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Pharmacology > Neurology > Flashcards

Neurology Flashcards

1
Q

Define Focal Injury.

A

A focal traumatic injury results from direct mechanical force to the head causing symptoms related to the area/region that was injured.
(ex. blow to the occipital lobe leads to loss of vision)

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2
Q

Define Global Injury.

A

A global traumatic injury yields larger effects and propagates throughout other areas of the body.
(ex. a head injury leads to loss of consciousness, coma, loss of reflexes etc)

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3
Q

What is the reticular activating system (RAS)?

A

RAS is the brain stem’s activating system, it promotes awareness and alertness in order to activate the cerebral cortex. It has the capability to control what is perceived within our conscious.

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4
Q

What are the sequelae when the RAS is damaged?

A

This kind of damage results from a traumatic brain injury. The damage will lead to;

  • Decreased Perfusion
  • Altered Metabolic State (metabolic acidosis)
  • Altered Consciousness (LOC)
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5
Q

Define Brain Death.

A

Brain death occurs when there is no motor, no brainstem reflexes and apnea when the patient is removed from the oxygen machine.

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6
Q

Vegetative State.

A

A vegetative state occurs when there is damage to the gray matter however, does not fully meet all requirements for brain death.
*There are maintenance brainstem reflexes; sleep-wake cycle, hypothalamic function adequate enough to meet basic demands *

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7
Q

Minimally Conscious State.

A

The patient has SOME self-awareness and presents simple responses to the environment.

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8
Q

Hypoxia.

A

Deficit of oxygen delivery to the tissues.

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9
Q

Hypoxemia.

A

Low oxygen levels in the bloodstream.

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10
Q

Ischemia.

A

The lack of oxygen within a tissue. This may be caused by a blockage or by low oxygen levels in the blood or tissue.

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11
Q

Global Ischemia.

A

Global ischemia occurs when there is no cardiac output, no nutrition delivery, and depletion of resources within 5minutes! All these factors lead to permanent brain and neuronal injury.

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12
Q

How does global ischemia contribute to cerebral edema?

A

The lack of nutrients and oxygen to the brain tissue causes altered cellular function. The decrease in cellular function causes a decrease in depolarization. The lack of electrolyte shifts (depolarization) will cause an electrolyte imbalance. The body addresses the imbalance by shifting fluids. The fluid shift will cause cerebral edema.

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13
Q

‘watershed infarcts’.

A

Aka ‘border zone infarcts’.

They represent the areas of tissue furthest from the arterial supply and thus are vulnerable to reduced perfusion.

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14
Q

Reperfusion injury.

A

Injuries due to inflammatory mediators. The inflammatory mediators become plentiful as the oxygen levels increase and can further injury
Mediators such as:
Catecholamines: The main catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine. These mediators in excess can cause the body to be stressed and cause further damage
Nitric Oxide: NO is a vasodilator and in excess will become a free radical and increase the damage

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15
Q

Cerebral edema.

A

Cerebral edema is brain swelling following a primary brain injury! Caused increase in fluid in the extravascular space and ICP.

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16
Q

Monro-Kellie Hypothesis.

A 
Intracranial pressure (ICP) is affected by CSF (cerebrospinal fluid) and works together to maintain cerebral perfusion pressure (CPP).
* if the volume of one of these structures increases, the others must decrease their volume to help alleviate pressure*
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17
Q

Vasogenic Edema.

A

This occurs when the blood-brain barrier is compromised. Mainly a result of head injury, hemorrhage OR CNS infection which leads to inflammation

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18
Q

Cytotoxic Edema.

A

Increased Intracellular fluid shifts into the cells, causing an increased ICP.

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19
Q

Range for Normal ICP.

A

Normal ICP= 0-15 mmHg

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20
Q

Cranial Perfusion Pressure Formula.

A

CPP= MAP- ICP
(this tells us how much blood pressure is required to perfuse the brain)

MAP: systolic + 2 Diastolic Divided by 3

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21
Q

What Occurs with increased Intracranial Pressure?

A
  • Limited cerebral blood flow due to decreased cerebral perfusion from building pressure in the brain.
  • The brain is getting squeezed and this leads to ischemia.
  • Increased ICP will cause a decrease in CPP
  • When CPP falls too low the body tries to increase systolic blood pressure to make more blood go to the brain, but this makes things worse!! Hence, leading to more swelling and even more ICP.
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22
Q

Signs and Symptoms of High ICP.

A
  1. Mental Status Change
  2. Irregular Breathing
  3. Nerve changes to the optic nerve
  4. Cushing’s Triad
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23
Q

Cuhsing’s Triad.

A
  • Increased systolic blood pressure (widening pulse pressure: increase in SBP and decrease in DBP), decreased heart rate, and abnormal breathing
  • Increased SBP (due to the body trying to get more blood to the brain)
  • Baroreceptor reflex (parasympathetic response by dropping the heart rate to decrease the blood pressure)
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24
Q

Sequelae of treatment for high ICP and cerebral edema.

A

Administer hypertonic saline solution, osmotic diuretics, reperfuse

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25
Q

Concussion.

A

A traumatic brain injury induced by a traumatic force OR by an acceleration-deceleration force!

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26
Q

Signs and Symptoms of a Consussion.

A
  • Headache
  • Amnesia
  • Confusion
  • Nausea
  • Irritability
  • Insomnia
  • Poor concentration/memory
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27
Q

Concussion Treatment.

A
  • Low stimulation (dim lights, low exposure to screens)
  • Return to ADL’s
  • Prevent Second Impact
  • If symptoms are severe focus on treatment for cerebral edema and high ICP
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28
Q

Define CNS Infection.

A

when a pathogen invades an anatomical structure. They are introduced into the body via direct entry/ exposure and spread via the bloodstream.

29
Q

Four sites of CNS Infection.

A

meninges = meningitis
Brain parenchyma = encephalitis
Spinal cord = myelitis
Brain and spinal cord= encephalomyelitis

30
Q

Meningitis.

A

Meningitis is an inflammation (swelling) of the pia mater, arachnoid, subarachnoid space (cerebrospinal fluid). It may be caused by a bacterial, viral or fungal infection.

31
Q

Pathology Sequalea of Meningitis.

A
  • Severe inflammation
  • The blood-brain barrier is compromised
  • Inflammation causes ‘capillary leaking’
  • The accumulation of fluid causes cerebral edema
  • Vascular Congestion: obstruction of the normal flux of blood within the blood vessels of the brain
  • Cellular death: due to lack of oxygen, nutrient and perfusion
  • Meningeal Thickening: the inflammatory response thickens the meninges
  • The CSF will be trapped within due to limited space of flow which is called (hydrocephalus)
32
Q

Signs and Symptoms of Meningitis.

A

Fever, headache, stiff neck, seizures

Petechial rash (emergency signs of sepsis)

33
Q

Meningitis Treatement.

A
  • Cephalosporins
  • Penicillins
  • Vancomycin
  • Glucocorticosteroids
34
Q

Glucocorticoids.

A

They have the ability to suppress histamine release and inhibit the synthesis of prostaglandins and COX-2! They also suppress phagocytes and lymphocytes (two major mediations of an immune reaction). This inhibition of the immune system reduces inflammation!

35
Q

Disorders Treated by Glucocorticoids.

A
  • Asthma
  • COPD
  • Rheumatoid arthritis
  • Chrones disease
36
Q

3 Common Glucocorticods.

A
  1. Fluticasone
  2. Predisone
  3. Methylprednisone
37
Q

Primary Brain Tumor.

A

A primary brain tumour is a tumor that starts in the brain. A primary brain tumor is often described as “low grade” or “high grade.”

  • A low-grade tumour generally grows slowly, but it can turn into a high-grade tumour.
  • A high-grade tumour is more likely to grow faster.
38
Q

Secondary Brain Tumor.

A

A secondary brain tumor is a cancerous tumor that started in another part of the body, such as the breast, lung, or colon, and then spreads to the brain.

39
Q

Neoplastic Meningits.

A

When cancer spreads to the cerebrospinal fluid and the meninges it is considered as neoplastic meningitis.

40
Q

Brain Tumor Diagnosis.

A

A brain tumor is diagnosed by CT scans or EEG

41
Q

Brain Tumor Treatment.

A
  • Surgery: Removal of the tumor
  • Gamma-Knife Radiation: uses many beams of radiation from multiple angles to target one specific area in the brain.
  • Radiation: Use of high-energy x-rays to destroy cells.
  • Chemotherapy: use of drugs to destroy cancer cells.
42
Q

Alkalizing Agents.

A

Medications such as alkylating agents destroy the DNA found in cancerous cells to inhibit replication.

43
Q

Side Effects of Alkylating Agents.

A

Hair loss, GI issues, bone marrow suppression and low blood cell count

44
Q

Seizure.

A

Abnormally synchronous electrical discharges from neurons in the cerebral cortex. It can cause changes in behaviour, movements or feelings, and in levels of consciousness.

45
Q

Focal (Partial) Seizure.

A

Occurs when a seizure begins in ONE area. The excess neuronal discharge occurs in one cerebral cortex.

46
Q

Generalized Seizure.

A

The aberrant electrical discharge diffuse throughout the entire cortex of both hemispheres.

47
Q

Absence Seizures.

A

Can cause individuals to blank out or stare into space for a few minutes. (Petit Mal Seizures)

48
Q

Tonic-Clonic Seizures.

A

These seizures allow the muscles and joints to stiffen and subsequently, the body will start to rhythmically jerk. (Gran Mal Seizures)

  • All the muscles stiffen.
  • The person loses consciousness and falls to the floor.
  • The arms and usually the legs begin to jerk rapidly and rhythmically
49
Q

Febrile Seizure.

A

Convulsions that occurs when a young child has a fever above 100.4 degrees F (38 degrees celsius)

50
Q

Signs and Symptoms of a Seizure.

A
  • Loss of consciousness
  • Aura (focal seizure)
  • Automatisms (repeating behaviour)
51
Q

Diagnosis of Seizures.

A

-EEG or MRI

52
Q

Seizure Treatment.

A
  • Benzodiazepines
  • Barbituates
  • Anticonvulsants
53
Q

How do Benzodiazepines work?

A

Work to calm or sedate a person, by raising the level of the inhibitory neurotransmitter GABA in the brain. Benzodiazepines= ‘sedativ-hypnotic” drugs.

54
Q

Common Benzodiazepenes.

A
  1. Chlordiazepoxide (Librium)
  2. Diazepam (Valium)
  3. Alprazolam (Xanax)
  4. Lorazepam (Ativan)
55
Q

Overdose Treatment for Benzos.

A

In cases of overdose adminster Flumazentil (Romazicon), a receceptor antagonist

56
Q

Benzo Used in Roofies.

A

Flunitrazepam (Rohypnol)

57
Q

Barbituates.

A

They produce a calming and sedative effect on the central nervous system. Most generic names end with barbital or ‘ital’. They increase the effects of GABA (an inhibitory neurotransmitter)

58
Q

Side Effects of Barbiturates.

A
  • Respiratory Depression
  • Altered LOC and CNS
  • High risk of overdose
  • Highly addictive
  • High degree of tolerance
59
Q

Anti-Convulsants.

A

Alter electrolyte movement – delay action potential, decrease neuronal activity. These medications decrease the flow of Calcium and Sodium ions across the neuronal membranes

60
Q

Side Effects of Anti-Convulsants.

A

Dizziness, drowsiness, tremors, nausea

61
Q

Status Epilepticus.

A

A seizure that lasts longer than 5 minutes, or having more than 1 seizure within a 5 minutes period, without returning to a normal level of consciousness between episodes.

62
Q

Status Epilepticus Treatment.

A

Treat with Benzodiazepeines via IV

-Diazepam or Lorazapam

63
Q

Anatomial Structures that Contribute to sleep.

A

RAS, thalamus, cerebral cortex, hypothalamic suprachiasmatic nucleus, pineal gland

64
Q

Melatonin.

A

Melatonin is produced naturally from the amino acid tryptophan, by the pineal gland. Tryptophan is converted into serotonin. Serotonin is the converted into melatonin (an inhibitory neurotransmitter)

65
Q

Sleep Stages.

A
  • nonREM stages: light to deep sleep progression

- REM: the brain becomes more active, the body becomes relaxed and dreams occur

66
Q

Insomnia.

A

A sleep disorder in which you have trouble falling and/or staying asleep.

67
Q

Populations at Risk for Insomnia.

A

-Elderly population, post-menopausal, people who use stimulants and patients who use glucocorticoids.

68
Q

Minimum CPP.

A

The minimum CPP is 45 mmHg

profound ischemia presents itself as a CPP less than 40 mmHg

Pharmacology (27 decks)

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