Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MED PHYS > Block 3 Trans Phys Review > Flashcards

Block 3 Trans Phys Review Flashcards

1
Q

Name the layers of vascular blood vessels from outside to inside.

A

Tunica Externa -> External Elastic Lamina -> Tunica Media -> Internal Elastic Lamina -> Tunica Intima

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

Explain the anatomical presence and complications of atherosclerosis.

A

Cholesterol can build up between the tunica intima and tunica media. When this builds up of cholesterol ruptures the tunica intima this may trigger a clotting response and cause a permanent calcification of the cholesterol. This calcification leads to a large near permanent blockage of the blood vessel.

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

Explain the physiological consequences of atherosclerosis.

A

At the site of rupture, the clotting can create a thrombus which further blocks blood flow and could potentially break off into the blood and become an embolism. Furthermore, the overall cross-sectional area of the vessel at the location of cholesterol build up will greatly reduce blood flow and increase blood pressure at that location.

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

What is the benefit of imaging the blood vessel where atherosclerosis is taking place?

A

The main benefit of imaging the blood vessel where atherosclerosis has taken place is that it can help identify which cholesterol build ups are too far gone and which ones are treatable. As long as either a thick cap or thin cap of endothelial cells exist to separate the cholesterol from the lumen of the vessel treatment can be administered. Likewise by imaging the plaque formation certain components like calcified tissue and necrotic cores can help determine whether or not the patient has other risk factors, needs monitoring, or if some treatment is now unavailable.

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

What are risk factors that can be found within the build up of plaque in atherosclerosis?

A

Necrotic core, TCFA or thin cap fibroatheroma, Spotty Calcification, and/or remodeling of the vessel, all indicate a high likelihood of rupture.

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

What is the danger of allowing a plaque formation like that found in atherosclerosis to continue growing?

A

Once any blockage of a blood vessel, plaque or otherwise, reaches 50% size of the lumen the chances of a heart attack increase dramatically. Likewise, in atherosclerosis once plaque formation reaches a size that is around 50% of the lumen the growth of the plaque formation increases substantially.

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

What are some potential imaging techniques that can be used in the diagnoses and treatment of atherosclerosis?

A

Coronary CT, Carotid Ultrasound, Brachial Artery Reactivity Testing, Myocardial Perfusion Imaging, and Invasive Vascular Imaging.

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

What are techniques used to measure the physiological response of a vessel with atherosclerosis?

A

Flow-Mediated Dilation, Hyperemic Flow, Myocardial Perfusion Imaging, and both invasive and noninvasive Fractional Flow Reserve.

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

Coronary CT

A

Using an Xray machine you can identify areas of calcification. However, by using computer tomography along with an injection of dye it is possible to get much better imaging.

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

Carotid Ultrasound

A

A carotid ultrasound involves using ultrasound near the carotid artery to identify increases in intima media thickness. This technique works very well for vessels near the skin but not as well for more embedded vessels.

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

Single Photon Emission Computed Tomography

A

Injection of a radioactive substance can image the blood vessel. By then furthering exercising the target location and comparing it at rest you can determine location and severity of the blockage.

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

Invasive Vascular Imaging

A

A camera is inserted directly into the vessel.
- Intravascular Ultrasound
- Optical Coherence Tomography

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

Brachial Artery Reactivity Testing

A

At sites of plaque build up nitric oxide release is needed to offset blood flow lost by the blockage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  • Flow Mediated Brachial Artery Dilation
A

Temporarily cutting off blood flow causes a delayed endothelial response in which they release nitric oxide. This measures the reactivity of the endothelial cells, if the reactivity is low this is a high-risk factor.

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

Flow independent Brachial Artery Dilation

A

Rather than cutting off blood supply an injection of nitroglycerin is administered instead.

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

Hyperemic Velocity

A

Measure of the speed of dilation.

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

Myocardial Infusion Testing

A

Rather than measure individual artery perfusion you instead measure the pre and post concentration of oxygen surrounding a target organ and the difference can be used to determine how impeded the blood vessel is.

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

Fractional Flow Reserve

A

The ratio between blood that can move through a vessel with a stenosis versus the blood flow of a vessel without a stenosis.
- This determines the percentage loss of blood flow caused by the stenosis.
- It is the max flow during exercise that is used for fractional flow reserve.

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

What is a normal Fractional Flow Reserve Value?

A

Anything greater than 0.80. The lower the FFR the higher the likelihood of cardiovascular disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe inotropy through the lens of someone attempting to understand heart failure.

A

Inotropy is the strength of contraction, it is influenced by the amount and affinity of calcium within the myocyte. The more calcium and the more affinity for calcium on troponin C then the higher the amount of inotropy.

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

What are current therapies that target inotropy specifically?

A

Digoxin – Improves Ventricular Filling but does not increase survival.
Calcium Sensitizer Levosimendan – Binds Troponin C when calcium is high.
cAMP Mediated Inotropic Stimulation
PDE Inhibitors

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

What is Omecamtiv Mecarbil?

A

Omecamtiv Mecarbil is a cardiac myosin activator that was tested as a potential heart failure medication. The idea behind the medication was that by strongly binding the myosin head with actin a stronger crossbridge can be formed and therefore a stronger contraction.

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

What was found in the mouse models of the Omecamtiv Mecarbil? Human model?

A

Omecamtiv Mecarbil was found to increase force generation at low calcium levels but increased the time it took to detach myosin from actin. In human models however, any beneficial effect provided by the medication was submaximal and hindered overall heart rate and diastolic filling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the three tubes used for collecting blood and how do you obtain them?
Red – No Chelator used to obtain serum for chemical analysis. - The plasma and RBC clot Purple – EDTA is administered which is an irreversible chelator and prevents all clotting used to obtain RBC counts. Blue – Sodium Citrate which is a reversible chelator is used to test coagulation by preventing plasma from coagulating.
26
Describe the elastic and compliant properties of Arteries, Arterioles, and Veins.
Arteries have low compliance and but are able to stretch to some degree but also have capabilities to bounce back. Arterioles are the main site of resistance it has a decreased radius without being in parallel and also has innervated smooth muscle. Veins are more compliant and easier to stretch at low pressures but at extremely high pressures lose the ability to be compliant.
27
What is the significance of cross-sectional area and velocity?
If cross sectional area decreases velocity must increase because it has to maintain blood flow.
27
Mnemonics for remembering what factors cause vasoconstriction and vasodilation.
Vasoconstriction - NEAE Near Gq G alpha P GAP PL-C Police Police called because PIP2 PP peepee exposed get arrested and much show them your ID IP3 and Dag, you are salty so it raises calcium o Near the Gap you expose your PP and the police ID you and you are salty about it Vasodilation - EAP Eat eating food gives you Gs G alpha s Gas too much gas you want to turn on AC, eat too much you go to fat cAMP camp exercise so you vasodilate o Eating to much food gives you gas and makes you want to turn on the AC but you have to go to fat camp where you exercise and increase blood flow. - Nitric Oxide NO no Guanylyl cyclase GC Game cube No gamecube cGMP can’t game multiplayer because no gamecube in PKG package no gaming so relax vasodilation o No gamecube so can’t play multiplayer game because its not in its packaging so may as well relax.
28
What happens if you increase the production of cAMP and cGMP in smooth muscle?
The smooth muscle relaxes and as a result produce a decrease in the strength of the contraction.
29
NEAE
Norepinephrine Epinephrine Angiotensin II Endothelin-1
30
EAP
Epinephrine Adenosine PG
31
What is a myogenic response?
Increasing transmural pressure causes an increase vascular smooth muscle constriction.
32
What is the only endothelial local promoter that promotes contraction?
ET-1 or endothelin
33
Explain endothelial response to shear stress.
When the endothelial cell undergoes shear stress caused by increased blood flow agonists react with the Gq Receptors to promote nitric oxide synthase production of Nitric Oxide from L-Arginine
34
What is a PDE? What happens when PDE receptors are blocked?
PDE is Phosphodiesterase which breaks down cGMP to cause vasoconstriction. By blocking PDE you promote vasodilation.
35
What is endothelial dysfunction and what is it a marker of?
Endothelial dysfunction is a sign of vascular disease in which flow mediated dilation is impaired this could be because of lower amounts of nitric oxide synthase, low nitric oxide, or oxidative stress. Endothelial cells that are dysfunctional are sometimes known as activated cells.
36
What three vital systems are heavily autoregulated when it comes to their blood circulation?
Coronary, Cerebral, and Renal.
37
Explain the basics of special circulation organ systems.
Coronary blood flow is autoregulated and will vasodilate when more blood is needed. The blood vessels get compressed during systole, so the blood supply in the heart occurs during diastole. Cerebral blood flow mainly senses high amounts of CO2 and will cause vasodilation in response. Skeletal muscle has the highest increase in blood flow during exercise. Skeletal muscle that is being used during exercise will vasodilate to receive more oxygenated blood while muscle not being used will vasoconstrict. Pulmonary vessels are usually the last to be taken into consideration when oxygen levels are low and will vasoconstrict to allow the oxygenated blood to be shunted to more metabolically demanding organs.
38
What is the main cause of heart failure?
The main cause of heart failure is chronic hypertension.
39
How do you diagnose someone with hypertension?
You obtain three separate readings of a heart pressure of 140/90 over several weeks.
40
What is the main correlation between heart failure and hypertension?
Hypertension causes thicker arteriole walls and ventricular muscle. This leads to increased resistance within the vessels which further increases blood pressure and lowers the effectiveness of of the heart’s ability to pump blood.
41
What is primary and secondary hypertension?
Primary hypertension also known as secondary hypertension is hypertension that is not associated with any underlying condition. Secondary hypertension is hypertension that occurs due to an underlying medical condition.
42
What is the definition of heart failure?
The inability for the heart to maintain cardiac output needed either because of systolic or diastolic dysfunction.
43
What is the most common cause of Right Sided Heart Failure?
Left Sided Heart Failure
43
Compare and contrast Systolic and Diastolic Dysfunction.
Systolic dysfunction is an impaired ability to pump blood which causes a decrease in stroke volume and cardiac output and a decrease in ejection fraction. This is the most common cause of myocardial infarction. Diastolic Dysfunction is an impairment in the filling of the heart, caused by ventricles being unable to properly relax. This leads to decreased stroke volume and cardiac output. However, the ejection fraction remains the same.
44
What are some different signs and symptoms of right and left heart failure?
Right sided heart failure causes fatigue and weight gain. The signs of right sided heart failure are hepatomegaly or an enlarged liver, likely due to the chronic increase of blood in circulation, jugular venous distension caused by blood getting backed up in the veins, and peripheral edema caused by the increase in peripheral blood volume. Left sided heart failure causes fatigue, paroxysmal nocturnal dyspnea, abnormal shortness of breath when sleeping, and general shortness of breath. The signs of right sided heart failure are the introduction of S3 and S4 sounds, tachycardia likely caused by the heart attempting to compensate for its inefficiency by increasing heart rate, and pulmonary congestion. Pulmonary congestion further shows itself as cough, crackles, wheezes, and/or tachypnea.
45
Define afterload and contractility. How do they relate to systolic dysfunction?
Afterload is the pressure necessary for the heart to pump blood out of the aorta. During heart failure however, the heart lacks any sort of compensation mechanism for increased afterload and does not increase its pressure like a functional heart would. Instead the amount released and pressure applied is just barely enough to overcome afterload. Contractility is how well the heart can eject blood and in hearts undergoing systolic dysfunction we see ESPVR or end systolic pressure volume relation decrease so not as much pressure is produced and less blood is pumped.
46
What are some consequences of impaired contractility?
Myocardial Infarction, ischemia, and chronic volume overload.
47
What are the consequences of increased afterload?
Aortic stenosis or blockage caused by the thickening of the walls and uncontrolled hypertension caused by the narrowing of vessels and increased blood pressure.
48
Explain left ventricular filling and relaxation. How does it relate to diastolic dysfunction?
Impaired relaxation of the left ventricle means that it always at a higher-than-normal pressure and experiences less filling. Stroke volume and cardiac output is decreased but does not affect the contractility.
49
What are the consequences of impaired relaxation?
Left ventricular hypertrophy, restrictive cardiomyopathy, and myocardial ischemia.
50
What are the consequences of obstruction to left ventricle filling?
Mitral Stenosis and pericardial constriction
51
Explain the pathophysiological cycle of heart failure.
Due to some factor, coronary heart disease, hypertension, or cardiomyopathy, the body wrongly assumes that there is less water in the blood. This preserved decrease in blood volume is due to decreased cardiac output and abnormal reflexes. As a result neurohormonal systems are activated in an attempt to remedy this. The neurohormones activated cause salt and water retention. However in retaining more water and salt when there is no need to the heart’s functions are further impeded and continue to go through this cycle which if unchecked leads to progressive heart failure.
52
What are the neurohormonal systems that contribute to heart failure?
Firstly, there is an increase in NE, Renin, ADH, ANP, and ET-1. RAAS systems are activated. RAAS systems cause a decrease in heart rate and increases water and salt retention. Natriuretic Peptides are impaired by ANP and as a result are unable to be used to remove excess salt and water effectively.
53
What are nonpharmacological treatments of heart failure?
Lifestyle changes and addressing any secondary disorders that may be present.
54
Beta Blockers
block beta receptors - Causes Negative inotrope and negative chromotrope activity - Prevents heart from over working itself - Can be used well with Ace inhibitors and diuretics
54
Diuretics
attempts to treat heart failure by causing an increase in sodium and water excretion to lower blood pressure. - Thiazide diuretics is most effective for hypertension - Loop diuretics are the most effective for volume decrease - All drugs combine well with diuretics
55
ACE Inhibitors and ARBs
- RAAS is activated to rescue MAP o Increases NaCL and Water retention. o Causes vasoconstriction. o Activates the CNS o Good during hemorrhage and acute blood loss o Very negative for heart failure and hypertension o Works by converting Angiotensin into Angiotensin II - ACE-I stops the conversion of angiotensin into angiotensin II. - ARB Blocks AT-1 Angiotensin II receptors
56
Calcium Channel Blockers
inhibits the flow of calcium into cardiac and smooth muscle cells. - Causes vasodilation - Decreases heart rate - Decrease contractility - Used to treat diastolic heart failure and hypertension o Not advised for systolic dysfunction because it would further decrease contractility
57
Cardiac Glycosides
inhibits the Na/K pump by disrupting gradient - NCX channel won’t be able to exchange sodium and calcium which causes more intracellular calcium to be in the cell and increase contractility. - Also activates the parasympathetic nervous system to decrease heart rate - Increases cardiac output without increasing heart rate
58
Further explain the RAAS system.
RAAS system is a system that is good for replenishing blood volume but is not needed to chronically be activated. It works by converting Angiotensinogen into Angiotensin I via Renin and Angiotensin I into Angiotensin II via ACE which is activated by Bradykinin.
59
What are some examples of calcium dysregulation in heart disease?
Decreased SERCA2a Expression – Decreased Calcium uptake into the sarcoplasmic reticulum Leaky RYR Reduced or reorganized T Tubules Oxidative Stress Hyperphosphorylation
60
What are cardiac alternans?
Alternans are the appearance of strong propagation followed by low propagation in a cyclic manner that does not increase HR. decrease contractile force, or cause apoptosis.
61
What is the danger of ventricular arrhythmia?
Ventricular arrythmia have an unknown cause but can cause death.
61
What causes/increases the risk of abnormal alternans?
Decreased SERCA
62
What is the relationship between mortality and ejection fraction?
As left ventricle ejection fraction decreases the chances for mortality increase. This matches the shape of mortality and arrhythmias.
63
Why do T tubules move inwardly within the cardiac muscle?
Allows for signals to propagate the entire myocyte as opposed to just the outer cells.
64
When are alternans shown in normal individuals?
During periods of higher-than-normal heart rate.
65
What are cytokines and what do they cause?
Cytokines are pro-inflammatory substances released by many different cell types but is especially worrying in failing mesenchymal stem cells. Can cause prolonged action potential, RYR leak, and reduce connexon expression.
66
What are two examples of cytokines?
Interleukin-1 and Tumor necrosis factor
67
What was found to happen when anti-IL-6 intervention was done?
Decreased risk of sudden cardiac death
68
What is the cardioprotective role of Mesenchymal Stem Cells?
Increase Serca activity. Decrease Ca alternans
69
Explain advanced cardiac life support.
First always start with CPR and determine whether or not you can shock the patient. The EAD will determine if possible. If no shock can occur administer epinephrine and continue checking for shock. Continue administering CPR for two minutes followed by checking for shock and administer epinephrine. When epinephrine has begun to allow for a shock go to the shock steps. If you can shock continue 2 minutes of CPR and administer cycles of norepinephrine and lidocaine every 3-5 minutes.
70
What is the American Heart Associations PICO system?
P-Population I-Intervention C-Comparator O-Outcome Used to determine CPR guidelines.
71
What can be done with compressions and shock to improves survivability?
Shortest possible duration between shock and compressions of about <25 seconds.
72
What can and cannot be shocked?
Shock if the heart is undergoing ventricular fibrillation or tachycardia. Shock can not be administered to Sinus rhythm, supraventricular contraction, or atrial fibrillation.
73
What are some drug therapies for cardiac life support?
Amiodarone – Treats Ventricular Arrhythmia Lidocaine – Blocks cardiac sodium channels Epinephrine – Increases heart rate and contractility Rotigaptide – Drug under investigation to treat arrhythmia
74
What are other ways to assist someone undergoing a cardiac arrest?
Advance airway and allow air to flow in and out of the lungs.
75
76
What causes of cardiac arrest can be reversed?
Hypo- causes Tension Tamponade Toxins Thrombus
77
What part of the action potential are cardiac alternans involved in?
The repolarization phase.
78
How can you fix cardiac alternans?
Increase gap junction coupling
79
Explain the pathophysiological timeline of cardiac arrest.
Cardiac Arrest -> 10 Sec Loss of Consciousness -> 20 Sec Isoelectric EEG -> 2-3 Min depletion of cerebral ATP -> Causes increase in intracellular potassium, cellular depolarization, and calcium influx -> 10-20 Min brain reperfusion -> Return of Spontaneous circulation -> 3 hrs systemic inflammatory response -> hemodynamic instability increase in arrhythmias -> 2-3 days increase in sepsis due to GI ischemia and subsequent reperfusion -> 7 days apoptosis can be seen after ischemic event in hippocampus

MED PHYS (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions