Midterm Flashcards
Aorta is derived from what embryonic structure
truncus arteriosus
pulmonary trunk is derived from what embryonic structure
truncus arteriosus
smooth part of R and left ventricle (concus cordis and aortic vestibule) are derived from what embryonic structure
bulbus cordis
L and R atrium are derived from
primitive atrium
smooth part of RA and oblique v. of L. atrium are derived from
sinus venous
where is M2 receptor found, G subunit and mechanism?
heart, Gi, decreased cAMP, increased K
Where is m3 found, g subunit, and mechanism
everywhere, Gq, increased ip3 and DAG
m4 found where? g subunit and mechanism
neurons, Gi, decreased cAMP, decreased ACh release
Alpha post ganglionic adrenergic affinity NE or EPI
NE>epi
Beta post ganglionic adrenergic affinity-NE or EPI
epi>NE
Alpha 1 g subunit
Gq
Alpha 2 G subunit
Gi
Beta 1-3 G subunit
Gs
Eyes sympathetic response-m. and receptor too
dilate
radial muscle-contracts-alpha 1, dilate pupil
ciliary muscle-relax and flatten- beta- allow distance vision
Cardiovascular sympathetic receptors
beta1> beta2
vasculature adrenergic receptors
alpha 1-vasoconstrict and send blood away
beta 2-dilate and increase blood flow
pulmonary adrenergic receptors
bronchodilation-beta 2
secretions- beta-2 humidify more air, alpha 1- decrease secretions
Gi tract sympathetic recptors
alpha 1- increase sphincter tone
alpha 1 and beta- decrease motility
alpha 2- decrease secretions
liver sympathetic response
alpha 1 and beta 2 to increase glucose release
adipose tissue sympathetic response
alpha1, beta 1, and beta 3 to increase FFA release
male sex organs sympathetic response
alpha- ejaculation
eyes parasympathetic resposne
M- activate sphincter muscle of eye- constrict pupil
M- contraction ciliary muscle muscle of lens-near vision
heart PS response
M2- decrease rate
smooth muscle PS receptor
M3-vasodilation except for abdominal viscera, kidneys and veins
lungs PS response
M3- bronchial SM contraction and gland secretion
digestive organs PS response
m3- increase motility, secretion and relax sphincter
male sex organs PS response
M-erection
urinary system PS response
m3-micturition
Smooth muscle has what receptors
mACHRs and adrenergic
ACh does what to SM
gut SM m. contraction, relaxation in other tissues
NE/epi does what to SM
vascular SM contraction, gut SM relaxation
NO does what to SM
inhibits SM
PKA is activated through what G protein and does what to SM
Gs, blocks myosin light chain kinase it results in inhibition of contraction (decreased cross bridge cycling)
Skeletal muscle Organization, innvervation, NTs, Action of NTs, mode of transmission and NT receptors
Thick/thin filaments organized, alpha-motorneuron, ACh, Excitatory only, Specialized NMJ, nAChRs at motor end plate
Smooth muscle Organization, innvervation, NTs, Action of NTs, mode of transmission and NT receptors
Thick/thin filaments randomly arranged, intrinsic and ANS innervation, NTs=ACh, NE/epi, NO, Excitatory or inhibitory, uses varicosities with no motor end plate, Multiple receptors located over cell membrane
What is Thrombopoietin, where is it from and where does it bind
From liver, stimulates megakaryocytes to make platelets and binds MPL receptor
What do platelets contain
Mitochondria Actin Myosin Cox1 Vesicles-contain serotonin
5 steps of hemostasis
Vascular spasm, Platelet plug, Blood clotting, repair and removal
Describe vascular spasm
platelets release serotonin which vasoconstricts
also release thromboxane A2 which is a prostaglandin that increases IP3 of SM, which leads to inc Ca++
Describe platelet plug
Vascular damage leads to collagen being exposed and binding/activating receptors on platelets
Platelet and collagen are held together via
Von willebrand factor and is associated with collagen type 6, collagen also binds to integrin to platelet membrane
What does an activated platelet do in platelet plug
swells, extends podocytes
then contracts, releases calcium, actin and myosin interact to squeeze out granules
ADP and thromboxane A2 are release which attracts other platelets
*may be sufficent to stop bleeding
Decribe clot retraction
requires platelets, which bind fibrin and contract to pull fibrin closer together,
also requires calcium and the final product squeezes liquid out which solidifies clot
what happens during repair of damage?
