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BMS200 > FUCK!!! > Flashcards

FUCK!!! Flashcards

1
Q

the AV valves between atria and ventricles

A

tricuspid and mitral valves

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2
Q

chronotropy

A

rate of depolarization; heart rate

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3
Q

ionotropy

A

aka contractility; Ca2+ binds troponin

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4
Q

preload

A

ventricular filling ~ end diastolic volume

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5
Q

blood flows from

A

high to low pressure

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6
Q

how much of ventricular filling is passive

A

80%

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7
Q

s3 and s4 heart sounds

A

s3 can be healthy or pathologic

s4 is pathologic; atria force blood into non compliant ventricle

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8
Q

which ventricle has the higher pressure

A

Left Ventricle

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9
Q

Aorta is 120/80mmHg so its

A

the blood pressure value

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10
Q

more force; atria or ventricles

A

ventricles

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11
Q

ACXVY for at the atria

A

A wave: atrial contraction (atrial systole)

C wave: tricuspid buldge

X-descent: atrial relax (atrial diastole)

V wave: passive filling (ventricular systol)

y-descent: atria empty into ventricles with open AV valves

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12
Q

dicrotic notch

A

division between 2 waves in aortic valves; when valve closes (elastic recoil)

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13
Q

Stroke volume

A

volume ejected with each heart beat

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14
Q

SV=

A

SV= EDV-ESV

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15
Q

cardiac output

A

volume ejected each systole x heart rate

–> give o2 and nutrients to tissues
–> equal in left and right ventricles

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16
Q

CO=

A

CO = SV x HR

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17
Q

ejection fraction

A

proportion of EDV ejected with each heart beat

–>estimated heart function in heart failure

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18
Q

EF=

A

EF= SV/ EDV
EF= (EDV-ESV)/ EDV

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19
Q

preload of 1 ventricle depends on ____ of other ventricle

A

cardiac ouput

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20
Q

treppe effect

A

accumulate Ca2+ in SR as HR increases (not enough time to remove calcium)

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21
Q

skeletal myocyte excitation- contraction coupling

A

Ach (nicotinic receptor) –> depolarize –> Na+ VGC open –> Ca2+ VGC open –> t tubules get AP deeper –> Ca2+ binds troponin and open the myosin binding site on actin by moving tropomyosin out of the way –> cross bridge formation

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22
Q

where does most of the calcium come from in skeletal muscle contraction

A

little bit from Ca2+ VGC

but the main action of Ca2+ VGC is to open ryanodine receptor in SR and the SR is where most of the Ca2+ is from

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23
Q

cardiac myocytes differences from skeletal myocytes

A

-no tetany bc long refractory period

-synctium; intercalated disks (gap junctions and desmosomes) = coordinated heart contraction

-t tubules less important; rely more on L-type Ca2+ channels

-1 nucleus, lots of mitochondria; ATP, oxidative metabolism with fats

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24
Q

automatic cells 4 phases

A

phase 4: unstable, funny current (Na+ and K+)

phase 0: depolarize by L-type Ca2+ channels (NOT Na+ VGC)

-no phase 1 or phase 2 plateau

-phase 3: repolarize; K+ efflux

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25
Q

where is there a delay in heart conduction

A

AV node; give atria time to eject blood to ventricles and time for ventricles to fill

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26
Q

bundle of His (AV bundle) purpose

A

carry AP along septum to ventricle

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27
Q

purkinje fibers carry AP to…

A

apex then base = ventricular contraction

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28
Q

fibrous skeleton so

A

atria and ventricles can only communicate through AV node

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29
Q

Bachman’s bundle

A

right and left atrium contract simultaneously

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30
Q

4 major types of APs in the heart

A
  1. myocyte APs (ventricular and atrial)
  2. purkinje cell APs (almost same as ventricular but unstable 4 like automatic cell)
  3. automatic cell APs
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31
Q

automatic cells

A

-SA and AV node
-depolarize without external stimuli

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32
Q

what cell takes over in complete heart block

A

purkinje cells give AP because cant go from atria to ventricles with AV node and SA

