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BMS200 > test 2 key > Flashcards

test 2 key Flashcards

1
Q

what are the 2 things that the force of a cardiomycote depends on with each systole

A
  1. ionotropy (contractility)
  2. optimal overlap between myosin and actin in diastole
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2
Q

what is ionotropy and what is it increased by

A

contractility from calcium binding troponin

increased by SNS, HR, cortisol, thyroid homrone

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3
Q

what is the optimal overlap between actin and myosin in diastole length? what’s it determined by?

A

(1.95-2.25)

Determined by preload (ventricular filling- end diastolic volume)

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4
Q

afterload

A

(pressure to overcome to eject blood into great arteries).
Tension the ventricles need to open aortic valve

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5
Q

what increases afterload

A

Increased by aortic stenosis, elevated BP

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6
Q

increasing afterload has what effect on stroke volume and ejection fraction

A

Increasing afterload decreases stroke volume and ejection fraction

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7
Q

if ionotropy decreases then what happens to ejection fraction and stroke volume

A

decreased ejection fraction  lower stroke volume

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8
Q

chronotropy

A

Rate of depolarization aka heart rate

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9
Q

how much of ventricular filling is passive

A

80%

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10
Q

which side of heart has lower pressure

A

right ventricle bc left ventricle goes into systemic

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11
Q

Atrial pressure curve

A
  • A Wave – Atrial contraction (atrial systole)
  • C Wave – Bulging of tricuspid
  • X Wave – Atrial relaxation (atrial diastole)
  • V Wave – Passive filling of the atria (ventricular systole)
  • Y Wave – Emptying of atria into the ventricles with the opening of AV valves (early diastole).
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12
Q

what is the dicrotic notch

A

2nd wave after aortic valve closes (elastic recoil)

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13
Q

s3 and s4 ok?

A
  • S3 in healthy people unless new emergence (MI)
  • S4 pathologic (non compliant ventricle)
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14
Q

what part of the heart has the highest pressure and is what causes our 120/80 blood pressure

A

aorta

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15
Q

what corresponds to preload

A

end diastolic volume

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16
Q

what is end diastolic volume

A

the volume in the ventricle at the end of diastole

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17
Q

what is end systolic volume

A

the volume in the ventricle at the end of systole

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18
Q

what is stroke volume

A

the volume ejected with each heartbeat

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19
Q

formula for stroke volume

A

SV = EDV – ESV

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20
Q

what is stroke volume impacted by

A
  • Preload
  • Contractility (inotropy)
  • Afterload
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21
Q

increasing afterload does what to stroke volume and ejection fraction

A

decreases stroke volume and ejection fraction (higher oxygen demand in hypertension)

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22
Q

cardiac ouput

A

is the volume ejected by each systole X heart rate

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23
Q

cardiac output formula

A

CO = SV X HR

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24
Q

what determines oxygen and nutrient delivery to tissues

A

cardiac ouput

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25
Q

what is cardiac output increased by

A

catecholamine, stretching of ventricles, increased HR and contractility, increased central blood volume, increased systolic BP, increased preload and venous return

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26
Q

what is the SNS trope effect and how does it increase cardiac output

A

accumulate Ca2+ in SR as HR increases; not enough time to remove Ca2+

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27
Q

what decreased cardiac ouput

A

PNS

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28
Q

why does cardiac output need to be equal in the left and right ventricle

A

ventricle to prevent pulmonary congestion and systemic hypoperfusion

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29
Q

what is ejection fraction

A

is the proportion of EDV that is ejected each beat

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30
Q

what is an estimate of heart function in heart failure

A

ejection fraction

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31
Q

what is a normal ejection fraction

A

> 50%

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32
Q

ejection fraction formula

A

▪ EF = SV/EDV = (EDV – ESV)/EDV

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33
Q

preload of one ventricles depends on ____ of the other

A

cardiac output

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34
Q

SERCA (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase)

A
  • Reuptake Ca2+ into SR after contraction
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35
Q

what happens if SERCA activity decreases

A

prolonged muscle relaxation (diastolic dysfunction), reduced Ca2+ release for contraction and weaker heartbeats (negative ionotropy)

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36
Q

Skeletal myocyte excitation contraction coupling

A
  1. Ach on nicotinic receptor  initial depolarization
  2. Na+ VGC open  depolarize sarcolemma (AP)  open Ca2+ VGC
  3. L type Ca2+ VGC opens ryanodine receptor in SR (T tubules get AP deeper into myocyte)
    a. Most Ca2+ that enters cytoplasm if from SR
  4. Increased cytosolic Ca2+ binds troponin  open myosin binding site on actin (move tropomyosin out of way)  cross bridge formed and force generation
  5. Ca2+ decrease when AP stop; pump Ca2+ into ECF or SR
  6. When Ca2+ decrease the tropomyosin covers myosin binding sites again  sarcomeres relax
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37
Q

what acts on nicotinic receptor to start excitation contraction coupling (in skeletal muscle)

A

Ach

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38
Q

what gets AP deeper into myocyte in skeletal muscles

A

t tubules

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39
Q

most of the Ca2+ that enters the cytoplasm is from the (in skeletal muscle)

A

SR

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40
Q

cross bridge cycle

A
  1. ADP + Pi on myosin head, allosterically inhibited by tropomyosin so cant bind actin
  2. Ca2+ binds troponin C so myosin can bind actin  rigor state  detach when ATP binds myosin head and is hydrolyzed
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41
Q

sarcomere

A
  • Thick (myosin) and thin (actin) filaments overlap for contraction and cross bridge
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42
Q

similarities in skeletal and cardiac myocutes

A
  • Striated, involve actin: myosin overlap
  • Parabolic isometric length: tension relationship
  • Peak isometric forces matches optimum passive resting length
  • T-tubules exist in both (get AP deeper into muscle fibers)
  • Ca2+ ATPase pumps to remove Ca2+ into SR
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43
Q

what is in cardiac myocytes that’s not in skeletal

A

no tetany in cardiac

have a syncytium

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44
Q

why no tetanic contraction in cardiac myocytes?

A

due to long electrical refractory period (extracellular calcium triggers intracellular calcium release)

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45
Q

syncytium in cardiac myocytes

A

cardiac myocytes are interconnected via branches and intercalated disks (gap junctions and desmosomes)

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46
Q

t tubules in cardiac myocytes

A

T tubules play a less important to the excitation- contraction coupling of cardiac cells; they are larger but fewer

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47
Q

cardiac cells; how many nuclei and mitochondria ? what form of metabolism?

