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BIOL 1080 > Part 2 > Flashcards

Part 2 Flashcards

1
Q

what are the methods of INTRACELLULAR COMMUNICATION?

A

DIRECT SIGNALLING –> gap junctions, membrane (tunnelling) nanotubes, mechanosignals
INDIRECT SIGNALLING –> chemical messengers

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2
Q

what are CONNEXONS?

A

subunits that FORM A GAP JUNCTION
very SMALL pores
permits PASSAGE of sugar, amino acids, and ions between cells (METABOLIC exchange)
found in virtually all cells (EXCEPT muscles)

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3
Q

what are INTERCALATED DISKS?

A

GAP JUNCTION in CARDIAC cells
allows for rapid and COORDINATED propagations of ACTION POTENTIALS for RHYTHMIC CONTRACTIONS
smaller than connexons
regulated by PHOSPHORYLATION/DEPHOSPHORYLATION

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4
Q

what are MEMBRANE NANOTUBES?

A

formed in plasma membrane
longer than gap junctions and have a larger pore diameter
TRANSFER of NUCLEIC ACIDS and SMALL ORGANELLES between cells
maybe transfer from stressed to healthy cells

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5
Q

what is MECHANOSIGNALLING?

A

conversion of MECHANICAL SIGNALLING to a CELLULAR RESPONSE
direct PHYSICAL STRESS to cells, eliciting a CHEMICAL/METABOLIC response

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6
Q

what are the types of CHEMICAL MESSENGERS?

A

paracrine signalling
neurotransmitters
hormones

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7
Q

describe PARACRINE SIGNALLING

A

acts on nearby cells
CLOTTING and GROWTH factors
many secreted hormones act in a paracrine and endocrine manner

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8
Q

describe NEUROTRANSMITTERS

A

SYNAPSE is a short distance
signal is TIGHTLY CONTROLLED
few molecules released
need AUTO SHUTOFF (REUPTAKE/DEGREDATION)

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9
Q

describe HORMONES

A

water or lipid soluble
must CROSS MEMBRANES
TARGET SPECIFICITY

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10
Q

describe HYDROPHILLIC hormones

A

stored in SECRETORY cells
DISOLVES in PLASMA –> NO CARRIER
secreted via fusing secretory vessels to membrane and releasing (EXOCYTOSIS)
binds to cell surface
ALTERS ACTIVITY of enzymes/proteins directly or via second messengers

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11
Q

describe HYDROPHOBIC HORMONES

A

made on demand
does not dissolve in plasma –> NEEDS CARRIER
can CROSS LIPID MEMBRANE
binds to cytosolic or nuclear receptors
TURNS ON GENES to make new PROTEINS

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12
Q

what are the main components of NEURONS?

A

axon terminals
axons
myelin sheath
schwann cells
nodes of ranvier
dendrite
soma
cell body
nucleus

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13
Q

what causes MULTIPLE SCLEROSIS

A

destruction of MYELIN SHEATH due to AUTOIMMUNE disorder
cell signals travel SLOWER without sheath

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14
Q

what are NEURONS?

A

signal specific TARGETING cells with a specific NEUROTRANSMITTER
release ONE neurotransmitter at a given PRESYNAPTIC neuron
diverge, converge and form NETWORKS

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15
Q

what is the difference between synaptic CONVERGENCE and DIVERGENCE?

A

CONVERGENCE = ONE nerve cell INFLUENCED by MANY others

DIVERGENCE = MANY nerve cells INFLUENCED by ONE cell

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16
Q

when does REMODELLING occur in the brain?

A

around 10 years
pruning away unused synapses
creating new synapses
increased DOPAMINE SENSITIVITY
increased MYELINATION (faster transmission speed)

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17
Q

describe the differences and similarities between OLIGODENDROCYTES and SCHWANN cells

A

BOTH - produce MYELIN

OLIGODENDROCYTES - span multiple axons and found in CNS

SCWANN cells - do NOT span multiple axons and found in PNS

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18
Q

what are ASTROCYTES?

A

STELLATE/starlike morphology
COMMUNICATION
more ABUNDANT than neurons

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19
Q

what are EPENDYMAL cells?

A

LINE VENTRICLES to form a barrier
produce CEREBROSPINAL fluid

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20
Q

what are MICROGLIA?

A

MOBILE, macrophage-like IMMUNE cells

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21
Q

what are the KEY FUNCTIONS of ASTROCYTES?

A
  1. Coordinate overall function of BLOOD BRAIN BARRIER and PROVIDE NUTRIENTS to neurons
  2. coordinate function of VENTRICLE EPITHELIUM (brain network)
  3. coordinate function at NODES OF RANVIER
  4. form TRIPARTITE SYNAPSES with neurons
  5. serve as SUPERHUBS for neural networks via syncytium formation and calcium signalling via GAP JUNCTIONS
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22
Q

what is the BLOOD BRAIN BARRIER?

A

TIGHT CONTROL over what gets into brain
PROTECTION against bacteria and toxins
fatty acids, alcohol, caffeine, and glucose (via transporter) can get through –> issue when creating targeting drugs

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23
Q

what is the role of HORMONES?

A

maintain HOMEOSTASIS
GROWTH and development
REPRODUCTION

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24
Q

what are the ORIGINS of HORMONES?

A

endocrine glands, nerves, organs

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25
Q

describe the interactions between the ENDOCRINE and NERVOUS systems.

A

form FOUNDATION of CCN
some NERVES release NEUROTRANSMITTERS into BLOODSTREAM (neurohormones)
primary ENDOCRINE glands and secondary endocrine tissues are innervated
NEUROTRANSMITTERS modulate HORMONE SECRETION
NEURONS in the CNS and PNS have HORMONE RECEPTORS

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26
Q

describe NEUROTRANSMITTERS

A

CHEMICAL MESSENGERS secreted by neurons
transmit signals to ADJACENT cells
act at a SYNAPSE

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27
Q

describe NEUROHORMONES

A

NEUROTRANSMITTERS that are released into the bloodstream by neurons
travel to DISTINCT TARGET CELLS
act BROADLY in the body (affect function of endocrine glands and hormone release)

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28
Q

describe the POSTERIOR PITUITARY

A

collection of nerve endings
RELEASES hormones made in HYPOTHALMUS
OXYTOCIN and ANTIDIURETIC hormones

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29
Q

describe OXYTOCIN (OT)

A

responsible for MILK EJACULATION, UTERINE CONTRACTIONS, POSITIVE MOOD
higher in BREAST FEEDING individuals
low levels associated with ASD, depression, anxiety, more perceived pain

30
Q

describe ADH

A

important role in BLOOD PRESSURE REGULATION
increased release with HEART FAILURE (supports blood pressure in response to reduced blood flow; causes water retention and fluid overload)
increase release in SEVERE BLOOD LOSS or DEHYDRATION

31
Q

describe the ANTERIOR PITUITARY

A

acts like a GLAND (has ENDOCRINE cells that RELEASE HORMONES)
multi organ-hormone axis
releases growth hormones

32
Q

describe GROWTH HORMONE

A

GHRH simulated by SEX HORMONES and DEEP SLEEP
insulin like growth factor 1 has ANABOLIC effects
skull and facial bones can still GROW under GH in adulthood (muscle not so much)

33
Q

why are STEROIDS/GH harmful?

A

effective dose is supraphysiological (more than what the body needs)
not timed to NATURAL HORMONE PRODUCTIONS and RHYTHMS

34
Q

what are the three main parts of the LOCAL SUPPORT and DEFENCE SYSTEM?

A

NON-SPECIFIIC:
1st Line: PHYSICAL and CHEMICAL BARRIERS
2nd Line: INTERNAL CELLULAR and CHEMICAL DEFENCE
SPECIFIC/ADAPTIVE:
3rd Line: IMMUNE RESPONSE

35
Q

what is the 2nd line of defence?

A

international resident cells, proteins, inflammation, and fever

identifies foreign matter but ISN’T SPECIFIC and DOESN’T DEVELOP A MEMORY

36
Q

what are PHAGOCYTES?

A

ENGULF/digest FOREIGN particles
NEUTROPHILS - first on the scene, CONSUME BACTERIA
MACROPHAGES - consume almost everything

37
Q

what are NON-PHAGOCYTES?

A

target particles that are TOO LARGE for phagocytosis
EOSINOPHILS - release ENZYMES that digest a target
NATURAL KILLER CELLS - constantly circulate and monitor for non-self cells; release PERFORIN and PROTEASES to destroy cells

38
Q

what is LYSIS by the complement system?

A

20+ proteins, synthesized in the LIVER
ACTIVATED by POLYSACCARIDES on bacteria surface or ANTIGEN/ANTIBODY complexes
deactivated by NATIVE PROTEINS
ENHANCE ability of ANTIBODIES and PHAGOCYTES to CLEAR microbes and damaged cells from body
PROMOTES INFLAMMATION and ATTACKS pathogen’s cell membrane

39
Q

why do red blood vessels widen?

A

PROMOTE INFLAMMATION
REDNESS - bloodflow carries nutrients and chemicals to damaged cells and tissue, removing toxins
HEAT - speeds up metabolic processes, speeding healing

40
Q

why do capillaries become more permeable?

A

PROMOTES INFLAMMATION
SWELLING - fluid containing defensive cells, nutrients, oxygen, and defensive chemicals seeps into area, promoting healing
PAIN - prevents movement

41
Q

what are PARENCHYMAL cells?

A

“FUNCTIONAL” cell type
most prominent

42
Q

what are STROMAL cells?

A

supportive and structural cells
make up LSDS

43
Q

what are MAJOR HISTOCOMPATIBILITY COMPLEX MARKERS?

A

PROTEINS expressed on CELL SURFACE
RECOGNITION of PATHOGENS (attack) in immune cells
identification of self (support) cells

44
Q

what are ANTIGENS

A

MOLECULE displayed on the surface of a PATHOGEN, which the immune system recognizes as a THREAT
MHCs display self and non self

45
Q

what are the first four steps of a MHC response?

A
  1. threat
  2. DETECTION - macrophage engulfs protein, place a piece of the invader on itself with the MHC marking
  3. ALERT - macrophage presents the antigen to a helper T cell
  4. ALARM
46
Q

what is the T-CELL response?

A

Building specific defence - T-CELLS DIVIDE
DEFENCE - T-cells TARGET and KILL foreign antigens using chemicals (perforin)
MEMORY - MEMORY T-CELLS stored for SURVEILLANCE

47
Q

what is the ANTIBODY response?

A

Naieve B cell divides into plasma cells
DEFENCE - PLASMA CELL (effector cytotoxic B cell) secretes antibodies, which neutralize foreign proteins, attract more compliments and macrophages; antibodies attack foreign antigens
MEMORY B-cells stored for SURVEILLANCE

48
Q

describe NEGATIVE FEEDBACK

A

“break for system”

T-SUPPRESSOR CELLS - suppress activation of immune cells; important for REGULATION
–> Too little suppressor response = autoimmune disease
–> Too high suppressor response = cancer

49
Q

what are AUTOIMMUNE DISORDERS?

A

body’s immune system ATTACKS and destroys HEALTHY CELLS
ex. celiac

50
Q

describe the LYMPHATIC SYSTEM

A

maintains FLUID BALANCE and supports immune system
FILTERS harmful substances from LYMPH and transports WBCs
return extra INTERSTITIAL fluid to bloodstream

51
Q

describe the FLOW OF BLOOD

A

DOB returns to the heart from the RIGHT ATRIUM from venus circulation
atrium receives blood
heart CONTRACTS, pumps blood into ventricle
from RIGHT ventricle to lungs
BLOOD BECOMES OXYGENATED
returns to LEFT ATRIUM
leaves LEFT VENTRICLE via AORTA
NOTE: OB in pulmonary VEINS and DOB in pulmonary ARTERIES

52
Q

where does EXCHANGE OCCUR?

A

capillaries –> large surface area, low velocity

53
Q

what is CARDIAC OUTPUT?

A

amount of blood PUMPED by heart per minute
heart rate x stroke volume

54
Q

how do VEINS work?

A

pump blood AGAINST gravity using PRESSURE GRADIENT
FACILLITATED BY:
EXPANSION of THORACIC cavity
CONTRACTION of skeletal muscules
VALVES

55
Q

what are VARICOSE veins?

A

often found in PREGNANT women
one way VALVE malfunction
allows BACKFLOW

56
Q

describe THE HEART

A

muscular PUMP
MYOCARDIUM cells
INVOLUNTARY, automatic
many GAP JUNCTIONS
high OXIDATIVE CAPACITY ~35% mitochondria

57
Q

what are the HEART VALVES?

A

AV VALVES: LUB sound, between atrium and ventricle, TRICUSPID and MITRIAL
SEMI LUNAR VALVES: DUB sound (2nd sound, louder), between ventricles and arteries, pulmonary and aortic

58
Q

what is STENOSIS?

A

NARROWING of a valve; can occur due to rheumatoid fever

59
Q

what are the problems with ARTIFICIAL VALVES?

A

can form CLOTS
can get STUCK
RESISTANCE to flow
vulnerability to BACKFLOW
biological valve TRANSPLANTS are also an option –> need IMMUNOSUPRESSANTS

60
Q

what factors influence FRS?

A

age
HDL-c
total-c
smoking
sex
diabetes diagnosis

61
Q

what is the CARDIAC CYCLE?

A
  1. contraction of ATRIA
  2. contraction of VENTRICLES
  3. a REST

contraction = SYSTOL; RELAXATION = DIASTOLE (120/80)

62
Q

describe CONDUCTION THROUGH the HEART

A

CARDIOMYOCTES are connection through INTERCALLATED DISKS (gap junctions) to produce a singular, functional organ

63
Q

how are ELECTRICAL SIGNALS PROPOGATED?

A

NODES –> sinoatrial nodes (electrical impulses generated, HEARTS NATURAL PACEMAKER)
NERVES –> bundle of HIS, bundle branches, purkinje fibers
INTERCALLATED DISKS

64
Q

describe ARRHYTHMIA

A

ABNORMAL SA FIRING: tachycardia (fast) or bradycardia (slow)
BLOCKS: prevent signal propagation, ventricles can pump independently
FIBRILLATIONS: cells polarize independently

65
Q

how does the ENDOCRINE SYSTEM effect HEARTRATE

A

SYMPATHETIC INNERVATION (norepinephrine) = INCREASED heart rate
PARASYMPATHETIC INNERVATION (acetylcholine) = DECREASED heart rate
EPINEPHRINE = INCREASED STRENGTH of contraction

66
Q

describe HEART ADAPTATIONS

A

ENLARGEMENT from overworking
HYPERTROPHY
ENDURANCE: increase in LV CHAMBER (increases output)
WEIGHTLIFTERS: increase in LV WALL and SEPTUM THICKNESS

67
Q

what is ATHERIOSCLEROSIS?

A

NARROWING of arteries due to CALCIFIED FATTY DEPOSITS
thickening of wall
cause HEART ATTACK or STROKE

68
Q

how are blockages treated?

A

BYPASS SURGERY - VEIN taken from are or leg; attached above and below blockage
ANGIOPLASY - inflated balloon and stent

69
Q

what is ARTERIOL BLOOD PRESSURE?

A

SYSTOLIC: maximum, when VENTRICLES contracts
DIASTOLIC: minimum, when heart relaxes, not zero due to elastic recoil

70
Q

what is VASOCONSTRICTION?

A

NOREPINEPHRINE and EPINEPHRINE attach to a2 adregenic receptors
blood pressure INCREASES

71
Q

what is VASODIALATION?

A

NOREPINEPHRINE and EPINEPHRINE attach to B2 adregenic receptors in skeletal muscles
blood flow INCREASES

BIOL 1080 (3 decks)

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