HTN 2 Drugs 1 Flashcards

(47 cards)

1
Q

Blood pressure is determined by the product of

A

BP = CO x PVR

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2
Q

CO=cardiac output which is equal to

A

SV X HR

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3
Q

The Primary physiologic factors that determine blood pressure are

A
Renin-angiotensin-aldosterone system
Sympathetic nervous system
Plasma volume (largely mediated by kidneys)
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4
Q

CO will Increase

A

Increase venous constriction:
Sympathetic nervous system overactivity
Excess stimulation of Renin-angiotensin aldosterone system

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5
Q

Increase in cardiac preload include

A

Increased Fluid volume from excess Na

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6
Q

PVR increase by these factors

A

Increasing vascular constriction and hypertrophy
Excess stimulation of RAAS
SNS overactivity
Endothelial dysfunction due to decreases Nitric Oxide and increases endothelial

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7
Q

Most pts with essential HTN have a normal CO but increased

A

peripheral resistance

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8
Q

Peripheral resistance is determined by small arterioles

A

responsible for blood flow distribution to organs

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9
Q

Arteriole walls contain layers of

A

endothelial cells

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10
Q

Vasodilator

A

Nitrico oxide

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11
Q

Vasoconstrictor are

A

ENDOTHELIUM and ANGIOTENSIN 2

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12
Q

When there is damage in endothelial

A

blood starts to aggregate in the damage part and become plaque

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13
Q

Angiotensin 2 positive and negative effects

A

The postive effects if angiotensin 2 are it plays the major part homeostasis, decrease thrombosis, decrease platelet aggregation but when endothilial is damage it does the oppsite cause thrombosis, platelet agregation and plaque.

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14
Q

Excess stimulation of Renin angiotensin-aldosterone

system (RAAS) can lead to:

A

Increased sympathetic activity
Increased PVR (arteriolar vasoconstriction)
Water / salt retention
Lead to elevated BP

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15
Q

Inhibiting RAAS leads to

A

lowering BP

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16
Q

ACE INHIBITOR MOA

A

block conversion of angiotensin 1 to angiotensin 2

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17
Q

The ace inhibitor also inhibits and break down

A

BRADYKININ

which means the bredykinin level increase

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18
Q

The inhibition of Bradykinin by ACE-1 leads to

A

Cough, hperkalemia and Angioedema

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19
Q

ACE inhibitor meds are

A

Lisinopril (Prinivil, Zestril) 10 – 40MG Daily

Enalapril (Vasotec) 5 – 40MG 1-2 times daily

20
Q

The ACE inhibitor is also considered

A

First-line therapy in HTN guidelines (without compelling indication)

21
Q

When someone already has a heart attack and they are established. what ACE will do

A

improves their chance of second heart attack and reduces hospitalization.

22
Q

Compelling use of an ACE inhibitor

A

Post-MI & HFrEF
renal protection for patients with protein-related DM DKD or CKD
Elevated UACR (> 30mg/g)
eGFR < 60

It helps patients with post-MIT, hfref AND protects kidney

When they already have it then we use it but we cannot use to prevent it from happening.

23
Q

When not to use ACE

A

HTN: less efficacy as monotherapy in Black patients, consider combo therapy when used (need adequate dose!)
Contraindicated in pregnancy Especially in the 2nd and 3rd trimester
Pt with Bilateral Renal Artery Stenosis

24
Q

ARB Angiotensin Receptor Blocker MOA

A

Block the activity of Angiotensin 2 at the Type 1 receptor

25
Stimulation of AT1 ________ Inhibiton of At1 _________
Vasoconstriction, Vasodilation
26
ARB does not cause what side effect
Bradykinin
27
ARB meds are
Irbesartan (Avapro) 150 – 300 Daily Lorsartan (Cozaar) 50 – 100 1-2 times daily Valsartan (Diovan) 80 – 320 Daily
28
Special compelling for ARB are
``` Compelling use in Post-MI & HF •Compelling use in renal protection for patients with protein-related DM DKD or CKD •Elevated UACR •eGFR < 60 ```
29
ARB has ONE extra advantage and why
•Consider losartan in pts with PMH of gout due to increased urinary uric acid excretion
30
ACEI / ARB Adverse Drug Events (ADE)
Slight rise in SCr at initiation (<30% rise from baseline acceptable) • Hyperkalemia have Increased risk in pt with CKD Dry Cough* (Can be DELAYED) --> Asian Americans have a higher incidence of ACE inhibitor–induced cough. Angioedema* (Rare: <1%)
31
Contraindicated: of ACEI / ARB are
Pregnancy Category D & Bilateral Renal | Artery Stenosis
32
cough and angioedema are less common with _____ but have a chance of happening
ARBs
33
Lisinopril-induced cough will not be effected by cough suppressant the solution is
Change to ARB.
34
Lisinopril-induced angioedema can be cure by
changing to ARB means wait 6 week wash out period. | than change to ARB
35
ACE/ARB Drug Interactions are
Effect k+ so not use with K+ sparing dieuretics or supplements
36
ACE/ARB monitoring include
B.P. SCr, BUN, K+, angioedema and cough | Asses blood test for electorlytes and renal function 2 to 4 weeks after initiating therapy
37
Direct Renin Inhibitor MOA
Block RAAS at its initial point of activation and prevent formation of ATI AND ATII
38
Direct Renin drug (cousin of ARB/ACE) name is
Aliskirn
39
One imporant thing about Direct Renin Inhibitor is
Do not use with ARB/ACE as it will increase K+ level
40
ALDOSTERONE Antagonist MOA
Inhibit aldosterone receptor in distal tubule, and increasing NaCl & H20 excretion while conserving K+. Block effect of aldosterone on arteriolar smooth muscle (Work on fluid balance and smooth muscle)
41
Aldosterone Antagonists are
Spironolactone (Aldactone) 25 – 100mg/day 1-2times/day
42
Aldosterone antagonist should be avoided in
someone has elevated K+ | or less kidney fuction
43
Alodosterone antagonist is effective in
Heart failure with reduce ejection fraction Primary aldostronsim ( elevated eldostrone) Resistant HTN
44
Spironolactone adverse effect are
``` Hyperkalemia Hyponaterima Gynecomastia ( main issue in males) impotence Hpotension ```
45
Excess stimulation of Renin-angiotensinaldosterone system (RAAS) can lead to
Increased sympathetic activity Increased PVR (arteriolar vasoconstriction) Water / salt retention Lead to elevated BP
46
Inhibiting RAAS lead s to
Leads to lowering BP
47
Adverse effects specific to Aldosteron antagonist are
Hyponaterima | Gynecomastia ( main issue in males)