PDGF released by platelets which stimulates fibroblasts to repair
Describe clot removal
Plasmin is an enzyme that digests fibrin
Plasminogen is inactive form of plasmin, made by liver, found in blood
tPA activates plasminogen-plasmin
tPA is released by damaged tissue
Delayed activation due to tPA inhibitor in blood… so you won’t actually start using tPA until the blood goes away/the damage is healed
*Protein C inactivates tPA inhibitor
How do endothelial factors within blood vessel prevent clots?
Smooth surface of vessel makes it harder for platelets to grab on
Membrane proteins on endothelial cells such as Glycocalyx repels platelets and clotting factors. Thrombomodulin inhibits thrombin and leads to protein C activation
How does Prostacyclin/PGI2 prevent clots?
It is made near the injury and causes vasodilation, which prevents agregation
How dose antithrombin III prevents clots?
anticoagulant, binds and inhibits thrombin
*Heparin: increases antithrombin efficacy-Heparin is from mast cells
What is happening in a systolic murmur?
Systolic: between S1 and S2
Mitral/tricuspid regurg: blood moving back into atria when AV valve should be closed
Aortic/pulmonic stenosis: hard to push blood out
What is happening in a diastolic murmur?
Diastolic: between S2 and S1
Mitral/tricuspid stenosis: hard to push blood through into
ventricle
Aortic/pulmonic regurg: blood moving back into ventricle when these valves should be closed
Define preload
end diastolic volume or right atrial pressure
define afterload
aortic/pulmonary a. pressure
what is frank starling relationship
increased preload=increase ventricular fiber length= increased tension and CO
Increased preload leads to what
increased SV and wider loop on chart
increased afterload leads to what
increased aortic pressure, decreased SV, higher LV pressure
increased contractility leads to what
greater tension during systole, which means higher SV, dec end systolic volume and higher LV pressure
increased TPR leads to what
decreased CO and decreased venous return for certain RA pressure
positive inotropy leads to what
increase CO and decrease RA pressure
phase 0 of ventricles, atria and purkinje myocytes
inward Na current and depolarization
phase 1 of ventricles, atria and purkinje myocytes
outward K current +
decreased inward Na current
rapid repolarization
phase 2 of ventricles, atria and purkinje myocytes
inward Ca current +(slow ca++ channels open)
increased outward K current(via calcium activated potassium channels, although closing of special, voltage gated K channel)
plateau
phase 3 of ventricles, atria and purkinje myocytes
decreased inward Ca current (ca channels close)
increased outward K current (special K channels open)
repolarization
phase 4 of ventricles, atria and purkinje myocytes
inward and outward K
currents are equal
RMP
Phase 4 of SA/AV node
inward Na current (“funny current,” activated by
repolarization from preceding AP)
slow depolarization
Phase 0 of SA/AV node
inward Ca current (opening of slow ca++ gates), closing of special K gates
depolarization
Phase 3 of SA/AV node
outward K current (opening special K+ gates)
closing of ca++ gates
repolarization
define inotropy
how hard the cardiac muscle contracts,
based off [intracellular Ca]
*Ejection fraction
define chronotropy
Chronotropy: how fast the cardiac muscle contracts,
based off firing rate of SA node
HR, length of phase 4 depolarization
define dromotropy
Dromotropy: the conduction velocity through the AV
node (PR interval)
What is happening in P wave, PR interval, QRS, T wave, QT interval and ST segment? and what phase is each one?
