Written by students who passed Immediately available after payment Read online or as PDF Wrong document? Swap it for free 4.6 TrustPilot
logo-home
Exam (elaborations)

NURS 5315: Advanced Pathophysiology Summer 2024 UTAH | Questions with Answers Verified 100% Correc

Rating
-
Sold
-
Pages
41
Grade
A+
Uploaded on
09-10-2024
Written in
2024/2025

NURS 5315: Advanced Pathophysiology Summer 2024 UTAH | Questions with Answers Verified 100% Correc

Institution
N5315 Advanced Pathophysiology
Course
N5315 Advanced Pathophysiology

Content preview

NURS 5315: Advanced Pathophysiology Summer
2024 UTAH | Questions with Answers Verified
100% Correct
Tetralogy of Fallot - ✔✔Most common cyanotic congenital heart defect


Tetralogy of Fallot involves four heart defects:
1. A large ventricular septal defect
2. Pulmonary stenosis
3. Right ventricular hypertrophy
4. An overriding aorta



Heart Failure Risk Factors - ✔✔-Age (most common over 65 y/o)
-Ischemic heart disease
-Obesity
-Diabetes
-Hypertension
-Excessive ETOH use
-Congenital heart disease
-Valvular heart disease
-Myocarditis
-Cardiomyopathy (stiffening of heart muscle)
-Renal failure



Heart Failure Clinical Manifestations - ✔✔-Volume overload
-Poor perfusion secondary to pump failure

,Heart Failure with REDUCED Ejection Fraction, SYSTOLIC Heart Failure, LEFT-SIDED heart failure
- ✔✔-LEFT-SIDED HEART FAILURE, SYSTOLIC HEART FAILURE, but right ventricular systolic
dysfunction can happen too
-IMPAIRMENT in LEFT VENTRICULAR CONTRACTION (SYSTOLE)
-Most common CAUSE is MYOCARDIAL INFARCTION. Other causes are myocarditis and
cardiomyopathies.
1. Decrease in contractility in left ventricle will decrease stroke volume (volume of blood
pumped from left ventricle with each beat).
2. Cardiac output (amount of blood pumped from heart per minute) decreases.
3. Left ventricular end diastolic (relaxation of heart) volume (preload) increases - not enough
blood got pumped out of left ventricle during systole (contraction), so more is hanging around
during diastole (relaxation).
4. Ventricular remodeling occurs.
5. Preload (amount of blood in ventricle during relaxation) further increases over time, causing
causing a dilation of the ventricle and further compromises contraction and cardiac output.
6. Myocytes deteroriate.


The systolic dysfunction (low cardiac output) results in 2 processes being triggered:


-Baroreceptor activation: Baroreceptors notify the medulla to turn on sympathetic nervous
system because heart is not pumping out enough blood. The catecholamines epinephrine and
norepinephrine cause vasoconstriction, increased afterload, increased blood pressure,
increased heart rate. This increases work loard of heart, causes hypertrophy & dilation of left
ventricle, and further impairs contractility.
-Renin Angiotensin Aldosterone System (RAAS): Activated by decreased renal blood flow.
Causes vasoconstriction, which increases afterload and blood pressure, but contributes to
worsening of left ventricular hypertrophy/dilation and worsens contractility.


Medications: BETA BLOCKERS to block the effects of chatecholamines in the heart. ACE
INHIBITORS and ARBS (angiotensin II receptor blockers) to block effects o


Heart Failure with PRESERVED Ejection Fraction (HFpEF),

,LEFT-SIDED heart failure - ✔✔-Diastolic heart failure (heart can't relax)
-Characterized by pulmonary congestion in the presence of normal left systolic ejection
fraction, stoke volume, and cardiac output.
-More common in WOMEN
-Most commonly caused by hypertension-induced hypertrophy or myocardial ischemia
resulting in remodeling
-Patho: Myocytes are unable to actively pump out CALCIUM, which IMPAIRS VENTRICULAR
RELAXATION.
-Pressure backs up into left atrium and pulmonary circulation, resulting in PULMONARY EDEMA.
-Over time, pulmonary hypertension and right-sided failure may develop.


Heart failure with Reduced Ejection Fraction combined with Heart Failure with Heart Failure
with Preserved Ejection Fraction (HFrEF combined with HFpEF) - ✔✔Combination of
SYSTOLIC & DIASTOLIC heart failure



Left-sided heart failure - ✔✔Same as HFrEF. Systolic heart failure.
Heart Failure with Reduced Ejection Fraction
*Systolic heart failure - avoid calcium channel blockers (Diltiazem & Verapamil)*



RIGHT-sided Heart Failure - ✔✔-Characterized by failing right ventricle which results in its
inability to pump blood forward to the pulmonary circulation
-Most common CAUSE is LEFT-sided heart failure, but it can occur without left-sided heart
failure
-When it happens without left-sided failure, it's usually the result of LUNG DISORDERS, such as
COPD, cystic fibrosis, ARDS, pulmonary fibrosis, pulmonary hypertension.
-When pressures are too high in left ventricle, the back flow of blood into the pulmonary
circulation against causes higher pressures in the pulmonary circulation against which the right
ventricle must pump.
-The right ventricle is unable to effectively pump against the increased pressure and it
ultimatately dilates and fails.

, -As a result, the pressure and volume backs up causing right atrial hypertrophy, JUGULAR VEIN
DISTENTION, hepatosplenomegaly, and peripheral edema.



Systolic heart failure patients should avoid what meds? - ✔✔Calcium channel blockers
(Diltiazem & Verapamil)*
In systolic heart failure, the contraction is weak. Calcium helps to strengthen the contraction
(systole), so you don't want the calcium blocked!



What increases contraction? - ✔✔*Systolic heart failure needs help contracting!*


-Catecholamines - epinephrine & norepinephrine make heart pump harder
-Increases in intracellular calcium
-Decreased sodium in blood (decreases activity of the sodium/calcium exchanger)
-DIGITALIS: increases intracellular calcium


What decreases contraction and promotes r? (improves diastolic heart failure) -
✔✔*Diastolic heart failure needs help relaxing!*


-Beta Blockers: Block effects of catecholamines. Metoprolol, Bystolic
-Acidosis
-Hypoxia/hypercapnia
-Calcium channel blockers



Systole - ✔✔Contraction of heart as it shoots blood



Diastole - ✔✔Relaxing of heart so it can fill with blood



Systolic heart failure - ✔✔Heart can't contract

Written for

Institution
N5315 Advanced Pathophysiology
Course
N5315 Advanced Pathophysiology

Document information

Uploaded on
October 9, 2024
Number of pages
41
Written in
2024/2025
Type
Exam (elaborations)
Contains
Questions & answers

Subjects

$13.99
Get access to the full document:

Wrong document? Swap it for free Within 14 days of purchase and before downloading, you can choose a different document. You can simply spend the amount again.
Written by students who passed
Immediately available after payment
Read online or as PDF

Get to know the seller

Seller avatar
Reputation scores are based on the amount of documents a seller has sold for a fee and the reviews they have received for those documents. There are three levels: Bronze, Silver and Gold. The better the reputation, the more your can rely on the quality of the sellers work.
QUINTER New York College Of Dentistry
Follow You need to be logged in order to follow users or courses
Sold
393
Member since
2 year
Number of followers
105
Documents
39291
Last sold
4 days ago

3.6

69 reviews

5
34
4
10
3
7
2
2
1
16

Recently viewed by you

Why students choose Stuvia

Created by fellow students, verified by reviews

Quality you can trust: written by students who passed their tests and reviewed by others who've used these notes.

Didn't get what you expected? Choose another document

No worries! You can instantly pick a different document that better fits what you're looking for.

Pay as you like, start learning right away

No subscription, no commitments. Pay the way you're used to via credit card and download your PDF document instantly.

Student with book image

“Bought, downloaded, and aced it. It really can be that simple.”

Alisha Student

Working on your references?

Create accurate citations in APA, MLA and Harvard with our free citation generator.

Working on your references?

Frequently asked questions