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Advanced Patho > Weeks 4 - 7 > Flashcards

Weeks 4 - 7 Flashcards

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
Q

What are some short term consequences of disrupted circadian rhythms?

A

• Cognitive deficit
• Poor vigilance
• Difficulty concentrating
• Inadequate performance of psychomotor skills

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26
Q

What are some long term consequences of disrupted circadian rhythms?

A

• Depression / anxiety
• Increased risk for cardiovascular disease
• Increased all-cause mortality

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27
Q

Define conductive hearing loss:

A

Interference in air conduction

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28
Q

What are some common causes of conductive hearing loss?

A

• Impacted cerumen
• Foreign bodies
• Benign tumors of middle ear
• Carcinoma of external auditory canal or middle ear

29
Q

What are symptoms of conductive hearing loss?

A

• Diminished hearing
• Soft speaking voice (bone conduction sound is louder)
• Better hearing in noisy environment

30
Q

What causes sensorineural hearing loss?

A

• 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
Q

Define presbycusis:

A

Age related hearing loss usually in the high frequencies.

32
Q

What is the most common form of hearing loss?

A

Presbycusis; most common in older adults

33
Q

What are some causes of presbycusis?

A

• 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
Q

What is the pathophysiology of multiple sclerosis?

A

• 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
Q
A

Destruction of myelin sheath; signals are not sent down nerve properly which leads to motor-type symptoms, weakness, slurred speech, autoimmune inflammatory disorder.

36
Q
A

Destruction of myelin sheath; signals are not sent down nerve properly which leads to motor-type symptoms, weakness, slurred speech, autoimmune inflammatory disorder.

37
Q

What is the pathophysiology of MS?

A

• 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
Q

What are MS symptoms?

A

Motor-type symptoms: weakness, slurred speech, autoimmune symptoms inflammatory disorder

39
Q

What causes Guillain-Barré syndrome?

A

A bacterial or viral infection triggers an autoimmune response (usually days or weeks after initial infection).

  • Vaccines may result in GBS
40
Q

What is the pathophysiology of GBS?

A

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
Q

What is the pathophysiology of Amyotrophic lateral sclerosis (ALS)?

A

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
Q

Symptoms of ALS:

A

• Muscle weakness
• Fasciculations (muscle twitching)
• Atrophy (muscle wasting)
• Loss of voluntary muscle control

  • Risk factors include family history
43
Q

Describe Bulbar onset disease:

A

Rapid and progressive course affecting muscles in the face and neck as well as swallowing, speech, and saliva production.

44
Q

What is the life expectancy for ALS?

A

Most commonly 3 to 5 years (death by respiratory failure)
10% live a decade or longer

45
Q

What physiology is affected by Parkinson’s?

A

The basal ganglia:
• Corpus striatum
• Globus pallidus
• Subthalamic nucleus
• Substantial nigra

46
Q

What physiology is affected by Parkinson’s?

A

The basal ganglia:
• Corpus striatum
• Globus pallidus
• Subthalamic nucleus
• Substantial nigra

47
Q

What physiology is affected by Parkinson’s?

A

The basal ganglia:
• Corpus striatum
• Globus pallidus
• Subthalamic nucleus
• Substantial nigra

48
Q

Define stage 1 cancer:

A

Confined to organ of origin

49
Q

Define stage 2 cancer:

A

Cancer that is locally invasive

50
Q

Define stage 3 cancer

A

Cancer that has spread to regional structures (ie lymph nodes)

51
Q

Define stage 4 cancer

A

Cancer has spread to distant sites (liver to lung, prostate to bone etc)

52
Q

Benign v. Malignant:
Cell Appearance

A

Benign: well differentiated
Malignant: poorly differentiated

53
Q

Benign v. Malignant:
Usual rate of growth

A

Benign: slow
Malignant: rapid w/ variability in size/shape

54
Q

Benign v. Malignant:
Vascularization

A

Benign: slight
Malignant: neovascularization through angiogenesis

55
Q

Benign v. Malignant:
Tissue structure

A

Benign: Maintained
Malignant: Changed

56
Q

Benign v. Malignant:
Ability to metastasize

A

Benign: no
Malignant: yea

57
Q

What is the hallmark pathological feature of Parkinson’s?

A

Dopaminergic deficiency in striatum, brain stem and cortex.

58
Q

What are some causes of secondary Parkinson’s?
(4)

A

Neurodegenerative and acquired disorders
• Pesticide exposure
• Heavy metals / herbicides
• Antipsychotic drugs
• Repeated head trauma

59
Q

When can we definitively diagnose Parkinson’s?

A

Post Mortem

60
Q

When can we definitively diagnose Parkinson’s?

A

Post Mortem

61
Q

What are classic motor manifestations of Parkinson’s? (Global)
(6)

A

• Pill rolling tremor
• Resting tremor
• Bradykinesia / akinesia
• Muscle rigidity
• Postural abnormalities
• Shuffling gait / side falls

62
Q

What are classic motor manifestations of Parkinson’s? (Facial)
(3)

A

• Wide - eyes / unblinking
• Smooth facial muscles
• Frequent drooling

63
Q

What is the primary role of IgA?

A

DOMINANT SECRETORY IMMUNOGLOBULIN

Prevents attachment and invasion of pathogens through mucosal membranes (GI, pulmonary and genitourinary tracts).

64
Q

Which system do migraines active?

A

Trigeminovascular system and associated changes in brain metabolism and blood flow.

65
Q

What are the neuroanatomic alterations of schizophrenia?

A

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
Q

What are the two types of immunity?

A

Innate: natural barriers and inflammation
Acquired (adaptive): humoral and antibodies

67
Q

What are the four cardinal signs of inflammation?

A

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
Q

What are the two types of adaptive immunity?

A

Humoral: B-cells produce antibodies
Cellular: T-cells (T-helper & Tc cells) - protects against cancer.

69
Q

What does viral replication rely on?

A

The ability to infect a permissive host cell.

Advanced Patho (3 decks)

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