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NURSING NUR 2063 Essentials of Pathophysiology - Exam 1 review sheet, Exams of Nursing

NURSING NUR 2063 Essentials of Pathophysiology - Exam 1 review sheet NURSING NUR 2063 Essentials of Pathophysiology - Exam 1 review sheet NURSING NUR 2063 Essentials of Pathophysiology - Exam 1 review sheet

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Download NURSING NUR 2063 Essentials of Pathophysiology - Exam 1 review sheet and more Exams Nursing in PDF only on Docsity!

Essentials of Pathophysiology – Exam #1 Review Sheet Covers Modules 1, 2, and 3 – Chapters 1, 2, 3, 7, 8, 9, 10, 24, 51, 52, 53

1. Define pathophysiology. What does the study of pathophysiology include? - PATHOPHYSIOLOGY : The study of all the abnormalities in physiologic function of living beings. o Derives from 2 disciplines :

Patho meaning Dx of diseases through exam of organs, tissues, and cells.

Physiology meaning Mechanical, physical, and biochemical functions. o There are FOUR parts of pathophysiology: 1- Etiology: causes/reasons of disease. This ID’s causal factors for Dz 2- Pathogenesis: Evolution of Dz from the initial stimulus to ultimate manifestations of the Dz. (GENESIS = CREATE)

2. Review terms such as signs, symptoms, acute, chronic, exacerbation, remission, convalescence, and sequela - Signs: objective/observed manifestations o Ex: rash, change in temperature - Symptoms: Subjective o Ex: pain, nausea - Acute: short-lived. - Chronic: lasts for months/years - Exacerbation : increase in severity - Remission: decrease in severity - Remission: decrease in severity - Convalescence: Stage of recovery - Sequela: subsequent pathological condition resulting from an illness o Ex: renal failure 2/2 HTN o

3. What is epidemiology? Review the different levels of disease prevention such as primary, secondary, and tertiary as well as examples for each. - Epidemiology is the study of study and analysis of the distribution, patterns and determinants of health and conditions in defined populations. o Primary level: altering susceptibility a. Ex: Immunizations o Secondary level” early detections/screenings a. Ex: Pap smears, breast exams, cancer screenings o Tertiary level: Rehabilitation (reduce disabilities) a. Ex: PT/OT after a stroke - Florence Nightingale was the first practicing epidemiologist.

4. Review the difference between homeostasis and allostasis. - Homeostasis: The process by which a state of internal, physiological equilibrium is maintained. o Ex: pH, concentration of ions in ECF, glucose levels, osmolality of ECF - Allostasis: Steps the body takes to re-establish homeostasis. Adaptation to a changing internal and external environment o Ex: HR, body core temperature, BP 5. Review the three different stages of the General Adaptation Syndrome (GAS) including the alarm stage, adaptation/resistance, and exhaustion stage. What hormones are released during the alarm stage and what effects do they have on the body? - Three stages of GAS: 1: Alarm Stage: Fight/Flight response. 2: Resistance/Adaptation: Activity of nervous/endocrine systems to return to homeostasis 3: Exhaustion: If stressor is not removed the body cannot return to homeostasis. The body will go into allostatic overload and organs tissues give out. o Ex: renal failure 2/2 HTN

Stressor Excites receptors

Hypothalamus relases

CRH + ACH This activates the SNS

Providing a surge of

energy

Adrenal Medulla releases catecholamines (epinepherine and Norepinepherine)

Increased cardiac output,

increased respirations,

enhanced blood coag.

increased BP, dialated

pupils, increadd BG (energy),

GI/GU supressed.

Adrenal Medulla releases cortisol due to ACTH. (^) Corticosteroids stabilize vascular

reactivitiy, inhibit glucose uptake, suppress protein sysnthesis

*inhibit release of CRH+ACH fron the hypothalamus

6. Review the differences between the sympathetic vs the parasympathetic nervous systems. What happens to the body during “fight-or-flight” response?

