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Pathology Exam 2 Study Guide: Integumentary System, Study Guides, Projects, Research of Nursing

This comprehensive study guide covers the integumentary system for pathology exam 2. It delves into the structure and function of the skin, its appendages, and various skin conditions. The guide includes detailed information on layers of the epidermis, dermal appendages, primary and secondary skin lesions, common skin diseases, and their causes, symptoms, and treatments. It also explores the respiratory system, covering topics like dyspnea, cough, hemoptysis, abnormal breathing patterns, and pneumonia.

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NR 283 Patho Exam 2 Study guide
Integumentary system
SKIN- largest organ, 20% of body weight
ACCESSORIES
1. hair 3. Gland
2. nails
1. PROTECTION
2. TEMPERATURE REGULATION
3. PROTECT AGAINST MICROOGRANISM
4. LOSS OF BODY FLUIDS
5. STRESS OF MECHANICAL FORCES
6. PRODUCTION OF VITAMIN D
7. IMMUNE SURVEILLENCE
8. PLEASUREABLE SENSATION
EPIDERMIS
Layers
1. superficial outer layer 4. stratum spinosum
2. stratum corneum 5. stratum germinativum
3. stratum lucidum 6. Stratum basale
Keratinocytes- keratin
Melanocytes- melanin
* Vitiligo- autoimmune related loss of melanocytes; depigmentation of patches of skin
Langerhan cells- present processed antigen to T- cells
Merkel cells- function as slowly adapting mechoreceptors
DERMIS
1. deeper layer, true skin
2. collagen, elastin, reticulum, and a gel-like ground substance
3. hair follicles, sebaceous glands, sweat glands, blood vessels, lymphatic vessels, nerves
4. Fibroblast- secrete collagen
5. mast cells- release histamine
6. macrophages- phagocytic immune cells
* Histocytes- loose connective tissue; phagocytize pigments and debris of inflammation
SUBCUTANEOUS LAYER
1. fat cell or adipocytes and connective tissue
2. dermal collagen is continuous w/ the subcutaneous collagen
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NR 283 Patho Exam 2 Study guide

Integumentary system  SKIN- largest organ, 20% of body weight  ACCESSORIES

  1. hair 3. Gland
  2. nails  1. PROTECTION
  3. TEMPERATURE REGULATION
  4. PROTECT AGAINST MICROOGRANISM
  5. LOSS OF BODY FLUIDS
  6. STRESS OF MECHANICAL FORCES
  7. PRODUCTION OF VITAMIN D
  8. IMMUNE SURVEILLENCE
  9. PLEASUREABLE SENSATION  EPIDERMIS Layers
  10. superficial outer layer 4. stratum spinosum
  11. stratum corneum 5. stratum germinativum
  12. stratum lucidum 6. Stratum basale  Keratinocytes - keratin  Melanocytes - melanin
  • Vitiligo- autoimmune related loss of melanocytes; depigmentation of patches of skin  Langerhan cells - present processed antigen to T- cells  Merkel cells - function as slowly adapting mechoreceptors  DERMIS
  1. deeper layer, true skin
  2. collagen, elastin, reticulum, and a gel-like ground substance
  3. hair follicles, sebaceous glands, sweat glands, blood vessels, lymphatic vessels, nerves
  4. Fibroblast- secrete collagen
  5. mast cells - release histamine
  6. macrophages - phagocytic immune cells
  • Histocytes - loose connective tissue; phagocytize pigments and debris of inflammation  SUBCUTANEOUS LAYER 1. fat cell or adipocytes and connective tissue
  1. dermal collagen is continuous w/ the subcutaneous collagen
  1. macrophages, fibroblast, fat cells, nerves, fine muscles, blood vessels, lymphatics, and hair root follicles  DERMAL APPENDAGES
  2. hair, nails
  3. Sebaceous glands - secrete sebum
  4. Eccrine sweat glands - thermoregulate and cool the body through evaporation
  5. Apocrine sweat glands – limited function  Blood supply and innervation
  6. papillary capillaries provide a rich supply of blood
  7. sympathetic nervous system regulates vasoconstriction and vasodilation through a- adrenergic receptors  PRIMARY LESIONS
  8. Macule- flat, circumscribed area that a change in the color of skin (freckles, measles)
  9. wheal- transient lesion w/ well defined and often changing borders caused by edema of the dermis ( insect bites, allergic reactions)
  10. Papule- elevated, firm, and circumscribed area, measures less than 1 cm (warts)
  11. Pustule- elevated, superficial lesion, filled with fluid ( acne, impetigo)  SECONDARY LESIONS
  12. Excoriation- loss of epidermis, linear, hollowed, crusted (scabies, scratches)
  13. Fissure- linear crack or break from the epidermis to the dermis, maybe moist and dry (athlete’s foot)
  14. Erosion- loss of a part of the epidermis, depressed area, moist, glisten, rupture of a vesicle or bulla (chicken pox, diaper dermatitis)
  15. Ulcer- loss of epidermis and dermis, concave, varies in size (pressure sore)
  16. pressure ulcer- result of an unrelieved pressure on skin, causing underlying tissue damage
  • shearing forces, friction, moisture
  • occlude capillary blood flow w/ resulting ischemia and necrosis
  • STAGE 1 – nonblanchable erythema of intact skin
  • STAGE 2- partial thickness, skin loss, involves epidermis or dermis
  • STAGE 3- full thickness, skin loss, involving damage or subcutaneous tissue
  • STAGE 4- Full thickness, skin loss w/ damage to muscle, bone, or supporting structures

*varicella- zoster virus ( VZV)

  • intitial infection w/ varicella, followed yrs later by herpes zoster
  1. pain and paresthesia localized to dermatom
  2. vesicular eruptions along a facial, cervical, or thoracic lumbar dermatome
  • compresses, calamine lotion, baking soda
  • anti-viral drugs w/in 72 hours
  • Topical lidocaine patch, anticonvulsant, tricyclic antidepressants  Basal cell carcinoma and squamous cell carcinoma (most common)  Malignant melanoma (most serious) most common cause of skin cancer
  1. chronic UV radiation
  2. sunscreen, protective clothing  Kaposi sarcoma vascular malignancy
  • drug-induced immunosuppression (after kidney transplant)
  • exhibited on lower legs of man (classic form)
  • epidemic and nonepidemic form related AIDS *Kaposi- associated herpes virus 8 (HHV-8) found in all forms *purpleish – brown macules, developing into plaques and nodules *local lesions- surgical removal
  • multiple disseminated- combination of immunomodulatory, cytotoxic, and antiviral drugs *highly active antiretroviral therapy (HAART) for AIDS  Aging skin *reflects environmental and genetic changes *thinner, dryer, wrinkles, and changes in pigmentation *# of capillary loops shorten and decrease
  • melanocytes and Langerhan cells decrease *sebaceous, eccrine, and apocrine gland atrophy *wound healing delayed *temp. regulation delayed
  • pressure, touch receptors, free nerve endings decrease  Pityriasis rosea- *Circular single lesion *well demorcrated

*salmon pink

  • secondary lesions extend over trunk and extremities  Vegetans pemphigus- large blisters in tissue folds of the axilla and groin area  Erythmea multiforme- “BULLS EYE” or target lesions  Acne Rosacea *inflammation of the skin *bulbous nose *conjunctivitis  Furuncles- inflammation of the hair follicles  Tinea capitis- fungal infection of the scalp  Scleroderma- massive deposits of collagen w/ fibrosis  Pulmonary disease *dyspen and cough * cyanosis
  • altered breathing * chest pain
  • Hyperventilation * clubbing
  • hemoptysis
  • abnormal sputum  Dyspnea *subjective sensation of uncomfortable breathing
  • severe dyspnea
  1. flaring nostrils
  2. use of accessory muscles of respiration 3.retraction of intercostal spaces
  • dyspnea on exertion
  1. shortness of breath w/ activity *orthopynea- dyspynea w/ lying down *paroxysmal nocturnal dyspnea- awaking at night and gasping for air (need to sit or stand up)  Cough- protective reflex that helps clear the airways by explosive expiration *acute cough- resolves in 2 to 3 weeks *chronic cough- lnger than 3 wks *abnormal sputum – changes in the amount, consistency, color, odor, provide information about disease  Hemoptysis- coughing up blood or bloody secretions

*infection and inflammation of parietal pleura accompanied by pleura stretch during inspiration and pleura friction rub  Chest wall pain may due to airway, muscle, or rib pain  Hypercapnia- increased carbon dioxide (Co2) in arterial blood *occurs from decreased drive to breathe or an inadequate ability to respond to ventililatory stimulation.

