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
describe the interactions between the ENDOCRINE and NERVOUS systems.
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
26
describe NEUROTRANSMITTERS
CHEMICAL MESSENGERS secreted by neurons transmit signals to ADJACENT cells act at a SYNAPSE
27
describe NEUROHORMONES
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)
28
describe the POSTERIOR PITUITARY
collection of nerve endings RELEASES hormones made in HYPOTHALMUS OXYTOCIN and ANTIDIURETIC hormones
29
describe OXYTOCIN (OT)
responsible for MILK EJACULATION, UTERINE CONTRACTIONS, POSITIVE MOOD higher in BREAST FEEDING individuals low levels associated with ASD, depression, anxiety, more perceived pain
30
describe ADH
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
describe the ANTERIOR PITUITARY
acts like a GLAND (has ENDOCRINE cells that RELEASE HORMONES) multi organ-hormone axis releases growth hormones
32
describe GROWTH HORMONE
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
why are STEROIDS/GH harmful?
effective dose is supraphysiological (more than what the body needs) not timed to NATURAL HORMONE PRODUCTIONS and RHYTHMS
34
what are the three main parts of the LOCAL SUPPORT and DEFENCE SYSTEM?
NON-SPECIFIIC: 1st Line: PHYSICAL and CHEMICAL BARRIERS 2nd Line: INTERNAL CELLULAR and CHEMICAL DEFENCE SPECIFIC/ADAPTIVE: 3rd Line: IMMUNE RESPONSE
35
what is the 2nd line of defence?
international resident cells, proteins, inflammation, and fever identifies foreign matter but ISN'T SPECIFIC and DOESN'T DEVELOP A MEMORY
36
what are PHAGOCYTES?
ENGULF/digest FOREIGN particles NEUTROPHILS - first on the scene, CONSUME BACTERIA MACROPHAGES - consume almost everything
37
what are NON-PHAGOCYTES?
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
what is LYSIS by the complement system?
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
why do red blood vessels widen?
PROMOTE INFLAMMATION REDNESS - bloodflow carries nutrients and chemicals to damaged cells and tissue, removing toxins HEAT - speeds up metabolic processes, speeding healing
40
why do capillaries become more permeable?
PROMOTES INFLAMMATION SWELLING - fluid containing defensive cells, nutrients, oxygen, and defensive chemicals seeps into area, promoting healing PAIN - prevents movement
41
what are PARENCHYMAL cells?
"FUNCTIONAL" cell type most prominent
42
what are STROMAL cells?
supportive and structural cells make up LSDS
43
what are MAJOR HISTOCOMPATIBILITY COMPLEX MARKERS?
PROTEINS expressed on CELL SURFACE RECOGNITION of PATHOGENS (attack) in immune cells identification of self (support) cells
44
what are ANTIGENS
MOLECULE displayed on the surface of a PATHOGEN, which the immune system recognizes as a THREAT MHCs display self and non self
45
what are the first four steps of a MHC response?
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
what is the T-CELL response?
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
what is the ANTIBODY response?
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
describe NEGATIVE FEEDBACK
"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
what are AUTOIMMUNE DISORDERS?
body's immune system ATTACKS and destroys HEALTHY CELLS ex. celiac
50
describe the LYMPHATIC SYSTEM
maintains FLUID BALANCE and supports immune system FILTERS harmful substances from LYMPH and transports WBCs return extra INTERSTITIAL fluid to bloodstream
51
describe the FLOW OF BLOOD
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
where does EXCHANGE OCCUR?
capillaries --> large surface area, low velocity
53
what is CARDIAC OUTPUT?
amount of blood PUMPED by heart per minute heart rate x stroke volume
54
how do VEINS work?
pump blood AGAINST gravity using PRESSURE GRADIENT FACILLITATED BY: EXPANSION of THORACIC cavity CONTRACTION of skeletal muscules VALVES
55
what are VARICOSE veins?
often found in PREGNANT women one way VALVE malfunction allows BACKFLOW
56
describe THE HEART
muscular PUMP MYOCARDIUM cells INVOLUNTARY, automatic many GAP JUNCTIONS high OXIDATIVE CAPACITY ~35% mitochondria
57
what are the HEART VALVES?
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
what is STENOSIS?
NARROWING of a valve; can occur due to rheumatoid fever
59
what are the problems with ARTIFICIAL VALVES?
can form CLOTS can get STUCK RESISTANCE to flow vulnerability to BACKFLOW biological valve TRANSPLANTS are also an option --> need IMMUNOSUPRESSANTS
60
what factors influence FRS?
age HDL-c total-c smoking sex diabetes diagnosis
61
what is the CARDIAC CYCLE?
1. contraction of ATRIA 2. contraction of VENTRICLES 3. a REST contraction = SYSTOL; RELAXATION = DIASTOLE (120/80)
62
describe CONDUCTION THROUGH the HEART
CARDIOMYOCTES are connection through INTERCALLATED DISKS (gap junctions) to produce a singular, functional organ
63
how are ELECTRICAL SIGNALS PROPOGATED?
NODES --> sinoatrial nodes (electrical impulses generated, HEARTS NATURAL PACEMAKER) NERVES --> bundle of HIS, bundle branches, purkinje fibers INTERCALLATED DISKS
64
describe ARRHYTHMIA
ABNORMAL SA FIRING: tachycardia (fast) or bradycardia (slow) BLOCKS: prevent signal propagation, ventricles can pump independently FIBRILLATIONS: cells polarize independently
65
how does the ENDOCRINE SYSTEM effect HEARTRATE
SYMPATHETIC INNERVATION (norepinephrine) = INCREASED heart rate PARASYMPATHETIC INNERVATION (acetylcholine) = DECREASED heart rate EPINEPHRINE = INCREASED STRENGTH of contraction
66
describe HEART ADAPTATIONS
ENLARGEMENT from overworking HYPERTROPHY ENDURANCE: increase in LV CHAMBER (increases output) WEIGHTLIFTERS: increase in LV WALL and SEPTUM THICKNESS
67
what is ATHERIOSCLEROSIS?
NARROWING of arteries due to CALCIFIED FATTY DEPOSITS thickening of wall cause HEART ATTACK or STROKE
68
how are blockages treated?
BYPASS SURGERY - VEIN taken from are or leg; attached above and below blockage ANGIOPLASY - inflated balloon and stent
69
what is ARTERIOL BLOOD PRESSURE?
SYSTOLIC: maximum, when VENTRICLES contracts DIASTOLIC: minimum, when heart relaxes, not zero due to elastic recoil
70
what is VASOCONSTRICTION?
NOREPINEPHRINE and EPINEPHRINE attach to a2 adregenic receptors blood pressure INCREASES
71
what is VASODIALATION?
NOREPINEPHRINE and EPINEPHRINE attach to B2 adregenic receptors in skeletal muscles blood flow INCREASES