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PATHO EXAM 2 > YOU GOT THIS > Flashcards

YOU GOT THIS Flashcards

1
Q

decrease blood flow to the kidneys is what CAUSE of AKI

A

prerenal cause

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2
Q

hypo perfusion of the kidneys

A

prerenal cause

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3
Q

RAAS stimulation causing concentrated pee is under what type of AKI cause

A

prerenal

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4
Q

glomerlunephritis, intersitial nephritis, acute tubular necrosis

A

infrarenal cause AKI

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5
Q

what type of pH change occurs during AKI

A

metabolic acidosis

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6
Q

obstruction of outflow

A

post renal cause AKI

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7
Q

evolving injury to kidneys

symptoms starting means end of phase

A

initiation kidney injury

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8
Q

low urine output

A

oliguria (maintenance stage)

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9
Q

increase urine output to rid everything in the body

A

diuresis stage

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10
Q

loss of 3.5g of protein

A

nephrotic syndrome

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11
Q

primary cause nephrotic syndrome and age category

A

idiopathic, 3-5 year old boys

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12
Q

secondary cause of nephrotic syndrome

A

systemic disease (lupus)

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13
Q

manifestations of nephrotic syndrome

A 
PERIORBITAL EDEMA
hyperthyroidism
hyperlipidemia
vit D deficiency
hypercoagulation
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14
Q

what type of protein is excreted in nephrotic syndrome

A

IgG’s, albumin, clotting protein

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15
Q

GFR normal

A

90ml/min

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16
Q

USG normal

A

1.001-1.025

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17
Q

normal Cr

A

53-106 M

44-97 F

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18
Q

normal BUN

A

3.6-7.1

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19
Q

main causes of chronic kidney injury

A

diabetes and HTN

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20
Q

stage 1 CKI

A

decrease renal reserve

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21
Q

stage 2 CKI

A

renal insufficiency 60-90%

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22
Q

stage 3 CKI

A

renal failure 30-60

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23
Q

stage 4 CKI

A

severe failure 15-30

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24
Q

ESKD

A

<15

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25
Q

BUN and Cr in CKI

A

increased! azotemia

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26
Q

UO during CKI

A

decreased. oliguria or even anuria

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27
Q

fluid and electrolytes during CKI

A 
increase:
K
P
Mg
Na
Volume
decrease:
Ca
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28
Q

why is decrease Ca

A

sticks to P, parathyroid notices increase P and tells PTH to release Ca from bones
also vitamin D deficiency from not working kidneys

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29
Q

why anemia with CKI

A

EPO decrease and hematuria

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30
Q

why HTN during CKI

A

its a risk factor and also because Renin notices decrease output of urine and thinks we are hypotensive which is not true, so increases blood pressure

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31
Q

most common type of bladder cancer

A

transitional cell carcinoma

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32
Q

type of kidney cancer

A 
renal carcinoma
renal adenoma (RF: smoking, obesity, HTN)
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33
Q

orthostatic hypotension drops systolic ___mmHg and diastolic __ mmHg within 3 mins of moving

A

20 & 10

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34
Q

loss of __g or more of protein albumin makes you more susceptible to

A

infection and water retention

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35
Q

stage of GAS

everything is increased, blood pressure vitals, pupils are dilated

A

alarm stage

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36
Q

what happens during the exhaustion allostatic phase of GAS

A

increase blood glucose
onset of disease
suppression of osteoblasts
decrease immune system from atrophy thymus
increase gastric ulcers
hypertrophy adrenal gland because of secretion of cortisol and catecholamines

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37
Q

GAS stage where everything is normalizing

A

adaptation

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38
Q

hypothalamus secretes

A

adrenocorticotrophin hormone

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39
Q

pituitary secretes

A

corticotrophin releasing hormone

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40
Q

adrenal gland secretes

A

glucocorticoids and catecholamines

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41
Q

what stimulates gluconeogenesis

A

cortisol

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42
Q

main stress hormone

A

cortisol

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43
Q

what hormone atrophies the thymus and inhibits unnecessary events for fight or flight

A

cortisol

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44
Q

regulates blood pressure

A

norepinephrine

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45
Q

regulates heart rate

A

epinephrine

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46
Q

fight or flight

A

acute stress

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47
Q

what is secreted in acute stress

A

catecholamines and glucocorticoids

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48
Q

what is secreted during chronic stress

A

glucocorticoids

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49
Q

response of acute stress

A 
increase BP
increase HR
dilated pupils
increase visual acuity
increase respirations
increase alertness
increase gastric ulcers
increase glucose
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50
Q

what system is stimulated during chronic stress

A

limbic system

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51
Q

cortisol promotes production of metabolic substances BUT

A

inhibits the use

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52
Q

triad of structural change

A

atrophy of thymus
increase gastric ulcers
hypertrophy adrenal

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53
Q

what type of pain is
localized
sharp
quantifiable

A

acute

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54
Q

neospinalthalamic tract

A

acute pain

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55
Q

long fast and myelinated fibers

A

A delta

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56
Q

releases substance P and glutamate (excitatory)

A

acute and chronic pain

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57
Q

can be visceral or somatic

A

acute pain

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58
Q

example of acute pain: referred

A

laproscopic exam

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59
Q

stimuli for acute pain

A

thermal/mechanical

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60
Q

3-6 months pain

A

chronic pain

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61
Q

poorly localized pain with emotions involved

A

chronic pain

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62
Q

fibers for chronic pain

A

C delta fibers

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63
Q

short and unmyelinated

A

C delta

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64
Q

tract for chronic pain

A

paleospinothalamic tract

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65
Q

neuropathic pain is a part of

A

chronic pain

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66
Q

stimuli for chronic pain

A

ischemia, inflammation or persistent acute pain

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67
Q

fibers that relieve pain by releasing inhibitory neutrons: by touching or rubbing

A

A beta fibers

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68
Q

describe the ascending pathway of ACUTE pain

A

nociceptor, 1st order neuron in dorsal horn, through substantial gel to second order neuron bringing to medulla and thalamus travelling to opposite site of the brain, thalamus is relay centre, goes to third order to the somatosensory area for location and meaning

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69
Q

pain on the right hand will travel to the

A

LEFT side of the brain

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70
Q

descending pathway involves

A

periaqual duct: stimulated by opioids to inhibit pain form travelling (control centre)

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71
Q

transduction

A

activation of nociceptor

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72
Q

transmission

A

conduction of impulse up dorsal horn

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73
Q

endogenous opioid

A

morphine like

BLOCKS the pain (excitatory)

74
Q

enkephalin (endomorphic)

A

agonist to opioid receptor (block transmission)

75
Q

endocanniboid

A

analgesic

76
Q

pain threshold

A

when stimulus=pain

77
Q

perceptual dominance

A

pain at one location increases threshold at another

78
Q

pain tolerance

A

duration of time or intensity of pain before initiation of response
the more you experience the worse it gets

79
Q

pathway or modulation:

A

descending (facilitation)
segmental:
diffuse noxious:
placebo

80
Q

descending pathway

A

activating opioids to inhibit pain

81
Q

segmental pathway

A

b fiber stimulates inhibitory neurons to decrease pain transmission

82
Q

noxious pathways

A

pain relief when 2 noxious stimuli occur at same time at different locations

83
Q

placebo

A

expectations

84
Q

occipital lobe

A

back of the brain responds to flashing lights

85
Q

temporal lobe

A

on the sides and is most responsible for seizure activity

for memory retrieval

86
Q

frontal

A

motor strip: marching

87
Q

partial seizure

A

only involves one hemisphere of the brain

88
Q

aura

A

visual cue right before seizure

89
Q

prodroma

A

days before seizure

90
Q

simple partial seizure

A

most aura occur
no loss of consciousness, usually memory
JACKSONIAN MARCH

91
Q

complex partial seizure

A

LOC, not much memory

92
Q

secondary generalized seizure

A

partial seizure that has spread to both sides of the brain

TONIC CLONIC

93
Q

generalized seizure

A

both hemispheres

LOC bilateral movement

94
Q

types of generalized seizure

A

atonic
myoclonic
absense
tonic clonic

95
Q

atonic seizure

A

loss of muscle tone (drop seizure)

96
Q

absense seizure

A

blank stare and lip smacking

97
Q

myoclonic seizure

A

jerking, short lasting

98
Q

tonic clonic

A

convulsions to relaxation of muscles
cry or groan because muscles are contracting and forcing air out of trachea increase ATP AND O2 need because you’re doing so much

99
Q

idiopathic unprovoked seizures

A

genetic? treat with anti epileptic medications

100
Q

provoked seizure

A

metabolic disorder, infection, tumour: treat with underlying cause

101
Q

sequence of tonic clonic

A 
depolarization
tonic contraction
LOC
clonic 
incontinence
cyanosis
hyperpolarization
seizure over
post ictial phase
102
Q

repeated seizure without break or several seizures back to back

A

status epilepticus

103
Q

classification of brain injury

A

primary and secondary

104
Q

primary brain injury

A

initial injury and displacement of the brain

105
Q

secondary brain injury

A

consequence from initial insult

106
Q

types of primary brain injury

A

focal
diffuse
contusion
concussion

107
Q

focal primary brain injury

A

close: one are (coup vs counter coup)
open: penetration

108
Q

diffuse brain injury

A

widespread: shearing force causing axon damage causes swelling and bruising
increases ICP, decrease O2, ischemia hypoxia and necrosis

109
Q

contusion

A

no Brian movement

bruising or leaking

110
Q

concussion

A

impact, movement of brain

111
Q

result of secondary brain injury

A

hemorrhage, increase ICP, death

112
Q

complications of brain injury

A

post concussion syndrome
post trauma seizure disorder
CTE (chronic traumatic encephalopathy)

113
Q

what is post concussion syndrome

A

weeks or moths after incident

anxious, dizzy anorexia, overstimulation

114
Q

why would someone be overstimulated with post concussion syndrome

A

damage to the RAS

this system controls and filters nonsense, without this you get overstimulated

115
Q

what is post trauma seizures

A

can be after brain injury or occur years after. you are hyper excitable, administer anti-seizure medications

116
Q

what is CTE

A

complication of brain injury from repeated brain trauma. occurs often with contact sport or work related injuries
results in dementing disease (diagnosed at death)

117
Q

cerebral death

A

brain stem and cerebellum still functioning, you are maintaining homeostasis but unresponsive- vegetative state

118
Q

brain death

A

no brain stem function, no homeostasis irreversible

119
Q

what is coup countercoup

A

the action of you brain hitting the back and front of your skull

120
Q

what would happen if you had a blow to the back of your head (coup or countercoup)

A

brain would hit the front of your skull, coup

121
Q

alterations in cerebral hemodynamics (blood flow)

A

increase ICP
cerebral edema
hydrocephalus

122
Q

increase ICP etiology

A

hemorrhage, tumor, CSF

123
Q

Monroe kelle theory

A

displacement of either hemorrhage tumor or CSF causes shift of other two

124
Q

stages of ICP

A

asymptomatic
increase pressure (compromises o2)
hypoxia to brain tissues (hypercapnia)
herniation and damage to tissue

125
Q

etiology of cerebral edema

A

tumor, meningitis, cancer

126
Q

types of cerebral edema

A

vasogenic edema
cytotoxic metabolic edema
interstitial edema

127
Q

what is vasogenic edema

A

a type of cerebral edema found in brain injury

at the site of the injury increasing permeability which leads to ischemia

128
Q

what is cytotoxic edema

A

a type of cerebral edema found in brain injury

toxic factors in grey matter make you lose K and gain water and sodium

129
Q

what is interstitial edema

A

a type of cerebral edema found in brain injury

CSF moves into ventricles

130
Q

what is hydrocephalus

A

type of alteration that is increase CSF causing accumulation

131
Q

etiology of hydrocephalus

A

blockage or increase fluid

132
Q

cells in wound healing

A

fibroblasts

133
Q

inflammation of skin cells that are red painful warm and edeamic

A

cellulitis

134
Q

hard necrotic tissue

A

eschar

135
Q

incision breaks

A

dehiscent

136
Q

organs out of wound

A

evisceration

137
Q

whiteness, wrinkled, soft skin due to exposure to fluid

A

masceration

138
Q

soft necrotic tissue

A

slough

139
Q

scar extending beyond wound

A

keloid

140
Q

abnormal tightening of skin

A

contracture

141
Q

scar on boundary

A

hypertrophy scar

142
Q

scar tissue binding to tissues and other organs

A

adhesion

143
Q

how to assess for circulation when wound healing

A

albumin
hemoglobin
bood glucose

144
Q

bad circulation

A

albumin less than 30
hemoglobin less than 100
blood glucose more than 7

145
Q

phases of wound healing

A

inflammation (hemostasis)
proliferation (new tissue being build)
remodelling (compensatory hyperplasia scar tissue)

146
Q

local acute inflammation

A

cell changes and vascular changes

147
Q

cell changes of local acute inflammation

A 
WBC
granulocytes 
- neutrophils
- basophils
- eosinophils
- mast cells
non-granulocytes
- lymphocytes
- monocytes
148
Q

neutrophils

A

1st responder

149
Q

basophils

A

mast cells

150
Q

eosinophils

A

parasites

151
Q

mast cells

A

release histamine

152
Q

monocytes

A

turn into macrophages then giant cells in presence of foreign body

153
Q

vascular changes of local acute inflammation

A

injury to tissue, then transient vasoconstriction to vasodilation

  • erythmea
  • increase permeability
154
Q

pain mediatory

A

prostaglandins and bradykinin (nociceptor)

155
Q

warmth/redness mediator

A

prostaglandin, histamine, nitric oxide (vasodilation)

156
Q

swelling mediator

A

histamine and leukotrienes (increase permeability)

157
Q

systemic acute inflammation

A

WBC response and acute phase response

158
Q

WBC response of acute systemic inflammation

A

macrophages phagocytize because opsonization

159
Q

acute phase response of systemic inflammation

A

blood work changes!!!!

increase ESR, CRP, Shift to the left increase WBC

160
Q

What is ESR

A

erythrocyte sedimentation rate- protein attached to RBC and how fast it falls

161
Q

CRP

A

increases where the inflammation is- type of protein

162
Q

shift to the left

A

immature neutrophils and a lot of them accumulate and cause shift to the left

163
Q

systemic acute inflammation causes

A

increase permeability, vasodilation, clotting (firbolysis)

164
Q

response to systemic acute inflammation

A

fever, malaise, heal OR abscess OR chronic inflammation

165
Q

how long does acute have to last to turn into chronic

A

2 weeks or more

166
Q

what happens to monocytes in chronic inflammation

A

turn into macrophages, then giant cells which surround and encapsulate foreign bodies

167
Q

what is nonspecific chronic inflammation

A

accumulation of nongranulocytes and proliferation of fibroblasts causing scary tissue. granulation formation from lots of macrophages and foreign bodies are surrounded.

168
Q

vascular response to inflamamtion

A

vasodilation and permeability mediated by plasma proteins

169
Q

plasma protein systems

A

clot complete, kinin

170
Q

components of inflammation

A

cell receptor

cytokines: regulate response of inflammation
erythrocytes: platelets or WBC

171
Q

mediators

A

leukotrienes (similar to histamine) prostaglandins (pain), platelet activating factor (like histamine)

172
Q

what are platelets activated by

A

tissue destruction and inflammation- they interact with coagulation factors to stop bleeding

173
Q

what do WBC do when they arrive at site of injury

A

adhere, engulf, phagosome, lysosome, destruct

174
Q

phases of wound healing

A

hemostasis, proliferation, remodelling

175
Q

referred pain is possible because it is carried on

A

same spinal segment

176
Q

normal Na

A

135-145

177
Q

normal K

A

3.5-5

178
Q

normal glucose

A

3.5-7.8

179
Q

normal platelets

A

150-4000

180
Q

normal HgB

A

120-160 f

140-180 m

181
Q

what happens in stress-age-syndrome

A 
increase catecholamines and cortisol
decrease thyroxine and testosterone
immunodepressed
hypercoagulation
free radical damage

PATHO EXAM 2 (1 decks)

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