P wave: atrial depolarization (phase 0 atrial m.)
PR interval: depends on conduction velocity through AV
node
QRS complex: ventricular depolarization (phase 0 ventricles)
T wave: ventricular repolarization (phase 3 ventricles)
QT interval: entire period of depolarization and
repolarization of ventricles (includes Q, R, S, T waves)
ST segment: period of ventricular depolarization (stops
right before T wave)
phase 0 of ventricles, atria and purkinje myocytes
inward Na current and depolarization
phase 1 of ventricles, atria and purkinje myocytes
outward K current +
decreased inward Na current
rapid repolarization
phase 2 of ventricles, atria and purkinje myocytes
inward Ca current +
increased outward K current
plateau
phase 3 of ventricles, atria and purkinje myocytes
decreased inward Ca current
increased outward K current
repolarization
phase 4 of ventricles, atria and purkinje myocytes
inward and outward K
currents are equal
RMP
st depression means
subendocardial problem- ischemia has not made it all the way through the wall, just endocardium
Phase 0 of SA/AV node
inward Ca current
depolarization
Phase 3 of SA/AV node
outward K current
repolarization
define inotropy
how hard the cardiac muscle contracts,
based off [intracellular Ca]
*Ejection fraction
define chronotropy
Chronotropy: how fast the cardiac muscle contracts,
based off firing rate of SA node
HR, length of phase 4 depolarization
how to measure turbulence
reynolds number= densitydiametervelocity/ viscosity
if greater than 2000 then turbulent (bruits and arteriosclerosis)
What is happening in P wave, PR interval, QRS, T wave, QT interval and ST segment?
P wave: atrial depolarization
PR interval: depends on conduction velocity through AV
node
QRS complex: ventricular depolarization
T wave: ventricular repolarization
QT interval: entire period of depolarization and
repolarization of ventricles (includes Q, R, S, T waves)
ST segment: period of ventricular depolarization (stops
right before T wave)
definition for compliance
Compliance= change in V/ Change in pressure
Septal leads are
V1 and V2
how is atrial pressure calculated
pulmonary wedge pressure
catheter measures pressure in pulmonary a (slightly overestimates)
lateral leads are? and look at what coronary artery?
I, aVL, V4, V5, V6 (l circumflex)
starling forces pushing fluid out are
capillary hydrostatic pressure +interstitial oncotic pressure = Pc + πi
st depression means
subendocardial problem- ischemia has not made it all the way through the wall, just endocardium
equation for blood flow
Velocity= flow rate (Q)/ area (cm) Q= pressure gradient/ resistance
equation for cardiac output
CO= SV x HR CO= (arterial-venous pressure)/ TPR
When muscles contract and temporarily compress arteries, the increased flow after relaxation is called
reactive hyperemia
Equation for resistance
R= (8n(viscosity)length)/ pir^4
how to measure turbulence
reynolds number= densitydiametervelocity/ viscosity
if greater than 2000 then turbulent (bruits and arteriosclerosis)
define shear
the difference in velocities of adjacent layers of blood, shear is higher at periphery because greatest difference of blood velocity of adjacent layers
definition for compliance
Compliance= change in V/ Change in pressure
Mean arterial pressure is calculated how
diastolic + 1/3 pulse pressure
how is atrial pressure calculated
pulmonary wedge pressure
catheter measures pressure in pulmonary a (slightly overestimates)
Starling forces keeping fluid in are
capillary oncotic pressure +interstitial hydrostatic pressure = πc + Pi
starling forces pushing fluid out are
capillary hydrostatic pressure +interstitial oncotic pressure = Pc + πi
what does histamine and bradykinin do
arteriolar dilation,venous constriction
it is released in response to tissue damage and increases capillary porosity. This can cause edema
what does serotonin do to blood vessels
arteriolar vasoconstriction
what do lactate, adenosine and inc K do to skeletal muscle
local vasodilation (active hyperemia)
When muscles contract and temporarily compress arteries, the increased flow after relaxation is called
reactive hyperemia
Name all the things angiotensin II does
aldosterone secretion by adrenal cortex leads to increased Na reabsorption and H2O follows
increases Na/H exchange in PCT in kidney-H2O follows
increases thirst-increased H2O intake
vasoconstriction of arterioles
stimulates ADH secretion from posterior pituitary-fluid retention +vasoconstriction
anterior leads are
v3-4
inferior leads are
2,3, avf
blood islands are first seen _____
in the Yolk sac
Blood islands arise from ___ and are induced to become___
mesoderm cells, hemangioblasts
what binds to mesenchymal cells to form hemangioblasts
FGF2
central cells become
HSC
peripheral cells become
angioblasts-endothelium of blood vessels
what arterial systems have only alpha receptors
skin and mucosa, salivary glands, and brain
Erythropoietin source, trigger for release, control of hormone, receptor, cells expression receptors and effect
kidney, low o2 to kidney, HIF accumulation in renal cell, receptor is EPoR, pluripotent stem cells and RBC precursors, increased erythroid division
thrombopoiesis source, trigger for release, control of hormone, receptor, cells expression receptors and effect
liver and possibly others, constitutive release, controled by internalization of TPO by plateltes, MPL is receptor, Platelets and Hematopoietic cell lines express receptor and it increases ALL blood cell lineages.
blood coagulation 3 steps
formation of prothrombin activator
activation of thrombin
creation of fibrin from fibrinogen
binding of thrombin to thrombomodulin activates ___?
____ can then inactive _____?
protein C, which can then inactive the plasmin inhibitor
what does primary heart field form
form left and right side
Atria, Left ventricle, and PART of right ventricle
secondary heart field forms
form remainder of right ventricle and outflow tract (consisting of conus cordis & truncus arteriosus)
where are timed k gates opening in the ventricles-atria
t wave
P WAVE ECG Characteristics
upright in 1,2 v4-6, AVF,
inverted in AVR
all others are variable
wolff parkinson white is
ventricular preexcitation syndrome
qrs duration, q duration and see 1-2 mm in which leads
.05-.11, .03, normal in 1 AVL, AVF, v5-6
t wave shape, height and leads seen in
1,2, v3-6, inverted in AVR
shape is slightly round and asymmetrical
heigh is not greater than 5 mm in standard leads and not greater than 10 mm in precordial leads
qrs greater than .12 sec
BBB
CUSHING REACTION
hypertension because of intracranial pressure too low and body tries to compensate
where do you see stemi
v2-v3 J point greater than 2mm (1.5 woman), or 1mm in 2 or more contiguous leads
describe nstemi
st segment depression, t wave inversion, chest pain and elevated cardiac enzymes
Zones of infarction- you see infarction, injury and ischemia at what respective waves/segments
infarction-q
injury-st segment shifts
ischemia- t wave changes
MI LAD- Area and leads
Anterior wall infarction v1-7
MI RCA- area and leads are
inferior wall infarction, 2,3,AVF
MI circumflex artery
Lateral wall, 1, AVL v5-6
posterior descending
posterior wall infarction v1-3
ekg first several hours post MI
T wave peak
EKG first day after MI
St elevation marked and r wave amplitude diminshing
EKG 2nd day after MI
R wave nearly gone, T wave inversion, St elevation may decrease and significant q wave
EKG after 2/3 days
No r wave, Deep t wave inversion, marked q wave, st may be at baseline
EKG weeks post MI
some r wave may return, t wave less inverted, st elevation may persist in aneurysm develops and q wave persists
lab values post MI
WBC increased 12-15000 hours to 2-4 days after
CRP increased and BNP increased because of ventricular wall stress and fluid overload
Caridac biomarkers of necrosis
troponin I (cTnI) or T 1-4 hours s/p MI 10-24 hours peak persists for 5-14 days renal failure may give false positive
