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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
hydropic
accumulation of water first manifestations of forms of reversible cell injury results from malfunction of Na-K pump Na ions in cell, water follows
26
Megaly
Generalized swelling in cells of particular organ with cause - megaly (increase in size and weight)
27
hepatomegaly
enlarged liver
28
Irreversible cell injury - Necrosis
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
29
Irreversible cell injury - Apoptosis
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
chain of transmission - agent/pathogen/microbe
causes disease
31
chain of transmission - reservoir
place where pathogen lives and reproduces could be human/water/food/mosquito
32
chain of transmission - portal of exit/entry
how it gets in and out of host
33
chain of transmission - mode of transmission
mechanism of how an agent is spread ``` droplet airborne surfaces bodily fluids animals, vectors oral fecal ```
34
chain of transmission - host
individual t risk for contracting organism
35
Symbiosis
benefit only human, no harm to microorganism
36
Mutualism
benefit both
37
Commensalism
benefit only microorganism, no harm to human
38
Pathogenicity
benefit microorganism, harms the human
39
Opportunism
benign microorganisms become pathogenic bc of decreased host resistance or location where they shouldn’t be
40
host characteristics - physical / mechanical barriers
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
host characteristics - risk factors
``` age (old & young) nutritional status (SDOH) chronic illness (diabetes) immunosuppressive chronic stress ```
42
agent characteristics - pathogenicity
ability to cause disease
43
agent characteristics - virulence
how severe
44
agent characteristics - adherence
difficult to treat | sticky - pili/fimbriae
45
agent characteristics - invasion
how they get access | where they replicate
46
agent characteristics - endotoxins (toxigenicity)
indirect injury- part of cell wall which is released when cell dies
47
agent characteristics - exotoxins (toxigenicity)
direct injury- excreted
48
agent characteristics - biofilms
microorganisms in highly organized extracellular matrix- tolerant and resistant to antibiotics and immune responses. Form on implantable devices and associated with chronic infections
49
agent characteristics - bacterial enzymes
degrade tissue; dissolve RBC | block immune response
50
agent characteristics - antiphagocytic factors
outside coating, not recognizable to leukocytes, also helps with adherence, capsules
51
agent characteristics - endospores
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
agent characteristics - mobility
chemotaxis | move toward nutrients and away from repellants (flagellum)
53
agent characteristics - antimicrobial resistance
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
bacteria
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
Fungi
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
infections cause by fungi are called...
mycoses, mycotic
57
parasites
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
viruses
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
incubation
period from initial exposure to onset of first symptoms communicable
60
prodromal
occurrence of initial symptoms (mild)
61
illness
pathogen is multiplying rapidly immune and inflammatory responses are being triggered development of symptoms specific to the pathogen
62
convalescence
immune and inflammatory systems have successfully removed agent and symptoms decline Latency phase with resolution until reactivation Fatal
63
acute
severe, short
64
chronic
last for months or years
65
subclinical
patient functions normally, even though disease processes are well established
66
exacerbation
sudden severity
67
remission
decline in severity
68
what is the hallmark of the clinical manifestations?
fever (except in young or old)
69
what are the majority of the signs and symptoms of infectious diseases from?
inflammation
70
toxigenicity
ability to produce toxins or endoxins. Microbes that can produce these are thought to be more virulent
71
Immunogenicity
ability of pathogens to induce an immune response toxins, enzymes

Pharmacology 1 (3 decks)

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