7. Review the functions of the various organelles of the cell such as the nucleus, mitochondria, ribosome, lysosome, endoplasmic reticulum, peroxisome, golgi apparatus - Nucleus - Control center or “brain” of the cell - DNA and genes stored here - Production of messenger RNA - Contains the instructions needed to build nearly all the body’s proteins Most cells contain only one nucleus

  • Some cells like liver and skeletal muscle cells contain more
  • Red blood cells contain no nucleus
    • Mitochondria - “Power house” of the cell
      • Provide energy to the cell in the form of ATP
      • More metabolically active cells have more mitochondria
    • Mitochondria are enclosed by two membranes
      • Outer membrane
      • Inner membrane has folds called cristae
      • Mitochondria are a unique organelle because they contain their own set of DNA
    • Ribosomes
      • Site of protein production - RNA produced in nucleus sent to ribosomes
      • RNA Protein = Translation
      • Found either floating in the cytoplasm (free) or attached to the endoplasmic reticulum (bound)
  • Endoplasmic Reticulum (ER)
    • Series of folded membranes that move proteins around the cell
    • Continuous with nuclear membrane of nucleus
  • Rough ER – ribosomes attached to ER
  • Site of protein synthesis
  • Production of integral proteins and phospholipids found in cellular membranes
  • Smooth ER – ribosomes not attached to smooth ER
  • Functions include:
  • Detoxification
  • Lipid metabolism
  • Synthesis of hormones
  • Calcium storage - Golgi Bodies (Golgi Apparatus)
  • Organelle made up of stacked, flattened membranes
  • Sorts and packages proteins produced in ER
  • Protein “packaging plant” – cell post office
  • Move materials within cell and out of the cell - Lysosomes
  • Lysosomes are spherical membranous organelles containing digestive enzymes
  • Lysis = breakdown
  • Digests particles taken in by endocytosis
  • Including bacteria, viruses, and toxins
  • Degrades worn-out or nonfunctional organelles and tissues - Peroxisomes
  • membranous sacs containing a variety of powerful enzymes such as oxidase and catalase
  • Oxidases use molecular oxygen (O 2 ) to detoxify harmful substances such as alcohol and f formaldehyde
  • Neutralize dangerous free radicals into hydrogen peroxide (H 2 O 2 ) ▪ Free radicals - highly reactive chemicals with unpaired electrons that can damage biological molecules
  • Catalase breaks down hydrogen peroxide (H 2 O 2 ) into H 2 O and O 2
  • Numerous peroxisomes found in liver and kidney cells 8. Review the differences between extracellular fluid and intracellular fluid. Which electrolytes are found in high concentration outside the cell versus inside the cell?
  • Water accounts for ½ body mass o Males: 60% o Females 50 % o Infants: 73%
  • Water occupies 2 main fluid compartments o ICF (75%): fluid within the cells o ICF has increased concentrations of K+, Magnesium, and HPO4. Has less NA and Cl.

o ECF (25%): Fluid in-between cells (interstitial fluid)

o Ex: blood plasma, CSF, lymph fluid, synovial fluid, GI secretions

o The ECF has increased concentrations of Na+, Cl, and HCO o Also contains plasma therefore has higher concentrations of proteins.

9. Review how fluid is transported across the plasma membrane of the cell. What forces drive the movement of water across the membrane? 1. Passive: Moves down a concentration gradient (HIGH - > LOW) 2. Active: Requires ATP (LOW -> HIGH) 3. Osmosis: movement of water between ICF and ECF. o Know osmolality: concentration of solutes o Water moves from area of low osmolality to an area of higher osmolality. o Ex: if ECF osmolality is decreased, water will move from the ECF into the cells o ICF volume is determined by ECF solute concentration.

  • Increase in plasma osmolality triggers: o Release of antidiuretic hormone (ADH) o Kidneys conserve water and excrete concentrated urine o Thirst - causing us to drink water
  • Decreased osmolality of plasma inhibits both thirst and ADH release o Results in output of large volumes of dilute urine 10. Review ways that fluids enter the human body (intake) versus ways fluid is excreted (output) out of the body.
  • Intake: Ingested Liquids/food, cellular metabolism
  • Output: Urine, sweat, feces, exhaled air 11. Review conditions that result in ECF volume deficit (dehydration) versus ECF volume excess (hypotonic hydration). What are signs, symptoms, and causes for each?

