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Pathophysiology Exam 1 > Pathophysiology Exam 1 > Flashcards

Pathophysiology Exam 1 Flashcards

1
Q

Clinical Manifestations of Inflammation:

A

Heat
Edema
Loss of Function
Pain
Redness

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2
Q

What is the function of Histamine?

A

*Released by degranulation of mast cells
*Vasodilation (redness, heat): vessels increase in size = more blood to area.
*Increased vascular permeability (edema): fluid dilutes agent and moves to interstitial spaces.
*smooth muscle contraction

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3
Q

Clinical Manifestations of Histamine Production:

A

Heat, edema, redness, itching

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4
Q

What are the four different types of hypersensitivity’s?

A

Type I
Type II
Type III
Type IV

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5
Q

Type I Hypersensitivity

A

*Immediate
*IgE and histamine
*Allergies, asthma, anaphylaxis reactions, eczema

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6
Q

Type II Hypersensitivity

A

*Cell specific
*Antibody mediated: IgG or IgM
*Hemolytic Anemia, Graves Disease, Guilain-Barre

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7
Q

Type III Hypersensitivity

A

*Immune Complex Mediated
*Systemic Lupus Erythematosus, Rheumatoid Arthritis

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8
Q

Type IV Hypersensitivity

A
  • Delayed
    *T-Cell Mediated (slow)
    *24-48 hours after exposure
    *TB skin test, Poison ivy
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9
Q

Primary Immune Deficiency:

A
  • Rare genetic disorders generally seen in children
    *Severe infections requiring hospitalization
    *Failure to thrive and poor growth in newborns
    *Wiskott-Aldrich Syndrome, Hypogammaglobulinemia, Severe Combined Immunodeficiency Disease (SCID)
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10
Q

Secondary Immune Deficiency:

A

*More Common
*Physiologic changes (aging, pregnancy, stress), illness (HIV, cancer, autoimmune diseases), malnutrition (drug use, alchoholism), medications (immunosuppressant, chemotherapy)

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11
Q

Difference between HIV and AIDs:

A

*HIV: Entry: Virus enters CD4+ nucleus and becomes part of DNA, Stage 1: Initial period of viremia and drop in blood level, Stage 2: Latent - virus replicates in body for 10-12 years.
*AIDs: Stage 3 of HIV when CD4+ count drops below 200. Client is severely immunocompromised.

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12
Q

What lab is used to determine if patient has progressed to AIDs?

A

*CD4+ Cell Count (<200 is AIDs)
*Western Blot of HIV

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13
Q

Nursing consideration for taking care of AIDs patient?

A

Infection Control

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14
Q

Difference between virus and bacteria?

A
  • Virus: Replicates inside host using cells own structures to manufacture new viruses - most are pathogenic
    *Bacteria: Replicates outside host cell - most not pathogenic
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15
Q

What is opportunistic infection?

A

Infections that occur more frequently and are more severe in people with weakened immune systems

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16
Q

What is the role of normal flora?

A

Prevent colonization of pathogens by competing for attachment and nutrients.

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17
Q

Examples of bacterial infection:

A

Cellulitis
Clostridium Difficile

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18
Q

Pathophysiology of Cellulitis:

A

*Infection of dermis and subcutaneous tissue usually as extension of wound or ulcers and commonly caused by Staphylococcus Aureus. Infected skin can get swollen, red, tender, and may have fever.

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19
Q

Pathophysiology of C. diff.:

A

*Exists outside of host as gram positive anaerobic bacteria (spore) - transmission usually from caregiver to client via fomites or can occur when antibiotics kill normal flora in GI tract. Diarrhea, fever, abdominal pain, nausea, and cramping can all occur.

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20
Q

Examples of viral infections:

A

Varicella Zoster, Herpes Zoster (Shingles)

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21
Q

Clinical Manifestation of Herpes Zoster:

A

*Red rash
*Fluid filled blisters
*Itching
*Pain, burning , tingling
*Lasting Complications: Post-Herpetic Neuralgia

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22
Q

First sign of pressure ulcer:

A

Discolored patches of skin that don’t change color when pressed

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23
Q

Risk factors for pressure ulcer:

A

*Immobile/bedridden patients
* Age 75 or older
*Impaired sensory perception
*Poor nutrition
*Any disease resulting in diminished or altered tissue perfusion
*Fecal/urinary incontinence

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24
Q

Shear

A

Forces that act up skin when gravity causes body to slide while under pressure (hospital bed in raised position)

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25
Q

Friction

A

Forces that pull at skin when body suddenly shifts movement from one direction to another (client repositioned in bed)

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26
Q

Stages of wound healing:

A
  1. Inflammatory (1-3 days): WBC’s enter wound to kill bacteria, macrophages enter to clear any debris and secrete proteins to attach other immune cells to wound for repair - edema, redness, pain
  2. Proliferative (3 days-2 weeks) Proliferates fibroblasts and collagen formation occurs. Granulation tissue formed from bottom to top and new blood vessel capillaries are formed (angiogenesis).
  3. Maturation (3 weeks to >6 months): Reepitheliazation: New tissue grows and grains strength/flexibility. Scar tissue may form over wound site.
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27
Q

What is granulation tissue and why is it important to wound healing?

A

Granulation Tissue: New connective tissue and blood vessels that form in wound during healing. Important because it fills the wound.

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28
Q

What kind of dressing would you use to protect granulation tissue?

A

Moist to prevent dehydration and enhance angiogenesis and collagen synthesis

29
Q

Full Thickness Wound:

A

Affects epidermis, dermis, and underlying fatty tissue/bones/muscles/tendons. Requires new tissue to fill wound and regeneration of epidermis - can take months to heal and may leave scar.

30
Q

Partial Thickness Wound:

A

Affects epidermis, and part of dermis. Bleeds. If left uncovered blood clot will cover wound and scab will form.

31
Q

What is the most severe complication of burns?

A

*Infections

32
Q

What degree of burn is the most painful?

A

Second degree because in third degree all nerve endings are destroyed so there’s no pain.

33
Q

What does rule of 9 do?

A

Helps give an idea of how much of a body surface is taken up by burns.

34
Q

Explain physiological process of production of erythropoietin:

A

Low blood oxygen stimulates the production of erythropoietin (hormone that stimulates RBC production) from the kidneys.

35
Q

Hemoglobin:

A

*Decreased levels indicate anemia, bleeding, or fluid overload
*Increased levels indicate dehydration, Polycythemia vera (PV)

36
Q

Hematocrit (% of packed RBC’s in total blood volume):

A

*SHOWS HYDRATION STATUS
*Decreased levels indicate anemia, bleeding, or fluid overload
*Increased levels indicate dehydration, Polycythemia Vera (PV)

37
Q

Clinical Manifestations of Anemia:

A

*Decrease in RBC’s (Anemia) = low hemoglobin - not enough O2 delivered to tissues
*Rate and depth of breathing increases due to hypoxia
*Fatigue
*Pallor
*Heart palpitations
*Cold hands/feet

38
Q

What is pernicious anemia?

A

*Anemia=low RBC’s
*Folic acid is required for DNA synthesis in RBC’s - needs assistance from B12 to transport to inside of RBC’s - B12 can’t be absorbed without intrinsic factor.
* Strophic gastritis causes causes lack of intrinsic factor so B12 is not available for adequate absorption.

39
Q

Pathophysiology of sickle cell disease and trigger for sickling:

A

*Genetic
*Inherited disorder of abnormal hemoglobin. Decreased O2 causes distortion in shape to RBC’s leading to early death of RBC’s. Sickle celled RBC’s stick together and occlude small vessels.
*RBC’s have shortened lifespan

40
Q

What is Polycythemia Vera?

A

*(many-cells-condition in blood) Absolute increase in total RBC mass accompanied by elevated WBC and platelet counts.
*Blood cancer
*Occurs in bone marrow
*Increased blood viscosity and low O2 to tissue due to decreased blood flow
*Treated via phlebotomy

41
Q

Common complication of Polycythemia Vera?

A

*Thromboembolism (blood clot) and hemorrhage
*CVA (Stroke)

42
Q

Characteristics of malignant cell:

A

*Don’t look or function like normal cells
*Lack capsules
*Have leg-like structures to infiltrate surrounding tissue
*Proliferate without limit
*Lack inhibition
*Don’t die to keep cell counts constant
*Invade multiple body systems

43
Q

Rick factors for cancer:

A

*Heredity
*Family history
*Obesity
*Chemicals
*Radiation
*Viruses

44
Q

Warning signs for cancer:

A

*Cough, blood in sputum, chest pain
*Lump in breast, thickening, dimpling
*Blood in stools, change in bowel movement, pain, anemia
*Weak or interrupted urine flow
*Lump in testicle, breast enlargement, lower back pain
*Enlargement of abdomen
*Change in wart or mole

45
Q

What is oncogenesis (carcinogenesis)?

A

Process through which healthy cells become transformed into cancer cells.

46
Q

Stages of oncogenesis (carcinogenesis):

A

Initiation: Damage to cell DNA (Where it starts)
Promotion: Tumor begins to develop
Progression: Proliferation and Angiogenesis

47
Q

What is the purpose of staging cancer?

A

It’s an attempt to describe the severity of an individual case by looking at factors: tumor size, degree of invasion, affected lymph nodes, metastasis

48
Q

What is angiogenesis?

A

Formation of new blood vessels. Bad in cancer because these vessel provide tumors with nutrients.

49
Q

Hodgkins Lymphoma:

A

*80% survival rate
*Signaled by presence of Reed-Sternberg cells (DIAGNOSTIC TEST) which are large, abnormal lymphocytes with multiple nuclei.
*Contigous (predictable) spread and single node
*Enlarged lymph node (painless), night sweats, fever, fatigue, weight loss
*Teens and adults >50

50
Q

Non-Hodgkins Lymphoma:

A

*Most common B cell lymphoma
*60% survive 10 years
*Strikes men over 60 and those with Epstein-Barrr Virus (EBV)
*Noncontiguous (Unpredictable spread) with localized painless lymphadenopathy and unpredictable spread
*Fever, sweats, fatigue, weight loss
*Treated with chemo

51
Q

Clinical manifestations of leukemia:

A

*Fatigue (Anemia - lack O2 from RBCs), repeated infections (Neutropenia -high WBC but non-functional), bleeding (thrombocytopenia - platelets), fever, night sweats, bone pain, splenomegaly, lymphadenopathy, hepatomegaly
*Anemia (low RBC)
*Thrombocytpenia (Low platelet)
*Neutropenia (low WBC)

52
Q

What are some cancers that have a genetic connection:

A

*Colon, Breast, Prostate Cancers

53
Q

Leukemia

A

Overcrowding of non-functioning WBC’s in bone marrow - impairs production of RBC’s (anemia) and platelets (thrombocytopenia).

54
Q

Pernicious Anemia Treatment:

A

Lifelong B12 by injection only - by mouth is wouldn’t be absorbed due to lack of intrinsic factor

55
Q

Clinical Manifestations of Sickle Cell Disease:

A

*Anemia and all CM of it
*Jaundice = due to early death of RBC’s and metabolizing them
Blood vessel occlusion

56
Q

Wound: Primary Intention:

A

*Wound with edges that are proximated (touching each other) - like a surgical opening - shorter healing time

57
Q

Wound: Secondary Intention:

A

*Wound edges aren’t touching each other - longer healing time -requires granulation tissue to fill it - typically cause by injury

58
Q

Stages of Infection:

A

*Incubation
*Prodomal
*Acute:

59
Q

What is the incubation stage of infection?

A

Pathogen gains access to host, spreads to target organs/tissues and proliferates outward

60
Q

What is the prodomal stage of infection?

A

When non-specific symptoms develop (joint pain, malaise, fatigue)

61
Q

What is the acute stage of infection?

A

Host develops specific symptoms as pathogen grows and destroys cells

62
Q

Onychomycosis:

A

Toenail fungus

63
Q

What plasma protein forms fibrous meshwork during inflammatory response?

A

Coagulation

64
Q

What is the physiological manifestation present in all anemias?

A

Hypoxia

65
Q

Why would a sickle cell anemia patient appear jaundiced?

A

Heme destruction exceeds liver’s ability to conjugate and excrete bilirubin

66
Q

Three ways cancer can move from one part of body to another?

A
  1. Direct Invasion
  2. Seeding Body Cavities
  3. Metastic Spread (lymphatics and blood vessels)
67
Q

What clinical manifestation is present in B12 deficient anemia and not iron deficient anemia?

A

Paresthesia (pins and needles sensation)

68
Q

How does the body compensate for anemia?

A

Increasing rate and depth of breathing

Pathophysiology Exam 1 (1 decks)

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