Patho Final PDF

1/4 Lecture (Injury Death) (3 q's) o o o Mechanisms of cell injury (there are 6 and how do they cause injury) § Mitochondrial dysfunction and damage depletion of ATP, reduced activity of ATP-dependent plasma membrane sodium pumps, accumulation of sodium intracellularly, osmotic gain of water, cellul...

1/4 Lecture (Injury Death) (3 q's) o o o Mechanisms of cell injury (there are 6 and how do they cause injury) § Mitochondrial dysfunction and damage depletion of ATP, reduced activity of ATP-dependent plasma membrane sodium pumps, accumulation of sodium intracellularly, osmotic gain of water, cellular swelling and dilation § Oxidative stress An imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants § Membrane changes Damaged by ROS (vulnerable double bonds --> peroxide --> autocatalytic reaction) Decreased phospholipid biosynthesis due to hypoxia or nutrient deprivation Increased degradation from increased phospholipase activation due to increased Ca Cytoskeletal abnormalities that disrupt the anchors for plasma membranes § Disturbance in calcium homeostasis Calcium ions are oftentimes second messengers Most intracellular calcium is sequestered in mitochondria and ER Excessive intracellular calcium can lead to activation of enzymes Increased mitochondrial calcium leads to increased permeability o Cytochrome c is released into the cytoplasm § Endoplasmic reticulum stress During protein synthesis, misfolded polypeptides are generated and targeted for proteolysis. But if too abundant then signals are released to initiate apoptosis Accumulation of misfolded proteins may be caused by increased production or decreased elimination Protein misfolding may cause disease by creating deficiency of an essential protein or by inducing apoptosis CHAT: When proteins are made, sometimes they don't fold properly and become misshapen. Usually, cells break down these misfolded proteins. But if there are too many misfolded proteins, cells send signals to start a process called apoptosis, which is like cell suicide. Misfolded proteins can build up because they're made too quickly or because the cell can't get rid of them fast enough. This buildup can lead to diseases either by causing a lack of important proteins or by triggering cell death. § DNA damage May be due to radiation, chemotherapy, ROS, or mutations Damage leads to accumulation of p53 P53 stops the cell cycle and allows DNA repair If too damages, then triggers apoptosis Types of necrosis and their associations § Coagulative - infarction of solid organ (except brain) Due to hypoxia Issue architecture is maintained, pale wedge-shaped with apex towards obstruction § Liquefactive – in the brain; bacterial, and some fungal, infections Enzymes from recruited leukocytes “liquefy” the tissue § Caseous – tuberculosis Tissue architecture is obliterated § Gangrenous – hypoxia wet or dry § Fat - abdominal trauma or pancreatitis Tissue architecture is obliterated Fatty acids combine with calcium to produce chalky white lesions focal areas of fat destruction § Fibrinoid - vasculitis, transplant rejection, severe hypertension complexes of antibodies and antigens or fibrin are deposited Cellular adaptations to stress and why they occur § Hypertrophy –Increase in cell size § Hyperplasia – Increase in number of cells § Atrophy- Decrease in cell size and number § Metaplasia – Change in function 1/9 Lecture (Inflammation & Repair) (4 q's) o Main components of acute inflammation (there are 3) and what their key mediators are § 1. Dilation of small blood vessels Most important mediator = histamine § 2. Increased permeability of microvascular Mediators are histamine, bradykinin, leukotrienes § 3. Emigration of leukocytes Mediators = adhesion molecules and cytokines o Acute inflammatory cytokine effects on the body § Local effects Endothelial activation: makes selectins, integrins, binding receptors, etc. Leukocyte recruitment Activation of leukocytes + others § Systemic effects Upregulate prostaglandins --> fever Accelerate release of cells from bone marrow