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Pathopharmacology Intro > Module 4 > Flashcards

Module 4 Flashcards

1
Q

What is hyperactive confusional state? How long does this develop over?

A

Acute disturbances in attention / awareness - develops over 2-3 days

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2
Q

What are the risk factors for hyperactive confusional state?

A

Medications, acute infection, surgery, hypoxia, electrolyte imbalances, and insomnia

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3
Q

How does hyperactive confusional state manifests?

A

Restless, irritable, difficulty concentrating, insomnia, tremors, poor appetite

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4
Q

What is fully developed delirium?

A

Hallucinations, completely inattentive, grossly altered perception

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5
Q

What is excited delirium syndrome

A

Combative, aggressive, pain, rapid breathing, can lead to death

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6
Q

How to treat hyperactive confusional state

A

Remove risk factors when possible

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7
Q

What is hypoactive confusional state associated with?

A

Right sided frontal basal-ganglion disruption

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8
Q

How does hypoactive confusional state manifest?

A

Decreased alertness and attention span, forgetfulness, apathetic, slow speech, frequently falls asleep

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9
Q

How do you treat hypoactive confusional state?

A

Remove causative agents if possible

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10
Q

Compare the onset of delirium and dementia

A

Dementia: slow and progressive
Delirium: acute (r/t hospitalizations)

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11
Q

Compare the course of delirium and dementia

A

Dementia: chronic, slow decline
Delirium: fluctuating and reversible

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12
Q

Compare the attention level for delirium and dementia

A

Dementia: intact early but declines later
Delirium: inability to focus or sustain attention

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13
Q

Compare the alertness and orientation level of dementia and delirium

A

Dementia: intact early and can be variable in later stages
Delirium: impaired

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14
Q

Compare the behavior between dementia and delirium

A

Dementia: intact early on
Delirium: agitated, withdrawn, depressed

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15
Q

Compare the speech habits between delirium and dementia

A

Dementia: word finding problems / aphasia
Delirium: incoherent, disorganized

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16
Q

What are the risk factors for Alzheimers

A

65+, family hx, existing mild cognitive impairment, head trauma, and isolation

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17
Q

What is the patho behind Alzheimers

A

Accumulation of neuritic plaques and intraneuronal neurofibrillary tangles of tau protein

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18
Q

In frontotemporal dementia what is progressive non-fluent behavior and semantic dementia

A

Progressive : problems with language and writing
Semantic: problems forming words and sentences

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19
Q

What is dopamine responsible for

A

pleasure, satisfaction

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20
Q

what is norepinephrine responsible for

A

increases alertness, arousal, and attention

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21
Q

what is serotonin responsible for

A

mood, sleep, sexual desire

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22
Q

what is GABA responsible for

A

reduces neuronal excitability by inhibiting nerve transmission

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23
Q

How does a dopamine deficit manifest

A

parkinson’s like symptoms and pleasure center dysfunction

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24
Q

how does a serotonin deficit manifest

A

OCD like symptoms and impulsivity

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25
Q

together how do serotonin and dopamine deficit manifest

A

depression and cravings

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26
Q

what is anticipatory anxiety

A

fearful expectation of panic anxiety onset

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27
Q

what is avoidance anxiety

A

personal strategies used to increase feelings of control and decrease the risk of panic

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28
Q

what is used as a second line therapy for panic disorders

A

benzos

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29
Q

what is generalized anxiety disorder and how long does it take to be diagnosed

A

excessive, uncontrolled, unrealistic worry accompanied by muscle tension, autonomic hyperactivity, exaggerated startle, difficulty concentrating
anxiety present for more than 6 months

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30
Q

what are the risk factors for GAD

A

excessive use of certain substances, childhood abuse / family trauma, genetics

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31
Q

what are the key characteristics of PTSD

A

vivid flashbacks, nightmares, emotional blunting, irritability, and exaggerated startle

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32
Q

what are the 4 main causes of PTSD in men and women

A

Men: rape, combat, childhood neglect, and childhood physical abuse
Women: rape, sexual molestation, physical attack, being threatened with a weapon

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33
Q

If a person takes propranolol for social anxiety how long before should they take it?

A

1-2 hours before

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34
Q

compare obsessions and compulsions

A

obsessions - repetitive unwanted thoughts
compulsions - repeated activities or rituals

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35
Q

What is a second line treatment (pharm) for OCD

A

Clomipramine

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36
Q

How does the brain pathways change with addiction

A

Addiction decreases dopamine pathways but with abstinence they do regenerate

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37
Q

What are the risk and protective factors of substance abuse?

A

Risk: aggressive behavior as children, lack of parental supervision, poor social skills, drug experimentation, availability of drugs at school
Protective: good self control, parental monitoring and support, positive relationship, good grades, school anti-drug policies

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38
Q

What is the safest way to manage acute withdrawal symptoms

A

medically assisted detoxification

39
Q

treatment programs for substance use also need to test patients for what

A

diseases that are associated with substance use disorders - like HIV / ADIS, hepatitis, TB, and endocarditis

40
Q

Antagonist or agonists - for buprenorphine and naloxone

A

Buprenorphine: partial opioid agonist
Naloxone: opioid antagonist

41
Q

What is the opioid withdrawal timeline

A

begins 12-24 hours after last dose, peaks at 72 hours, physical symptoms start to lessen at 1 week
cravings and depression can last through months

42
Q

What is included in supportive treatment for opioid withdrawal

A

Tylenol and anti-diarrhea

43
Q

what are the serious symptoms related to benzo and alcohol withdrawal

A

seizures, hallucinations, delirium tremens (tachycardia, hypertension, fever, agitation, diaphoresis), wernikes encephalopathy (profound disorientation, inattention, oculomotor dysfunction)

44
Q

What is the benzo withdrawal timeline

A

first symptoms start 6-12 hours after last dose, peaks at 2 weeks

45
Q

what is the alcohol withdrawal timeline

A

8 hours - anxiety, insomnia, nausea, and abdominal pain
1-3 days is the peak - high blood pressure, increased body temperature

46
Q

with alcohol withdrawal what vitamin needs supplementation

A

B1

47
Q

What is the purpose of acute pain

A

protective, promotes withdrawal from painful stimuli, teaches avoidances, allows injured parts to heal

48
Q

what are the three pathways that are involved with pain sensation, perception, and response

A

afferent pathways - take impulses from spinal cord to cortex
interpretive centers - interpret impulse as pain
efferent pathways - physical / mental response to pain

49
Q

what is nociceptive pain

A

stimuli of a certain intensity that causes or could potentially cause tissue injury

50
Q

what happens at the transduction phase of pain

A

stimuli converted to action potentials - happens at A-delta and C-fibers

51
Q

What does prostaglandin do when activated

A

lowers the pain threshold - when prostaglandin is suppressed it decreases the pain by raising the pain threshold.
promotes inflammation, pain, and fever
protects lining of stomach from acid, promotes clotting factors (activates platelets), and affects kidney function

52
Q

what fibers are myelinated

A

a-delta

53
Q

what fibers are non-myelinated

A

C-fibers

54
Q

if pain activate the a-delta fibers what does the pain feel like

A

sharp, stinging, cutting, and pinching - these are localized

55
Q

if pain activates the c-fibers what does the pain feel like

A

dull, burning, aching - these are poorly localized

56
Q

what fibers do not transmit pain

A

A-alpha and A-beta

57
Q

compare tolerance and threshold in relation to pain

A

tolerance - greatest intensity of a pain a person can handle
threshold - lowest intensity of pain that a person can recognize

58
Q

intense pain at one location may decrease or increase the pain threshold in another site

A

decreases

59
Q

what is the gate control theory

A

if we block the pain before it gets to the brain we can stop/lower the pain perception

60
Q

pain < 3 months is considered

A

acute

61
Q

pain >3-6 months is considered

A

chronic

62
Q

what type of pain stimulates the ANS

A

acute - can change HR, BP, sweating, and cause dilated pupils

63
Q

compare the stimuli for nociceptive and neuropathic pain

A

nociceptive - outside the CNS
neuropathic - inside the CNS

64
Q

compare the causes of nociceptive and neuropathic pain

A

nociceptive - activated in response to actual / impending tissue injury
neuropathic - arises from direct injury to NERVES

65
Q

visceral pain activates only which pain fiber

A

C

66
Q

cutaneous / somatic pain involves what system and has what complaints

A

musculoskeletal pain

constant, achy

67
Q

what is the localization of cutaneous / somatic pain

A

well localized in skin and subcutaneous tissue but less well localized for bones

68
Q

visceral pain involves what system and has what complaints

A

involves organs

cramping, splitting, N/V, diaphoresis

69
Q

what is the localization of visceral pain

A

poorly localized

70
Q

neuropathic pain involves what system and has what complaints

A

nerves

shooting, burning, electric shock, sharp, numb, weakness

71
Q

what is the localization of neuropathic pain

A

poorly localized

72
Q

compare referred and phantom pain

A

referred - pain felt at a distance from the actual pathology (common in visceral pain)
phantom - sensation of pain that originates from an amputated part

73
Q

nonselective COX inhibitors decrease what

A

gastric acid protection and platelet function

74
Q

does acetaminophen have anti-inflammatory effects

A

no

75
Q

what enzyme is responsible for the production of prostaglandins

A

COX

76
Q

chronic alcohol users should limit their acetaminophen to how much

A

2 g / day

77
Q

when administering an opioid when should you wait and assess for level of sedation

A

if RR is less than 10

78
Q

how does initial drowsiness change with more doses of opioids

A

diminishes

79
Q

0.1 mg of IV fentanyl is how much morphine

A

10 mg IV morphine

80
Q

define myoclonic

A

brief, shock-like jerks of a muscle of groups

81
Q

what is the cause of primary seizures

A

don’t know the cause - they are idiopathic

82
Q

what is the etiology of secondary seizures

A

chemical imbalances, fever, brain injuries

83
Q

What is the caveat to diagnosing epilepsy

A

must have no evidence of a reversible metabolic cause

84
Q

what is seizure threshold

A

persons likelihood to have a seizure

85
Q

what is a generalized onset seizure

A

neuronal activity simultaneously in both hemispheres on the brain

86
Q

tonic vs clonic

A

tonic - prolonged skeletal muscle contraction
clonic - alternating skeletal muscle contraction and relaxation

87
Q

what are absence seizures

A

brief loss of awareness that commonly occurs with repetitive spasmodic eyes blinking for up to 30 seconds

88
Q

what is a focal onset seizure

A

seizure originating in a localized part of the brain (one lobe)

89
Q

what is the prodromal phase of seizure

A

signs / activities that usually come before a seizure starts

90
Q

what is that aural, ictal, and post-ictal phases of seizures

A

aural - sensory warning
ictal - seizure
post-ictal - recovery

91
Q

what is status elipepticus

A

a continuing series of multiple seizure without a recovery period, lasts 30 minutes or more and can lead to respiratory arrest

92
Q

how long must a patient go without a seizure to be be eligible to decrease dose or stop their anti-epileptic meds?

A

1-2 years

93
Q

are pregnant women able to take anti-epileptic drugs

A

no, they are teratogenic

Pathopharmacology Intro (6 decks)

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