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Pathophysiology > Disorders of the Neurological System > Flashcards

Disorders of the Neurological System Flashcards

1
Q

Where are action potentials initiated?

A

Junction between the cell body and the axon (if enough excitatory info)

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2
Q

Where does the action potential go from there?

A

Down the axon until the axon terminals, will then signal to release neurotransmitters

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3
Q

What are the two vessels that bring blood to the brain?

A

Internal carotid artery and the middle cerebral artery, form an anastomosis

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4
Q

What is the purpose of the blood brain barrier?

A

Serves as a physical barrier to chemicals

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4
Q

What elements compose the blood brain barrier?

A

Endothelial cells connected by tight junctions (rest on the basement membrane), astrocyte foot processes (surround the capillaries, help regulate) and pericytes (embedded within the basement membrane)

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5
Q

What are the meninges?

A

Layers of connective tissue that help to stabilize the brain and protect the structures from hitting surrounding bones

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6
Q

What are the components that make up the meninges?

A

Dura matter, arachnoid matter, pia matter

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7
Q

Which layer of the meninges is the thickest?

A

The dura matter which is the outermost region

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8
Q

What is found within the arachnoid matter?

A

Subarachnoid space which holds CSF

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9
Q

Where is the pia matter located?

A

On the surface of the brain itself, this layer is fine and delicate

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10
Q

What are the two types of ischemic stroke that can occur?

A

Thrombotic (more common, thrombus formed within the cerebrovasculature) and embolic (thrombus formed outside of the brain that breaks off and travels to, usually obstructs smaller vessels)

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11
Q

What are the two areas that develop when an infarction occurs?

A

Ischemic core (most severe area, neuronal and glial death within moments) and penumbra (surrounding area to this core, can survive for hours with full recovery)

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12
Q

Which area do therapeutic strategies target?

A

Penumbra!

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13
Q

Where does the ischemic cascade start?

A

Within the penumbra

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14
Q

What are the three elements of the ischemic cascade?

A

Excitotoxicity, oxidative stress, inflammation

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15
Q

What occurs during excitotoxicity in the ischemic cascade?

A

Sustained activation of neurons within penumbra, Ca2+ enters neurons, stimulates NT release, but when accumulates b/c cannot be pumped out= death signal. Neurons won’t have enough energy to maintain action potential, remain excited and cannot repolarize

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16
Q

How does inflammation impact the blood brain barrier?

A

Disrupts it and makes it more permeable= cerebral edema

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17
Q

What pathologic changes occur in hemorrhagic strokes?

A

Pooling of blood results in compression of surrounding tissues and this can disrupt blood flow= ischemic cascade activation. Hemoglobin is toxic to neurons!

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18
Q

What are common causes of hemorrhagic strokes?

A

Uncontrolled hypertension or ruptured aneurysms

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19
Q

What clears away the blood in a hemorrhagic stroke?

A

Macrophages and astrocytes, results in a cavity with dense glial scarring

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20
Q

What are oligodendrocytes?

A

Glial cells that produce a lipid-rich substance called myelin, wrap it around axon of the neuron

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21
Q

What is the purpose of myelin?

A

Serves as an insulator, prevents electrical information from leaking out

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22
Q

What are the Nodes of Ranvier?

A

Gaps in the myelin, allow ions to move in and out to propagate the action potential down the axon

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23
Q

What occurs in multiple sclerosis?

A

Autoimmune targets cells that produce myelin, resulting in myelin degeneration and loss of axons/killing off of oligodendrocytes

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24
Q

What are potential causes of MS?

A

Genetics, epigenetics, infectious component (infection may precipitate the autoimmune response–many positive for the EBV which has viral proteins that resemble myelin)

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25
Q

What is the pathophysiology in MS?

A

Immune cells attack oligodendrocytes, cytokines and ROS damage axons. Have Th1 and Th17 CD4+ cells involved, CD8+, macrophages and plasma cells

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26
Q

What are the types of MS?

A

Relapsing and remitting (65-80%), primary progressive (10-20%)

27
Q

What are some of the clinical manifestations of MS?

A

Sensory or motor abnormalities- numbness, tingling, pain, weakness, slurred speech, etc., usually asymmetrical, can lead to brain atrophy, mood disorders, etc.

28
Q

What region of the brain does Parkinson’s affect?

A

Primarily basal ganglia

29
Q

What is Parkinson’s disease?

A

Chronic and progressive neurodegenerative disorder, results in motor deficits and lose neurons within the basal ganglia (less able to help coordinate movement)

30
Q

Which gene places individuals at greater risk for Parkinson’s?

A

Abnormal a-synuclein gene

31
Q

What occurs in Parkinsons?

A

Substantia nigra releases dopamine, there is a destruction of these neurons in the pars compacta of the substantia nigra

32
Q

What are Lewy bodies in Parkinson’s disease?

A

Intracellular accumulations of the a-synuclein protein, gets mutated and aggregates which is toxic to neurons

33
Q

What pathophysiological processes occur in Parkinson’s?

A

Presence of Lewy bodies, dopaminergic neuron loss, mitrochrondrial dysfunction and ROS

34
Q

What are some of the clinical manifestations of Parkinson’s?

A

Motor related- asymmetric, regular, rhythmic tremors, rigidity, bradykinesia (lack of ability to produce smooth motions), postural abnormalities, constipation, oil skin, impulse control, difficulty forming thoughts, other non-motor symptoms

35
Q

What is Alzheimer’s disease?

A

Progressive neurodegenerative disorder that results in memory loss and overall decrease in intellectual function. Loss of neurons but in higher functioning areas

36
Q

What characterizes Alzheimers?

A

Senile plaques, neurofibrillary tangles, neuronal death, loss of synapses

37
Q

What are senile plaques?

A

Aggregation of AMYLOID-B PEPTIDES, toxic to neurons, can become surrounded by activated microglial and astrocytes coming to contain damage

38
Q

What are neurofibrillary tangles?

A

Aggregate of TAU protein (insoluble, hyperphosphorylated), toxic, start to form insoluble masses

39
Q

What prompts neuronal damage in Alzheimers?

A

Senile plaques and neurofibrillary tangles along with mitochondrial dysfunction and ROS, inflammation, cerebrovascular abnormalities (decrease in oxygen/nutrients, accumulation of aggregates around blood vessels, leaky BBB)

40
Q

What are some clinical manifestations of Alzheimers?

A

Become progressively more forgetful, decline in concentration/problem solving/judgement, behavioural abnormalities, motor abnormalities

41
Q

What is a protective measure against Alzheimers?

A

Estrogen- blocks some harmful effects of Amyloid-B protein

42
Q

What are two infections of the CNS?

A

Meningitis and encephalitis

43
Q

What occurs in viral meningitis?

A

Enters CNS, spreads through subarachnoid space and causes inflammation, resolves on its own and can be caused by numerous viruses (Enterovirus, measles, mumps, herpes, etc)

44
Q

What occurs in bacterial meningitis?

A

More severe, high incidence in neonates, reaches the subarachnoid space through blood, causes severe inflammatory response, purulent exudate impairs the removal of CSF and cerebral edema occurs

45
Q

What are the likely causes of bacterial meningitis?

A

In neonates= E.Coli and Group B strep, in adults= Streptococcus pneumoniae, Nesisseria meningitidis, H. Influenza

46
Q

What occurs in encephalitis?

A

Inflammation of brain parenchyma (actual brain tissue), can occur alongside meningitis

47
Q

How are traumatic brain injuries characterized?

A

Mild, moderate, severe concussion

48
Q

What characterizes a severe TBI?

A

GCS <8, LOC >24 hours, brainstem involvement, permanent deficits

49
Q

What characterizes moderate TBI?

A

GCS 8-13, LOC >30 min, no brainstem involvement, long duration amnesia, some permanent deficits

50
Q

What characterizes a mild TBI?

A

GCS 13-15, may or may not have LOC (momentarily if anything), <24 hours amnesia

51
Q

What is a TBI?

A

Traumatic brain injury, alteration in brain function caused by external force

52
Q

What is a closed injury?

A

Striking of head on hard surface, rapidly moving object striking head, blast waves. Results in focal injury, may be coup or contrcoup, can result in contusions and hematomas

53
Q

What types of hematomas can occur in TBI?

A

Epidural hematoma, subdural hematoma, intracerebral hematoma

54
Q

What is an open injury?

A

Skull fracture, break in dura= exposure of cranial contents to environment

55
Q

What two types of fractures can occur in an open injury?

A

Compound skull fracture, basilar skull fracture

56
Q

What is often the cause of diffuse TBI?

A

Mechanical effects(whiplash, rotational forces) that result in stretching and shearing of axonal fibers

57
Q

What are Schwann cells?

A

Provide support for neuronal processes in PERIPHERAL nervous system

58
Q

What does the Wernicke area do?

A

Interpreting speech

59
Q

What is the corpus callosum?

A

Transverse fiber tract that connects two cerebral hemispheres

60
Q

What is the pons region in the brain?

A

Located below midbrain and above medulla- transmits info from cerebellum to brain stem and b/t two hemispheres

61
Q

What is the vagus nerve?

A

A part of the PNS, stimulates results in PNS activity

62
Q

Sympathetic motor neurons at the neuromuscular junction relase what?

A

Norepinephrine

63
Q

What is an effect of Alpha-1 receptor stimulation?

A

Constriction of the coronary arterioles

64
Q
A

Pathophysiology (12 decks)

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