Dehydration: H20 output exceed intake. H20 from ECF is LOST

Osmolality of ECF increased and H20 moves from ICF to the ECF o Common after N/V/D, hemorrhage, burns, sweating o Due to DM/Diabetes insipidus

- S/S of Dehydration: o Dry mouth, thirst, decreased urine output o If prolonged: weight loss, hypovolemic shock, fever, confusion

Hypotonic Hydration: Over Hydration.

o Occurs with rapid water intake OR decreased renal activity. o Concentration of water in ECF is increased and osmolality of ECF is decreased

  • S/S of Hypotonic Hydration: N/V, muscular Cramps o N/V, Muscular cramps, cerebral edema. o Treatment: IV hypertonic saline solution (pulls water out of the cells)

12. What is edema? Review the various factors that can contribute to edema.

  • Edema: The accumulation of fluid in the interstitial space due to the increase in forces that move fluid from capillaries to interstitial compartment. OR decreased forces that move fluid from interstitial compartment to capillaries. Factors Contributing to Edema:

o Inflammation, CHF, HTN, decrease in plasma proteins, blockage of lymphatic drainage, increase in hydrostatic pressure.

13. Why are electrolytes important?

  • Control fluid movement
  • Provides minerals for secretory activity
  • Permeability of cells o Regulation of Sodium Balance: o Normal Level (125 – 145) o Enters Body: Foods + Fluids o Leaves Body: feces, urine, perspirations o Kidneys play an important role in sodium regulation.

o Regulation of Potassium o IMPORTANT FOR CARDIAC CONDUCTIVITY o Normal level 3.5 – 5. o The heart is sensitive to K+ levels o Plays role in neuromuscular function and metabolic activities

o Regulation of Calcium o 99% of calcium is found in the bones o Important in blood clotting o Closely regulated by PTH.

4

14. What hormones play a role in regulating electrolyte levels?

Aldosterone: Retains Sodium o When aldosterone concentrations increase Na+ is reabsorbed by the kidneys ▪ Promotes sodium and H2O retention PTH is important for calcium regulation.

  • Decrease in plasma levels of Ca2+^ stimulates release of PTH
  • Promotes an increase in calcium levels by targeting: o Bones - PTH activates osteoclasts which break down bone matrix ▪ Increased release of Ca2+^ and HPO 2 –^ to the blood 15. What are electrolyte reservoirs? What electrolytes are found stored in bones? - C, K, and Magnesium found in bones

16. What are the cardinal signs and symptoms of inflammation? What lab tests can detect inflammation in the body?

▪ The five cardinal signs are o Redness, Heat, Swelling, Pain, and Loss of function ▪ Lab tests that can detect inflammation o ESR – measures the rate at which the RBC’s (erythrocytes) settle at the bottom. o Increases with inflammation o CRP – will be elevated with inflammation

17. Review the role of histamines, prostaglandins, and leukotrienes. What effect do they have on the body during an immune response? - Histamines, Prostaglandins Leukotrienes result is s/s of inflammation o They are chemical mediators that cause vasodilation o This increases blood flow and capillary permeability o Allows for movement of leukocytes to site of tissue injuries 18. Review the differences between innate and adaptive immunity, which is specific? Which is nonspecific? - Innate: born with – body is equipped with mechanisms - Ex: skin barrier, mucous membranes (secretions, tears, saliva), low PH of stomach - Non-specific - Immune response occurs on initial exposure to antigen o Sx involve fever, inflammation, phagocytes, and natural killer cells - Adaptive: things that can evolve over time - Specific - Slow to develop - More efficient on subsequent exposures o Includes B-cells and T-cells 19. Review the following terms: virulence, invasion, exotoxin, endotoxin, and antimicrobial resistance. What factors contribute to antimicrobial resistance in microorganisms? How can we prevent the spread of microorganisms? - Exotoxins o Excreted by a living cell, with high concentrations in liquid

  • Endotoxin o Integral part of the bacterial cell wall o Released upon cell death/destruction ▪ Either due to immune response or antimicrobials o Can be fever producing, lead to sepsis/septic shock
  • Virulence - microorganism’s ability to cause severe disease
  • Invasion - how the microorganism invades the host
  • Usually through the skin
  • Antimicrobial Resistance - resistant strains of microorganisms emerge following exposure to antibiotics
  • Caused by excessive use of antibiotics or subtherapeutic dosing
  • Susceptible strains die, creating a drug-resistant infection **20. Review the difference between active and passive immunity, know examples for each type.
  1. What is a hypersensitivity? Review the four different types of hypersensitivities: Type I (Anaphylactic), Type II (Cytotoxic), Type III (Immune complex), Type IV (Delayed cell-mediated). Know examples and mediating factors for each type.
  2. Review the differences between benign and malignant tumors.
  3. What are the three steps of carcinogenesis?**
  • Initiation o Initiating events include: ▪ Genetic mutations which inappropriately activate proto-oncogenes ▪ Inactivate tumor suppressor genes, ▪ Each type of cancer has its own combination of mutations that lead to malignancy
  • Promotion ▪ Stage during which mutant cell proliferates ▪ Activation of another oncogene ▪ Inactivation of tumor suppressor gene ▪ Nutritional factors ▪ Infection o Regulated by many hormonal growth factors ▪ Such as estrogen and testosterone ▪ Cancer cells produce telomerase ▪ Allows immortality in cancer cells - Progression o Mutant, proliferating cells begin to exhibit malignant behavior o Cells whose phenotype gives them a growth advantage proliferate more readily o Evolved tumor cells differ significantly from the normal tissue

24. Review the effects of cancer on the body including terms: cachexia, anemia, leukopenia, and thrombocytopenia.

Pain – possible result of metastasis, tissue destruction/inflammation Cachexia - overall weight loss and generalized weakness o Loss of appetite (anorexia) o Increased metabolic rate o Nausea/vomiting Bone marrow suppression - caused by invasion and destruction of bone marrow cells, poor nutrition, and chemotherapy. contributes to anemia, leukopenia, and thrombocytopenia o Anemia - deficiency in circulating red blood cells o Leukopenia - deficiency in circulating white blood cells o Thrombocytopenia - deficiency in circulating platelets

25. Review the various infections of the skin discussed in class including: warts, herpes simplex virus, herpes zoster, fungal infections, impetigo, and leprosy.

  • Warts (verrucae ): benign papilloma’s caused my DNA containing papillomaviruses o Can be characterized as thickened composition of skin o Treatment: Liquid Nitrogen, Cryotherapy, Salicylic acid, topical blistering agents, immunomodulators, intralesional injections
  • Herpes Simplex Virus: o TWO TYPES : HSV-1 and HSV- o HSV-1: common on the lips, face, and mouth ▪ Include cold sores – heals in 10-14 days o HSV-2: genital o Usually beings with a burning or tingling, vesicular formations/erythema. Crusts before healing o No cure, analgesics for pain, antivirals to shorten duration of outbreaks.
  • Herpes Zoster o SHINGLES: acute localized inflammatory dz of a dermatomal segment of the skin caused by varicella zoster o Results from reactivation of the latent virus o Causes eruption of painful vesicles with erythematous bases typically unilateral. Causes paresthesias o Treatment: Antiviral drugs o Prevention: vaccination
  • Fungal Infections o Superficial Fungal Infections o Three main types infect human skin: Microsporum Trichophyton Epidermophyton o Infection (tinea) named after location: Tinea capitis (scalp)

tinea barbae (beard) tinea faciei (face) tinea corporis (trunk) tinea manus (hand); tinea cruris (groin) tinea pedis (foot) o Erythematous macules or plaques with peripheral scaling and central clearing o Topical antifungal such as clotrimazole usually effective, systemic therapy for resistant infections such as fluconazole (Diflucan)

  • Yeast Infections o Candida albicans common source of superficial skin infections o Manifests as thrush (infants), intertrigo (infants and bedridden patients), and mucocutaneous candidiasis (immunocompromised) o Treatment : Oral candidiasis - nystatin mouth rinse and clotrimazole troches Topical antifungals/systemic meds if severe
  • Bacterial Infections
  • Impetigo: o Acute contagious skin disease characterized by vesicles, pustules, and yellowish crusts; usually caused by staphylococci or streptococci o Treatment: Topical application of 2% mupirocin ointment or 1% retapamulin ointment Oral antibiotics for large area of infection or if febrile
  • Syphilis: o Sexually transmitted disease caused by Treponema pallidum Primary syphilis - single chancre on genitalia Secondary syphilis - disseminated rash Tertiary - permanent cardiac and CNS damage o Diagnosis - serum antibodies (VDRL), microscopic evaluation of exudate from pustules for spirochete o TREATMENT: Penicillin very effective in eradicating primary and secondary syphilis
  • Leprosy o Chronic infectious disease caused by the intracellular bacillus Mycobacterium leprae o Diagnosis - skin biopsy o Treatment: Usually responsive to sulfone drugs. Corrective orthopedic surgery may be required

26. Review the various inflammatory conditions of the skin discussed in class including: lupus, psoriasis, atopic and contact dermatitis.

