Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SUM'20 - Anatomy & Physiology > Week 1 - Neuroanatomy 3 of 4 (exam 1) > Flashcards

Week 1 - Neuroanatomy 3 of 4 (exam 1) Flashcards

1
Q

Fentanyl, alfentanil, and sufentanil are lipophilic opioids that can be placed neuraxial, what does this mean in relation to diffusion?

A

readily diffuse through lipid membrane.

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

Intrathecal (spinal) placement of lipophilic opioids: Tell me the rate of diffusion out of the CSF? The rate of onset and duration for analgesia? When does depression of ventilation take place?

A

Rapid diffusion out of CSF Rapid onset and short duration of analgesia Early depression (within 2 hrs) of ventilation due to significant uptake by systemic circulation Due to rapid diffusion out of CSF, little left in CSF for rostral spread, therefore, late depression of ventilation does NOT occur

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

True or False, Epidural placement of lipophilic opiods is NOT similar to Spinal placement of lipophilic opioids?

A

False! Epidural placement is similar to Spinal (Intrathecal) placement. Thus Rapid onset and short duration of analgesia and early depression of ventilation NOT late.

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

Tell me all the side effects of opioids that you know?

A

Pruritus

Nausea

constipation

Urinary retention

Addiction

Respiratory depression

Sedation

CNS excitation

Viral reactivation

Sustained erection

Thermoregulatory dysfunction

Sexual dysfunction

Ocular dysfunction ‘PPP’

Neonatal morbidity

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

Why do opioids cause pruritus?

A

due to histamine release

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

Tell me why opioids can cause urinary retention?

A

inhibit sacral (parasympathetic) nerve

Bladder relaxation leads to retention

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

If a patient has respiratory depression from opioid use, what will you do next? (three answers)

A

Monitor pulse ox Give supp. 02 Prophylactic Naloxone

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

Spinal analgesia, what is the dominant receptor? (what receptor is responsible for giving you the desired pain relief)

A

Mu-2 is the dominant receptor (even though it is mediated by all receptors technically.)

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

What has to be suppressed in order for spinal analgesia to take place?

A

Transmission of pain through Substantia Gelatinosa (L II) has to be suppressed.

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

To be considered spinal analgesia the opioid has to act on what structures after IV administration?

A

opioid acts on periventricular and periaquaductal gray, locus ceruleus, raphe magnus − spinal analgesia (don’t call this supraspinal analgesia)

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

What structures must opioids act on in order to be considered Supraspinal Analgesia?

A

Opioids act on limbic system, hypothalamus and thalamus.

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

What is the dominant receptor for supraspinal analgesia?

A

Mu-1 is the dominant receptor. (also mediated by kappa and delta but Mu-1 is dominant)

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

True or False, opioids produce both spinal and supraspinal analgesia?

A

True!

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

After IV administration of opioids a patient may say?

A

“I feel pain but I do not care”

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

Which opioid receptor only produces spinal analgesia ( 3 receptors have spinal and supraspinal but one receptor has only spinal analgesia)

A

Mu-2 can only cause spinal analgesia, does not cause supraspinal analgesia.

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

Which opioid receptor is responsible for Respiratory depression and Addiction?

A

Mu-2 (delta is resp. depression and physical dependence)

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

Which opioid receptor is responsible for marked constipation and which one has minimal constipation?

A

marked constipation = mu-2 minimal constipation = delta

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

Which opioid receptor is resp. for euphoria and which causes dysphoria?

A

euphoria = mu-1 dysphoria = kappa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which two opioid receptors have low abuse potential? (two answers)

A

mu-1 and kappa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tell me all the “responses” caused by the different opioid receptors being stimulated, That you know (chart is the answer, see how many you know!)

A

ppt 122

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

Name some opioid agonists?

A

Morphine, fentanyl (sublimaze), codeine, heroin, methadone, meperidine (demerol), dextromehtophan, hydormorphone (Dilaudid) Sufentanil (sufenta), Remifnetanil ( Ultiva)

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

Mechanism of action of opioids?

