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PHGY 350 > Final Exam Practice Questions > Flashcards

Final Exam Practice Questions Flashcards

1
Q

Which cell type is particularly susceptible to damage during chemotherapy?

a) enteric neurons
b) interstitial cells of Cajal
c) enterocytes
d) commensal bacteria
e) vascular endothelium

A

c) enterocytes

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2
Q

Diarrhea results from…

a) dysfunctional internal anal sphincter
b) increased colonic water absorption
c) enhanced colonic segmentation activity
d) all of the above
e) none of the above

A

e) none of the above

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3
Q

Hepatitis leads to…

a) infection by 3 viruses
b) increased portal pressure
c) increased lipid absorption
d) increased colonic bile salt absorption
e) none of the above

A

b) increased portal pressure

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4
Q

Which of the following is not a symptom of Thiamine deficiency?

a) ST memory loss
b) weakness
c) heart failure
d) peripheral neuropathy
e) anemia

A

e) anemia

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5
Q

Which GI pathogen produces a toxin that indirectly stimulates the CFTR Cl- channel?

a) C. difficile
b) H. pylori
c) V. cholera
d) E. coli 0157
e) Fecalibacterium prausnitzii

A

c) V. cholera

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6
Q

Which mediators have been implicated in pain due to IBS?

a) acetylcholine and histamine
b) acetylcholine and serotonin
c) GLP-1 and serotonin
d) acetylcholine and microbial proteases
e) serotonin and histamine

A

e) serotonin and histamine

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7
Q

Blocking the actions of which mediator or signaling pathway would not be expected to reduce IBD severity?

a) TNF alpha
b) IL-23
c) TGF beta
d) alpha 4 beta 7 integrin
e) JAK

A

e) JAK

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8
Q

Case 1: John - 40yo teacher has burning sensation in chest’s center. Sometimes he gets a flood of bitter tasting fluid in his mouth that burns his throat. He was on proton pump inhibitors for a while and they helped, but now his symptoms are getting worse.

What might be the cause of these symptoms?

A

Gastroesophageal reflux disease with a possible gastric ulcer

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9
Q

What regulates lower esophageal sphincter tone?

A
  • Myogenic tone e.g. its default state is contraction/closure, blocks food passage between stomach and esophagus except during a meal, belching or vomiting
  • Reflux = loss of myogenic tone
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10
Q

What are the molecular targets of drugs that inhibit acid secretion?

A
  • K+ H= ATPase (aka proton pump)
  • Histamine reception - 2 antagonist
  • Antacids provide temporary relief
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11
Q

What is a microbial cause of gastric ulceration? Describe how this microbe is thought to cause ulcers?

A
  • Helicobacter pylori (distal stomach)
  • Chemotaxis and flagellae - swims deeper into mucous and away from acid
  • Urease - converts urea to CO2 + ammonia
  • Evokes inflammatory response and release of gastrin, which causes acid secretion
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12
Q

What diseases present with diarrhea?

A
  • Infectious disease
  • IBD
  • IBS
  • Food sensitivities
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12
Q

Is weight loss more common among patients with IBS, IBD, or celiac disease?

A

IBD or celiac disease

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13
Q

What changes in motility and absorption/secretion cause diarrhea?

A
  • Increased motility reduces time for fluid absorption
  • Damage to mucosa leads to decreased fluid absorption
  • Increased water and electrolyte secretion e.g. cholera
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13
Q

Describe the pain pathways from the gut? How are gut stimuli sensed?

A
  • Sensory axons in gut lack specialized endings but can respond directly to changes in tension/inflammation - activated by release of enteroendocrine substances e.g. serotonin (pain relation)
  • Subset of DRG neurons respond to noxious stimuli e.g. nociceptors
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13
Q

What are the causes of these 3 diseases: celiac disease, IBD, and IBS?

Are there differences in the parts of the GI tract affected? Are there systemic manifestations?

A

Celiac disease - small intestine
- Autoimmune inflammation following injection of BROW
- Systemic manifestations (rash)

IBD - any part of GI tract (mouth to anus)
- Autoimmune disease (not quite - more like chronic inflammation)
- Systemic manifestations

IBS - small and large intestines
- Functional disorder (no obvious tissue damage)
- Other pain syndromes, anxiety and depression (associations not necessarily result of IBS)

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14
Q

True of False? We have >800 billion cells in our brain

A

True

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15
Q

True or False? Brain messages travel as fast as 400km/hour

A

True

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16
Q

True or False? We only use 10% of our brain

A

False

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17
Q

True of False? Once we reach adult age, our brain’s structure does not change anymore

A

False

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18
Q

True or False? A spermaceti whale has the largest brain in the world

A

True

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19
Q

What is the main excitatory NT?

A

Glutamate

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20
Q

What is the main inhibitory NT?

A

GABA

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21
Q

What are the 3 types of pain?

A
  1. Cutaneous - shock, trauma, burn
  2. Somatic - tendon, muscle, joint
  3. Visceral - organs
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22
Q

What is allodynia?

A

Pain triggered by a stimulus that is normally painless e.g. sunburn

  • Clinically important due to inability to do daily dask e.g. getting dressed
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23
Q

What is hyperalgesia?

A

Increased pain to painful stimulus e.g. hammer

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24
Q

What is the resting potential of neurons?

A

-60 to -80mV

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25
Q

What type of nerve fiber is the main nerve transmitting pain?

A

C (mechanical, thermal, and chemical pain) - non-myelinated (smallest diameter and slowest conduction speed)

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26
Q

What are the 3 main receptors of glutamate?

A
  1. AMPA receptor
  2. NMDA receptor - blocks MG pore so AMPA signals
  3. Metabotropic receptor (GPCR)
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27
Q

Afferent neuron - transfer info. orthodromic vs antidromic way?

A

In general afferent - ascending pathway = periphery to brain

Orthodromic - periphery to brain
Antidromic - brain to periphery

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28
Q

What does the term “sprout” mean?

A

Lamina III grow into Lamina II = pain sensation (consq. = touch perceived as painful)

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29
Q

What are the steps for neuro-immune interaction?

A
  1. Tissue damage (cut skin)
  2. Significant cell death (local)
  3. Immune cell influx
  4. Activation of immune cells
  5. Releases pro-inflamm mediators
  6. Activation and sensitization of sensory fibers
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30
Q

What is gate theory?

A
  • Beta sensory fibers inhibit C fibers
  • Massage sore area
    E.g. phantom limb (touching does not change level of pain due to massive A-B fiber sprouting)
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31
Q

How is acupuncture related to this course?

A
  • Stimulates A beta and A alpha fibers (activates inhibitory neuron in spinal cord like rubbing)
  • Releases GABA (explains acute effect)
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32
Q

What is pain?

A

Not a stimulus but an experience - interpretation of the brain

*Expression of an unpleasant sensory and emotional experience involving existing or potential tissue damage

  • # 1 MD consultation
  • Acute = danger detection
  • Can be chronic = pathology
  • Precise location, emotion, and context dependent
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33
Q

What are the stages of pain transmission?

A

Transduction: Conversion of painful stimuli into electrical impulses by sensory receptors.
- Coding to be routed in poterior horn of spinal cord

Transmission: Conduction of these impulses along nerves to the spinal cord and brain.
- Marrow to thalamus

Modulation: Regulation of pain signals in the spinal cord and brain, either amplifying or dampening them.
- Plasticity - local and central sensitization/negative feedback pathway

Perception: Processing of the impulses in the brain, resulting in the conscious experience of pain.
- Brain - emotional component

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34
Q

What are pain receptors?

A

Also known as nociceptors - specalized sensory receptors detecting potentially harmful stimuli and transmit signals to brain, resulting in perception of pain.

E.g. ionoceptors (ion channels nociceptors) and GPCR (metabotropic nociceptors)

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35
Q

What’s the difference between NT and NP?

A

NT - small, fast synaptic transmission - rapid signaling
- Synthesized and stored in synaptic vesicles within the presynaptic neuron, released into the synaptic cleft, and bind to receptors on the postsynaptic neuron

NP - large (AA chains), slower signaling
- Synthesized as larger precursor molecules in the cell body, transported to the axon terminals, and released along with NT

36
Q

What is neurogenic inflammation and an example of neuroimmune interaction?

A

Triggered by sensory nerve activation, leading to the release of neuropeptides and subsequent inflammation.

E.g. migraines - contributes to pain and other symptoms through vasodilation and immune cell recruitment

37
Q

What is pain synapse plasticity?

A

Ability of synapses in NS involved in pain processing to undergo changes in structure and function.
- Signicant role in development and maintence of chronic pain by altering sensitivty pain pathways and contributing to amplification

38
Q

What is a feedback mechanism - in the context of pain (central inhibition)?

A
  • Body’s ability to regulate pain signals within CNS (when excessive or unecessary)
  • Modulate or inhibit signals through a variety of mechanisms, e.g. releasing NT like endorphins or activating descending inhibitory pathways)
  • Maintain homeostasis
39
Q

What is the placebo effect? What is released during this process?

A

Taking medication or vehicle activates periaqueductal gray matter neuron
- Release glutamate to activate neurons
- Activates descending nerve fibers in spinal cord
- Release of opioid and adrenaline blocking neuronal activity

NOTE: Pts with more pain are more likely to respond to placebo effect

40
Q

What is the stress paradox?

A

Very high stress situation - e.g. injured soldiers or athletes who do not feel pain for awhile

  • Stress leads to activation of descending pain pathways
  • Local opioid release in dorsal horn of spinal horn
  • Activates pre- and postsynaptic mu (Gi/o) receptor
  • AMP/c production block
  • Decreased neuronal activation
41
Q

What are the accessory digestive organs?

A
  • Salivary glands
  • Exocrine pancreas
  • Liver (gall bladder)
42
Q

List the parts of the small intestine from most to least distal.

A

Ileum, Jejunum, Duodenum

43
Q

What does the esophagus connect?

A

Pharynx to stomach

44
Q

Where do most gut cells arise?

A

Myenteric plexus

45
Q

Difference between afferent and efferent neurons?

A

Afferent - sensory signals from intestine
Efferent - autonomic nervous system (parasymp and symp)

46
Q

Difference betweem parasympathetic and sympathetic NS?

A

Parasymp - rest and digest (Para for peaceful process)
Symp - fight or flight (decreased BS)

47
Q

What is the largest interface between the body and the outside world?

A

Mucosal surface

48
Q

Where does the majority of absorption occur in the GI tract?

A

Small intestine

49
Q

How are the liver and gall bladder realted to bile?

A

Liver - produces and secretes bile
Gall bladder - stores and concentrates bile - releases into duodenum in response to meal (x5 more concentrated here)

50
Q

What is the motility of the GIT regulated by?

A

ENS and interstitial cells (in between other cells) of Cajal (all along gut)

51
Q

What is segmentation?

A

Contraction of circular muscle in order to mix food without propelling food along GIT - SQUISHES (mix with enzymes during digestion)

52
Q

What is peristalsis?

A

Corrdinated contraction of circular and lingutudinal muscle to propel food down GIT

53
Q

What is the process of vomiting?

A
  • Glottis closes
  • LES relaxes
  • Reverse perisatlatic waves
  • Abdominal msucles contract
54
Q

What happens during LES contraction and relaxation?

A

Contraction - Occurs after swallowing, prevent stomach acid and contents from flowing back up (reflux)

Relaxation - Occurs when swallowing food or liquids (allows to pass from esopahgus to stomach)

55
Q

What is jaundice caused by?

A

Liver inflammation (dysfunction/damage) or gallbladder dysfunction
- High blood levels of bilirubin

56
Q

What are the 2 functions of the pancreas?

A
  1. Exocrine secretion of enzymes and bicarbonate (food digestion)
  2. Endocrine secretion of insulin, glucagon, and somatostatin
57
Q

What are the 4 main modalitites of the somatosensory system?

A
  • Touch
  • Propioception
  • Thermal sensation
  • Pain
58
Q

What are the 2 main physiological roles of pain?

A
  • Danger detection
  • Avoid/escape (survival)
59
Q

What is nociception versus pain?

A

N - Biochemical process allow you to detect danger - process info

P - perception/emotional experience of detection

60
Q

What are the origins of chronic pain?

A

Idiopathic - no known cause
Inflammatory - tissue damage
Neuropathic - nerve damage

61
Q

What does local cell death cause?

A

Activation of sensory neurons - immune cells

62
Q

Give an example of cutaneous, somatic, and visceral pain.

A

C - cut or burn
S - sprain
V - heart attack

63
Q

Give a few examples of inflammatory pain.

A

Stretching, twisting, bruising (back pain), arthritis, cancer, migraine

64
Q

Give a few examples of neuropathic pain.

A

Post-herpetic neuralgia, diabetic neuropathy, phantom limb pain

  • Nerve damge and immune cell influx
65
Q

What do each of the following innervate: lumbar (DRG), inf. vagud nerve (ND), and trigeminals (TRG)

A

DRG - skin
ND - viscera and organs
TRG - face

66
Q

What are ion channels sensitive to?

A

Heat, cold, chemical moelcules, amd pressure - can also detect bacteria

67
Q

Is wasabi an example of TRPA1 (chemical) or TRPV1 (heat)?

A

TRPA1

68
Q

What is the consequences of phosphoyrlating ion channels of sensory neruons?

A

Lower activation threshold - easier to activate and generate pain (RTK)

69
Q

What are the non-painful receptors?

A

Mechanoreceptors
Thermoreceptors
Propioceptors

70
Q

Where does the transmission stage of pain direct information to and from?

A

Periphery to brain (afferent)

71
Q

List the transmisssion nerve fibres in order of largest/fastest to slowest/smallest.

A

A-alpha, A-beta, A-delta, C

72
Q

What is another name for a neuropeptide?

A

Neuromodulator (activates GPCRs)

73
Q

What is GABA’s precursor?

A

Glutamate

74
Q

What are the signs and symptoms of inflammation?

A

pain, redness, heat, edema, loss of function

75
Q

What are the 4 steps of the local response of neurogenic inflammation?

A

1) activation of sensory fibers (e.g. cut)
2) activates capillaries - vasodilation, increased BP
3) chemotacis of immune ceels (increased influx)
4) extravasation of immune cells near nerve endings

76
Q

What are the 5 causes of central sensitization?

A

1) reduction in effectiveness of inhibitory synapses (GABA)
2) new synapses between A B fiber and C fiber - “sprout”
3) A B fiber de novo expresses inflammatory mediators
4) overexpression of new ion channels
5) genesis of ectopic discharge

77
Q

What can you do to help stop allergic reactions?

A
  • Block cyotkine receptor on nerve
  • Block peptide receptor on T cells
  • Block nerve
78
Q

What does IL-10 always block?

A

Block inflammation - type of M2 microglia

79
Q

List examples of M1 microglia that are pro-inflammatory.

A

IL-1 B, IL-6, TNF alpha

80
Q

List some neuroendocrine effects.

A

Glucocorticoid - blocks immune cells
Catecholamine - hypertension
Decreased ghrelin - decreased appetitie
Decreased melatonin - difficulty sleeping
Decreased Insulin - glucose intolerance (diabetic)

81
Q

What is the purpose of acute pain?

A

Warn the host - defend from danger (use reflex arc)

82
Q

Why does chronic pain occur?

A

Chronic activation of nerve fibers - not supposed to happen (negative consequence)

83
Q

Does active inflammation occur within IBD or IBS?

A

IBD

84
Q

What type of NT is released in the LES?

A
  • Major inhibitory (relaxatory) NT released in LES = nitric oxide gas
85
Q

What senses are the nonpainful: mechanoreceptors, thermoreceptors, and propioceptors involved with?

A

Mechanoreceptors - touch, light pressure
Thermoreceptors - warm cold
Propioceptors - change in length and tension of muscles

86
Q

Waking during night is common with IBS or IBD?

A

IBD

87
Q

Is pain more often relieved after bowel movements for patients with IBS or IBD?

A

IBS

88
Q

What is oily and undigested stool related to?

A

celiac/Crohn’s ileitis

89
Q
A
90
Q

What can a pain synapse plasticity occur in response to?

A

Various stimuli: injury, inflammation, chronic pain

91
Q

Can you match dorsal horn and ventral horn with antidromic/orthodromic afferent neurons?

A

Orthodromic - periphery to brain (dorsal horn)
Antidromic - brain to periphery (ventral horn)

PHGY 350 (4 decks)

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