Disorders
Dermatitis
Non-neoplastic
Rash
Psoriasis
Inflammatory skin disease
Scaling skin condition
Psoriasis: Angiogenesis
VEGF
Released from keratinocytes
Stimulate epidermal hyperplasia vascular growth, leukocyte infiltration
Psoriasis: Verucae
Verrucae
Squamoproliferative
Generally self limiting
Pemphigus
Autoimmune formation of blisters
Foliaceus
Subcorneal lesion
Vulgaris
suprabasal lesion
Bullous Pemphigoid
Subepidermal, nonacantholytic lesion
Mendelian Disorders
Monogenic Disorders
Generally rare (usually incompatible with life)
Single gene defect causes disorder
High penetrance
Chromosomal Abnormalities
Uncommon
Extra chromosomal material (or lacking)
Complex Multigenic DIsorders
Far more common
Complex interaction of geentic defect with environmental factors
Predisposition
Autosomal
Located on chromosomes 1-22 rather than X or Y (sex linked)
Penetrance
Whether or not the variant genotype can be inferred on the basis of defined phenotypic criteria
Can you infer genotype from phenotype
Can you identify disorder based on appearance or clinical observation
Autosomal Recessive
Recessive need both copies to express
Nondisjunction
Failure of two homologus chromosomes (or two sister chromatids) to separate at metaphase of meiosis I (or meiosis II/mitosis)
Autosomal Dominant
Only need one copy of gene to express characteristic
If you have the gene you will express it
Sex-Linked
characteristics (or traits) that are influenced by genes carried on the sex chromosomes
Males will express because they only have one X
Phenylalanine Hydroxylase
Catalyzes conversion of Phe to Tyr
Mutated in PKU