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General Med 1 > Physiology - Exam 3 and 4 > Flashcards

Physiology - Exam 3 and 4 Flashcards

1
Q

What are the major classes of plasma lipids?

A

a) Cholesterol
- synthesized from acetyl-CoA
- structural role in membranes
- precursor for:
- bile salts
- steroids
- vitamin D
- Exogenous – dietary
- Endogenous – formed in liver

b) triglycerides
- glycerol + 3 FAs
- storage and transport form of energy
- fat deposits – insulation, protection

c) phospholipids
i. Lecithins
ii. Cephalins
iii. Sphingomyelins
- glycerol + 2 FAs
- membranes, lipid transport, nerve, cell signaling, thromboplastin

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2
Q

What are the 3 options for triglycerides once absorbed through GIT?

A
  • storage in liver
  • adipose tissue
  • used as fuel
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3
Q

What are the major classes of lipoproteins and what are their characteristics?

A

Exogenous pathway:

  1. chylomicron
    - TG rich
    - t1/2: 5-30 mins
    - Apo-B48
  2. CM remnants

Endogenous:

  1. VLDL
    - TG rich
    - t1/2 – 12 hrs
    - Apo-B48 and Apo-B100
  2. IDL
  3. LDL
    - main carrier of cholesterol from liver to tissue
    - t1/2 – 3 days
    - Apo-B100
    - atherosclerosis

Reverse cholesterol transport:

  1. HDL
    - 50% protein, little TGs
    - t1/2 – 5-6 days
    - ApoA-1 is major apo
    - protects against atherosclerosis
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4
Q

What is a chylomicron?

A
  1. lipoprotein complex that carries lipids from SI through circulation
  2. large (75-1,200 nm)
  3. Composition:
    - apoproteins
    - phospholipids
    - triglycerides (85%)
    - cholesterol, cholesterol esters
  4. Composition modifies as they mature in the blood stream
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5
Q

How are lipids absorbed?

A
  1. dietary lipids absorbed by small intestine
  2. bile secreted into the SI lumen
  3. Contains bile salts and lecithin (phospholipid) which emulsify lipids and create much smaller droplets.
  4. Absorbed by intestinal cell
  5. Transported into blood stream by chylomicron
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6
Q

What is the chylomicron lifecycle?

A
  1. Nascent chylomicron:
    - created by SI enterocytes
    - exocytosed into lacteals (SI lymphatic vessels) then secreted into bloodstream (thoracic duct)
  2. Mature chylomicron (circulating)
    - HDL donates Apo-CII and Apo-E (apoproteins)
    - Apo-CII is the cofactor for lipoprotein lipase (in capillary lumen)
    - Lipoprotein lipase empties TGs from circulating CMs – muscle, adipose tissue
  3. Chylomicron remnant – once TG stores are distributed
    - CM returns Apo-CII to HDls
    - now only 30-50nm
    - endocytosed and broken down by liver. Anything left over can be stored in the liver

EXOGENOUS PATHWAY
Density is increasing as lipids unloaded
T1/2 = 5 mins

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7
Q

What is the endogenous pathway?

A

Liver – LDL – IDL – LDL: goes from liver to tissues
HDL – goes from tissues to liver

LDL t1/2 – 1-2 days
HDL t/12 – 5-6 days
Therefore if someone is fasting, you can measure LDL and HDL levels.

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8
Q

What are apoproteins?

A

Basically signaling molecules on outside of these lipoprotein complexes

  1. maintenance of lipoprotein structure
  2. regulate lipoprotein metabolism
  3. cofactor for enzymes of lipid metabolism
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9
Q

*What are 5 of the different apoproteins and what do they do?

A
  1. Apo-CII
    Lipoprotein: HDL, CM, VLDL, IDL
    Function: Cofactor for lipoprotein lipase
  2. Apo-E
    Lipoprotein: HDL and remnants
    Function: Ligand for LDL receptor
  3. Apo-B100
    Lipoprotein: VLDL, LDL
    Function: Synthesized in the liver; ligand for LDL receptor
  4. Apo-B48
    Lipoprotein: CM and remnants
    Function: Synthesized in intestine, receptor-binding domain is absent, so it can target areas without actually binding to receptors
  5. Apo-Al
    Lipoprotein: HDL
    Function: Enzyme activator (LCAT), reverse cholesterol transport
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10
Q

What are both CMs and VLDLs rich in?

A

Triglycerides

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11
Q

What is the only apoprotein in LDLs?

A

Apo-B100

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12
Q

What are LDL levels strongly associated with?

A

Atherosclerosis. They have a very long half-life and they are the main carrier of cholesterol from liver to tissue.

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13
Q

Why do HDLs solve the problems of LDLs?

A

Clean up damage. They reverse cholesterol transport and take it back to liver. Protects against atherosclerosis.

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14
Q

What is the VLDL/LDL lifecycle?

A
  1. VLDL synthesized in liver
    - loaded with TGs, cholesterol, PLs
    - Apo-B100
    - secreted directly into circulation
    - modified: addition of Apo-E and Apo-CII from HDLs
  2. VLDL – IDL – LDL in circulation
    - Apo-CII activated Lipoprotein Lipase (LPL)
    - TGs removed by LPL present on tissue cells
    - as TGs decrease, density increases
    - modified: removal of apo-E and apo-CII to HDLs
  3. LDL removal
    - apo-B100 receptor-mediated endocytosis (liver, tissues)
    - lysosomal degradation – deposits cholesterol
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15
Q

The LDL receptor pathway


A
  • LDLs express apo-B100, a ligand for the LDL receptor
  • When there is binding – endocytosis. Endosome of entire LDL
  • Endosome – lysosome – FA’s, amino acids and cholesterol extracted
  • This feeds back onto our body’s own cholesterol synthesis – if we are getting enough from this mechanism we don’t need anything else. It also switched off expression of LDL receptors.
    - It inhibits the HMG-CoA reductase pathway
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16
Q

/Why is LDL such a problem?

A
  • packed full of cholesterol and circulating for days
  • oxidise readily
  • taken up by macrophages in artery walls
  • damage to endothelium and underlying smooth muscle
  • restricted blood flow, increased BP, endothelial dysfunction
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17
Q

/What factors contribute to the accumulation of LDL?

A
  • LDL receptor saturation
  • Familial hypercholesterolaemia – defective/absent B/E receptors
  • Familial defective ApoB:ApoB100 mutation
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18
Q

What is the HDL lifecycle?

A
  1. Lipid-poor or nascent HDL disc structures

    - secreted by liver and intestine (CM/VLDL biproduct)
  2. HDL discs pick up lipids from peripheral cells (via ABCA1)
  3. Lipid-loaded discs are converted to mature plasma HDL by 
LCAT (lecithin cholesterol acyltransferase: C - CEs)
  4. CEs transferred to other lipoproteins (via CETP)
  5. Taken up by liver via HDL receptor (SR-B1)
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19
Q

/What are normal cholesterol ranges?

A
  • Total: 1

- LDL/HDL ratio

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20
Q

*What is large fibre sensory neuropathy?

A

Large fibers are fast.

Elderly patients-poor postural control, high likelihood of falls. Extreme cases have great difficulty in moving. Muscle strength normal

Degeneration of mechanosensitive myelinated nerve fibres from muscles and joints deprives motor control systems of information about joint and limb position

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21
Q

Explain stimulus features encoded by sensory system


A

a) Modality
- specific sense that we can perceive
- light, sound touch, pain, heat, cold, smell, taste, sense of limb position

b) Spatial information
- body location for touch and pain
- location in external space for light and sound

c) Intensity
- threshold (minimum detectable intensity)
- perceived strength above threshold

d) Quality
- i.e. colour, sharpness of pain, pitch of sound etc

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22
Q

In terms of modality, what forms of stimulus energy can actually be detected?

A
  1. Mechanical - sense of touch, limb position, hearing, balance etc.
  2. Chemical - taste, smell
  3. Photic - vision
  4. Thermal - sense of hot and cold
  5. Noxious – pain. Also a function of overcooking any of the other senses

There are specific sensors for each sense.

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23
Q

Explain detection and transmission of sensory stimuli


A

Sensory receptors – specialized cells that generate graded potentials called receptor potentials in response to a stimulus.

5 major types:

  1. mechanoreceptors
  2. thermoreceptors
  3. photoreceptors
  4. chemoreceptors
  5. nociceptors
Sensory transduction (conversion of one type of stimuli to another):
-	receptors transform external signal to membrane potential

What are the two types of sensory receptor cells?

  • nerve cell
  • a specialized cell + afferent neurone
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24
Q

Discuss the ‘labeled line’ concept of sensory transmission

A

Each sensory nerve fibre transmits only one modality of sensation to a specific location.

Receptor does not dictate what the brain will understand, the location of the afferent nerve does.

Action potentials in labeled lines generate specific sensory perception

If a pain fibre is stimulated, you will perceive pain no matter what type of stimulus excites the fibre.

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25
Q

Explain encoding of sensory stimulus intensity

A

Stimulus intensity is encoded by action potential firing rate.

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26
Q

Understand that the somatosensory cortex has a topographic map

A

x

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27
Q

Describe the Ascending sensory pathways:

A
  1. Dorsal column-medial lemniscal pathway
    - large fibers (30-110 m/s)
    - more special organization
    - decussation (crossing over) occurs later
  • localized tough
  • fine grade tough
  • vibration
  • movement against skin
  • joint position
  • fine pressure
  1. Anterolateral pathway
    - Thinner fibers (
28
Q

List the classification of somatic senses.

A

Somatic sensation from skin, muscles bones, tendons and joints.

  • Tactile sense (touch, pressure, vibration, tickle)
  • Temperature (warm, cold)
  • Propriocept (static position, rate of movement)

Initiated by a variety of somatic receptors:

  • mechanoreceptors
  • thermoreceptors
  • nociceptors
29
Q

*What are the somatosensory receptor types in the skin?

A
  1. Free nerve endings
    - pain, warm, cold
    - slow adapt
    - Aδ or C fibers
  2. Meissner’s corpuscle
    - sensitivity to light touch, especially finger pads, spatial characteristics
    - rapid adapt
    - Aβ fibers
  3. Expanded tip Receptors (Merkel’s Disks)
    - continuous touch
    - slow adapt
    - Aβ fibers
  4. Pacinian Corpuscle
    - deep pressure, vibration
    - Rapid adapt
    - Aβ fibers
30
Q

What determines stimulus duration?

A
  1. Rapidly adapting receptor (phasic)
    - neurones respond poorly to steady stimuli, but very well to dynamic
  2. Slowly adapting receptor (tonic)
    - neurones detect continuous stimuli, but not dynamic
31
Q

*First order neuron determines whether conduction is fast or slow. What are the primary afferent axons and their details?

A
  1. Aα
    Diameter (um): 13-20
    Speed (m/s): 80-120
  2. Aβ
    Diameter (um): 6-12
    Speed (m/s): 35-75
  3. Aδ
    Diameter (um): 1-5
    Speed (m/s): 5-35
  4. C
    Diameter (um): 0.2-1.5
    Speed (m/s): 0.5-2
32
Q

What causes stimulus acuity?

A

Ability to distinguish between two spatially separate stimuli

Depends on:

  • density of peripheral receptors
  • size of receptive fields
  • central convergence and lateral inhibition

Lateral inhibition restricts spatial spread of excitation as dominant neuron suppresses neighbors.

33
Q

How are mechanosensitive neurones stimulated?

A

Stretch activated ion channels – stimulated when muscle stretched

34
Q

What are the types and ranges of thermoreceptors?

A
  1. Warm receptors
    - 30-45 degrees
  2. Cold receptors
    20-35 degrees
35
Q

What are the positional sense receptor types?

A
  1. Golgi tendon organs
    - compression, stretch
    - joint position, reflex response to over flexion
    - rapid adapt
    - Aα/Aβ fibers
  2. Muscle spindles
    - compression, stretch
    - rate of change and muscle stretch
    - rapid or slow (for posture)
    - Aα/Aβ fibers
  3. Pacinian corpuscles and Ruffini’s endings in Joint capsule
36
Q

Define analgesia, hyperalgesia and allodynia.

A

Analgesia:
- pain relief and/or attenuation

Hyperalgesia:

  • normal response
  • sensitization: enhances sensation to noxious stimuli following injury
  • stimulus provided by noxious mechanical, thermal or chemical input

Allodynia:

  • abnormal response
  • sensitization: abnormal response to touch
  • caused by lesions or trauma to nerve or CNS
37
Q

Broadly speaking, what are the two types of pain?

A
  1. Somatogenic
    - pain with cause
    - localized in body tissue
    a) nociceptive pain
    b) mixed type
    b) neuropathic pain (similar to allodynia)
  2. Psychogenic
    - no known physical cause but processing of sensitive info in CNS disturbed
38
Q

Describe the types of somatogenic pain.

A

a) Nociceptive
- caused by activity in neural pathways in response to potentially tissue-damaging stimuli

b) Mixed type
- combo of primary injury and secondary effects

c) Neuropathic
- initiated or caused by primary lesion or dysfunction in the nervous system
- no stimulation of nociceptors but something has gone wrong higher up so you perceive pain the same as you would for nociceptive pain.

39
Q

What are the various classes of pain?

A

a) Mechanical – pricking, stabbing, pinching
b) Thermal – burning, freezing
c) Chemical – aching, stinging, soreness
d) visceral – actually chemical and mechanical

40
Q

What are the 3 categories of pain perception?

A
  1. Fast Pain
    - sharp and well localized
    - transmitted by myelinated axons (Aδ fibers)
    - neurotransmitter = glutamate
    - extremely rapid acting
    - very short duration (milliseconds)
  2. Slow Pain
    - dull aching sensation, not well localized
    - transmitted by unmyelinated axons (C fibers)
    - Neurotransmitter: Substance P
    - slower acting
    - long duration (minutes to hours)
  3. Visceral
    - very poorly localized
    - referred pain
41
Q

Describe mechanical nociceptors.

A
  • specialized for painful mechanical stimuli
  • NS: nociceptive specific
  • Aδ fibers
  • Glutamatergic
  • Excited by strong pressure, pinch or squeezing
  • Mediate pain from skeletal muscle of viscera due to excessive stretch or contractile force
  • Most respond to noxious heat (T>45)
42
Q

What types of chemicals do nociceptors respond to?

A

a) Exogenous chemicals that penetrate skin

b) Intracellular molecules released by cell injury
- cations (K+, H+]
- peptides, neurotransmitters
- prostaglandins, histamine, bradykinin

c) Pathological substances released by diseased tissue

d) Toxins
- microorganisms, insect bites, venom

43
Q

What are polymodal nociceptors?

A
  • nociceptors that respond to thermal, chemical and mechanical stimuli
  • C fibers
  • Glutamate and/or Substance P
  • Express multiple receptors
44
Q

/How does tissue damage and inflammation stimulate nociceptors?

A
  • NGF
  • Bradykinin
  • Serotonin
  • ATP
  • H+
  • Lipids
  • Heat
  • Pressure
45
Q

/What signals sensitize nociceptors to low-threshold nociceptors?

A
  • Bradykinin
  • Serotonin
  • H+
  • Norepinephrine
  • Histamine
  • K+
  • Prostanoids
  • Purine
  • Interleukins
  • TNF
  • Neuropeptides
  • Leukotrienes
46
Q

What are the names of the fast and slow pain tracts?

A

Neospinothalamic tract: Fast, Sharp

Paleospinothalamic tract: Slow, Burn

47
Q

Describe the Neospinothalamic tract.

A
  • Aδ fibers synapse with neurons in Lamina 1 of the dorsal horn
  • 2nd order neurones decussate immediately
  • ascend anterolateral spinothalamic tract to brainstem
  • carries info to:
    o midbrain
    o thalamus
48
Q

Describe the Paleospinothalamic tract.

A
  • C fibers synapse with neurons in Lamina 2 and 3 of dorsal horn
  • Project to lamina 4
  • 2nd order neurones decussate
  • ascend anterolateral spinothalamic tract to brainstem
  • much more emotional and long term learning about pain – aversion to pain learnt
  • reticular formation
  • carries info to
    o pons
    o limbic system
    o mid brain
    o PAG
49
Q

/Where are different aspects of pain experienced in the brain?

A
  • pain locatization: somatosensory cortex
  • sensation: dorsal insular cortex
  • emotion: enterior cingulate cortex
  • body physical response and subjective memory: Hippocampus and limbic cortex
50
Q

Describe the efferent analgesic system.

A

Inhibits afferent pain signals.

  • pain afferents stimulate neurons
  • activates descending anti-nociceptive pathways transmitted through the spinal cord to the dorsal horn
  • analgesic neurotransmitters released
    o serotonin, noradrenaline
    o enkephalins - opioids
    o endorphins – opioids
  • inhibit or block transmission of nociceptive signals
51
Q

What are the endogenous opioid peptides?

A
  1. leucine-enkephalin
  2. methionine-enkephalin
  3. β-endorphin
  4. dynorphin
52
Q

What is the theory of pain suppression in the dorsal horn level?