  • caused by
  1. disease of medulla
    1. large airway obstruction
    2. thoracic cage abnormalities
    3. depression of respiratory center  Hypocapnia *assessed for sever anxiety *results in alkalosis *confirmed by PaCO2/sub>36mmHg  Hypoxemia- *shunting
  • alvelolar dead space – area where alveoli are ventilated but not perfused  Pneumonia- infection of lower respiratory tract *responsible for more disease and death than any other infection *streptococcus pneumonia- community acquired pneumonia)
  • healthcare associated pneumonia *ventilator – associated pneumonia
  • ROUTES OF INFECTION- aspiration, inhalation, endotracheal tubes, and suctioning  Pneumoccal pneumonia- acute lung injury (ALI), resulting in inflammatory cytokines and cells, causes alveolar edema *edema aids in the spread of infection into adjacent portions of lung *involved lobe undergoes consolidation *PHASES
  1. consolidation
  2. red hepatization
  3. grey hepatization
  4. Resolution  Viral Pneumonia *seasonal, mild, self-limiting
  • can set the stage for secondary bacterial infection *Influenza *chills, malaise, pleuritic chest pain, cough, fever, dyspnea, proceeded upper respiratory infection
  • vaccination, antibiotics, isolate, deep breathing, hydration, adequate O2, anti-viral/anti-fungal in severe cases  Nosocomial pneumonia- pseudomas aeruginosa ( pathogen)

 Aspiration pneumonia risk factors *amount, size, pH, of aspirate *bacterial content present in aspirate  Small cell carcinoma= antidiuretic hormone producing lung tumor  Acute respiratory distress causes *TB, inhalation of excessive amounts of coal dust, Reumatoid arthritis(pulmonary fibrosis)  Chronic cough resulting from viral infection: *return for treatment if cough persists after 8 wks *acess for GERD *acess for allergic rhinitis  Risks for chronic upper airway obstruction *congenital malformations *subglottic stenosis  Tuberculosis *Myobacterium TB *acid-fast bacillus *leading cause of death from a curable infectious disease

  • air borne *granulomatous lesion *causeous necrosis (cheese-like material) *may remain dormant or cause disease *isolation of bacilli *latent TB = asymptomatic *fatigue, weight loss, anorexia, low grade fever in after noon, night sweats, purulent cough
  • PPD, chest x- ray, sputum culture *Isoniazid, Rifampin, Pyrazinamide, Ethambutol (for 18 mths, review at 6)  Obstructive pulmonary disease *airway obstruction is worse w/ respiration *emptying lungs is slowed, more force/ time is required to expire *wheezing, dyspnea *increased work of breathing *perfusion mismatching *decreased in FEV (Forced expiratory volume) in 1 sec *can lead to asthma, chronic bronchitis, emphysema, COPD  Asthma- chronic inflammatory disorder of the bronchial mucosa *causes bronchial hyperrepsoniveness, constriction of airways, obstruction
  • one half of all cases develop in childhood *hygiene hypothesis *familial disorder *bronchospasm attacks, bronchial inflammation, mucosal edema, increased mucosal production *Early asthmatic response ***IgE responses

*loss of elastic recoil *primary emphysema (genetic) *secondary ( smoke, environment)

  • destruction of alveoli
  • oxidative stress *apoptosis of lung’s structural cell *alveolar destruction produces large air spaces w/ in lung parenchyma (bullae) and air spaces adjacent to pleurae (bleb) *dyspnea, tachypnea, BARRELL CHEST, leans forward to increase lung capcity
  • O2, inhaled bronchodilators, oral or inhaled corticosteroids, antibiotics, anticholinergenics, beta agonist  Pulmonary vascular disease- any condition that affects the blood vessels along the route between the heart and lungs. *causes may be due to pulmonary arterial hypertension, pulmonary venous hypertension, pulmonary embolism, chronic thromboembolic disease  RIGHT HEART FUNCTION
  1. pumps blood throughout the lungs (pulmonary circulation)
  2. delivers bloods to the lung for O
  3. low pressure system  LEFT HEART FUNCTION
  4. pumps blood (oxygenated) through the circulation
  5. delivers metabolic waste products to lungs, kidneys, and liver
  6. high pressure system  Arteries- carry blood away from the heart (thick walls, oxygenated)  Veins- carry blood to the heart (deoxygenated)  Capillaries- exchange fluids between the blood and interstitial space  Pericardium *double walled membranous sac *parietal- surface layer *visceral- inner layer (epicardium) *prevents displacement, acts as a physical barrier, pain & mechanoreceptors, brings force to normalize BP  Pericardial cavity *space between parietal and visceral layers *contains pericardial fluids (20mL)  Thoracic duct receives lymph from most of the body  Angiotension II - vasoconstriction  CHAMBERS OF THE HEART

*right atrium *left atrium *interatrial septum *right ventricle *left ventricle *interventricular septum *thickness of each chamber depends on pressure or resistance it must over come to eject blood  Atrioventricular valves (AV’S)- one way blood flow from the atria to ventricles  Semilunar valves- one way flow from ventricles to either pulmonary artery or aorta  Distole- relaxation (ventricles fill)  Systole- contraction (blood leaves ventricles)  CARDIAC CYCLE *PHASE1- atrial systole or ventricular diastole *PHASE2- isovolumetric ventricular systole *PHASE3- ventricular ejection ( semilunar valves open) *PHASE4- isometric ventricular relaxation (aortic valves close) *PHASE5- passive ventricular filling (mitral and tricuspid valves open)  S1- “LUB”  S2-“DUB”  S3-ventricular gallop (early diastole)  S4- atrial gallop (late diastole)  Caridiac output- HR X STROKE VOLUME = CO  BLOODFLOW

  1. right atrium from superior vena cavae 8. left ventricle
  2. tricuspid valve 9. aortic valve
  3. right ventricle 10. systemic
  4. pulmonary trunk 11. inferior vena cavae
  5. pulmonary arteries
  6. Pulmonary viens
  7. left atrium  Coronary circulation – supplies oxygen and other nutrients to the myocardium *coronary arteries protect form ischemia and formed by arteriogenesis or angiogenesis
  • coronary capillaries- where gas exchange of O2 and other nutrients takes place *coronary viens- coronary sinus, great cardia vein, posterior vein of left ventricle  CONDUCTING SYSTEM

 Myocardial contraction- represents the intrinsic ability of the heart/ myocardium to contract. Changes in the ability to produce force during contraction result from incremental degrees of binding between myosin (thick) and actin (thin) filaments.  Excitation contraction coupling- process where action potential triggers the cycle of events, leading to a cross bridge activity and contraction *requires calcium

  • calcium troponin complex facilitates contraction  Myocardial relaxation- *calcium, troponin, tropomysin needed to facilitate
  • troponin release of calcium begins relaxation *vital to optimal cardiac function  Cardiac output- volume of blood flowing through wither systemic or pulmonary circuit *HR X STROKE VOLUME= CO
  • ejaction fraction- amount of blood ejected per minute ( 55% or higher in normal adult)
  1. indicator of ventricular function
  2. stroke volume/ end diastolic volume
  • preload- pressure generated at the end of diastole
  1. AKA- LEFT VENTRICULAR END DIASTOLIC PRESSURE (LVED)
  2. determined by 2 factors
  3. amount of venous return to ventricle
  4. blood left in ventricle after systole or end systolic volume
  5. when preload exceeds physiologic range, further muscle stretching causes a decline in CO2.
  • Afterload
  1. resistance to ejection during systole
  2. aortic systolic pressure is a good index of afterload for the left ventricle
  3. decrease afterload, heart contracts more rapidly
  4. increase afterload, slows contractions and increase work load  Frank’s starling law *volume of blood at the end of diastole *myocardial stretch determines force (more stretch= increase force of contraction) *major way that the right and left ventricles maintain equal minute outputs, despite stroke output variation  Myocardial contractibility *stroke volume *changes in stretching of ventricular myocardium caused by changes in ventricular volume (preload) *alterations in nervous system input to the ventricles *adequate of myocardial O2 supply:
  5. inotropic agent- increase the force of contraction
  6. norepinephrine – from sympathetic nerves
  7. epinephrine – from adrenal cortex
  8. thyroid hormone and dopamine
  9. negative inotropic agents- decrease the force of contraction
  10. acetycholine- releases from vagus nerve
  11. hypoxia- decreases contractility

 Hear rate- 70 BPM *cardiovascular control center *neural reflexes

  1. sinus arrhythmia
  2. baroreceptors reflex- when BP fall, heart rate increases, arterioles constrict
  3. brainbridge reflex- changes in heart rate from IV infusions
  • atrial receptors *hormones and biochemical  Cardio inhibitory center- parasympathetic excitatory neurons  Systemic circulation *arteries *viens *arterioles *peripheral vascular system – systemic circulation that *capillaries supplies skin and extremities *venules  Angiogenesis- growth of new vessels that branch from existing vessels (branches from small vessels)  Arteriogenesis- branching from larger vessels  Vasculgenesis- growth of vessels from progenitor or stemlike cells that originate in bone marrow and other body tissue  Cigarette smoke can increase thrombotic state  Endothelium Roles *transport *coagulation *antithrombogenesis and fibrolysis *immune system function
  • tissue growth and wound healing
  • vasomotion – contraction and relaxation of vessels  Velocity and viscosity affect blood flow  Hypertension – (high BP)- increase cardiac output or total peripheral resistances or both *120-130 systolic/ 80-90 diastolic *older age *hypertension can cause damage to the arteries *can cause heart disease, stroke, kidney disease, bone loss *risk factors- obesity, race, gender, high sodium, sedentary lifestyle, stress, age, family history, congestive heart failure (secondary occurenc)  CORONARY ARTERY DISEASE (atherosclerosis) *fatty streak, raised fibrous plaque, smooth cell proliferation *insufficient blood supply to the heart, the heart muscle does not receive the oxygenated blood it requires *antiplatelets- nitrates, beta adrenergic blockers, calcium channel blockers *chest x ray, lipid level, ECG, stress test, LDH, coronary angioplasty, tomography, cardiac troponin

 Deep vein thrombosis- destruction of venous flow leading to increase venous pressure ( venous stasis can be factor)  CONGESTIVE HEART FAILURE- cardiac dysfunction that result in inadequate perfusion of tissues w/ blood borne nutrient *systolic heart failure- pulmonary congestion, left EJ will be greater than 40, filling defect *right heart failure- commonly caused by a diffuse hypoxic pulmonary disease *high output failure- heart can’t keep up w/ demand  Mitral regurgitation- *can be due to abnormalities of valves, annulus, chordae, tendinae, papillary muscle of LV *common causes can be degenerative (myxomatous) disease, ischemia heart disease, infectious endocarditis  Pericardial effusion- (blood effusion) *endocardium inflamed by staphylococcus aureus *resulting in the presence of frank blood (coagulation defect)  Infectious endocarditis *SLE, Marfan’s syndrome, Danlos syndrome *A-fib *forceful, displaced, systolic thrill *soft S1, S *Pansystolic *Barlow’s syndrome- floppy mitral valve  Aortic regurgitation *asymptomatic for yrs *develop LV failure (dyspnea, orthopnea, fatigue) *collapsing pulse, laterally displaced apex beat (thrusting), wide pulse pressure *CORRIGAN’S SIGN- carotid pulsations *DE MUSSET’S SIGN- head nodding w/ each beat *QUINCKE’S SIGN- capillary pulsations

