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Pathology > Module 1 (Exam 1) > Flashcards

Module 1 (Exam 1) Flashcards

Cellular Function and Immunity

1
Q

What are the substances that cell allow free passage to (3)?

A

enzymes (1), glucose (2), & electrolytes (3)

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2
Q

What are electrolytes?

A

charged conductors when dissolved

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3
Q

What is diffusion?

A

the movement of particles from a higher solute concentration to a lower solute concentration

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4
Q

What is facilitated diffusion?

A

diffusion with the help of a transport molecule/carrier protein/channels; requires atp

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5
Q

What is osmosis?

A

passive movement of water and solute to lower concentrations with osmotic pressure

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6
Q

What is cell lysis?

A

osmosis; cell swells with water and causes it to burst

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7
Q

What is cell crenation?

A

osmosis; water leaves the cell which causes it to shrivel and shrink

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8
Q

What is active transport?

A

movement against the concentration gradient; endocytosis (phagocytosis and pinocytosis)

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9
Q

How is ATP created?

A

the breakdown of glucose/triglycerides/protein (only when nothing else is available)

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10
Q

How can ATP be stored?

A

by building larger molecules, like in the Krebs cycle and aerobic/anaerobic respiration

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11
Q

What is cell proliferation?

A

when cells divide and reproduce; meiosis and mitosis

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12
Q

What is cell differentiation?

A

occurs when cells become specialized; stem cells

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13
Q

Why are stem cells less differentiated?

A

it allows them to differentiate and fill different roles in the body as needed

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14
Q

What is epithelial tissue?

A

simple and stratified; tightly packed cells (squamous, cuboidal, & columnar)

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15
Q

What is connective tissue?

A

tissue that supports and connects; extracellular matrix (loose and dense)

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16
Q

What is muscle tissue?

A

tissue that contracts for movement; cell fibers with contractive proteins (actin and myosin)

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17
Q

What is nervous tissue?

A

tissue that senses, processes, and responds to stimuli; neurons and neuroglia

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18
Q

What is neoplasm?

A

“new growth”; uncontrolled and unregulated cell growth

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19
Q

What is carcinogenesis impacted by?

A

hereditary oncogenes and carcinogens

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20
Q

Three steps of carcinogenesis: Initiation

A

introduction of the agent

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21
Q

Three steps of carcinogenesis: Promotion

A

the initiation of uncontrolled growth

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22
Q

Three steps of carcinogenesis: Progression

A

permanent malignant changes

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23
Q

What are some ways to detect cancer?

A

change in elimination habits (1), sores that aren’t healing (2), weird bleeding or discharge (3), thickening/tissue lumps (4), change in warts or moles (5)

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24
Q

What are some complications of cancer?

A

cachexia, fatigue, infection, pain, anemia, leukopenia, thrombocytopenia

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25
Q

What is cachexia?

A

cancer changes appetite, causing muscle and fat loss

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26
Q

What is leukopenia?

A

low level of WBCs in the blood

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27
Q

What is thrombocytopenia?

A

lower number of platelets in the blood

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28
Q

What are some ways to diagnose cancer?

A

biopsy (1), tumor markers (2), imaging procedures (3)

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29
Q

How is cancer classified?

A

by stage and grade

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30
Q

What is cancer staging?

A

based on disease spread; TNM (tumor node metastasis)

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31
Q

What is cancer grading?

A

I-IV, according to histological findings of tumor differentiation

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32
Q

Treatment goals are…

A

curative, palliative, and prophylactic (intended to prevent disease); treatments range from surgery to radiation

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33
Q

What is a cancer prognosis?

A

the likelihood of survival

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34
Q

What is cancer remission?

A

when the cancer is considered under control

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35
Q

Atrophy

A

lowers functionality (lower workload lowers organelle size, which lowers energy usage)

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36
Q

Hypertrophy

A

lowers functionality (higher workload, higher organelle size and contractility)

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37
Q

Hyperplasia (higher number of cells)

A

raises functionality (higher workload, higher tissue size due to cell proliferation)

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38
Q

What is metaplasia?

A

the replacement of normal cells with abnormal cells

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39
Q

What is dysplasia?

A

the mutation of normal cells to abnormal cells

40
Q

What are some cell injury causes?

A

physical, chemical, biological agents; radiation; nutritional imbalances; apoptosis

41
Q

Necrotic cell death

A

coagulative, liquefactive, caseous, or fatty

42
Q

What is gangrene?

A

necrosis by severe hypoxia injury (coagulative, liquefactive, or gas pathologies)

43
Q

Congenital and genetic disorders are…

A

caused by mutations (1), and characterized by patterns of transmission (2)

44
Q

Autosomal DOMINANT disorders

A

• 50% chance of transmission (unaffected offspring don’t pass on disorder)
• delayed onset
• abnormalities with structural proteins

45
Q

Marfan syndrome

A

autosomal DOMINANT disorder with FBN1 (chromosome 15), increases growth factor

46
Q

Autosomal RECESSIVE disorders

A

Rare, as both members of the
gene pair must be affected (homo/heterozygous alleles are carriers)
* early onset (deficient enzyme)

47
Q

Cystic Fibrosis

A

Progressive disorder of the
mucus and sweat glands
* Primarily affects the lungs
and pancreas

AUTOSOMAL RECESSIVE

48
Q

X-linked disorders

A

Males have a 50% chance of getting the
disorder from their affected mother,
females have a 50% chance of being a
carrier for the disorder
* Female offspring of affected males are
carriers, male offspring are not

49
Q

Fragile X Syndrome

A
  • FMRI sequence repeated 200 times
  • affects synaptic development (intellectual disability and learning issues, long face, large mandible, ears, and balls due to connective tissue)
50
Q

Multifactorial Inheritance Disorders

A
  • common but unpredicatable
  • cleft palate (diagnosed with prenatal ultrasound)
51
Q

Trisomy 21 (Down Syndrome)

A
  • diagnosed with prenatal screening
  • manifestations include upward slanted eyes, varying degrees of disability, organ defects/complications, and a strong relation to Alzheimer’s disease
52
Q

Monosomy X (Turners Syndrome)

A
  • no ovaries, aortic coarctation (narrow aorta)
  • deletion of X chromosome diagnosed through serum hormones and genetic tests
53
Q

Polysomy X (Klinefelter’s Syndrome)

A
  • diagnosed in males with multiple X chromosomes through genetic testing but often undetected
  • small genitals, higher vulnerability to osteoporosis and breast cancer
54
Q

Stress: General adaptation syndrome stages

A

Alarm (body mobilizes resources), resistance, exhaustion (resistance depleted)

55
Q

Stress: Local

A

damage to one specific area

56
Q

The immune system is…

A

self-regulating and self limiting (antigens); must be able to distinguish self from nonself)

57
Q

Innate Immunity: Barriers

A

IMMUNITY YOURE BORN WITH
Nonspecific but immediate: recognizes nonself but not specific pathogens
⚬Includes skin and mucous membranes, chemicals, and microbiome

58
Q

Innate Immunity: Inflammatory Response (Nondiscriminatory)

A

Vascular reaction from damage or trauma to body
tissue (mast cells trigger inflammation)
⚬Nondiscriminatory: same sequence regardless of
cause, local and systemic

59
Q

Innate Immunity: Inflammatory Response (Acute)

A

immediately after injury, until threat is eliminated (vasodilation and vasoconstriction, phagocytosis, fibrinogen)

60
Q

Innate Immunity: Inflammatory Response (Chronic)

A

if acute does not resolve issue, lasts until healing is complete (often occurs in presence of resistant organisms)

61
Q

Innate Immunity: Pyrogens

A

released by bacteria after exposure, causes fever

62
Q

Innate Immunity: Interferons

A

released from virus-infected cells which binds to unaffected cells that release enzyme to prevent replication

63
Q

Innate Immunity: Complement proteins

A

enhance antibodies, activated by antigens

64
Q

Adaptive (acquired) Defenses

A

pursue those that escape innate immunity
• specific to organisms (memory)
• distinguishes self from nonself

65
Q

Adaptive Immunity: Cellular

A

• DESTROY THE ANTIGEN
• T regulator cells (helper T and suppressor T) and T effector cells (cytotoxic killer Ts) are PRODUCED in marrow and MATURE in the thymus
• viruses, cancer, hypersensitivity reactions and transplant rejections

66
Q

Adaptive Immunity: Humoral

A

• PRODUCE ANTIBODIES AGAINST ANTIGEN
• B cells (memory cells and immunoglobulin secreting cells produce antibodies 72 hrs after exposure)
• active and passive acquired immunities

67
Q

Memory cells

A

quicker response to the same antigen in the future

68
Q

Immunity: Infancy

A

• based on maternal IgG for 3-6 months, granting temporary passive immunity (though low affinity)
• breastfeeding can transfer IgA (+ vaccines)
• newborns respond effectively to protein antigens (NOT GLYCOPROTEINS OR POLYSACCHARIDES) so limited functions

69
Q

Immunity: Adolescence

A

hormone changes effect B cells and macrophages
• risk for inflammatory and autoimmune diseases rise
• immune dimorphism

70
Q

What is immune dimorphism?

A

sexes respond differently to infection and vaccination

71
Q

Immunity: Aging

A

• lower B and T cells but higher rate of apoptosis
• higher risk of autoimmune disorders due to misinterpreting signals

72
Q

Type I (IgE mediated) Hypersensitivity Reaction

A

• immediate; local or systemic, within an hour
• T cells stimulate B cells to produce IgE antibodies that sensitizes mast cells and basophils
• REQUIRES EXPOSURE MORE THAN ONCE
• systemic anaphylaxis

73
Q

Type II (cytotoxic) Hypersensitivity Reaction

A

• immediate, targets single cell
• IgG/IgM antitbodies bind to individuals own cells, triggering antibody production in macrophages
• cell lysis due to activation of complement proteins and phagocytosis
• erythroblastosis fetalis (hemolytic anemia), blood transfusions

74
Q

Type III (immune complex) Hypersensitivity Reaction

A

• delayed, local or systemic, 1-3 weeks
• circulating IgG antigen-antibody complexes that haven’t been cleared are deposited in tissues, which triggers inflammatory response (+ anaphylaxis)
• SERUM SICKNESS, SLE (lupus)

75
Q

Type IV (cellular) Hypersensitivity Reaction

A

• delayed, 2 phases (sensitizing and effector), days to weeks
• antigen presentation causes T cells (cytotoxic and helper) to release cytokines that activate inflammation
• can cause chronic inflammation, tissue loss and fibrosis
• POISON IVY RASH, SJS

76
Q

Type IV Hypersensitivity Reaction First Exposure

A

• no reaction
• sensitization stimulates T cells which produces memory T’s that become activated on future exposures

77
Q

Type IV Hypersensitivity Reaction Second Exposure

A

memory T’s are reactivated which produces inflammatory cytokines that stimulate macrophages and cytotoxic T cells to induce a lesion which can inflict long term damage

78
Q

Transplant Reactions: Allogeneic

A

donor/recipient are related/unrelated, similar tissue types; most common

79
Q

Transplant Rejections: Syngeneic

A

D/R are identical twins

80
Q

Transplant Rejections: Autologous

A

D/R are same person (most successful method)

81
Q

Transplant Rejections: Xenogenic

A

D/R are different species

82
Q

Hyperacute tissue rejection

A

nearly immediate; due to complement system and causes necrosis

83
Q

Acute tissue rejection

A

occurs within 3 months, is treatable, manifests in fever and edema

84
Q

Chronic tissue rejection

A

4 months+, antibody-mediated, due to ischemia in vessel walls of tissue

85
Q

Host vs. Graft Disease

A

either tissue may have immune response, can be treated with lifelong immunosuppression if the tissue is a match

86
Q

Lupus (autoimmunity)

A

• potentially due to B cells producing antibodies and autoantigens
• symptoms: butterfly rash, pain and swelling joints, fatigue, headaches

87
Q

Immunodeficiency (autoimmune)

A

• diminished or absent immune response which raises vulnerability to opportunistic infections (acute or chronic)

88
Q

Immunodeficiency: Primary

A

defect with the immune system (inherited)

89
Q

Immunodeficiency: Secondary

A

underlying disease or factor that is suppressing immune system (Iv drug abuse, malnutrition, HIV/AIDS)

90
Q

HIV

A

• retrovirus infecting CD4 and macrophages
• transmitted via blood and fluids
• HIV-1 most prevalent strain

91
Q

HIV Asymptomatic phase

A

allows the virus to reproduce for years, CD4 is destroyed and symptoms increase

92
Q

HIV Progression

A

• immunodeficiency (opportunistic infections)
• autoimmunity (arthritis)
• neurologic dysfunction (AIDS dementia)

93
Q

NAT (nucleic acid tests)/ antigen-antibody tests

A

detects viral load but is expensive and nonroutine; rapid and home antibody tests

94
Q

AIDS Categories

A

1: >500 CD4 cells
2: 200-499 cells
3: < 200
A: asymptomatic
B: less serious manifestations of immunodeficiency
C: AIDS illnesses present

95
Q

Necrosis vs Apoptosis

A

necrosis is unplanned cell death that results in cell lysis that affects many cells, apoptosis is programmed cell suicide that results in cell shrinkage and doesn’t induce inflammatory response

Pathology (8 decks)

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