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Stack #291180

QuestionAnswer
Macule freckle
Papule elevated solid area
Vesicle tiny blister (5mm or less) ie: chicken pox
bulla normal blister more that 5 mm
putule acne dicrete pus filled raised area
scale dry, horny, plate like excrecience, usually the reult of cornification
lichenification thickened skin charecterized by skin markings; from repeated rubbing
excoriation raw area usually due to scratching
acute inflammatpry dermatosis Urticaria(hives) Mast cells release vasoactive mediators via immoglobulin antibodies ie: pollen, foods , drugs, insect venom, some opiatess, antibiotics lessions vary fom small pruitic papules to edematous plaques (reddening and vascular dilation
acute inflammatpry dermatosis Acute eczematous dermatitis Allergic contact atopic, drug related, and sun related CD4 cells remember and create an inflammatory response - Red oozing plaques and crusted lessions that can turn into raised plaques
Chronic Inflammation psorasis T cells secrete cytokines and growth factors that induce Keratinocyte hyper- proliferation resulting in lessions
Infectious dermatosis (impetigo) Bacterial infection ( Staph aureus and Strepto pyrogenes
Infectious Dermatosis (Verrucae) warts HPV
Infectious Dermatosis Superfiscial Candida Yeast fungus (Candida albicans) caused by warmth moisture (Thrush) found in newborns mouths (Candida Viginitis) common in women on the pill (Candida esphagitis) AIDS pts (Cutaneous candidasis) -diaper rash
Benign premalignant epithelial lessions Seborrhecic Keratosis Benign skin tumor- FGF receptor 3 Fibroblast Growth factor F: round stuck on velvetty stuck -on coin like plaques
Benign premalignant epithelial lessions Actinic Keratosis (sun related)UV light damage Mutation of p53 may result in a carcinoma F: Cytologic atypia in lower parts of epidermis
Malignant Tumors Squamous cell carcinoma C: UV light exposure F: defined red scaling plaques
Malignant Tumors Basal cell carcinoma C: Associated with dys- regulation of Sonic Hedgehog or PTCH F: Pearly papules often containing prominant dilated subepidermal blood vessels
Tumors or tumor like lesions of melanocytes Common Nevus ( beauty marks) C: Genes (BRAF or NRAS) transformation of highly dendritic melanocytes
Tumors or tumor like lesions of melanocytes Melanoma C: Sun light , genes prexising NEVI F: change in color and size can occur in esophagis and eye or meninges
ABCDE for melanomas Assymetry, Border, Color, diameter, evolution
Radial growth melanoma initially grow horizontally and within the superfiscial dermal layers
Vertical growth melanomas after time grows downward into deeper dermal laayers
Chronic inflammatory dermatitis (Atopic Dermatitis) C: associated with Rhinitis and asthma some food allergies F: Pruitis scaly lessions
Chronic inflammatory dermatitis ( Seborrheic dermatitis) C: Fungus Pityrosporum ovale may be involbed it follows sebacious glands F: Inflammatory waxy lesions with waxy yellowish/brownish scaling
Chronic inflammatory dermatitis (Acne vulgaris) C: Increased hormonal stimulation of the production of Sebum(oil) and plugged hair follicles due to keratinization
Bacterial infections (Necrotizing Fasciitis) Flesh Eating disease Anaerobic bacteria like Vibrio Vulnificus F: Deep subcutaneous, deep fascia, and underlying skeletal muscle Comp: sever fevers large wounds, death amputation
Viral skin infections (Varicela) chcken pox comp: corneal lessions pnuemonia encephalitis
Viral skin infections Herpes zoster (Shingles) Varicella reaches the ganglion cannot spread shingles but can spread chickenpox
Viral skin infections Herpes 1 and 2 remains in the ganglion if transmitted during childbirth ca cause neonatal encephalitis
Fungal skin infections Tinea Corporis Ringworm C:Microsporum, Trichopython, and Epidermpphyton person to person animal to person soil to person
Fungal skin infections Tinea capitis Fungal infection of the scaalp and hair may produce a kerion most common dermophytosis in children
Fungal skin infections Tinea Versicolor caused by Malassezia fulfur part of normal skin flora
Fungal skin infections THRUSH candida albicans which commonly exists in the GI tract
Fungal skin infections Candida diaper dermatis candida albicans intense red plaques with sharp demarcated borders and satelite papules
Scabies Sarcoptesscabiei spread by physical contact female mite burrows between superfiscial and deep layers of epidermis laying eggs and depositing feces Intense pruitis and red papules in a linear pattern
Chronic inflammatory dermatitis Acne Rosaccea Flushing redness from heat emotion or alcohol can become permanent.