A

cells have 1 single nucleus and LOTS of mitochondria

Oxidative metabolism (use fats), little glycogen stores

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48
Q

4 APs in the heart

A

myocyte:
1. atrial
2. ventricular

  1. purkinje
  2. automatic cell
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49
Q

4 phases of myocyte APs

A
  • Phase 4= resting membrane potential (RMP)
  • Phase 0= rapid depolarization (upstroke)
  • Phase 1 and 2= prolonged depolarization/plateau
  • Phase 3= repolarization
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50
Q

what’s shorter; atrial or ventricular APs?

A
  • Atrial APs shorter than ventricular, allowing for faster contraction cycles
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51
Q

purkinje fibers have an unstable phase _

A

unstable phase 4; can spontaneously generate APs in abnormal conditions

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52
Q

automatic cells are :

A

pacemaker cells (SA and AV nodes)

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53
Q

automatic cells have an unstable phase _ and depolarize via __________

A

unstable phase 4 to spontaneously depolarize via funny currents (If)

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54
Q

which node sets the HR

A

SA node

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55
Q

where is SA node located

A

SA nodes in right atrium close to entrance of superior vena cava

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56
Q

phase 4; what is open? memebrane potential?

A

resting membrane potential
o (leaky K+ channels are open)
o Nernst= -84mV

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57
Q

phase 0; what opens?

A

rapid depolarization
o open VGC Na+; Na+ influx

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58
Q

phase 1

A

initial rapid repolarization
o close Na+ VGC
o open fast K+ VGC allowing K+ efflux
o membrane potential close to 0

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59
Q

phase 2

A

plateau
o open L-type Ca2+ channels that allow Ca2+ to influx
o No summation is possible due to the prolonged depolarization of the myocyte, no further action potential can be delivered to the cardiac myocyte
o Plateau bc Ca2+ channels (in) and slow K+ channels (out) cancel each other out

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60
Q

phase 3

A

: slow repolarization
o Close Ca2+ channels
o open slow K+ VGCs

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61
Q

calcium spark

A

1 Ca2+ VGC opens and elicits small amount of Ca2+ release from neighbouring ryanodine receptor on SR  summation of these to increase cytosolic Ca2+

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62
Q

how to get ca2+ into SR? regulated by?

A
  • SERCA get Ca2+ into SR

Regulated by phospholamban (phosphorylate to increase activity)

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63
Q

how is calcium removed from cytoplasm

A

Calcium sequestered by sarcolemma calcium ATPase (ca2+ out) and sodium-calcium exchanger (3 Na in, 1 Ca out; depolarize)

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64
Q

activation of SNS has what effect on contractility

A
  • Active SNS (Beta 1 receptors)  increase cAMP  phosphorylate phospholamban and troponin and l-type Ca2+ VGC

SNS
- Increases cytosolic calcium release with each AP  greater force of contraction
- Increase relaxation after  reduced troponin affinity and increased SERCA activity
- Net: quick, forceful contraction and quicker relaxation

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65
Q

atria vs ventricular myocyte AP

A
  • Atria don’t need to generate as much force
  • RMP (phase 4) is slightly more depolarized (reduced K+)
  • Lower plateau (phase 2) (lack of Ca2+ channels)
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66
Q

what are the pacemakers

A
  • SA node, AV node, Purkinje fibers: generate APs spontaneously (no external stimuli)
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67
Q

primary pacemaker? bpm? backup?

A

a. SA node= primary pacemaker (60-100bpm)

i. AV node as backup
ii. Purkinje in pathologic states

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68
Q

heart rate is determined by

A

which cell depolarizes most frequently - SA node

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69
Q

phase 4 RMP in automatic cells

A

not stable; funny current from gNa+ and gK+ open during hyperpolarization and closed in depolarization

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70
Q

which phases are missing in automatic cells

A

phase 1 and 2

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71
Q

which phases are in automatic cell APs

A

phase 4, 0, 3

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72
Q

phase 0 and phase 3 in automatic cells

A
  • Depolarization in phase 0 if from L type Ca2+ channels NOT Na+ VGC (closed)
  • Phase 3: Ca2+ VGC close, K+ open (efflux = more negative)
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73
Q

PNS impacts on automatic cell AP

A
  • Increase K+ = hyperpolarize
  • Decrease Ca2+ influx= slow depolarization
  • Increased atrial refractory period= decrease HR and decrease cardiac output
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74
Q

negative and positive ionotropy

A
  • Positive ionotropy (contractility) = SNS increases rate of depolarization, RMP more +
  • Negative ionotropy= PNS decrease rate of depolarization, RMP more –
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75
Q

where in the conduction system is there a delay

A
  • Delay at AV node: time for atria to eject blood into ventricle prior to ventricular contraction
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76
Q

what carries the AP along the septum of the heart

A
  • Bundle of His (AV bundles)
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77
Q

where do purkinje fibers carry AP to

A

to apex and base of heart  ventricles contract

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78
Q

fibrous skeleton of heart purpose

A

isolates atria and ventricles and prevents direct conduction (so that only communication is via AV node)

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79
Q

Bachman’s bundle

A

allows for rapid conduction from right to left atrium = simultaneous atrial contraction

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80
Q

ECGs measure what

A

electrical differences across the heart

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81
Q

baseline in an ECG

A

= whole heart is either repolarized or depolarized

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82
Q

wave in an ECG

A

different electrical state in 2 separate areas of the heart

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83
Q

little box in an ECG

A

0.1mV high x 0.04 seconds wide

(big box= 0.5 mV x 0.2 seconds)

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84
Q

P wave

A

atrial depolarization (via SA node)

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85
Q

PR interval

A

time it takes for impulse to travel from SA node through atria and AV node to ventricles

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86
Q

QRS complex

A

ventricular depolarization (conduction pathway via Bundle of His and Purkinje fibers)

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87
Q

ST segment

A

when ventricles are fully depolarized, before they repolarize

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88
Q

T wave

A

ventricular repolarization

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89
Q

QRS interval

A

time it takes for AP to travel from end of AV node and throughout ventricles

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90
Q

QT interval

A

ventricular depolarization and repolarization

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91
Q

heart failure

A
  • Contractility is significantly impaired resulting in reduced ejection fraction (how much is pumped out versus how much remains in the ventricle)
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92
Q

cardiac arrest

A
  • Heart suddenly and unexpectedly stops pumping, often caused by ventricular arrhythmia’s, such as ventricular fibrillation or ventricular tachycardia
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93
Q

angina

A
  • Pain brought on by ischemia, that doesn’t result in permanent heart damage
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94
Q

tachyarrhythmia

A

Abnormal heart rhythm (arrhythmia) with a heartbeat of >100 beats per minute (tachycardia)

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95
Q

3 layers of walls of veins and arteries (in to out)

A

tunica intima
tunica media
tunica externa/adventitia

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96
Q

what’s in the tunica intima

A

a. Simple squamous endothelium, subendothelial CT, internal elastic lamina

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97
Q

what’s in the tunica media

A

a. Thickest layer in arteries
b. Smooth muscle cells and fibroelastric CT, external elastic lamina

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98
Q

what’s in the tunica advnetitia/externa

A

a. Outermost layer
b. Thickest layer in veins
c. Dense irregular CT
d. Houses vasa vasorum (blood vessels to supply tunica adventitia and media)

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99
Q

which layer is thickest in veins? in arteries?

A

arteries- tunica media
veins- tunica externa/adventitia

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100
Q

elastic arteries

A

have most elastic membranes (for high pressure blood flow from heart)
a. Aorta, pulmonary arteries, common carotid arteries, subclavian arteries, common iliac arteries

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101
Q

muscular arteries

A

have more smooth muscle (in tunica media) for regulating blood flow
a. Radial artery, femoral artery, brachial artery, coronary arteries, popliteal artery

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102
Q

arterioles

A

control flow into capillary beds and regulate BP through constriction or dilation

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103
Q

metarterioles

A

are transitional vessels between arterioles and capillaries (via precapillary sphincters to regulate blood flow)

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104
Q

what regulated blood flow to capillaries

A

pre capillary sphincter

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105
Q

3 types of capillaries

A

continuous
fenestrated
sinusoidal

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106
Q

what type of capillary is the majority

A

continuous capillaries

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107
Q

which capillary is the least permeable

A

continous capillarie

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108
Q

which capillary is the most permeabel

A

sinusoidal capillaries

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109
Q

continuous capillaries

A
  • Least permeable, majority of capillaries
  • Intercellular junction for flow of water-soluble substances
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110
Q

fenestrated capillaires

A
  • Moderately permeable (filtration and absorption organs i.e. kidneys, endocrine glands)
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111
Q

kidneys, endocrine, pancreas, intestines are which type of capillary

A

fenestrated

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112
Q

sinusoidal capillaries

A
  • Highly permeable to large particles (i.e proteins), in specialized organs (liver, spleen, etc)
  • Discontinuous basal lamina, big gap junctionsw
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113
Q

what type of capillaries are CT, muscle, neural, brain

A

continuous capillaries

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114
Q

what type of capillaries are bone marrow, spleen, lymph

A

sinusoidal capillaries

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115
Q

large veins

A
  • i.e. vena cava, pulmonary veins, portal vein
  • tunica intima has prominent subendothelial layer
  • tunica media is thin with few muscle cells
  • tunica adventitia is thickest layer with dense CT, collagen, elastic fibers, vasa vasorum
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116
Q

function of large veins

A

return deoxygenated blood to heart from systemic

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117
Q

medium veins

A
  • i.e. femoral vein, renal vein, brachial vein
  • tunica intima is think subendothelial layer
  • tunica media is thin and scattered smooth muscle cells
  • tunica adventitia is thickest layer with collagen and elastic fibers
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118
Q

what do medium veins have to prevent back flow

A
  • valves in limbs to prevent backflow of blood due to low pressure
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119
Q

function of medium veins

A

drain blood from organs and limbs using valves to direct blood flow towards heart

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120
Q

small veins (venules)

A

i.e. postcapillary venules, collecting venules
- tunica intima: thin basal lamina
- tunica media: few layers of smooth muscle or absent
- tunica adventitia: thin layer of CT

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121
Q

function of small veins (venules)

A

collect blood from capillaries and begin process of returning it to larger veins

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122
Q

how are valves made in medium and large veins

A

via reflections in tunica intima (esp lower extremities)

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123
Q

how much of the body blood volume is in systemic veins and why

A
  • lumen of veins is larger (and don’t constrict much) than arteries; 2/3 of body’s blood volume is in systemic veins
    a. can restrict via catecholamines
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124
Q

poiseuilles law for blood Flow through a tube

effect of radius, length, viscosity

A

a. smaller radius= higher resistance and decreased flow
b. increased length and viscosity= higher resistance (i.e. dehydration)
c. only applicable in laminar flow (not turbulent)

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125
Q

turbulent flow is increased by

A

turbulent flow at high velocities or area with bifurcations and atherosclerotic plaques (sharp changes in vessel diameter)
a. use Reynolds number for turbulent flow
b. pathologies increasing turbulent flow: atherosclerosis, stenosis, hypertension, aneurysm, valvular heart disease

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126
Q

Bernoulli principle

A

pressure is constant in a system, regardless of velocity

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127
Q

two types of circulation

A

series and parallel

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128
Q

series circulation

A

one vessel to another; less common (ie. heart to aorta)
a. total resistance= sum of resistances of each individual vessel= higher overall resistance and less efficient blood flow

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129
Q

what is the more common arrangement of circulation in body; series or parallel

A

parallel

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130
Q

parallel circulation

A

blood flow through multiple vessels simultaneous; majority arrangement in body (i.e. capillary beds)
a. total resistance is less, each additional pathway provides alternative rout for blood flow; more efficient
b. capillaries have higher resistance due to small radius but in parallel it decreases it

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131
Q

total blood volume in body? when is it?

A
  • total =5 L
    a. 80% systemic circulation  60% systemic veins and 20% small arteries and capillaries
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132
Q

veins are ____ and easily distend to hold lots of blood

A

floppy

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133
Q

compliance

A
  • How much pressure is required to change the diameter (volume) of blood vessel
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134
Q

high compliance

A

small amount of pressure  large change in volume

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135
Q

what is more compliant; veins or arteries

A
  • Veins more compliant than arteries (less muscle, more floppy) “blood reservoir”
    a. Arteries stiffer, esp. atherosclerosis, calcify
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136
Q

low compliance in

A

in arteries; don’t stretch easily bc of muscle and elastic fibers to help maintain high BP and efficient flow of blood

a. Compliant, yet elastic arteries decrease cardiac work

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137
Q

central blood volume (25%). (most is systemic

A
  • Vena cavae, heart, pulmonary circulation
  • Determines preload
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138
Q

upright posture; how to get blood back to heart

A
  • Valves in leg veins of lower body
  • Skeletal muscles contract when standing and surround leg veins
  • Inhale decreases intrathoracic pressure and draws blood up
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139
Q

mean arterial pressure

A
  • Average of systolic and diastolic
  • 1/3 of cardiac cycle is in systole
  • MAP= DP + 1/3(SP-DP)
140
Q

how much of cardiac cycle is spent in systole

A

1/3

141
Q

microcirculation

A
  • Distributing artery (branches) when go to organ  further branching into arterioles (regulate blood flow, resistance, BP)  metarterioles (discontinuous muscle) (pre-capillary sphincters to regulate blood flow)  capillaries (site of nutrient and gas exchange) (type IV collagen in basement membrane)
142
Q

basement membrane in capillaries

A

type Iv collagen

143
Q

continuous capillaries allow for

A

least permeable) are leaky and allow free movement of small, water-soluble substances across

144
Q

exception for continuous capillaries

A

blood brain barrier and blood testes barrier

145
Q

what is in the blood brain barrier and blood testes barrier that reduces permeability

A

i. Tight junctions from occludins and claudins

146
Q

pinocytosis

A

endocytose extracellular fluid  vesicles that allow for regulated exchange of substances between bloodstream and tissue; even if tight junctions

147
Q

pinocytic vesicles can coalesce and form

A

vesicular channels

148
Q

what increases pinocytosis

A

i. Increased pinocytosis and permeability in inflammation to transport immune cells to affect area

149
Q

caveolae “small caves” in continuous capillaries of

A

i. Endocytosis and transcytosis of macromolecules
ii. Intercellular clefs for small molecules (albumin wont get through- albumin keeps water in capillary)

150
Q

starling forces; oncotic pressure and hydrostatic pressure

A

i. Hydrostatic pressure pushes fluids out
ii. Oncotic pressure pulls fluids in

151
Q

too much movement across capillaries

A

edema

152
Q

how to reduce edema

A

i. Reduced by glycosaminoglycans (absorb water) and lymphatics

153
Q

auto regulation; caused by what?

A

intrinsic ability of capillaries to regulate blood flow via local tissue factors

a. Metabolic factors: CO2, O2, H+, lactate, adenosine, K+ = vasodilate

154
Q

myogenic regulation of blood flow in capillaries

A

a. Constant rate of tissue flow despite changes in mean arterial pressure (via dilate or constrict)

155
Q

myogenic regualtion vs autoregulation

A

myogenic- dilate or constrict

auto regulation- local tissue factors to regulate blood flow (i.e. CO2, K+)

156
Q

nitric oxide is made by? and released by? to vasodilate

A
  • Made by endothelial cells and released by shear stress (force on blood vessel)
157
Q

steps of nitric oxide vasodilation

A
  • NO  guanylyl cyclase cGMP  PK G  relax smooth muscle
158
Q

what causes vasodilation

A
  • Histamine: vasodilate arterioles, constrict venules  edema
  • Bradykinin: via inflammatory signals
  • Prostaglandin E2 and I2
  • Epinephrine and norepinephrine via beta 2 receptors
159
Q

what cause vasoconstriction

A
  • Epinephrine and norepinephrine via alpha 1 receptor
  • Serotonin via tissue damage
  • Thromboxane A2 and prostaglandin F
  • Angiotensin II
  • ADH
  • Reaction to damage (platelet plug formation)
160
Q

for NE and E which receptors do vasodilate and which do vasoconstrict

A

beta2= vasodilate
alpha1= vasoconstrict

161
Q

which metabolic factors override the ANS in exercise

A
  • Lactate: anerobic; increase blood flow and oxygen delivery
  • K+: vasodilate and increase blood flow
  • Adenosine: result of ATP breakdown; vasodilate
162
Q

cerebral blood flow regulated by

A

pH and adenosine

163
Q

Cushing reflex in brain

A

increased intracranial pressure decreases perfusion

164
Q

pulmonary circulation is controlled by

A
  • Controlled by O2
    a. Decreased= constrict
    b. OPPOSITE TO MOST VASCULAR BED which dilate in low oxygen
    c. This allows for gas exchange efficiency
165
Q

effect of oxygen on pulmonary (opposite to most other vascular beds)

A

vasoconstrict

166
Q

which receptors in skin to constrict? purpose?

A
  • SNS alpha 1 receptors = constrict  regulate body temperature
167
Q

coronary - mechanical compression during systole doses what to blood flow

A

decrease

168
Q

stimulating hemorrhage via lower body negativee pressure

A

Lower Body Negative Pressure (LBNP) simulates hemorrhage by redistributing blood into the lower extremities.

  • Key Concept: Mimics central hypovolemia without physical blood loss
169
Q

5 causes of edema

A

increased blood hydrostatic pressure (push water out of vessel)

drop in oncotic pressure (pull water into vessel)

increased vascular permeability

blocked lymphatic drainage

sodium and water retention

170
Q

increased hydrostatic pressure causing edema causes?

A
  • Increased blood hydrostatic pressure (pushing force to move water out of vessel into tissue)
    a. i.e. malignant hypertension, cushings (increase aldoterone)
171
Q

drop in blood oncotic pressure causing edema- causes?

A
  • drop in blood oncotic pressure (pulling force to draw water into blood vessel)
    a. albumin for oncotic pressure
    b. nephrotic syndrome= leak albumin from glomerulus
    c. hepatic failure,
172
Q

transudate

A

low protein, low cellular content from pressure imbalances

173
Q

exudate

A

high protein, high cellular content caused by inflammation and vessel damage

174
Q

transudate vs exudate in edema

A
  • Transudate= low protein, low cellular content from pressure imbalances
  • Exudate= high protein, high cellular content caused by inflammation and vessel damage
175
Q

angioedema

A

edema in deep layers of skin esp seen in face

176
Q

anasarca

A

= edema in many body parts

177
Q

anasarca vs angioedema

A
  • Anasarca= edema in many body parts
  • Angioedema= edema in deep layers of skin esp seen in face
178
Q

arterial vs venous side; which has greater oncotic or hydrostatic pressure

A
  • Arterial side: hydrostatic pressure > oncotic pressure (fluid into interstitum)
  • Venous side: hydrostatic pressure < oncotic pressure (filtered fluid is recaptured by osmosis)
179
Q

hyperemia and congestion are both caused by

A

increased blood volume

180
Q

hyperemia

A

arteriolar dilation leads to increased blood flow

a. Erythema
b. i.e. blood flow returns when warm after being out in cold

181
Q

congestion

A

passive process = reduced outflow of blood from a tissue (passive hyperemia)

a. systemic (heart failure) or local (venous obstruction)

182
Q

hemosiderin in congestion how?

A

b. cyanosis from red cell stasis  eventually extravasate/ breakdown and cause hemosiderin (degradation product of hemoglobin found in macrophages)

183
Q

long standing/ chronic passive congestion

A

a. hypoxia, cell death, fibrosis, congestion, hemorrhage, phagocytose and catabolise debris  accumulate hemosiderin-laden macrophage

184
Q

pulmonary congestion acute vs chronic

A

a. acute: alveolar capillaries engorged with blood, nutmeg appearance
b. chronic: septa become thickened and fibrotic and have hemosiderin laden macrophages

185
Q

hepatic congestion

A

a. acute: hepatocytes degenerate, sinusoids and venules are distended with blood  hypoxia and fatty change

186
Q

infarct

A

tissue necrosis from lack of blood supply, oxygen, ischemia

187
Q

white infarct

A

organs with only a single blood supply (i..e kidney or spleen)

188
Q

red infarct

A

organs with dual blood supply (i.,e. lung, intestine)

189
Q

what causes a red and white infarct

A

red= venous occlusion

white= arterial occlusion

190
Q

pulmonary infarct

A

complication of pulmonary embolus in congestive heart failure
- cant provide oxygen to larger lung structures  necrosis and hemorrhage

191
Q

shock is from

A
  • from trauma, MI, hemorrhage, PE, sepsis…
192
Q

hemodynamic and metabolic disturbances in shock

A

circulatory system fails to supply adequate microcirculation to perfuse vital organs

193
Q

distributive shock

A

anaphylactic and neurogenic shock

194
Q

myocardial pump failure in schock

A

decrease blood volume, increase vasodilation, increase vascular permeability

195
Q

types of shock

A

cardiogenic (i.e MI)
hypovolemic (i.e. hemorrhage)
septic
anaphylactic
neurogenic

196
Q

septic shock

A
  • high levels of pro-inflammatory cytokines. Leukocytes, activate coagulation and complement cascades
  • dysregulated vascular reflexes
  • warm skin
197
Q

distributive shock

A

too many vessels dilated, not enough blood to keep the pressure up

198
Q

symptoms in hypovolemic and cardiogenic shock

A
  • hypotension, weak rapid pulse, tachypnea, cool clammy cyanotic skin
199
Q

2 stages of shock

A

I- compensated
II- decompensated

200
Q

compensated stage of shock

A

a. tachycardia, but BP normal (compensatory mechanisms to increase HR and peripheral vasoconstriction)

201
Q

decompensated stage of shock

A

a. tachycardia and hypotension

202
Q

decompensated vs compensated stages of shock

A

compensated has tachycardia but normal BP

decompensated is tachycardia and hypotension

203
Q

ishcemic heart disease

A
  • inadequate blood supply to myocardium
204
Q

most common cause of ishcemic heart disease

A

atherosclerosis of coronary arteries

205
Q

stable angina

A

when lumen on large artery reduced 50-75% and IHD symptoms increase during activity
i. occlusion from plaque or thrombosis

206
Q

unstable angina

A

lumen reduced 80-90%, symptoms at rest
i. from thrombus that forms and is broken down

207
Q

unstable vs stable agina

A

stable= only symptoms at activity

unstable= symptoms at rest and thrombus broke down

208
Q

what exacerbates ishcmeic heart disease

A

increase metabolic demand ie. a. increase HR, wall tension, contractility

209
Q

what are the 2 components to acute coronary syndrome

A

unstable angina and MI

210
Q

Prinzmetal angina (vasospastic or variant angina)

A
  • unstable angina, but with better prognosis
  • caused by coronary artery spasm
  • occurs in morning, unrelated to exertion
  • responds well to vasodilators
211
Q

adaptations to chronic heart ischemia

A
  • hypertrophy and changes in contraction
  • develop coronary collateral circulation
212
Q

acute infarction

A
  • heart only gets oxygenated blood during diastole
213
Q

what type of angina is more likley to cause myocardial infarction/heart attack

A

unstable angina

214
Q

symptoms of MI

A

chest pain, heartburn, interscapular pain, dyspnea…

215
Q

time course of MI

A
  • first few minutes: cells and mitochondria swell, lose glycogen
  • 30-60 minutes: irreversible ischemia myocyte injury
  • Day 2-3: neutrophils enter necrotic tissue, edema, hemorrhage
  • Day 5-7: neutrophils replaced by macrophages, myofibroblasts deposit collagen (scar tissue)
  • Week 1 >: collagen depositions
  • Week 3: scar tissue  remodel
216
Q

vessels most often involved in MI

A
  • Anterior descending branch of left coronary artery (50%)
  • Right coronary artery (30-40%)
  • Left circumflex artery (15-20%)
217
Q

which artery is most often involved in MI

A
  • Anterior descending branch of left coronary artery
218
Q

reperfusion injury in MI

A

damaged cardiomyocytes after blood flow is restored to ischemic tissue

219
Q

what happens to contraction band in reperfusion injury (MI)

A
  • Contraction band necrosis (along Z disk, disorganized sarcomeres) from Ca2+ flooding sarcolemma and ROS damaging mitochondria
220
Q

2 types of MI

A

STEMI (st elevation)
NSTEMI (non-st elevation)

221
Q

STEMi vs NSTEMI

A

STEMI: - Permanent occlusion/ complete blockage of coronary artery

NSTEMI: - Partial blockage of coronary atery
- Global hypoxia, small vessels occluded, transient occlusion

222
Q

what’s worse STEMI or NSTEMI

A

STEMI is generally worse than NSTEMI due to the complete blockage of a coronary artery and the larger area of heart muscle affected.

223
Q

ischemicc heart disease symptoms

A
  • Asymptomatic
  • Chest pain- angina pectoris (refer to left arm, scapular, sternal etc)  crushing/sqeueezing pain
  • Dyspnea, fatigue, palpitations, diaphoresis (sweat)
  • Complication : MI
224
Q

acute ischemic heat disease

A
  • Stable or unstable angina, MI, sudden cardiac death
    a. Stable angina: chest or arm pain, reproduced with exertion or stress, relieved with rest and nitroglycerine
    b. Unstable angina: chest or arm pain, occurs and not relieved at rest
    c. Cardiac death: from dysrhythmia
225
Q

ischemic heart disease diagnosis

A
  • ECG : ST elevations…
  • Cardiac enzymes ; troponin, CK-MB (creatine kinase) (most reliable)
  • Angiogram
  • Echocardiogram
  • Nuclear medicine imagine
226
Q

what is the most reliable blood marker for ishemic heart disease

A

creatine kinase MB (CK-MB)

227
Q

ishcemic heart disease treatment

A
  • Treat causes of imbalance of energy supply and demadn to myocardium
    a. ASA aspirin (antiplatelet agent), antihypertensives, beta blockers, calcium channel blockers, nitroglycerine, blood glucose control…
228
Q

different treatment for STEMI vs NSTEMI

A
  • NSTEMI: no clot busting drugs (bc partial blockage)
  • STEMI: clot busting drugs, thrombolytic drugs
  • For both; revascularization (angioplasty or stent), resuscitation
229
Q

2 characteristics of a normal ventricles

A

compliant (diastolic filling at low atrial pressure), strong (ventricles generate enough force)

230
Q

cardiomyopathies

A

damaged myocardium- decreased compliance and contractility

231
Q

reasons for heart failure

A
  • Increased afterload (ventricles hypertrophic and decrease contractility)
  • Impaired oxygen; ischemic heart disease
  • Cant relax/ reduced compliance bc fibrosis
  • Cardiomyopathies= damaged myocardium- decreased compliance and contractility
232
Q

risk for heart failure

A
  • Hypertension, MI, valve disease, diabetes…
233
Q

2 types of heart failure

A

HFrEF (systolic dysfunction)
HFpEF (diastolic dysfunction)

234
Q

HFrEF (heart failure with reduced ejection fraction)

A

AKA systolic disfunction

b. Impaired contractility  reliance on elevated preload for adequate cardiac output

235
Q

HFpEF (heart failure with preserved ejection fraction)

A

AKA diastolic dysfunction

b. Elevated diastolic pressures; good contractility, maybe impaired EDV
c. Impaired compliance

impaired diastolic function — meaning the heart is unable to relax and fill with blood properly.

236
Q

HFrEF vs HFpEF

A

HFrEF is primarily a systolic dysfunction with a reduced ejection fraction, leading to significant heart muscle damage and worse prognosis without treatment.

HFpEF is a diastolic dysfunction with preserved ejection fraction, where the heart struggles to fill properly due to stiffening or thickening of the heart muscle, often seen in older adults or those with chronic hypertension or metabolic conditions. impaired diastolic function — meaning the heart is unable to relax and fill with blood properly

237
Q

forward flow vs backward flow problem in chronic heart failure

A

Forward flow problems in chronic heart failure involve inadequate perfusion to the body’s organs and tissues, leading to fatigue, dizziness, and organ dysfunction.

Backward flow problems occur when blood backs up into the lungs or body due to the heart’s inability to pump blood effectively, leading to symptoms like shortness of breath, edema, and organ congestion.

238
Q

what part of the heart is usually first to fail in chronic heart failure

A

usually left ventricle because greatest afterload

then pulmonary congestion icreases and the right ventricle will faail

239
Q

when the right ventricle fails first what happens

A

o Cor pulmonale: pulmonary hypertension from COPD, OSA

o Lung disease causes hypoxia and pulmonary vasoconstriction

240
Q

cor pulmonale

A

pulmonary hypertension from COPD, OSA

right ventricle problem

Cor Pulmonale refers to right-sided heart failure that occurs as a result of chronic lung disease or pulmonary conditions that cause increased pressure in the pulmonary arteries (pulmonary hypertension).

241
Q

low oxygen concentrations in pulmnonary microcirculation causes

A

constriction

  • Different than other vascular beds; help redirect blood flow to regions with higher oxygen; optimize gas exchange
242
Q

concentric vs eccentric hypertrophy

A

Concentric hypertrophy is a response to pressure overload, resulting in thickened ventricular walls with preserved or reduced chamber size. This type of hypertrophy is often seen in diastolic heart failure (HFpEF) and can lead to diastolic dysfunction.

Eccentric hypertrophy results from volume overload, leading to dilated heart chambers with thinned walls. This type of hypertrophy is typically associated with systolic heart failure (HFrEF), where the heart becomes less efficient at pumping blood.

243
Q

concentric hypertrophy

A

thicken ventricular wall; increased afterload

244
Q

eccentric hypertrophhy

A

dilate or thin ventricular wall; volume overload

245
Q

ventricular remodelling in chronic heart failreu

A

o Myosin use more ATP
o Increase TGF beta
o Myocytes enlarge and less

246
Q

in chronic heart failure what happens to angiotensin II

A
  • Angiotensin II increases as cardiac output to kidneys decrease

o AT II binds myocytes and causes hypertrophy and CT deposits
o Increase volume and vasoconstriction = edema and afterload

247
Q

what happens to beta adrenergic receptors in chronic heart failure

A

downregulated
o Hypertrophy and fibrosis of myocytes
o SNS in short term improves cardiac but long term bad

248
Q

inflammatory cytokines in chronic heart failure

A

o JNK and MAPK – remodel and apoptosis

249
Q

calcium changes in chronic ehart failure

A

o Release less Ca2+ per AP
o SERCA Ca2+ uptake is limited
o Elevated diastolic Ca2+ and impair Ca2+ spikes in contraction

250
Q

whicvh pathway for chronic heart failure is good for healthy hypertrophy

A

o Activate IGF-1 and PI3K

251
Q

impacts of SNS and RAAS in chronic heart failure

A
  • Activate SNS and RAAS
    o Increase HR, BP, contractility
    o Retention of Na+ and water
     Increase preload and cardiac output
  • Over time bad… excessive vasoconstriction and volume retention
    o Baroreceptors that increase pressure, decrease PNS
    o Increase ADH= increase volume
    o Excess SNS= decreased renal perfusion = chronically elevated renin and AT II to maintain kidney blood flow
252
Q

in chronic heart failure which 2 things aren’t released by stretched ventricles to protect against fluid overload

A
  • Protection against fluid overload: ANP and BNP (released by stretched ventricles)
    o In heart failure, become resistance to BNP and ANP
    o No longer leads to Na+ and water loss
253
Q

chronic heart failure symtpoms

A
  • Fatigue
  • Left side: orthopnea, dyspnea, angina, impaired cognitive function
  • Right side: edema, RUQ pain
254
Q

chronic heart failure signs

A
  • Pitting edema
  • Hepatosplenomegaly
  • Elevated JVP (Right sided heart problem)
  • S3 or S4
  • Crackles, wheezing, pleural effusion
255
Q

class I to class IV chronic heart fialure

A

class II- good at rest but physcical activityh causes fatigue, palpitations, dysnpenea, angina

classs IV- heart failure and aging at rest and worse with activity

256
Q

heart failure diagnosis

A
  • BNP
  • Echocardiography
  • Chest x-ray: cardiomegaly and pulmonary edema
257
Q

HFrEF and HFpEF %

A
  • HFrEF: reduced ejection fraction; <50 %
  • HFpEF- normal (>50%) but left ventricle hypertrophy, atrial enlargement
258
Q

what is the most common cause of heart failure?

A
  • Chronic IHD (coronary artery disease)
259
Q

second most common cause of chronic heart filaure? what does it present as HF_EF?

A
  • Second most common cause is chronic hypertension
    o Myocardial hypertrophy and fibrosis
    o Presents as HFrEF
260
Q

concentric or eccentric LV hypertrophy in chronic hypertension leading to heart failure

A

concentric (can process to eccentric)

261
Q

atherosclerosis pathophysiology

A
  • Fatty streak  deposit oxidized LDL  activate macrophages  calcify, accumulate cholesterol, foam cells, fibrous cap w necrotic tissue, stenosis of lumen
262
Q

risks for atherosclerosis

A

smoking, high BP (hypertension), oxidative stress
o Lp(a)
-diabetes and dyslipidemia (LDL and AGES)

263
Q

Lp(a)

A

increase endothelial damage via immune cell recruitment and plaque formation
 Also inhibits clot breakdowns

264
Q

which receptor do beta blockers work in for congestive heart failure

A

beta 1 receptors to block NE and SNS

265
Q

effect that beta blockers have on heart

A

(beta 1/NE – block SNS, NE)
o IHD: reduce cardiac oxygen demand
o CHF: reduce and reverse cardiac remodeling

266
Q

cardiac glycoside (digoxin) is a medication fro CHF and does what

A

o Inhibit Na+/K+ pump
o Increase cytosolic Ca2+  Increase contractility
 Via Na+/Ca2+ exchanger

267
Q

diuretics for CHF

A

o Reduce blood volume- increase water and Na+ loss
 Loop and thiazide diuretics
 Spironolactone
 ACE inhibitors

268
Q

2 types of calcium channel blockers for CHF

A

o Dihydropyridine = cause vasodilation

o Nondihydropyridine= slow AV conduction (HR) and decrease contractility

269
Q

nitrates medication for CHF

A

o NO = vasodilate
o Decrease preload and afterload and vasodilate

270
Q

HMG CoA reductase inhibitors (statins) do what

A

o Reduce hepatocytes ability to produce cholesterol  upregulate LDL receptor and increase its clearance
 Decrease circulating TG, reduce oxidative stress

271
Q

PCSK9 is a medication to do what in CHF

A

o Block PCSK9 protease in hepatocytes
o This protease degrades LDL receptor
o More LDL receptors available to clear LDL

272
Q

ezetimibe medication for CHF

A

o Reduce absorption of dietary and bilary cholesterol

273
Q

niacin for CHF

A

o Inhibit lipolysis in adipose tissue; less FFA release so less VLDL and LDL production

274
Q

damage to valves from?

A
  • Congenital disorders, wear and tear, inflammation, ishcemia, aortic dissection, idiopathic
275
Q

stenosis of a valve

A

narrowed valvve= impair outflow

276
Q

regurgitation in a vlave

A

backflow across valve

277
Q

how does regurgitation effect EDV and preload and outflow

A

backflow across the valve results in

  • Increased EDV and preload and impair outflow
278
Q

2 types of regurgitation

A

incompetence
prolapse

279
Q

incompetence in valve

A

valve doesn’t close completely

280
Q

prolapse in valve

A

backwards valve movement into proximal chamber

281
Q

most common valve pathology

A

mitral valve prolapse

282
Q

mitral valve prolapse goes into which part of the heart

A

left atrium

-Enlarged valve leaflets and redundant and billow into LA systole

283
Q

rheumatic heart disease from what

A

group A strept infection

284
Q

PAGE 34-35 FOR CHARTS

A
285
Q

3 types of cardiomyopathies

A
  1. restritcive
  2. hypertrophic
  3. dilated
286
Q

most and lease common form of cardiomyopathy

A

most common= dilated

least common= restrictive

287
Q

restrictive cardiomyopathy

A

The heart muscle becomes stiff and less flexible, making it difficult to fill with blood between heartbeats. This is the least common type of cardiomyopathy, but it can occur at any age.

288
Q

hypertrophic caardiomyopathy

A

The heart muscle thickens, making it harder for the heart to work. This condition can start at any age, but it mostly affects the heart’s main pumping chamber.

289
Q

dilated cardiomyopathy

A

The heart’s chambers thin and stretch, causing the heart to grow larger. This condition usually starts in the heart’s main pumping chamber, making it difficult for the heart to pump blood to the rest of the body. It can affect people of all ages.

290
Q

what happens to septum in hypertrophic cardiomyopathy ? how is outflow impacted?

A

Septum overgrown; outflow obstruction in left ventricle (i.e. entry to aorta blocked)

291
Q

causes of hypertrophic cardiomyopathy

A

Autosomal dominant; common

Genetic deficits in sarcomere proteins

Gain of function mutation in sarcomere proteins

292
Q

clinical features of hypertrophic cardiomyopathy

A

Asymptomatic
-athletes heart (sudden cardiac death from dysrhythmias)
-with aging; angina, dyspnea, syncope (sudden loss of consciousness from impaired cerebral hypoperfusion)

293
Q

is hypertrophic cardiomyopathie HFpEF or HFrEF

A

HFpEF (can develop into HFrEF)

294
Q

hypertrophic, dilated and restrictive cardiomyopahty are
HFpEF or HFrEF

A

hyper- HFpEF (can progress to HFrEF)
dilated- HFrEF
restrictive- HFpEF

295
Q

mortality rate for restrictive cardiomyopthy

A

High mortality rate bc heart failure

296
Q

which cardiomyopathy has high mortality

A

restrictive cardiomyopathy

297
Q

severity for dilated cardiomyopthy?

A

Can reverse damage if eliminate initial insult (i.e. alcohol use)

not as good if genetic…

298
Q

ir restrictiva cardiomyopthy HFpEF or HFrEF

A

isolated diastolic dysfunction, HFpEF picture – stroke volume is normal in most cases

299
Q

causes of dilated cardiomyopathy

A

SO MANY! that’s why its most common

Genetic deficits in sarcomere proteins or infection, inflame, toxic
toxicities (i.e. alcohol, catecholamine, cancer therapy)
-peripartum
-genetics
-inflammatory (infection, sarcoidosis)

300
Q

is dilated cardiomyopathy HFrEF or HFpEF

A

HFrEF

300
Q

symptoms of dilated cardiomyopathy

A

Asymptomatic –> heart failure symptoms (fatigue, exercise intolerance, dyspnea, dependent edema)
-mitral regurgitation
-palpitations/syncopal episodes from dysrhythmias

301
Q

microscopy of dilated cardiomyopthy

A

Microscopy can alternate between hypertrophy and atrophic/fibrotic sections of myocardial cells

302
Q

what does heart look like in dilated cardiomyopthy

A

Heart is massive (2-3x size)
-ventricles dilated more than atria
-heart wall appears flabby
-regurgitation of AV valves

303
Q

restrictive caridomuopthy

A

Characterized by restricted ventricular filling, reduced diastolic volume in one or both ventricles, and normal or near-normal ventricular systolic function and wall thickness

304
Q

causes of restrictive cardiomyopathy

A

Some are autosomal dominant mutations

Most secondary causes from outside the heart:
-amyloidosis (accumulate abnormal proteins in various tissues; i.e kidneys)  form beta pleated sheets from liver or antibody fragments  proteins deposit extracellularly
-hemochromatosis (accumulate iron in cardiomyocytes)
-sarcoidosis (granuloma disease infiltrate wall of ventricle)

305
Q

where is Lp(a) made

A

in the liver

306
Q

what does Lp(a) look like?

A

LDL

307
Q

what do Lp(a) and LDL both contain

A

apo(b)

308
Q

what is Lp(a) made of

A

kringle units

309
Q

what makes lp(a) pathogenic

A
  • Transports oxidized phospholipids
310
Q

what does Lp(a) do

A
  • causes coagultation, unstable plaques, activates monocytes, pro inflammatory cytokines (IL-6)
311
Q

what is an unstable plaque

A

unstable fibrous cap thats prone to rupture

312
Q

how to increase stability in a plaques cap

A

via collagen

o activated platelets release growth factor for collagen deposition

313
Q

what breaks down a fibrous cap on a plaque

A
  • activated macrophages produce metalloproteinases that degraded collagen
314
Q

delusion

A

belief despite evidence against

315
Q

hallucination

with or without?

formed vs unformed?

A

sensory perception in absence of stimuli

  • with insight (aware) or without insight (thinks is real)
  • formed (i.e. voice making command) or unformed (i.e. non specific sound)
316
Q

DSM criteria for schizophrenia

A
  • need 2+ symptoms, 1 month active symptoms and 6 months of signs
  • delusion OR hallucination OR disorganized speech (must be one of these)
  • disorganized or catatonic (psychomotor) behaviour
  • negative symptoms (decreased function ie.. limited speech and emotion)
317
Q

which 1/3 symptoms must be in shcizeophrenai

A
  • delusion OR hallucination OR disorganized speech
318
Q

speech issues in schizophrenia

A

derailment: loose association
poverty of speech
tangentiality: go off topic
lack of logic
perseveration: repetitive thoughts or speech
neologism: made up word
thought blocking: stop abrupt in middle of speaking
clanging: rhyme or alliteration
echolalia: repeat or mirror words

319
Q

behavioural issues in schizophrenia

A

incoherent or erratic behaviour
inappropriate emotional responses
difficulty planning or sequencing
motor immobility
stupor: unresponsive
rigidity: muscle stiffness
strange postures: catalepsy
excessive motor activity
echopraxia: imitate or mirror movements

320
Q

what system is dyregulated//hyperresponsive in schizophrenia

A

dopaminergic system

321
Q

which monoamines in dopaminergic syste

A

dopamine, NE, serotonin

322
Q

antipsychotic drugs block what receprot

A

D2 dopamine receptor

323
Q

drugs that increase dopamine increase

A

psychosis

324
Q

what is the last interneuron to be incorporated into the developing brain and is therefore vulnerable to insults like oxidative stress

A

GABA

325
Q

dopaminergic system- which areas of the brain release dopamine

A
  • Neuronal cell bodies that release dopamine are in midbrain
    o Ventral tegmental area (VTA) and substantia nigra
326
Q

which dopamine area of the brain for reward and motivation and projects where

A

VTA –>nucleus accumbens and ventral striatum (of basal ganglia)

327
Q

which dopamine area of the brain for motor and projects where

A

substantia nigra –>  striatum (of basal ganglia

328
Q

which dopamine area of the brain for executive function and projects where

A

VTA and dorsal substantia nigra –> many cortical areas

329
Q

which type of firing is at rest in dopamine system

A

tonic firing

330
Q

tonic firing

A

dopamine neuron fire in slow pacemaker fashion at rest

331
Q

what slows down the tonic firing of dopamine system

A

o Ventral pallidum release GABA and slows it down
o Hyperfunctioning tonic firing in hippocampus in schizophrenia and reduced GABA
o Stress in early childhood reduces GABA and overactivates amaygdala

332
Q

phasic firing in dopamine system is caused by?

A

RAS detects stimulus  glutamate release onto dopamine neurons  rapid action potentials

333
Q

what increases phasic firing in the dopamine ssytem

A
  • Stronger phasic firing in response to new or stressful stimulus: activate hippocampus (subiculum) to enhance tonic firing
334
Q

chronic stress impact on the firing of dopamine system

A
  • Decrease tonic and phasic firing in chronic stress –> activate amygdala
335
Q

pro infallmatory cytokines involved in psychosis in schizophrenia

A

TNF alpha, IL6, IL1beta

336
Q

what do profinlmatory cytokines produce that causes psychosis

A

TNF alpha, IL6, IL1beta –> kyureneic acid production –> block NMDA receptor –> psychosis

337
Q

microglial cells and schizophnreia

A

cogntiive dysfunction

338
Q

migraine has pain from what input

A

trigeminovascular input

339
Q

pathophysiology of migraine

A
  • Pain from trigeminovascular input
  • Meningeal vessels  trigeminal ganglion  syanpses on second order neurons in trigeminocervical complex in brainstem  thalamus  cortex
340
Q

what modulates pain in migraine and causes vasoconstrict or dilate in migraines

A
  • Modulate pain by midbrain nuclei (dorsal raphe nucleus, locus coeruleus, nucleus raphe magnus)
341
Q

which medications act on pain pathway in migraines

A

o 5-HT1 receptors: bind serotonin in trigeminal nucleus
o CGRP; vasodilate to modulate pain on efferents

342
Q

neuromuscular theory of migraines

A

o Primary neural dysfunction= wave of spreading depression (slowly travelling wave of neural excitability) throughout cortex, activates trigeminal complex

343
Q

pro inflammatory cytokines in migraines

A
  • Pro-inflammatory cytokines  release nerve growth factor (NGF) from mast cells  increase BDNF from C fibers = pro-pain in dorsal horn
344
Q

pain pathway in migraines

A

o Orthodromic (periphery to SC)
o Antidromic (SC to periphery)

345
Q

c fibers release what in migraines

A

o C fibers release substance P (mast cell, edema, vasodilate) and CGRP (vasodilate) –> inflammation

346
Q

migraines and microbiome?

A

o H pylori
o IBS- visceral hypersensitivity; food intolerances, high serotonin
o Dysbiosis  permeability  LPS leak  pro inflame cytokines

BMS200 (46 decks)

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