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Pharmacology 1 > exam 1 > Flashcards

exam 1 Flashcards

1
Q

when presented with a challenge what do cells do?

A

adapt, injury, die

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2
Q

examples of adaptations

A

Atrophy, Hypertrophy, Hyperplasia, Metaplasia, Dysplasia

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3
Q

examples of cell death

A

Necrosis, Apoptosis

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4
Q

is cell death reversible?

A

no

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5
Q

cellular adaptations

A

Responses to Increases or Decreases in Functional Demand

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6
Q

atrophy

A

decrease in cell size and potential reduction in their differentiated function

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7
Q

hypertrophy

A

increase in cell size accompanied by augmented functional capacity (cardiac, liver skeletal muscle)

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8
Q

hyperplasia

A

increase in number of cells by mitotic division (liver, high altitudes, estrogen, BPH)

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9
Q

metaplasia

A

replacement of one differentiated cell type with another (smoking, HPV, cancer)

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10
Q

dysplasia

A

abnormal appearance of cells because of abnormal variations in size, shape and arrangement (chronic, cancer)

lives btw injury/adapt
most likely to turn into cancer
look for on biopsy

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11
Q

hypoxia

A

poor oxygenation
cell can adapt
single most common cause of tissue injury

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12
Q

Ischemia

A

interruption of blood flow
worse than hypoxia
most common cause of hypoxia
cell cannot adapt

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13
Q

mechanism of action

A

ATP production in cell to stall
ATP dependent pumps fail
NA accumulates and brings water inside cell
Excess Ca in the mitochondria interferes
Glycogen stores are depleted
Lactate is produced
pH falls- cellular components more dysfunctional

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14
Q

how is cell death caused by ischemia/hypoxia?

A

Plasma, mitochondrial and lysosomal membranes critically damaged

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15
Q

Re-perfusion injury - calcium overload

A

trigger apoptosis
breaks down membranes
mitochondrial decreases ATP

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16
Q

re-perfusion injury - oxidative stress

A

cell membrane damage
breakdown protein
changes to genetics

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17
Q

re-perfusion injury - inflammation & complement activation

A

chronic inflammation

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18
Q

nutritional cellular injuries - deficiencies

A

malabsorption
iron deficiency
malnutrition

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19
Q

nutritional cellular injuries - excess

A

obesity
diabetes
high cholesterol

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20
Q

chemical cellular injuries

A

lead, mercury
air pollution
alcohol and substance use

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21
Q

physical / mechanical cellular injuries

A

deep sea diving (bends) - abrupt changes in atmospheric pressure
cars, guns, suicide
radiation - damage to DNA creates free radicals
electrical - burns, shock
temperature extremes

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22
Q

cell injury - intracellular accumulations

A

excessive amounts of normal cellular substances - water, lipids, carbs, fats

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23
Q

cell injury - intracellular accumulations

A

Accumulation of abnormal substances produced by cell b/c of issues - byproducts of abnormal metabolism

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24
Q

examples of cell injury caused by intracellular accumulation

A

diabetes, gallstones, build up of bilirubin

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25
Q

hydropic

A

accumulation of water
first manifestations of forms of reversible cell injury
results from malfunction of Na-K pump
Na ions in cell, water follows

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26
Q

Megaly

A

Generalized swelling in cells of particular organ with cause - megaly (increase in size and weight)

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27
Q

hepatomegaly

A

enlarged liver

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28
Q

Irreversible cell injury - Necrosis

A

Consequence of toxic injury or ischemia
disruption of plasma membrane
contents will spill out and cause inflammation
monitor - increase WBC, fever, pain, increase HR

examples - gangrene, abscess / cyst

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29
Q

Irreversible cell injury - Apoptosis

A

Activate a chain of events that leads to cell killing itself
minimal disruption to surrounding tissue
cell membrane intact
no inflammation
normal cell function - self regulation
phagocytosis

30
Q

chain of transmission - agent/pathogen/microbe

A

causes disease

31
Q

chain of transmission - reservoir

A

place where pathogen lives and reproduces

could be human/water/food/mosquito

32
Q

chain of transmission - portal of exit/entry

A

how it gets in and out of host

33
Q

chain of transmission - mode of transmission

A

mechanism of how an agent is spread

droplet
airborne
surfaces
bodily fluids
animals, vectors
oral fecal
34
Q

chain of transmission - host

A

individual t risk for contracting organism

35
Q

Symbiosis

A

benefit only human, no harm to microorganism

36
Q

Mutualism

A

benefit both

37
Q

Commensalism

A

benefit only microorganism, no harm to human

38
Q

Pathogenicity

A

benefit microorganism, harms the human

39
Q

Opportunism

A

benign microorganisms become pathogenic bc of decreased host resistance or location where they shouldn’t be

40
Q

host characteristics - physical / mechanical barriers

A

Epithelial cells- skin , gi, gu, respiratory
constant shedding removes organisms
Mucous membrane lining- sticky traps, layer of separation from sterile to non sterile
Cough, sneeze, pee & poop
Acidic environment of skin, urine, vagina
HCl acid in stomach
Sweat, saliva, mucus, tears- have antimicrobial chemicals that inhibit bacteria

41
Q

host characteristics - risk factors

A 
age (old & young)
nutritional status (SDOH)
chronic illness (diabetes)
immunosuppressive
chronic stress
42
Q

agent characteristics - pathogenicity

A

ability to cause disease

43
Q

agent characteristics - virulence

A

how severe

44
Q

agent characteristics - adherence

A

difficult to treat

sticky - pili/fimbriae

45
Q

agent characteristics - invasion

A

how they get access

where they replicate

46
Q

agent characteristics - endotoxins (toxigenicity)

A

indirect injury- part of cell wall which is released when cell dies

47
Q

agent characteristics - exotoxins (toxigenicity)

A

direct injury- excreted

48
Q

agent characteristics - biofilms

A

microorganisms in highly organized extracellular matrix- tolerant and resistant to antibiotics and immune responses. Form on implantable devices and associated with chronic infections

49
Q

agent characteristics - bacterial enzymes

A

degrade tissue; dissolve RBC

block immune response

50
Q

agent characteristics - antiphagocytic factors

A

outside coating, not recognizable to leukocytes, also helps with adherence, capsules

51
Q

agent characteristics - endospores

A

ability to form an internal store that is in a resting state, resistant to heat and chemicals. When conditions are better- nutrients return- then they will reactivate

52
Q

agent characteristics - mobility

A

chemotaxis

move toward nutrients and away from repellants (flagellum)

53
Q

agent characteristics - antimicrobial resistance

A

mutation which allow microbes to survive in presence of antibiotics. develop in response to excessive use or subtherapeutic dosing of antibiotics
MRSA (methicillin resistant staph aureus, VRE (vancomycin resistant enterococcus), tuberculosis

54
Q

bacteria

A

Single cell, rigid wall, no internal organelles

Characteristics:
Shapes: cocci (spherical), bacilli (rod or comma), spiral (twisted)
Gram stain: positive (dark blue), negative (pink), acid fast (resist stain)
Oxygen requirement: anaerobic or aerobic

Gram stain- tells us about cell wall components- different drug choices have to be used to penetrate the walls.

55
Q

Fungi

A

Eukaryotic, contains organelles, form complex structures, thick rigid cell wall
difficult to treat
Superficial & cutaneous (tinea)
Subcutaneous (ulcers or abcesses)
Systemic (Invasive heart, lungs, other organs)

56
Q

infections cause by fungi are called…

A

mycoses, mycotic

57
Q

parasites

A

Establish themselves WITH another organism & benefit from the other
Protozoa (single celled)- plasmodium (malaria), trichamonis (STI)
Helminthes (roundworms and flatworms- pinworms, hookworms, tapeworms)
Arthropods (invertebrate animals with jointed appendages)- ticks, lice, scabies
Common sites of infection- skin and GI tract

58
Q

viruses

A

most common
Simple microorganisms- no metabolism, incapable of independent reproduction
Need to infect a permissive host cell to replicate- turn those cells into replication machine
Can bypass many defense mechanism b/c they develop intracellularly (protected)

59
Q

incubation

A

period from initial exposure to onset of first symptoms

communicable

60
Q

prodromal

A

occurrence of initial symptoms (mild)

61
Q

illness

A

pathogen is multiplying rapidly
immune and inflammatory responses are being triggered
development of symptoms specific to the pathogen

62
Q

convalescence

A

immune and inflammatory systems have successfully removed agent and symptoms decline
Latency phase with resolution until reactivation
Fatal

63
Q

acute

A

severe, short

64
Q

chronic

A

last for months or years

65
Q

subclinical

A

patient functions normally, even though disease processes are well established

66
Q

exacerbation

A

sudden severity

67
Q

remission

A

decline in severity

68
Q

what is the hallmark of the clinical manifestations?

A

fever (except in young or old)

69
Q

what are the majority of the signs and symptoms of infectious diseases from?

A

inflammation

70
Q

toxigenicity

A

ability to produce toxins or endoxins. Microbes that can produce these are thought to be more virulent

71
Q

Immunogenicity

A

ability of pathogens to induce an immune response toxins, enzymes

Pharmacology 1 (3 decks)

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