Bacterial infections Impetigo staph aureus and strep pyrogenes (Scalded skin syndrome)
Bacterial infections Folliculits Staph aureus common where hair is
Bacterial infections Furnicle staph aureusinfection deep in the hair follicle pyogenic infection
Bacterial infections Carbuncle begins as folliculits than becomes a mass of pus
Bacterial infections Erysipelas Strep inflammation of the face or scalp causes fever
Bacterial infections Cellulitis acute inflammation of the subcutaneous tissue strep
Proptosis forward diplacement of the eye caused by a disease that increases orbital contents C: enlargement of the lacrimal glands from inflammation or neoplasm
Dfference between herodeolums (styes) and chalazions H: softer and not chronoio points to the lid margin spah infection usually a follicle C: solid and chronic usually needs to be exised, usually points inside the lid rather than the lid margin, refer specifically to the meibowian glaand
Basal cell carcinoma most common neoplasm of the lower eyelid
Causes of Conjunctivitis 1Stap and Strep particularly Strep. 2(Gonococcul usually through genitals(Chlamydial Keratoconjunctivitis) also neo natal Neissaria Ghonorhea 3 Viral Conjunctavitis adenovirus type 3 4 allergic 5 Trauma
Distinguish between Pinguecula and Ptergium PING: Elderly from sunexposure- epithelial atrophy thickened yellow area in conjunctivita benign PTER: Vascularized connective tissue stetching from limbus -cornea may cause visual impairment
Keratitis Corneal ulcers infection and inflammation of the cornea results in scarringC: Herpes simplex virus(dendritic) Herpes Zoster, Chlamydia Trachoma, most common cause of blindness, Bacterial (Pseudomonas aeruginosa) Fungal, Acanthamoeba(contact wearers)
Process of Cataract formation and causes C: Diabetes Meletis, fetal infection(Rubella), Wilsons disease, Hypoparthyroidissm, radiation Trauma, overuse of steroids, glaucoma Form: Opifacation due to chages in lens proteinslens my liquefy
Glaucoma distinctive changes in the visual field and in the cup of the optic nerve. Increased intra ocular pressure caused by obstruction to outflow of the aqueous humor
Differences between acute closure Glaucoma and Chronic Glaucoma ACG: Older age group, rapid onset of severe pain and profound visual loss (halos around lights) Red eye, steamy cornea, dilted pupil, hard eye when palpate, Rare. pt have shallow ant chambers with narrow angles
chronic glaucoma open angle CG: No symptoms in early stage, Insidious progressive bilateral loss of peripheral vision, tunnel vision with preeserved visual acuities, Pathologic cupping o f the optic discs, persistant elevation of intra ocular pressure. Genetically determ, death
2 most common predisposing causes of vascular disease Hpertention, and Diabetes mellitus
Diabetic retinopathy Usually after 10 -20 years from onset, disease of the microvasculature, caused by ischemia, start with capilary microaneurysims, retinal edema, hemmorage, small vessels hemmorage, fibrosis, retinal detachment, vision loss
Age is the most common cause of irreversible vision loss AMD environmental exposure, vascular pathogy, AMD effects Macula (part of the eye that sees fine detail.
Rhinoblastoma (cats eye reflex) occurs in children malignant introcular tumor, germline mutation of the RBI gene. cause germ cell mutations that are passed along. whitish hue
Acute Otitis media C: bacterial infection of mucosally lined air containing spaces of the temporal bone. Strep Pn, Haemonphilus Influenzae, and Strep Py occurs in kidsredness and decreased mobility of thetympanic membrane
Chronic Otitis Media Infection of the middle ear and mastoid C: P auriginosa, Proteus, Staph A, Pussy discharge, not tons of pain, hearing loss
Serous Otitis Fluid in the middle earneg. pressure produced by altered Eustachean tub function. common in children with narrow e. tubes. Assoc. with feeding while lying down, URI and Chronic rhinitis The tymp membrane is dull.
Otitis media complications mastoidits, can gain access to CNS meningitis, or brain abscess, facial paralysis, or pain from pressure on nerves cholestoma rupture of TM, chronic infection
Choestoma prolonged auditory tube disfunction chronic negative middle ear pressure, creates a sac that becomes obstructed and filled with desquamated keratin and becoes infected, can errode bone as they penetrate the mastoid and ossicular chaiin-inner e. and fac. n
Otoschlerosis familial, unknown cause, bilateral, most common cause of progressive hearing loss in adults with normal TM, lessions involving footplate of the stape
Acoustic Neuroma benign tumor arrising from Scwann cells 8th cranial nerve usually have tinitus and unilateral sensensoinueuarl hearing loss
Infectiions Rhinitis Common cold Viruses
Allergic Rhinitis Hay fever allergens
Acute and chronic sinusitis consequeces : bone-osteomylitis, cranial vault- septic thrombophebitis.
Thrush Candida albicans debillitated pts HIV, diabetes, steroids for asthma, lack of normal flora
causes of acute Pharyngitis common cold more sverly hemolytic streptococci and adenovirus. also eptien Barr (Mono) may lead to peritonsillar abcesses and scute rhummatis fever
Croup Babies parainfluenza virus could cause respiratory failure Barking cough Larynx
Epiglotits Bacterial in babies H Influenza Hib vaccine also Larynx
Smoking Laryngeal carcinoma , tongue , oral cavity,
Neoplasm growth persits after cessation of stimuli often called a tumor
oncology study of tumors
2 components of tumors parenchyma(neoplastic cells) stroma (connective tissue, blood vessels and host derived inflammatory cells
Benign localized and cannot spread and is amiable to surgery oma
Cystadenoma hollow cystic masses usually seen in the ovary
Sarcoma neoplasm arrising from mesenchymal tissue or its derivatives
mixed tumors pleomorphic adenoma neoplastic cells are differentiated
Tera tomas contain tissues representative of more than one germ cell layer and sometimes all three
Benign vs Malignant 4 features differentiation and anaplasia, rate of growth, local invasion, and metastasis Benign are well differentiated cells that closely resemble their normal counterparts
Anaplasia vary in size and shape lac differentiation giant nuclues
Dyspalsia disorderly but not usually neoplastic usually in the epithelium
Carcinoma in situ dysplastic changes are marked and involve entire thickness of the epithelium
3 pathways of metastasis seeding within body cavity, lymphatic spread(carcinomas- epithelia), hematogenous spread(Sarcomas- mesenchymal)liver and lungs
Cancer incidence # of cases per year
cancer deaths # of deaths per year
Factors that affect cancer Age, genes, geography
Carcinogenesis Initiation (genetic changes introduced Promotion induction of cell prolifferation, Progression- initiatd cells acquire secondary genetic abnormalities- dysregulation, autonomus cell growth
Oncogenes produced by mutations promote autonomic cell growth without normal growth promoting signals
Factors that affect cancer Age, genes, geography
Carcinogenesis Initiation (genetic changes introduced Promotion induction of cell prolifferation, Progression- initiatd cells acquire secondary genetic abnormalities- dysregulation, autonomus cell growth
Oncogenes produced by mutations promote autonomic cell growth without normal growth promoting signals
Sustained angiogenesis the process in which cancer cells stimulate growth of new vessels from preexisting capillaries it contributes to metastesis
Cancers caused by chemical or radiation exposure Tobacco, polycyclic hydrocarbons, aromatic amines and azo dyes, mold, nitrites, , houshold chemicals, Atomic Bomb, UV light
Cancer caused by Viral and bacterial infection HPV, Epstein Barr, AIDS, Hep B and C,
immune surveilance host defence against tumors recognize tumor cells as not self
Tumors effect on a host Bleeding, impingement, hormone production, cachexia(loss of fat and lean body mass), paraneoplastic syndromes
Grading and staging of tumors TNM staging Grading based on level of differentiation and # of mitosis's I to IV, Staging- T-T1-4 primary tumor N- 0-3regional lymph node involvement M- metastses 0-1
Sampling approaches to diagnose tumors Biopsy, Ctologic smears, immunocytochemistry, Tumor markers, Cytometry
Tumor markers check for tumor related enzymes biochemical assay Prosatic PSA
Tumor markers check for tumor related enzymes biochemical assay Prosatic PSA
Hypertrophy adaptation to stress increase in size of cells while number remains the same skeletal and cardiac tissues Thyroid gland enlarges during pregnancy-
Hyperplasia Adaptation Increase in number of cells not skeletal, cardiac, and nerve cells ---hormones Parathyroid increase when serum calcium levels are low pregnancy
Atrophy Addaptation of reducing size and volume of cells
metaplasia reversible replacement of one adult cell with another adult cell ie epithelial cells
Irreversible Injury chronic and apoptosis membrane damage anf nuclear dissolution occur
Necrosis unnatuarl cell dearth cell enlarges and explodes into extracellular
Apoptosis progammed cell death phagocytes clean up crew
Casseous necrosis TB cheese lie
Fat Necrosis Soaps Pancreitis
Mechanisms of cell injury ATP depletion, Mitochondrial damage, Influx of calcium, Accumulation of reactive oxygen species, Increased permeabilty of cellular membrae, Accumulation of damaged DNA and misfolded proteins trigger apoptosis
Fatty change (steatosis) free triglycerides excess intake or defective tranport
Cholesterol (atherosclerosis) defective catbolism and excessive intake smoothe muscle of vessel walls
Iron (hemochromatosis) hemosiderosis
Calcium (atheromas, heart valves, hypercalcemia) usually too much parathyroid hormone
major steps of the inflammatory response Recognition, recruitment, removal, regulation, resolution
Things that effect wound healing Infection, Diabetes, Type of wound, volume of wound, Location of injury
First intention wound healing clean, small minimally invasive
Second intention wound healing more extensive, large clot or scab
Repair in connective tissue Formation of new blood vessels, angiogenesis, Migration and prolifferation of fibroblasts, Deposition of the extracellular matrix(scar formation/collagen synthesis)
Systematic effects of Inflammation Fever, Leukocytosis, Severe: septic shock production of acute phase proteins
ganulomatous inflammation groupings of activated Microphages(granuloms)ie: TB, Leprosy, cat scratch disease, sarcoidosis, crohn disease, syphilis
Chronic inflammation Prolonged host response to persistant stimuli
serous inflammation/effusion outpouring of watery, protein poor fluid, blister
Fibrinous inflammation/resolution and organization serious injury lining of body cavitieslar (firogen pass through endothelial layer results in ingrowth of fibroblasts and blood vessels result in fbrous scar tissue
suppurative inflammation/ abscesses and ulcers large amounts of puscaused by pyrogenic organsms
Stereotypic healing response of vessel walls to injury injury recruitment, smoothe muscles prolifferate, elaboration of ECM
risks of artherosclerosis not changeable- age, male, genetic, family history C: Hyperlipidema, smoke, diabetes, c reactive protein, other; obecity, lack of exercise pneumonoia, menapause, stress
Atherosclerosis Arteries supplting the heart brain kidm=neys and legs primarily effects elastic arteries(aorta and carotid) and large and med sized arteries coronary and popliteal)
BP regulators Kidney (renin)and adrenals
Things that influence BP Heart rate, Cardiac output(blood volume- sodium),peripheral vascular resistance(arterioles)
Hypertension accelerates atherogenesis increases rate of aortic dissection and cerebrovascular hemmorage HT changes the structure of the vessel walls
Essential HT combo of genetic and environment
Secondary HT Biproduct of primary disease usually renal disease
Aneurysm/ arterial dissection abnormal dilation of a blood vessel at the heart/ blood enters the wall of the vessel and separates the layers
abdominal arortic aneurism/aortic dissection Complication of atherosclerosis-Leads to dilation and maybe rupture of vessel----Rupture causing fatal hemorrhage in abdomen
abdominal arortic aneurism/aortic dissection Tear causes blood to enter the vessel wall, bisecting the layers and either bleeding into tissue (e.g. cardiac tamponade or hemothorax) or into body cavity
Varicose veins Varicose veins are abnormally dilated, tortuous veins
Risk factors for deep veinous thrombosis of the legs Risk factors for DVT include congestive heart failure, neoplasia, pregnancy, obesity, the postoperative state, prolonged bed rest or immobilization, and genetic hypercoagulability syndromes.
ANgina chest pain
acute Myocardial infarction Heart attack
syndroms of Ischemic Heart Disease and Coronary artery disease Chronic Ischemic Heart Disease: Development of progressive congestive heart failure as a consequence of long-term ischemic myocardial injury cardiac arrest (death)
acute plaque changes and thrombosis can cause acute coronary syndrome
complications of MI Contractile dysfunction, pericardities, erythmias, mycocardial rupture, infarct expansion, mural thrombis, ventricular aneurism, papillary muscle dysfunction and progressive light heart failure.
relationship of chronic hypertension and cardiac hypertrophy Chronic hypertension causes hypertrophy – the heart has to work harder to pump blood
Cor pulmonale A disease of the right-sided cardiac chambers caused by pulmonary hypertension resulting from pulmonary vascular disease.    Two types: acute and chronic.
general effect of valvular stenosis and regurgitation Causes hypertrophy – heart has to work harder to pump blood out.
Calcific Aortic Stenosis Sclerosis and calcification of the aortic valve.   Aortic valve leaflets are rigid and deformed by irregular calcified masses.loud murmur
Mitral Valve Prolapse accumulation of loose ground substance within the mitral valve, causing the valve to become “floppy” and incompetent during systole.click
Rheumatic Valvular Disease Rheumatic fever may cause chronic valvular deformities
Clinical Features: Acute RF appears most often in children aged 5-15 years
Infective Endocarditis Begins with unexplained fever, septicemia, heart failure, or embolic infarct. Due to virulent organism -- can occur on a normal heart valve. The bacteria proliferate and cause necrosis, generating thrombotic vegetation.
Define cardiomyopathy Disease of the heart muscle
Hypertrophic cardiomyopathy Walls of heart thicken substantially and asymmetrically. May present angina and/or breathlessness upon exertion or fainting. Famously known for sudden cardiac death of young athletes. Often inherited.
pericarditis inflammation of the pericardium
Pericardial effusion accumulation of fluid in the pericardial cavity. Can be caused by blunt chest trauma, a heart malignancy, ruptured MI, aortic dissection, etc. Can restrict heartbeat if pressure gets high enough (cardiac tamponade)
events in hemostasis at the site of vascular injury Arteriolar Vasoconstriction,Primary Hemostasis (aka primary hemostatic plug,Secondary Hemostasis, Antithrombotic Counter-Regulation
hree primary influences on thrombus formation (Virchow’s triad), Endothelial injury,Abnormal blood flow: stasis or turbulence, Hypercoagulability
Mural Thrombi thrombi in heart chambers or aortic lumen. Promoted by abnormal myocardial contraction, ( arrhythmias, dilated cardiomyopathy, or myocardial infarction (including rheumatic heart disease)) or endomyocardial injury (caused by myocarditis, catheter trauma)
Arterial thrombi: thrombi in arterial system. frequently occlusive. produced by platelet and coagulation activation. friable meshwork of platelets, fibrin, erythrocytes, and degenerating leukocytes, usually on athrerosclerotic plaque.
veinous thrombosis (red, stasis thrombi): thrombi in venous system. invariably occlusive. Results from coagulation cascade activation and platelets. Generally occur in veins of the lower extremity.
four possible outcomes of thrombosis: propagation, embolization, dissolution, and organization.
correlations of venous thrombosis Venous thrombi can cause congestion and edema in vascular beds distal to an obstruction. They occur in superficial or deep veins of the leg. Superficial thrombi may varicose ulcers. Deep thrombi may embolize to lungs (pulmonary embolismdeath).
correlations of arterial thombi Arterial thrombi can embolize and cause downstream tissue infarction.(Atherosclerosis). brain, kidneys and spleen are prime targets because of large volume of blood flow. Occlusion at coronary vessel myocardial infarction.
Pulmonary thromboembolism pulmonary arteries or arterioles. (primarily from lower extremity deep vein thrombosis. can cause sudden death, right heart failure, pulmonary hemorrhage, or infarction.
Systemic thromboembolism arterial circulation. (Travel to wide variety of sites, derived from cardiac mural or valvular thrombi, aortic aneurysms, or atherosclerotic plaque. Major sites for systemic emboli are the lower extremities, brain.
Fat embolism microscopic fat gobules in circulation after long bone fractures or other soft-tissue trauma. Pulmonary insufficiency, neurological symptoms, anemia, and thrombocytopenia. Involves mechanical obstruction after skeletal injury
Air embolism gas bubbles within the circulation (can obstruct vascular flow and cause distal ischemic injury. Decompression sickness
Amniotic fluid embolism uncommon complication of labor and the immediate postpartum period. (High mortality rate (20-40%) Sudden severe dyspnea, cyanosis, and hypotensive shock followed by seizures and coma
infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. Nearly 99% of all infarcts result from thrombotic or embolic events, and almost all result from arterial occlusion.
effects of shock (reduced cardiac output, and reduced blood volume) Hypertension, impaired tissue perfusion, cellular Hypoxia
Cardiogenic Shock pump failure
Hypovolemic Shock blood loss
Septic shock hypoperfusion from complicated host innate immune response to bacterial/fungal infection
Neurogenic shock anesthetic accident or spinal cord injury loss of vascular tone, peripheral blood pooling sepsis
Anaphylactic shock immunoglobin E hypersensitivity (allergic) reaction systemic vasodilation, increased vascular permeability sepsis
Endotoxic shock septic shock from gram-negative infections
Clinical Triad of septic shock hypotension, DIC, Metabolic disturbance Hypoxia - systemic vasodilation from cytokine cascade /DIC- activation of coagulation system, culminating in disseminated intravascular coagulation /Metabolic disturbances- hypoxia (insufficient O2)
Identify common causes of heart failure congenital heart diseases, IHD (coronary artery disease), hypertensive heart diseases, heart disease caused by intrinsic pulmonary diseases, valvular heart disease, and primary myocardial disease systolic dysfunction(contraction)
systolic dysfunction- progressive deterioration of myocardial contractile function Diastolic dysfunction- the heart contracts normally but relaxation is abnormal
Forward failure- inadequate cardiac output, almost always accompanied by backward failure. Backward failure- increased congestion of the venous circulation.
L sided heart failure- most common in (coronary artery disease), systemic hypertension, symptoms are primarily related to pulmonary congestion and edema. L Sided CHF results in the progressive damming of blood within pulmonary circulation system Right sided heart failure- is most commonly due to left sided heart failure or to primary pulmonary diseases; it is associated with peripheral edema and visceral congestion.
Created by: mmanges
 

 



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