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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
Q

Describe the Dinecephalon

A

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

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26
Q

Describe the functions of the Brainstem

A

Midbrain, pons and medulla oblongata

Midbrain = visual/ auditory reflexed

Pons = conveys ascending/descending information

Medulla = autonomic CV and respiratory rhythm control

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27
Q

Describe the structure and function of the Cerebellum.

A

Two hemispheres and divided into lobes

Autonomic processing center

Coordinates balance and posture and programs ongoing movements

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28
Q

Define and describe pharmacodynamics.

A

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.

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29
Q

Describe and define pharmacokinetics

A

Describes the fate of the drug

Absorption, distribution, metabolism and distribution

What body does to the drug

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30
Q

Describe and define pharmacotherapeutics

A

Use of drug treatment to cure disease, delay progression and alleviate signs/symptoms of disease

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31
Q

Define and describe side effect and adverse drug effects

A

Side effect

Drug effects not the primary purpose for giving the drug

Adverse drug effect

Unintended and undesirable response to a drug

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32
Q

What are the main groups of molecular targets for drugs?

A

Proteins

Nucleic acids

Miscellaneous targets

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33
Q

What are the four types of protein molecular targets

A

Receptors
ion channles
enzymes
carreir molecules

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34
Q

What are the 4 receptors of protein targets?

A

Ligand gated Ionotropic

Metabotropic (GPCR)

Kinase-linked

Nuclear receptors

35
Q

What do protein receptors do?

A

enhance, mimic, inhibit ot modulate signals.

Drug actions = agonists, antagonist and allosteric modulators.

36
Q

describe ion channel molecular targets, how they act on drugs and an example.

A

Transmembrane pores that regulate the flow of ins

Drug actions: Block and modulate

local anaesthetics and tetradoxin

37
Q

Describe enzyme molecular targets, how they act on drugs and examples

A

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
Q

Describe carrier molecules (transporters) molecular targets, how they act on drugs and example.

A

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
Q

Give examples of ligand-gated, GPCRs, Kinase-linked and Nuclear receptors

A

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
Q

Outline an example of an Ion Channel protein target

A

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
Q

Outline the three actions of drugs acting at receptors

A

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
Q

What does a lower Ka indicate interms of affinity?

A

higher affinty
produce effects at low concentartions

43
Q

Do agonists of equal affinity produce the same size response?

A

not always

44
Q

What is an example of a drug that uses antagonising endogenous neurotransmitters and hormones?

A

B-blockers

45
Q

A drug that is more potent will….

A

deliver a response at a lower dose

46
Q

What are the main routes of administartion?

A

oral
Parenteral
Inhalation
Epithelial
Sublingual
Rectal

47
Q

what are the four types of parenteral modes of administration?

A

Intravenous: directly into blood

Intramuscular: injected into muscle

Subcutaneous: injected under the skin

Intrathecal: injected into the subarachnoid space of the spine

48
Q

what are the benefits and disadvanatges of intravenous?

A

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
Q

Describe ionisation and pH

A

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
Q

Define Volume of Distribution

A

Volume of fluid in which amount of drug in the body need to be uniformly distributed to produce observed concertation.

51
Q

What is the calculation of VD?

A

Vd = total amount of drug in body/plasma drug concentration

52
Q

What are the functionalisation reactions of Phase I metabolised catalysed by?

A

Catalysed by a group of hepatic microsomal enzymes = Cytochrome P450 mono-oxygenase system

53
Q

Describe phase I reactions of drug metabolism.

A

Functionalization reactions: functional group added/ exposed

Results in loss of pharmacological activity = more reactive products

Important for prodrugs

54
Q

Describe phase II drug metabolism

A

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
Q

What may the conjugatefof Phase II reactions in Drug metabolism be og?

A

glucuronic acid, sulphate, glutathione, amino acids, methyl groups or acetyl groups.

56
Q

What is an exmaple of Phase I and phase II drug metabolism?

