Translational Physiology Block 2 Flashcards Preview

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Flashcards in Translational Physiology Block 2 Deck (110):
1

What is a dysraphism?

Incomplete closure of the neural tube

2

When do the anterior and posterior pores in the neural tube close in humans?

Closure of the neural tube in humans normally occurs between 26 and 28 days of gestation.

3

What is the most serious dyraphism? Describe it.

anancephaly: the cerebral hemispheres are absent and the rest of the brain is severely malformed. Overlying malformations of the skull, brain coverings, and scalp are present (effects both ectoderm (skin, nervous tissue) and mesoderm (skull))

4

Which dyraphism of the posterior pore does not result in a pathological condition? Approximately where in the spinal cord is this malformation?

Spina bifibida occulta; fifth lumbar or first sacral vertebra

5

What is it term used for when the dura and arachnoid membranes herniate (i.e., protrude) through the vertebral defect? if the spinal cord also herniates?

spina bifida cystica; myelomeningocele

6

What is it term used for when the dura and arachnoid membranes herniate (i.e., protrude) through the cranial defect? if the brain also herniates?

meningocele; cephalocele

7

What protein is elevated in dyraphisms?

alpha fetoprotein

8

What are the known causes of dyraphisms?

folic acid deficiency, maternal heat exposure, and polygenic mutations

9

Describe the steps in axonal degeneration.

Step 1: Synaptic transmission occurring at the axon terminal fails within hours because this complex process is dependent on material provided by axonal transport; Step 2: entire distal segment of axon is destroyed and removed (Wallerian); Step 3: myelin degenerates (Schwann cell may secrete trophic factors that help in recovery); Step 4: macrophages and Schwann cells in the PNS scavenge the debris created by the breakdown of the axon and its myelin; Step 5: After axonal injury, most neuron cell bodies swell and undergo a characteristic rearrangement of organelles called chromatolysis. The nucleus also swells and moves to an eccentric position. The endoplasmic reticulum, normally close to the nucleus, reassembles around the periphery of the cell body. Chromatolysis is reversible if the neuron survives and is able to re-establish its distal process and contact the appropriate target.

10

What is retrograde degeneration? anterograde?

the neuron that synapses on the injured cell undergoes degeneration; neuron that received synaptic contacts from an injured cell degenerates

11

What are general symptoms of neuropathies?

numbness (sensory), weakness (motor), parathesias (tingling or pain)

12

How do neuropathies usually present in patients?

Neuropathies are first presented in the feet (longest axon) and spread upwards and later more proximally

13

What are two signs of motor neuron injury (LMN) and muscle atrophy?

Fasciculations: muscle cells may twitch in unison. These small twitches can be seen under the skin (result of spontaneous action potential in injured motor neurons); Fibrillations: individual muscle fibers may twitch spontaneously (in the absence of motor neuron (LMN); suggestion that Schwann cells may release acetlycholine)

14

Understand different types of hydrocephalus, and the location of blockage which would affect the size of the ventricle(s) and drainage

Communicating hydrocephalus occurs when the flow of CSF is blocked after it exits the ventricles. This form is called communicating because the CSF can still flow between the ventricles, which remain open (problem absorbing CSF into SSS through arachnoid granulations); Damage to the arachnoid villi can occur most commonly from infection or inflammation of the meninges or from the presence of an irritating substance, such as blood in the CSF after a subarachnoid hemorrhage (normal pressure hydrocephalus: LP reveals normal ICPs; enlargement of all four ventricles on MRI, characterized by progressive dementia, urinary incontinence, and gait disturbance); Non-communicating hydrocephalus — also called "obstructive" hydrocephalus — occurs when the flow of CSF is blocked along one or more of the narrow passages connecting the ventricles. One of the most common causes of hydrocephalus is "aqueductal stenosis." In this case, hydrocephalus results from a narrowing of the aqueduct of Sylvius, a small passage between the third and fourth ventricles in the middle of the brain; Hydrocephalus ex-vacuo occurs when stroke or traumatic injury cause damage to the brain. In these cases, brain tissue may actually shrink.

15

How is hydrocephalus treated?

shunting

16

Describe a lumbar puncture.

A hollow needle for sampling of CSF can be safely inserted into the subarachnoid space at the level of the L3-L4 interspace (cord ends at L1). With the patient lying on the side, normal (opening) pressure varies from 100 to 180 mm H 2 O (in this position lumbar CSF pressure corresponds to intracranial pressure); Queckenstedt test: gently compressing the external jugular veins in the neck for 10 seconds (rapidly increases intracranial pressure because it increases the volume of intracranial venous blood. It quickly leads to an increase in lumbar pressure)

17

What can cause increased CSF pressure? What procedure should a physician not do in this case?

CSF pressure can become elevated because of a pathological mass within the cranium, such as a tumor or collection of blood, or because the brain is swollen as a result of injury or infection; i. Attempting a lumbar puncture in these patients is risky, since a small loss of CSF or CSF leak following lumbar puncture can cause brain herniation (pressure gradient that results from low lumbar CSF pressure)

18

Describe cerebral edema.

increase in BECF where extra fluid comes from intravascular compartment; If the cerebral edema is generalized, it can be tolerated until intracerebral pressure exceeds arterial blood pressure, at which point blood flow to the brain stops; Symptoms: headache, vomiting, altered consciousness; Body responds by raising blood pressure, hyperventilating (alkolosis and vasoconstriction); treatment: mannitol (increases blood osmolarity)

19

What can cause increased extracellular glutamate? Why is this a pathologic condition?

ischemia, anoxia, hypoglycemia, or trauma; The action of rising levels of extracellular glutamate causes increased uptake of sodium into neurons causing swelling; excitotoxicty also damages astrocytes (swelling resulting from potassium uptake and water)

20

What is vasogenic edema? What causes it?

Vasogenic edema occurs when there is a leak in the BBB allowing protein to cross drawing water osmotically to increase the volume of BECF and ICF

21

Know types of glial cells and role of myelin in the CNS

oligodendrocytes, astrocytes, and microglia; myelin speeds up conduction by insulation (saltatory)

22

Immunopathogenesis of multiple sclerosis

Cell-mediated immunity: CD4 helper 5 cells release cytokines causing tissue damage; Humoral immunity: B lymphocytes secrete autoantibodies and serve as antigen presenting cells; Immunoregulatory cells: decreased activity of regulator cells

23

Basic pathology of multiple sclerosis

active plaques, multiple areas of demyelination + gliosis + inflammation + initial relative axonal preservation; lymphocyte infiltration: more CD8 cytotoxic T lymphocytes and fewer CD4, beta, and plasma cells

24

Is remylelination a feature of early MS?

Yes

25

Does nerve degeneration and axonal loss happen early in MS? Why is primary stage of the disease have milder symptomology to later stages?

Yes; Resolving inflammation, remyelination of axons, and the relative plasticity of the CNS initially compensate for axonal injury (once these fail (much like Diabetes) disease and disability from it become progressive)

26

What are the major causes of axonal and neuronal loss from MS?

Cortical and meningeal inflammation, Wallerian degeneration, and either ischemia or edema

27

Know basics of clinical and MRI diagnosis of MS

Dissemination in time, space, or both (more than one T2 lesion, new lesion at follow-up); sites of lesions: periventricular, corpus callosum, cerebellum, juxtacortical (GM-WM junction)); other features: black holes (atrophy), flame-shaped, perpendicular to ventricles and parallel to longitudinal axons, larger than 0.5 cm

28

How does a physician treat multiple sclerosis?

prednisone (steroid, anti-inflammatory) is used to MS relapses (does not prevent new attacks); Immunomodulators: BG-12, laquinimod, teriflunomide; Reduction in immune cell proliferation: Alemtuzumab; T cell adhesion and transmigration prevention: Natalizumab; future directions: stem cell therapy and remyelination

29

What are symptoms associated with multiple sclerosis?

sensory and motor deficits, visual loss, ataxia (loss of balance), diplopia, vertigo

30

Why is gadolinium an important diagnostic tool for MS?

Gadolinium enhancement of a MS lesion on MRI represents BBB damage, which enables infiltration of inflammatory cells into the CNS

31

How does the length constant change in patients with MS?

Decrease in length constant via a decrease in membrane resistance (axoplasmic resistance unchanged)

32

A patient complains of blurry vision in their left eye and is diagnosed with optic neurtis? Where is the nerve damage?

Left optic nerve (inflammation); may also cause diplopia (symptoms can be related to MS)

33

What explains the remission/relapse component of MS?

inflammation attacks (resolution of these attacks)

34

How can MS, a demyelinating disease, result in gray matter injury?

Axonal injury leading to chromatolysis

35

Why do MS patients feel relief from their disease burden at cooler temperatures?

Action potential duration is slower at colder temperatures

36

Would K+ voltage gated channel blockers called aminopyridines be useful in treatment of an MS patient?

Yes, because repolarization would be slowed

37

What would be the expected result on an EMG of an MS patient?

Normal peripheral conduction velocity

38

In another inflammatory demyelinating disease, Guillain-Barre Syndrome, the peripheral nervous system is attacked. Would the patients muscle tone and reflexes remain intact?

No; muscle flaccidity and hyporeflexia

39

What would be the expected findings in the CSF of a MS patient? How are remyelinated axons of different from the from the damaged axons?

elevated IgG levels; Nav1.2 channels may replace Nav1.6 channels in demyelinated axons. Conduction is often barely adequate under normal circumstances and may become inadequate under stressful situations, such as illness, emotional stress, and exhaustion.

40

What are risk factors for stroke?

hypertension (other cardiac history), smoking, prior stroke, diabetes, blood-borne diseases (sickle-cell), obesity, alcohol (non-modifiabled: age, race, gender, genetics)

41

Describe major blood flow in the brain.

Anterior circulation: supplies cerebral hemispheres (fed by carotid arteries); posterior circulation: supplies brainstem & occipital lobe (fed by basal artery (anastomose of vertebral arteries)); most arteries are interconnected (anterior and posterior; left and right) by an intact Circle of Willis

42

What are the different type of stroke?

Hemorrhagic (20%)- 60% ICH, 40% SAH; ischemia (80%)- 20% cardiac embolism, 20% large vessel, 25% lacunar (small vessel) (blood flow is blocked)

43

What are common causes of ischemic stroke?

arteriosclerosis plaques, atrial fibrillation, other heart failure

44

What are common cause of hemorrhagic stoke?

hypertension, AVMs, anticoagulants (warfarin) (arteriolar lipohyalinosis results from chronic HTN; more likely to rupture); SAH are caused by ruptured aneurysms

45

What are the most common signs of stroke?

Sudden, Painless, Focal neurological dysfunction; Sudden, severe, uncharacteristic headache (sometimes LOC)

46

T/F: Depressed consciousness and headaches are a sign of infarcts or ischemic events?

False; hemorrhagic

47

Mean arterial pressures above the point of cerebral blood flow autoregulation result in what two pathophysiologies?

edema and hemorrhage (below a certain point, ischemia occurs); hypertensive patients have a curve shifting to the right

48

Who are ideal candidates for iv t-PA treatment? What is t-PA treatment?

Tissue plasminogen activator (breaksdown clots); no hemorrhage apparent and no history of chronic hypertension (may result in reperfusion hemorrhage) with the patient arriving at the hospital within a 4.5 hour time window following ischemic onset

49

Looking at a patient’s chart, you note that he has had a previous occlusion in the most proximal segment of his anterior cerebral artery, which of the following symptoms would you expect he had at the time?

Nothing; Collateral blood flow from the contralateral anterior cerebral artery through the communicating artery

50

Describe the pathophysiology of axonic brain injury

Cessation of cerebral circulation results in depletion of oxygen stores within 20 sec; Cessation of synaptic activity and action potentials (LOC); Within 5 min, brain glucose and ATP stores are depleted (loss of NaK pump; cell depolarization, later causes neurotoxicity); oxidative free radicals, lactic acidosis, and prostaglandins/thrombaxane A2


51

What is the pathophysiology of reperfusion injury?

hyperfusion followed by hypoperfusion; Formation of oxygen free radicals, cytokines, apoptosis; poor blood flow due to viscosity of blood and perivascular edema; inability of pericytes to regulate vessel size (no-reflow phenomenon)

52

Which parts of the brain are selectively vulnerable to hypoxia/ischemia?

most important: thalamus, reticular formation, periaqueductal gray area; CA1 & CA4 regions of hippocampus (memory), amygdala, cerebellar vermis, and caudate nucleus

53

Describe the role of the thalamus and cortex in coma recovery and ways to explore this connectivity

reperfusion injury is followed by dysregulated or aberrant thalomcortical activity (needed to respond to external stimuli; arousal); these could be tested by inducing and recording somatosensory evoked potentials in the ventroposterior lateral nucleus of the thalamus and somatosensory cortex (stimulate a sensory nerve)

54

What are predictors of poor prognosis for patients post cardiac arrest? How do these predictive markers change in patients undergoing hypothermia treatment?

myoclonic status epilepticus, absence of bilateral N20 somatosensory evoked potentials, high expression of neuron-specific enolase in blood (poor predictor), absence of pupillary and corneal reflexes as well as extensor posturing or no movement to noxious stimuli 3 days after the cardiac event; patient must have at least predictors of poor outcome (suggested to conduct a neural exam following 4-5 days)

55

What is Cushing's triad?

increase to increased intracranial pressure; heart rate decreases to increase MAP; respiratory dysfunction (shallow breathing)

56

What is the Monroe-Kellie doctrine?

The Monro-Kellie hypothesis states that the cranial compartment is incompressible, and the volume inside the cranium is a fixed volume. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another (The easiest thing to displace, that which requires the least amount of force, is venous blood followed by CSF and then arterial blood)

57

Describe the intracranial pressure waveform.

P1 (percussion wave): arterial pulsation; P2 (tidal wave): (normally a smaller peak) intracranial compliance; P3 (dicrotic notch): aortic valve closure; if P2 is higher than P1 - it indicates intracranial hypertension.

58

ICPs should be kept below which point?

20 mm Hg

59

What are Lundberg waves?

predictor of poor prognosis; three waveforms (A waves are pathological. There is a rapid rise in ICP up to 50-100 mm Hg followed by a variable period during which the ICP remains elevated followed by a rapid fall to the baseline and when they persist for longer periods)

60

How does breathing effect the autoregulation of cerebral blood flow?

breathing decrease CO2 (increases blood pressure); this results in cerebral vasoconstriction (decreased blood flow)

61

What can cause increased intracranial pressure?

intracranial etiologies: ICH, tumor, pseudotumor, infection, trauma, and hydrocephalus

62

What is the equation for cerebral perfusion pressure? What are normal values for CPP?

CPP = MAP (1/3 systolic + 2/3 diastolic pressure) - ICP; 50-150 mm Hg

63

Which brain region receives the highest normal cerebral blood flow? Does white matter or gray matter receive greater normal blood flow?

neurohypophysis; gray matter

64

A mean arterial pressure of 125 mm Hg or above causes what pathophysiology? below 50 mm Hg?

in both situations, cerebral autoregulation is not intact; for high MAPs, edema will ensue (vessels remain dilated); for low MAPs, ischemia (vessels remain constrict)

65

How does hypertension effect the autoregulation of blood flow?

The of MAPs on the x axis and CBF on y axis is shifted to the right

66

What happens to vessel size with increasing MAPs in situations of autoregulatory failure?

Vasodilation and increase in both cerebral blood flow and intracranial pressure

67

How does a neurointensivist treat a patient with intracranial pressure above 25 mm Hg?

Targets: cerebral perfusion pressure of 60-70, ICPs below 20; position patient with head up 30-45 degree angle, ventilation (mild hyperventilation), mannitol (osmotherapy), sedatives (barbituates), hypothermia, and decompressive craniectomy

68

Why is hypothermia effective treatment for brain injury?

minimizes apoptosis, reduction of oxidative free radicals, decrease disruption of BBB, prevents excitotoxicity

69

Describe the basic pathology and symptoms of Parkinson's disease.

characterized by motor symptoms: rigidity, bradykinesia (slowness in execution of movement), tremor (occur at rest and disappear during activity), and postural instability (shuffling gait); pathologic progression: olfactory system (loss of smell) followed by autonomic system (loss of GI function), limbic system, sensorimotor system; loss of dopaminergic neurons from substantia nigra pars compacta

70

Describe the general features of the basal ganglia and thalamocortical networks

When you take away the dopamine, activity
in the direct pathway (striatal cells to GPi to thalamus) goes down, and motor activity goes down (dopamine excites striatal cells); dopamine normally inhibits the indirect pathway (striatal cells to GPe to subthalamic nucleus to GPi to thalamus); acetylcholine has opposite effect to dopamine

71

Describe the basic biophysics of electrical stimulation in the brain. Are there alternatives?

DBS pulses: 100 Hz, 2-5 V with the hope that they form bidirectional action potentials in the neighboring neurons (surgical target: subthalamic nucleus; complications: avoiding overstimulation or stimulation of the internal capsule nearby; alternative therapy: pallidotomy

72

Define dementia. What are the types of dementia?

acquired loss of cognitive abilities occurring in clear consciousness; Alzheimer's disease, prion disease, chronic traumatic encephalopathy

73

Is dementia acute or progressive?

progressive; intermediate state: mild cognitive impairment

74

How is dementia diagnosed?

One of more of aphasia, agnosia (loss of recognition), apraxia (inability to do skilled movements), executive functions (not related to a single event like urinary tract infection); MRI evidence of black spots (neuronal atrophy); impairment in contrast-sensitivity

75

How is Alzheimer's diagnosed?

PET scanning; beta amyloid plaques (derived from APP cleavage Chr. 21, may present 15 years prior to disease onset, low AB in the blood, first targets association cortex of parietal lobe and prefrontal cortex, extracellular); tau protein neurofibrillary tangle (intracellular component of actin-microtubule complex, prion-like spreading cell to cell, evident in CTE, familial mutations have been discovered, first targets entorhinal cortex of temporal lobe); APOE4: impairment of microglia to clear out beta amyloid plaques

76

What are treatments for Alzheimer's disease?

Acetylcholinesterase inhibitors (loss of acetylcholinergic neurons from basal forebrain results in dementia? seems to be necessary for memory function); NMDA receptor inhibitors (neurotoxicity (too much extracellular glutamate leading to neuronal cell death; sustained activation of NMDA receptors) are suggested causes of Alzheimer’s disease symptoms; Mematine is proposed to return NMDA receptors to normal physiologic ranges where magnesium is capable of blocking ion entry; too much inhibition is not beneficial such as usage of PCP and ketamine)

77

T/F: Some Alzheimer's patients lack beta amyloid plaques?

True

78

Besides multiple sclerosis, what are other known demyelinating diseases?

progressive multifocal leukoencephalopathy: occurs in patients with AIDs, infection of oligodendrocytes with polyomavirus (fatal); central pontine myelinolysis: demyelination following rapid correction of hyponatremia with salt infusion or rapid correction of hypernatremia; Guillan-Barre: patients may recover because it effects the peripheral nerves, which can re-generate

79

What is the importance of the PHOX2B gene?

A transcription factor required for development of visceral control systems (not in preganglionic sympathetic neurons)

80

What is congenital central hypoventilation syndrome (CCHS)? Hirschprung disease? Name of the syndrome for the combined pathophysiologies?

heterozygous mutation in PHOX2B gene characterized by breathing problems during sleep (Deficiency in detection of oxygen and carbon dioxide by chemoreceptors or dysfunction of NTS); enteric nervous system does not develop properly in colon; Haddad syndrome

81

How does a vagus nerve stimulator help epilepsy patients?

vagal afferent input (influences many rostral brain structures); May reduce number of seizures by half (stimulates the nerve daily or can be mechanically stimulated prior to an aura)

82

Describe Horner's syndrome

Combination of unilateral ptosis, miosis (small pupil), and anhidrosis (lack of sweating); syndrome of the sympathetic neurons innervate the smooth muscle that elevates the eyelid, the pupillary dilator, and the sweat glands of the face; First-order Horner syndrome: affects the hypothalamus or the axons traveling down from the brain to the ipsilateral intermediolateral column (other brainstem abnormalities can be co-expressed); Second-order Horner syndrome: disruption of axonal signal from lateral intermediolateral column to the paravertebral column; Third-order Horner syndrome may result from a complication during a carotid artery dissection (damage to the wall of the artery) (affects postganglionic neuron)

83

What are the tests to diagnose Horner's syndrome?

Test 1: administration of cocaine (block NE uptake); in a healthy person, this would cause pupil dilation (not in a patient with Horner’s); Test 2: administration of hydroxyamphetamine (Paredrine) (releases NE from synaptic terminals) (no pupil dilation in a patient with Horner’s)

84

Describe the various color-blind diseases.

result of mutation in visual pigment genes (opsins); i. L or M pigment mutations: X-linked recessive (less common mutation is S pigment on Chr. 7); A single abnormal pigment can lead to either dichromacy (the absence of one functional pigment) or anomalous trichromacy (the absorption spectrum of one pigment shifted relative to normal), often with a consequent inability to distinguish certain colors.

85

What can damage the cochlea?

genetic factors, a variety of drugs (e.g., some antibiotics, including quinine), chronic exposure to excessively loud sounds

86

How can a cochlear implant improve hearing? Who are the best candidates for the device?

electric cochlea (nerve must be intact): cochlear implant exploits the tonotopic arrangement of auditory nerve fibers; Young children and older children or adults whose deafness was acquired after they learned some speech.

87

What is the difference between paresis and paralysis?

paresis: weakness; paralysis: loss of motor function

88

Are reflexes present in patients with lower motor neuron injury?

No

89

What happens when a nerve (innervating a muscle) is transected?

muscles become flaccid (atonia) and eventually develop profound atrophy (loss of muscle mass) because of the absence of trophic influences from the nerves.

90

T/F: Complete transection of the spinal cord leads to profound paralysis above the lesion?

False

91

Complete transection of the spinal cord affecting the both legs is called? both legs, trunk, and arms? only one side is affected? Describe the consequences of such a transection

paraplegia; quadraplegia; hemiplegia; For a few days after an acute injury, there is also areflexia and reduced muscle tone (hypotonia), a condition called spinal shock. The muscles are limp and cannot be controlled by the brain or by the remaining circuits of the spinal cord (days to months); following spinal shock, patient presents with exaggerated muscle tone ( hypertonia ) and heightened stretch reflexes ( hyperreflexia ) with related signs—this combination is called spasticity (loss of brain modulation)

92

Where are the different sources for neural stem cells in the developing and in the adult brain?

developing: SVZ, external germinal layer (cerebellum); adult: SVZ, subgranular zone (hippocampus)

93

What are characteristics of stem cells?

multipotent, ability to self-renew, anti-apoptotic, surrounded by a niche

94

Describe some of the basic methodologies (cultured cells vs. transgenic animal models) used in investigating cancer stem cells.

