Brainscape's Knowledge GenomeTM

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


See full index

Medicine Unit 4 > UNIT 4 REVISION > Flashcards

UNIT 4 REVISION Flashcards

1
Q

left shift

A

decreased temp
decreased H+
CO

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

right shift

A

reduced affinity
oncreased temp
ioncreased H+

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

somatic sensory

A
  • Receptor
  • Afferent
  • Ventral/Dorsal ramus
  • Spinal nerve
  • Dorsal root
  • Spinal cord
  • Synapse in the dorsal horn of grey matter
  • Neurotransmitter: acetylcholine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

somatic motor

A
  • Ventral horn of grey matter
  • Efferent
  • Ventral root
  • Spinal nerve
  • Dorsal/ ventral ramus
  • Synapse at the effector
  • Neurotransmitter: acetylcholine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

sympathetic efferent

A

thoracolumbar outflow
- Preganglionic sympathetic fibre in the lateral horn of grey matter
- Ventral root
- Mixed spinal nerve
- White ramus of communicans (myelinated)
- Synapse in the sympathetic ganglion
- Meets the post ganglionic fibre
- Post ganglionic passes through the grey ramus of communicans (not myelinated)
- Target tissue
- Neurotransmitter: in presynaptic it is acetylcholine and in post it is noradrenaline

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

parasympathetic efferent

A

craniosacral outflow
- Efferent through the ventral horn of grey matter
- Ventral root
- Spinal nerve
- Dorsal/ventral ramus
- Synapse in the ganglion before the target tissue
- Neurotransmitter: acetylcholine

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

where do splanchnic nerves synapse

A

pre vertebral ganglia

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

p wave

A

atrial depolarisaiton

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

pr interval

A

time taken for electrical activity to move between atria and the ventricles

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

QRS

A

depolarisation of the ventricles

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

ST segment

A

isoelectric line
time between depolarisation and repolarisation of the ventricles

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

T wave

A

ventricular repolarisation

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

RR interval

A

peak of one r wave to peak of next R wave

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

QT complex

A

ventricles to depolarise then repolarise

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

passive ventricular filling

A

pressure in ventricles lower than in atrai
tricuspid opens
ventricles passively fill with blood

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

atrial ejection

A

atria contract
rest of blood to the ventricles
semilunar close as pressure higher in arteries than ventricles

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

isovolumic contraction

A

ventricles contract
tension building
pressure higher in ventricles than atria
AV slam shut
pressure not high enough to open aortic and puilmonary

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

ventircular ejection

A

pressire in ventricles higher than arteries
aoritc and pulmonary valves open

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

isovolumetric ventricular repolarisation

A

ventricles astart to relax
pressure lower in the ventricles than the arteries
aortic and pulmonary valves slam shut
ventricular pressure higher than the atria
AV valves still shut

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

isotonic contraction

A

same tension, length changes

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

isometric contraciton

A

same length, tension changes, occurs if load is too heavy to move

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

length tension relaitonship

A
  • Cardiac muscle will only operate on the ascending limb of the curve
  • As cardiac muscle is stiffer than skeletal
  • Preload for left ventricle is EDV
  • Afterload is the aortic pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

frank starling relationship

A
  • Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole
24
Q

stroke volume

A

volume of blood ejected on each beat, EDV- ESV, roughly 70ml

25
Q

ejection fraction

A

fraction of the EDV ejected in one storke volume, storke volume divided by EDV

26
Q

cardiac output

A

total volume ejected by the ventricle per unit time, equal to venous return

27
Q

what factors affect storke volume

A

prelaod
contractility and afterload

28
Q

preload and SV

A

`- Changes in stroke volume occur following changes in resting ventricular muscle fibre length (preload)
- Mechanism intrinsic to the heart

29
Q

contractility and SV

A
  • Inotropic effect
  • Changes in stroke volume without changes in resting ventricular muscle fibre length (no change in preload)
  • Mechanism extrinsic to the heart
30
Q

afterload and SV

A
  • Changes in aortic pressure
31
Q

absolute refractory

A
  • closure of inactivation gates of sodium channel in response to depolarisation
  • gates closed position until cell is depolarised back to resting membrane potential and Na+ have recovered to closed but available state
32
Q

relative refractory

A
  • action potential can be elicited
  • only if a greater than usual depolarisation current
  • higher K+ conductance than is present at rest
  • membrane potential is closer to K+ equilibrium potential
  • more inwards current needed to bring membrane to threshold for next action potential to be initiated
33
Q

ion currnt

A

occurs when there is movement of an ion across the cell membrane

34
Q

when will ions move across the cell membrane

A

when there is 1. driving force on the ion
2. membrane has conductance to the ion

35
Q

cardiac action potential

A

Phase 0: upstroke, rapid depolarisation, Na+ influx
Phase 1: initial repolarisation, Na+ influx stops, K+ efflux
Phase 2: plateau, stable depolarisation, Ca2+ influx via L-type calcium channels, k+ efflux
Phase 3: repolarisation, Ca2+ influx stops, K+ efflux
Phase 4: resting membrane potential, close but not equal to K+ equilibrium potential

36
Q

SAN action potentia

A

Phase 0: upstroke, rapid depolarisation, Ca2+ influx
Phase 3: repolarisation, Ca2+ influx stops and K+ efflux
Phase 4: influx of Na+ through funny channels which is turned on by repolarisation from previous AP, gradient restored

37
Q

features of SAN actrion potentials

A

Features of SAN action potentials:
1. automaticity: spontaneous AP generation without neural input
2. unstable resting potential
3. no sustained plateau

38
Q

chronotropic effects

A

effects on autonomic nervous system on the heart rate , increase is sympathetic

39
Q

dromotropic effects

A

: effects on the autonomic nervous system on conduction velocity, increase is the increase in conduction velocity through AV node

40
Q

inotropism

A

intrinsic ability of myocardial cells to develop force at a given muscle length, increase will increase contractility

41
Q

amount of Ca2+ depends on what

A
  1. size of inward Ca2+ current
  2. amount of Ca2+ previously stored in the SR for release
42
Q

phases of ventricular pressure volume loops

A

isovolumetric contraction is 1 to 2
ventricular ejection is 2 to 3
isovolumetric relxation is 3 to 4
ventircular fillng is 4 to 1

43
Q

diastolic pressure

A

pressure during ventricular relaxation, lowest pressure

44
Q

systolic pressure

A

: highest pressure, pressure after the blood has been ejected

45
Q

dicrotic notch

A

when aortic valve closes, brief period of retrograde flow towards valve, briefly decreasing aortic pressure below systolic

46
Q

pulse pressure

A

difference between diastolic and systolic

47
Q

mean arterial pressure

A

Pa, average pressure over complete cardiac cycle, DP + 1/3 pulse pressure, 70-100 mmHg

48
Q

blood floq

A

Q= different in pressure / resistance

49
Q

total peripheral resistance

A

resistance of entire systemic vasculature (TPR) or systemic vascular resistance (SVR)
R a 1/r4 (remember this!)

50
Q

baroreceptors

A

carotid sinus
aortic arch

51
Q

carotid sinus baroreceptors

A

glossopharyngeal
nucleus tractus solitarus
cardiac decelerator
parasympathetic
SAN

52
Q

aortic arch baroreceptors

A

vagus
nucleus tractus solitarus
decreases careidac acceleratory and vasoconstriction
increases SAN, contractility, arterioles and venous vasodilation

53
Q

carotid sinus massage

A
  • Massage carotid sinus distends the barorecpetors
  • Increases vagal outflow to the heart
  • Slows SA firing and AV conduction
  • AVN conducts fewer action potentials through ventricles
  • Less QRS complexes, ventricular rate slows from dangerously high rates
54
Q

diving reflex

A
  • Cold water stimulates the sensory receptors of the trigeminal nerve and receptors in the nasopharynx and oropharynx
  • Resulting in:
    1. Apnoea
    2. Bradycardia
    3. Peripheral vasoconstriction
55
Q

procedure of valsalva manoeuvre

A
  1. Inhale deeply and then hold the breath.
  2. Imagine that the chest and stomach muscles are very tight and bear down as though straining to initiate a bowel movement.
  3. Hold this position for a short time, usually about 10 seconds.
  4. Breathe out forcibly to release the breath rapidly.
  5. Resume normal breathing
56
Q

physiology of valsalva

A
  1. Increased intrathoracic pressure increases blood flow from the pulmonary circulation into the left atrium. This increases left ventricular EDV and SV. There is also compression of the aorta, increasing blood pressure.
  2. High intrathoracic pressure impedes venous return, decreasing SV and therefore also blood pressure. During this period, there is a baroreceptor-mediated increase in heart rate.
  3. When the manoeuvre is released, compression on the aorta is stopped and left ventricular filling pressures are reduced temporarily as the pulmonary vessels re-expand. This causes a drop in blood pressure.
  4. VR is restored, increasing cardiac filling pressures and SV. This increases BP, resulting in a baroreceptor reflex-mediated bradycardia and subsequent fall in BP to normal levels.

Medicine Unit 4 (19 decks)

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