Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

HSC2008 Pathology & Pharmacology > Week 1 > Flashcards

Week 1 Flashcards

(139 cards)

Start Studying
1
Q

body defense system

A
  1. non-specific / general
  2. specific
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what mediates specific defense system

A

B-cells = humoral immunity = antigen specific ABs

T-cells = cell-mediated immunity = triggers apoptosis in infected cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

irreversible injury leads to __

A

necrosis & apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cellular adaptation types

A

Hand HM

  1. hyperplasia
  2. atrophy
  3. neoplasia
  4. dysplasia
  5. metaplasia
  6. hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

atrophy

A

size reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hyperplasia

A

increase in number of cells due to cell proliferation stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hypertrophy

A

increase in cell size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

metaplasia

A

healthy mature cells replaced by different kind of mature cells in same tissue such as changes in morphology & function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

dysplasia

A

abnormal growth of other cells types within tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

neoplasia

A

uncontrolled growth of tissues which may be malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cell injury causes

A

genetics, environment, infections, damage, foreign body, electrolyte imbalance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

phases of repair in acute wound healing

A

hemostasis > inflammation > proliferation > remodeling

HIPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how long does inflammation take

A

0.1 - 10 days after wounding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how long does cell proliferation & matrix deposition

A

1 - 30 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how long does matrix remodeling occur

A

1 - 300 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hemostasis

A

clot formation to stop bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

primary vs secondary hemostasis

A

primary = initial clot to form primary platelet plug

secondary = strengthening clot via coagulation cascade such as fibrinogen > fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

aim of inflammation

A
  1. eliminate initial cause of injury
  2. initiate repair process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

inflammatory response steps

A
  1. injury
  2. chemical mediators released
  3. vasodilation
  4. increased capillary permeability
  5. leukocytes move to injury
  6. phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

list 2 hormones that promote inflammation

A

bradykinin & histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

vascular events of acute inflammation

A

redness > head > swelling > pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

erythema

A

redness of skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

cellular events of acute inflammation

A

fluid exudation > stasis > margination > diapedesis > chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

stasis

A

RBC engorgement in vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
margination
WBC accumulate & adhere to vessel wall
26
diapedesis
oozing of WBC out of blood vessel
27
chemotaxis
directional migration of WBC to injury site
28
leukocyte examples
neutrophils, basophils, eosinophils
29
neutrophil function
microbe phagocytosis
30
basophil function
histamine release causing inflammation
31
eosinophils function
enhances allergic response
32
lymphocyte examples
T-cells, B-cells, macrophages
33
T-cell function
activates cell mediated immune response
34
B-cell function
antibody production
35
macrophages function
matured monocytes for phagocytosis
36
how is injury cause eliminated during inflammation
degradation & removal of necrotic tissue via neutrophils & macrophages
37
how does differential count assist with inflammation diagnostic testing
distinguish type of bacterial infections
38
high eosinophil count indicates
allergic response
39
high neutrophil count indicates
pyogenic bacterial infection
40
high lymphocyte count indicates
viral infection
41
high basophil count indicates
parasitic infection
42
how does cell enzymes assist with inflammation diagnostic testing
locate site of necrotic cells
43
what parameters are monitored for inflammation screening
plasma proteins, C-reactive proteins, increased ESR
44
what parameters are unable to determine site of inflammation
plasma proteins, C-reactive proteins, increased ESR
45
when does C-reactive protein production increase in blood
24-48hrs
46
anorexia
appetite loss
47
characteristic differences between acute & chronic inflammation
A has more exudation & swelling than C A involves migration of leukocytes but C has more presence of lymphocytes, macrophages, fibroblasts C has more severe damage and scar tissue than A
48
causes of chronic inflammation
persistent infection, persistent indigestible material, immune mediated reactions, repeated/continuous acute inflammation PRIP
49
acute management of inflammation
RICE = rest, ice, compression, elevation
50
non selective COX inhibitors
Naproxen + ibuprofen
51
selective COX inhibitors
Diclofenac, Etoricoxib
52
Arachidonic Acid breaks down into
COX-1 & COX-2
53
which COX is present in normal tissues
COX-1
54
which COX is induced during inflammation
COX-2
55
what are the products of COX-1
PGI2 & TXA2
56
PGI2 function
Gastric protection
57
TXA2 function
platelet function
58
what are the products of COX-2
PGE2
59
PGE2 effects
pain, inflammation, fever
60
which inflammatory stimuli stimulates COX-2
IL 1,6,8
61
which anti-inflammatory stimuli controls COX-2
IL-10
62
pharmacological effects of NSAIDs
anti-inflammatory, anti-pyretic, analgesic
63
how do NSAIDs have anti-inflammatory effect
decrease synthesis of prostaglandins involved in increasing vasodilation
64
how do NSAIDs have anti-pyretic effect
- inhibits COX-2 in hypothalamus - IL-1 stimulates prostaglandins in hypothalamus which increases body temp
65
how do NSAIDs have analgesic effect
reduces peripheral prostaglandin synthesis which sensitizes nociceptors to inflammatory mediators
66
diff ways to administer glucocorticoids
- PO; orally - intramuscularly - intravenous - topical - inhalation - rectal - inject into joints
67
anti-inflammatory mechanisms of glucocorticoids
inhibits NKfB = inhibits production of inflammatory cytokines, chemokines, adhesion molecules inhibits phospholipase A2 & cox enzyme = decreases PG, thromboxane production increases transcription of anti-inflammatory
68
ASA
aminosalicyclic acid
69
ASA mechanism of anti-inflammatory action
irreversibly inhibits COX-1 & 2 weakly selective to COX-1
70
Acetaminophen mechanism of anti-inflammatory action
selective COX-2 inhibitor property
71
NSAID mechanism of anti-inflammatory action
competitive inhibitor of COX-1 & 2 both ibuprofen & naproxen weakly selective to COX-1
72
glucocorticoids mechanism of anti-inflammatory action
inhibits NFkB increases transcription of anti-inflammatory proteins, IL-1 antagonist, & IL-10
73
COX-2 mechanism of anti-inflammatory action
competitive COX-2 inhibitor at therapeutic dose
74
NSAID
non-steroid anti-inflammatory drug
75
common synthetic corticosteroids
cortisone/hydrocortisone prednisone/prednisolone dexamethasone betamethsaone
76
half life of cortisone/hydrocortisone
6-12 hrs
77
half life of prednisone / prednisolone
12 - 36 hrs; 5x more potent than hydrocortisone
78
half life of dexamethasone
36 - 72 hrs; 25x more potent than hydrocortisone
79
half life of betamethasone
36 - 72 hrs; used topically to manage skin inflammation
80
3 Rs of healing
resolution, regeneration, replacement
81
tissue healing is achieved by __
cell regeneration & replacement process
82
resolution happens in tissues that are ___
capable of regeneration with intact extracellular matrix framework
83
regeneration occurs by
replacement of damaged tissue by identical tissue via mitosis
84
replacement occurs when __
tissues cannot regenerate and replaced by connective tissue scars
85
types of tissues
labile, stable, permanent
86
what are labile tissues
stem/undifferentiated cells
87
what are stable tissues
normally low proliferative activity unless stimulated to
88
what are permanent tissues
left cell cycle and cannot proliferate
89
cell proliferation process
granulation tissue formation > collagen synthesis + laydown by fibroblasts
90
what is granulation tissue metabolically active with
angiogenesis & fibroblast proliferation
91
key building blocks of tissue healing
fibronectin, proteoglycans, elastin, collagen
92
function of fibronectin + proteglycans
forms scaffolding that provides tensile strength and glues cells together
93
function of elastin
cross linking to form fibrils that provide tissue elasticity
94
function of collagen
structural support & tensile strength; main determinant of structural stability of extracellular matrix
95
MMP
matrix metalloproteinases
96
type of collagen for early & late scars
early = type III late = type I
97
3 determinants of complete healing
tissue type, injury nature, extent of injury
98
difference between necrosis & apoptosis in terms of cell size
n = enlarged a = reduced
99
difference between necrosis & apoptosis in terms of nucleus
n = clumped a = fragmented
100
difference between necrosis & apoptosis in terms of plasma membrane
n = disrupted a = intact
101
difference between necrosis & apoptosis in terms of cellular content
n = enzymatic digestion a = intact & packaged into apoptatic body
102
difference between necrosis & apoptosis in terms of inflammation
n = frequent a = none
103
difference between necrosis & apoptosis in terms of causes
n = pathological a = physiological & pathological
104
coagulate necrosis
coagulation of dead cells
105
liquefactive
liquidifcation of dead cells
106
gangrenous
lack of blood supply
107
caseous
cheese-like necrosis
108
factors affecting healing
age, nutrition, circulation, existing tissues
109
when does collagen synthesis & fibroblast laydown occur
3-5 days post injury & continues for weeks depending on wound size
110
as collagen mass increases, cellularity & vascularity __
decreases
111
what specific plasma proteins do we look out for during diagnostic testing for inflammation
fibrinogen & prothrombin
112
what happens when COX-2 selective NSAIDs inhibit COX-2
decreased gastric & platelet function
113
analgesic
pain relief
114
pyretic
fever
115
other effects of glucosteroids
- increased blood sugar - decreased serotonin, immunity, Ca2+ absorption - regulates metabolism - retains Na+
116
vascular events of injury
vasodilation & capillary permeability
117
cellular events of injury
leukocyte migration, phagocytosis
118
which process is important for recovery & mobility
cell proliferation
119
examples of labile cells
epithelial, hemopoietic stem cells
120
examples of stable cells
parenchymal / mesenchymal cells
121
examples of permanent tissues
skeletal / cardiac cells
122
what are essentials for recovery
Protein, Vitamin A & C
123
exacerbation
disease worsens
124
sequelae
unwanted outcome of primary condition
125
healing process
blood clot > inflammation > granulation tissue formation > epithelial regeneration > fibroblast laying collagen fibers > angiogenesis > cross-linking & realigning collagen fibers
126
pyknosis
clumped
127
karyorrhexis
fragmented
128
karyolysis
dissolution
129
clean vs dirty cell death
clean = apoptosis dirty = necrosis
130
remodelling primarily mediated by __
matrix metalloproteinases
131
which enzyme indicates myocardial infarction
CK-MB isoenzyme
132
which enzyme indicates liver
ALT
133
adverse effects of NSAIDs
GI distress, stomach ulceration, allergies, blood clot delays
134
adverse effects of ASA
GI distress, stomach ulceration, allergies, blood clot delays
135
adverse effects of glucocorticoids
GI distress, stomach ulceration, allergies, blood clot delays, increased risk of infection, edema, increased BP
136
adverse effects of acetaminophen
none
137
which drug has no anti-inflammatory effect
acetaminophen
138
which drug has no anti-pyretic & anti-analgesia
glucocorticoids
139
which synthetic glucocorticoid is used topically for skin condition
betamethasone

HSC2008 Pathology & Pharmacology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions