Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cells 2 Systems General Revision > Bits and Pieces > Flashcards

Bits and Pieces Flashcards

1
Q

What is the difference between a generalised and a localised system, give an example of each.

A

Generalised - distrib through body i.e. cardiovascular

Localised - in one area only i.e. reproductive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between the carotid artery and the jugular vein

A

Carotid: heart to head
Jugular: head to heat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give examples of amorphous extracell. and fibrous extracell. material

A

Amorphous: jelly like - blood, lymph or solid - cartilage and bone
Fibrous: collagen, reticular, elastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can be found on the apical, lateral and basal surfaces of epith. cells

A

apical: cilia, microvilli, stereocilia
lateral: interdigitation or junctional complexes
basal: striations, basement membrane, hemidesmosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the embryonic origin layers for skin, gut and cavities?

A

Skin: ectoderm
Gut: endoderm
Cavities: mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the difference between flexion, extension and hyperextension in terms of body movement (feet/hands)

A

flexion; folded up like when asleep

extension: straight line from ante brachium/crus
hyperextension: dorsal flexion/plantigrade stance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The pectoral limb: scchurc’mp

probs of no help but to me :)

A

scapula, clavicle, coracoid, humerus, ulna, radius, carpal bones, metacarpals, phalanges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

The pelvic limp: iiapfpft’mp

probs of no help but to me :)

A

ilium, ischium, acetabular bone, pubis, femur, patella, fibula, tibia, tarsal bones, metatarsal, phalanges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What solutes are high intracellularly?

A

K+, Mg2+, phosphates, proteins,

maintained by active transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What solutes are high extracellularly?

A

Na+, Cl-, Ca2+, HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where are discontinuous capillaries found?

A

bone marrow, liver and spleen - permeable to large molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What three things make up ficks law

A

SA, conc. difference, thickness of diffusion pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List the 4 functions of the lymphatic system

A

1) control blood vol and extract vol (return oncotic protein to blood)
2) absorption of fat
3) immune surveillance
4) metabolism and turnover of extracell matrix constit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is there no lymphatic tissue?

A

CNS, eye and bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is lymphodema? How does it occur?

A

obstruct of lymph drainage = build up of lymph fluid can be from lack of sufficient lymph vessels, radiotherapy destroyed or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where do platelets come from?

A

fragments of megakaryocytes from one marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a Heamopoietic stem cell and how is it controlled?

A

multipotent precursor of amyloid, lymphoid or erythroid cells.
regulated by stream fibroblast, osteoblast, endoth, cell and extracell matrix - receptor binding needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the three roles of EPO

A

shortens cell cycle
increases rate of maturation
increases rate of release from bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why and where is EPO released from?

A

from kidney

why: fall of RBC’s, tissue hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do platelets form? What stimulates this?

A

megakaryocytes increase DNA and cytoplasmic volume –> platelets bud off
stimulated by thrombopoietin (TPO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where are monocytes stored

A

they are not stored - released into blood after production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

List the four things the immune system requires to be functional

A

1) inactivity to itself
2) specificity - be able to recognise non-self
3) recognition of microbes and proteins - antigens, PAMPS
4) be able to destroy foreign/abnormal material - phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where are B cells derived from?

A

bone marrow, peyers patches in ruminants and bursa of Fabricius in birds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does mast cell action vary between GI tract, Airways and Blood vessels?

A

GI tract: increase fluid secretion and peristalsis
Airways: decrease diameter, increase mucus
Blood vessels: increase blood flow, increase permeability = higher lymph flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are some common autacoids?

A
  • histamine
  • bradykinin and substance P –> vasodilation, itch and pain
  • cytokines
  • Eicosanoids - PGs, thromboxanes and leukotrienes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How can leukocytes migrate into tissue to cause inflam?

A

toxins and proinflam cytokines activate endothelium = expression of cell adhesion molecules = leukocytes stick and slowed down –> emigration into tissue where they release enzymes and ROS = clear dead tissue and microbes (init good)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the differences between serous, catarrhal, fibrinous and suppurative inflam?

A
  • serous - minimal increase in permeabil. forms serous exudate
  • catarrhal - exudate formed on mucosal surface. serous fluid with mucus, inflam cells and cell debris
  • fibrinous - greater permeabil fibrinogen out = fibrin –> yellow gel like bread and butter
  • suppurative = pus, thick and creamy with neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a phlegmon?

A

diffuse suppurative inflammation in loos connective tissue (cellulitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is an empyema?

A

assume of pus in body cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What cell population change happens in chronic vs acute inflam?

A

neutrophils –> macroph. (3 days) to lymphocytes and plasma cells (7-10 days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does granulation tissue look like - is it the same as granulomatous inflammation? When does it occur?

A

Not the same as granulomatous inflammation = macrophage rich
It is pink, soft, moist and bumpy, well vascularised (angiogenesis occurs) but no nerves = no pain. It occurs in the repair of inflammation - fibroblasts eventually migrate through = fibrin scaffold and collagen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the difference between primary and secondary intention healing?

A

primary - if directly opposing wound edges
secondary - extensive tissue loss need greater volume of granulation tissue, more extensive scar contraction - may restrict movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is proud flesh?

A

excessive proliferation of granulation tissue, tumour like masses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is keloid?

A

unsightly proliferation of scar tissue - very dense collage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How can a low energy balance cause hydraulic degeneration?

A

Na+/K+ ATPase is the main regulator for electrolyte balance that then drives water uptake/exit. With low energy this ATPase doesn’t function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What happens to fatty acids that enter the liver?

A
  • oxidised in mitochondria
  • used for cholesterol and phospholipids
  • oxidised to ketone bodies
  • esterified to make VLDL to go into circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How is VLDL made and what problem occurs if a step is compromised?

A

fatty acid –> esterified to triacylglyceride –> bound with apoprotein —> packed into VLDL –> circulation
if this is compromised (apoprotein synthesis or packaging into VLDL) = fatty change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What does a corticosteroid do?

A

induces transcription of glycogen synthetase = excessive storage of glycogen = steroid hepatopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are hyaline droplets and what do they stain as?

A

they are accumulations of proteins within cytoplasm. Eosinophilic staining.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What do glyoproteinoses, sphingolipidoses, glycogenoses and ceroid-lipofuscinoses have in common?

A

All inherited lysosomal storage disorders where substrate cannot be broken down (enzyme disfunction/absence or absence of activator protein) - accumulate in lysosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Can lysosomal storage disorders be acquired?

A

Yes - exogenous toxins such as swainsonin/alkaloid inhibiting lysosomal alpha mannosidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How can you identify amyloidosis?

A

It is an amorphous, eosinophilic extracell. material. Stains red with Congo red stain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the two main forms of necrosis?

A

a) oncotic = death by swelling, membrane breakdown = leak. More common and pathological, involves immune response.
b) apoptosis = cell suicide, death by shrinkage - chromatin, fragmentation –> phagocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the pathogenesis of Apoptosis?

A

Suicide - uses cells own caspase enzymes –> cleaves cytoskeletal proteins, activates endonuclease, cleaves nuclear proteins. Flipping of phospholipid membrane = abnormal –> phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the pathogenesis of oncotic necrosis?

A

cell membrane injury = influx of calcium into cell = intracellular messenger and enzyme activator.
- phospholipases active = membrane destruction
- Atlases accelerate ATP depletion
- proteases - destruct membrane and cytoskeleton
- endonucleases - degrade nuclear chromatin
Cell death = release of cellular contents - stimulate immune response. Degradation by own lysosomal enzymes (autolysis) or recruited leukocytes (heterolysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

List the three different appearances of the nucleus

A

pyknosis: shrunken, dark staining
karyorrhexis: rupture of nuclear envelope
karyolysis: fading nucleus (RNA/DNAases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How can you grossly see oncotic necrosis?

A 
Sharply demarcated from viable tissue as active inflamm reaction. 
red border (hyper perfusion), internal white border (leukocytes with lysosomal enzymes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the two types of gangrenous necrosis, what do both stem from?

A

Both from coag necrosis.

1) dry - mummified by dehydration
2) wet/gas - necrosis then colonisation by bacteria –> liquefaction and putrefaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are differences between liquefactive and caseous necrosis?

A

liquefactive - from rapid degradation of cells and accumulation of neutrophils = pus
Caseous - dry debris +/- mineralisation often with rim of inflammation or fibrous tissue capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are some causes of fat necrosis?

A
  • lipolytic enzymes from necrotic exocrine pancreas
  • trauma
  • ROS damage as deficient in Vit. E and selenium
  • hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is dystrophic mineralisation?

A

Accumulation of calcium salts in tissues with oncotic necrosis = gritty, hard, chalky foci

intracel - accum of Ca2+ in mitochondria of dead cells
extracell = ca2+ to membrane phosphates of disintegrating cells = mycrocrystal formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Give an example of an environmental signal

A

light = change in rhodopsin (photoreceptive protein) -> activates transducin -> cGMP lowered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the function of a tropic hormone?

A

to regulate hormone production of another cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Where is the pituitary gland located and how is it divided?

A

it is in the sella truck, connected to the hypothalamus by the sella turcica. Divided into anterior and posterior pituitary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

which pituitary portion receives portal venous inflow? What does this breach?

A

Only the anterior pituitary - breaches BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Where does the hypophyseal artery enter?

A

In the primary capillary plexus - in lower hypothalamus, takes up inhabit or releasing hormones –> portal system to secondary capillary plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the factors influencing release of Growth Hormone?

A

Growth hormone releasing hormone
Somatostatin (inhibits)
Ghrelin (peptide hormone from stomach, stimulates)
stress, exercise, nutrition, sleep, GH itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is ACTH and what does it do once in the bloodstream?

A

Adrenocorticotrophic hormone
To adrenal cortex = glucocorticoid release (cortisol, adrenal androgens)
Influenced by stress, circadian rhythms, feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the half life of a peptide hormone like?

A

short as unbound to plasma protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What to thyroid hormones and catecholamines have in common? How are they different?

A

Both amino derived
Thyroid - lipid soluble = intracel. target
Catecholamins - hydrophilic - alpha and beta surface receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What inhibits prolactin release?

A

Dopamine from hypothalamus - if stalk cut = no dopamine, so prolactin levels rise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What does low affinity mean in terms of the number or receptors to ligands?

A

High conc. of receptors to ligands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is meant by a molecular switch?

A

It means activation/inactivation by binding of molecules

  • activation by phosphorilation
  • guanine nucleotide to G protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the 6 steps to signal transduction?

A

1) recognition of signal
2) transduction (extracell. message to intracell)
3) transmission of second messengers
4) modulation of an effector (altering enzyme activity)
5) appropriate response
6) termination of response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Explain the activation of a G protein coupled pathway acting via adenylate cyclase (Gi/Gs)

A

ligand binds = conformational change of receptor. The Ga subunit binds to G protein and releases GDP, binds GTP. Gy and Gb components dissociate. G protein active until GTP is hydrolysed.
Active G protein activates adenylate cyclase allowing ATP –> cAMP
cAMP = secondary messenger: activates PKA to activate other certain enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How to adrenaline and prostaglandin act antagonistically in terms of G proteins?

A

Both act on adenylate cyclase
adrenaline activates it
prostaglandin inhibits it
They bind to two different G proteins (Gi and Gs) but have the same second messenger.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How does cholera toxin act with G proteins?

A

The bacterium secretes a toxin that can form a very similar activator to adenylate cyclase as G protein. Decays much slower so pathway not turned off.
In gut adrenaline to G protein receptor - adenylate cyclase activation = H2O and chloride secretion (with cholera this continues) = diarrhoea and dehydration

Give adrenaline antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What type of G proteins act via phospholipase C? What are the second messengers?

A

Gq proteins
Activation of phospholipase C = activation of IP3 and DAG
IP3 = intracell Ca2+ release
Ca2+ + DAG = protein kinase C activatiom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How are calmodulin and protein kinase C linked?

A

Protein kinase C subunit = calmodulin

if binds with Ca2+ = more catalytic efficiency/accelerating protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Can the Gyb subunit have a role?

A

Yes - while parasymp. ACh at the heart causes Gi protein activation, Gyb goes on to open K+ channels aiding in depolarisation - slowing of heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Explain the role of G proteins and NO signalling to increase blood flow

A

ACh/bradykinin/adenine nucleotides –> Gq at vascular endothelial cell –> IP3 –> Ca2+ and calmodulin
Ca2+ and calmodulin activate NO synthase = NO production
NO out od endothelial cell –> adjacent smooth muscle and activates guanylyl ciclase –> cGMP = phosporylation of muscle proteins = relaxation = vasodilation and increased blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the difference between a receptor tyrosine kinase and a tyrosine kinase linked receptor?

A
  • receptor tyrosine kinase: receptors themselves are protein kinases - cross-phosporilate with dimerisation then phosphorylate tyrosine residues on intracell. enzymes/proteins
  • tyrosine kinase linked receptor: don’t have intrinsic enzyme activ bind/dimerise first then bind cytoplasmic tyrosine kinase -> phosphorylate target proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is meant by the term desensitisation?

A

if a particular signal persists, the threshold to elicit transduction increases - down regulate receptors, alter receptor (lower affinity) or make it unable to initiate changes in cellular function

74
Q

How does skeletal muscle move bone?

A

Through muscle tendon complex

muscle contraction = pulling on tendon = pulling on bone

75
Q

What do muscle spindles allow perception of?

A

Stretch = sensory nerve stimulation = perception of position, velocity and acceleration of contraction

76
Q

what is the role of the fascia adherens?

A

To anchor actin to nearest sarcomere (cardiac muscle)

77
Q

What determines the size of the cell body of a neuron?

A

the level of activity and length of processes it has to support

78
Q

Why would we want to reduce astrocyte activity with spinal chord injury?

A

They are the scar forming cells = block reinervation

79
Q

What is a satellite cell?

A

Glial cell covering ganglion cells, thought to have similar role to astrocytes in CNS

80
Q

Why will the resting membrane potential not decrease to equilibrium potential of potassium?
How is this RMP maintained?

A

Even though more permeable to K+ (dif. out of cell), sodium will diffuse into the cell down conc. gradient
these gradients are maintained by Na+/K+ ATPase (2K+ in, 3Na+ out)

81
Q

What is the absolute refractory period?

A

Period after action potential where Na+ permeability changes

82
Q

What determines the velocity of an action potential?

A

diameter of axon and myelination of neuron

83
Q

Why is the location of the synapse also of importance for the outcome (action potential or not)

A

The postsynaptic cell body has resting membrane potential much closer to threshold
spacial summation can also occur

84
Q

What does binding of ACh at nicotinic receptor on skeletal muscle do?

A

Sodium channel opening = depolarisation

85
Q

How is the number of fibres in a motor unit related to fine control of muscle?

A

If less fibres controlled by motor unit = finer control

86
Q

What is the release of ACh from neuron dependent on?

A

Action potential –> calcium influx presynaptically allowing fusion of vesicles

87
Q

What is the role of calcium in skeletal muscle contraction?

A

It is released from the sarcoplasmic reticulum by depolarisation (Na+ influx) - then bins to troponin = shift of tropomyosin = actin myosin binding.
Need Ca2+ removal back into sarcoplasmic reticulum to stop contraction (Ca2+ ATPase)

88
Q

What has to happen for muscle to relax?

A

Ca2+ must be moved out of cytoplasm and action potential has to be stopped (ACh degradation)

89
Q

What are the three roles of ATP

A

1) energy for power stroke
2) breaking of cross bridge (binds to myosin)
3) drives Ca2+ ATPase pump

90
Q

When are more motor units recruited?

A

In increased intensity of stimulation - recruit more motor units until all activated

91
Q

What are the three cells found in heart muscle?

A

myocardial cells, pacemaker and parking fibres

92
Q

Does smooth muscle have t-tubules and a sarcoplasmic reticulum?

A

No they have calveoli (membrane invaginations) - sarcoplasmic reticulum only if rudimentary, have very low stores of intracell. Ca2+

93
Q

Where is multiunit smooth muscle found?

A

large airways of lungs, ciliary muscle of eye

94
Q

What role does calcium play in smooth muscle contraction?

A

Mostly extracell calcium, in through ligand gated ion channel. Binds to calmodulin in cytoplasm
Ca-clamodulin -> myosin light chain kinase active –> phosphorylation of myosin cross bridges = binding with actin filaments

95
Q

What is the difference between Golgi tendon organs and muscle spindles?

A

Golgi: in tendons, reports tension and force of muscle contraction
Muscle spindles: in muscle, report stretch

96
Q

What does the muscle spindle detect?

A

rates of change in stretching of muscle and changes in length of muscle - constant feedback and minute adjustments

97
Q

What are motor neurons are intrafusal and extrafusal fibres supplies by?

A

Intrafusal: gamma motor neuron
Extrafusal: alpha motor neuron
normally coactivation of both

98
Q

Describe the stretch reflex and reciprocal innervation

A

muscle spindle detects stretch –> synapses with alpha motor neurone in spinal chord –> contraction of muscle that was stretched

reciprocal innervation: in spinal chord synapses with inhibitory interneuron –> relaxation of antagonistic muscle

99
Q

In stretch reflex and Golgi tendon response - is the brain made aware of what has happened?

A

yes but often after response has occurred, from spinal chord - signal to brain for appraisal of change

100
Q

Describe the tendon reflex

A

contraction of muscle –> synapses with inhibitory interneuron –> motor nerve to relax contracted muscle

reciprocal innervation: excitatory interneuron at spinal chord –> motor nerve –> contraction of antagonistic muscle

101
Q

What is the EC50 a measure off?

A

the potency of a drug, how much to give

102
Q

What is Vd?

A

Volume of distribution = X/C, where X is drug administered and C is concentration measured after administration.
shows us extent of distribution but not location. To determine initial dose.

103
Q

What is Clearance?

A

The irreversible removal of drugs by excretion or metabolism

104
Q

What can t1/2 be used for?

A

To determine dosing interval

105
Q

What neurotransmitter is found in the ganglia of the autonomous nervous system?

A

ACh binding to nicotinic receptors

106
Q

What neurotransmitter is used at the target for parasympathetic postganglionic neurons? and what receptor?

A

ACh to Muscarinic receptor

107
Q

What kind of muscarinic receptors are there and where are they found?

A

M2: cardiac, Gi = inhibitory by opening K+ channels, decrease heart rate
M3: smooth muscle/glandular, Gq = stimulatory, IP3 = increase in Ca2+ increase contraction of GIT and secretion

108
Q

What type of receptor do sweat glands have? Are they parasympathetic or sympathetic? What is the postganglionic neurotrans?

A

Muscarinic, Sympathetic, bound by ACh

109
Q

What are the different types of adrenoceptors?

A

a1 - smooth muscle contraction
a2 - inhibitory, pre junctional, contraction of smooth muscle
b1 - heart, increase in contractility
b2 - airways, dilation of muscle/blood flow
b3 - fat - lipolysis

110
Q

How is Adrenaline synthesised

A

From tyrosine
tyrosine –> (into cell) L-Dopa –> Dopamine –> (into synaptic vesicle) NA –> Adr (into blood - stimulation of release by sympathetic NS)

111
Q

What do the adrenal glands secrete

A

Adr, NA, Aldosterone

112
Q

Is NA found in the blood?

A

No - mainly neurotransmitter at postganglionic parasymp. nerves

113
Q

How can NA action be increased?

