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Advanced Patho > Weeks 4 - 7 > Flashcards

Weeks 4 - 7 Flashcards

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1
Q

What are the main functions of the nervous system?
(4)

A

• Pain
• Temperature regulation
• Sleep
• Sensory function

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2
Q

Define Nociceptors:

A

• Sensory receptors that are activated by noxious stimuli that damage or threaten the body’s integrity

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3
Q

Where are nociceptors located?
(5)

A

The peripheral nervous system:
• Skin
• Muscles
• Joints
• Bones
• Internal organs

Abundant in fingertips, none in cartilage

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4
Q

How are nociceptors activated?

A

Painful stimuli - they send electrical signaling messages to the dorsal horn of the spinal cord.

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5
Q

What is the most commonly diagnosed sleep disorder?

A

Obstructive sleep apnea syndrome

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6
Q

What age does the occurrence of sleep apnea increase?

A

60 years and above

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7
Q

What are major risk factors for sleep apnea?
(6)

A

• Obesity
• Male sex
• Older age
• Postmenopausal status
• Craniofacial anomalies
• Increased size of tonsillar and adenoid tissues

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8
Q

Clinical presentation of obstructive sleep apnea (or symptoms)?
(3)

A

• Loud excessive snoring
• Gasping
• Multiple apneic episodes that last 10 seconds or longer.

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9
Q

Define Central Sleep Apnea:
What is the pathology regarding O2 and CO2?

A

• The temporary absence or diminution (lessening) of ventilatory effort during sleep.
• Decreased sensitivity to carbon dioxide and oxygen tensions with decreased airway dilator muscle activation.

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10
Q

What are major risk factors and/or associations for Central Sleep Apnea?
(4)

A

• Heart failure
• Neurologic disease
• High altitude
• Narcotic medications

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11
Q

Define Obesity hypoventilation syndrome:

A

A combination of obesity, daytime hypercapnia, and sleep disordered breathing not caused by other disorders of hypoventilation.

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12
Q

What are the short term consequences of the sleep apneas?
(4)

A

• Apneic breathing causes
arousal,
interrupted sleep cycles,
decreased sleep time, and
REM deprivation.

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13
Q

What are the long term consequences of the sleep apneas?
(11)

A

• hypercapnia
• low O2 saturation
• polycythemia
• pulmonary hypertension
• systemic hypertension
• stroke
• RHF
• dysrhythnias
• liver congestion
• cyanosis
• peripheral edema

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14
Q

What is the difference in source between acute and chronic pain?

A

Acute pain is a protective mechanism to warn of actual or impending injury; the external agent and/or internal disease is usually known.

The source of chronic pain is often unknown - if known, treatment is often prolonged and ineffective.

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15
Q

How long does acute pain last versus chronic pain?

A

Acute pain is transient and may last up to 6 months.

Chronic pain is prolonged and persistent (months to years).

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16
Q

What are the clinical signs of acute pain?
(5)

A

Sympathetic response:
• Increased HR
• Increased BP
• Increased RR
• Diaphoresis
• Dilated pupils

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17
Q

What are the clinical signs of chronic pain?

A

Sympathetic response is usually unresponsive due to adaptation therefore fewer overt symptoms (HR, BP normal) patient presents as calm.

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18
Q

What is the prognosis of acute pain versus chronic pain?

A

Acute pain has a likelihood of eventual complete relief whereas complete relief with chronic pain is usually not possible.

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19
Q

How does temperature work as a protective mechanism?
(5)

A

Moderate fever:
• Raised body temperature kills or adversely affects the growth of pathogens.
• Decreased serum levels of iron, zinc, and copper (minerals needed for bacterial replication).
• Lysosomal breakdown and auto destruction of cells (preventing viral replication).
• Increased lymphocytic transformation and motility of polymorphonuclear neutrophils (ramps up immune response).
• Phagocytosis is enhanced and production of antiviral interferon is augmented.

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20
Q

What is the danger in prolonged fever?
(4)

A

Prolonged hyperthermia can cause:
• Nerve damage
• Protein coagulation
• Convulsions
• Death

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21
Q

What are pyrogens?

A

Fever causing substance.
Exogenous pyrogens are produced by pathogens.
Endogenous pyrogens are mostly produced by phagocytes cells (prostaglandin and interleukins).

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22
Q

What does fever look like in the elderly?

A

Subtle / atypical responses accompanied by dehydration.
• Feeling cold / warm
• Strange body sensations
• Headache
• Vivid dreams
• Hallucinations
SEVERE systemic infection may cause alternating hypo/hyperthermia in 24H period.

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23
Q

What does fever look like in children / infants?

A

Infants: less than 60 to 90 days old present with fever and no other symptoms (differential diagnosis is difficult).
Children: Develop higher temperatures than adults for minor infections any skin vasoconstriction can lead to rapid increase in body temperature.

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24
Q

What are some causes circadian rhythm sleep disorders?
(3)

A

• Rapid time zone changes (jet lag syndrome)
• Alternating sleep schedule involving 3 hours or more (rotating work shifts)
• Changing total sleep time from day to day.

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25
What are some short term consequences of disrupted circadian rhythms?
• Cognitive deficit • Poor vigilance • Difficulty concentrating • Inadequate performance of psychomotor skills
26
What are some long term consequences of disrupted circadian rhythms?
• Depression / anxiety • Increased risk for cardiovascular disease • Increased all-cause mortality
27
Define conductive hearing loss:
Interference in air conduction
28
What are some common causes of conductive hearing loss?
• Impacted cerumen • Foreign bodies • Benign tumors of middle ear • Carcinoma of external auditory canal or middle ear
29
What are symptoms of conductive hearing loss?
• Diminished hearing • Soft speaking voice (bone conduction sound is louder) • Better hearing in noisy environment
30
What causes sensorineural hearing loss?
• Impairment of the organ of corti or its central connections • Congenital / hereditary factors • Noise exposure • Aging • Ototoxicity • Systemic disease (syphilis, paget disease, collagen diseases, DM).
31
Define presbycusis:
Age related hearing loss usually in the high frequencies.
32
What is the most common form of hearing loss?
Presbycusis; most common in older adults
33
What are some causes of presbycusis?
• Atrophy of the basal end of the organ of corti • Loss in the number of auditory receptors • Vascular changes • Stiffening of the basilar membranes
34
What is the pathophysiology of multiple sclerosis?
• Chronic inflammatory disease - autoimmune response to self-antigens - B cells produce myelin specific antibodies - plaques develop when T cells recognize myelin as auto-antigens. • Degeneration of central nervous system myelin • Scarring of formation of plaque • Loss of axons
35
Destruction of myelin sheath; signals are not sent down nerve properly which leads to motor-type symptoms, weakness, slurred speech, autoimmune inflammatory disorder.
36
Destruction of myelin sheath; signals are not sent down nerve properly which leads to motor-type symptoms, weakness, slurred speech, autoimmune inflammatory disorder.
37
What is the pathophysiology of MS?
• Chronic inflammatory disorder causing destruction of central nervous system myelin sheath because B cells produce myelin specific antibodies • Scarring / formation of plaque (due to T cells recognizing myelin as autoantigens) & loss of axons.
38
What are MS symptoms?
Motor-type symptoms: weakness, slurred speech, autoimmune symptoms inflammatory disorder
39
What causes Guillain-Barré syndrome?
A bacterial or viral infection triggers an autoimmune response (usually days or weeks after initial infection). * Vaccines may result in GBS
40
What is the pathophysiology of GBS?
The immune system attacks healthy nerves (myelin and axons) in peripheral nervous system * Some chemicals seen on bacteria and viruses resemble those on nerve cells.
41
What is the pathophysiology of Amyotrophic lateral sclerosis (ALS)?
Motor neuron disease originating in cortical motor neurons characterized by degeneration and death of upper and lower motor neurons including neuromuscular junction. • Amyotrophic: lower motor neurons experience poor muscle nutrition causing progressive muscle wasting. • Lateral sclerosis: scarring of spinal cord causing upper motor neurons experience symptoms.
42
Symptoms of ALS:
• Muscle weakness • Fasciculations (muscle twitching) • Atrophy (muscle wasting) • Loss of voluntary muscle control * Risk factors include family history
43
Describe Bulbar onset disease:
Rapid and progressive course affecting muscles in the face and neck as well as swallowing, speech, and saliva production.
44
What is the life expectancy for ALS?
Most commonly 3 to 5 years (death by respiratory failure) 10% live a decade or longer
45
What physiology is affected by Parkinson’s?
The basal ganglia: • Corpus striatum • Globus pallidus • Subthalamic nucleus • Substantial nigra
46
What physiology is affected by Parkinson’s?
The basal ganglia: • Corpus striatum • Globus pallidus • Subthalamic nucleus • Substantial nigra
47
What physiology is affected by Parkinson’s?
The basal ganglia: • Corpus striatum • Globus pallidus • Subthalamic nucleus • Substantial nigra
48
Define stage 1 cancer:
Confined to organ of origin
49
Define stage 2 cancer:
Cancer that is locally invasive
50
Define stage 3 cancer
Cancer that has spread to regional structures (ie lymph nodes)
51
Define stage 4 cancer
Cancer has spread to distant sites (liver to lung, prostate to bone etc)
52
Benign v. Malignant: Cell Appearance
Benign: well differentiated Malignant: poorly differentiated
53
Benign v. Malignant: Usual rate of growth
Benign: slow Malignant: rapid w/ variability in size/shape
54
Benign v. Malignant: Vascularization
Benign: slight Malignant: neovascularization through angiogenesis
55
Benign v. Malignant: Tissue structure
Benign: Maintained Malignant: Changed
56
Benign v. Malignant: Ability to metastasize
Benign: no Malignant: yea
57
What is the hallmark pathological feature of Parkinson’s?
Dopaminergic deficiency in striatum, brain stem and cortex.
58
What are some causes of secondary Parkinson’s? (4)
Neurodegenerative and acquired disorders • Pesticide exposure • Heavy metals / herbicides • Antipsychotic drugs • Repeated head trauma
59
When can we definitively diagnose Parkinson’s?
Post Mortem
60
When can we definitively diagnose Parkinson’s?
Post Mortem
61
What are classic motor manifestations of Parkinson’s? (Global) (6)
• Pill rolling tremor • Resting tremor • Bradykinesia / akinesia • Muscle rigidity • Postural abnormalities • Shuffling gait / side falls
62
What are classic motor manifestations of Parkinson’s? (Facial) (3)
• Wide - eyes / unblinking • Smooth facial muscles • Frequent drooling
63
What is the primary role of IgA?
DOMINANT SECRETORY IMMUNOGLOBULIN Prevents attachment and invasion of pathogens through mucosal membranes (GI, pulmonary and genitourinary tracts).
64
Which system do migraines active?
Trigeminovascular system and associated changes in brain metabolism and blood flow.
65
What are the neuroanatomic alterations of schizophrenia?
Lateral and third ventricle enlargement abnormal amygdala connectivity Alterations in dopamine pathways Progressive loss of frontal lobe volume = difficulty in appropriate social judgements, decline in cognitive functioning, difficulty in emotional processing
66
What are the two types of immunity?
Innate: natural barriers and inflammation Acquired (adaptive): humoral and antibodies
67
What are the four cardinal signs of inflammation?
Edema: vasodilation increases blood flow Warmth/redness: increased blood flow and increased RBCs cause warmth Pain: biochemical mediators (Histamines, Bradykinins, Leukotrienes, Prostaglandins) Neutrophils: phagocytize pathogenic microbes remove cellular debris / dead cells.
68
What are the two types of adaptive immunity?
Humoral: B-cells produce antibodies Cellular: T-cells (T-helper & Tc cells) - protects against cancer.
69
What does viral replication rely on?
The ability to infect a permissive host cell.

Advanced Patho (4 decks)

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