  • TRAUBE’S- “pistol shot” sound over a femoral A. *AUSTIN FINT MUMUR- mid diastolic murmur over cardiac murmur  Aortic stenosis- orifice of the aortic semilunar valves narrow causing diminishing blood flow from left V into aorta  Mitral stenosis- impaired blood flow from left atrium to left ventricle  Dyslipidemia- low lipoproteins (VLDL) triglycerides and proteins  Cellular injury of myocardium – myocardial cells remain viable if blood returns in 20 min.  Hemoglobin carries oxgen  Hematopoiesis- production of blood cells and platelets  Agranulocytes- lymphocytes and monocytes  Granulocytes- neutrophils, basophils, eosinophils

 Erythropoietin – a hormone released by the kidneys that stimulate RBC production  Reticulocyte- immature erythrocyte  Thrombopoiesis- endothelial cells primary produced in the liver  Red bone marrow- primary site for production and maturation of blood cells and platelets in adults  Leukocytosis- increase WBC’s  Neutrophilia- increase neutrophil  Neutropenia- decrease neutrophil  Lymphocytosis- increase lymphocytes  Leukopenia- low white blood cell count  Ansiocytosis- RBC’s vary in size  Polychromasia- insufficient hemoglobin w/in the cell  Basophilic stippling- caused by intense regenerative anemia or lead poisioning  Rouleaux- grouping of RBC’s in stacks, when increase globulin and fibrinogen  Anemia *fewer circulating RBC’S * hemmorage *decreased PCV *decreased HgB *decreased production  Regenerative anemia- bone marrow able to respond, increase production, releases reticulocytes  Non- regenerative anemia- bone marrow doesn’t respond, no reticulocytes  Hypoxia- blood loss/anemia, decrease in RBC OR Hb  Polycythemia- excess EPO production by kidneys  Micocytic hypochromic anemia- *iron metabolism *globin synthesis *parphyrin synthesis *heme production  B12- required for nerve myelination, extended deficiency can cause neurological damage

  1. absorption of B
    1. complex w/ intrinsic factor
    2. transported to ileum
    3. B12 combines w/ transcobalamin II to be transported to PB and tissues
    4. stored in liver
  • distributed by TC1 (plasma), TC2 ( cells), TC3 ( liver)
  • causes of B12 deficiency
    1. pernicious anemia 6. Ideal resection and
    2. lack of intrinsic factor and Coron’s diease

 Gaucher’s disease- accumulation of glcusycoramide in lysosomes of reticuoendothelial cells due to glucocerebrosidase deficiency  Kostmann’s syndrome- neutropenic disease  Thalassemia major- anemias w/ bone deformities  Stromtolites present in alcoholism and liver disease  Factors in increase Iron absorption *acids * iron deficiency *vitamin C * primary hemochromatosis *inorganic iron *sugars/ amino acids  Factors in decrease Iron absorption *alkalis * excess iron *Antacids * decrease utilization *organic iron *gastroectomy *Ferric iron *achlohydria

  • phytates *intestinal mucosal abnormalities *tea  Duodeum and upper jejunum – site of iron absorption  Iron deficiency- caused by altered heme synthesis in erythiod cells *hemoglobin of 7g/dl to 8g/dl accompanied by pallor *common in children due to their extremely high need for iron for normal growth  Infectious mononucleosis is commonly caused by EBV ( Epstein Barr virus)  Lymphoma- palpable and tender nodes  Hodgkins lymphoma- peak incidence occurs in the early 20’s through 30’s and then later in life  Burkitt lymphoma- fast growing tumor of the jaw and facial bones  Spontaneous bleeding w/out trauma is possible when platelet count is less than 10,  Heparin is most common drug induced thrombosytopenia  Thrombocytopenic Pupura (TTP) *more common in females
  • caused by platelet aggregates *occurring more frequently  Analgesics – used for chest pain  Triad of Virchow *injury to endothelium *abnormalities to blood flow *hypercoagulability of the blood  Spinal cord damage will result in VASOGENIC SHOCK