postmitotic reserve pool --> leukocytosis Upregulate acute-phase proteins High [TNF] = vasodilation, decreased myocardial contractility TNF promotes lipid and protein mobilization, suppresses appetite --> cachexia Insulin resistance in skeletal muscle T-cell activation Upregulate acute-phase proteins Accelerate release of cells from bone marrow o Chronic inflammation morphologic features and key cells § Morphologic features Infiltration of mononuclear cells Tissue destruction Attempts at healing through angiogenesis and fibrosis § Predominant cells = macrophages Mediators--> Interferon gamma, interleukin-12, interleukin-17 o Granulomatous inflammation § Collections of activated macrophages, sometimes associated with central necrosis = granuloma § An attempt to contain difficult to eradicate offending agents --> avoid it from spreading Microbes or foreign bodies o Phases of wound healing (there are 4) and what their key characteristics are § Phase 1 = hemostasis Tissue factor released --> coagulation cascade activation (platelets, complement, kinins activated) --> fibrin clot (scab) § Phase 2 = inflammation Begins within minutes --> continues for 6-48hrs DAMPs and chemokines are released by the injured cells § Phase 3 = proliferation and new tissue formation 3-4 days after injury --> 2 weeks Macrophages clean-up site and release numerous growth factors (VEGF – vascular endothelial growth factor, PDGF – platelet derived growth factor) ---> angiogenesis Granulation tissue grows into the wound from surrounding healthy tissue Fibroblasts secrete collagen and other connective tissue proteins § Phase 4 = remodeling and maturation 2-3 weeks after injury --> months to years Increases strength, decreases size (contraction) Fibroblasts deposit type I collagen (as opposed to the original type III collagen 1/11 Lecture (Hypersensitivity & Reactive derm) (4 q's) o Hypersensitivity reactions § Type I: Immunoglobulin-E (IgE) mediated Two phases o Immediate response (5-30 minutes subsiding in 60 minutes) § Mediated by vasoactive amines (histamine), lipid mediators (leukotrienes) o Late phase (2-8 hours later; may last days) § Mediated by cytokines o Initiated by entry of antigen (also called allergen) o Severity varies (e.g. runny nose (rhinitis)----> anaphylaxis o Susceptibility is genetically predetermined o Atopy= exaggerated immune response to harmless substances o Environmental pollutant exposure is a predisposing factor § Type II: Tissue specific Caused by antibodies directed against target antigens Antigens may be normal cellular components or exogenous substances Typically IgG and IgM antibodies are involved o Activate complement cascade and bind to phagocytes § Type III: Immune complex-mediated Antigen-antibody complexes in circulation activate complement Antigens can be exogenous or endogenous Tend to lead to systemic diseases Preferentially involve the kidneys, joints, small blood vessels Pathogenesis o 1. About 1 week after introduction of antigen---> antibodies form o Antibodies are secreted in blood and bind to antigens o Antigen-antibody complexes deposit in various tissue o An acute inflammatory reaction is initiated via complement pathway § Leads to consumption of C3 during active phase of disease § Type IV: cell media o All the reactive skin dermatoses (focusing on pathogenesis and clinical manifestations) § Type I hypersensitivity Urticaria: o Hives o Pathogenesis: Mediated by localized mast cell degranulation o Manifestations: Erythematous, edematous and pruritic plaques=wheals Eczematous dermatitis: o Pathogenesis: Type 1 hypersensitivity o Manifestations: Erythematous papules with overlying vesicles that ooze and crust----> coalesce into raised, scaling plaques o Hallmark: lichenification in the flexural regions § Type II hypersensitivity Pemphigus Vulgaris o Pathogenesis: IgG autoantibodies deposition along intercellular desmosomal proteins (desmoglein type 1 and 3) o Manifestation: § Painful, flaccid superficial vesicles or bullae filled with clear fluid Bullous Pemphigoid o Pathogenesis: IgG