Transgenic: hyperplasia of EGL in non-neoplastic cells can form tumors, loss of Hedgehog pathway proteins can be a precursor to cancer, p53 and NF1 in GBM; cultured: many groups have shown that culturing patient-derived tumors in neural stem cell conditions form tumors in vivo; potential markers (refuted): CD133, side population (ABC transporter)

95

Define cancer stem cells and describe studies in support and against their role/importance in cancer.

"stem-like" tumor cells (also known as tumor-initiating cells); combined activation of KRas and AKT only forms tumors in CSC cells (not in differentiated populations), aberrant EGFR signaling (down-regulated Ink4a/Arf) can transform cells with either CSC phenotype or differentiated phenotype; resistant to radiation/chemotherapy;

96

Describe the concepts of “dedifferentiation” and “cell of origin”

ability of differentiated cells to acquire the ability to self-renew; exogenous EGF can dedifferentiate non-neoplastic differentiated cells of the brain; cell of origin describes the cell thought to have acquired for the first mutation or mutational program in the development of cancer

97

What embryonal signaling pathways have been shown to play a role in cancer?

EGFR, Notch, Hedgehog (patched & Gli; inhibited by Smo), Wnt

98

What are the two competing models regarding tumor heterogeneity?

stochastic: Cancer cells of many different phenotypes have the potential to proliferate extensively, but any one cell would have a low probability of exhibiting this potential in an assay of clonogenicity or tumorigenicity; cancer stem cell: a subset of cancer cells consistently proliferate extensively in clonogenic assays and can form new tumours on transplantation

99

Describe the four steps (in order) that help clinicians reach the final or pathological diagnosis in a patient with neurologic symptoms, and which one of these steps is the most important.

phenomenology (signs and symptoms; most important), physiologic disturbance, anatomical diagnosis, pathological diagnosis

100

List the main rubrics of the neurological examination.

arousal and orientation, cranial nerves, neurovascular, motor, sensory, stance & gait, reflexes, ANS

101

List the various categories of disease processes that may affect the nervous system

trauma, infection, immune/inflammatory, neoplasm, vascular, metabolic, and degenerative

102

What is an acute focal lesion of the CNS? subacute? chronic?

stroke from either an infarct or hemorrhage; seizure; migraine; infection or inflammation; mass

103

What is an acute diffuse lesion of the CNS? subacute? chronic?

cardiac event or seizure; meningitis or metabolic disorder; degenerative syndrome

104

A stroke is a decrease in brain function due to what?

disturbance in arterial blood flow to the brain

105

Do subarachnoid hemorrhages present with focal symptoms?

No

106

T/F: If a patient presenting with a stroke does not experience loss of consciousness, the stroke is most likely a result of an infarct

True

107

T/F: Cerebral blood flow only occurs if MAP is above ICP

True

108

What causes a coma?

Most severe: bicortical dysfunction; less severe: damage to reticular activating system (thalamus and periaqueductal gray)

109

A patient comes to the ER with headache and vomiting. MRI reveals generalizaed cerebral edema. Which of the following is likely true of the patient?

in this case, the patient has elevated intracranial pressure; if the patient's cerebral blood flow remains autoregulated, then the goal of the body is to raise cerebral perfusion pressure in opposition of the high ICPs; this can be done by raising the mean arterial pressure by hyperventilating (decreased CO2 increase blood pressure)

110

Describe the Circle of Willis

Anterior-posterior: anterior cerebral artery (interconnected by ACOM) connects MCA through the ICA; basilar artery (anastomosis of vertebral arteries) gives rise to the posterior cerebral artery and connects to anterior circulation by PCOM