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SEM2 > BIOL1080 midterm #2 (7-14) > Flashcards

BIOL1080 midterm #2 (7-14) Flashcards

1
Q

Direct communication mechanisms of intercellular communication

A

gap junctions, membrane (tunnelling) nanotubes, mechanosignals

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2
Q

Indirect communication mechanisms of intercellular communication

A

chemical messengers

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3
Q

Explain the use of connexons for gap junctions in direct intercellular communication

A
  • The subunits that form a gap junction
  • Pore size is very small
  • Permits passage of sugars, amino acids, & ions between cells i.e. metabolic & electric exchange
  • Found in virtually all cells except mature skeletal muscle
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4
Q

Explain the use of intercalated disks for gap junctions in direct intercellular communication

A
  • Type of gap junction in cardiac muscle
  • Allows for rapid & coordinated propagation of action potentials for rhythmic contractions
  • Smaller than connexons
  • Can be acutely regulated (activated/deactivated) by phosphorylation/ dephosphorylation
  • Phosphorylation causes a cascade, allowing bands to open
  • Inside of muscles
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5
Q

Explain membrane nanotubes in direct intercellular communication

A
  • Formed from the plasma membrane
  • Longer than gap junctions & have a larger pore diameter
  • Transfer of nucleic acids & even small organelles between cells
  • Might be a way to transfer cellular components from stressed to healthy cells
  • Microscopic bridge/tunnel
  • Healthy cell generally sends to stressed cells (but could also send to a healthy cell)
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6
Q

Explain mechanosignal transduction of direct intercellular communication

A
  • Conversion of mechanical stimuli into a cellular response
  • Direct physical stress to cells eliciting a chemical or metabolic response
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7
Q

Give some examples of mechanosignal transductions

A
  • hearing: Conversion of a soundwave into an electrical signal
  • Pulsatile & shearing stresses from blood flow on arterial endothelial cells
  • Mechanical stress to muscle fibers from weightlifting resulting in increased protein synthesis
  • Remodeling of bone & cartilage through physical stresses (such as weight lifting)
  • Conversion of pressure on skin into a neural (electrical) impulse
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8
Q

Elaborate on this example of mechanosignal transductions: Pulsatile & shearing stresses from blood flow on arterial endothelial cells

A
  • Can induce formation of new blood vessels
  • If excessive, mediates vascular inflammation & progression of atherosclerosis
  • frictional force generated by blood flow in endothelium
  • cells receive force from blood rushing through blood forces
  • fast blood flow helps cells survive turn over and align in blood flow direction
  • healthy strong blood flow is good for cells
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9
Q

What are the 4 types of chemical messengers in indirect intercellular communication (and identify the 3 main ones)

A

MAIN: paracrine signalling, neurotransmitters, hormones
4. neuroendocrine signalling

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10
Q

Why is autocrine not labelled directly as a chemical messenger in indirect intercellular communication (and what is it)

A
  • considered more of direct communication
  • when a messenger acts back on the cell that produced the chemical messenger
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11
Q

Explain paracrine signalling of chemical messengers of indirect intercellular communication

A
  • Acts on a nearby cell
  • Clotting factors, growth factors e.g. estrogen (promotes ovary maturation)
  • Many secreted hormones can act in both a paracrine & endocrine manner
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12
Q

Explain neurotransmitters of chemical messengers of indirect intercellular communication

A
  • Synapse is a short distance
  • Neurotransmitter signal must be tightly controlled
  • Not too many molecules released
  • Need an auto shutoff (reuptake or degradation)
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13
Q

Explain hormones of chemical messengers of indirect intercellular communication

A

Can be water or lipid- soluble
* Must cross membranes
* Have target (receptor) specificity

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14
Q

Describe what hydrophilic hormones are (in reference to chemical messengers of indirect intercellular communication)

A
  • E.g. insulin, epinephrine, serotonin
  • Typically stored in secretory cell
  • Dissolves in plasma i.e. no need for carrier
  • Generally secreted by fusing secretory vesicles to membrane & releasing (exocytosis)
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15
Q

Describe what hydrophobic hormones are (in reference to chemical messengers of indirect intercellular communication)

A
  • E.g. steroid & sex hormones (estrogen, testosterone, cortisol)
  • Storage typically more limited (i.e. made on demand)
  • Cannot dissolve in plasma i.e. needs a carrier
  • No issue crossing a lipid membrane
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16
Q

What is response based on?

A

receptor specificity

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17
Q

Explain receptor specificity

A
  • Cells express many different types of receptors
  • There may be hundreds or thousands of a given receptor type on
    a cell surface (i.e. amplification)
  • Amount of a receptor is controllable i.e. can be up- or down- regulated
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18
Q

Where do hydrophilic chemical messengers bind and what is the goal of the attachment?

A
  • to cell surface (plasma membrane) receptor
  • Alters activity of existing enzymes/ proteins directly or via second messengers
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19
Q

Where do hydrophobic chemical messengers bind and what is the goal of the attachment?

A
  • binds to cytosolic or nuclear receptors
  • turns on genes to make new proteins (ex: enzymes)
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20
Q

What is the central nervous system?

A
  • brain and spinal cord
  • “mission control”
  • sends info down to motor neurons
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21
Q

What is the peripheral nervous system?

A
  • cranial and spinal nerves
  • liaison between CNS and body
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22
Q

What is the autonomic nervous system?

A
  • involuntary response control
  • lowers blood pressure (without you having to think about it)
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23
Q

What is the somatic nervous system?

A
  • voluntary movement control
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24
Q

What is sensory (afferent) in the nervous system?

A
  • sensory neurons
  • conducts signals from receptors to CNS
  • baroreceptors
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25
Q

What is motor (efferent) in the nervous system?

A
  • composed of motor neurons
  • conducts signals from CNS to effectors
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26
Q

What is sympathetic in the nervous system?

A
  • “fight or flight” respons
  • mobilizes bodily systems
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27
Q

What is parasympathetic in the nervous system?

A
  • “rest and digest” response
  • conserves energy
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28
Q

What are the major cell types of the adult human central nervous system?

A
  1. Neurons

“Glial” or non-neuronal cells:
2. Oligodendrocytes(CNS)& Schwann cells (PNS)
3. Astrocytes
4. Microglia
5. Ependymalcells

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29
Q

Explan the anatomy of a neuron

A

Receiving end (near cell body) vs sending end (near axon terminal)
- Dendrites pick up info from other neurons (neurotransmitters
- Cell body inputs this, axons transmit/conduct the neurons away from body
- Axon terminal release the neurotransmitters

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30
Q

What happens in multiple sclerosis?

A
  • destruction of myelin sheath due to autoimmune disorder
  • Unmyelinated axon – 0.5 to 2m/s
  • Myelinated axon – 6 to 120m/s
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31
Q

How do neurons work in the central nervous system?

A
  • Signal specific target cells with a specific neurotransmitter
  • Typically release one type of neurotransmitter at a given pre-synaptic neuron (e.g. dopamine, serotonin, norepinephrine, acetylcholine, etc.)
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32
Q

Explain the summation of inputs of neurons in the CNS

A
  • neurons receive several signals: are either excitatory or inhibitory
  • Net response is based on overall (summation) effect of all inputs
  • neuron summation is combined effect of all signals, determining whether an action potential will be generated
  • dopamine: related to rewards
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33
Q

Explain synaptic divergence and synaptic convergence of neurons

A
  • Synaptic divergence: many other nerve cells influenced by one
  • Synaptic convergence: one nerve cell influenced by many others
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34
Q

When do neurons start to diverge, converge, and form networks?

A

Beginning at ~10 years of age in humans, there is a lot of remodeling within the brain’s neural network
* Developing new synapses
* Pruning away unused synapses

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35
Q

What are some key changes in the teen/emerging adult brain?

A
  • Growth in size 90% complete but massive reorganization & development of synapses i.e. networking
  • Increased sensitivity to dopamine – does this explain why teens respond strongly to social reward?
  • Large increase in myelination i.e. increase in transmission speed of neurons
  • These changes should facilitate learning & social networking which are important for survival – does it also explain risky behaviour?
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36
Q

Explain what oligodendrocytes and schwann cells do and where they are found

A
  • Produce myelin
  • Oligodendrocytes span multiple axons & are found in the CNS
  • Schwann cells do not span multiple axons and are found in the PNS
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37
Q

Explain the function and location of astrocytes

A
  • Stellate (starlike) morphology
  • Many functions but very important
    for communication
  • More abundant than neurons
  • allow multiple neurons to connect together
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38
Q

Explain the function and location of ependymal cells

A
  • Line ventricles to form a barrier
  • Produces cerebrospinal fluid
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39
Q

Explain the function and location of microglia

A
  • Mobile, macrophage-like, immune cells
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40
Q

What are the 5 key functions of astrocytes (according to the astrocytic super-network theory)

A
  1. Coordinate overall function of the blood brain barrier (BBB) & provide nutrients to neurons
    2.Coordinate function of the ventricle epithelium (brain network)
  2. Coordinate function at the Nodes of Ranvier
  3. Participate in/form tripartite synapses with neurons
  4. Serve as “superhubs” for neural networks via syncytium formation (cytoplasm containing many nuclei & enclosed in cell membrane), & calcium signaling via gap junctions (astrocyte clouds)
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41
Q

Explain the blood brain barrier and what it does

A
  • Very tight control over what gets through to the brain
  • Very good protection against most bacteria & toxins
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42
Q

What can get through the blood brain barrier?

A
  • Very small lipid-soluble compounds (essential
    fatty acids)
  • Caffeine & alcohol
  • Glucose via specific glucose transporter GLUT1 (not insulin-sensitive)
  • An issue when targeting drugs for the brain
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43
Q

Who is Phineas P. Gage, 1823-1860?

A

“man who began neuroscience”
- Intense brain surgery, where a metal rod went through his frontal lobe
- He survived, but his personality had changed so much “an almost different person entirety”
- Helped better understand what the frontal lobe does in relation to personality
- Example of emergent properties (looking at the total sum)

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44
Q

What did Phineas Gage’s condition help prove?

A
  • Early evidence that different areas of the brain are “networked” to create our personality
  • The brain is segregated yet networked in a way to make it responsible for creating emergent properties such as personality, rational decision making, & the process of emotion
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45
Q

What are two modern imaging techniques?

A

Positron Emission Tomography (PET) and Functional Magnetic Resonance Imaging (fMRI)

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46
Q

How do PET scans work?

A

tracks glucose uptake i.e. glucose tracer
- Glucose is needed to power the brain
- Radioactive form of glucose: glucose tracer to track movement of glucose
- Gamma rays make a 3D model of where the glucose has moved (they light up)

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47
Q

How do fMRI scans work?

