B3W3 Flashcards

1
Q

What are the clinical markers for hypertension diagnosis

A

three measurements of 140/90 over several weeks

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2
Q

Pathophysiology of HTN

A

hypertension leads to the thinning of arteriole walls and narrowing of arteriole lumen

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3
Q

Primary v secondary hypertension

A

primary - has no known cause
secondary - due to underlying chronic illness (such as DM, cushings, pheochromocytoma, sleep apnea, increased alcohol, increased Na

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4
Q

Largest risk factor for HF

A

hypertension

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5
Q

HF decreases or increases cardiac output

A

decreases

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6
Q

Systolic v diastolic heart failure

A

systolic: impaired ability to pump blood into circulation leading to decreased CO, decreased SV, decreased EF, decreased contractility

diastolic: impaired filling of the blood (decreased ventricular wall relaxation , decreased EDV, decreased SV, NO CHANGE IN EF

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7
Q

Clinical symptoms of (R) sided heart failure

A

fatigue and weight gain

hepatomegaly (large liver), peripheral edema, JVD

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8
Q

Clinical symptoms of (L) sided HF

A

fatigue, orthopnea/PND (paroxysmal nocturnal dyspnea, shortness of breath

S3/S4 heart signs, cyanosis, tachycardia, pulmonary congestion (crackling, wheezes, tachypnea and rales)

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9
Q

How do you distinguish (L) and (R) sided HF clinically?

A

where edema is present.

(L) = pulmonary circulation is backed up

(R) = systemic circulation is backed up

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10
Q

How does the PV loop move when you have systolic dysfunction

A

down and to the right
(decreases in SV, CO, EF, MAP, contractility)

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11
Q

What are the clinical causes of systolic dysfunction

A

MI, ischemia, chronic volume overload (from aortic or mitral valve regurgitation) and increased afterload (from aortic stenosis or uncontrolled HTN)

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12
Q

What happens to the ESPVR during systolic dysfunction

A

slope moves down

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13
Q

What happens to the ESPVR during diastolic dysfunction

A

nothing. no change in EF leads to no change in this relationship

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14
Q

What are the clinical causes of diastolic dysfunction

A

Impaired (L) ventricle relaxation, (L) ventricle hypertrophy, restrictive cardiomyopathy, myocardial ischemia

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15
Q

How can the left ventricle have clinical obstructions of filling?

A

Mitral stenosis, pericardial constriction (tampanade)

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16
Q

How does the PV loop change in diastolic dysfunction

A

left and up because there is decreased ventricular filling

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17
Q

How does a decrease in left ventricular function lead to salt and water retention

A

Decreased LV function leads to decreased CO which gives the false sense of hypovolemia. This creates abnormal reflexes to cause neurohormonal activation which will lead to the RAAS system to activate hormones to salt and water retention of the body to increase blood volume

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18
Q

What are the substances that are released by the neurohormonal activation pathway to cause water and salt retention

A

NE, renin, ADH, ANP (renal dilation),ET-1

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19
Q

Give a list of the medications that are used in HF patients

A

-adrenergic agonists
-adrenergic antagonists
-RAAS inhibitors
-Ca Channel blockers
-Dieuretics
-Mineralcorticoids
-Combined therapy
-Cardiac glycosides

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20
Q

How do adrenergic agonists act on cardiac muscle

A

alpha 1 - vasoconstriction
beta 1-2 - increases HR, contractility, dilation of vasculature
beta 2- vasodilation/bronchodilation

21
Q

Phenylephrine
Isoproternol
Albuterol

A

adrenergic agonists

22
Q

How do adrenergic antagonists act on cardiac muscle

A

negative ionotropic and chronotropic effects - aids in prevention of the heart working too hard, can reduce cardiac remodeling caused by neurohormonal activation

23
Q

What are the types of medications that reduce mortality in HF patients

A

beta blockers, ACE inhibitors

24
Q

What are the non pharmacological treatments for HF

A

Dietary decrease in Na, decrease in smoking, alcohol, maintain body weight, exercise, or treating underlying illnesses for secondary hypertension

25
Explain how RAAS inhibitors act on the heart to aid HF patients
ACE inhibitors- prevents the transition from ANG1 to ANG2, increases H2O and Na excretion Angiotensin Receptor Blockers- blocks AT1 receptors which are located in the body to promote vasoconstriction and blocks in the heart which normally promote cardiac remodeling (decreases BP and water retention)
26
Prazosin Propanolol Metoprolol Atenolol
Adrenergic antagonists
27
Enalapril Losartan
RAAS inhibitors
28
How do Ca channel blockers influence the cardiovascular system
inhibits Ca voltage gated channels on cardiac and VSMCs to arteriodilation and decrease TPR and BP, HR, and contractility increases ventricular compliance
29
What type of patients would you not use Ca Channel blockers on
systolic dysfunction patients (because they already have a decreased EF)
30
Amlodipine Verapamil
Ca Channel blockers
31
How do cardiac glycosides affect the heart
Digioxin -inhibits the Na-K pump which increases intracellular Ca, stops the NCS and leads to more forceful contractions, increase CO indirectly digioxin leads to no rise in HR but has vagus efferents that increase ventricular fill rate
32
Digioxin
Cardiac glycoside
33
How do mineralcorticoids
receptor blocker that promotes diuresis, increases K specific and non specific
34
Spironolactone Eplerenone
mineralcorticoid
35
How do combination therapies aid in HF patients
sacubitril and valsartan prevents natriuretic breakdown, and angiotensin blocker
36
Entrusto
combination therapy
37
How do diuretics aid HF patients
aids in the net Na and H2O excretion to decrease BP, aids in edema tx can be combined with other drugs synergistic effects
38
Difference between Thiazide and loop diuretics for clinical tx
thiazide- HTN loop- HF
39
hydrochlorothiazide
thiazide diuretic
40
Go through CICR
-T tubules bring down AP -Ca enters the cell through Ica -Internal rise in Ca leads to RYR to open (CICR) To get rid of Ca -SERCA uptake (phosphorylation of PLB) -NCX (3 Na in, 1 Ca out)
41
Why is there dysregulation of Ca in HF patients
-decrease in SERCA expression in heart disease patients -decrease in Ca uptake allows for more Ca to stay in thce cell which can lead to EAD/DAD -a leaky RYR (Ca back into the cell) -disorganized T tubules (leads to oxidative stress)
42
What are cardiac alternans
rhythmic oscillations that can lead to SCD
43
How does a disruption of Ca lead to cardiac alternans
with reduced SERCA uptake there are different levels of Ca being taken up leading to abnormal impulse propagation and abnormal conduction
44
Where can you see calcium transient alternans on the ECG
T wave
45
Describe heart alternans in normal patients and HF patients
normal - at high heart rates HF patients - lower threshold for alternans because of a decreased SERCA
46
What are some of ways that inflammation affect the heart
myocarditis, sarcoidosis, a-fib, MI, heart failure, sepsis, obesity, exercise, arrhythmogenic (R) ventricular cardiomyopathy, COVID 19
47
How do MSC cells work in normal patients
MSC activate paracrine activity to increase SERCA to aid in decreasing the risk of Ca alternans
48
How do fMSC cells work in HF patients
Remodeling of MSC to have them release interleukins that are harmful 1. I1B - prolongs AP duration 2. I6 - reduces connexon expression
49
What is the antibody which is being shown to decrease risk of SCD
anti IL 6