YOU GOT THIS Flashcards
1
Q
decrease blood flow to the kidneys is what CAUSE of AKI
A
prerenal cause
2
Q
hypo perfusion of the kidneys
A
prerenal cause
3
Q
RAAS stimulation causing concentrated pee is under what type of AKI cause
A
prerenal
4
Q
glomerlunephritis, intersitial nephritis, acute tubular necrosis
A
infrarenal cause AKI
5
Q
what type of pH change occurs during AKI
A
metabolic acidosis
6
Q
obstruction of outflow
A
post renal cause AKI
7
Q
evolving injury to kidneys
symptoms starting means end of phase
A
initiation kidney injury
8
Q
low urine output
A
oliguria (maintenance stage)
9
Q
increase urine output to rid everything in the body
A
diuresis stage
10
Q
loss of 3.5g of protein
A
nephrotic syndrome
11
Q
primary cause nephrotic syndrome and age category
A
idiopathic, 3-5 year old boys
12
Q
secondary cause of nephrotic syndrome
A
systemic disease (lupus)
13
Q
manifestations of nephrotic syndrome
A
PERIORBITAL EDEMA hyperthyroidism hyperlipidemia vit D deficiency hypercoagulation
14
Q
what type of protein is excreted in nephrotic syndrome
A
IgG’s, albumin, clotting protein
15
Q
GFR normal
A
90ml/min
16
Q
USG normal
A
1.001-1.025
17
Q
normal Cr
A
53-106 M
44-97 F
18
Q
normal BUN
A
3.6-7.1
19
Q
main causes of chronic kidney injury
A
diabetes and HTN
20
Q
stage 1 CKI
A
decrease renal reserve
21
Q
stage 2 CKI
A
renal insufficiency 60-90%
22
Q
stage 3 CKI
A
renal failure 30-60
23
Q
stage 4 CKI
A
severe failure 15-30
24
Q
ESKD
A
<15
25
BUN and Cr in CKI
increased! azotemia
26
UO during CKI
decreased. oliguria or even anuria
27
fluid and electrolytes during CKI
```
increase:
K
P
Mg
Na
Volume
decrease:
Ca
```
28
why is decrease Ca
sticks to P, parathyroid notices increase P and tells PTH to release Ca from bones
also vitamin D deficiency from not working kidneys
29
why anemia with CKI
EPO decrease and hematuria
30
why HTN during CKI
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
31
most common type of bladder cancer
transitional cell carcinoma
32
type of kidney cancer
```
renal carcinoma
renal adenoma (RF: smoking, obesity, HTN)
```
33
orthostatic hypotension drops systolic ___mmHg and diastolic __ mmHg within 3 mins of moving
20 & 10
34
loss of __g or more of protein albumin makes you more susceptible to
infection and water retention
35
stage of GAS
| everything is increased, blood pressure vitals, pupils are dilated
alarm stage
36
what happens during the exhaustion allostatic phase of GAS
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
37
GAS stage where everything is normalizing
adaptation
38
hypothalamus secretes
adrenocorticotrophin hormone
39
pituitary secretes
corticotrophin releasing hormone
40
adrenal gland secretes
glucocorticoids and catecholamines
41
what stimulates gluconeogenesis
cortisol
42
main stress hormone
cortisol
43
what hormone atrophies the thymus and inhibits unnecessary events for fight or flight
cortisol
44
regulates blood pressure
norepinephrine
45
regulates heart rate
epinephrine
46
fight or flight
acute stress
47
what is secreted in acute stress
catecholamines and glucocorticoids
48
what is secreted during chronic stress
glucocorticoids
49
response of acute stress
```
increase BP
increase HR
dilated pupils
increase visual acuity
increase respirations
increase alertness
increase gastric ulcers
increase glucose
```
50
what system is stimulated during chronic stress
limbic system
51
cortisol promotes production of metabolic substances BUT
inhibits the use
52
triad of structural change
atrophy of thymus
increase gastric ulcers
hypertrophy adrenal
53
what type of pain is
localized
sharp
quantifiable
acute
54
neospinalthalamic tract
acute pain
55
long fast and myelinated fibers
A delta
56
releases substance P and glutamate (excitatory)
acute and chronic pain
57
can be visceral or somatic
acute pain
58
example of acute pain: referred
laproscopic exam
59
stimuli for acute pain
thermal/mechanical
60
3-6 months pain
chronic pain
61
poorly localized pain with emotions involved
chronic pain
62
fibers for chronic pain
C delta fibers
63
short and unmyelinated
C delta
64
tract for chronic pain
paleospinothalamic tract
65
neuropathic pain is a part of
chronic pain
66
stimuli for chronic pain
ischemia, inflammation or persistent acute pain
67
fibers that relieve pain by releasing inhibitory neutrons: by touching or rubbing
A beta fibers
68
describe the ascending pathway of ACUTE pain
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
69
pain on the right hand will travel to the
LEFT side of the brain
70
descending pathway involves
periaqual duct: stimulated by opioids to inhibit pain form travelling (control centre)
71
transduction
activation of nociceptor
72
transmission
conduction of impulse up dorsal horn
73
endogenous opioid
morphine like
| BLOCKS the pain (excitatory)
74
enkephalin (endomorphic)
agonist to opioid receptor (block transmission)
75
endocanniboid
analgesic
76
pain threshold
when stimulus=pain
77
perceptual dominance
pain at one location increases threshold at another
78
pain tolerance
duration of time or intensity of pain before initiation of response
the more you experience the worse it gets
79
pathway or modulation:
descending (facilitation)
segmental:
diffuse noxious:
placebo
80
descending pathway
activating opioids to inhibit pain
81
segmental pathway
b fiber stimulates inhibitory neurons to decrease pain transmission
82
noxious pathways
pain relief when 2 noxious stimuli occur at same time at different locations
83
placebo
expectations
84
occipital lobe
back of the brain responds to flashing lights
85
temporal lobe
on the sides and is most responsible for seizure activity
| for memory retrieval
86
frontal
motor strip: marching
87
partial seizure
only involves one hemisphere of the brain
88
aura
visual cue right before seizure
89
prodroma
days before seizure
90
simple partial seizure
most aura occur
no loss of consciousness, usually memory
JACKSONIAN MARCH
91
complex partial seizure
LOC, not much memory
92
secondary generalized seizure
partial seizure that has spread to both sides of the brain
| TONIC CLONIC
93
generalized seizure
both hemispheres
| LOC bilateral movement
94
types of generalized seizure
atonic
myoclonic
absense
tonic clonic
95
atonic seizure
loss of muscle tone (drop seizure)
96
absense seizure
blank stare and lip smacking
97
myoclonic seizure
jerking, short lasting
98
tonic clonic
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
idiopathic unprovoked seizures
genetic? treat with anti epileptic medications
100
provoked seizure
metabolic disorder, infection, tumour: treat with underlying cause
101
sequence of tonic clonic
```
depolarization
tonic contraction
LOC
clonic
incontinence
cyanosis
hyperpolarization
seizure over
post ictial phase
```
102
repeated seizure without break or several seizures back to back
status epilepticus
103
classification of brain injury
primary and secondary
104
primary brain injury
initial injury and displacement of the brain
105
secondary brain injury
consequence from initial insult
106
types of primary brain injury
focal
diffuse
contusion
concussion
107
focal primary brain injury
close: one are (coup vs counter coup)
open: penetration
108
diffuse brain injury
widespread: shearing force causing axon damage causes swelling and bruising
increases ICP, decrease O2, ischemia hypoxia and necrosis
109
contusion
no Brian movement
| bruising or leaking
110
concussion
impact, movement of brain
111
result of secondary brain injury
hemorrhage, increase ICP, death
112
complications of brain injury
post concussion syndrome
post trauma seizure disorder
CTE (chronic traumatic encephalopathy)
113
what is post concussion syndrome
weeks or moths after incident
| anxious, dizzy anorexia, overstimulation
114
why would someone be overstimulated with post concussion syndrome
damage to the RAS
| this system controls and filters nonsense, without this you get overstimulated
115
what is post trauma seizures
can be after brain injury or occur years after. you are hyper excitable, administer anti-seizure medications
116
what is CTE
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
cerebral death
brain stem and cerebellum still functioning, you are maintaining homeostasis but unresponsive- vegetative state
118
brain death
no brain stem function, no homeostasis irreversible
119
what is coup countercoup
the action of you brain hitting the back and front of your skull
120
what would happen if you had a blow to the back of your head (coup or countercoup)
brain would hit the front of your skull, coup
121
alterations in cerebral hemodynamics (blood flow)
increase ICP
cerebral edema
hydrocephalus
122
increase ICP etiology
hemorrhage, tumor, CSF
123
Monroe kelle theory
displacement of either hemorrhage tumor or CSF causes shift of other two
124
stages of ICP
asymptomatic
increase pressure (compromises o2)
hypoxia to brain tissues (hypercapnia)
herniation and damage to tissue
125
etiology of cerebral edema
tumor, meningitis, cancer
126
types of cerebral edema
vasogenic edema
cytotoxic metabolic edema
interstitial edema
127
what is vasogenic edema
a type of cerebral edema found in brain injury
| at the site of the injury increasing permeability which leads to ischemia
128
what is cytotoxic edema
a type of cerebral edema found in brain injury
| toxic factors in grey matter make you lose K and gain water and sodium
129
what is interstitial edema
a type of cerebral edema found in brain injury
| CSF moves into ventricles
130
what is hydrocephalus
type of alteration that is increase CSF causing accumulation
131
etiology of hydrocephalus
blockage or increase fluid
132
cells in wound healing
fibroblasts
133
inflammation of skin cells that are red painful warm and edeamic
cellulitis
134
hard necrotic tissue
eschar
135
incision breaks
dehiscent
136
organs out of wound
evisceration
137
whiteness, wrinkled, soft skin due to exposure to fluid
masceration
138
soft necrotic tissue
slough
139
scar extending beyond wound
keloid
140
abnormal tightening of skin
contracture
141
scar on boundary
hypertrophy scar
142
scar tissue binding to tissues and other organs
adhesion
143
how to assess for circulation when wound healing
albumin
hemoglobin
bood glucose
144
bad circulation
albumin less than 30
hemoglobin less than 100
blood glucose more than 7
145
phases of wound healing
inflammation (hemostasis)
proliferation (new tissue being build)
remodelling (compensatory hyperplasia scar tissue)
146
local acute inflammation
cell changes and vascular changes
147
cell changes of local acute inflammation
```
WBC
granulocytes
- neutrophils
- basophils
- eosinophils
- mast cells
non-granulocytes
- lymphocytes
- monocytes
```
148
neutrophils
1st responder
149
basophils
mast cells
150
eosinophils
parasites
151
mast cells
release histamine
152
monocytes
turn into macrophages then giant cells in presence of foreign body
153
vascular changes of local acute inflammation
injury to tissue, then transient vasoconstriction to vasodilation
- erythmea
- increase permeability
154
pain mediatory
prostaglandins and bradykinin (nociceptor)
155
warmth/redness mediator
prostaglandin, histamine, nitric oxide (vasodilation)
156
swelling mediator
histamine and leukotrienes (increase permeability)
157
systemic acute inflammation
WBC response and acute phase response
158
WBC response of acute systemic inflammation
macrophages phagocytize because opsonization
159
acute phase response of systemic inflammation
blood work changes!!!!
| increase ESR, CRP, Shift to the left increase WBC
160
What is ESR
erythrocyte sedimentation rate- protein attached to RBC and how fast it falls
161
CRP
increases where the inflammation is- type of protein
162
shift to the left
immature neutrophils and a lot of them accumulate and cause shift to the left
163
systemic acute inflammation causes
increase permeability, vasodilation, clotting (firbolysis)
164
response to systemic acute inflammation
fever, malaise, heal OR abscess OR chronic inflammation
165
how long does acute have to last to turn into chronic
2 weeks or more
166
what happens to monocytes in chronic inflammation
turn into macrophages, then giant cells which surround and encapsulate foreign bodies
167
what is nonspecific chronic inflammation
accumulation of nongranulocytes and proliferation of fibroblasts causing scary tissue. granulation formation from lots of macrophages and foreign bodies are surrounded.
168
vascular response to inflamamtion
vasodilation and permeability mediated by plasma proteins
169
plasma protein systems
clot complete, kinin
170
components of inflammation
cell receptor
cytokines: regulate response of inflammation
erythrocytes: platelets or WBC
171
mediators
leukotrienes (similar to histamine) prostaglandins (pain), platelet activating factor (like histamine)
172
what are platelets activated by
tissue destruction and inflammation- they interact with coagulation factors to stop bleeding
173
what do WBC do when they arrive at site of injury
adhere, engulf, phagosome, lysosome, destruct
174
phases of wound healing
hemostasis, proliferation, remodelling
175
referred pain is possible because it is carried on
same spinal segment
176
normal Na
135-145
177
normal K
3.5-5
178
normal glucose
3.5-7.8
179
normal platelets
150-4000
180
normal HgB
120-160 f
| 140-180 m
181
what happens in stress-age-syndrome
```
increase catecholamines and cortisol
decrease thyroxine and testosterone
immunodepressed
hypercoagulation
free radical damage
```
