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Pathophysiology > Week 3 Jan 20-24 > Flashcards

Week 3 Jan 20-24 Flashcards

1
Q

what is a side effect of hypokalemia associate dwith H+

A

metabolic alkalosis
- if potassium is low in blood mmore is drawn out of cell into blood in exchange more H+ enters cel, therfore decreas in H+ in blood

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2
Q

alaklosis is associated with ___ in tmers of K+ because of ___

A

hypokalemia a
an antiporter

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3
Q

Explain conenction betwen K+ and H+

A

A side effect of hypokalemia (decrese K+ in blood) is metabolic alkalosis
Potassium low in blood, bring more potassium out of cell into blood, in exchange more H+ enters the cell, herfoer decrease in H+ in blood = metabloc alkalosis
Hyperkalemia can cause acidsosi - antiporter (H+/K+ interchange)
K+ increase in blood, goes into cell exchange h+ goes into blood, cinreaisng H+ in blood

Because of ANTIPORTER - passive transport based on changes - also can go other way around

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4
Q

A prolonged state of metabolic acidosis often
leads to:
a) Hypercalcemia
b) Hyperkalemia
c) Hyponatremia
d) Hypokalemia

A

hyperkalemia

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5
Q

is pain a sign or sympom

A

symptom

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6
Q

is pain always a result of peripheral stimulus?

A

no - sources and type of pain vaireis

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7
Q

our experienvce of pain can be described bhw hat 2 components?

A

sensory component = nocireceptors activated by pain stimules

affective cognitive componenet - brain experiencing pain from context

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8
Q

definition of pain?

A

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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9
Q

what are the 3
sources of apin - desctib each

A

Nocireceptive pain - from actual tissue damge. (chemical, thermal, mechanica)

somatic - whithin skin or bones/joints/msucle where somatosensory nerved detect pain stim

neuropathic pain - dysfunction of NS. OFten no tissue damage - present in many diff ways

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10
Q

waht is pain threshold?

A

the lelvel of stimualtion needed to activate the pain pathway and achieve a pereivable signal to the brain

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11
Q

what is pain tolerance. What is it modulated by?

A

ability to withstand pain - dpendent on intensity and time

modualted by endorphins, (increased pain tolerance),
fatigue, stress, mental health (decrease pain tolerance)

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12
Q

endorphins ____ pain threshold, also known as ____

A

increase pain throshold - endogenous opiods

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13
Q

what are the three key poitns sfor recdoneptualizing pain accoreing to moseley?

A

1) pain not porpotionate ot tissue injurt
2) pain modulated by many facotrs
3) relationship between pain and state af tissue is less predictable as pain persists

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14
Q

what are hte 2 types of affernt fibres that carry pain signals?

A

A delta (larger, myelinated)
- low threshold pain (mechanocal and thermal) - sharp, locaized pain

C fibres (small, unmyelinated)
- high threhsold, thermo, maechano, chemo
- dull, throbbing, aching, burning, poorly localized

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15
Q

at type of afferent pain telated fibrees are found in most tissues?

A

C fibres

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16
Q

draw the pain pathway

A
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17
Q

explain the pain pathway - starting wiht pain stimulus

A
  1. pain stiimulus (mechanical, thermal, chemical) -
  2. nocireceptor to afferent fiber ithru dorsal ganliion + root
  3. synpase in spincal chord (substance P)
  4. lateral spinothalmic tract
  5. brainstem (reic formation - awareness/aletrt)
  6. thalamus - relays
    • to hypothal Istress response - Hr, BP…)
      5o limbi system (emotion/ememory resp)
      primary somatosens ( awareness + loaclization)
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18
Q

waht are the 2 ways pain can be inhibiter

A

1) other mechanical/ touch stimuli coming into the sc at the same time
2) descending signals from brain block pain

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19
Q

what happens when the gate is closed in the gate control theory - what 2 substances are involved?

A

when the gate is closed, and interneuron is activated by descining(effeernt signals) from the brain or afferent touch signals ) this enkpahlin(an endorph

Stimulates the release of enkephalin form interneuron

opiate receptors are blocked and substance P cannot be released, the gate is closed and transmission cannot travel tot he brain

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20
Q

Which of the following substances plays a role in inhibiting pain signals by binding to opioid receptors in the spinal cord? a) Substance P
b) Enkephalins
c) Serotonin
d) Acetylcholine

A

enekephalin - endophin - andogenous opioid

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21
Q

The brain’s release of serotonin in response to pain can help inhibit pain transmission by:

A

enhancing action of enkephalins to inhibit pain signals

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22
Q

explain seratonins role on the gate control theory?

A

seratonin is released by the brainstem and it
1) directly inhibits nocirecepor (substane P)
2) indirectly - activates inteuron and icnreaes enkephalin release inhibtinh substance P

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23
Q

does release of enkephalin comploetely inhibit painrepose?

A

no it just inhibits release of substnace P, reducing intensity if pain feeling

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24
Q

What machine is based on gate control theory and what does it do?

A

TENS mahine - distract area of spincal chord by adding other senory input hwich releases enkephalin and inhibts substance B decreasing intensity of pain repsonse

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25
explain how seratonin. boith directly and indirectly inhibits pain
Desceingin signals form teh brain Directly - inhibits the release of substance P on 1st order afferent (eg delta C fibers) indirectly - via interneuon stimulatees release of enkephalin which inhibtis substance P
26
what is shared in the thory behind referred pain?
shared second order afferent - incorrect coding
26
explain how referred pain occurs
pain signal synapse on the same second order afferent and brain misinterprets signals as the pain felt form a diffenet area
27
according to WHO chronic pain lsts more than ____
3 months
28
true or false - chronic pain is usually an extensin of acute?
false - differnt underlying mechanisms + treatment
29
true or false pain is a resuult of solely peripheral stimulus?
no - it can also be localized in the CNS - neurpathic pain
30
what does current research show the caue of chronic pain being
inflmattion og NS - malfuncitoning glial cells tratment - fish oil, exercise, neuromodulation
31
what are the 2 types of pharmacological treatment of pain ? what do each decreaes? a
analgesics - pain perception by blocking pathway anethetcis - anethetic block snesation
32
analgesics block ____ and anethetics block ___
perception, sensation
33
what are teh 4 P's in treatment of pain - examples of each
Prevention - Sleep management, nutrition, education, goal setting Psychological - Mindfulness, relaxation, cognitive behavioural therapy Retrain your brain Physical - Learn your body, safe moecemtnt, elarn your pain Safe movement and exercise Evidecne that exercise help desensitzie the sensitized NS Exercise is antiinflammatory Helps to visulaize moevemt
34
what is neuromodulation?
Transcranial magnetic stimulation Use and electromagnetic coil to deliver a magnetic pulse that that stimulates nerve cells in specific regions of the brain Shown to be effective treatment for chronic depression and chronic neuropathic pain
35
encephalitis is inflmmation of the___
brain
36
hepatitis is inflammationof the
liver
37
how can exercise help pain
releases endorphins (enkephelin) can help mange chronic pain - also can reduce the effect of acute pain - makes u feel like ur not in pain and keep going (runners hihg)
38
inflammation is an important ___ of the body
defense mechanism
39
what are the two type of stimuli that can cause. inflammtion
pathogen (ciru, funfus, bacvteria), allergen, toxin, irritants physical damage - any cell damage, bone break/soft tissue sprain, exercise
40
what is the goal of inflammation
respond to stimuli and resotr balance
41
what are the 5 cardinal signs of acute inflammation
pain, heatm, redness, swelling, loss of fucntion
42
diffenece between local and sytemic inflmamation
local is speciic area of bod, ssytemic is entire body and invovles immune system
43
what are the three steps of the acute inflammatory response?
1) intitiation and amploification - chemical mediators eleased into blood at side of injury by resident immune cells + more immune cells recruited to aresa 2) destruction - neutralization of the injury and debris removal by chemical mediators and immuen cells 3) termination - cytokines and chemokines end the inflammatory response
44
what are the 3 local actions of chemical mediators in teh acute inflammatory response?
1) pain response - bidn to nocireceptors 2) vascular response - casodilation + increase capillary permeability 3) cellular response - attract immune cells to cite of injury (chemotaxis)
45
what are cytokines?
Proteins that coordinate the immune response * Some are pro-inflammatory and some are anti-inflammator
46
cytokines are antinflammatory.. true or flase?
flase they are pro and anti
47
name 4 cells involved in the inflammatory response?
platelets - release blood-clotting proteins at the wound site (if needed) mast cells - secrete chemical mediators neutrophils - migrate to the site and secrete factors that kill pathogens, phagocytosis to remove pathogens and debris macrophages - secrete cytokines, phafocytosis to remove apthogens and debris
48
platlets only relased in..
physical teat
49
draw diagram of cells and what each secrete
50
what do mast cells secrete. What common action do all three of these share?
histamine prostaglandins leukotrines all caues vasodilation + incr capillary permeability
51
the actions of histamines are: it is secreted by ___
icnrease cap perm vasodilation secreted by mast cells
52
actions of prostaglandin are
cap perm incr vasodilation pain fever
53
actions of leukotrines
vasodilation, incr capillary perm, chemotaxis
54
what chemcial mediators do macrophages secrete? what are its actions ?
cyrokines - fever, chemotaxis, leukocytosis (recruit more WBCs)
55
what are neutrophils
a type of WBC that mitigate to cite and secrete facots that kill aothgens, phagocytosis to remove pathogens and degree
56
wehat chemical mediators do plaetelets secrete?
pleatelet activating facteor - paltelet agregation(blood clotting)
57
what 4 chemical mediators do plasma proteins secrete?
bradykinin complemetn sytem c-reactive proteine prothombin and fibrogen
58
what does bradykinin do and what secretes it?
bradykinin - vasoilation _ incr cap perm, pain plasma proteins secrete
59
what does complement system do - secrete dby what?
vsosdilation, icnr cap perm, chemotaxis
60
whta does c reactive protein do (CRP)
Secretion of more cytokines, activates complement system, chemot
61
what do prothrombin and fibrinogen do?
blood clotting
62
what chemical mediators do vasodialtion and incr cap perm
histmaine, prstaglandin, leukotrine, bradykinin, compleem system,
63
what is exudate?
intersitial fluid colleceted in the area of inflamtion
64
what are the 4 characteristics of exudat
serous, ibrinous, purulent, hemmorhagic
65
what type of exudate is prsent in a common edema during inflamttion
serous - watery, fluid _small amothnf if pretin and WBC
66
in fibrinours exudate ___ and ___ content are higher and it looks___
cell and fibrin - thick and it looks thick and sticky
67
what tupe of exudate suggests a bacterial infection? characteristcs of it?
purulent - thicka nd yellow-green 0 higher wBC and debris
68
what is na abscess?
Pocket of purulent exudate in a solid tissue
69
what is antipiurite drugs? example of drug that does not do this but reduces inflammation
reduce fever - glucocoticoid
70
what are some non-pharmaceutical treatment for inflammation?
compression, cold, hot, elebatopm, rest
71
what 3 fates are there for healing
resolution - damged cells recover regeneration - damged cells replace dby identical type (they divide by mitosis) (epithelial) replacement - damged cells replaced by conn tissue (scar tissue). Loss opf function in area
72
scar tissue is ___ crosslinking
collagen crosslinking (fibrosis)
73
is there an antinflmamatory component in chronic inflammation?
no ther eis not only in acute
74
what immune cells are mostly involved in acute inglammation
neutrophils mainly
75
what immune ells are mainly involved in chronic inflamtion
monocytes, macrophages, lumphosyte
76
true or glase chronic inflammtion awlays develops ar result of acute
false - could be some kind of irration/toxins, autoimmune, inflammtory stress
77
what are 2 proinflammatory cytokines?
CRP +interleukin 6
78
what can chronic inflammation result form
acute -that didnt resolve exposure to irritant autoimune inflammator/bicohemcal inducers cause oxiadtice stress + mito fisfunction
79
what are some non-pharmacologic treatment for chronic inflmamation?
nutrition - antiinflammatory foods - avoid alcohol, sugar, carbs, trans fats consumer whole grains, ewwhole foods, veg, fish aerpobic/resitance exerice sleep stress redcution

Pathophysiology (11 decks)

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