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CTL > Revision deck -7-12 > Flashcards

Revision deck -7-12 Flashcards

wks 7-12 from revsion slides

1
Q

What are the three factors to consider in the creation of membrane potentials?

A

Ionic concentrations- Na higher on outside
Electrical forces- opposites attract
ion channels allow ions to move - passive, gated

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2
Q

What are the 4 types of membrane ion channels and how do they open?

A

Passive- always open
chemically-gated: via binding of neurotransmitter
voltage-gated: response to changes in MP
mechanically gated: physical deformation of rceptors

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3
Q

what does ion flow create?

A

electrical current and voltage change across the membrane.

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4
Q

What is the RMP due to?

A

Difference in ICF and ECF ionic concentration

Differential permeability of the membrane to Na and K.

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5
Q

What are ionotropic Receptors, what is their time line and what are some examples?

A

ligand-gated ion channels

Excitatory receptors = for small cations (Na) for depolarization.

Inhibitory receptors for Cl influx evoking hyperpolarisation

Milliseconds

Nicotinic and ACh receptor

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6
Q

What are Metabotropic GPCRs

A

GPCRs

Ligand binds to GPCR –> GDP echnage for GTP –> active sub unit –> a-GTP dissociates and activates second messenger –> G inhibits or stmulates cAMP/PLA pathway

seconds long ( indirect, prolonged and complex)
examples are muscarinic and ACh receptors

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7
Q

Describe the ionic bases of resting state of AP

A

Na and K+ channels closed

Small build-up of negative charges along inside surface equal to build up positive outside.

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8
Q

What is the mechamims of AP propagation?

A

Local AP currents depolarize adjacent membrane in the forward direction. Can’t travel backwards due to inactivationvoltage-gated ion channels during the refractory period.

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9
Q

What are the five steps of synaptic neurotransmission?

A

depolarisation by AP (nerve impulse) opens VG Ca2 channels at the presynaptic terminal

Ca influx triggers fusion of synaptic vesicles with the membrane → exocytosis

NTs diffuse across the synaptic cleft

NTs activate postsynaptic LGIC → excitatory/ inhibitory event (graded potential - PSPs)

NT effects terminated by reuptake, degradation, or diffusion

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10
Q

What are the two types of Synaptic potentials

A

excitatory (EPSP) = depolarising (net positive influx) = closer to threshold potential

inhibitory (IPSP) = hyperpolarising (net negative influx)= further from 0mV

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11
Q

What are the 4 types of neurotransmitters?

A

Ach
Catecholamines
Idolamines
Amino Acids

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12
Q

What are the actions of ACh?

A

neuromuscular junction (excitatory) and some ANS/CNS synapses (cardiac= inhibitory)

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13
Q

What are some catecholamines and what do they act on?

A

Epinephrine, norepinephrine, dopamine

Act on adrenergic receptors

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14
Q

Name 2 inodlamine and 2 amino acid neurotransmitters

A

Indolamines

Serotonin and histamine

Amino Acids

Glutamate and GABA

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15
Q

Is GABA an excitatory or inhibitory neurotransmitter?

A

Inhibitor of the CNS
reduce neuronal excitability via inhibiting nerve transmission

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16
Q

Compare and contrast ionotropic and metbotropic.

A

Similarities
- both use ACh
-moth mechanism of cell communication via receptors

Differnces
- I = Breif and immediate, M= complex and prolonged

-I = excitatory and inhibitory receptors on ion channels M= GPCR and second messenger

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17
Q

describe the effects of hypokalemia

A

hypokalemia (low ECF ) = extracellular K^ → greater electrochemical gradient driving K^ efflux → hyperpolarisation (MP becomes more negative)

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18
Q

What is the fastest fibre type?

A

Aa- somatic motorneurons (Skletal)

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19
Q

Describe, in general terms, the neural reflex arc

A

Sensory receptor – site of stimulus

Sensory neuron – afferent impulses

Integrating center – monosynaptic or polysynaptic within CNS

Motor neuron – efferent impulses towards effector

Effector – muscle fiber/ gland that contracts or secretes in response

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20
Q

What are the two sensory/motor reactions in the patellar reflex?

A

Sensory neuron synapse:

Excitatory motor inputs = quadricep stimulation

inhibitory motor neuron = hamsiting inhibiton

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21
Q

Describe the patellar reflex

A

Stimulus: Patellar tendon of quadricep muscle stretches in response to being tapped (mechanically gated)

Sensory receptor: Strech is detected by the muscle spindle fibers in the quadriceps AP sent to sensory neuron

Sensory neuron synapses with excitatory motor inputs stimulate quadriceps – monosynaptic integration

Sensory neuron synapses with inhibitory motor neuron inhibit hamstring inhibition of antagonistic muscle allows extension of agonist (quadricep) to be unopposed.

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22
Q

Outline B Fibre classifications

A

Small diameter, myelinated = slower than A

preganglionic ANS axons (from CNS autonomic ganglia)

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23
Q

Outline C fibre classifications

A

Smallest diameter and unmylelinated = slowest

ANS postganglionic axons (from ganglia to target)

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24
Q

Describe the major functions of the cerebrum

A

Site of conscious thought, sensation, intellect and memory

processes sensory and motor information

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25
Describe the Dinecephalon
Thalamus and hypothalamus Overall Centres for drives and emotional & behavioral patterns Hypothalamus: Autonomic regulation of homeostasis Thalamus: relay station for sensory impulses passing to cortex
26
Describe the functions of the Brainstem
Midbrain, pons and medulla oblongata Midbrain = visual/ auditory reflexed Pons = conveys ascending/descending information Medulla = autonomic CV and respiratory rhythm control
27
Describe the structure and function of the Cerebellum.
Two hemispheres and divided into lobes Autonomic processing center Coordinates balance and posture and programs ongoing movements
28
Define and describe pharmacodynamics.
The action of the drug: what it does to the body Qualitative = HOW to produce effects Quantitative = Magnitude of response. = potency, therapeutic efficacy and tolerance.
29
Describe and define pharmacokinetics
Describes the fate of the drug Absorption, distribution, metabolism and distribution What body does to the drug
30
Describe and define pharmacotherapeutics
Use of drug treatment to cure disease, delay progression and alleviate signs/symptoms of disease
31
Define and describe side effect and adverse drug effects
Side effect Drug effects not the primary purpose for giving the drug Adverse drug effect Unintended and undesirable response to a drug
32
What are the main groups of molecular targets for drugs?
Proteins Nucleic acids Miscellaneous targets
33
What are the four types of protein molecular targets
Receptors ion channles enzymes carreir molecules
34
What are the 4 receptors of protein targets?
Ligand gated Ionotropic Metabotropic (GPCR) Kinase-linked Nuclear receptors
35
What do protein receptors do?
enhance, mimic, inhibit ot modulate signals. Drug actions = agonists, antagonist and allosteric modulators.
36
describe ion channel molecular targets, how they act on drugs and an example.
Transmembrane pores that regulate the flow of ins Drug actions: Block and modulate local anaesthetics and tetradoxin
37
Describe enzyme molecular targets, how they act on drugs and examples
Endogenous protein that catalyzes biochemical reactions Inhibits or act as a false substrate = inhibits synthesis of normal product and converted into metabolite paracetamol (COX 1, COX –2 inhibitors, prevents synthesis of PG (FA mediator of inflammation))
38
Describe carrier molecules (transporters) molecular targets, how they act on drugs and example.
Because many endogenous components are too polar to cross Drug action = inhibits and can act as false substrate = inhibition of substrate transport SSRIs- blocks serotonin reuptake channels of postsynpatic neurons Amphetamines: binsd to catecholamine transporters, taken into neuron and inhibits VMAT-2= increased number of NT released into synaptic cleft
39
Give examples of ligand-gated, GPCRs, Kinase-linked and Nuclear receptors
Liand gated Ionotropic- nicotinic ACh (post ganglionic), GABA A, Glutamate ionotropic receptors. Metabotropic (GPCR) - Muscarinic ACh = parasympathetic effectors, Adrenoceptors (sympathetic), peptide receptors, Kinase-linked – JAK-STAT, Cytokines, IGF/Insulin Nuclear receptors- Estrogen receptors , steroid/thyrpid receptors
40
Outline an example of an Ion Channel protein target
e.g. GABA A Cl- channel: GABA antagonsist binds to blocks GABA binding: Vallium = modulator that turns control up --> GABA allows more Cl into cells.
41
Outline the three actions of drugs acting at receptors
Agonists - stimulate receptors and mimic messengers - affinity and efficacy Antagonist -block receptors and prevent signal being sent Allosteric modulators -act at modulatory site on receptor -volume control of response to endogenous chemical
42
What does a lower Ka indicate interms of affinity?
higher affinty produce effects at low concentartions
43
Do agonists of equal affinity produce the same size response?
not always
44
What is an example of a drug that uses antagonising endogenous neurotransmitters and hormones?
B-blockers
45
A drug that is more potent will....
deliver a response at a lower dose
46
What are the main routes of administartion?
oral Parenteral Inhalation Epithelial Sublingual Rectal
47
what are the four types of parenteral modes of administration?
Intravenous: directly into blood Intramuscular: injected into muscle Subcutaneous: injected under the skin Intrathecal: injected into the subarachnoid space of the spine
48
what are the benefits and disadvanatges of intravenous?
intravenous injections are: common provide almost immediate effect deliver large amounts of drug over time used for drugs that can't be taken orally and avoids first-pass metabolism Disadvtatges - difficult to adminsiter
49
Describe ionisation and pH
Drug will be ionized when exposed to pH of oppose pKa Acidic drugs more ionized with higher pH Must be unionised from to cross membrane
50
Define Volume of Distribution
Volume of fluid in which amount of drug in the body need to be uniformly distributed to produce observed concertation.
51
What is the calculation of VD?
Vd = total amount of drug in body/plasma drug concentration
52
What are the functionalisation reactions of Phase I metabolised catalysed by?
Catalysed by a group of hepatic microsomal enzymes = Cytochrome P450 mono-oxygenase system
53
Describe phase I reactions of drug metabolism.
Functionalization reactions: functional group added/ exposed Results in loss of pharmacological activity = more reactive products Important for prodrugs
54
Describe phase II drug metabolism
Covalent linkage made between functional group of drug or metabolite from Phase I Produce highly polar molecules which are rapildy excreted in urine Usually = decreased activity and more active metabolites
55
What may the conjugatefof Phase II reactions in Drug metabolism be og?
glucuronic acid, sulphate, glutathione, amino acids, methyl groups or acetyl groups.
56
What is an exmaple of Phase I and phase II drug metabolism?
Phase I: Aspirin -- oxidation, hydroxylation, dealkylation, deamination, hydrolysis ---> Salicylic acid (derivative) -- Conjugation--> Glucuronide
57
What is first pass metabolism AKA
presystemic metabolism
58
How does first-pass metabolism limit oral administartion?
higher dose is needed large individual variation some drugs can't be given orally at all
59
Compare innate and adaptive immune response.
Innate is nonspecific whilst adaptive in specific innate uses first and second but adaptive uses a third line of defense innate is the immediate response that is limited and has a lower potency, adaptive is longer and stronger Adaptive involves the activation of
60
What are the granular and agrnaular leukocytes?
granular = neutrophils, eosinophils and basophils agranular = lymphocytes and monocytes
61
What are the three types of Antigen-presenting cells?
Dendritic cells, macrophages and B cells
62
Describe Dentric cells
Mobile sentinels of boundry tissue Phagocytoise pathogens, then enter lymphatics to present T cells to lymph nodes Link between innate and adaptive
63
How do macrophages act as antigen presenting cells?
Widely distributed Present antigens to activate other T cells Activated macrophage = voracious phagocytic killer Triggers powerful inflammatory responses
64
Who do B cells present antigens to?
Helper T cells
65
What cells produce Antiboides (which ones create and which ones secterte)
Lymphocytes produce them: B cells= create Plasma cells= secrete
66
Differentiate between the 1st and 2nd line of defences
Both are innate 1st = surface barriers (skin, mucous) 2nd = internal defences (phagocytes, NK cells, Inflammation, Antimicrobial proteins and fever)
67
What cells are used in humoural immunity vs cell-mediated immunity?
humoral = B Cell mediated = T
68
What is adaptive immunity?
Ability to defend against a specific invading agent Highly evolved responses that are stimulated by exposure to infectious agent and increase in magnitude
69
What are the two ways in which lymphocytes of Cellular immunity act?
Indirectly releasing chemicals that enhance inflammatory response OR activating other lymphocytes or macrophages
70
Describe what happens to the antigen after it recognised and bound in cell-mediated immunity.
small number of T cells proliferate and differentiated it clone of effector cell antigen is eliminated
71
Describe the action of humoral immunity on antigens
Lymphocytes produce antiboides which circulate freely in the blood Antigen recognised and bound Marked for destruction by phagocytes Helper T cells constimulte the B cell ---> B cell proliferates and differentiates --> clone of effector produces antibodies --. antigen eliminated
72
Describe the mechanism of action of Naturally Acquired immuity
contact with pathogen --> Antigen recogition by B cells and T cells --> formation of antibody secreting plasma cells, cytotoxic T cells, B and T memory cells.
72
What are two modes of natrual passive immunity
IgG transferred from mother to foetus across placenta . IgA from mother to baby via breast milk.
73
Describe Artificially acquired active immunity with an example.
Vaccine (dead or attenuated) --> stimulates cell mediated and humoral immune response --> production of memory cells (immunogenic) 
74
What are two examples of Artificially acquired passive immunity?
intravenous injections of IgG antibodies and anti-venom for snake bite
75
What does patholody involve?
causes (aetiology) and underlying mechanisms (pathogenesis)
76
When is cell injury reversible?
in the early stages or mild forms or in functional and morphological changes if the stimulus is removed
77
When does cell injury become irreverisble and what does it lead to?
when there is continued damage and leads to cell death as the cells can't recover.
78
Outline the stages in the cellular response to stress and noxious stimuli
Stress --> Adaption -- (inability to adapt) --> cell injury) Cell injury reversible --> normal cell Cell injury irreveirble --> necrosis/ apoptosis
79
What are the hallmarks of reversible cell injury?
Reduced oxidative phosphorylation = depletion of ATP Cellular swelling from changes in ion concentrations and water influx Intracellular organelles show alterations
80
Outline the steps in the development of disease.
Etiology --> pathogenesis (mechanism) --> abnormalities in cells and tissue (molecular, functional and morphologic) --> clinical manifestations
81
Compare necrosis to apopotosis
necrosis = pathological, Apoptosis = physiological necrosis= enlarged cell size Apoptosis = reduced cell size necrosis: plasma membrane disrupted, Apoptsois = plasma membrane altered strcutre but in tact
82
what are the five stages of phagocytosis?
Chemotaxis, adherence, ingestion, digestion, and killing

CTL (11 decks)

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