A

tracks blood flow i.e. oxygenated blood (oxyhemoglobin) vs deoxygenated blood (deoxyhemoglobin)
- Changes in blood flow and oxygenation: fMRI
- Can activity that stretches from one lobe to the other

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48
Q

What did the use of PET and fMRI imaging make apparent?

A

areas of activity (function), do not always precisely coincide with defined anatomical zones i.e. they can stretch across different regions of the brain

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49
Q

What does mesocortical mean (neurotransmitter-driven network)?

A

involved with cognition, memory, attention, emotional behavior, learning

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50
Q

What does nigrostriatal mean (neurotransmitter-driven network)?

A

involved with movement and sensory stimuli

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51
Q

What does mesolimbic mean (neurotransmitter-driven network)?

A

involved with pleasure and reward seeking behaviors: addiction, emotion, perception

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52
Q

How do neutransmitter-driven networks work?

A
  • Networks are identified by neurons using the same neurotransmitter
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53
Q

Name 4 neurotransmitters

A

norepinephrine, serotonin, acetylcholine, dopamine

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54
Q

What does the norepinephrine network modulate?

A
  • Attention
  • Arousal
  • Sleep-wake
  • Learning
  • Memory
  • Pain
  • Anxiety
  • Mood
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55
Q

What are psychostimulants of the norepinephrine network?

A
  • Methamphetamine
  • Caffeine
  • Ritalin (this along with Adderall are used for ADHD treatment, but are also used by some college/university students – nootropics)
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56
Q

What does the serotonin network modulate?

A

pain, sleep-wake cycle, emotion (contributor to feelings of well-being and happiness)

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57
Q

How do antidepressants work?

A

increasing serotonin levels

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58
Q

What are low serotonin levels associated with?

A

migraines

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59
Q

What does the acetylcholine network modulate?

A
  • Arousal
  • Sleep-wake
  • Learning
  • Memory
  • Sensory information
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60
Q

Explain Alzheimer’s Disease in correlation to the acetylcholine network

A
  • Massive loss of cholinergic neurons
  • Low acetylcholine levels
  • Various drugs available in Canada – cholinesterase inhibitors (cholinesterase enzyme rapidly breaks down acetylcholine in the synapse)
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61
Q

What are neurons of acetylcholine called?

A

cholinergic neurons

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62
Q

What does the dopamine network modulate?

A
  • Motor control
  • Reward/pleasure centers
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63
Q

Explain the advancements of Parkinson’s disease in correlation to the dopamine network

A
  • Loss of dopamine network
  • Dopamine agonists used to increase healthspan of patients
  • Too much medication can cause problems controlling impulses (e.g. gambling)
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64
Q

How do agonists fit into receptors?

A

Dopamine fits into receptor like lock and key; agonists do the same (“copy of a key”)

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65
Q

Explain the dopamine network and drugs

A
  • Dopamine = feel good i.e. the “pleasure network”
  • Network typically associated with addictions
  • Can be increased by various addictive drugs such as cocaine (blocks dopamine reuptake)
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66
Q

How can dopamine be increased?

A

natural endorphins: exercise-induced euphoria, food

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67
Q

What happens after dopamine is released into synapse

A

it must be cleared (can go through reuptake; cocaine blocks the transporter zo that dopamine cannot get in, causing an increase in effective dopamine)

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68
Q

What are origins of hormones?

A

endocrine glands, nerves, organs (produce hormones as a secondary function)
* bones + skeletal muscles and fat + adipose tissue also produce lots of hormones

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69
Q

Explain dopamine and GABA as neurotransmitters, and in correlation to addiction

A

Dopamine is an excitatory neurotransmitter (turns the signal on) GABA is an inhibitory neurotransmitter (turns the signal off)

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70
Q

Explain phenylketonuria (PKU)

A
  • Autosomal recessive
  • Deficiency of hepatic enzyme phenylalanine hydroxylase (PAH), which normally catalyzes the hydroxylation of phenylalanine to tyrosine
  • Accumulation of phenylalanine leads to decreased production of myelin, dopamine, norepinephrine, & serotonin
  • Children develop profound intellectual disability without treatment (rare)
  • Usually found right at birth, and if so, can do rigours treatment to reverse it, leading the child to live a normal life
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71
Q

What do hormones modulate?

A
  • Growth & development
  • Homeostasis
  • Reproduction
  • Many other roles in the CCN e.g. neurodevelopment & immunity
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72
Q

Explain the graph of the endocrine system (placebo vs rHuEPO)

A
  • EPO is ergogenic
  • rHuEPO is an enhancement medicine
  • rHuEPO will increase oxygen in body before a race will improve physical performace, so it is banned
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73
Q

What does oxytocin do in the posterior pituitary?

A

uterine contractions, milk ejection, positive mood (bliss, love, bonding)

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74
Q

What are neurohormones and what is their function?

A
  • Neurotransmitters that are released into the bloodstream by neurons
  • Travel to distant target cells or glands where they exert their effects
  • Act more broadly on the body, influencing the function of endocrine glands & the release of hormones
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75
Q

Explain the interactions between the nervous and endocrine system

A
  • Interact to form foundation of the CCN
  • Some nerves release their neurotransmitters directly into the
    bloodstream (neurohormones)
  • All primary endocrine glands & secondary endocrine tissues are innervated by neurons of the autonomic nervous system
  • Neurotransmitters can modulate hormone secretion e.g. norepinephrine increases epinephrine & decreases insulin
  • Neurons in the CNS & PNS have receptors for many hormones e.g. insulin, estrogen, testosterone, etc.
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76
Q

Explain neurotransmitters and what is their function?

A
  • Chemical messengers released by nerve cells (neurons)
  • Transmit signals to adjacent cells (typically within the nervous system)
  • Act at synapses i.e. the junctions between nerve cells & their target cells (neuron, muscle, gland)
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77
Q

What are the two hormones of the posterior pituitary?

A

oxytocin (OT) and andidiuretic hormone (ADH / vasopressin)

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78
Q

What does ADH do in the posterior pituitary?

A

retention of fluid by the kidneys

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79
Q

What does the posterior pituitary do?

A
  • Releases neurohormones made in the hypothalamus
  • Isn’t really an endocrine gland, more like a collection of nerve endings that release OT & ADH into the pituitary’s circulation i.e. neuroendocrine
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80
Q

What are low levels of oxytocin associated with?

A
  • Conditions such as ASD (implicated in social cognition &
    behaviour)
  • Depression, anxiety, & stress
  • Higher levels of perceived pain
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81
Q

When does oxytocin increase?

A
  • breastfeeding individuals
  • Initiate let-down & milk ejection
  • Calming effect on mother
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82
Q

What is the role of ADH?

A

important role in blood pressure regulation

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83
Q

What does ADH increase its release?

A

heart failure:
* Mechanism to support blood pressure in response to reduced blood flow
* Leads to water retention & fluid overload that tends to worsen heart failure symptoms

severe blood loss or dehydration:
Mechanism to try to increase water retention & maintain blood
pressure
* Hypovolemic shock (even in low volumes) can be life threatening

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84
Q

How does the anterior pituitary act like a gland?

A
  • Contains endocrine cells that release many hormones
  • has a multi-organ hormone axis
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85
Q

Briefly explain some hormones of the anterior pituitary (also refer to graph)

A
  • plus sign means stimulus
  • minus side means inhibitory
  • RH is releasing (stimulatory)
  • IH is inhibitory
  • Dopamine suppresses release of prolactin, to keep them low when breastfeeding does not occur
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86
Q

What does anabolic mean?

A

build up

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87
Q

What is the growth hormone stimulated by?

A

sex hormones and deep sleep

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88
Q

What does catabolic mean?

A

break down

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89
Q

Can bone and muscle still grow under influence of GH in adulthood>

A
  • skull and facial bone can
  • Muscle not as much, except when administered in cases of deficiency
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90
Q

What is IGF-1?

A

insulin-like growth factor 1), has anabolic effects

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91
Q

How are anabolic steroids/GH harmful?

A
  • Effective dose is supraphysiological
  • Dose of the hormone/hormone agonist is generally not timed to mimic natural hormone production
  • Hormones are released according to complex ultradian, circadian, & infradian rhythms
92
Q

How can hormones be used as aids?

A

ergogenic aids, many banned due to significant health risks

93
Q

What are neurohormones in reference to neurotransmitters?

A

neurotransmitters that influence hormone release

94
Q

What is the Innate vs Adaptive immune system

A

Innate: natural, not learned through experience
Adaptive: holds onto memory of specific pathogens so it can elicit a greater defense upon later exposure

95
Q

What lines of defense are nonspecific and innate?

A

Nonspecific and innate: 1st and 2nd
Specific and adaptive: 3rd

96
Q

What is the 1st line of defence?

A

physical and chemical surface barriers

97
Q

What is the 2nd line of defence?

A

internal cellular & chemical defense (if pathogen penetrates barriers)

98
Q

What is the 3rd line of defence?

A

immune response (if pathogen survives nonspecific, internal defenses)
- like a superhero response
- a specialized team that comes into action when the 1st and 2nd line can’t defend

99
Q

What are examples of the 1st line of defense?

A

external physical barriers: Skin, stomach acid, saliva, urine (low pH: protects against pathogens), respiratory epithelium, bacteria in gut

100
Q

What are examples of the 2nd line of defense?

A

Internal resident cells, proteins, inflammation, & fever

101
Q

Elaborate on the 2nd line of defense

A

Identifies foreign (non-self) matter, but isn’t specific & doesn’t develop a memory
- Pathogen has already gotten through physical barriers

102
Q

How does cell-based defense work by?

A

destruction by phagocytocis

103
Q

What are 2 phagocytes and what do they do?

A

engulf/digest particles/foreign bodies
neutrophils, macrophages
- Some phagocytes already on site, some migrate

104
Q

What do neutrophils do in cell-based defense?

A

first on the scene, consume bacteria

105
Q

What do non-phagocytes do in cell-based defense and what are the 2 types?

A

target pathogens/invade organisms that are too large for phagocytosis
eosinophils, natural killer cells

106
Q

What do macrophages do in cell-based defense?

A

consume almost anything

107
Q

What do eosinophils do in cell-based defense?

A

discharge enzymes that digest target

108
Q

What do natural killer cells do in cell-based defense?

A

constantly circulate & “patrol” for non-self; release perforin & proteases to destroy cells

109
Q

What does the complement system do?

A

It is a protein-based defence, performs lysis

110
Q

Explain the complement system in reference to protein-based defense

A
  • 20+ proteins synthesized mainly in liver; released in inactive form
  • Become activated by i) polysaccharides on bacteria surface, or ii)
    antigen/antibody complexes (adaptive immune response)
  • Normally deactivated by native proteins in the blood & the surface of the body’s own cells
  • Enhances the ability of antibodies & phagocytic cells to clear microbes & damaged cells from the body
  • Promotes inflammation & attacks the pathogen’s cell membrane
111
Q

What chemical signals does injured tissue release (inflammation) as a defensive process?

A

Blood vessels widen (redness and heat), Capillaries become more permeable (swelling and pain)
- Inflammation is to help overcome pathogens

112
Q

Explain more about redness and heat when blood vessels widen during inflammation

A

Redness – blood flow carries defensive cells & chemicals to damaged tissue, removing toxins
Heat – increases the metabolic rate of cells in the injured area to speed healing

113
Q

Explain more about swelling and pain when capillaries become more permeable during inflammation

A

Swelling – fluid containing defensive chemicals, blood-clotting factors, oxygen, nutrients, & defensive cells seeps into injured area
Pain – hampers movement, allowing the injured area to heal

114
Q

What is RICE and how does it fit into the 4 key signs of inflammation?

A

Rest
Ice (reduces pain and heat)
Compression (reduces swelling)
Elevation

115
Q

What is acute vs chronic inflammation?

A

Acute: bruises and torn tissue
Chronic: disease states such as arthritis, obesity, etc

116
Q

Can fever occur in the absence of an infection?

A

Yes, called fever of unknown origin (endocrine disorders, autoimmune disorders, cancer)

117
Q

What are functional vs support cells in the local support and defense system (LSDS)?

A

Functional: parenchymal (critical portion of the tissue, like gland/organ)
Framework: stromal (support parenchymal cells, forming LSDS)

118
Q

What is the islet of langerhans?

A

irregularly shaped patches of endocrine tissue located within the pancreas of most vertebrates

119
Q

What do beta cells do?

A

secrete insulin

120
Q

What do F cells do?

A

secretes pancreatic polypeptide

121
Q

What do Alpha cells do?

A

secretes glucagon

122
Q

What do delta cells do?

A

secretes somatostatin

123
Q

What is the capillary made of?

A

non-parenchymal cells, they support

124
Q

Elaborate on parenchymal cells and give some examples

A
  • Usually the most prominent cell type in terms of mass
  • E.g. liver = hepatocyte; skeletal muscle = myocyte; heart = cardiomyocyte; brain = neuron; adipose tissue = adipocyte; pancreas = various secretory cells
125
Q

Give examples of stromal (non-parenchymal) cells

A

E.g. astrocytes (support neural function, BBB); capillary endothelial cells (control blood flow, provide nutrients, oxygen); lymphoid cells (resident T/B cells, NK cells); myeloid cells (neutrophils, macrophages); fibroblasts (make extracellular matrix & collagen); stem cells (divide & replace parenchymal cells); gap junctions (communication between parenchymal cells e.g. intercalated disks between cardiac cells)

126
Q

What can you see in the stromal view of the pancreas?

A

cholinergic neurons (dark brown), fibroblasts (light brown), macrophages (dark spots), E-cadherin protein i.e. gap junctions (brown webs)

127
Q

When is the LSDS functioning?

A

always, doing multiple tasks

128
Q

Give some examples of the tasks of the LSDS, beyond invading microbes

A
  • Local tissue damage by processes that are not due to infectious
    pathogens
  • Normal tissue turnover (cell death, tissue repair & regeneration during wound healing)
  • Looks out for appearance of transformed cell populations (cancer)
129
Q

What are MHC markers and what is their purpose?

A
  • Proteins expressed on the surface of a cell
  • Used primarily in the recognition of pathogens (attack) in immune
    responses
  • Also used in self (support) recognition
  • IMAGINE: it “identifies a badge of every cell in a city”
130
Q

What are the 3 steps that MHC markers go by

A

Threat, detection, alert

131
Q

What are antigens?

A
  • Molecule, often on the surface of a pathogen, that the immune system recognizes as a specific threat
  • IMAGINE: “one cell in the city gets attacked by bacteria, it eats it up, it takes a piece of pathogen and stick it on its badge” “immune system sees the identity badge and will see that something inside it does not belong”
132
Q

What does the MHC display?

A

both self and non-self antigens

133
Q

Elaborate on step 1 of how MHC markers work (threat)

A
  • an invader enters the body
133
Q

Elaborate on step 3 of how MHC markers work (alert)

A
  • Macrophage presents antigen to helper T cell & secretes chemical that activates it
  • Complex set of signals to activate helper T cell (recognition + verification to ensure it’s responding to non-self)
134
Q

Elaborate on step 2 of how MHC markers work (detection)

A
  • A macrophage encounters, engulfs, & digests the invader (antigen e.g. a bacterium)
  • Macrophage places a piece of the invader (antigen) on its surface with the self (MHC) marker
135
Q

When do antibody and cell mediated responses get activated?

A

during step 3 (alert)- helper T cell divides and transforms into effector helper T cell

135
Q

What happens during step 4, when antibody and cell mediated responses get activated?

A

Alarm
- effector helper T cell activates:

A. Cell-mediated (T cell) response
(Naïve cytotoxic T cell activated)

B. Antibody-mediated (B cell) response
(Naïve B cell activated)

136
Q

What are steps 5, 6, and 7 for cell-mediated (T-cell) response

A

Building specific defenses, defense, continued surveillance

136
Q

Elaborate on step 5 (building specific defenses) of A: cell-mediated T-cell response

A
  • Naïve cytotoxic T cell divides (amplification) into effector cytotoxic T cell and memory cytotoxic T cell
137
Q

Elaborate on step 6 (defense) of A: cell-mediated T-cell response

A
  • Effector cytotoxic T cells targets cells displaying foreign antigen and kills them by chemical means

EX: (cells infected with intracellular pathogen, cancer cells, cells of organ transplants, etc.) (BY perforins (punch holes in the target cell membrane))

137
Q

Elaborate on step 7 (continued surveillance) of A: cell-mediated T-cell response

A

Memory T cells stored for continued surveillance

138
Q

Elaborate on step 5 (building specific defenses) of B: antibody-mediated (B-Cell) Response

A

Naïve B cell divides (amplification) into plasma cell (effector cytotoxic B cell) and memory B cell

138
Q

Elaborate on step 6 (defense) of B: antibody-mediated (B-Cell) Response

A

Plasma cell (effector cytotoxic B cell) secretes antibodies (amplification), neutralizes foreign proteins (toxins), triggers release of more complement, & attracts macrophages
* Antibodies attack the foreign antigens when found – circulation, tissues, etc. (B cells themselves don’t engage)
* Antibodies target pathogens or toxins outside of cells by binding to the specific antigen(s) that initiated prior events

139
Q

Elaborate on step 7 (continued surveillance) of B: antibody-mediated (B-Cell) Response

A

Memory B cells stored for continued surveillance

140
Q

How long are memory B cells stored for?

A

hopefully a lifetime, can be only 8 months
- Ex: Memory B cells remain for 2 years after COVID-19 (it is such a dangerous disease, to provide a longer protection period)

140
Q

Do all B cells turn into useful cells?

A

No

141
Q

How to antibodies identify cells with pathogens?

A

they put tags on them, notifying other cells to kill them

141
Q

Name the 3 types of memory cells

A
  1. Memory helper T cells
  2. Memory cytotoxic T cells
  3. Memory B cells
142
Q

Where are memory cells stored?

A

in the bone marrow & thymus

143
Q

What does having memory cells help with?

A

provides a quicker & more robust response in subsequent encounters

144
Q

What is negative feedback?

A

A “brake” for the system

145
Q

What do T suppressor (regulatory, Foxp3+) cells do?

A
  • Suppress activation of the immune system, particularly production of T helper cells
  • Important in allowing tolerance to self antigens
146
Q

What happens if there is too little T suppressor response?

A

association with autoimmune disease,
allergies, graft rejection, inflammatory bowel disease

147
Q

When do autoimmune disorders occur and how many types are there?

A

Occur when the body’s immune system attacks & destroys healthy body tissue by mistake
- 80+ types

147
Q

What happens if there is too much T suppressor response?

A

possible connection to cancer & increased incidence of infectious diseases

147
Q

Explain the autoimmune disorder: Celiac Disease (causes digestive issues when consuming gluten)

A
  • Gluten describes the protein fraction of wheat, barley, & rye which have high concentrations of glutamine & proline (cannot be completely digested by humans)
  • Partially-digested peptides initiate innate & adaptive immune response in those with Celiac Disease
  • Immune system attacks peptides in small intestine, damaging it & hindering its function
  • Non-celiac gluten sensitivity – pathophysiology not yet understood
148
Q

What is the cardiovascular system made of (its 3 main components)?

A
  1. Heart – muscular pump
  2. Blood vessels – conduits for blood to flow
  3. Blood – fluid that circulates through the body & carries materials between the cells i.e. communication
148
Q

List some affiliated organs/tissues to the cardiovascular system

A
  • Lymph, cerebrospinal fluid (CSF), extracellular fluid
  • Lymph & CSF vessels
  • Kidney (erythropoietin, filtering)
  • Spleen, thymus, tonsils (reservoirs for blood/immune cells) * Lungs (O2, CO2 removal)
  • Bone marrow (stem cell pool)
149
Q

What is the circulatory system?

A

Cardiovascular System + Lymphatic System

150
Q

How does the lymphatic system work?

A

Lymph- fluid derived from interstitial fluid and white blood cells

  • Lymph nodes, lymphatic vessels, spleen, tonsils, & thymus
  • Filters harmful substances from lymph & transports white blood
    cells
  • Lymphatic vessels return excess interstitial fluid & substances to bloodstream i.e. balance between fluid intake & output
150
Q

What does the cardiovascular and lymphatic systems both do?

A

Cardiovascular: transports blood
Lymphatic: maintains fluid balance & supports immune system

151
Q

Give some examples of cardiovascular disease (CVD)

A
  • Coronary artery disease
  • Stroke
  • Heart attack (myocardial infarction)
  • Heart failure
  • Hypertension
  • Diabetes
151
Q

How do blood vessels conduct blood in continuous loops?

A
  • Deoxygenated blood returns to right side of heart (enters right atrium) from venous circulation
  • Atria receive blood
  • Heart contracts, pumps blood to ventricles
  • From right ventricle to lungs, then left atrium
  • Oxygenated blood leaves left ventricle via the aorta
  • Note the deoxygenated blood in the pulmonary artery & the oxygenated blood in the pulmonary vein
152
Q

What are the 5 characteristics of blood vessels?

A

arteries > arterioles > capillaries > venules > veins

153
Q

What are arteries?

A
  • Thick, muscular walls (smooth muscle) designed to handle high pressures
153
Q

What are arterioles?

A
  • A bit less muscle (pressures dropping)
  • Lots of innervation to control vessel diameter through smooth muscle contraction (main
    site of BP regulation)
154
Q

What are capillaries?

A
  • No muscle i.e. no control over diameter
  • No connective tissue i.e. no ability to withstand high pressures * Movement of fluid & solutes maximized
  • Nutrients, waste, fluid exchange at local level
155
Q

What are venules?

A
  • Main site of lymphocytes (white blood cells) crossing from blood to lymph nodes
156
Q

What are veins?

A
  • Thin-walled & fairly muscular for easy expansion & recoiling
157
Q

Where is the majority of blood in the body?

A

systemic veins/venules
- As soon as blood is dumped out of hemoglobin, it rushes to heart via veins

158
Q

What is dyslipidemia?

A
  • imbalance of lipids such as cholesterol, low-density lipoprotein cholesterol, (LDL-C), triglycerides, and high-density lipoprotein (HDL)
  • Blockages lead to issues in heart, and brain (the final target organ doesn’t get the oxygen it needs)
159
Q

How do blood vessells differ?

A

By velocity and area
- large surface area and low velocity gives optimal exchange

159
Q

What does a high velocity and small surface area (exchange of deoxygenated and oxygenated blood) cause?

A

direct, rapid conductance of blood

160
Q

What is cardiac output?

A
  • The amount of blood pumped by the heart per minute * A product of heart rate x stroke volume
160
Q

What happens to blood flow when resting vs exercise (cardiac output goes from 5 L/min to 25L/min)

A

skeletal muscle takes up the majority of cardiac output during exercise (compared to around equal amount with kidneys, brain, GI tract, and others when resting)
(view graph)

161
Q

What direction does blood move in veins?

A

Blood is moving against gravity, toward the heart by pressure gradient between left & right side of heart

161
Q

What is blood movement in veins facilitated by?

A
  • Expansion of the thoracic cavity during breathing
  • Contracting skeletal muscles
  • Valves (prevent blood flowing backwards)
162
Q

What are varicose veins caused by and what does it result in?

A
  • One-way valves malfunction
  • Allow backwards flow of blood & pooling
  • Generally occurs in superficial veins in thigh & calf (saphenous vein – longest vein in the body)
162
Q

What is the heart made of?

A

cardiac muscle tissue (myocardium)

163
Q

What is neural input in heart?

A

involuntary, autonomic

164
Q

What is neural conduction in heart?

A

gap junctions (very fast, contract as a unit)

165
Q

What is metabolism in heart?

A

very high oxidative capacity
* Many mitochondria (~35% of volume compared to ~5% in skeletal
muscle)
* Fatigue resistant (beats ~3 billion times over a lifetime)

165
Q

What happens when AV valves close in reference to blood flow?

A
  • “LUB” (1st heart sound)
  • AV valves located between each atrium &
    ventricle
  • Closure of tricuspid valve (right) & mitral valve (left)
166
Q

What happens when semilunar valves close in reference to blood flow?

A
  • “DUB” (2nd heart sound, louder)
  • Semilunar valves located between each
    ventricle & its artery
  • Closure of pulmonary & aortic valves
166
Q

What is stenosis (heart valve problems)?

A
  • Narrowing of a valve
  • May be congenital, due to calcification, or scarring from rheumatic fever
  • Seriousness varies
  • Can cause fatigue & shortness of breath, exercise intolerance, or in more serious cases, heart failure
167
Q

What are issues with artificial valves?

A
  • Durability – in theory, material could last 1000s of years (carbon, titanium)
  • Clot formation – requires consistent anticoagulant therapy
  • Can get stuck
  • Resistance to flow; vulnerability to backflow & regurgitation
  • Biological valves are an alternative, usually porcine – need immunosuppressive drugs
168
Q

How many aortic valve replacements are there per year?

A

300 000

169
Q

What does the Framingham Risk Score (FRS) determine?

A

estimation of 10-year cardiovascular disease risk

170
Q

What factors influence FRS?

A
  • Age
  • HDL-c
  • Total-c
  • SBP
  • Smoking status
  • Diabetes diagnosis
    At the same FRS, risk in males is greater than in females
171
Q

How does age, HDL-C (high density), total-c, SBP, smoking affect FRS?

A

increases as they increase/occur

172
Q

How does diabetes diagnosis affect FRS?

A

statin-indicated condition

173
Q

Does very low HDL-C also cause higher FRS?

A

Yes

174
Q

What are the 3 parts of the cardiac cycle?

A
  1. contraction of atria (atrial systole)
  2. contraction of ventricles (ventricular systole)
  3. a rest (diastole) where neither chamber is contracting
175
Q

What is the systole (systolic blood pressure)?

A

contraction: the upper number of arterial BP (<120 in normal, the maximum)
- when Kortkoff number is first heard: ventricles contract, sending blood into arteries

176
Q

What is the diastole?

A

relaxation: the lower number of arterial BP (<80 in normal, the minimum)
- when Kortkoff number is last heard, when the heart relaxes between beats (not 0 due to elastic recoil of arterial wall)

177
Q

What is afterload?

A

Diastolic arterial pressure
the pressure against which the heart must work to eject blood during systole (systolic pressure)

178
Q

What is cardiac muscle consisted of?

A

Individual cardiomyocytes connected by intercalated discs (gap junctions) working together as a single, functional organ

179
Q

What is electrical signal propagated by?

A

Nodes, nerves, intercalated discs (gap junctions)

180
Q

What are the 2 nodes that electrical signal is propagated by through the heart?

A

SA (sinoatrial) node: where electrical impulses are generated (heart’s natural pacemaker)
AV (atrioventricular) node: connects the electrical systems of the atria and the ventricles

181
Q

What are the 3 types of nerves that electrical signal is propagated by through the heart?

A
  • bundle of his
  • bundle branches (left and right)
  • purkinje fibres (small)
182
Q

What does miscommunication result in?

A

arrhythmia (irregular heartbeats)

183
Q

What can arrhytmia cause?

A

abnormal sinoatrial (SA) node firing, blocks, fibrillations (most serious)

183
Q

What can abnormal synoatrial (SA) node firing result in?

A
  • tachycardia (fast), bradycardia (slow)
184
Q

What can blocks cause and describe them?

A
  • ex: at AV node
  • vary in terms of degree of blockage
  • can slow down or prevent signal propagation from atria to ventricles
  • ventricles can contract independently (bundle of His, 40 bpm)
185
Q

What are fibrillations and what can they cause?

A
  • Heart is supposed to contract at the same time, something wrong with communication, causes cells to depolarize independently
  • Atrial fibrillation (A-fib) – a quivering or irregular heartbeat (arrhythmia)
  • Ventricular fibrillation (V-fib) – considered most serious cardiac rhythm disturbance
186
Q

How does sympathetic innervation (norepinephrine) affect heart rate?

A

increases heart rate

187
Q

How does Parasympathetic innervation (acetylcholine) affect heart rate?

A

decreases heart rate

188
Q

How does Epinephrine affect contraction strength?

A

increases strength of each contraction

189
Q

How does heart rate and cardiac output increase from rest to exercise?

A

Heart rate: increase to nearly 200 bpm (max HR= 220 bpm - age)
Cardiac output: increase from 5-25 L/min (40 L/min in elite athletes)

190
Q

What causes enlargement of the heart?

A

over-working heart, endurance athletes, weightlifters

191
Q

How does over-working the heart enlarge the heart?

A

Heart muscle responds with hypertrophy (similar to skeletal muscle after weight-lifting)

191
Q

How do endurance athletes have an enlarged heart?

A

Mostly an increase in LV chamber (need to increase cardiac output)

192
Q

How do weightlifters have an enlarged heart?

A

Mostly increased LV wall & septum thickness (need to overcome increased afterload i.e. the amount of pressure needed to eject blood during ventricular contraction)

193
Q

Is enlargement of the heart good or bad?

A

neither/both!
bad:
- causes high blood pressure and narrowing of aortic valve
- heart must work harder to overcome this
good:
- an appropriate adaption for athletes: Athlete’s heart

194
Q

What is atherosclerosis?

A
  • Narrowing of arteries due to calcified fatty deposits (plaque) & thickening of the wall
  • Triggered by damage to arterial wall (inflammation)
  • Can lead to heart attack or stroke
  • Coronary artery disease
    = atherosclerosis in the arteries of heart muscle
195
Q

What are atherosclerosis contributing factors?

A
  • Elevated blood lipids
  • Hypertension (high blood pressure)
  • Inflammatory mediators (C-reactive protein)
  • Diet (sodium, potassium, saturated/trans fats)
  • Smoking
  • Physical inactivity
  • Obesity/diabetes
  • Age
  • Genetics
196
Q

How can you treat coronary artery blockages?

A
  • bypass surgery (left)
  • angioplasty (right)
197
Q

Explain bypass surgery

A
  • vein taken from arm or leg
  • one end attached above blockage and the other below
198
Q

What is vasodilation?

A
  • Blood vessels in skeletal muscles lack alpha-receptors
  • Norepinephrine & epinephrine bind to β2 adrenergic receptors in arteries of skeletal muscles
  • Dilates vessels of the skeletal muscles (vasodilation) so they can receive increased blood flow
  • E.g. during exercise
198
Q

What is vasoconstriction

A
  • redirects blood flow towards exercise muscle
  • Alpha-receptors are located on
    arteries
  • Norepinephrine & epinephrine
    bind to α2 adrenergic receptors
  • Causes arteries to constrict
    (vasoconstriction)
  • Increases blood pressure
  • E.g. during exercise
198
Q

Explain angioplasty

A

less invasive, insert catheter in artery or vein, on its end is a deflated balleon with a mesh, inflate balloon to fully open vein with plaque, and then a stent will hold it open

A blockage can be fully removed, but can be dangerous (if we remove plaque, but some is left loose, it will flow in blood and cause worse conditions: strokes, etc)
less invasive, insert catheter in artery or vein, on its end is a deflated balleon with a mesh, inflate balloon to fully open vein with plaque, and then a stent will hold it open

A blockage can be fully removed, but can be dangerous (if we remove plaque, but some is left loose, it will flow in blood and cause worse conditions: strokes, etc)

199
Q

How does cardiac output increase during exercise?

A

5x, up to 8x in elite athletes

199
Q

Does blood pressure increase dramatically during exercise?

A

Not really
* Distribution of blood does not increase proportionally i.e. blood flow is diverted where it is needed during exercise (the working muscles)
* Dilation of vessels to skeletal muscle & heart increases blood flow to muscles (β2 receptors & local metabolites)
* Constriction of vessels to the gut & kidneys decreases blood flow to these organs (α2 receptors)
* Dilating vessels in the muscle decreases resistance & we have a lot of muscle mass

200
Q

What is the Valsalva maneuver?

A
  • common for weightlifters
  • holding your breath increases intrathoracic pressure during the lift
  • temporarily raises blood pressure and slows heart rate
200
Q

How does resistance exercise (weightlifting) affect blood pressure?

A

can cause dramatic increases in blood pressure- up to 345/245 mmHg

SEM2 (4 decks)

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