A

Act on opioid receptors (u=morphine, d= enkephalin, k = dynorphin) Modulate (decrease intensity) synaptic transmission by opening K+ channels and closing Ca++ channels leading to decrease synaptic transmission and decreasing release of neurotransmitters (Ach, NE, glutamate, substance P)

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

clinical uses of opioids?

A

Pain , cough suppression (dexomethorphan), diarrhea ( loperamide, diphenoxylate), acute pulmonary edema, maintenance program for addicts (methadone)

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

toxicity to opioids can cause?

A

Addiction, respiratory depression, constipation, pinpoint pupil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name some opioid antagonist?

A

Naloxone (Narcan), Naltrexone ( Trexate), Nalmefene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What kind of antagonists of the opioid receptor are the below? Naloxone (Narcan), Naltrexone ( Trexate), Nalmefene

A

competitive antagonist (does not activate the receptor, therefore naloxone reverses the effects of opioid agonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Side effects of opioid antagonists?

A

(increased sympathetic activity) Reversal of analgesia Excitement / Dysphoria Tachycardia Hypertension Dysrhythmias – V fib Pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Nalorphine (Nalline) ,Dezocine(Dalgan), Buprenorphine ( Buprenex), Nulbuphine (nubain) , Butorphanol (Stadol), Pentazocine (Talwin) The above drugs are what kind of drugs?

A

mixed agonist/antagonist (stimulate one opioid receptor but block another (they block Mu))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

mixed agonist/antagonist for opioids block which receptor?

A

they block Mu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

mixed agonist/antagonist for opioids are unlikely to have what negative effect that you can see in opioids?

A

severe resp. depression is unlikely because no Mu effect!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

opioid mixed agonist/antagonist mediate their effects through what receptors?

A

kappa and delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Can opioid agonist/antagonist reverse opioid induced respiratory depression?

A

yes, due to agonistic action on mu receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Site of action of various pain killers: LA? (3 answers)

A

Nerve endings

primary afferent nerve

dorsal root ganglion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Site of action of various pain killers: NSAIDS?

A

Nerve endings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Site of action of various pain killers: a2 agonists?

A

dorsal root ganglion descending noradrenergic and serotoninergic inhibitory fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Site of action of various pain killers: opioids?

A

dorsal horn

descending noradrenergic and serotoninergic inhibitory fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Site of action of various pain killers: ketamine and gabapentinoids?

A

dorsal horn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Site of action of various pain killers: TCAs, SSRIs

A

descending noradrenergic and serotoninergic inhibitory fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where are the sites of action of various pain killers? (picture in the answer to label)

A

ppt 126

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the risks associated with Posterior Fossa Surgery?

A

Risk of obstructive hydrocephalus, brain stem injury pneumocephalus, venous air embolism , air is entrained into the circulation -Paradoxical air embolism through existing ‘hole’ in heart (PFO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

During Posterior Fossa Surgery you will monitor for air bubble with? (3 answers)

A

Esophageal Echocardiography (most sensitive), droppler, end-tidal CO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Treatment for air bubbles during Posterior Fossa Surgery?

A

Notify the surgeon , so that surgical field can be flooded with N/S. Packing and bone wax, JV compression Discontinue nitrous oxide, give 100% O2 Aspiration with multi- orificed catheter placing tip 2 cm below the SVC – atrial (cavoatrial) junction. Aspiration with single- orificed catheter placing tip 3 cm above the SVC – atrial junction Left lateral position, 15 degrees head down IV fluid to increase CVP Vasopressor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Where is the Cavoatrial Junction? (picture for answer)

A

slide 128

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How would you describe the position for seated posterior fossa surgery?

A

knees at the level of the heart and neck not hyperflexed. (slide 130)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What causes a venous air embolism?

A

Due to negative pressure in open veins and dural sinuses (-10 mmHg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Pathophys of venous air embolism? (what are some causes)

A

Ischemic injury Reflex vasoconstriction Release of inflammatory substances Pulmonary HTN increased PCO2 Arrhythmia Circulatory collapse Paradoxical AE through hole in heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What kind of things would use or do to monitor a venous air embolism?

A

Doppler – most sensitive non-invasive PA catheter ETCO2 ETN2 Transesphageal echo (TEE) – most sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How would you prevent a venous air embolism?

A

Proper positioning Use of bone wax Avoid N2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Treatment of a Venous air embolism intraoperatively?

A

Notify surgeon immediately D/C N2O, increase O2 flow Modify the anesthetic Flood surgical field with NS Jugular vein compression Aspirate right atrial cath CV support Change the position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

post op goals with a venous air embolism? (what can you do post op to help)

A

Supplemental O2 Cx, EKG, ABG Hyperbaric O2 compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What occurs in relation to calcium levels and Trauma?

A

with trauma you will have an influx of calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Will a trauma patients ICP and CPP increase or decrease?

A

Increased ICP Decreased CPP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

If a trauma patient has cerebral edema what are your two goals?

A

Osmotic diuresis by mannitol Prevent secondary ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Treatment for Trauma patients can include? (four answers)

A

Lower ICP, Reduce vasospasm, Maintain blood flow, Clot extraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Craniocerebral injuries can happen in a number of ways, can you name a few? (will also have a picture)

A

Cranium distorted by forceps (birth injury). Gunshot wound of the brain. Falls (also traffic accidents). Blows on the chin (“punch-drunk”). Injury to skull and brain by falling objects. (slide 135)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Total volume of CSF = ?

A

150ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Specific gravity and pH of CSF?

A

SG 1.002-1.009 pH 7.32

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pressure of CSF?

A

5-15 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What two structures are responsible for the formation of CSF? How much is made in a day?

A

Formation of CSF by the choroid plexus epithelium and ependymal cells = 500 ml/day @ 30 ml/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Of the substances below tell me which freely cross the BBB and equilibrate btwn blood and CSF? (3 answers) -CO2 -O2 -NaCl -H20 -Polyethlyne -ions

A

lipid soluble substances such as CO2, O2, H2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How do other substances that are not freely diffusable end up in the CSF?

A

Other substances are transported by carriers in the choroid plexus epithelium. They may be secreted from blood into CSF or absorbed from the CSF into blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What two molecular structures are excluded from CSF because of their large size?

A

Protein and cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

True or False CSF does NOT function as a cushion to protect the brain, it only acts as a lubricant?

A

False Provides ‘cushion’ to brain-protection against trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

True or False CSF is absorbed through the lymphatic system.

A

False Absorb through Arachinoidal villi (Brain and spinal cord have no lymphatic system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How would you sample CSF?

A

With a Lumbar puncture at L3-L4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What kind of issues would cause CSF pressure to increase? (3 answers)

A

brain tumor, hemorrhage or infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is papilledema?

A

Chronic Intracranial hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

For a local anesthetic to result in spinal anesthesia or subarachnoid block what must occur?

A

the LA injected into the subarachnoid space must mix with CSF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Vasodilation can occur with sensory block, motor block, and sympathetic block, this is an undesirable side effect, how would you avoid this?

A

give fluids and vasoconstrictor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

CSF vs. Blood Know what substances in CSF and blood are equal, what substances are greater in CSF compared to blood and what substances are lower in CSF compared to blood. (graph/picture for answer)

A

slide 138

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What spaces in the brain contain CSF? (picture for answer, just be able to point it out in case its on the test I guess?)

A

slide 141 - easy to identify, all the water/blue looking areas. also shows the flow path.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the volume of the cranial vault? (CSF is 150ml)

A

1600ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

500ml of CSF is formed each day mainly by what sturcture?

A

choroid plexus in lateral ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What does the brain float in?

A

CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Be able to loosely label the ventricular system. (diagram for answer)

A

slide 142

76
Q

Tell me the pathway of flow for CSF? (board question) (written out and also has a picture)

A

Choroid Plexus–> Lateral Ventriclue –> Foramina of Monro –> Third Ventricle –> Aqueduct of Sylvius –> Fourth Ventricle –>then it can go in two direction either to the Foramina Lushka or the Foramina Magendie which both lead to the Subarachnoid space of the Spinal cord –> brain –> Arachnoid Villi (will also add a diagram/picture)

77
Q

Dumb acronym I made up to remember pathway of CSF. “Can Lisa fix the aqueduct for for for some boy already?” (my acronym has a speech problem)

A

Choroid Plexus–> Lateral Ventriclue –> Foramina of Monro –> Third Ventricle –> Aqueduct of Sylvius –> Fourth Ventricle –>then it can go in two direction either to the Foramina Lushka or the Foramina Magendie which both lead to the Subarachnoid space of the Spinal cord –> brain –> Arachnoid Villi

78
Q

Another picture for the pathway of cerebraospinal fluid flow of a hydrocephalus head where the subarachnoid space is narrowed.

A

slide 145

79
Q

What two types of hydrocephalus is there?

A

Communicating – dysfunction of CSF absorption Non-communicating – obstruction of ventricular system

80
Q

What is hydrocephalus, what does it cause?

A

Increased CSF leading to increased ventricle size

81
Q

what type of hydrocephalus is a dysfunction of CSF absorption?

A

Communicating

82
Q

What type of hydrocephalus is an obstruction of the ventricular system?

A

non-communicating

83
Q

What are some causes of hydrocephalus?

A

Intraventricular hemorrhage Infection Congenital malformation Brain tumor

84
Q

How does hydrocephalus present?

A

Irritability Increased head circumference Lethargy Vomiting Sun downing (can’t look up)

85
Q

How do you diagnose or what do you use to diagnose hydrocephalus? (three answers)

A

CT MRI U/S

86
Q

What therapy is available for hydrocephalus? (two answers)

A

Spinal tap and shunting

87
Q

Know what a hydrocephalus baby looks like. (picture as answer in case he makes us pick one out?)

A

slide 146

88
Q

Tell me where a ventriculoperitoneal shunt is used for? Where would it be placed? How does it work?

A

used for accumulation of CSF in brain, such as is the case with hydrocephalus. Tube is inserted into lateral ventricle through hole in skull. Drainage tube, usually introduced into peritoneal cavity, with extra length to allow for growth of child. (slide 147)

89
Q

What percentage of the brains oxygen requirements is for neuronal electrical activity and what percentage is for cellular integrity?

A

60% neuronal electrical activity 40% cellular integrity (slide 148)

90
Q

What percentage of the total body oxygen does a normal brain require to produce ATP that is needed?

A

20% of total body oxygen is required in the brain to produce ATP.

91
Q

What does CMRO2 stand for?

A

Cerebral Metabolic Rate Oxygen consumption

92
Q

Brain consumes what percentage of total body 02?

A

20%

93
Q

If the brain consumes 20% of total body 02, that would come out to how much 02 in ml/min (the 02 is in the blood) and ml/g brain tissue?

A

50 ml/min (3.5 ml/100 g brain tissue)

94
Q

Due to increased consumption and decreased reserves, interruption of cerebral perfusion results unconsciousness within how long?

A

within 10 sec.

95
Q

What is the primary source of energy to the brain?

A

glucose!

96
Q

If the brain can not extract glucose (such as during starvation) what is an alternative source of energy the brain can use?

A

ketones

97
Q

True or False Glucose supply to the brain is not insulin dependent?

A

True!

98
Q

For how long can the brain handle an interruption in glucose supply (energy)?

A

3-8 min which will then lead to irreversible brain damage.

99
Q

what is the process for what occurs when the brain goes without glucose (energy)?

A

No ATP leads to pump failures leading to decreased intracellular potassium, increasing intracellular sodium and calcium. Release of glutamate that further increases Ca++ leading to release of toxic substances e.g. prostaglandins and leukotrienes leading to vasodilation

100
Q

What medication blocks the effects of glutamate on the NMDA receptors?

A

Ketamine

101
Q

True or False Hypoglycemia is as fatal as hypoxia?

A

TRUE!

102
Q

We know that hypoglycemia is dangerous, but is hyperglycemia dangerous?

A

hyperglycemia can lead to cerebral acidosis which can cause hypoxic brain injury.

103
Q

If a patient has hypothermia, a 1 degree C decrease in temp would equal a what percentage decrease in CBRO2?

