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Human Pathophyisology: Midterm > Lecture 1: Inflammatory Processes > Flashcards

Lecture 1: Inflammatory Processes Flashcards

1
Q

cell membrane damage early on; destruction of organelles and leakage of cytoplasm; causes inflammation

A

necrosis

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2
Q

programmed cell death; does not cause inflammation; cell shrinks and cellular fragments are packaged into pieces of cell membrane and dispersed

A

apoptosis

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3
Q

area adjacent to the ischemic core where cells undergo apoptosis

A

ischemic penumbra

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4
Q

evolutionary ancient immune response; immediate activation with inflammation

A

innate immunity

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5
Q

immune response that targets specific structure via antibodies and cytotoxic T cells; slow

A

adaptive immunity

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6
Q

cause direct injury at site of infection or release toxins that can cause systemic illness

A

bacteria

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7
Q

nucleic acids surrounded by protein coat that invade cells to produce copies of themselves

A

viruses

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8
Q

need to live off a host to complete life cycles

A

parasites

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9
Q

What are some physical barriers to infection?

A
  • skin
  • respiratory tract
  • GI tract
  • genitourinal system
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10
Q

How does the skin protect from infection?

A
  • keratinized epithelium
  • normal cutaneous microbial flora (inhibit colonization of other bacteria)
  • normal sebaceous and sweat glands (secretions are acidic, antimicrobial, contain anti-fungal fatty acids, lactic acid, lysosome, and antibodies)
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11
Q

How does the respiratory tract protect from infection?

A
  • cough and sneeze reflexes
  • mucociliary escalator
  • antibodies
  • collectins
  • alveolar macrophages
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12
Q

How does the GI tract protect from infection?

A
  • epithelial barrier
  • the microbiome
  • low gastric pH
  • peristaltic movement
  • antibodies
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13
Q

If pathogens do make it through the GI tract, whats another method of protection?

A

they enter the blood which is rerouted to the liver – destroyed by Kuppfer cells (liver macrophages)

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14
Q

How does the genitourinal tract protect from infection?

A
  • physical flushing of urine
  • low vaginal pH
  • normal vaginal flora
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15
Q

What are the characteristics of inflammation?

A
  • rugor (redness)
  • calor (warmth)
  • dolor (pain)
  • tumor (swelling)
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16
Q

What do neutrophils do?

A
  • first on scene
  • release mediators to promote inflammation and vasodilation
  • chemotaxis
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17
Q

What are macrophages and what do they do?

A
  • derived from monocytes (enter tissue and change into macrophages)
  • phagocytize and destroy foreign cells/particles
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18
Q

What are dentritic cells and what do they do?

A
  • similar to macrophages but not derived from monocytes
  • in CNS –> microglia
  • clean up debris and maintain other cells
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19
Q

Where is histamine released from and what does it do?

A
  • released from mast cells in tissues

- vasodilation and increased vascular permeability

20
Q

Where are eicosinoids released from and what do they do?

A
  • produced by virtually all cells

- includes prsotaglandins and leukotrienes (aspirin inhibits these)

21
Q

Where is neuropeptide released from and what does it do?

A
  • released from sensory C-fiber neurons

- increases sensitivity of noniceptors (increased pain sensation)

22
Q

Where are cytokines released from and what do they do?

A
  • released from immune cells
  • examples: IL-1, IL-6, TNF, interferons
  • regulate immune response (activate and inhibit)
  • can act locally or systemically
23
Q

cytokine that is a non-specific blocker of viral replication

A

interferon

24
Q

Where are plasma proteins released from and what do they do?

A
  • produced in liver in response to cytokines
  • complement – antibody production
  • clotting proteins
  • C-reactive protein – facilitates phagocytosis
25
Q

What are some of the effects of an immune response?

A
  • vasodilation
  • increase capillary permeability
  • chemotaxis
  • complement (antibodies)
  • phagocytosis
  • tissue repair via blood clotting and proliferation of fibroblasts
26
Q

What are the symptoms of an immune response?

A
  • fever
  • decrease plasma iron levels
  • lethargy and loss of appetite
  • increase production of certain plasma proteins by liver
27
Q

How can an infection cause damage?

A
  • direct injury from site of infection
  • release of toxins
  • triggering of a strong host response
  • viruses can alter DNA to promote cancer
28
Q

What immune cells attacks/binds specifically to pathogens making it easier for other immune cells to attack it?

A

-B cell/antibodies

29
Q

What cell is able to identify and kill infected host cells?

A

cytotoxic T cell

30
Q

What immune cell is responsible for an allergic reaction?

A

IgE

31
Q

someone with this is predisposed to allergic responses to allergens (possible explanation: hygiene hypothesis)

A

atopy

32
Q

when immune cells do NOT attack molecules associated with the cells of one’s own body

A

tolerance

33
Q

What are some ways autoimmune diseases can develop?

A
  • modification of molecule on host cell (via drugs or pathogens)
  • molecular mimicry (cloaked pathogens; antibodies attack normal cells by accident)
  • exposure of a sequestered antigen (ex. sperm)
  • inappropriate activation of lymphocytes
  • imbalance of suppressor T cells (inhibit) and helper T cells (activate)
  • genetic factors
34
Q

Examples of causes of chronic inflammation?

A
  • autoimmune disease
  • persistent injuries
  • persistent infections
  • obesity
35
Q

What is adiponectin and what role does it play in inflammation?

A
  • anti-inflammatory; produced by healthy adipose tissue
  • down-regulated by dysfunctional adipocytes
  • low in obese patients
  • inhibited by cytokines
  • decreases risk of diabetes
36
Q

What is SFRP5 and what role does is play in inflammation?

A
  • anti-inflammatory
  • helps maintain normal normal metabolic functioning of fat cells
  • inhibited by inflammation and insulin resistance
37
Q

What is M1 and how does it relate to adipocytes?

A
  • cells found in high levels in DYSFUNCTIONAL adipocytes
  • pro-inflammatory
  • produces cytokines TNF and IL-6
38
Q

What is M2 and how does it relate to adipocytes?

A
  • cells found in high levels in HEALTHY adipocytes
  • anti-inflammatory
  • repairs damaged tissues and promotes resolution of inflammation
39
Q

How do adipocytes become susceptible to inflammation?

A
  • enlargement increases distance from blood supply
  • cells in more interior region become hypoxic and necrotic –> promotes inflammation
  • enlarged adipocytes produce more leptin
40
Q

What is leptin and what is its role in inflammation?

A
  • produced by adipose tissue
  • “appetite suppressing hormone”
  • leptin resistance when levels are consistently high
  • pro-inflammatory; increases TNF and IL-6 and activates immune cells
41
Q

How does insulin resistance results from obesity?

A

-damaged adipose tissue is less sensitive to insulin

42
Q

the “wear and tear” on the body from continually having to deal with stress

A

allostatic load

43
Q

What are some responses to acute stress?

A
  • increase HR and contractility
  • increased gluconeogenesis
  • mobilization of amino acids
  • decreased fatigability
  • cortisol and ACTH promote learning and memory
  • activation of immune system (initially… suppressed long-term)
44
Q

What are consequences of chronic stress?

A
  • immune suppression (high cortisol levels)
  • cognitive impairment
  • metabolic changes (increased appetite, weight gain)
  • increased risk for CHD (promotes atherosclerosis and hypertension)
  • physiological effects - addiction, depression, PTSD
45
Q

the expected maximal load a structure is able to handle

A

safety factor

Human Pathophyisology: Midterm (6 decks)

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