autoantibodies & C3 deposition along subepidermal cleft (hemidesmosomes) ----> inflammatory infiltrate o Manifestation: § Pruritic, tense subepidermal bullae filled with clear fluid § Overlying epidermis lacks acantholysis § Type IV hypersensitivity Contact dermatitis Psoriasis o Pathogenesis: Sensitized skin-homing Th1 and Th2 cells accumulate in the epidermis---> cytokine and growth factor----> hyperproliferation o Manifestation: Most commonly affects the skin of the elbows, knees, posterior, scalp, lumbosacral areas, intergluteal cleft, penis, and vulva o Acanthosis: Marked epidermal thickening Lichen planus o Pathogenesis: CD8 + cytotoxic T cells responding to unknown antigens expressed by basal keratinocytes or deposited at dermo epidermal junction o Manifestation: § Usually symmetrically distributed § Pruritic, purple, polygonal, planar papules, plaques § White dots/lines= Wickham striae Erythema multiforme o Pathogenesis: Cutaneous and mucosal basal cell (Keratinocytes) injury mediated by skin homing CD8+ cytotoxic T cells o Manifestations: May include macules, papules, vesicles, bullae o Targetoid appearance Stevens Johnsons Syndrome/Toxic epidermal necrolysis o Patho: Extensive Keratinocyte cell death due to cytotoxic T cells o Manifestations § SJS 30% of BSA § Prodrome= fever, headache, malaise, sore throat, cough § Vesicles and bullae form----> sloughing----> secondary erosions, crusts 1/16 Lecture (Infective dermatoses) (4q's) o Mechanisms of bacterial, viral, and fungal invasion/damage § Bacterial: key toxin and biofilms Pili (fimbria) = adhesion Flagella = motility Toxins o Exotoxins = secreted protein enzymes that cause direct injury o Endotoxins = contained in outer membrane of gram-negative bacteria and released when lysed Enzymes = proteases, lipases, DNAases, hyaluronidases Capsules = outer coating to evade phagocytosis Biofilms = excreted matrix acting as a protective structure § Viral: key is enzyme and specific more varied than bacteria Mostly production/release of enzymes More specific to each individual virus Severity of symptoms is dictated by level of inflammatory response § Fungal: key enzymes, inflammatory response, dermatophyte Similar to bacteria Direct injury via secretion of enzymes (e.g., keratolytic proteases) Mycotoxins can cause disease without infection Indirect injury via inflammatory response Dermatophytes = Fungi that invade skin, hair, and nails Phagocytes and T cells are important in controlling fungal infections o How anatomy determines the name of the infectious dermatosis o Clinical manifestations of infectious derms § Bacterial Impetigo: kids, superficial, red scab, dried serum, face/extremities Erysipelas: superficial, well-defined erythema, sharply demarcated, bright red, legs/face/arms Cellulitis: fat to skin surface, muted in color, less defined margins Folliculitis: inflammatory nodule involving hair follicle Pilonidal disease: abscess involving hair follicle near butt crack Necrotizing fasciitis: Fournier’s Gangrene = necrotizing fasciitis of perineum and genitals; blackblue discoloration, anaerobic microbes, spread fast and toxins released --> life threatening Scalded skin syndrome: neonates; staph toxin not bacteria itself; desquamation (desmoglein and ketinocyte adhesion molecule attacked) Toxic shock syndrome: hypotension; macular erythema --> desquamation; mucocutaneous involvement; superantigen (TSST toxic shock syndrome toxin/SPE strep pyrogenic exotin) Scarlet fever: strep superantigen; exudative pharyngitis, fever, blanchable erythematous rash § Viral Cold sores: HSV-1, orofacial lesions, HSV-2 = genital Chicken pox: VZV (herpes 3) Shingles Warts: verrucae Mollucsum contagiosum: kids, warm climates, umbilicated, dome-shaped papules Exanthems § Fungal: scaly, pruritic, erythematous Cradle crap: tinea capitis, babies heads Ringworm: tinea corporis Jock itch: tinea cruris Athlete's foot: tinea pedis Nail fungus: tinea unguium/onychomycosis Candida, forms white plaques with shallow ulcer, intertringous region o Thrush o Yeast infection Other Acne vulgaris: inflammation and rupture of follicle; anaerobic bacteria; androgen-related Hidradenitis suppurvita: “inverse acne”; recurring scarring disease of pilosebaceous follicular ducts, intertriginous area Seborrheic dermatitis: “dandruff, cradle cap”, relapsing inflammation of skin rich in sebaceous glands, genetic predisposition + Malassezia fungal o hyperkeratosis, acanthosis Acne rosacea o Skin mites/microbes o Inappropriate dilation (redness and warmth); middle aged women with fair skin § 1/23 Lecture (neoplasia) (3 q's) o Cancer terminology § Neoplasia = spectrum of diseases characterized by abnormal cell growth, loss of tissue homeostasis, and distorted architecture § Neoplasm = new growth (ex. tumor) § Tumor = abnormal growth caused by uncontrolled proliferation § Benign = well-differentiated, well-organized cells encapsulated by connective tissue § Malignant = “cancer” = neoplasia that involves tissue invasion and destruction --> NOT well-differentiated (not the cells they should be) § Anaplasia = Loss of cellular differentiation § Pleomorphic = Marked variability in size and shape of cells § Dysplasia = “precancerous” = abnormal changes in size, shape, and organization of mature cells § Metaplasia = abnormal cell reprogramming to appear and function like a different cell type § Metastasis = spread of a tumor to sites physically discontinuous with primary tumor § Carcinoma = arise from epithelial cells (MOST cells) § Sarcoma = arise from mesenchymal cells (muscle, bone, CT) § Lymphoma = arise from lymphatic tissue (lymph nodes) § Leukemia = arise from blood-forming cells (myeloid, lymphoid) § Carcinoma in situ (CIS) = pre-invasive epithelial tumor of glandular or squamous cell origin (still contained by basement membrane, no invasion) § Germline mutations = mutations inherited from parents and present in ALL cells § Somatic mutations = mutations acquired during life in specific cells § Clinical phase = overt signs and symptoms of malignancy § Preclinical phase = asymptomatic (or vaguely symptomatic) where malignancy is unknown o Cancer fundamentals and hallmarks (on a 35,000-foot view kind of level) § Fundamentals Disordered regulation results in loss of: Control over cell growth, Differentiation, Spatial confinement (DNA mutations, exposure to environmental carcinogens) Error in corrective measures or apoptosis § Cancer hallmarks 1. Sustaining proliferative signaling: oncoproteins, RB = key negative regulator of cell cycle, inactive RB = DNA transcription starts and continues into S phase 2. Evading growth suppressors: TP53 (tumor suppressor gene, most mutated in cancer) 3. Reprogramming energy metabolism: aerobic glycolysis (cancer) is used instead of oxidative phosphorylation (healthy cell) 4. Resisting apoptotic cell death 5. Enabling replication immortality 6. Inducing angiogenesis: insulin growth factor, PDGF, VEGF 7. Activating invasion and metastasis 8. Evading immune destruction: cancer immunoediting, immune checkpoints, CAR-T cells 9. Genomic instability: DNA repair is defective in inherited disorders, BRCA-1, BRCA-2 10. Tumor-promoting inflammation o TNM staging system (what do the letters mean) --> valuable clinically, extent of spread § T = size of primary tumor and it’s invasion into local tissues T0-T4 § N = regional lymph node involvement N0-N3 § M = presence of metastases M0-M1 § Carcinoma in situ – STAGE 0 CANCER § ***Stage 4 --> automatically when there is metastasis*** --> pleural effusion, free fluid in belly, metastasis 1/25 Lecture (Autoimmune & deficiencies) (4 q's) o Autoimmune disorders clinical manifestations and Antibodies § Systemic Lupus Erythematosus Clinical Manifestations: Depends on injury to skin, joints, kidneys, serosal surfaces o Joint pain=nonerosive serositis o Butterfly rash on face (sun exposure) = erythema on nose and cheeks o Lupus nephritis=Immune complex-mediated glomerulonephritis---> major morbidity and mortality for those with SLE Antibodies: o Anti-dsDNA antibodies (correlates with disease activity) o Anti-Smith antibodies (most specific for SLE) o Anti-phospholipid antibodies (binds to plasma proteins) ----> increases thromboses) § Sjogren Syndrome Clinical Manifestations: o Dry eyes: blurry vison, itchy, thick secretions o Dry mouth: difficulty swallowing, cracks, poor dentition Antibodies o Anti-SS-A (RO) antibodies (associated with extra glandular manifestations o Anti-SS-B (La) antibodies o Rheumatoid factor (RF) = antibody reactive to self-IgG § Systemic Sclerosis (Scleroderma) CREST SYNDROME o Calcinosis o Raynaud phenomenon o Esophageal dysmotility o Sclerodactyly o Telangiectasia Antibodies: o Anti-nuclear antibodies (ANA) o Anti-centromere antibodies (specific for crest syndrome) o Anti-SCL70 antibodies (associated with diffuse disease) o Transplant rejection pathogenesis § Process in which T lymphocytes and antibodies against the graft react with and destroy the graft o What cells are impaired/absent in the primary immunodeficiencies § Combined Immunodeficiency Defects that directly affect development of both B and T lymphocytes § Antibody Immunodeficiency Defects in B-cell maturation or function (results in low levels of circulating immunoglobulins IgG, IgM, IgA, IgE 1/30 Lecture (Oral Cavity) (4 q's) o Etiologies, pathogenesis and clinical manifestations of dental caries, periodontal dz, inflammatory lesions, diseases of the salivary glands, and proliferative lesions of the oropharynx § Dental caries “cavities” Etiology/pathogenesis = acids generated during fermentation of sugars by bacteria Clinical manifestations = Cavities and tooth loss before 35 years old § Periodontal disease Etiology = poor hygiene that affects the gingival bacteria composition Pathogenies = Pathogen mediated inflammation Clinical manifestations = Gums can pull away from the tooth, bone can be lost, teeth may loosen or even fall out § Inflammatory lesion: aphthous ulcers “canker sore”, herpes simplex infection “fever blisters” or “cold sores”, oral candidiasis “thrush” Aphous ulcer = canker sore o Etiology = unknown, associated with IBD/Behcet disease o pathogenesis = unknown, maybe cell-mediated immune o Clinical manifestations = annoyingly painful, common in first 2 decades of life, superficial mucosal ulcerations with hyperemic base, recur Herpes simplex o Etiology = HSV1, HSV2 o Pathogenesis = Target keratinocytes due to glycoproteins on cell membrane o Clinical manifestation = inflamed and painful vesicles on erythematous base Oral candidiasis o Etiology = not in slide? Opportunistic, budding yeast o Pathogenesis = Uses keratolytic proteases to invade o Clinical manifestations = forms white plaques (or spots) with shallow ulcers, readily scrape off the mucosa § Disease of the salivary glands: parotid, submandibular, sublingual --> Xerostomia: dry mouth o Etiology = medication (also autoimmune disease, radiation therapy) o pathogenesis = directly suppresses the CNS from producing ACh or occupies the muscarinic/adrenergic receptors o Clinical manifestations = dry mucosa, fissures/ulcerations on tongue, dental caries, oral candidiasis, difficulty swallowing/speaking Sialadenitis: inflammation of salivary glands o Etiology = Trauma, viral or bacterial infection, autoimmune o pathogenesis = inflammatory infiltration of the salivary gland interstitium o Clinical manifestations = firm, diffusely tender gland; erythema and edema overlying skin; bad taste (halitosis); +/- express pus from duct Sialolithiasis: salivary stone o This is under the same slide as previous condition. I think just know what the word means. Mucocele: looks like bubble o Etiology = Usually trauma o pathogenesis = Blockage or rupture of the salivary duct o Clinical manifestations = toddlers, young and old adults; painless; fluctuant swelling of lower lip; bluish translucent color § Proliferative lesions of oropharynx Leukoplakia o Etiology = prolonged irritation without a known cause § Associated with tobacco use, alcohol consumption, vitamin deficiency o pathogenesis = hyperkeratosis of the oral mucosa, may be dysplastic o Clinical manifestations = more common male; 40-70 y/o; well-demarcated hyperkeratotic plaques; tongue; gray-white, DOES NOT SCRAPE OFF Squamous Cell Carcinoma of the OP o Etiology = high-risk variants of HPV (16 and 18), tobacco and alcohol use o pathogenesis = genetic mutations to TP53 and RAS o Clinical manifestations = raised, film, pearly plaques OR irregular, roughened, verrucous thickenings (warts) 2/1 Lecture (Special senses (4 q's) o Pathogenesis and clinical manifestations of vision loss (the flow chart essentially) o Pathogenesis of hearing loss § Conductive Hearing loss Inability to transmit sound waves to the cochlea § Sensorineural Hearing loss Impaired conduction of sound waves from organ of Corti (hair cells to brain) 2/6 Lecture (interstitial lung dz) (4 q's) o Pathogenesis and clinical manifestations of ARDS and interstitial lung diseases § Aspiration: passage of fluids or solid particles into the lungs Pathophys: host defense responds to foreign substance in the lung tissue Clinical manifestations: lands in the right lobe most often o Small items: pneumonia, bronchitis o Larger items: chocking, cough, wheezing, stridor § Atelectasis: Collapse of lung tissue (not complete collapse) Pathogenesis o Obstructive: hyperventilated alveoli gradually absorbs air into blood and deflate o Compressive: external pressure causes collapse of alveoli o Surfactant impartment: decreased production of alveoli Clinical manifestation: dyspnea, cough § Bronchiolitis Pathophys: inflammation and fibrosis of bronchioles due to infection or chronic insult Clinical manifestation: rapid ventilation rate with accessory muscle use, nonproductive cough, +/wheezing § Idiopathic Pulmonary Fibrosis Pathophys: repeated injury and defective repair of alveolar epithelium --> fibroblastic proliferation Risk: smoking, viral infections, GERD Clinical manifestation: Seen in older individuals, dyspnea on exertion § Pneumoconiosis Pathogenesis: deposition of inorganic dust particles leading to chronic inflammation and scarring of the alveocapillary membrane Clinical manifestations: Chronic productive cough , Dyspnea, Decreased lung volume, wheezing § Sarcoidosis Pathogenesis: Genetic predisposition causing noncaseating granulomatous inflammatory respond to unidentified antigen driven by CD4 T helper T cells Clinical manifestation: seen in younger pt. Asymptomatic. 2/3 of symptomatic pt have SOB, dry cough. Eye and skin symptoms. Hypercalcemia due to vit D granuloma-producing macrophages § ARDS Pathogenesis: injury to epithelial/endothelial lining of alveocapillary membrane --> neutrophil (main player) activation, proinflammatory cytokines --> loss of surfactant --> stiffens alveolar unit --> hypoxemia Clinical manifestations: dyspnea and hypoxemia, hyperventilation and respiratory alkalosis, less tissue perfusion and metabolic acidosis, increased work of breathing and less tidal volume, hypercapnia due to hypoventilation, re ZZZZZspiratory acidosis and worsening hypoxemia, multiorgan failure --> death 2/8 Lecture (obstructive dz) (4 q's) o Pathogenesis of obstructive lung diseases: Obstructive lung disease TLC is unchanged, FEV1/FVC lowers the threshold of the subendothelial vagal receptors to irritants (making it easier for bronchoconstriction) Status asthmaticus: asthma attack o Severe asthma attack does not respond to therapy § Can cause hypercapnia, acidosis and sever hypoxic § COPD Emphysema: permanent enlargement of the distal to terminal bronchioles o Destruction without significant fibrosis o Centriacinar (centrilobular) most common pattern Chronic bronchitis: persist productive cough o Pathophys: hypersecretion of mucus in the large airways § Hypertrophy of the mucous gland § Increased mucin-secreting goblet cells § Inflammation infiltrated by macrophages--> may lead to fibrosis § May hear wheezing § Cystic Fibrosis Etiology: autosomal receive mutation of the CFTR gene Pathophys: defective chloride ion transport--> thick dehydrated mucus secretions § Bronchopulmonary Dysplasia Pathogenesis: poor formation of airway epithelium leading to decreased surface area for gas exchange. Risk: premature birth, perinatal O2 supplementation 2/13 Lecture (Lower resp infections) (4q's) o Acute Bronchitis: inflammation of the bronchus § Patho: acute inflammatory response to a pathogen, usually a virus Cough may be dry or productive ABSENCE of dullness to percussion o Pneumonia: infection of lower resp tract § Etiology: virus or bacteria, also from fungi parasites § Presence of dullness to percussion egophony crackles, decreases air sounds o Pulmonary abscess: Usually bacterial § Risk factors: alcohol abuse, seizure disorders, swallowing disorders § Pathophys: acute inflammation that leads to necrosis § Clinical manifestations: fever, chills, malodorous sputum o Tuberculosis: bacterial infection § Pathophys: localized nonspecific inflammation in the upper lobes. Makes caseating granulomas § Risk: People who are incarcerated, experience homelessness, institutionalized, substance abuse § Symp: latent is asymptomatic, active TB: night seats, fatigue, weight loss, low grade fever 2/20 Lecture (Pleural dz) (4 q's) o Transudative vs exudative effusions and etiologies § Transudative: low protein content Due to heart failure, liver disease or kidney disease Pathophys: changes in the hydrostatic or oncotic pressures o Fluid backs up into capillaries o Decreased protein --> decrease oncotic pressure § Exudative: High protein content Due to infection, malignancy, pancreatitis Leukocytes and proteins migrate to the affected tissues o Other types of effusions and their pathogenesis § Empyema: pus Due to: pneu0monia, trauma, bronchial obstruction Pathophys: exudative effusion that has microbes. o S. Aureaus, E. coli, K. pneumonia, Anaerobes § Hemothorax: blood Pathophys: Blood in the pleural space due to damage in the blood vessel wall such as Trauma, surgery, cancer § Clyrothorax: Chyle or lymph fluid in the pleural space Due to surgery or cancer Pathophys: injury to the thoracic duct § Pneumothorax: air Rupture of the visceral or parietal pleura pr both: Disrupts the elastic recoil of the lung and chest wall o Primary: unexpected rupture of bleb in a healthy person: tall young males o Secondary: unexpected bled in a person with lung disease o Traumatic: Penetrating trauma disrupting pleura o Tension vs open: tension is a one-way valve air flows in and out § Obesity hypoventilation syndrome Associate with obesity, sleep apnea Pathophys: related to leptin resistance, leptin is produced in the adipose tissue o Mesothelioma: asbestos exposure § Pathophys: mesothelial lung cancer, arises from parietal or visceral pleura. Develops 25-40 years after exposure to due slow driver mutation. Leads to pleural fibrosis and plaque formation. 2/22 Lecture (Pulm vessel dz) (4 q's) o It's 14 slides...but I would focus on pathogenesis and associated diseases/conditions § Pulmonary Htn Mean arterial pressure >25% Group 1: pulmonary arterial HTn due to vascular remodeling and overproduction of vasoconstrictors Group 2: left hearted dieses--> due to back up of blood from the left heart Group 3: chronic lung disease--> hypoxemic pulmonary vasoconstriction and parenchymal damage Group 4: Chromic thromboembolic pulmonary HTN § Cor pulmonale Pathophysiology: chronic pressure overload of the RV leading to hypertrophy § Pulmonary embolism Pathophysiology: thrombus lodges in pulmonary artery --> inflammatory mediators --> widespread vasoconstriction--> v/q mismatch § ANCA-associated vasculitis (anti-neutrophil cytoplasmic antibodies) Pathophys: ? Drugs or cross-reactive microbes, inflammation upregulates the expression of pr3 and MPO o 2 important ANCAS § Anti-proteinase 3 granulomatous with polyangiitis --> necrotizing vasculitis of small vessels § Anti-myeloperoxidase Microscopic polyangiitis --> necrotizing vasculitis of capillaries Eosinophilic granulomatosis with polyangiitis--> small vessels vasculitis associated with asthma and allergic rhinitis o Peripheral eosinophilia o GI bleeding o Affects the upper respiratory and lower resp tract--> kidneys o Know the antibodies and which diseases they belong to (above)