A

Gate-Control theory

  • Pain can be suppressed in the dorsal horn level
  • ‘gate’ = inhibitory interneuron
  • Normally, inhibitory interneurons inhibit ascending pathways for pain
  • Fibers from nociceptors synapse on the inhibition interneuron
  • When activated, the fibers override the interneurons inhibition, pain travels to the brain
53
Q

What is lateral inhibition?

A
  • lateral inhibition from sensory fibers activate inhibitory interneurons
  • if both pain stimulus and non-pain stimulus arrive at the same time, there will be partial inhibition of pain transmission
54
Q

What are some interventions that can be used to control pain?

A
  1. Opiates
    - act centrally by inhibiting neurotransmission of afferent neurones
  2. A2-adrenergic antagonists – i.e. Clonidine
    - act centrally
    - stimulate endogenous anti-nociceptive neurones
  3. Local anaesthetics
    - block action potential conduction in nociceptive nerve fibers
    - i.e. ion channel inhibitors (i.e. lidocaine)
  4. Anti-inflammatory drugs + aspirin
    - can reduce hyperalgesia and allodynia
    - blocks prostaglandin production

Drugs acting on brain:

  • opioids
  • a2-adrenergic antagonists

Drugs acting at dorsal horn:

  • opioids
  • a2-adrenergic antagonists
  • local anesthetics

Drugs acting on peripheral nerve:
- local anesthetics

Drugs acting on site of trauma:

  • local anesthetics
  • anti-inflammatory drugs
55
Q

What is congenital analgesia?

A

Nociceptive stimuli are not processed and/or integrated at a level of brain (patient does not feel pain)

56
Q

What is congenital sensoric neuropathy?

A

Nociceptive signals are not transmitted by peripheral nerves or by spinal afferent tracts (patient does not feel pain)

57
Q

What are the sub-modalities of somatosense?

A
  • touch
  • pressure
  • vibration
  • pain
  • temperature
58
Q

What is the threshold for discrimination of two simultaneously applied touch stimuli?

A

Threshold for two-point discrimination can be taken as the distance between the points of the stimuli for which the subject just felt two points of contact. In other words, the smallest distance between two points that still results in the perception of two distinct stimuli.

59
Q

Why is the threshold for two-point discrimination lower in the index finger than in the back?

A

Two factors:

  • receptor density
  • size of receptive fields

In terms of receptor density, the receptors must be packed closely enough so that a probe stimulates one or more of them.
In terms of the size of the receptive fields, two-point discrimination requires that neighboring receptors be connected to different CNS neurones. For a given neurone, the less receptors it is connected to, the smaller the receptive field (i.e. the smaller the area of skin it receives information from).

Fingertips have higher receptor density and the neurones have smaller receptive fields.

Examples:
Fingertips: 2-3mm
Arm and back: 35-40mm

60
Q

Why are some spots on the skin particularly sensitive to thermal stimulus whereas others are not?

A

This illustrates the discreet nature of cutaneous sensation.

The cold and warmth receptors are located immediately under the skin at discrete separated spots. In most areas of the body, there are 3 to 10 times as many cold spots as warmth spots, and the number in different areas of the body varies from 15 to 25 cold spots per square centimeter in the lips to 3 to 5 cold spots per square centimeter in the finger to less than 1 cold spot per square centimeter in some broad surface areas of the trunk.

61
Q

What are the 4 classes of peripheral receptors contributing to the sense of kinaesthesis (our sense of limb position and movement)?

A
  • joint receptors
  • tendon organs
  • muscle spindles
  • skin receptors
62
Q

What is proprioception?

A

Information arising from only the joints, tendons and muscles

63
Q

How is the angle of the joint and the speed of movement detected?

A

If a joint is passively flexed, the receptors on the extensor side are stretched and their firing rate increases, while the receptors on the flexor side are unloaded. This change in receptor activity is the basis for the detection of the angle of the joint, and the speed of the movement.

If a joint is actively flexed, the receptors on the extensor side are stimulated in essentially the same way as in the passive situation; however, the muscle spindles (through gamma efferent activity), tendon organs and joint receptors on the flexor side are now loaded owing to the active muscular contraction. Hence in the active situation, the receptors around a joint can detect the angle of the joint and the speed of movement.

64
Q

What is kinaesthetic acuity?

A

The accuracy with which an individual can detect change in joint angle

65
Q

What is kinaesthetic perception and memory?

A

This refers to how well the individual can interpret perceived kinaesthetic information and how efficiently that information is encoded and stored for later use.

General Med 1 (24 decks)

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