A

Phase I: Aspirin – oxidation, hydroxylation, dealkylation, deamination, hydrolysis —> Salicylic acid (derivative) – Conjugation–> Glucuronide

57
Q

What is first pass metabolism AKA

A

presystemic metabolism

58
Q

How does first-pass metabolism limit oral administartion?

A

higher dose is needed
large individual variation
some drugs can’t be given orally at all

59
Q

Compare innate and adaptive immune response.

A

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
Q

What are the granular and agrnaular leukocytes?

A

granular = neutrophils, eosinophils and basophils
agranular = lymphocytes and monocytes

61
Q

What are the three types of Antigen-presenting cells?

A

Dendritic cells, macrophages and B cells

62
Q

Describe Dentric cells

A

Mobile sentinels of boundry tissue

Phagocytoise pathogens, then enter lymphatics to present T cells to lymph nodes

Link between innate and adaptive

63
Q

How do macrophages act as antigen presenting cells?

A

Widely distributed

Present antigens to activate other T cells

Activated macrophage = voracious phagocytic killer

Triggers powerful inflammatory responses

64
Q

Who do B cells present antigens to?

A

Helper T cells

65
Q

What cells produce Antiboides (which ones create and which ones secterte)

A

Lymphocytes produce them:
B cells= create
Plasma cells= secrete

66
Q

Differentiate between the 1st and 2nd line of defences

A

Both are innate

1st = surface barriers (skin, mucous)

2nd = internal defences (phagocytes, NK cells, Inflammation, Antimicrobial proteins and fever)

67
Q

What cells are used in humoural immunity vs cell-mediated immunity?

A

humoral = B

Cell mediated = T

68
Q

What is adaptive immunity?

A

Ability to defend against a specific invading agent

Highly evolved responses that are stimulated by exposure to infectious agent and increase in magnitude

69
Q

What are the two ways in which lymphocytes of Cellular immunity act?

A

Indirectly releasing chemicals that enhance inflammatory response

OR
activating other lymphocytes or macrophages

70
Q

Describe what happens to the antigen after it recognised and bound in cell-mediated immunity.

A

small number of T cells proliferate and differentiated it clone of effector cell
antigen is eliminated

71
Q

Describe the action of humoral immunity on antigens

A

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
Q

Describe the mechanism of action of Naturally Acquired immuity

A

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
Q

What are two modes of natrual passive immunity

A

IgG transferred from mother to foetus across placenta . IgA from mother to baby via breast milk.

73
Q

Describe Artificially acquired active immunity with an example.

A

Vaccine (dead or attenuated) –> stimulates cell mediated and humoral immune response –> production of memory cells (immunogenic)

74
Q

What are two examples of Artificially acquired passive immunity?

A

intravenous injections of IgG antibodiesand anti-venom for snake bite

75
Q

What does patholody involve?

A

causes (aetiology) and underlying mechanisms (pathogenesis)

76
Q

When is cell injury reversible?

A

in the early stages or mild forms or in functional and morphological changes if the stimulus is removed

77
Q

When does cell injury become irreverisble and what does it lead to?

A

when there is continued damage and leads to cell death as the cells can’t recover.

78
Q

Outline the stages in the cellular response to stress and noxious stimuli

A

Stress –> Adaption – (inability to adapt) –> cell injury)

Cell injury reversible –> normal cell

Cell injury irreveirble –> necrosis/ apoptosis

79
Q

What are the hallmarks of reversible cell injury?

A

Reduced oxidative phosphorylation = depletion of ATP

Cellular swelling from changes in ion concentrations and water influx

Intracellular organelles show alterations

80
Q

Outline the steps in the development of disease.

A

Etiology –> pathogenesis (mechanism) –> abnormalities in cells and tissue (molecular, functional and morphologic) –> clinical manifestations

81
Q

Compare necrosis to apopotosis

A

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
Q

what are the five stages of phagocytosis?

A

Chemotaxis, adherence, ingestion, digestion, and killing

CTL (11 decks)

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