A

Decreasing reuptake of presynaptic neutron with drugs
- cocaine
- desipramine
By stimulating non exocytotic release (not calcium dependent) with sympathomimetics
- amphetamine
- Epinephrine

114
Q

Name a selective agonist and antagonist of alpha 1 and their effects. (a1pp)

A

Agonists: phenylephrine –> constriction of blood vessels.
Increases BP, decongests, reflex bradycardia = decreased heart rate

Antagonists: Prazosin –> dilation of blood vessels
Decreases BP

115
Q

Name a selective agonist and antagonist of alpha 2 and their effects. (a2cy)

A

Agonist: clonidine –> decrease peripheral vascular resistance = decrease BP

Antagonist: yohimbine –> at low doses causes increase in BP

116
Q

Name a selective agonist and antagonist of beta 1 and their effects. (b1da)

A

Agonist: Dobutamine –> (treat heart failure) - increases contractility and cardiac output

Antagonist: Atenolol –> decreases heart rate and workload (treat hypertension)

117
Q

Name a selective agonist and antagonist of beta 2 and their effects.

A

Agonist: Salbutamol –> relaxation of smooth muscle

118
Q

How is ACh synthesised?

A

Choline –> (into cell) binds with acetyl (from acetyl CoA) –> ACh –> into vesicle

119
Q

What are the actions of muscarinic receptors?

A

SLUD, sweating, slowing of heart, bronchoconstriction, vasodilation

120
Q

Name agonists of muscurinic receptors

A

pilocarpine
carbachol (in GIT and bladder paralysis)
bethanecol (obstruction)

121
Q

What are methods to increase ACh action?

A

Anticholinesterases (drugs)

  • physiostigmine
  • neostigmine (more active at NMJ) - use for myasthenia gravis (more ACh for decreased number of receptors) and can reverse blockage by tubocurarine)
122
Q

How can release of ACh be modulated?

A
  • need calcium for exocytosis

- drug: Botulinum toxin used to cleave snare proteins = cannot bind vesicles

123
Q

Name to muscarinic antagonists and when you would use them

A

Atropine: antiSLUD: can increase heart rate - but if very fit and parasymp. NS dominates heart muscle tone - will cause tachycardia. Reduces secretions.

Hyoscine: motion sickness

124
Q

What does physostigmine do?

A

is an anti cholinesterase - increases ACh action

125
Q

What does neostigmine do? Where does it act?

A

is an anti cholinesterase - more active at NMJ

126
Q

What is a H1 receptor antagonist known as? What are they used for?

A

Antihistamines

For hayfever, anaphylaxis, atopic dermatitis

127
Q

How can peptic ulcers be treated?

A

H2 receptor antagonist (cimetidine, ramitidine)

Block receptor on parietal cell for Histamine = decrease acid production

128
Q

What is Bradykinin? What does it do?

A

local peptide released with plasma exudation

Action: increases vascular permeability = inflam. and stimulates sensory nerve endings = pain

129
Q

What are prostanoids?

A

All from arachidonic acid and COX pathway

prostglandins and prostacyclins

130
Q

Are eicosanoids stored?

A

No produced on demand

131
Q

What do leukotrienes cause?

A
  • chemoattractant

- constriction of bronchi

132
Q

What are the actions of PG’s?

A

vasodilation and pain (PGI), mast cell degranulation (PGD), platelet aggregation (TXA), fever and pain (PGE)

133
Q

How is blocking the COX pathway beneficial? What blocks this?

A
  • NSAIDs block - no PGE2 = no pain, no fever = enhanced clinical benefits - but also decreased mucous production
  • Glucocorticoids (also at many other levels)
134
Q

What are the four decisions an embryogenic cell must make

A

1) division to increase in number
2) differentiate
3) cell morphology change
4) apoptosis

135
Q

What are the three broad periods of gestation?

A

ovum
embryo
foetus

136
Q

What is a morula? What does this turn into?

A

Morula = ball of cells

–> Blastomere = beginning of differentiation, loose spherical shape

137
Q

What is gastrolation broadly?

A

Formation of three germ layers

- ectoderm, mesoderm and endoderm

138
Q

What is cleavage?

A

Division of cells without increasing in volume (hyperplasia)

139
Q

What is a blastocyst?

A

3 layers:
embryonic disc: inner cell mass
trophoblast cells: absorb nutrient (and enzymes that degraded the zone pellucida)
cavity: blastocoele

140
Q

What is the chorion?