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33
Q

SA node is

A

pacemaker; HR = 60-100bpm

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34
Q

4 typical phases of myocyte APs

A

phase 4- resting membrane potential, leaky K+, Nernst = -84mv

phase 0- rapid depolarization, Na+ VGC open; influx

phase 1- initial repolarization, close Na+ VGC, K+ VGC open= efflux

phase 2- plateau- open L-type Ca2+, influx (Ca2+ and K+ balance out)

phase 3- slow repolarization; close Ca2+, open slow K+ VGCs

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35
Q

calcium spark

A

1 Ca2+ VGC opens and elicits small Ca2+ release from neighbouring ryanodine receptor on SR –> summation = increase in Ca2+ in cytosol (some contribution from ECF)

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36
Q

3 things remove Ca2+ from cytosol

A

-SERCA
-Na+ Ca2+ exchanger; 3 Na in, 1 Ca out
-sarcolemma calcium ATPase; Ca out

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37
Q

what is SERCA regulated by

A

phospholambdin phosphorylation

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38
Q

beta 1 receptors (SNS)

A

beta 1 –> cAMP –> phospholambdan –> phosphorylate troponin –> L-type Ca2+ VGC –> Ca2+ influx –> enhance contractility and quicker Ca2+ reuptake into SR

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39
Q

ECG measures? what is a little box?

A

electrical activity
-little box is 0.1mV high and 0.04 seconds wide

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40
Q

P wave

A

atrial depolarization via SA node

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41
Q

PR interval

A

impulse from SA node through atria and AV node to ventricles (AV node delay for ventricular filling)

AP from SA –> AV node

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42
Q

QRS complex

A

ventricular depolarization (via bundle of His and Purkinje)

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43
Q

ST segment

A

ventricles fully depolarized, before they depolarize

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44
Q

T wave

A

ventricular repolarization

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45
Q

QRS interval

A

AP from end of AV node to throughout ventricles

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46
Q

QT interval

A

ventricle depolarize and repolarize

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47
Q

3 layers of blood vessels

A

tunica intima
tunica media
tunica externa/adventitia

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48
Q

tunica intimia is made of

A

simple squamous endothelium

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49
Q

tunica media is made of

A

muscle cells

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50
Q

which layer is thickest in arteries

A

tunica media

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51
Q

which layer is thickest in veins

A

tunica externa/adventitia

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52
Q

tunica externa/adventitia components

A

vasa vosaorum (blood vessels), fibroelastic CT

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53
Q

4 types of arteries

A

elastic arteries/conducting
muscular arteries/distributing
arterioles
metaarterioles

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54
Q

elastic arterioles/ conducting

A

i.e. aorta, pulmonary trunk

elastic fibers for high pressure near heart, major pressure reservoirs

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55
Q

muscular arteries/ distributing

A

i.e. brachial and femoral arteries

smooth muscle, most abundant in body

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56
Q

most common artery in body

A

muscular arteries/ distributing

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57
Q

arterioles

A

constrict and dilate, control systemic BP

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58
Q

metaarterioles

A

regulate flow into capillaries via pre capillary sphincters

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59
Q

3 types of capillaries

A

continuous capillaries
fenestrate capillaries
sinusoidal capillaires

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60
Q

which are the majority of capillary in the body

A

continuous capillaries

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61
Q

what is least permeable and most permeable capillary

A

least- continuous capillary

most- sinusoidal capillary

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62
Q

continuous capillaries

A

least permeable, majority, intercellular junctions for water soluble substances to pass

exception: BBB, BtestesB –> tight junctions (Claudius and occluding)

caveolae (caves): endocytosis of macromolecules

intracellular cleft; for small (albumin cant go through)

coalesces and make vesicular channels –> pinocytosis and endocytose ECF –> increase in inflammation to transport antibodies and nutrients

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63
Q

3 types of veins

A

large
medium
small (venules)

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64
Q

large veins

A

vena cava, portal vein, pulmonary veins

thick tunica advanetitia with dense CT, collagen, elastic fibers, vasa vasorum

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65
Q

medium veins

A

femoral, renal and brachial veins

valves to prevent back flow to limbs

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66
Q

small veins (venules)

A

post capillary and collecting venules

collect blood from capillaries

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67
Q

valves formed via

A

reflection of tunica intima

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68
Q

lumen bigger in vein or artery

A

vein

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69
Q

2/3 blood in

A

systemic vein

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70
Q

veins can somewhat constrict via

A

catecholamines

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71
Q

poiselles law vs Reynolds #

A

poiselles; laminar flow

Reynolds; turbulent flow (i.e. atherosclerosis, hypotension)
–> likely if increased blood velocity, decreased or irregular diameter and decreased viscosity (faster)

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72
Q

pressure and velocity in arteries, capillaries and veins

A

arteries- high pressure, fast velocity

capillaries- low pressure, slow velocity

veins- low pressure, moderate velocity

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73
Q

basement membrane of capillaries

A

type IV collagen

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74
Q

series circulation vs parallel circulation

A

series- higher resistance

parallel- majority, reduce resistance even though small radius i.e. capillaries

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75
Q

lower resistance in parallel or series circulation

A

parallel

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76
Q

compliance

A

amount of pressure need to change volume

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77
Q

high compliance

A

small amount of pressure= large change in volume

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78
Q

what are more complaint; veins or arteries

A

veins; blood resevoir

arteries have low compliance to maintain high BP

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79
Q

mean arterial pressure MAP

A

MAP= DP + 1/3 (SP-DP)

1/3 of cardiac cycle in systole

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80
Q

edema

A

too much movement across capillary walls

albumin keeps H2O in capillary

glycosaminoglycans absorb H2O and reduce edema

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81
Q

what reduces edema

A

albumin and glycosaminoglycans

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82
Q

2 ways capillary blood flow is regulated

A
  1. autoregulation
    2.myogenic regulation
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83
Q

autoregulation of capillaries

A

capillary bed regulates flow via local tissue factors

h2o, o2, co2, [lactate, K+, adenosine= exercise] all vasodilate

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84
Q

myogenic regulation of capillaries

A

constant flow despite changes in MAP because if pressure drops then dilate and if pressure increases then constrict

Increased Blood Pressure (Stretch):
When blood pressure increases, it causes the walls of arterioles (the small arteries leading to capillaries) to stretch.
The smooth muscle cells in the walls of these arterioles respond to this stretch by contracting (a phenomenon known as the myogenic response). This constriction reduces the diameter of the arteriole, thereby decreasing the flow of blood into the capillaries.
This is a protective mechanism to prevent overdistention of the capillaries and potential damage to delicate capillary walls.
Decreased Blood Pressure (Reduced Stretch):
When blood pressure decreases, the walls of the arterioles are less stretched. In response, the smooth muscle cells in the arteriole walls relax, causing the arterioles to dilate.
This dilation helps maintain blood flow through the capillary network by preventing the pressure in the capillaries from becoming too low, ensuring adequate perfusion to tissues.

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85
Q

NO effect and pathway

A

vasodilate via shear stress

NO –> guanylyl cyclase –> cGMP –> PKG –> dephosphorylate myosin and relax

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86
Q

vasodialtors of capillaries

A

histamine
bradykinin
prostaglandin E2 and I2
NE, E via beta 2 receptors

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87
Q

vasoconstriction of capillaries

A

NE, E alpha 1 receptors
serotonin
ADH
AT II
thromboxane A2 and prostaglandin F

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88
Q

NE and E 2 receptors

A

beta 2= vasodilate
alpha 1= vasoconstrict

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89
Q

cerebral blood flow is regulated by

A

ph and adenosine

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90
Q

cushing reflex in the cerebrum

A

increased intracranial pressure will decrease perfusion

91
Q

pulmonary capillaries are unique- low oxygen causes

A

vasoconstriction; for efficient gas exhange

92
Q

skin receptors

A

SNS alpha 1, body temperature

93
Q

coronary capillaries regulated by

A

oxygen and adenosine

94
Q

causes of edema

A

increased hydrostatic pressure (from increased arterial pressure i.e. malignant hypertension, decrease venous drainage)

decreased oncotic pressure (albumin, i.e. nephrotic syndrome and hepatic filature)

increased vascular permeability

blocked lymph (malignancies, surgeries)

increase Na+ and H20 retention via ADH and aldosterone

damaged endothelium

95
Q

transudate vs exudate in edema

A

transudate- low protein and cell content from pressure imbalances

exudate- high protein and cell content from inflammation and vessel damage

96
Q

arterial and venous; is hydrostatic or oncotic pressure greater

A

arterial: H > O
venous: O > H

97
Q

anasarca and angioedema

A

anasarca- generalized edema in body

angioedema- in deep layers of face

98
Q

what is most severe edema

A

pulmonary and brain

99
Q

hyperemia and congestion are both from

A

local increase in blood volume

100
Q

hyperemia

A

arteriol dilation increases blood flow; erythema i.e. blood flow when warmed up after being in cold outside

causes local increase in blood flow

101
Q

congestion

A

passive hyperemia; decreased blood outflow from a tissue; cyanosis because of red blood cell stasis

can be systemic or local

RBC breakdown and get hemosiderin= hemoglobin degrade in macrophage

local increase in blood volume

102
Q

long standing congestion

A

hypoxia, apoptosis, fibrosis, hemosderin laden macrophages

103
Q

pulmonary vs hepatic congestion causes

A

pulmonary- left heart failure

hepatic- right heart failure

104
Q

nutmeg liver from

A

hepatic congestion

105
Q

infarct

A

tissue death from ischemia

106
Q

white vs red infarct

A

white= organs with single blood supply (kidney or spleen)

red= dual blood supply (lung, intestine, testis)

107
Q

arterial or venous occlusion for white and red infarcts

A

white infarct= arterial occlusion (cause white appearance; abrupt and severe damage since cut off only blood supply)

red infarct= venous occlusion (blood pools and causes red/blue colour, slow process because dual blood supply)

108
Q

shock

A

inadequate blood flow to organs

109
Q

types of shock

A

cardiogenic- MI, myocarditis, cardiac tamponande, pulmonary embolus

hypovolemic- hemorrhage, diarrhea, dehydration

septic- infection

distributive (too much dilation; not enough pressure= anaphylactic and neurogenic)

anaphylactic; type 1 hypersensitivity

neurogenic- brain damage or spinal cord injury

110
Q

in shock the myocardial pump fails causing

A

decreased blood volume, vasodilation, increased vascular permeability

(inadequate blood flow to organs)

111
Q

stage 1 (compensated) vs stage 2 (decompensated) shock

A

compensated= tachycardia with normal BP

decompensated= tachycardia and hypotension

112
Q

symptoms in ischemic heart disease

A

asymptomatic or chest pain, dyspnea, fatigue, palpitations

113
Q

what is the mechanism in ischemic heart disease

A

blood flow to the myocardium is inadequate

114
Q

main cause of ischemic heart disease (90%)

A

atherosclerosis

115
Q

what makes ischemic heart disease worse

A

things that increase heart metabolic demands; HR, Ca2+ contractility, wall tension

116
Q

stable angina

A

IHD symptoms during activity, 50-75% of lumen decreases, Bette with rest and worse with exercise, fixed with nitrgoclycerine

117
Q

unstable angina

A

IHD symptoms at rest, 80-90% of lumen decreased, not better with rest or nitroglycerine

thrombus breaks down

118
Q

acute coronary syndrome

A

unstable angina + MI

119
Q

acute IHD

A

-stable or unstable angina
-MI
-sudden cardiac death (dysrhythmia)

120
Q

chronic IHD can lead to

A

heart failure

121
Q

IHD diagnosis

A

ECG
cardiac enzymes; CK-MB, troponin T and I
angiogram
echocardiogram

122
Q

IHD treatment

A

ASA antiplatelet agent (decrease thrombus)
antihypertensive
beta blocker
nitroglycerine (decrease preload and afterload; vasodilate)
Ca2+ channel blocker (decrease contractility)

123
Q

IHD complications

A

MI

124
Q

chronic IHD can lead to

A

congestive heart failure

125
Q

pritizmetal angina (vasospastic or variant angina) cause

A

coronary artery spasm

126
Q

pritizmetal angina (vasospastic or variant angina) symptoms

A

at rest in the morning

respond to Ca2+ blockers and nitroglycerine

127
Q

adaptations in chronic ischemia of the heart

A

hypertrophy and collateral circualtion

128
Q

MI symptoms

A

pain could be in scapula, heart burn, dyspnea, fatigue- not typical presentation always

129
Q

cells in MI

A

cells and mitochondria swell and lose glycogen

130
Q

what opens in MI

A

MPTP (mitoahcondria pore) opens from an increase in Ca2+ –> please H+, no ATP, more Ca2+ in cytosol

131
Q

time frame in MI

A

30-60 min: irreversible, coagulative necrosis (Ca2+ accumulate, ROS, decrease ATP, open MPTP)

2-3 days: neutrophils in necrotic tissue, edema, hemorrhage

5-7 days: scar tissue, replace neutrophils with macrophages, myofibroblasts deposit collagen

132
Q

reperfusion injury after MI

A

damage cardiomyocytes if restore blood to quick after ischemia

contraction band necrosis

133
Q

transmural infarcts/ STEMI

A

blocked coronary artery

use clot busting drugs

134
Q

non-transmural infarct/ NSTEMI

A

partially blocked coronary artery; transient occlusion

135
Q

what to do in STEMI and NSTEMI

A

revascularize- angiopalsty or stent

136
Q

MI most common vessel effected

A

anterior descending branch of left coronary artery (50%)

137
Q

diagnose heart failure

A

ECG

BNP

HFrEF, decreased ejection fraction <40%

HFpEF, EF >50%, left ventricle hypertrophy

138
Q

2 most common cause of heart failure

A
  1. chronic IHD (HFrEF)
  2. hypertension (concentric LV hypertrophy)
139
Q

mechanisms of heart failure

A

-increased afterload –> hypertrophic ventricles

-chronic ischemia from low oxygen

-decreased compliance (cant relax)

-cardiomyopathy- damaged myocardium impairs compliance and contractility

140
Q

2 types of heart failure

A

systolic dysfunction/ HFrEF

diastolic dysfunction/ HFpEF

141
Q

HFrEF (heart failure with reduced ejection fraction)/ systolic dysfunction

A

impaired contraction, rely on increased preload

142
Q

HFpEF (heart failure with preserved ejection fraction)/ diastolic dysfunction

A

impaired EDV (compliance), elevated diastolic pressure, but contraction OK

143
Q

forward flow vs backward flow problem in heart failure

A

forward= impaired cardiac output

backward= congestion

144
Q

what is first to fail in heart failure

A

left ventricle because greatest afterload

145
Q

what is it called when the right ventricle fails first in heart failure

A

cor pulmonale (COPD, OSA, pulmonary hypertension)

146
Q

pulmonary microcircualtion

A

constrict if low O2

147
Q

concentric vs eccentric hypertrophy usually happens 1st

A

concentric

148
Q

concentric hypertrophy

A

ventricular wall thickens, no increase in chamber size

149
Q

eccentric hypertrophy

A

myocytes increase length and the chamber enlarges

150
Q

ventricular remodelling in heart failure via

A

increased TGF b

151
Q

2 main pathways in CHF

A

RAAS and SNS

152
Q

angiotensin II in CHF

A

AT II increases when cardiac output to kidneys decrease

causes vasoconstriction, edema, increased BP

153
Q

SNS in CHF

A

beta adrenergic

154
Q

endothelin 1 in CHF

A

vasoconstriction

155
Q

JNK and MAPK in CHF

A

inflammation and apoptosis

156
Q

Ca2+ in CHF

A

less released for contraction, inhibited uptake (increased in diastole and decreased in systole)

157
Q

IGF1 and PI3K in CHF

A

hypertrophy

158
Q

ANP and BNP in CHF

A

become resistant to them and no longer lead to Na+ and H2O loss

159
Q

signs in CHF

A

pitting edema
increased JVP
s3,s4
crackle, wheeze
hepatosplenomegaly

160
Q

3 causes/ mechanisms in atherosclerosis

A

-diabetes (AGEs)
-dislipidemia (LDL)
-Lp(a)- increased endothelial damage via immune cells and plaque formation also inhibits clot breakdown

161
Q

lp(a) mechanism

A

increased endothelial damage via immune cells and plaque formation also inhibits clot breakdown

162
Q

medications for CHF and angina

A

-beta blocker (SNS- NE)

-cardiac glycosides (digoxin): inhibit Na/K+ pump which decreases Na+ Ca2+ exchangers = increased Ca2+ in systole

-diuretics: increase water and sodium loss

163
Q

angina medications

A

-Ca2+ channel blockers
–> dihydropyridine: vasodilate
–> nondihydropyrine: slow AV conduction (HR) and contractility

-nitrates (NO): vasodilate

164
Q

medications for dyslipidemia

A

-HMG CoA reductase inhibitors (statins); decrease hepatocyte cholesterol production

-PCSK9 inhibitors: block the degradation of LDL receptors

-ezetimibe: decrease cholesterol absorption

-niacin B3: inhibit lipolysis

165
Q

valve pathologies

A

stenosis (narrow)

regurgitation (backflow)
–> incompetence: valve doesnt close
–> prolapse: valve into proximal chamber

166
Q

aortic stenosis/sclerosis

A

very common, >65yrs

from congenital bicuspid aortic valves

calcific aortic stenosis: myofibroblast become osteoblast like –> valve calcifies which increases afterload and causes concentric hypertrophy

167
Q

aortic regurgitation

A

related to aortic stenosis, ankylosing spondylitis, rheumatic heart disease, infective endocarditis

can cause shock

168
Q

most common valve pathology

A

mitral valve prolapse

169
Q

mitral valve prolpase

A

go back into left atrium

enlarged annulus and chord tendinae, myxomatous CT, proteoglycans, redundant leaflets

cadherin deficit, CT problem

170
Q

mitral valve regurgitation

A

from chronic mitral valve prolapse

papillary or chordae tendinae rupture

171
Q

rheumatic fever cause

A

autoimmune from group A strep (strep thoat or strep skin)

M protein

172
Q

rheumatic heart disease (group A strep)

A

affect all cardiac layers (Endo, myo, peri)

2-3 weeks after infection

inflammation –> valvular stenosis
= mitral (chordae tendinae)
=aortic stenosis (bicuspid)
most common

173
Q

most common valve pathologies from rheumatic heart disease

A

= mitral (chordae tendinae)
=aortic stenosis (bicuspid)

174
Q

3 types of cardiomyopathies

A
  1. dilated cardiomyopathy
  2. hypertrophic cardiomyopathy
  3. restrictive cardiomyopathy
175
Q

most common cardiomyopathy

A

dilated

176
Q

HF_EF in the cardiomyopathies

A

dilated= HFrEF
hypertrophic= HFpEF (can delve into HFrEF)
restrictive= HFpEF

177
Q

dilated cardiomyopathy causes

A

genetic sarcomere, infection, inflammation, toxic (alcohol, catecholamines, sarcoidosis, x linked)

178
Q

what happens in dilated cardiomyopathy

A

heart muscle enlarges and weakens; LV enlarges most- mitral regurgitation

179
Q

what valve issue in dilated cardiomyopathy

A

mitral regurgitation (LV enlarged most)

180
Q

symptoms of dilated cardiomyopathy

A

hypertrophy and fibrosis of cells

asymptomatic –> heart failure (fatigue, dyspnea), palpitate, syncope

181
Q

hypertrophic cardiomyopathy cause

A

-genetic deficit in sarcomere (gain of function)

182
Q

mechanism in hypertrophic cardiomyopathy

A

overgrown septum; obstruct outflow of LV to aorta

183
Q

symptoms in hypertrophic cardiomyopathy

A

asymptomatic, syncope (lose consciousness bc cerebral hypoperfusion)

184
Q

least common cardiomyopathy

A

restrictive cardiomyopathy

185
Q

causes of restrictive cardiomyopathy

A

deposits of ECM, amyloidosis (accumulate protein), hemochromatosis (iron), sarcoidosis (granuloma infiltrate), autosomal dominant

186
Q

mechanism in restrictive cardiomyopathy

A

restricted ventricular filling, decreased diastolic volume, normal systole

187
Q

where is Lp(a) made and in response to

A

made in liver bc increased IL6, cytokines (inflammation)

188
Q

what is a key feature in lp(a)

A

kringel units

189
Q

what does lp(a) look like

A

LDL - both contain apo(b)

190
Q

what is the pathogenic factor of lp(a)

A

transports oxidized phospholipids

191
Q

unstable plaques

what degrades collagen and makes the cap weaker

A

-rupture and release pro-coagulant molecules

weaker cap: macrophages make metalloproteinases to degrade collagen

192
Q

more stable cap

A

increase collagen via growth factors

193
Q

hallucination

A

sensory perception

formed (voice commands), unformed (non specific sounds)

with insight (aware) or without insight (think is real)

194
Q

schizophrenia DSM5

A

> 2 symptoms for 6 months or 1 month active symptoms (1-4), need 1 of the 1st 3

  1. delusion
  2. hallucination
  3. disorganized speech
  4. disorganized or catatonic behaviour
  5. negative symptoms
195
Q

cause of schizophrenia

A

dysregulated dopaminergic system- hyperactive tonic firing and reduced GABA in hippocampus

196
Q

2 things that back up schizophrenia and dopamine hypothesis

A
  1. antipsychotics block D2 receptors
  2. drugs that increase dopamine (l-dopa, amphetamines) increase psychosis
197
Q

GABA interneurons

A

inhibit dopamine in schizo- develop last and are damaged by ROS

198
Q

monoamines in the dopaminergic system

A

NE, serotonin, dopamine

199
Q

what part of the brain releases dopamine

A

midbrain- VTA and substantial nigra

200
Q

reward/motivation for dopamine

A

VTA –> nucleus accumbens and ventral striatum

201
Q

motor for dopamine

A

substantia nigra –> striatum

202
Q

executive function in dopamine

A

VTA and substantia nigra –> many cortical areas

203
Q

tonic firing for dopamine

A

slow, at rest, pacemaker via ventral palladium

slower by GABA

204
Q

phasic firing in dopamine system

A

RAS: glutamate release onto dopamine –> AP

in response to stimuli

205
Q

phasic firing changes

A

stronger via hippocampus if new stimuli

weaker phasic and tonic firing via amygdala in chronic stress

206
Q

schziophrenia and inflammation

A

-kyurenic acid blocks NMDA receptor= psychosis

activate microglial cells - prune synapses

207
Q

what causes pain in migraine

A

trdigemiocervical complex (TCC) –> thalamus –> cortex

208
Q

things that cause pain in migraine

A

serotonin and CGRP (vasodilate)

209
Q

medication for migraine

A

5HT-1 receptors for serotonin are blocked by “-triptans”

block CGRP (vasodilate)

210
Q

cause of migraine

A

spreading depression wave (excitability) through cortex and activate TCC

211
Q

central sensitization in migraine

A

central sensitization: cytokines –> release nerve growth factor from mast cells –> BDNF in C fibers –> pro pain

c fibers release CGRP and substance P

212
Q

c fibers release (in migraines)

A

c fibers release CGRP (vasodilate) and substance P (edema, vasodilate, mast cell degranulation)

213
Q

stomach microbiome and migraines

A

-h pylori triggers CGRP release

IBS increase serotonin

gut permeability –> LPS –> infalmmatory cytokines

214
Q

POTS (Postural orthostatic tachycardia syndrome)

A

lying to standing; HR increases > 30bpm with no hypotension or drop in blood pressure

or HR >120bpm

215
Q

if from lying to standing and HR increases and BP drops what is it

A

orthostatic hypotension

216
Q

symptoms of POTS

A

light headed, blurry vision, weak, nausea, palpitations

217
Q

who does POTS effect more

A

women > men

218
Q

test for POTS

A

tilt table test

219
Q

3 types of POTS

A

neuropathic POTS
hypovolemic POTS
hyperadrenergic POTS

220
Q

neuropathic POTS

A

lower limb blood pool because of less NE in the limbs

221
Q

hypovolemic POTS

A

decrease blood volume
-elevated renin and AT II
-inadequate aldosterone
-deconditioning

222
Q

hyperadrenergic POTS

A

increase NE
beta 1 and 2 autoantibodies

223
Q

4 heart sounds in order from right to left top to bottom

A

APTM

224
Q

location of SA, AV and purkinje

A

SA node: superior right atrium- sends signal to both atria

AV node: inferior RA- connect atria and ventricles
AV bundle of HIS sends signal to ventricles

Purkinje in ventricles

BMS200 (40 decks)

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