A

6% a decrease of 1 degree C = a decrease of 6% CBRO2

104
Q

What is the most effective method for protecting brain during focal (incomplete) or global (complete) ischemia?

A

Hypothermia

105
Q

An interruption in cerebral blood flow for 5-10 sec. can cause what?

A

unconsciousness, circulatory arrest.

106
Q

Average CBF?

A

50 ml/100 g/min (~ 750-900 ml/min)

107
Q

a decrease in cerebral blood flow (CBF) can lead to?

A

irreversible hypoxic injury

108
Q

Factors affecting CBF?

A

PCO2 -major regulator

H+

PO2

Sympathetic or parasympathetic play little or no role

109
Q

What substance (measurment) is the major regulator of CBF?

A

PCO2

110
Q

True or False Sympathetic or parasympathetic play a large role in CBF?

A

False, they play little or no role in CBF.

111
Q

What is the formula below? CO2 + H20–> H2CO3 –> H+ + HCO3

A

turning carbon dioxide and water into carbonic acid which can then yield hydrogen ions and bicarb.

112
Q

What ions cause vasodilation of cerebral blood vessels?

A

hydrogen ions (H+)

113
Q

would increased or decreased blood flow “wash away” CO2 and other acids?

A

increased blood flow will wash away CO2 and other acids.

114
Q

Does hypoxia cause or stop vasodilation?

A

hypoxia causes vasodilation which leads to an increase in CBF.

115
Q

If your P02 is below 20mmHg what will occur?

A

diminished neuronal activity or COMA!

116
Q

What would your PO2 level have to be in order to cause COMA?

A

BELOW 20mmHg

117
Q

What three mechanisms are responsible for regulation of CBF? (red in the power point, maybe important)

A

Cerebral Perfusion Pressure (CPP)

Autoregulation

Extrinsic Mechanism

118
Q

What would be examples of extrinsic mechanisms that regulate CBF?

A

Respiratory gas tension

Temperature

Viscosity

Autonomic influence

119
Q

Cerebral Perfusion Pressure (CPP) is regulated by two forces, what are they?

A

Mean arterial pressure – pushing the blood into the brain Intracranial pressure – keeps the blood out

120
Q

CPP = ?

A

CPP = MAP - ICP (or CVP, whichever is greater)

121
Q

What is the normal value for CPP?

A

100 mmHg

122
Q

what will an increase in ICP do to the CPP and CBF?

A

increased ICP will decrease CPP and CBF

123
Q

What occurs if the CPP is below 25mmHg?

A

irreversible brain damage, flat EEG

124
Q

What will you monitor closely in head injury patients, you want to make sure it does not increase?

A

Watch for increase in ICP in head injury there is increase ICP which will effect perfusion pressure. Even drain CSF to lower down ICP. (How Mo worded it)

125
Q

MAP =?

A

MAP= Diastolic + 1/3 Pulse pressure

126
Q

CBF remains constant between MAPs of ??

A

MAP of 60-160 mmHg

127
Q

Increased arterial pressure can cause what in relation to the brain?

A

rupture of cerebral vessels which disrupts BBB leading to brain edema and cerebral hemorrhage.

128
Q

What is one condition to the brain that disrupts autoregulation?

A

ischemia

129
Q

Cerebral vasculature rapidly adapt to changes in CPP: Thus if CPP increases what occurs to the vasculature and if CPP decreases what occurs to the vasculature?

A

increased CPP leads to vasodilation decreased CPP leads to vasoconstriction

130
Q

What tissue metabolites are responsible for vasodilation?

A

nitric oxide, adenosine, PGs

131
Q

if the MAP is below 60 mmHg what is likely to occur?

A

cerebral ischemia

132
Q

If the MAP is above 160 mmHg what is likely to occur?

A

disrupt BBB, cerebral edema and hemorrhage can occur

133
Q

Vasopressor will increase CBF only when MAP is?

A

below 60 or above 160 mmHg (apparently according to the PPT)

134
Q

Respiratory gas tension is part of the Extrinsic Mechanisms for regulation of CBF: What mechanisms fall under Respiratory gas tension?

A

PCO2– the most important factor Cerebrum > cerebellum > spinal cord CO2 crosses BBB ,therefore acute change in PCO2 affect CBF CBF is directly proportional to PCO2 between 20-80 mmHg 2% increase for each mmHg PCO2 PO2 – Severe hypoxia increases CBF

135
Q

Does severe hypoxia increase or decrease CBF?

A

increases CBF

136
Q

What is the most important factor to regulate CBF under the umbrella of extrinsic mechanisms?

A

PCO2

137
Q

CBF is directly proportional to PCO2 between ?-?mmHg

A

20-80mmHg

138
Q

How does temperature affect CBF? Will CBF increase or decrease with hypothermia and hyperthermia?

A

hypothermia will decrease CBF Hyperthermia will increase CBF 5%-7% increase per 1 degree C

139
Q

if your Hct decreases then your viscosity will decrease, so what will happen to your CBF?

A

Increased CBF (the reverse is true of polycythemia)

140
Q

Autonomic Influences that regulate CBF

A

Sympathetic parasympathetic vasospasm following brain injury and stroke

141
Q

Sympathetic and parasympathetic autonomic influence to regulate CBF: which one vasoconstricts and which one vasodilates?

A

sympathetic - vasoconstriction parasympathetic-vasodilation

142
Q

A normal cerebral autoregulation curve looks like what?

A

Cerebral blood flow at 50ml/100g/min will be steady between 60 and 160 mmHg. (slide 157)

143
Q

Myogenic cerebral autoregulation: as blood pressure increases from 60mmHg to about 160mmHg the CBF stays constant but what happens to the diameter of the artery?

A

as blood pressure increases the artery diameter would decrease. (Slide 158)

144
Q

Cerebral autoregulation in a patient with chronic hypertension: what changes about the CBF?

A

In patient with chronic HTN, the curve is shifted to right. In these patient decreasing the BP leads to decreased cerebral perfusion (slide 160)

145
Q

What can cause a autoregulatory failure in relation to CBF?

A

Hypoperfusion and ischemia hyperperfusion and circulatory breakthrough reperfusion injury cerebral steal Therapies that enhance perfusion

146
Q

What would be some examples of therapy for enhanced perfusion. (3 answers)

A

Maintain high perfusion pressure Hypocapnia Barbaturates (according to ppt, may reword after lecture)

147
Q

Breaking of BBB Swelling Rupture of blood vessels Hemorrhage The above are all examples of what?

A

Hyperperfusion and circulatory breakthrough examples in relation to autoregulatory failure.

148
Q

What volatile anesthetics increase CBF?

A

halothane, isoflurane, enflurane (What Mo has listed, but I think all have a dose dependent increase)

149
Q

What volatile anesthetic is containdicated in head injury because it dilates cerebral vessels up to 200%?

A

Halothane

150
Q

What do you want to maintain the PCO2 at or around in order to not change CBF?

A

maintain PCO2 25-30mm Hg

151
Q

True or False Hyperventilation (hypocapnia) can blunt the effects of increased CBF and ICP?

A

True! Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP

152
Q

Tell me all the agents which decrease CBF?

A

I/ V anesthetics (thiopental) propofol, benzodiazepines and etomidate. Decreased CMR

153
Q

How does Thiopental decrease CBF and ICP?

A

Thiopental decreases CBF (and ICP) by vasoconstriction, increasing CSF absorption , suppressing free radical formation. Thiopental does NOT affect CO2 reactivity at clinical doses.

154
Q

What is the only IV anesthetic that dilates cerebral vessels and increases CBF and ICP? (board question)

A

KETAMINE C/I in patients with head injuries!

155
Q

Does Nitrous oxide increase or decrease CBF?

A

Increases CBF

156
Q

What is ICP actually?

A

It is CSF pressure in lateral ventricle or cerebral cortex.

157
Q

Normal ICP?

A

5 to 15 mmHg

158
Q

Increased ICP results from decreased ??

A

CPP CPP = MAP - ICP

159
Q

What is the fixed volume of the skull?

A

1500-1600ml

160
Q

Minor variations in volume of its contents i.e. brain (80%), blood (12%) or CSF (8%), will affect ??

A

ICP

161
Q

Increased ICP can compress veins, and hence, can increase capillary hydrostatic pressure, causing brain to swell, what will then follow as a natural progression if nothing is done?

A

Brain herniation leading to death

162
Q

True or False Normally, increases in volume are initially well-compensated?

A

True

163
Q

True or False A point is reached where slight increase in volume decrease ICP?

A

False it will increase ICP NOT decrease ICP.

164
Q

Once ICP increases to a point in order to decrease CPP what may occur?

A

focal ischemia occurs

165
Q

The skull has a fixed volume of 1500-1600ml, if the volume goes above this then what can happen?

A

global ischemia occurs

166
Q

What is the most common cause of death after head injury?

A

Elevated ICP

167
Q

In the image, at what point do the S/S of increased ICP appear? (slide 167)

A

at point 3

168
Q

What is Cushing’s triad? What is it caused by?

A

Cushing’s triad is a clinical triad variably defined as having: Irregular, decreased respirations (caused by impaired brainstem function) Bradycardia. Systolic hypertension (widening pulse pressure) caused by slight elevation in ICP.

169
Q

What do space occupying lesions do to the adjacent brain tissue?

A

puts pressure on the adjacent brain tissue causing damage.

170
Q

Tell me the intracranial pressure cycle that Trauma, Tumors, and infection can cause?

A

image from ppt slide 168 to go here

171
Q

What is papilledema?

A

Search Results Featured snippet from the web Papilledema is a serious medical condition where the optic nerve at the back of the eye becomes swollen. Symptoms can include visual disturbances, headaches, and nausea. Papilledema occurs when there is a buildup of pressure in or around the brain, which causes the optic nerve to swell.

172
Q

Be able to identify a normal optic nerve compared to an optic nerve with edema (picture as answer)

A

slide 169

173
Q

If any type of herniation occurs that produces brainstem compression what will then occur?

A

coma and ultimately death will result.

174
Q

What issue caused by increased ICP is the opposite of shock?

A

Cushing Triad

175
Q

What ICP value is considered intracranial hypertension?

A

ICP of more than 15 mmHg

176
Q

What can cause Intracranial hypertension?

A

Due to mass lesion, hematoma , head trauma.

177
Q

with intracranial hypertension you are in danger of what occuring? (think herniation)

A

Danger of herniation through tentorial notch , foramen magnum.

178
Q

Acute intracranial hypertension will result in the following S/S (issues).

A

Irregular respiration Bradycardia Hypertension Ipsilateral (same side of mass) III cranial nerve compression leading to ipsilateral fixed, dilated pupil Cushing’s Triad Irregular respiration, bradycardia, hypertension (increased systolic)

179
Q

Chronic intracranial hypertension will cause what? (think eyes)

A

Papilledema

180
Q

Intracranial hypertension treatments?

A

ABCs Intubation plus hyperventilation Maintain PCO2 level of 25 mmHg Mannitol Norcotics for sedation Steroids

181
Q

What can occur to the ICP when ventilation is slowed?

A

Monitor ICP as ventilation slowed. ICP may rise again when ventilation slows down.

182
Q

True or False If a patient has intracranial hypertension you will try to wean them from the ventilator as quick as possible?

A

False, slowly wean from ventilator.

183
Q

hyperventilation causes hypocapnia which causes what?

A

vasoconstriction

184
Q

What are the different ways you can monitor ICP? (picture on next page)

A

slide 173

185
Q

When is ICP monitoring indicated? (6 examples given)

A

Trauma Subarachnoid hemorrhage Glasgow coma score < 7 Hydocephalus Pseudo tumor cerebri AV malformation

186
Q

If a patient has increased ICP, what can you do to REDUCE ICP? (10 answers given)

A

Fluid restriction Corticosteroid Hyperventilation Thiopental for induction Avoid Ketamine Head-up position Diuretics CSF drainage Avoid PEEP Hypothermia

SUM'20 - Anatomy & Physiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions