PHAR 121 Exam Practice Material: Blank Practice Exams and Answers
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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.
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
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
-
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
+
- -
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
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