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Case 1 > Case 1 > Flashcards

Case 1 Flashcards

1
Q

Name the types of pain (x7)

A 
nociceptive
cutaneous 
somatic 
visceral
referred 
neuropathic 
inflammatory
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2
Q

nociceptive pain definition

A

response to tissue injury

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3
Q

cutaneous pain definition

A

originates from skin

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4
Q

somatic pain definition

A

generated from deeper connective tissue and muscles

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5
Q

visceral pain definition

A

from internal organs

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6
Q

referred pain definition

A

perceived in an area away from the organ site

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7
Q

neuropathic pain definition

A

pain from damage / disease in somatosensory nervous system

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8
Q

inflammatory pain definition

A

activation / sensitisation of nocioceptive pain pathway die to IL-1/6 and TNF alpha

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9
Q

describe gate control theory

A

emotions influence pain / perception of it
pressure is also by inhibitory neurone (rubbing decreases pain)
noradrenaline suppresses pain by receptor inhibition

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10
Q

Phases of pain - transduction (1)

A

converting chemical info into electrical info in spinal cord = action potential

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11
Q

Phases of pain - transmission (2)

A

from nociceptive fibres to dorsal horn of spinal cord to brainstem to thalamus and cortex

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12
Q

Phases of pain - perception (3)

A

conscious experience of discomfort when pain threshold is reached

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13
Q

Phases of pain - modulation (4)

A

release of pain inhibiting neurochemicals ANALGESIA

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14
Q

types of pain fibres (x3)

A

A delta fibres
C fibres
B fibres

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15
Q

A delta fibres

A

noxious stimuli + sharp/localised pain
primary afferent neurons
slow / thin as unmyelinated

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16
Q

C fibres

A

noxious stimuli
free nerve endings
slow / thin unmyelinated
dull / throbbing pain

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17
Q

B fibres

A

large / FAST

from mechanoreceptors

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18
Q

Dorsal horn grey matter laminae 1

A

presynaptic terminal of A and C fibres / 2nd order

- thalamus + somatosensory cortex

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19
Q

Dorsal horn grey matter laminae 2

A

presynaptic terminal of C

- inhibiting signals to 1

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20
Q

Dorsal horn grey matter laminae 3/4

A

presynaptic terminal of A and B and dendrites from 5

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21
Q

Dorsal horn grey matter laminae 5

A

presynaptic terminal of A and 2nd order neurones

- hypothalamus and amygdala

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22
Q

Process of pain transmission (steps 1-4)

A

1 nociceptive action potential ( C and A fibres) reaches presynaptic dorsal horn

2 C and A fibres release pro nociceptive (excitatory NT) into synaptic cleft

3 C fibres release GLUTAMATE activating post-synaptic AMPA receptors

4 causing SP then NK1 receptor activation / CGRP pathways

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23
Q

CGRP receptors (x3)

A

ATP
Glutamate
Nitric oxide

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24
Q

Limbic system parts?

A

anterior angulate gyrus

right ventral prefrontal cortex

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25
Q

Pain threshold definition

A

point where sufficient pain transmitting stimuli has reached the brain to trigger action potential

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26
Q

pain tolerance definition

A

amount of pain a person can endure

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27
Q

affect of distraction on pain perception

A

interrupts pain signal lowering pain level perceived

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28
Q

reticular system function in pain pathway

A

warning individual by looking at damage (motor / autonomic response)

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29
Q

somatosensory cortex function in pain pathway

A

perception and interpretation of sensation (intensity / type / location)

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30
Q

limbic system function in pain pathway

A

emotional and behavioural response to the pain

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31
Q

mechanism of modulation of pain

A

descending inhibition - releasing inhibitory NT to either partially / completely block pain impulse ANALGESIA

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32
Q

Pain mechanism (COX)

A

1 ) phospholipids are converted to ARACHIDONIC ACID by phospholipase A2

2 ) COX (cyclooxygenase) combines amino acids and O2 to make PROSTALANDIN G2

3 ) G2 converted to H2 prostaglandin (peroxidase reaction)

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33
Q

What functions is COX 1 responsible for?

A

homeostasis
renal blood flow
liver function
gastric mucosal lining

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34
Q

What functions is COX 2 responsible for?

A

fever
inflammation
pain

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35
Q

PGH1 function

A

GI tract
chronic pain
inflammation

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36
Q

PGH2 function

A

reproductive things
chronic pain
inflammation

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37
Q

PGE2 function

A

sensitises A delta + C neurons to serotonin

38
Q

PGE2 function

A 
GI mucosa
renal protection (local vasodilation)
39
Q

PGD2 function

A

bronchoconstriction

antiplatelet activity

40
Q

PGF2 function

A

bronchoconstriction

urterine contraction

41
Q

TXA2 function

A

platelet aggregation

local vasoconstriction

42
Q

PGI2 function

A

INHIBITS
platelet aggregation
local vasoconstriction

43
Q

Name some NSAIDS

A 
ibuprofen
codeine 
rofecoxib 
asprin 
celecoxib
44
Q

What does NSAIDS stand for

A

Nonsteroidal anti-inflammatory drugs

45
Q

ibuprofen mechanism

A

non-selective inhibitor of COX1/2

is a competitive inhibitor of the AA for COX domain involved in prostanoid production

46
Q

Ibuprofen

A

T = pain / inflammation / fever

SE = indigestion / heart burn / vomiting / diarrhoea

DT = stomach ulcer / Crohns disease / asthma / liver failure/ hypertension / heart problems/ clotting issues

47
Q

codeine

A

opioid receptor antagonist

T =pain relief

SE = constipation / dry . ought / nausea / sweating

DT = kidney problems / thyroid or adrenal gland problems / gallstones / inflammatory bowel problems / breathing problems (COPD / asthma )

48
Q

rofecoxib

A

selective COX 2 inhibitor

T = osteoarthritis and pain

been withdrawn from market (MI / stroke risk)

49
Q

aspirin

A

irreversible inhibition of COX1/2

T = fever / pain / aches / excessive clotting (prevention)

SE = indigestion / nosebleeds

DT = asthma / stomach ulcer / below 16 (REYES DISEASE) / haemophilia / kidney or liver problems / heart failure / thyroid problems

50
Q

celecoxib

A

selective COX 2 inhibitor

T = pain / inflammation / osteoarthritis / rheumatoid arthritis

SE = dizzy / diarrhoea / indigestion / hypertension / UTI / peripheral oedema

DT = under 18 / asthma / stomach ulcer / hypertension / clotting issues / heart conditions / kidney and liver problems

51
Q

NSAID side effects on GI mucosa

A

COX 1

  • peptic ulcers
  • GI bleeding
52
Q

NSAID side effects on kidneys

A

COX 1 / 2

  • NA+ and H2O retention
  • hypertension
  • acute kidney damage
53
Q

NSAID side effects on cardiovascular

A

COX 1/2

  • stroke
  • MI
54
Q

inflammation function

A

eliminates cause of cell injury
clears out necrotic cells
initiates tissue repair

55
Q

acute inflammation mechanism

A

initial response to stimuli characterised by increase movement of plasma and leukocytes to injury site by hyperplasia / hypertrophy / atrophy

56
Q

vascular effect of inflammation

A

1 transient vasoconstriction preventing initial blood loss

2 vasodilation (histamine / NO) increasing vessel permeability (endothelial cells part too)

3 white blood cells enter

57
Q

cellular response

A

1 damaged tissue releases cytokines / C5a

2 attracts neutrophils into dilated vessels DIAPEDESIS

3 B and T cells migrate towards chemotaxis signals

4 phagocytosis / degranulation occurs

5 histamine / lysosome / prostaglandin synthesis

6 Increase in IP3

7 increase in Ca2+

8 cell movement

58
Q

chronic inflammation

A

macrophages (from monocytes) largely present
simultaneous destruction / healing of tissue
increase in white blood cells (tissue destruction)

59
Q

chronic inflammation cause

A

persistent infection

autoimmune disorder

60
Q

name the two phases of clotting

A

primary / secondary haemostasis

61
Q

Primary haemostasis steps (1-7)

A

1 damage to epithelium exposing collagen

2 von Willebrand (vW) factor binds to collagen

3 platelets (activated by thrombin / ADP ) bind to vW / collagen - SOFT CLOT

4 platelets activate and increase their surface area

5 degranulation of granules increase step 3/4

6 negative phospholipids bind to coagulation factors

7 smooth muscle contraction (decrease blood loss)

62
Q

secondary haemostasis

A

CLOT STABILISATION
coagulation of soft plug
fibrin forms mesh that traps platelets / erythrocytes

63
Q

intrinsic secondary haemostasis pathway

A

Factor XII to XI to IX to VIII to Factor X and V

64
Q

extrinsic secondary haemostasis pathway

A

Factor III to VII to Factor X and V

65
Q

common pathway secondary haemostasis pathway

A

prothrombin (Factor X + V) to thrombin

fibrinogen (thrombin) to fibrin

66
Q

Haemophilia types (x3)

A

A VIII deficiency
B IX deficiency
C XI deficiency

67
Q

Name steps of clotting cell based model (x3)

A

initiation
amplification
propagation

68
Q

initiation (1) clotting cell based mode

A

Small amounts of thrombin
Factor IXA made
EXTRINSIC PATHWAY

69
Q

amplification (2) clotting cell based mode

A

thrombin activated Factor XI / VIII INTRINSIC
and factor V COMMON
generating factor XA

70
Q

propagation (3) clotting cell based mode

A

increase in thrombin generated INTRINSIC

71
Q

function of thrombin in clotting cell based mode

A

increased thrombin converts fibrinogen - fibrin and factor VIII stabilising it

72
Q

definition of 1st intention healing

A

stitching together of wound and cleaning

73
Q

definition of 2nd intention healing

A

separated edges increase inflammation / scar tissue

74
Q

laceration definition

A

tearing of soft body tissue

75
Q

steps of laceration healing (x4)

A

haemostasis
inflammation (macrophages)
proliferation
maturation

76
Q

haemostasis laceration healing (1)

A

1 vasoconstriction (adrenaline) in first 10 mins

2 vasodilation (histamines)

3 exposed collagen = platelet activation

4 chemokines activated by platelets

5 inflammatory cells attracted

77
Q

inflammation laceration healing (2)

A

1 macrophages secrete collagen / elastase causing injured tissue breakdown

2 release of cytokines which release platelet derived growth factor

3 chemotaxis / fibroblast proliferation attracts endothelial cells

4 ANGEOGENESIS

78
Q

proliferation laceration healing (3)

A

1 epitheliazation / fibroplasia / angiogenesis

2 formation of granulation tissue

79
Q

maturation laceration healing (4)

A

collagen forms tight cross links increasing the tensile strength of scar tissue

80
Q

Bruising definition

A

type of haemotoma caused by crushing of connective tissue / ruptured capillaries without broken skin

81
Q

damage capillaries endothelium in bruising function

A

releases endothelia causing vasoconstriction to reduce bleeding

82
Q

damaged endothelium in bruising function

A

exposing the the vW factor causing coagulation to being - temporary clot - normal tissue reformed

83
Q

bruise colour sequential degradation steps (not indicative of injury age)

A

RED BLUE - haemoglobin
GREEN - biverdin
YELLOW - bilirubin
BROWN - hemosiderin

84
Q

graze / abrasion definition

A

wound caused by superficial damage to skin ( no deeper than epidermis ) with minimal bleeding

85
Q

serous wound definition

A

produces clear fluid from plasma and mesothelial cells

86
Q

fibrinous wound definition

A

after serous - increase fibrin / vascular permeability

87
Q

suppurative / purulent wound definition

A

++ dead tissue / WBS = pus

88
Q

ulcers wound definition

A

damage through epithelial layers leaving a cavity

89
Q

Grade 1 sprain injury

A

slight ligament damage / stretching

still able to keep knee joint stable

90
Q

Grade 2 sprain injury

A

stretches ligament causing it to loosen (partial tear)

91
Q

Grade 3 sprain injury

A

complete ligament tear = unstable knee joint

Case 1 (1 decks)

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