  • Lupus Erythematosus o Two types Discoid lupus: scaly red plaques with scarring that involves sun- exposed skin; slow healing under therapy Systemic lupus: butterfly-shaped erythema involving the cheeks and nose; affects many other organs
  • Psoriasis o Papules and plaques with overlying silvery scale o Inherited condition with immune system involvement o Characterized by: Lesions on knees, elbows, lower back, scalp, nails o Treatments: no cure, topical corticosteroids, vitamin D derivative, ultraviolet light, tar, systemic psoralen, methotrexate, hydroxyurea, or injectable biological agents
  • Atopic Dermatitis o Atopy: genetic component, form of eczema o Most common in children, usually improves with age o Lesions pruritic, oozing, crusting, thickening of the skin or lichenification occurs o Treatment - decrease frequency of bathing, use tepid water in baths, eliminate alkaline soaps, topical steroids, antihistamines, immunomodulatory agents for more severe cases
  • Contact Dermatitis o Cutaneous reaction to topical irritation or allergy, usually results from chemicals or plants o Allergic contact dermatitis indicates delayed acquired hypersensitivity to a specific allergen o Treatment - topical steroids or cooling shake lotions of camphor and menthol, corticosteroids for 10 to 14 days 27. Review parasitic infections of the skin/hair including: lice, scabies, ticks, and bedbugs.
  • Parasitic Skin Infections
  • Scabies

o Sarcoptes scabiei is a mite

o Begins with eggs laid in the epidermis, hatch into larvae within 3 to 4 days o Contracted after close contact with an infested individual o Characterized by linear burrows, small erythematous papules with overlying dry scale or crust o Treatment - topical creams Permethrin (Elimite), γ-benzene hexachloride (Lindane), or crotamiton (Eurax)

Stage I

Stage II

Stage III

Stage IV

Full-thickness tissue loss with exposed bone, muscle, or tendon

Full-thickness tissue loss with visible fat

Partial-thickness skin loss involving epidermis, dermis, or both

Intact skin with nonblanchable redness

  • Lice o Phthirus pubis (crab lice), Pediculus humanus var. capitis (head lice) and Pediculus humanus var. corporis (body lice) are most common in humans o Surface dwelling, usually readily seen o Eradication possible with permethrin cream rinse or pyrethrin and piperonyl butoxide liquid, gel, or shampoo 28. What are pressure ulcers? How are the staged and how can we prevent them?
  • Ulcers o Localized areas of cellular necrosis resulting from prolonged pressure between any bony prominence and an external object such as a bed or wheelchair o Pressure sores or decubitus ulcers most common in bedridden or elderly patients Risks - poor nutrition, aging, immobility, superficial sensory loss, bowel/bladder incontinence
  • Category/Stage I: Nonblanchable Redness. Intact skin presents with nonblanchable redness of a localized area usually over a bony prominence. Discoloration of the skin, warmth, edema, hardness, or pain may also be present. Darkly pigmented skin may not have visible blanching but its coloring may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue.
  • Category/Stage II: Partial-thickness. Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled or serosanguineous filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising. Bruising indicates deep tissue injury.
  • Category/Stage III: Full-thickness Skin Loss. Full-thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a

Category/Stage III pressure ulcer varies by anatomical location. Bone/tendon is not visible or directly palpable.

  • Category/Stage IV: Full-thickness Tissue Loss. Full-thickness tissue loss with exposed bone, tendon, or muscle. Subcutaneous fat may be visible but bone, tendon, or muscle are not exposed. Slough or eschar may be present. Often includes undermining and tunneling. The depth of a Category/Stage IV pressure ulcer varies by anatomical location. Exposed bone/muscle is visible or directly palpable.
  • Unstageable/Unclassified: Full-thickness Skin or Tissue Loss—Depth Unknown. Fu- thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Until enough slough and/or eschar are removed to expose the base of the wound, the true depth cannot be determined, but it will be either a Category/Stage III or IV.
  • Suspected Deep Tissue Injury—Depth Unknown. Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear_._ The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may be rapid even with optimal treatment. 29. What is compartment syndrome? Why does it occur and what are the signs? Remember the 5 P’s
  • Compartment Syndrome o Dangerous complication of soft-tissue injury - results from swelling of injured tissue within a restrictive fascia o Causes - decreased compartment size, increased compartment content, or externally applied pressure o Edema causes increased pressure in the compartment; pressure reduces capillary flow; muscle and nerves become ischemic. o If pressure not reduced, tissue necrosis occurs 30. Review diseases of the bone including: osteomyelitis, osteosarcoma, osteomalacia, and osteoporosis
  • Osteomyelitis o Severe pyogenic infection of bone and local tissue