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Pathophys: Unit 1 Exam > Patho Intro > Flashcards

Patho Intro Flashcards

1
Q

Define pathogenesis.

A

Pathogenesis refers to the development of the disease or the sequence of events involved in the tissue exchange related to specific disease process.

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2
Q

Define Acute.

A

Sudden, short term illness that develops quickly with marked signs. Ex. Gastroenteritis.

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3
Q

Define Insidious.

A

A gradual progression with only vague or very mild signs. Ex. Hepatitis.

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4
Q

Define Chronic.

A

Develops gradually but lasts for a long time with more permanent tissue damage, ex. RA

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5
Q

Define Subclinical.

A

Disease presents w/ no signs but pathological change occurs perhaps because of the great capacity of some organs, ex. renal failure

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6
Q

Definite Latent Stage.

A

Silent stage w/ no signs evident, AKA incubation period

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7
Q

Define Prodromal Stage.

A

Aware of change disease has elicited, signs nonspecific

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8
Q

Describe how a disease is manifested/manifestation of a disease

A

Manifestations is the clinical evidence or effects, the signs and symptoms of a disease.

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9
Q

Describe Local Disease Manifestation.

A

Signs and symptoms found at the site of the problem; ex. redness, swelling (edema), heat, pain, exudate (collection of interstitial fluid formed in the inflamed area)

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10
Q

Describe Systemic Disease Manifestation.

A

Signs and symptoms that are general indicators; ex. mild fever (pyrexia), malaise, fatigue, headache, anorexia

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11
Q

Define the term Sign. List examples of signs.

A

Signs can be observed and measured
Ex. Blood pressure, fever, rash, heart rate

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12
Q

Define the term Symptoms. List examples of symptoms.

A

Symptoms are subjective and hard to measure, we rely on patient’s reports.
Ex. pain, nausea, headache, feelings like depression or anxiety

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13
Q

Identify some systemic signs of disease.

A

Fever, elevated blood pressure, rashes

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14
Q

Define Prognosis.

A

The probability or likelihood for recovery or other outcomes; the average outcomes

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15
Q

Define Etiology.

A

The cause, set of causes, or manner of causation of a disease or condition.

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16
Q

Define Hypertrophy.

A

Increase in the SIZE of individual cells, resulting in an enlarged tissue mass.

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17
Q

Define Hyperplasia.

A

Increase in the NUMBER of cells, resulting in an enlarged tissue mass.

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18
Q

Define Anaplasia.

A

Cells that are undifferentiated with variable nuclear and cell structures and numerous mitotic figures, ex. malignant tumors.

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19
Q

Define Dysplasia.

A

The term applied to tissues in which the cells vary in size and shape, large nuclei are frequently present, and the rate of mitosis increased, ex. Pap smear irregular cells.

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20
Q

Define Atrophy.

A

Decrease in the size of cells, resulting in a reduced tissue mass.

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21
Q

Define Apoptosis.

A

Programmed cell death; self-destruct, digest themselves enzymatically.

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22
Q

Define Regeneration.

A

The healing process that occurs in damaged tissue in which the cells are capable of mitosis.

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23
Q

Define Latent Stage.

A

The “silent” stage in which no clinical signs are evident.

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24
Q

Define Predisposing Factor

A

The tendencies that promote development of a disease in an individual; indicates a high risk for the disease but not certain developmental. Includes age, gender, inherited factors, occupational exposures, certain dietary practices.

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25
Q

Define Incidence.

A

Indicates the number of new cases in a given population noted within a stated time period.

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26
Q

Define Precipitating Factor.

A

A condition that triggers an acure episode, such as seizure in an individual w/ seizure disorder; differs from predisposing factors; ex. predisposed to CAD because of high cholesterol diet, heart attack can be precipitated by shoveling snow on a very cold day.

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27
Q

Describe first line of defense.

A

One nonspecific or general defense mechanism is a mechanical barrier, such as skin of mucous membranes that blocks entry of bacterial or harmful substances into tissues.

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28
Q

Describe second line of defense.

A

Nonspecific processes of phagocytosis and inflammation.

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29
Q

Describe third line of defense.

A

The body’s specific defense mechanism; provides protection by stimulating the production of unique antibodies of sensitized lymphocytes.

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30
Q

Describe specific defenses.

A

Immune responses, cell mediated and humoral.

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31
Q

Describe nonspecific defenses.

A

Inflammation, fluids, skin/mucous membrane, phagocytosis, interferons.

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32
Q

Describe how the inflammatory process is initiated.

A

When tissue damage/injury occurs.

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33
Q

List the chemical mediators released during the inflammatory response (8).

A

Histamine
Chemotatic factor
Platelet-activating factor
Cytokines (interleukins, lymphokines)
Leukotrienes
Prostaglandins
Kinins
Complement system

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34
Q

List, in chronological correct order, the events in the inflammatory response.

A
  1. Injury
  2. Cells release chemical mediators
  3. Vasodilation (increased blood flow)
  4. Increased capillary permeability (pro/water leave capillary, form exudate)
  5. Leukocytes move to site of injury
  6. Phagocytosis (removal of debris in preparation for healing, macrophage engulf debris)
35
Q

Define fever and list some things that cause it.

A

1) Release pyrogens in circulation. 2) Reset hypothalamic control -> high. 3) Body responds to increase body temperature (shivers, chills, vasoconstriction in skin e.g. pallor, increased BMR, increased HR, curl up body). 4. Body reaches new high temperature. 5. Treatment to remove pyrogens. 6. Reset hypothalamus to normal. 7. Body responses that increase heat loss (vasodilation, sweating, lethargy, extended body). 8. Body returns to normal temperature.

Causes can be extensive inflammation, infection.

36
Q

Explain how the body reacts to reduce fever.

A

By reversing the mechanisms of fever production.

37
Q

Describe some local and systemic effects of inflammation.

A

Local effects: the cardinal signs of inflammation are redness, heat, swelling, pain, loss of function.

Systemic: mild/low grade fever (or pyrexia), malaise (feeling unwell), fatigue, headache, anorexia.

38
Q

Describe the composition of scar tissue.

A

Cross-linking and shortening of collagen fibers.

39
Q

List some things that promote rapid tissue healing.

A

Youth
Good nutrition (protein, vitamins A and C)
Adequate hemoglobin
Effective circulation
Clean, undisturbed wound
No infection or further trauma to the site

40
Q

Define superficial burn, partial thickness burns, full-thickness burns, deep burn.

A

Superficial burn: 1st degree burns; damage the epidermis and may involved the upper dermis; red, painful, w/out scar tissue, ex. sunburn.

Partial-thickness burns: 2nd degree burns; destruction of the epidermis and part of the dermis; red, painful, edematous, blistered, hypersensitive and painful; easily infected.

Full-thickness burns: destruction of all skin layers; charred, coagulated, hard and dry on surface.

Deep burn: extends to the underlying tissues.

41
Q

Explain the rule of nines that approximates the percentage of body surface burned.

A

A method for rapid calculation of the percentage of body surface area (BSA) for treatment purposes; it assigns a percentage to body parts as a value of nine or a multiple of nine; ex. head and each arm 9%, anterior and posterior surface 18%, each leg 18%, groin area 1%.

42
Q

Explain why blood pressure decreases when a large area of the body is burned.

A

Large burns cause an inflammatory response that results in a massive shift of water, protein, and electrolytes into the tissues, causing fluid excess or edema; loss of water and protein from the blood leads to decreased circulating blood volume, low blood pressure, and hypovolemic shock.

43
Q

Explain what isoenzymes in the blood indicate.

A

Isoenzymes of creatine kinase with myocardial component (CK-MB) is specific for myocardial infarction.

44
Q

Define diapedesis.

A

The movement of leukocytes out of the circulatory system and towards the site of tissue damage or infection, typically accompanying inflammation. Neutrophils and later monocytes and macrophages collect along the capillary wall and then migrate out through wider separations in the wall into the interstitial area.

45
Q

List the different kinds of exudates.

A

Serous
Fibrinous
Purulent
Abscess

46
Q

List examples of the following exudates.
Serous
Fibrinous
Purulent
Abscess

A

Serous: water exudate consists primarily of fluid with small amounts of protein and white blood cells; ex. those that occur with allergic reactions or burns.

Fibrinous: exudate that is thick and sticky and has high cell and fibrin content; increases the risk of tissue in the area.

Purulent: exudate that is thick, yellow-green in color and contains more leukocytes and cell debris as well as microorganisms; ex. pus from bacterial infection.

Abscess: a localized pocket of purulent exudate or pus in a solid tissue; ex. around a tooth or in the brain.

47
Q

Identify the role of Neutrophils.

A

Phagocytosis of microorganisms

48
Q

Identify the role of Macrophages.

A

Active in phagocytosis; these are mature monocytes that have migrated into tissues from blood.

49
Q

Identify the role of Cytokines.

A

Increased plasma protein, erythrocyte sedimentation rate; induce fever, chemotaxis, leukocytosis.

50
Q

Identify the role of Memory cells.

A

Remember antigen and quickly stimulate immune response on re-exposure.

51
Q

Identify the role of Basophils.

A

Release of histamine leading to inflammation.

52
Q

Explain the differences between humoral immediate vs. cell-mediated immunity.

A

Humoral: B cells
Cell-Mediated: cytotoxic T cells

53
Q

Explain Active natural immunity.

A

May be acquired by direct exposure to an antigen; ex. when a person has an infection and then develops antibodies.

54
Q

Explain Active artificial immunity.

A

Develops when a specific antigen is purposefully introduced into the body, stimulating the production of antibodies; ex. a vaccine, a solution containing dead or weakened organisms that stimulate the immune system to product antibodies but do not result in the disease itself.

55
Q

Explain Passive immunity.

A

When antibodies are transferred from one person to another; these antibodies are effective immediately but offer only temporary protection because memory has not been established in the recipient and the antibodies are gradually removed from circulation.

56
Q

Explain Passive natural immunity.

A

When IgG is transferred from mother to fetus across the placenta; breast milk also supplies maternal antibodies; these protect the infant for the first few months of life.

57
Q

Explain Passive artificial immunity.

A

Results from the injection of antibodies from a person or animal into a second person; an example is the administration of rabies antiserum or snack anti-venom.

58
Q

Explain Type 1 hypersensitivity reactions.

A

Allergic reactions that begin when an individual is exposed to a specific allergen and for some reason develops IgE antibodies from B lymphocytes; these antibodies attach to mast cells in specific locations creating sensitized mast cells; worsens upon re-exposure.

59
Q

Explain why anaphylaxis is considered a critical situation.

A

It is a severe, life-threatening, systemic hypersensitivity reaction resulting in decreased blood pressure, airway obstruction, and severe hypoxia; can result in loss of consciousness, severe oxygen deficit to the brain, and death.

60
Q

Explain some of the causes of autoimmune diseases.

A

Exact causes are still unknown; other possible causes, loss of immune tolerance following tissue destruction and subsequent formation of antibodies to the damaged cell components, aging, genetic factors.

61
Q

Explain the etiology of lupus (SLE).

A

Specific cause has not been established, appears to be multifactorial and includes genetic, hormonal (estrogen levels), and environmental factors (UV light exposure).

62
Q

Describe a major systemic distinguishing feature of SLE.

A

A characteristic facial rash, which is erythematous and occurs across the nose and cheeks, resembling the markings of a wolf; the rash is now often referred to as a “butterfly rash” reflecting its distribution.

63
Q

Identify what HIV targets.

A

CD4-positive T helper lymphocytes

64
Q

Explain the diagnosis of HIV positive and how it is confirmed.

A

An individual is considered HIV positive when the virus and its antibodies are present in the blood, but few, if any, clinical signs have developed. HIV confirmed by blood test from antibodies that form in 2-10 weeks post-exposure (causes difficulty in detecting the infection following exposure).

65
Q

Explain how HIV is transmitted.

A

HIV must find entry into the circulating blood of the recipient; the virus is transmitted in body fluids, such as blood, semen, and vaginal secretions. Blood contains the highest concentration of the virus, with semen next. HIV is not transmitted by casual contact. Also transmitted by infected mothers to infants before, during, or after birth.

66
Q

Identify serious opportunistic infections that occur in patients with AIDS.

A

Opportunistic infections, malignant tumors/cancers, or AIDS encephalopathy (general brain dysfunction).

67
Q

Explain the function of helper T cells.

A

To activate B and T cells; to control or limit specific immune responses.

68
Q

Define seroconversion in relation to HIV and AIDS.

A

Seroconversion: window period, virus in blood, no antibodies, mild symptoms (initial months). HIV-positive: more antibodies form, small amounts of virus in blood, asymptomatic (months to years). AIDS: active infection, decreasing CD4 count, AIDS indicator diseases (opportunistic infections, lymphoma, wasting syndrome, dementia) (many years after exposure).

69
Q

Define bacterial capsule.

A

An external capsule or a slime layer is found on some, but not all, bacteria. The capsule found outside the cell wall in gram-positive bacteria and outside the outer membrane in gram negatives, offering additional protection to the organism, as well as adhesion to surfaces. It also interferes with phagocytosis by macrophages and other WBCs in the human body.

70
Q

Define bacterial endospore.

A

A latent form of the bacterium with a coating that is highly resistant to heat and other adverse conditions; these bacteria can survive long periods in the spore state, but they cannot reproduce when in spore form. Ex. tetanus and botulism.

71
Q

Identify structures are found in human cells but not in bacterial cells.

A

Human cells do not have cell walls and have nuclear membranes and membrane-bound organelles.

72
Q

Describe the structure of a virus.

A

A very small obligate intracellular parasite; need living tissue, living host. Virion (extracellular virus particle) has a protein coat, or capsid, and a core of either DNA or RNA, sometimes additional protective envelope.

73
Q

Describe how fungi reproduce.

A

The long filaments or strands of a fungus are hyphae, which intertwine to form a mass called the mycelium, a visible mass. Fungi reproduce by budding, extending the hyphae, or producing various types of spores. Spores can spread easily through the air and are resistant to temperature change and chemicals.

74
Q

Define normal or resident flora.

A

Areas of the body (such as skin, nasal cavity, and mouths) that have a resident population of mixed microorganisms, primarily bacteria.

75
Q

List areas of the body that are sterile.

A

Lungs, brain, blood, bladder, and kidneys.

76
Q

Define the term opportunistic infections and explain why it develops.

A

When certain microbes that are not pathogenic under normal circumstances but may cause disease if they are transferred to another location in the body, if the balance among the species is not maintained (ex. one variety becomes dominant, or if the body’s defenses are impaired (ex. in immunodeficiency states).

77
Q

Define the term vaccine.

A

A type of acquired immunity (an artificial active) that involves having a live or attenuated organisms that are injected into a person; they do not produce illness, but antibodies are able to form.

78
Q

Describe some local signs of infections.

A

Swelling, erythema (redness), pain, tenderness, lymphadenopathy, exudate, purulent.

79
Q

Describe some systemic signs of infection.

A

Fever, leukocytosis, elevated erythrocyte sedimentation rate, fatigue, weakness, anorexia, headache, arthralgia.

80
Q

Define a culture and sensitivity test.

A

Culture tests: using specific specimens such as sputum to identify organisms causing disease; ex. sputum in patients with tuberculosis. Sensitivity tests: checks to see what kind of medicine, such as an antibiotic, will work best to treat an illness or infection.

81
Q

Identify the causative organisms in the following conditions: tinea pedis, trichomoniasis, candidiasis, malaria, TB, herpes zoster, Rocky Mountain spotted fever, gonorrhea, pneumocystis carinii. (Matching).

A

Tinea pedis: fungi
Trichomoniasis: protozoa
Candidiasis: fungi
Malaria: protozoa
TB: bacteria
Herpes zoster: virus
Rocky Mountain spotted fever: bacteria
Gonorrhea: bacteria
Pneumocystis carinii: fungi

82
Q

Identify components of the immune system and their function: Helper T cells, Memory T cells, Neutrophils, Basophils, Macrophages, Phagocytosis.

A

Helper T cells: Activate B and T cells; control or limit specific immune responses
Memory T cells: Remember antigen and quickly stimulate immune response on re-exposure.
Neutrophils: WBCs for phagocytosis; nonspecific defense; active in inflammatory process.
Basophils: WBCs that bind IgE, release histamine in anaphylaxis.
Macrophages: Phagocytosis; process and present antigens to lymphocytes for the immune response. (Matching)

83
Q

Another Anaplasia definition.

A

A severe loss of cell differentiation, often associated with aggressive and malignant tumors

84
Q

Another Dysplasia definition.

A

An abnormal growth and disorganization of cells within a tissue, considered a pre-cancerous condition

Pathophys: Unit 1 Exam (1 decks)

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