A

extra-embryonic membrane
trophoectoderm and mesoderm derived
attach to uterus, sac around everything

141
Q

How does gastrulation progress?

A

thickening of the embryonic disk and delamination –> two layers. Trophoblast, amnionic cavity and bilaminar embryonic dic. with inner epiblast and outer hypoblast.

Formation of primitive streak - head and tail/axis. epiblast and hypoblast separate. Epiblast through streak –> endoderm and mesoderm. Hypoblast week replaced by endoderm.

Mesoderm splits into two layers: coelum
somatic mesoderm - attached to ectoderm
splanchnic mesoderm - attached to endoderm

142
Q

What is the yolk sac?

A

extra-embryonic membrane
primitive endoderm derived,
regresses with time

143
Q

What is the allantois?

A

extra-embryonic membrane
primitive gut derived
collects waste from embryo and fuses with chorion –> foetal contribution to placenta

144
Q

What is the allantois?

A

extra-embryonic membrane
primitive gut derived
collects waste from embryo and fuses with chorion –> foetal contribution to placenta

145
Q

What is the notochord?

A

A rod shaped aggregation of cells cranial to primitive streak in mesoderm.
Marks location for future spinal chord.
Directs procesesses (head formation)

146
Q

What is neurolation?

A

Initial development of gut, heart and formation of NS

147
Q

How is the neural tube formed?

A

Thickening of ectoderm over notochord forming neural plate. Elevation = neural folds converge at midline.

148
Q

What are neural crest cells?

A

Cells at the lateral margins of the neural tube - go on to form other structures

149
Q

What are somites? And what are the tissues called moving laterally?

A

Balls of mesoderm tissue that form spine and limb buds. Can be used for waging.

tissue closest to neural tube/paraxial mesoderme = somite –> intermediate mesoderm (urinary and reproductive system) –> lateral mesoderm (somatic and splanchnic - forming cavities)

150
Q

What occurs following gastrulation?

A

The embryo becomes C shaped

  • surface ectoderm invaginate = pharyngeal clefts
  • internal endoderm evaginates = pharyngeal pouches
  • cardiac bulge
  • limb buds
151
Q

What is the difference between aplasia and hypoplasia

A

None really can be used interchangeable

= failure to grow

152
Q

Why would a cell change in structure and function?

A

To adapt to physiological stress or adverse stimuli - to find a new steady state and survive

153
Q

What are some causes of atrophy?

A 
decreased workload
loss of innervation
decreased blood supply
loss of endocrine stimulation
obstruction of secretory ducts
inadequate nutrition 
ageing
154
Q

What is serous atrophy of fat?

A

In emaciated animals - rapid mobilisation of fat stores = gelatinous, pale pink transformation
If very advanced - serous atrophy of bone marrow

155
Q

What is serous atrophy of fat?

A

In emaciated animals - rapid mobilisation of fat stores = gelatinous, pale pink transformation
If very advanced - serous atrophy of bone marrow

156
Q

How can small intestinal villous atrophy occur? What clinical signs might you see?

A
  • loss of enterocytes from villi
  • necrosis/imparied mitosis of crypt stem cells
  • dysregulation of crypt stem cell proliferation and enterocyte maturation

Clinical signs: diarrhoea (decreases SA, osmotic drag)

157
Q

What is abiotrophy?

A

Genetically programmed premature or accelerated degeneration of mature cells

158
Q

What is meant by replicative senescence? What enzyme can prevent this and where is it present?

A

Cells have a fixed number of divisions determined by the length of their telomeres.

Telomerase can extend these, found in tumour cells

159
Q

What are senile cataract and how are they related to ageing?

A

Accumulation of abnormally folded protein causing blindness

Protease function declines with age = persistence of these proteins.

160
Q

Is it grossly possible to distinguish between hypertrophy and hyperplasia?

A

No - need a microscope

161
Q

In what tissues can hyperplasia occur?

A

Only in those capable to mitotically divide

162
Q

How is hyperplasia different to neoplasia

A
  • responds to stimuli

- excess cells will be deleted by apoptosis

163
Q

What is metaplasia? Why would this occur?

A

It is the transformation (better: replacement) of a fully mature cell type into another mature cell type - through mitotic division.
Often occurs in order to form more resistant cell type in exchange for specialised function

164
Q

Where can metaplasia be seen?

A
  • with chronic irritation of epithelium/mucosa i.e. urinary tract with uroliths: epithelium may become stratified squamous
  • with chronic irritation - can get mucus secreting cells in fundic mucosa (decrease HCL secretion = decrease digestion)
165
Q

What is cellular pleomorphism?

A

Lack of uniformity - variation in cell and nuclear size, shape and appearance.
Seen with dysplasia

166
Q

What is Stroma?

Is it neoplastic?

A

The connective tissue supporting neoplastic cells.

Not neoplastic, will not grow without neoplastic cells.

167
Q

What are the four means to distinguish between benign and malignant neoplasia?

A

1) invasion into adjacent tissue
2) metastasis
3) degree of differentiation
4) growth rate

168
Q

What are the three pathways of metastasis?

A

1) haematogenous (favoured by sarcoma)
2) lymphatic (favoured by carcinoma)
3) implantation

169
Q

What would you call a benign epithelial neoplasm:

  • that is glandular
  • that is non-glandular
A

glandular: –adenoma

non-glandular: –papilloma

170
Q

What would you call a malignant epithelial neoplasm:

  • that is glandular
  • that is non-glandular
A

glandular: –adenocarcinoma

non-glandular: carcinoma

171
Q

What is the difference in naming: –oma vs. –sarcoma?

A

Both mesenchymal neoplasms.

  • -oma: benign
  • -sarcoma: malignant
172
Q

What is a teratoma?

A

Neoplasm with cells of more than one germ layer (multipotent cells, testes and ovaries) - have well differentiated tissue - bone, teeth

173
Q

What is a choristoma?

A

Malformation, normal cells at abnormal location. Not neoplastic

174
Q

What is meant by paraneoplastic syndrome? Give examples

A

Diseases seen with neoplasm but not directly caused by neoplasm

  • pyrexia (pro-inflam. cytokine in response to neoplasm)
  • autoimmune response (antigen expressed in tumour cells, can cause cross reactive antibodies with host as v similar morphology –> immune mediated haemolytic anaemia)
  • hormone secretion (parathyroid related hormone stimulating bone resorption to increase blood Ca2+)
175
Q

What are the 4 normal regulatory genes of growth/division?

A

1) proto-oncogenes
2) tumour supressor genes
3) genes involved in DNA repair
4) genes regulating apoptosis

176
Q

What are the 8 Hallmarks of Neoplasia?

A

1) No need for growth signals/produce own
2) No response to growth inhib signals
3) No apoptosis
4) Have telomerase = immortality
5) Angiogenesis - can vascularise themselves
6) can survive with glycolysis always
7) Avoid immune response
8) Can invade and metastasise

177
Q

What are the three categories of chemical carcinogens?

A

1) initiators - direct DNA damage
2) promoters - increase proliferation of mutated cells, increase chance of survival;
3) complete - initiate and promote (ionizing radiation)

178
Q

How do viruses cause cancer? Give some examples.

A
  • altering expression of normal regulatory genes
  • introducing virally encoded homologues of proto-oncogenes
  • inducing chronic inflam = oxidative DNA damage

e.g. retroviridae = feline leukaemia virus

179
Q

What bacterium is neoplasia causing?

A

H. pylori –> gastric adenocarcinoma and lymphoma

180
Q

What is tubocurarine?

A

Nicotinic recpetor antagonists = skeletal muscle relaxant. Can still get contraction with direct stimulation. Reversible.

181
Q

What is tetrodotoxin?

A

Voltage operated Na+ channel blocker

182
Q

What is Suxamethonium and what happens if ACh is increased in the synapse? Or if directly stimulated?

A

Nicotinic receptor agonist - constant depolarisation = unable to contract,
even if increase in ACh (neostigmine) as sodium channels are open = constant depolarisation.
Direct stimulation would not cause contraction either.

Cells 2 Systems General Revision (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions