Exam (elaborations)

PHAR 121 Exam Practice Material: Blank Practice Exams and Answers

16 views 0 purchase

Course
PHAR 121 (PHAR121)

Institution
University Of Saskatchewan (USask )

Practice Exams and Summaries for Module 1, Module 2 and Final Exam for PHAR 121 (pathophysiology and pharmacology) to help with exam studying. Notes cover all material learned through the course.

[Show more]

Preview 3 out of 26 pages

View example

Uploaded on August 11, 2024
Number of pages 26
Written in 2022/2023
Type Exam (elaborations)
Contains Questions & answers

practice
practiceexam
answers
recall
quiz
study
material
studymaterial
pharmacy
pharmacology
pathophysiology
cardiovascular
diabetes
exam

CA$6.86

Add to cart

Add to wishlist

100% satisfaction guarantee
Immediately available after payment
Both online and in PDF
No strings attached

Hypertension Part 1 – 1. General Review of CV System
Is the right heart or left heart more concerning in terms of heart failure? Why?
left heart=
systemic-venous system
right heart-pulmonary only arterial -

system
Describe the first pass effect:
circulation and to liver where metabolized before
Drugs enter go they are

circulation
entering
Draw a schematic of the heart and associated venous and arterial systems to help you
remember: N -
pulmonary
vein

J
Vend
Cara

14 Right Left
Vein-back to heart Atum
↳ deoxygenated except
pulmonary vein
from heart
~ Tricuspid
valve

value

artery away
-

↳
oxygenated except Right Left

ventricle
-

pulmonary artery ventricle
-Aorta
pulmonary
partery I
Name the heart valves associated with each:
Left atrium -> Left Ventricle: mitral value
Right atrium -> Right Ventricle: tricuspid valve
Left ventricle -> Aorta: aortic value
Right ventricle -> Pulmonary Artery: Pulmonary value
What would dysfunction in left atrium -> left ventricle cause?
Reduced Cardiac output (Co) -

problems wand heartbeat (Lub Dab)
Differentiate between capillaries in the following tissues:
Endocrine, small intestine, kidney: leaky holes vary size free passage up to 600nm
,
in -

Skeletal muscle and cardiac muscle: Free passage up to lonm
Brain: Tight junctions between endothelial cells little passive transport except water
- and CO2

Describe venules and veins: lower pressure ↳ less chance for
things to get in brain + cause CNS

values prevent backflow effects

More pliable venous tone influences venous return to the 8

Contain lots of blood at one time

Describe lymphatic system:

3
Small endomelial tubes w/contractile walls small clusters of
vacuum up
surrounding
tissues
Drain into venous system
Immune cells

checkpoint
like
dysfunction >
-
fluid
pooling
a edema
What is blood pressure? Pressure in arterial wall

Systolic (systole)
to
:
pressure in arteries when heart beats =

or lower is considered
Diastolic normal
:
pressure between beats/rest (diastole)
What is the issue with manual BP measurements? Describe the principles behind BP
measurement: Unconscious bias for multiples of 5
and closed artery is Silent while blood
Principle is that blood moving through fully open
Shut artery is turbulent
flow
through slightly
can't hear any turbulent flow
I .
Pump cuff to close brachial artery-pump until
you
. Watch dial and release cuff
2 slowly pressure
. As
3 soon as hear noise >
systolic pressure
-

you
4. Continue to watch
guage monitor noise
+

. Noise
5 diastolic pressure
stops-fully Should be measured at rest
>
open
-

Feet flat on ground
Arm out
⑮

, Based on this schematic, what is the blood pressure? beats
as it
as soon
T

Frelaxed
slightly high
Normal BP and resting HR: BD =
120/80 HR =
70BPM

What is the benefit of intermittent high blood pressure?
Increased blood flow O2 and cells that need it
, ,
glucose to in that
moment ↑protein mitochondria
~ But we don't want this chronically
cellular X's -> 8 hypertrophy
1.2 High Blood Pressure/Hypertension
Is high blood pressure a disease itself? Why or why not? If not, why do we care about it?
No It is not a disease itself but is a risk factor for diseases
other of the Clu system such as

heart attack ,
stroke , heart failure ,
atrial fibrillation

Differentiate between sustained and intermittent high blood pressure:
Sustained E to do specific tissues Kells
: bp always ,
even when
sleeping-takes this-wasted-damages >
-

hypertension
↳ consistent high
Intermittent : needed for E-no consequences on body/vessels
at rest
Spreadings
What are the two main consequences of high blood pressure that result in damage?
- Increased afterload
- arterial damage
What are some of the other consequences of sustained hypertension?
-

left ventricularSystolic dysfunction (LVSD)-decreased Co due to poor contraction

hard-muscle increases
hypertrophy (LVH)-left constantly working
ventricle in size
-

left ventricular
↳ we want maration runner not
Strongman

cannot relax and accept blood-reduced co
Diastolic dysfunction-ventricles
-

increase In myocardial Oxygen requirements due to muscle hypertrophy
-

Describe afterload. How can afterload be affected without the presence of high BP?
Afterload is the increase in resistance
against blood expulsion

High blood pressure can cause increase in afterload
(very common cause

Other heart conditions such
,
as aortic value Stenosis ,
can cause increased

afterload wout presence of
high blood pressure

Healthy blood vessel walls are lined with a blanket of _____________
endothelial ______.
cells What happens to
this structure with damage from high BP? Which diseases are arteries vulnerable to due to this
damage/dysfunction?
BP
Endothelial cells are
damaged from high
Without endothelial cells present , arteries are susceptible
to
-
Atherosclerosis (lesions due to
plaque buildup) and
of Vessel walls (aneurysm) -
Intering
risk factor for rupture and bleeding
Glomerular nephritis (damage) + high pressure causing
holes in
glomerulus
m e
-

and weaken its filtration abilities
to
get larger

, Antihypertensive drugs target natural pathways

Kidneys-fluid and
1. electrolyte balance

. Hormones
2 Sympathetic NS RAAS
-

,

. Direct
3 Targets-vasodilation and contractility

Hypertension Part 2 – 1.2 Pharmacology of Antihypertensives
Name the possible pathophysiology of HTN:
fluid retention Nat retention
> Kidney dysfunction >
- -
-

i s

>
-
Hormone Imbalance -
too much Epi/NE or renin >
-

Stimulate increase in BP to
organs /muscles
use
> Arterial
-

dysfunction
-

NO response/production > -

Vasoconstriction
is

The Kidney
How can the kidney play a role in HTN?
Fails to eliminate fluid -> builds up in vessels > -

bp increased

How is edema different from volume in vessels?
Edema is leakage of
lymph into tissues

What do diuretics do?
Increase fluid excretion
-> increase urine production
Distal Tubule , Proximal Tubule and
contribute
,
Ascending loop of henle all
to fluid relention In the nephron

Why is sodium absorption a part of our physiology if too much Na+ is a problem in diets?
Because previously ,
Nat was not
heavily in diets so our bodies needed a

Mechanism to reabsorb Nat as it is essential for electrical gradients and action potentials

Where are the three locations that Na+ reabsorption happens?
Distal Tubule
Proximal Tubule
of Henle
Ascending Loop
Describe what normal kidney function looks like:
-

fillers 120 mL/min into tubules

-
makes Urine at 1mL/min

-

Over 99 % of filtered fluid is reabsorbed
↳ Nat is major driver
How is sodium handled in different parts of the kidney?
Proximal Tubule reabsorbs 65 % of filtered Nat > No diuretics
target this
system
-
-

loop reabsorbs 25 % of filtered Nat
Ascending of Henle
-

small amount of Nat reabsorbed at distal tubule
>
very Afferent arteriolet ascending
-

connected by
loop of Henle are

Describe tubuloglomerular feedback: Maculadensa
↳ Specialized epithelia
-

Macula densa Senses [Na] in nephron that senses [Nat] in nephron
-

results in vasoconstriction via afferent arteriole vasoconstriction
↳ ↑ [Nat] used to don't want to filter and lose H2O
mean
dehydration
-

-
> decrease renal blood flow

What are the different classes of diuretics?
1.Loop diuretics (Nat-k -2C1-symport inhibitors) Strong (loop-25 %) only used in those Chronic Kidney Disease
+
- -

2. Thiazide thiazide-like diuretics (Nat-Cl-Symport Inhibitors) weaker-best diuretic for otherwise healthy
+ -

3. # sparing diuretics used to prevent potassium loss NOT used
+ -
diuretic -

as

4. carbonic anhydrase used for
-

hypertension (just
not know MOA)

5. Osmotic diuretics
Only used
-

hospital in

Loop Diuretics
What system do these diuretics inhibit? Explain
Ascending loop
In of Henle-Nat-K +
-2C-
Symporter is inhibited
↳ Inhibits Nat reabsorption here

> Note after loop there is not for Nat reabsorption
that a lot of
opportunity again
-

Nat needs channels to pass from lumen to interstitial space and back into blood

>
-
as a consequence .
CI- is not moved to interstitual space either

The benefits of buying summaries with Stuvia:

Guaranteed quality through customer reviews

Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.

Quick and easy check-out

You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.

Focus on what matters

Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!

Frequently asked questions

What do I get when I buy this document?

You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.

Satisfaction guarantee: how does it work?

Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.

Who am I buying these notes from?

Stuvia is a marketplace, so you are not buying this document from us, but from seller tanillenyeste. Stuvia facilitates payment to the seller.

Will I be stuck with a subscription?

No, you only buy these notes for CA$6.86. You're not tied to anything after your purchase.

Can Stuvia be trusted?

4.6 stars on Google & Trustpilot (+1000 reviews)

56326 documents were sold in the last 30 days

Founded in 2010, the go-to place to buy study notes for 14 years now

Start selling